A system of practical medicine. By American authors. Vol. 1 (part 6 of 8)

A system of practical medicine. By American authors. Vol. 1 (part 6 of 8)

Diphtheritic paralysis is invariably complicated by anæmia and debility, and the diet and medical treatment must be regulated accordingly. However, neither overfeeding nor a sameness of diet are to be permitted, for not rarely the muscular coat of the stomach suffers with the rest of the muscular tissue, and the secretion of gastric juice is very deficient in anæmic individuals. While, therefore, iron is indicated, we must not neglect to pay particular attention to nutrition and digestion, and to aid the latter with pepsin and moderate amounts of muriatic acid, well diluted. Quinia in small doses and stimulants are appropriate whenever there is no contraindication to their employment. The treatment of the paralysis itself will naturally depend on the diagnosis of the condition present in each individual case, which we have seen to differ considerably. This alone can explain why various modes of treatment, the electric current among others, after being recommended by some authors, are branded by others. Where we have to deal with those rare changes in the brain and spinal cord, the utmost care is necessary in order not to make the condition still worse; and in such cases there would be a contraindication to the use of the faradic current, though this would not hold true with regard to the use of the galvanic current in short sittings. Besides, central paralyses are by no means so frequent as peripheral ones. In most cases there is not the slightest elevation of temperature during the course of the paralytic phenomena. I lay great stress upon this point, for I am aware that many cases of central congestion and even of inflammation exhibit but very insignificant elevations of temperature. But, as the diagnosis will depend on a positive knowledge of whether there have been changes of temperature, I rely on the rectal temperature only, for many a myelitis runs its course with no greater elevation above the normal than one-half or one degree. In all cases in which the temperature is normal or subnormal, I do not hesitate for a moment to employ the faradic or the galvanic current. In addition to the internal administration of iron I advise by all means the employment of strychnia. When there is no necessity for haste, we may give moderate doses, gradually increasing them, and using iron in combination. When there is danger in delay, recourse ought to be had to subcutaneous injections of the sulphate of strychnia, once or twice daily. They are mainly indicated in paralysis of the muscles of deglutition and of respiration. Of course, where the former are affected it is necessary to nourish the patient artificially, partly perhaps by nutrient enemata, but principally by means of the stomach-tube. In using the latter it is unnecessary to introduce it into the stomach, as it only requires to be passed a few inches below the affected parts, when the oesophagus will usually be found able to undertake the further disposal of the food. In these cases strychnia should be injected subcutaneously in the neck, {714} once or twice daily. In a similar manner it should be injected in the region of the chest, diaphragm, or neck in paralysis of the respiratory muscles or of the glottis. In paralysis of the muscles of accommodation (in which Scheby-Buch claims to have seen the process cut short by the use of the Calabar bean, considered as inert by Hassner) they may be given in the forehead or temples.

Frictions dry and alcoholic, hot bathing, friction with hot water, kneading of the affected parts, will be found beneficial and pleasant.

{715}

CHOLERA.

BY ALFRED STILLÉ, M.D., LL.D.

DEFINITION.--Cholera is an epidemic disease, characterized by the transudation of serum into the stomach and bowels, and usually by the profuse discharge by vomiting and purging of a liquid resembling rice-water, followed by a tendency to collapse. It is endemic in India, but has been conveyed thence to almost every part of the world.

SYNONYMS.--Cholera algida, C. asiatica, C. asphyxia, C. maligna, C. spasmodica. In English it is generally spoken of as Asiatic cholera.

HISTORY.--It is sometimes stated that Hippocrates, Galen, Celsus, and the Greek, Roman, and Arabian medical writers generally record "the fact of the presence of cholera in the various countries in which they lived" (Macnamara). Nothing could be more contrary to the truth. All of these writers describe "cholera morbus" in nearly identical terms; they all include bilious discharges among its symptoms, and no one of them speaks of it as a mortal or even as an epidemic disease. (Compare, especially, Celsus, Aretæus, Cælius Aurelianus, and Paulus Ægineta.) Their description of sporadic cholera morbus is very precise. For example, Cælius Aurelianus says: "Cholericam passionem aiunt aliqui nominatam a fluore fellis, per os et ventrem effecto."[1]

[Footnote 1: Acut. Morb., lib. iii. cap. xix.]

Asiatic epidemic cholera is a very different disease. It seems to have been known in India from a very remote period, but no detailed account of it was published until the beginning of the sixteenth century. During that century many successive descriptions of the disease exhibited its extreme violence and mortality. It is believed to have occurred repeatedly, if not annually, in the same localities down to the present time. The invasion of India by the Portuguese, and afterward by the English, contributed to spread the disease throughout the Peninsula, partly by military occupation and partly through commercial channels, by which it was also carried to the islands in the Indian Ocean. It prevailed in Batavia in 1629. Between 1768 and 1790 numerous epidemics of cholera occurred. About the former date no less than 60,000 persons are said to have perished near Pondicherry, and in 1783 it is reckoned that 20,000 victims to the disease fell in a single week during the religious gathering at the sacred city of Hurdwâr, where, as will be seen hereafter, it became in later years more fatal still. The English armies extended their conquests in Hindostan, and established commerce between that country and Western Asia and Europe, and by the year 1817 opened new channels of {716} communication in every direction, both within and beyond the Peninsula. Along them the disease was carried; it invaded Ceylon and the Burmese empire, and extended to Batavia, Java, and China on the east, and advanced westward to Persia in 1821. In that year also it was carried from Arabia into Africa, and at various later periods penetrated more and more deeply into the Dark Continent, always following the track of pilgrims returning from Mecca, the routes of armies engaged in war, or those of trading caravans.[2]

[Footnote 2: Christie, Cholera Epidemics in Africa, 1876.]

In these cases, as in others elsewhere, the spontaneous origin of the disease has been assumed by certain writers, but at every stage of its progress careful investigation led uniformly to the conclusion that it was propagated directly or indirectly from pre-existent cases of cholera. From Persia it moved northward as far as the shores of the Caspian Sea, and westward to the Levant in 1823, and there for a time its ravages were stayed. Meanwhile, it prevailed at various places throughout Hindostan, and, assuming a greater degree of violence in 1826, it advanced steadily in a north-western direction across Afghanistan and Persia in the following year. In 1829 it reached Orenburg, to the north of the Caspian Sea, and was speedily conveyed into the interior of the Russian empire, where it raged with great violence in 1830. In 1831 it prevailed at Mecca among the pilgrims, who had brought it from India, and so virulently that one-half of them are computed to have perished. Hence it speedily passed with returning pilgrims to Alexandria and Constantinople, and was carried to St. Petersburg, to Sweden, to Hamburg, and other places in Northern continental Europe. From Hamburg and other seaports it was conveyed to commercial towns on the eastern coast of England, whence it extended to Edinburgh in the north and London in the south.

In 1832 cholera prevailed in France, and within the year caused 120,000 deaths, 7000 of which occurred in Paris in the space of eighteen days. In the spring and summer of that year it was reproduced in England, and extended to Ireland. From Liverpool, Cork, Limerick, and Dublin five vessels filled with emigrants sailed for Quebec, Canada, and they, together, lost 179 passengers by cholera during the voyage.

The immediate results of this importation and first appearance of cholera on the American continent are described by Dr. Peters as follows: "All these ships and their passengers were quarantined at Grosse Isle, a few miles below Quebec. On June 7th the St. Lawrence steamer Voyageur conveyed a load of these emigrants and their baggage, some to Quebec, but the majority to Montreal on the 10th. The first cases of cholera occurred in emigrant boarding-houses in Quebec on the 8th, and the same pest-steamboat, the Voyageur, landed persons dead and dying of cholera at Montreal, a distance of two hundred miles, in less than thirty hours. Over this long distance, thickly inhabited on both shores of the St. Lawrence, cholera made a single leap, without infecting a single village or a single house between the two cities, with the following exceptions. A man picked up a mattress thrown from the Voyageur, and he and his wife died of cholera; another man, fishing on the St. Lawrence, was requested to bury a dead man from the Voyageur, and he and his wife and nephew died. The captain of a passing boat requested an Indian to bury a man from on board; this man and five other Indians were attacked {717} and died. The town of Three Rivers, halfway between Quebec and Montreal, forbade steamers to land, and escaped for a long time. From Montreal the great influx of emigrants were forwarded away, by the Emigrant Society, as fast as they arrived, and by them the pestilence was sown at each stopping-place. Kingston, Toronto, and Niagara soon became affected. In the end, over 4000 persons died of cholera in Montreal, and more than an equal number in Quebec. The epidemic reached Detroit in the same way, ... and continued west along the Great Lakes, until in September it reached our military posts on the Upper Mississippi.... Fort Dearborn, near Chicago, was temporarily reoccupied in 1832, and it was here that epidemic cholera displayed its most fatal effects among our troops. Out of 1000 men, over 200 cases were admitted into hospitals in the course of seven or eight days.... When these troops again marched for the Mississippi, they appeared in perfect health, yet the cholera broke out again on the way, and when the command reached the Mississippi it had been as fatal as it had been at Fort Dearborn."

Meanwhile, an emigrant ship with cholera on board reached New York, whence the disease spread up the Hudson River, and was also carried southwardly to Philadelphia and the West. The mortality in New York City from this epidemic is stated at 3500. In 1833 the disease broke out in the cities of Havana and Matanzas in Cuba, and is said to have destroyed one-tenth of the entire population. Hence it was carried to Mexican and American towns on the Gulf of Mexico, and up the Mississippi and Ohio as far as the western border of Pennsylvania. In the following year it was again introduced at the port of Quebec by a vessel filled with emigrants, of whom many had died during the passage. It prevailed in Canada and the State of New York and spread over the whole country in 1835 and 1836. In the former of these two years it was confined to several Southern cities, whither it was brought, as on a former occasion, directly from Cuba. It then gradually subsided, and at last disappeared for the space of nearly ten years.

But in 1845 it was known to be advancing on its former path, which it steadily pursued, and entered England in October, 1848, at Sunderland, the very town at which it first appeared in 1831. "During the second epidemic in Europe, in 1848, two vessels sailed from Havre, where cholera prevailed--one, the New York, for New York, and the other, the Swanton, for New Orleans. Both contained large numbers of German emigrants. On one vessel the cholera appeared when it was sixteen days out, with fourteen deaths; on the other, in twenty-six days, with thirteen deaths. The New York arrived at Staten Island Dec. 2, 1848, and a severe epidemic broke out, but was confined to the quarantine grounds. The Swanton arrived at New Orleans Dec. 11th; no quarantine was instituted, and in two days its sick were taken into the Charity Hospital. This was the beginning of a severe epidemic, which increased in power all winter, till, in June, 1849, 2500 died of it in New Orleans. December 20, 1848, it reached Memphis by steamboat from New Orleans, and for twenty-five days was confined to the landing-place of the former city, whence it afterward spread. In the spring it was carried to St. Louis and Cincinnati and the whole Mississippi Valley. In October it reached Sacramento, Cal., by means of overland emigrants, and, almost at the same time, San Francisco, by the U.S. steamer Northerner from {718} Panama. The Chinese of California suffered most severely" (Peters). In April, 1849, cholera reappeared in the public stores at the quarantine station, Staten Island, N.Y., and in the city of New York, where it was fatal to 5000 persons.

A pause now took place in the ravages of the disease which lasted until 1853. In that year it destroyed no less than 11,000 persons in the Persian city of Teheran. At Messina its victims numbered 12,000, in France 114,000, and in England about 16,000. In 1854 it was introduced by emigrant ships into New York, causing a mortality of 2000 persons, and was carried to Philadelphia, where its victims numbered 500. It extended to many towns in New England and westward along the great channels of emigration. In Montreal the deaths were 1300, and in the then small town of Detroit, 1000.

After an interval of quiescence longer than any previous one the cholera again broke out among the pilgrims to Mecca in December, 1864. It appeared in Alexandria during May, 1865, and thence was carried to many parts of Europe, and from them to North America and the West Indies. This period of exemption included that of the Civil War in the United States, when, if ever, the local causes which have been erroneously assigned to the disease existed in all their forms and in the most intense degree. It was only when its specific germs were once more imported that cholera began to prevail again. Official records show that in 1866 it was introduced from Europe into Halifax, N.S., the city of New York, and the military posts of New York harbor. Thence it was carried in troop-ships to various Southern ports, from which its progress could be traced to Texas and other Gulf States, and to the towns on the Mississippi and Missouri Rivers. From New York, also, the disease travelled westward to Cincinnati and the U.S. barracks at Newport, on the opposite side of the Ohio River, whence it advanced in a south-westerly direction to meet the trail that, coming from the South, followed the great rivers of the Mississippi Valley. During the summer of 1867 cholera again prevailed, although less fatally, at most of the points, especially of the Mississippi Valley, which had been invaded the previous year, and some cases occurred at the military posts around New York in recruits who had shortly before arrived from places in the West where cholera prevailed. Thus did the disease complete the circuit of the United States.

Meanwhile, cholera prevailed to a greater or less extent in the east of Europe between 1865 and 1874. After the latter date it seems to have been confined to Syria, Arabia, and the African shore of the Mediterranean. In 1877-78 it existed to a limited extent among the pilgrims at Mecca, and since then it has not been known in Europe. The latest appearance of cholera in the United States was in 1873, when it occurred at three points far distant from one another. It was introduced in the effects of immigrants. The vessels that brought them were in a perfect sanitary condition. The passengers themselves were healthy, and remained so after landing and until they reached the distant points of Carthage, Ohio, Crow River, Minn., and Yankton, Dak., where their goods were unpacked. At each place, "within twenty-four hours after the poison particles were liberated, the first cases of the disease appeared, and the unfortunates were almost literally swept from the face of the earth" (E. McClellan).

{719} In 1881 cholera was brought from Hindostan to Arabia by pilgrims on their way to Mecca, where it soon afterward broke out and caused the death of about 8000 persons. In the following year several vessels from Bombay evaded the quarantine and reached Djeddah, the port of Mecca, and the pilgrims on reaching the latter city disseminated the disease. The unusually small number of persons who were there at the time, and their prompt dispersion before the danger, limited the mortality, and gradually cases of cholera ceased to appear. In 1882, the English at that time carrying on war in Egypt, very rigid sanitary precautions against the importation of cholera were enacted and successfully enforced, but in the following year, the same urgent necessity no longer commanding, they were considerably relaxed. At the end of June, 1883, the cholera made its appearance at Damietta (at one of the mouths of the Nile), and soon afterward at Rosetta, Port Said, and Mansourah. During July it spread to various places in direct communication with those named. At Cairo it was peculiarly fatal, and on July 20th it was reported to have caused 600 deaths. For several days the daily mortality varied between 500 and 600. The disease prevailed somewhat in Alexandria during the height of the epidemic, and near the end of October it was fatal to numerous European residents of that city, and some deaths occurred in the British army of occupation. In all Egypt, during the week ending Aug. 13th, the total mortality is said to have been 5000, but in the following week it fell to 2000. It is estimated that the epidemic destroyed at least 20,000 lives. The germ of this epidemic has not been accurately determined. Some regard it as a survival of the cholera of the previous year--a supposition which is at least plausible and sufficient; but certain "sanitarians" have attributed the outbreak to the ordinary causes of disease intensified by the civil war which had recently devastated Egypt. It is sufficient here to say that while such causes have in all ages generated typhus and typhoid fevers and dysentery, they never produced cholera. Some, more unwise than judicious, declared that the Egyptian disease of 1883 was not cholera. It is alleged, on the one hand, that several East Indian merchants from Bombay arrived at Damietta on June 18th, or three days before the disease was recognized in that city. It is also said that a stoker from on board an English steamer from Bombay introduced the cholera into Damietta. But the judgment of Surgeon-General Murray carries with it greater weight.[3] He is of the opinion that the Egyptian epidemic of 1883 was simply a revival of the Arabian epidemic of 1882. He shows that cholera existed in several villages on the Damietta branch of the Nile in the latter part of May and during June, and that it broke out in the capital itself, during a fair which had lasted for eight days, on the 22d of June, and was spread by the people on their return from Damietta to their villages. This, adds Mr. Murray, "is a literal transcript of the accounts of many of the severe epidemics that have raged over India." It also appears from M. Proust's narrative[4] that the Ottoman government had already, as early as April, notified the government of Egypt that certain Indo-Javanese pilgrims were on their way to Mecca, and that ought not to be allowed to land without quarantine. The French delegate to the sanitary council also begged that those of the pilgrims who reached Suez without previous quarantine should be isolated and kept under {720} surveillance for three days. But owing to the opposition of the English delegates these measures were not duly enforced, the council did not meet again, and no protective system was adopted.

[Footnote 3: Times and Gazette, Feb., 1884, p. 209.]

[Footnote 4: Le Cholera, 1883.]

ETIOLOGY.--The essential cause of cholera is unknown, unless the investigations of Koch, described below, may have revealed it. Its secondary causes, or the conditions of its dissemination, are better understood. Some general propositions concerning them will here be laid down, and illustrated so far as the argument requires and the available space will allow.

Cholera is endemic in no other country than India, and more particularly in Bengal. When it has occurred elsewhere it has invariably been carried from India. The cholera poison has been imagined to be of an aërial nature, but its diffusion has no relation whatever to the velocity or the direction of the wind. In no instance whatever has its rate of progress exceeded that of man on land or water, nor has it ever taken a direction different from that of commercial or military movements. On land it has usually crept from place to place, and if sometimes it has seemed to leap across wide spaces, and even seas and oceans, it has never invaded any inland town or seaport without having been brought thither from a point already affected with the disease. Nor, having once entered an inland or seaboard town, does it spread equally therein in all directions, but prevails chiefly in the quarter immediately surrounding the place of its entrance. If appropriate sanitary measures are enforced, it is sometimes confined to that quarter, and, in the case of quarantine stations, it has repeatedly been prevented from extending beyond them. This statement may be illustrated by the fact that of fourteen epidemics of cholera at Staten Island, the quarantine station of New York, all but four were prevented from reaching that city.[5] When the disease does overleap the barrier opposed to it, its origin and subsequent course can usually be traced.

[Footnote 5: Peters's Notes, etc., 2d ed., p. 94.]

A high atmospheric temperature is everywhere associated with the prevalence of cholera. Its origin in the hot climate of Hindostan and its general progress prove this conclusively. In nearly all of the places where a great difference exists between the summer and the winter temperature the disease has disappeared during the cold season, and attained its greatest intensity during the hot months of the year. The only apparent exception to this rule is, that cholera has prevailed in several Russian, Swedish, and Norwegian cities during the winter. But these very exceptions confirm the rule; for in the countries mentioned the intense cold of the winter compels the inhabitants to seal their houses by every possible means, while the atmosphere within them is kept at a high temperature by huge stoves, which hinder ventilation, and indeed render it almost impossible. Difference of temperature likewise explains the fact that of two cholera-ships arriving from Havre, the one at New York and the other at New Orleans, in December, 1848, the former did not disseminate the disease, but the latter formed the starting-point of an epidemic which lasted all the winter.

A good deal has been written of the predisposing causes of cholera, and poverty, crowding, filth, intemperance, and depression of spirits have been given prominent places in the catalogue. But to any one familiar {721} with the history of epidemic diseases it will at once be apparent that every one of these conditions favors the spread of all communicable infectious diseases. There is not the slightest evidence that these agencies, singly or combined, can generate cholera or favor its spread apart from the presence of the specific poison of the disease and the facility with which it is transmitted from the sick to the well whenever the population is crowded, poor, of filthy habits, and weakened by dissipation. Because among such people intemperance prevails, this vice has been regarded as predisposing to cholera. Apart from the brutish mode of living of drunkards, there is nothing to show that they are more liable to cholera than the most abstemious of water-drinkers. On the contrary, it is notorious that during cholera epidemics drunkards in the better classes of society enjoy a certain degree of immunity from the disease; which it is easy to explain on the ground that they imbibe but little water, which is the main channel through which the infectious principle of the disease is spread.

The specific cause of cholera is taken into the alimentary canal, and acts through it to produce the characteristic symptoms of the disease. It is conveyed from the sick to the well by means of the gastro-intestinal discharges, either moist or dry; in the former state, by means of drinking-water, and in the latter through the air, whose suspended noxious particles are received into the fauces and swallowed. There is reason to believe that the poison does not enter the system through the lungs, or through any other channel than the gastro-intestinal canal. W. B. Carpenter[6] appears to hold, however, that the poison may be absorbed through the lungs. To this view there are two objections: 1, That whatever is taken into the mouth or throat by inspiration may very well be swallowed; and, 2, that all the primary lesions of cholera affect the digestive and not the respiratory apparatus. It is not at all necessary to the propagation of cholera that its excreta should be furnished by persons laboring under the fully-formed disease. A specific choleraic diarrhoea is as infectious as the evacuations which occur in completely developed cholera. But neither will propagate the disease through the air to a distance. The tendency to its propagation in this manner depends chiefly upon the concentration of the poison; thus, it much more frequently occurs in close than in well-ventilated rooms or than in the open air. It has been argued that cholera is not contagious, because so few, comparatively, of the attendants upon cholera patients contract the disease. On the other hand, as some of them are attacked, this positive fact outweighs an indefinite number of negative instances. It should also be noted that different diseases enter the system and infect it through different channels--some through the lungs, others through the alimentary canal, etc. Small-pox, the most contagious of all diseases, is introduced through the air-passages, and is probably harmless when its virus is taken into the stomach. That the converse of this proposition applies to cholera is sustained by the whole history of the disease. Cholera poison may be taken to considerable distances in either a moist or a dry condition. In the former state it is mainly conveyed by water, as in rivers, water-pipes, etc.; in the latter, by fomites and especially by clothing saturated or merely soiled with cholera discharges, and which may retain their infectious quality for an indefinite time.

[Footnote 6: The Nineteenth Century, Feb., 1884.]

{722} Great stress has been laid upon the humidity and foulness of the soil, a damp atmosphere, filth, crowding, etc., as elements in the production of cholera, but in reality they have no more essential relation to it than to any other disease that occurs epidemically. Cholera may prevail whether they are present or absent. It is evident that from the earliest historical periods all of these causes of disease have existed, and in Europe much more generally and excessively than during the present century, and that they have never been removed in Asia Minor, Egypt, Arabia, and Africa. Yet cholera never was known in any of these countries until it was brought into them about the end of the first third of the present century.

According to Pettenkoffer, cholera is most prevalent when the subsoil water is lowest, and least so when the subsoil water is highest. It would be more descriptive of the fact to say that, so far as cholera has anything to do with the condition of the soil, it is most apt to be severe and prevalent when very dry weather follows a very wet period. Such circumstances are the most favorable to putrefactive fermentation and the dissemination of its products, which thus reach wells of drinking-water, and even rivers, especially when sewers empty into the latter. The identity of this explanation with that which is generally accepted for the dissemination of typhoid fever is too evident to be insisted upon. We might go farther, and say that, in typhoid fever as in cholera, the disease is communicated, although exceptionally, by the air of the sick room and by the exhalations of the soiled fomites of the patient. Now, if typhoid fever resembled cholera not only in being transmitted by means of the dejections, but also in its poison being derived from one primary source only, the analogy between the causes of the two diseases would be very striking indeed. But, in point of fact, the typhoid-fever poison may probably be generated de novo by fecal fermentation and other forms of putrefaction, and the disease is only exceptionally communicable; whereas, the poison of cholera, once received, is conveyed from man to man and far and wide through various channels; but, so far as is known, it has but one primary source, and that is in India. Lebert states that he did not find the localities that are the ordinary seats of typhoid fever peculiarly liable to invasions of cholera. But it must be noted that typhoid fever is very far from being exclusively a disease of the poor, squalid, and vicious. Like death itself, "regum turres pauperumque tabernas æquo pede pulsat;" while cholera much more commonly plants itself and disseminates its seeds in the rank soil of moral and physical degradation.

All morbid causes whatever, derived from race, climate, religion, dwellings, food, clothing, habits of living, etc., have no more to do with the development of cholera than with that of the eruptive fevers, and even less than with the causation of typhus and typhoid fevers and dysentery. The eruptive fevers are caused, as cholera probably is, by specific germs which no known combination of natural causes has ever developed, while the poisons of the other diseases named appear to be generated anew whenever certain more or less definite physicial conditions coexist. It would seem that cholera differs radically from all of these affections by the fact that its cause does not enter the circulation, but confines its direct operation to the gastro-intestinal mucous membrane. In this way it becomes intelligible that while, on the one hand, physicians and nurses of {723} cholera patients, although often, in fact, yet in relation to their numbers, are comparatively seldom infected, provided they duly observe proper sanitary rules, the disease, on the other hand, spreads like wildfire among those who drink water polluted by cholera excretions, and only a little less rapidly among people crowded into ill-ventilated apartments along with cholera patients.

The special fomites of the cholera poison are articles of clothing and furniture soiled with the discharges of the sick, and the emanations from privies, sewers, etc. into which these discharges have been cast. Many considerations render it probable that a very small quantity of cholera matter may suffice to render infectious a very large quantity of liquid, and especially of matters in process of putrefactive fermentation, and that the gaseous or vaporous emanations from them become diffused in the atmosphere and infect all who imbibe them. But water contaminated by cholera discharges is the most rapid and efficient agent in disseminating the disease. Innumerable instances of this mode of action are furnished by its history in Asia and Africa, where water is often scarce, and naturally so impure that its additional defilement by cholera dejections is apt to pass unnoticed. From the illustrations of this proposition which might be adduced only a few of the more striking will here be selected.

Hurdwâr is a town in Northern India at the base of the Himalayas, where the Ganges begins its course in the plains. It is the seat of a great Hindoo pilgrimage, which takes place annually in April, when sometimes from 2,000,000 to 3,000,000 of people occupy an encampment of about twenty-two square miles, comprising a low flat island in the Ganges and the opposite banks of the river. Bathing in the sacred stream on a certain day is the main object of the devotees; which day, in the year 1867, fell on the 12th of April. The bath was taken early in the morning. From noon on that day the pilgrims began to disperse so rapidly that on the morning of the 15th the encampment was quite deserted. It appears that up to the former date the health of the encampment was excellent, and it was the opinion of the reporter (Dr. Cunningham) that cholera was introduced into the camp by pilgrims from the neighboring districts going late to the fair. He believed that the cholera excreta may have been buried in the trenches and carried by a heavy rain into the river, and there swallowed by the pilgrims; for to drink of the water of the Ganges as well as to bathe in it is a religious obligation.

Immediately after the breaking up of the camp cases occurred in the surrounding districts, the epidemic widening in all directions. The pilgrims were almost always the first persons attacked in any locality, and the cholera attended them on their route wherever they went. In all the districts where the disease prevailed no cases occurred until ample time had been given for the pilgrims to reach them. In a word, "the cholera first showed itself among them; it followed their lines of route only, and did not outrun them; their progress was its progress, and their limits its limits." The mortality caused by this epidemic among the whole civil population of the North-western Provinces of the Punjâb has been estimated at about 117,181.[7] The history of the religious festival of 1879 {724} was identical with that just sketched, except that the number of the pilgrims was smaller and the deaths proportionally less.[8]

[Footnote 7: Brit. and For. Med. Chir. Rev., Jan., 1870, p. 137.]

[Footnote 8: Murray, Practitioner, xxvi. 309.]

Out of the numberless illustrations of the manner in which cholera is disseminated by water the following may be cited: In 1865 about 100,000 pilgrims were assembled at Mecca, of whom from 10,000 to 15,000 fell victims to the disease, two-thirds of them within a period of six days. Some cause acting simultaneously upon the whole number of persons must be admitted to account for so extraordinary a fact, and such a cause is not far to seek. At a certain sacred well "one hundred thousand people had skinfuls of water poured over them at the side of the well, and every one of them then drank largely of water drawn from the well. Much of the water poured over the pilgrims must have found its way by soakage back into the well, and if any of the pilgrims were at the time suffering from cholera, or had cholera-tainted garments about them, the well would be exposed to pollution."[9]

[Footnote 9: Christie, Cholera Epidemics in East Africa, p. 488.]

In the cholera epidemics of Zanzibar the disease produced the greatest havoc among the negroes, the Persians, and the East Indians; very few Europeans were attacked, and quite as few of the sect of the Banyans, who drank only water drawn from their own wells. The persons among whom the disease prevailed so fatally used chiefly the water of a certain well which was highly prized, but which on this occasion had become polluted by soakage from an adjacent cesspool into which the dejections of cholera patients had been thrown. It appears, also, that in Zanzibar the streams are very rarely bridged, and hundreds of negroes, in passing backward and forward, wade through them and pollute them. In these streams, also, the negroes wash their clothes and all the foul clothing of the contiguous town. While this business is going on "a gang of negroes may be at work at not many hundred yards' distance filling water-casks for the shipping." Subsequently to the watering of the ships in this manner sailors were attacked with cholera, and others who used water drawn from the stream below the place where it became polluted were attacked, and many of them died; while Europeans living on shore, and who drank the water of the same stream, but drawn from a much higher point in its course and after having been filtered, escaped the disease.[10]

[Footnote 10: Ibid., pp. 320, 492.]

The history of the disease in Europe furnishes a multiplicity of similar cases, and even more distinctly exhibits the dissemination of cholera by contaminated water.[11] In Holland not less than five epidemics of the disease occurred between 1832 and 1869, all of them causing a great mortality, to which the epidemic of 1866 alone contributed not less than 20,000 deaths. This was about 55 deaths for every 10,000 inhabitants. Such exceptional mortality over so wide a territory has been ascribed to the extreme porosity and humidity of the soil, which is nearly all below the level of the sea. Such a soil must necessarily retain longer than other soils whatever it absorbs, and thus tend to render the well-water habitually impure. If, then, to the ordinary impurities a specific {725} poison is added, its characteristic effects may assuredly be looked for. The conditions now stated explain the conclusions of Ballot of Rotterdam, drawn from a study of the several epidemics referred to. They are as follows: "1. Holland is highly affected by the cholera at every epidemic, chiefly in those parts where they drink water directly from the rivers and canals or from ground saturated with sewage. 2. In places where rain-water is generally drunk the disease is far less violent. 3. Places where there is no other drinkable water but rain-water are not affected by the epidemic; the single cases occurring there are imported. 4. When places affected by the cholera were supplied with pure water instead of the vitiated water the disease disappeared."[12] In like manner, we find that the cholera epidemic of 1873 in Germany seemed specially to select those situations where the subsoil was impregnated with decomposing organic matter; and it is evident that, in cities especially, such situations would include the most poverty-stricken districts, while the higher, drier, and at all times more salubrious localities are inhabited by the classes enjoying the greatest material prosperity.[13]

[Footnote 11: It is of interest to note that on the first appearance of cholera in England, at Sunderland, in 1831, a surgeon of that place, Mr. Ainsworth, collected and published conclusive proofs of the importation of the disease, of its communication from the sick to the well, "and of its propagation by clothes, and even by emanations, from the dead" (Observations on the Pestilential Cholera, London, 1832).]

[Footnote 12: Med. Times and Gaz., May, 1869, p. 459; June, 1869, p. 626.]

[Footnote 13: "Report of the German Imperial Commission," Practitioner, xxvi. 153.]

This mode of infection has been traced in numberless individual cases of cholera. In London there was a certain well into which the liquid contents of a sewer had been percolating for months. Of the water of this well hundreds of persons had been drinking without obvious injury. At last a case of cholera occurred hard by; the discharges were thrown into a privy which communicated with the sewer and indirectly with the well, whereupon more than 500 persons who drank water drawn from that particular well were attacked with cholera within three days. So in 1856 cholera prevailed in the county jail of Oxford, Eng., the drain from which emptied into a pool from which the water was drawn to supply the city prison. In the latter institution cholera began to prevail, but declined as soon as the pipes conveying the water were cut off, and soon afterward ceased entirely.[14] Again, in Constantinople in 1865 the clothes, mattrasses, etc. of cholera patients were washed at a fountain the basin of which was divided into two parts by a wall; one part was used for washing clothes and the other for drinking purposes. Unfortunately, the waste-pipe of the former being obstructed, the foul water of one side communicated with the clean water of the other, and in one day 60 people died of cholera in the small portion of the city which was supplied from the infected source. The striking case has often been cited which occurred at Epping, Eng., where a woman brought the disease from a distance into a perfectly healthy house and neighborhood, and of ten persons affected with it seven died, including a physician in attendance upon one of them. An examination of the premises "discovered, below the pipes leading from the water-closet and from the eye-hole of the sink through which the choleraic dejections had been passed, a leakage which extended under the foundations of the building and entered the well. The sewage was distinctly traceable on the side of the well corresponding with the leakage in the drain." After this discovery and the disuse of the foul water not another case occurred.[15] In 1868, Dr. {726} Farr, in his History of the London Cholera Epidemic of 1866, showed that water into which cholera dejections find their way produces cases of cholera all over the district in which it is distributed for a certain period of time, and that if the distribution is in any way cut short the deaths from cholera begin to decline within about three days of the date at which the distribution is stopped.[16]

[Footnote 14: Edinb. Med. Jour., i. 1122.]

[Footnote 15: Trans. of the Epidemiological Soc., ii. 428.]

[Footnote 16: Lancet, April, 1868, p. 217.]

Analogous instances are furnished by every cholera epidemic of which the history has been accurately observed, including that which extended so widely over the United States in 1873. Most of the following are cited from the official reports prepared, under the direction of the Surgeon-General of the army, by Surgeon Ely McClellan and Dr. John C. Peters. Several of the first cases, however, are foreign.

In 1861, at a station in India, some fresh cholera dejecta found their way into a vessel of drinking-water. Early on the following morning a small quantity of this water was swallowed by nineteen persons, five of whom were attacked with cholera between the first and the third day afterward.[17] In 1876 an outbreak of cholera took place in a village in Hindostan, which followed the arrival of wedding-guests, one of whom was attacked, and from whom it rapidly spread. The soiled clothes of one or more of the patients were washed in a pool from which all the villagers obtained their drinking-water, and on the discontinuance of this source of water-supply cholera speedily diminished in frequency and fatality.[18] In the German epidemic of 1873 many cases occurred where persons deriving their drinking-water from special sources were attacked with cholera, while their neighbors, supplied from a different source, remained free. Again, it has frequently happened that outbreaks of cholera have been checked by the prohibition of the suspected water and the substitution of a pure supply.[19] It seems probable that a very small portion of cholera discharges suffices to infect a very large body of water and maintain its infectiousness for a considerable time.

[Footnote 17: Macnamara, op. cit., p. 196.]

[Footnote 18: Surg.-Major Cornish, Practitioner, xxiv. 215.]

[Footnote 19: Practitioner, xxvi. 159.]

In December, 1871, an outburst of cholera occurred which was confined to the inmates of three excellent houses in a fine block of buildings in Calcutta. There had been no cholera in that neighborhood for four years. Within forty-eight hours a majority of the lodgers were sick, and on investigation it was found that the disease was carried in the drinking-water and in the milk diluted with it.[20] The particular locality in which Dr. Koch made the discovery of the microscopic representative of cholera furnishes an example of the same nature: "At Saheb Ragau, a locality which has repeatedly been visited by cholera during the last hundred years, numerous cases of the disease were reported, and these, on inquiry, were found exclusively in the huts situated round a certain tank. Of the few hundred people who dwelt in these huts, as many as seventeen died of cholera, though the disease was not at that time prevalent in the neighborhood, or indeed in the whole police district of Calcutta. It was proved that, as usual in such cases, the dwellers around the tank used it for bathing, and drew thence their drinking-water; it was also elicited that the linen of the first fatal case, befouled with cholera dejections, had been washed in the tank."[21] In June, 1873, a new {727} hotel was opened at Vienna, and many of the guests became affected with diarrhoea that was attributed to the drinking-water, which was offensive to the taste and smell. After a fortnight a gentleman died of cholera in the hotel, and two days later several of the guests were attacked with the disease, of whom fourteen died. The gentleman who first died was believed to have brought the poison with him into the hotel, so that the drinking-water, which previously had been polluted with ordinary fecal discharges, became specifically affected through him.[22] The discharges of one ill of cholera were thrown into, and the vessels used by him were washed near, a well from which all the residents of a farm-house drank. The wooden curbing of the well had rotted, and the ground immediately around had sunken; a heavy rain burst the curb, overflowed the well, and washed into it the entire surface-drainage of the surrounding ground. No attention was paid to this, and the water was used as before. It became so offensive that its use was forbidden, but too late to save the family, nine of whom died of cholera.[23]

[Footnote 20: U.S. Report, p. 85.]

[Footnote 21: Times and Gaz., April, 1884, p. 527.]

[Footnote 22: Times and Gaz., p. 86.]

[Footnote 23: Ibid., p. 140.]

At Farmington, Tenn., a man arrived who had contracted the cholera at Nashville; his illness ran its course at a point just forty paces from a well. Families that obtained their water from this well suffered in nearly all their members; where only certain members drank of it, they alone were affected.[24] At Huntsville, Ala., during an epidemic of cholera, the city authorities forbade the use of well-water, and supplied pure water from another source, but only for one week. During this time no new cases of the disease occurred, and the negroes, thinking themselves secure, resumed the use of the well-water, and within four days six fatal cases of cholera occurred in the vicinity. The use of the well-water was again prohibited, and again the progress of the disease was arrested.[25]

[Footnote 24: Ibid., p. 172.]

[Footnote 25: Ibid., p. 408. For other examples of the spread of cholera by means of drinking-water see Macnamara, p. 149 and seq.]

It has already been intimated that the cholera poison may be diffused through the air from either moist or dry sources, and especially from contaminated clothing, and then be taken into the throat and swallowed. Dr. Richardson refers to a local epidemic in England in which "the persons most constantly and fatally attacked were the women who washed the clothes of the sick;" and this circumstance has been largely confirmed by other observers.[26] In a village not far from Marseilles, and in an isolated place, a peasant and his wife who had not left the country sickened and died of the disease. The woman, who was a laundress, had received a bundle of linen belonging to a person recently arrived from Egypt, and the husband opened the bundle and unfolded the pieces. During the Crimean War many of the washermen attending to the washing of the French hospitals were attacked by cholera. In the post-office at Marseilles none of the clerks who handled the outgoing mails were attacked, but of those who sorted the mails coming from the East, where the disease prevailed, one after another suffered from cholera.[27]

[Footnote 26: Trans. Epidem. Soc., ii. 429.]

[Footnote 27: Read, Boston, 1866.]

The cholera was introduced into Guadaloupe by clothing contained in a trunk belonging to a person who died on the voyage thither from Marseilles, where the cholera then prevailed. The woman who washed the clothing died, with all her family. Attracted by the circumstances of {728} the case, many came to her house, and of these several died. From this point the disease spread over the island.[28] A sailor died at some port in Europe of Asiatic cholera in 1832. A chest containing his personal effects, clothing, etc. was sent home to his family, who lived in a small straggling village on the Atlantic coast of the State of Maine. It reached them about Christmas, and was opened on its arrival. The inmates of the house were all immediately and suddenly seized with a disease resembling Asiatic cholera in all its malignity, and died. There had been no cholera in the State. The last case of cholera that occurred in the garrison at Malta in the epidemic of 1865 was that of a woman who had stolen a chemise the property of one who had died of the disease. She put on this fatal garment, probably soiled with cholera discharges, and certainly unwashed, many days after the death of its former possessor; she took the disease and died.[29]

[Footnote 28: Med. Times and Gaz., April, 1874, p. 387.]

[Footnote 29: Lancet, Feb. 17, 1866.]

It is sometimes said, and oftentimes repeated, that cholera is not directly contagious--is not communicated by the sick to the well. No statement could be more unfounded. The whole history of cholera proves that the physicians and nurses of cholera patients are often affected by the disease. "In Constantinople no less than twenty-seven physicians and medical assistants were attacked and died during their attendance on cholera patients; and in Paris and Toulon similar results followed. At Halifax, N.S., two of the physicians who volunteered in aid of the steamer England, which put in there disabled by the ravages of cholera among the officers and crew, as well as among the steerage passengers, took the disease, and one died" (Read). In 1832 the cases of cholera in Edinburgh were in the proportion of 1 to every 1200 of the population of the city, while among those in attendance upon the sick the proportion was 1 to 5. In 1848-49 one-fourth of the nurses employed in the cholera hospital took the disease, while in the general hospital, only a few paces distant, where no cholera patients were received, not a single attendant was attacked. In the London Hospital, in 1866, none of the medical officers, volunteer nurses, or sisters were attacked. Of the (regular) nurses five contracted the disease, and of these four died.[30] In 1849 a severe and fatal epidemic broke out in the Philadelphia Almshouse. The resident physicians of the hospital were abundantly occupied with the care of the sick of other diseases, and it was thought prudent not to allow any, even an indirect, communication between them and the cholera patients. The latter were therefore removed to an isolated building in the middle of the quadrangle, and attended by physicians from the city who had volunteered their aid. Three or four of these physicians had attacks of cholera, and two of them died.[31] At this time there was no cholera at all in the city, and the young physicians could not have become infected outside of the almshouse. They were attacked while attending the sick of cholera, but the regular house-physicians, who seldom visited the cholera patients, escaped altogether.

[Footnote 30: London Hosp. Rep., iii. 439.]

[Footnote 31: Philada. Med. Examiner, Nov., 1849.]

The importance of recognizing the communicability of cholera is so great that no apology need be made for introducing the following additional illustrations of it furnished by Griesinger in his article on the dangers of cholera to medical men. They are the more important because {729} in many other instances cholera physicians have suffered little for their devotion to duty: "At Moscow, in 1840, hospital attendants contracted the disease to the extent of 30 or 40 per cent., while in the general population only 3 per cent. were attacked; at Berlin, in 1831, in Romberg's hospital, 54 out of 115 persons were attacked: in 1837 one-fifth of the attendants took the disease, and on one occasion no less than seven of them fell ill on a single day. In La Charité Hospital in Paris, in 1849, one-sixth of the attendants had the disease, while only one-twenty-fifth of the general population of the city suffered from it; at Mittau, in 1848, one-half of the physicians took the disease; in 1842, at Toulon, ten health officers out of thirty-five were ill with cholera, and five of them died, while of thirty workmen who were employed to carry the dead bodies one-third succumbed; at Stockholm, in 1853, of 536 attendants one-eighth took the disease, and half of that number died; at Vienna, in 1854, out of thirty-six nurses, seven caught the disease, and seven men employed in removing the dead became affected with a prolonged and exhausting diarrhoea; in 1849, at Strasburg, five nurses out of ten were attacked, etc." ... "Physicians, nurses, students, etc. are less frequently affected, however, than patients ill with other diseases who are lying in the wards where cholera patients are treated, and are therefore more constantly exposed to the emanations from the discharges; and physicians usually suffer less than the attendants who are constantly waiting on the cholera patients."[32]

[Footnote 32: Traité des Maladies infectieuses, 1868, p. 409.]

It may be added that Surgeon-General John Murray, who served continuously for thirty-eight years in British India, caused upward of five hundred circulars to be addressed to the local governments and filled up by the local medical officers. From these returns it appeared that the belief in the communicability of cholera, in one way or another, was practically unanimous; for of the whole number, those who believed that it is conveyed from person to person were 75 per cent.; from place to place, 85 per cent.; through the atmosphere, 80 per cent.; with the drinking-water, 85 per cent.; by the evacuations, 92 per cent.; and by clothing, 98 per cent.[33] This gentleman has more recently furnished additional facts supporting the same conclusion. For example: Out of fourteen cases that occurred at Ramleh during the Egyptian epidemic, eleven occurred in patients already in the hospital for other diseases. In 1856, after visiting the dead-house where the bodies of fourteen cholera patients lay, as he entered the cholera ward he felt a sudden shock in the epigastrium, followed by a deadening sensation that rapidly spread over the whole body. On another occasion he saw a clergyman who was talking to a cholera patient suddenly seized with vomiting of a watery liquid. Several analogous instances are related by him.[34]

[Footnote 33: Practitioner, xix. 470.]

[Footnote 34: Med. Times and Gaz., March, 1884, p. 281.]

It has been objected to the communicability of cholera that its dissemination does not always follow the deposit of cholera discharges in privies, wells, etc., and also that when infection does take place, it may occur between remote extremes as to time, and therefore cannot be attributed to infectious germs. Such objections are frivolous, because we know nothing of the nature or vitality of cholera-germs, and they are, moreover, drawn from exceptional cases. The power of infected fomites to develop {730} the disease has been preserved, in a journey from Arabia into Africa, for at least twelve days, and for even a longer period in passing from Germany to Chicago, as already related. It is true of every infectious and contagious disease that it may possess one or both of these qualities in various degrees--that at one time it is only exceptionally communicated, and that at another time it appears to propagate itself virulently. So the phenomena of cholera may consist of little more than a watery diarrhoea, which may be so mild as hardly to disable the patient from working, while at other times the attack may include all those terrible and fatal symptoms which have won for the disease the name of malignant. That a certain quantity, or "dose," of the cholera poison is required to develop the disease, but one that varies considerably in different cases, may be inferred from these facts: 1. Out of a certain number of persons equally exposed to receive the disease, only a portion may be attacked at all, and these in very unequal degrees. 2. Persons so slightly affected as to be ignorant of the nature of their sickness, and believing it to be an ordinary diarrhoea, may nevertheless become the innocent, because ignorant, disseminators of cholera. The explanation of such facts may be manifold: they may depend upon the dose or upon the energy of the morbid poison, on various possible conditions of its recipient, and so on; but, however explained, their reality is none the less certain. The receptivity of persons exposed to the contagion of cholera is very different. It is well known that some persons appear to be proof against other contagious diseases, while others seem never to acquire an immunity from them. On this very important point the conclusions of Fauvel directly bear.[35] They include the following propositions: The East Indian ports where cholera exists as an endemic disease are never the seat of an extensive epidemic among the native population. But strangers to these localities are liable to the disease, and such are the Mussulman pilgrims who come to Bombay to take ship for Mecca. A severe epidemic of cholera confers upon the locality in which it has taken place an immunity which in India appears to be of several years' duration. Such an epidemic in any country is a proof that the cholera is not endemic there.

[Footnote 35: Mémoire lu à l'Académie des Sciences, 1883.]

If a contagious disease preserved its virulence undiminished, it might continue to prevail indefinitely. But we know that all other contagious epidemics do come to an end sooner or later, and hence we must conclude that their specific cause progressively loses its virulent qualities. There is every reason, therefore, to believe that the same is true of cholera. Its communicability, and therefore its diffusion, may vary with climatic, seasonal, local, personal, and other conditions; but of what nature those conditions are, and especially of the last and most important, the personal, hardly anything is known. Nor need we too curiously investigate them, so long as the fact remains that outside of, and independent of them all, there is but one essential cause of cholera--a morbid poison as specific in its nature as that of any of the eruptive fevers--a poison which no determinable conjunction of circumstances has ever engendered, and which was unknown in Europe and America before it was carried to them from India. In just such a way did small-pox first arise in the Western World. It had never appeared in Europe until the latter part of the {731} sixth century, when for a short time it prevailed in Marseilles and the neighboring country. Afterward it was not heard of until it was reintroduced by the Crusaders on their return from Palestine in the twelfth century, since which period it has hardly ever ceased. The history of the diffusion of cholera is closely analogous to this in several particulars, and we may reasonably expect that what was in the last generation a new disease will henceforth be liable to prevail again and again as the intercourse increases between the nations of the West and the immemorial source of cholera in Hindostan.[36]

[Footnote 36: Additional illustrations of the communicability of cholera are contained in the Brit. and For. Med. Chir. Rev., July, 1872, p. 56.]

In the preceding discussion of the origin and dissemination of cholera the broad facts of its specific nature and its contagion by means of excreta have been chiefly insisted upon. Little has been said either of the nature of the contagium or of the conditions that modify its activity. These points will be considered hereafter. But it is proper in this place to state that, in the opinion of most investigators, the contagious element has the power of multiplying itself, not only within the body, but wherever it is in contact with decomposing organic matter, provided that the degree of heat and amount of moisture present are adapted to promote such a change, which is certainly analogous to fermentation, if not identical with it. And the facts already mentioned may be recalled, which show that the contagium cannot be a light and subtle substance, since, as has been stated, the immediate attendants upon cholera patients are not as apt as might be expected, on that hypothesis, to contract the disease, while washerwomen inhaling, and probably swallowing, the moist fumes from cholera fomites much more frequently do so; that fomites saturated with the dried discharges are very infectious; and that water is the principal vehicle by which cholera-germs are carried into the stomach.

SYMPTOMATOLOGY.--Like other diseases, cholera occurs under very dissimilar aspects and with various degrees of gravity. Like those especially which are caused by specific morbid poisons, it may be so insignificant as to escape recognition, or, on the other hand, it may give rise to violent and distressing symptoms which come on without warning and hurry the patient to inevitable death. Whenever epidemic diseases present such opposite extremes of severity in their symptoms, it may reasonably be inferred that the differences depend mainly upon the quantity of the poison that has been received into the system, precisely as the dose which has been taken of a narcotic or acrid poison may be estimated by the gravity of its effects. Individual peculiarities, constitutional or acquired, may modify the characteristic phenomena, and sometimes a careful inquiry may be necessary even to detect their existence; but a study of cholera in all its grades shows that its symptoms are all the effects of one and the same cause, and that the cholera poison acts primarily upon the gastro-intestinal mucous membrane. It follows, as a matter of course, that, being thus applied, it will occasion symptoms differing in degree and in kind according to the energy of its action, and that this, again, will depend partly upon the inherent virulence of the agent and partly upon its quantity. In fact, this feature in the clinical history of the disease can be explained only by the operation of a special irritant acting with different degrees of power upon the gastro-intestinal {732} mucous membrane. In other words, the different forms under which it is convenient clinically to recognize and describe cholera are nothing more than different degrees of the operation of one and the same poison, modified more or less by the peculiarities of individual patients. In the most typical of the fully-formed cases of cholera there is a stage of diarrhoea, a stage of cholera morbus--i.e. of vomiting and purging--with more or less evidence of stagnation of the blood, which is followed either by reaction and recovery or collapse and death. The phenomena of those several stages will now be described, after which certain symptoms will be more particularly considered.

It has more than once been pointed out that, however mild an attack of cholera may be, the dejections accompanying it are infectious, and may produce in other persons the gravest types of the disease. Hence the importance, not only to the patients, but also to others, of recognizing it in the earliest stage; for while this knowledge may suggest measures for preventing an extension of the disease, it leads to the prompt use of remedies at the only period in which their success can at all be counted upon. The characteristic of this stage, which has generally been called either choleraic diarrhoea or cholerine, is a diarrhoea remarkable for its profuseness and the frequency and serous quality of the stools, which are, however, of a more or less yellow color. They are preceded by rumbling and gurgling noises in the abdomen, are voided without colic or tenesmus, and are followed by a remarkable sense of exhaustion or faintness, which is sometimes also accompanied with nausea, and, if they are very frequent and copious, cramps are apt to be felt in the calves of the legs. In this variety or stage of the attack, as a rule, there is not any vomiting; there is complete anorexia, but urgent thirst, a white and clammy tongue, and a peculiar alteration of tone, a huskiness, faintness, or hoarseness of the voice. The stools vary from six to twelve a day, and, as above stated, are slightly yellow; they are also alkaline, and on standing deposit a granular sediment which consists largely of the débris of intestinal epithelium. Unless the attack is very severe the temperature is not lowered by much more than 1° F. The symptoms now described, especially in their milder grades, may last for a week or even longer, and then, according to circumstances, end either in cure or in fully-developed cholera; but under appropriate treatment they usually subside in a day or two, and more or less rapidly according to the degree of damage done to the digestive mucous membrane.

Between the above, which is the mildest type of epidemic cholera, and the fully-developed disease must be placed that grade of the disease which is more appropriately called cholerine, comprising cases in which vomiting occurs as well as purging, with increased debility and a tendency, more or less decided, to collapse. The matters vomited, after the rejection of undigested food, are at first bilious, but they gradually become less and less so the longer the attack lasts, and, together with the stools, assume the appearance of rice-water--i.e. they consist of a pale grayish, semi-transparent liquid in which white flocculi are suspended. Its reaction is alkaline, and it has a faint albuminous or spermatic smell. Along with these symptoms the other effects of serous depletion arise--debility with pallor, duskiness, coldness, profuse perspiration, and a sodden condition of the skin, while the secretion of urine is diminished, {733} and all the symptoms that belong to the first stage of cholera are present in an aggravated degree.

A curious feature of this disease is that sometimes the onset even of its graver forms is not attended by any evacuations, although the stomach and intestine may be filled with liquid. It is perhaps chiefly in such cases that the patient experiences a rapid depression of all the mental and physical faculties. The senses are irritable, the head aches and is confused, there is a disinclination to sleep, the limbs totter under the weight of the body, the pulse is frequent and feeble, occasionally fainting takes place; the skin is cool and bedewed with perspiration. In other cases, again, the attack is sudden; the patient is smitten with an unaccountable feebleness, speedily followed by profuse vomiting and purging and general spasms, and dies without any suspension of the symptoms or any tendency to reaction.

But more usually the attack begins with the diarrhoea and vomiting described above, which then assume, more or less rapidly, a high degree of violence, expressed by their frequency and excess. The stools with proportionate rapidity lose all their fecal qualities and acquire the rice-water appearance before mentioned, and the liquid rejected by vomiting in all respects resembles them. It is poured forth less by an ordinary act of vomiting than by gushes, as if it overflowed from the throat and mouth; and it often escapes from the stomach and the bowels at the same instant. Such profuse evacuations necessarily occasion an urgent thirst which cannot be satisfied, for liquids are thrown up immediately on being swallowed. Sometimes a distressing hiccough accompanies these symptoms. It is indeed only one of the many spasms which may affect the muscular system. They generally begin in the fingers and toes, which become bent and stiff; they seize upon the muscles of the calves of the legs, and render the muscular wall of the abdomen as hard as a board. The pain they produce is extremely severe, and unless the patient is exceedingly prostrated he endeavors to assuage it by a constant change of position.

At this period the debility is very great, and progressively increases, and the patient is unable to rise, or even to move at all except under the stimulus of the painful spasms. The features are shrunken; the nose is sharp and pallid, and bent to one side; the dusky, lack-lustre, and sunken eyes, the thin lips, the hollow cheeks, and the contracted muscles that stand out like cords under the tense and clammy skin, present a physiognomy that belongs to no other disease in the same degree. The hands and feet grow cold, and steadily the coldness creeps upward toward the trunk; the temperature falls to 94° or 95° F.; the feeble and even flickering pulse ranges from 100 to 120. The integuments of the limbs are shrivelled and damp, and look as if they had been macerated in water; and if a fold of the skin is pinched up it subsides very slowly indeed. The eyes grow dull and dry, the tongue has a pasty or sticky feel, and the urine is almost suppressed. If any of this excretion can be obtained for examination, it is found to contain both albumen and sugar. As the attack advances the patient falls into a dull, listless, and motionless state, which may be mistaken for insensibility or even unconsciousness but is really due to exhaustion of all the faculties of mind and body. He may express no interest in anything, and hardly notice the {734} attention or the distress of his friends, yet he will generally give clear, although languid, answers to questions, and fall again into an inert and unobservant state.

As these symptoms continue and the fluids of the body decrease, the blood accumulates and stagnates in the veins, giving to the hands and feet, the nose and lips and other features, to the neck, and even to the entire surface of the body, a bluish, leaden, or violet tint, precisely like that of cyanotic children. The pulse, that was already weak and thready, is no longer perceptible; the carotids even and the impulse of the heart cease to be felt, and the second sound of the latter becomes inaudible. The skin is everywhere cold; the hands, feet, and face are sometimes of an icy coldness, and yet the patients seldom perceive that they are so; indeed, complaint is more apt to be made of suffering from internal heat. Even the breath as it issues from the nostrils feels cold. The blood no longer circulates, and the heart seems still. If a vein is opened a few drops of black and viscid blood will trickle from the wound, which if it coagulates, yields but little serum, and in place of a firm clot only a diffluent jelly. The voice has sunk to a mere whisper or is quite extinct. The features assume a distorted and frightful expression; the temples and cheeks are hollowed; the nose is twisted and pointed, and the nostrils are obstructed with dry and powdery crusts; the eyes are also dry, dull, and sunken behind the half-closed and purple lids; the conjunctiva is no longer moistened by its secretion and becomes bloodshot; the temperature in the mouth may fall to 79° or 80° F.; a viscid exhalation bedews the icy and marbled skin; and the whole body is so shrunken from its natural proportions as to lose all the marks by which its identity has been recognized. From this pulseless, exhausted, cold, and cyanotic condition there can be but one step to death. It generally comes on gradually, the patient sinking into the state of apparent insensibility before mentioned; on the other hand, he may expire suddenly on attempting to make some unusual effort.

At any period in the progress of cholera, except that of complete asphyxia, the contest between the system and the disease may be decided in favor of the former. If this occurs before profuse evacuations have taken place or blueness of the skin appeared, the recovery may be gradual and present no special phenomena. The pulse regains by degrees its natural force; the skin grows warm again, first upon the trunk and afterward upon the extremities; the breathing becomes easy, and, the diarrhoea having already ceased, convalescence is established. But in proportion to the severity of the symptoms, the intensity and duration of the cold stage, the cramps, and the evacuations, will there be a tendency to febrile reaction, with more or less passive congestion of the internal organs, and therefore a slower return to health. If the attack has been very severe, and particularly if the algid stage has been prolonged, fever of a low type is apt to occur, and indeed may terminate fatally. This fever presents all the characters of the typhoid state, and is marked by dryness of the tongue, a brown crust upon the teeth and gums, jerking of the tendons, delirium, and coma. These symptoms are partly evidences of exhaustion, of inability of the system to resume its normal action, and perhaps also they denote the retention of the effete products of nutrition in the blood; but sometimes they appear to be associated {735} with, and caused by, a local and latent inflammation of low grade, established usually in the lungs. Again, the nervous system seems to bear the brunt of the reactionary effort, and the patient is attacked by convulsions or perishes in an apoplectic fit. These phenomena appear to be due in most instances, if not in all, to renal obstruction, and, as it is supposed that their immediate cause is the retention of urea in the blood, they have received the title of uræmic. In other cases a wasting diarrhoea, due probably to the damaged state of the intestinal mucous membrane, is superadded to the already existing typhoid state. Occasionally the parotid glands become enlarged and painful, and sometimes a measly or roseolous eruption appears upon the skin.

It frequently happens that the convalescence from cholera is slow and irregular. The system seems to be shattered by the trial it has passed through; the nervous susceptibility is for a long time morbidly increased, or, what is still more usual, the digestive function is greatly impaired. The appetite is capricious and the digestion feeble. The mouth is pasty, the abdomen tympanitic, the bowels are irregular and alternately confined and relaxed. Finally, patients who leave the bed too soon or indulge prematurely in their ordinary diet are liable to a relapse, perhaps fatally, into the original disease. It has sometimes happened that such a relapse has taken place several days after an apparent restoration to perfect health.

COMPLICATIONS AND SEQUELÆ.--In a small proportion of cases, as above stated, cutaneous eruptions have been observed during the attack of cholera, or rather during its decline, for they coincide with the reaction or follow it, and may be regarded as indications of increasing vitality. They belong to the exanthematous class, and comprise roseola, erythema, urticaria, and rarely vesicular eruptions.[37] But, instead of them, there may occur destructive tissue-lesions in the form of abscesses or ulcers. These affections are more usual on the limbs than on the trunk or face, but some of them may appear even in the mouth or fauces. Profuse sweats have been noticed elsewhere, and the important fact that they carry off large quantities of urea, which they deposit upon the skin. Diphtherial exudation has also been met with upon tender parts of the skin and in the fauces, as well as in the stomach and intestine. In some epidemics of cholera suppuration of the parotid gland is occasionally observed, while in others it may be entirely absent. Instances have been reported of double parotitis, and in several of them the termination of the attack was fatal. Still more rarely suppuration of the submaxillary or the cervical glands has been met with. Another sequela of cholera is a tetanic contraction of the flexor muscles of the limbs. Between the tenth and fifteenth days of convalescence the patient is attacked with a tearing, rending pain in the hands and forearms, the legs and feet, followed by tonic contraction of the flexor muscles of these parts. The sensibility is not impaired. The attack lasts for one or several days, and seems always to end in recovery (Guterbock).

[Footnote 37: Compare London Hosp. Reports, iii. 457.]

* * * * *

Some of the individual symptoms of cholera call for a more detailed notice than they have received in the foregoing epitome, in which the continuity of the narrative could not be interrupted by a description of variations depending upon the stage and grade of the disease.

{736} The first to be considered is the temperature. The animal temperature in cholera varies according to the part of the body at which it is taken more than in any other disease. In cases of average severity it rarely falls below 95° F. in the axilla. The temperature under the tongue does not furnish trustworthy indications. In the stage of asphyxia it seldom exceeds 87.8° F., and even in cases that recover it may fall to about 78.8° F. (Wunderlich). In the cold stage it is not uncommon for a difference of temperature to be noted of nearly ten degrees between the axilla and the rectum. In a female aged thirty-two the temperature in the axilla was 93° F., and that in the vagina 102.8° F. (Mackenzie). In other cases a vaginal temperature of 104° F., and even of 108.32° F., has been reached (Guterbock). Such high temperatures furnish an unfavorable prognosis. As Wunderlich has pointed out, during the algid stage temperatures taken in the mouth do not give an accurate idea of the general temperature; the rectal and vaginal temperatures are more nearly correct. The following are some results of thermometry in 74 cases of cholera: Lorain found the minimum rectal temperature in 1 case 93.2° F., in 2 cases 95°, and in 10 cases 96.8°. In 47 cases the normal temperature was preserved; in 27 it rose to 100.4°; in 15 cases to 102.2°; and in 1 to 104° F. Leubuscher gives the average temperature in the armpit 92.7° F.; under the tongue, 90.5°; upon the tongue, 81.5°, in the nostrils, 79.2°; and on the palm of the hand, 84° F. These numbers, however, only represent averages. It should be noted that the low temperature of the mouth and nostrils is caused not only by the evaporation from the surface of those cavities, but also by the relative coldness of the expired air, due to the partial suspension of the passage of blood through the lungs, and therefore to the heating of the air contained in them. According to Leubuscher also, the lowest temperature is found in the nostrils, and next under the tongue, and at the latter point it may vary from 79° F. to 90.5° F. In death by asphyxia the vaginal and rectal temperatures may rise to 104°-108° F. The axillary fluctuates less than the internal temperature. It is remarkable that during the algid stage the patients, at least before the temperature has reached its minimum, are not conscious of their coldness, but, on the contrary, complain of internal heat, precisely as happens in the congestive forms of periodical fever. When the febrile reaction assumes a typhoid type the temperature in many cases is normal or only slightly elevated, and it is of serious import if the temperature then sinks again below the normal grade (Wunderlich). On the whole, the maintenance of a uniform temperature, neither much above or below 90° F. in the axilla or under the tongue, may be regarded as favorable, yet recoveries have taken place even when the temperature at these points has fallen to 79° F. If the temperature of the parts just mentioned should rise rapidly to 104° F., it may be regarded as a very unfavorable sign.

The skin, as has elsewhere been described, is pallid, bluish, shrunken, and cold, and quite destitute of its natural firmness and elasticity, so that when it is pinched into folds they subside very slowly, as if they had been made on the skin of a corpse. It is curious that, although the drain of liquids through the bowels is so great, the skin not only remains moist, but generally is bathed in a profuse cold sweat. Although the secretion of urine is reduced or quite suspended, that of milk is said to be not {737} always so. Large quantities of urea have been found in the urine, and in some cases it has been visible upon the skin in the form of white scales. During convalescence the skin may be the seat of the various eruptions already enumerated. Of a graver nature, but, fortunately, of rarer occurrence, are erysipelas, boils, abscesses, ulcers, and gangrene. These several affections seem to result from the alternate obstruction and freedom of the cutaneous circulation. They commonly appear first upon the limbs, and afterward upon the face or trunk; they may affect even the cavity of the mouth. Some observers have noted a relatively frequent occurrence of diphtherial exudations in this disease, while others do not allude to their existence. The former describe the false membrane as affecting not only the mouth and fauces, but also the stomach, the intestine, and the female organs of generation. A case is reported by Joseph of a young man who, after an attack of cholera, was affected with a blenorrhoea, due to a diphtherial inflammation of the urethra.

The character of the heart- and pulse-beats in this disease is quite peculiar. Their rate does not increase indefinitely, as it does after hemorrhage; the pulse usually varies from 90 to 110, and indeed seldom exceeds 120, but its volume, tension, and force progressively decline until the beats become imperceptible at the wrist, and even in the brachial and femoral arteries. At the same time, the rhythm of the heart is interrupted, the energy of its impulse declines until it can no longer be felt, and its sounds grow weaker and weaker until they become quite inaudible. Sometimes, it is said, a pericardial friction sound may be heard, which is attributed to the dryness of the pericardium. That the decline and suspension of the heart's sounds and impulse are due not only to the weakness of the cardiac muscle, but also to the lessened volume of the circulating blood, is proved by the fact that they persist, sometimes for many hours, after reaction has commenced, and only become audible again when the arteries have been replenished with blood.

In the description of the symptoms of cholera it has been mentioned that the cyanotic color of the skin is produced by an accumulation of blood in the veins. Many years ago Magendie, and after him Dieffenbach, on examining the arteries of persons in the advanced stage of cholera, found those vessels empty of blood. It might be supposed that, under the circumstances, not only the right side of the heart, but also the lungs, would be gorged with blood, and that extreme dyspnoea would result. But, in point of fact, the respiration in cholera is hurried and shallow rather than oppressed and labored, while after death the lungs are not engorged with blood, but rather in a bloodless condition. The pulmonary artery and its branches are also empty, although the right side of the heart may be filled with dark and soft coagula. These singular conditions seem to be due, on the one hand, to the greatly diminished mass of the blood in the vessels, and to its accumulating and stagnating in various parts of the venous system, and, on the other hand, to the weakness of the heart, which is shown by its suppressed impulse and sounds, and which lessens its power to propel the venous blood into the lungs. The infarction of the systemic veins and the threatening suspension of the circulation necessarily impair the activity of all the functions, including those of nutrition and disintegration, so that the effete detritus of the economy tends to accumulate in the blood. This tendency is {738} doubtless counterbalanced not only by the diarrhoea, but also, more or less, by the almost total suspension of nutrition, due to the inability of the cholera patient to digest or even to retain food, as well as by the diminished oxidation of the blood in the lungs. It has already been observed that, to a certain extent, the impediment to the passage of the blood from the right side of the heart into the ramifications of the pulmonary artery tends to prevent congestion and infarction of the lungs. But this obstruction is precisely what occurs during the stage of reaction in many cases, which then terminate fatally by asphyxia, as in the previous stage still more perish by apnoea.

In the milder attacks of cholera vomiting may not occur, and in the most severe it not unusually is suspended for some time before death, although the diarrhoea may continue. In the most malignant cases, indeed, there may be no vomiting at all, in consequence of the extreme muscular exhaustion, although the stomach may be distended with liquid. When rejected, the liquid has the general aspect of rice-water, which the stools also present. Its reaction is alkaline or neutral, and it is said to contain a less proportion than the stools of solid matter, but a larger proportion of urea. The act of vomiting is strictly one of regurgitation, which is performed without effort or pain. Sometimes, indeed, it seems to relieve the sense of weight caused by the accumulated contents of the stomach. It is readily excited by attempts to drink, and even by slight changes of posture. The vomited liquid at first contains the various articles of food the patient may have eaten. Their half-digested remains have sometimes suggested the announcement of strange specific forms of cholera germs. The liquid, after ceasing to be colored brownish or greenish, becomes gray, and subsequently, in favorable cases, more or less green again; while during the stage of reaction in grave and ultimately fatal cases it is more or less reddened by an admixture of blood. Its most usual and characteristic appearance is that of a grayish liquid containing whitish flocculi. The nature of this liquid, whether discharged by vomiting or by purging, has been variously estimated. Formerly, some persons held the white granules to be leucocytes, but the greater number agree that they are mainly epithelial fragments. When the vomited liquid is allowed to stand, a sediment forms in it which is composed almost entirely of epithelial scales, more or less modified in their appearance by the accidental contents of the stomach, and a film covers its surface in which globules of fat and phosphatic crystals may be detected. They are frequently associated with sarcinæ, produced by fermentation in the contents of the stomach, and after standing for some time the liquid becomes crowded with vibrios (Lindsay).

Although the propensity of the sick to discover a cause for every symptom often leads cholera patients to attribute their diarrhoea to some particular exposure to cold, error of diet, etc., yet, in fact, this symptom, so far as it belongs to cholera, is primarily an effect of the cholera poison alone, although it may be aggravated by causes like those mentioned. It is of great practical importance to bear in mind that a specific choleraic diarrhoea--that is to say, a diarrhoea produced by the cholera poison alone--may continue to be very slight as long as it lasts, which may be for several weeks; and hence, as elsewhere insisted upon, a person who is not suspected of being affected with cholera may, quite ignorantly, sow {739} the seeds of a deadly epidemic of the disease. The danger in cholera is proportioned to the volume of the discharges rather than to their frequency, just as a single profuse hemorrhage is more serious than the loss of an equal amount of blood divided among several successive days. The special danger, however, is not, as in hemorrhage, from syncope, but from the progressive loss by drainage of the water of the blood, rendering it unfit to circulate, and therefore causing it to stagnate in the veins. The spoliative operation of the diarrhoea has occasionally been productive of benefit instead of injury, as in the following case of Barlow: A man suffering from dropsy was attacked with cholera, "and passed gallons of liquid by stool, had cramps, and became livid and clammy, but his pulse did not disappear, as in profound collapse, and he eventually rallied, and left the hospital apparently well. When he began to recover from cholera his appearance was almost ludicrous, from the manner in which the integument hung loosely about him."

The stools pass through a series of changes corresponding to those of the matters vomited, being fecal at first, and then becoming colorless and watery. During reaction, if that occurs, they regain more or less of their proper color, but if typhoid febrile symptoms prevail they are usually bloody. Decomposed blood sometimes renders them dark, tarry, and fetid; this condition has caused them sometimes to be described as being composed of vitiated bile, which is, however, a product not of the liver, but of the imagination.

In the intestine after death considerable quantities of epithelium are found floating in the contained liquid or else loosely adherent to the mucous membrane. It is usually in flocculi, but sometimes in fragments large enough to form a continuous membrane. A microscopic examination of cholera stools shows that their turbidness depends chiefly upon desquamated epithelium, with which is mixed white corpuscles and bacteria. It is remarkable that although the stools are drained directly and so rapidly from the blood-vessels, they nevertheless contain but little albumen, indeed hardly more than a trace of it. If, however, blood is mixed with the stools, as happens in rare instances, more albumen is present. Oil-globules are most abundant in cases that have passed beyond the stage of collapse into that of reaction with fever. In these it is said that oily matter may be found either in concrete masses or as a scum of liquid oil. Of inorganic constituents they contain crystals of the triple phosphate of ammonium and magnesium and chloride of sodium in greatest abundance, but the proportion of ammonium and potassium salts is small. Indeed, the total amount of solids does not exceed 2 per cent. As the quantity of water in the blood and solids is limited, and as in this disease the stomach will not receive nor retain any liquid, it follows that the more profuse the evacuations are, the shorter must be the duration of the attack, for the sooner then does the blood become too thick to circulate.

It has several times been stated that in cholera the urine is diminished, and that, therefore, the blood retains a larger proportion of effete products than in health. But it has also been remarked that the amount of these products is abnormally small, on account of the interference with nutrition of the abnormal state of the circulation. Doubtless, as in other cases of renal obstruction, an increased proportion of effete matter is eliminated by the skin, if not by the bowels. When the amount of {740} urine excreted is only diminished, its specific gravity may vary between remote extremes, as 1.012 and 1.030. Usually, however, when its quantity is very greatly reduced, symptoms which are described as uræmic are apt to arise, and the urine is found to contain the usual products of renal congestion--viz. albumen, sometimes traces of blood, hyaline and granular casts, and epithelial scales, with less chloride of sodium and more urea than normal. It is remarkable that at the beginning of convalescence the urine, which had been suppressed or greatly diminished, may become for a time abnormally abundant. Rarely, if ever, does the derangement of the kidneys now described denote or produce an organic lesion in those organs. Like the disorders elsewhere, these are due to the loss of balance between the arterial and the venous sides of the circulation; both, indeed, have lost their functions more or less, the one by lack of blood, the other by an excess of blood unfit for circulation.

The occurrence of cramps in cholera, which has bestowed upon the disease one of its titles, spasmodic, has, however, no distinctive relation to the Asiatic disease. Spasmodic phenomena occur in many cases of poisoning by corrosive and irritant agents and in ordinary cholera morbus, and in cholera infantum they are among the most alarming symptoms, assuming, as they often do, the character of general convulsions. In most of these cases they are clonic and general, and therefore probably of central origin, primary or reflected; but the spasms of cholera are tonic, and affect the muscles of the upper and lower limbs, and most frequently the flexor muscles of these parts, and especially those of the fingers and toes, which become rigidly bent. The larger muscles contract into hard lumps, and even those of the chest and abdomen do not escape the terrible spasms. When they are severe they extort cries from patients who at other times seem quite apathetic. It is stated by Macnamara that the natives of Southern Bengal and other people of relatively loose fibre are much less apt to be attacked by them than the natives of the upper country or than Europeans. It may be debated whether their immediate cause is a reflex irritation emanating from the gastro-intestinal mucous membrane; or whether it is due to the rapid diminution of the supply of blood to the nervous centres, or to the infarction of those centres with thick and imperfectly oxygenated blood; or, finally, whether it is occasioned by a diminished supply of blood, and that blood of bad quality, to the muscles themselves. Probably all of these factors are associated causes in producing the spasmodic phenomena of cholera. It is well worthy of notice, however, that spasms, which are so frequent in all infantile diseases, and especially in those affecting the stomach and bowels, rarely attack children suffering from cholera. This would seem to prove that the spasms in question are not reflex, but either central and spinal, or else muscular--an inference which is strengthened by their being tonic and not clonic. As stated, the spasms, or cramps, frequently affect the limbs, but comparatively seldom involve the muscles of the chest or abdomen, and those of the face hardly ever. They are almost the only causes of pain in the disease, which in not a few instances runs its whole course, even to a fatal termination, without their occurrence.

As a rule, the abdomen is not so much retracted as might be expected from the profuse discharges. Probably in some degree its form is maintained by the constantly recurring accumulation of liquid in the {741} gastro-intestinal cavity. In protracted cases, however, the abdomen becomes sunken and hollowed. At all stages of the disease it is somewhat sore under pressure, especially at the epigastrium, and it generally has a doughy feel. As to the functions of the digestive organs, they are completely suspended during a typical attack of the disease. Not only are these organs incompetent to digest food, but they cannot even retain it.

Throughout such an attack not only is sleep apt to be prevented by the pain of the cramps and the frequent evacuations, but, as a rule, the patient is wakeful, and yet, apart from the restlessness which accompanies the paroxysms of pain, there is, on the whole, a tendency to a placid quietness. Mental excitement and delirium are probably unknown during the primary attack, but sometimes a degree of somnolence or of apathetic tranquillity exists, which, however, is quite distinct from coma. When the attack is prolonged, and especially when it merges into a typhoid state, the eyes become inflamed by their exposure to the air. The conjunctiva then grows blood-shot, and occasionally the cornea is ulcerated.

MORBID ANATOMY AND PATHOLOGY.--The appearance after death of a person who has died in the collapse of cholera is very characteristic. It comprises a shrunken aspect of the whole body, its prevalent grayish or leaden pallor contrasting with the livid hue of the abdomen and back, the fingers and toes, the lips and eyelids, and ears; the eyes are sunken deeply in their orbits; the nose is sharp and bent, the temples are hollow, and the skin seems to cling tightly to the bones beneath it. The connective tissue is very dry, and the muscles are hard as well as dry, and, owing to the wasting of the softer parts, stand prominently out. In consequence of the absence of moisture decomposition takes place very slowly. Cadaveric rigidity is very marked and persistent. A very notable phenomenon is the occurrence of muscular contraction after death. It may be excited mechanically or may occur spontaneously. A case is related (Eichhorst) in which three hours after death the fibres of the biceps were observed to move tremulously, and then the entire muscle contracted, causing flexion of the forearm. Even the fingers performed movements like those made in piano-playing. The lower jaw has also been observed to move, causing the mouth to open and shut repeatedly. The late Sir Thomas Watson long ago described this singular phenomenon as follows: "A quarter or half an hour, or even longer, after the breathing had ceased, and all other signs of animation had departed, slight, tremulous, spasmodic twitchings and quiverings and vermicular motions of the muscles would take place, and even distinct movements of the limbs, in consequence of these spasms."[38] It was carefully studied by Barlow, from whose narrative the following is taken: The patient was a strong man; the course of his attack was rapid, and he suffered most cruelly from cramps. "Within two minutes of his ceasing to breathe muscular contractions began, becoming more and more numerous. The lower extremities were first affected. Not only were the sartorius, rectus, vasti, and other muscles thrown into violent spasmodic movements, but the limbs were rotated forcibly and the toes were frequently bent. The motions ceased and returned; they varied also: now one muscle moved, now many. Quite {742} as remarkable were the movements of the arm: the deltoid and biceps muscles were peculiarly influenced; occasionally the forearm was flexed upon the arm--flexed completely, and when I straightened it, which I did several times, its position was recovered instantly. The fingers and thumbs were now and then contracted, and at times the thumbs were separately moved. The fibres of the pectoral muscles were often in full action; distinct bundles of them were seen at intervals beneath the skin.... After I had taken leave of the body the nurse was horrified by a movement of the lower jaw, which was followed by others; and I thought for a moment that the man was alive. The facial muscles became generally affected, and at length all was still."[39] These muscular contractions succeed one another in a regular order, beginning in one lower extremity and extending to the other, then to the upper limbs, and finally to the face. Their degree varies from a slight quivering to a powerful contraction, and their duration from a minute or less to an hour and a quarter. Cases have occurred in which the legs were so forcibly retracted that they could with difficulty be straightened again. In one case, six hours after death movements took place in one leg, and the hand was drawn across the chest; in another, "the forearms were powerfully flexed, and the hands, approximating, gave the attitude of praying to the body."[40] Again, Mr. Ward reports: "I saw the eyes of my dead patient open and move slowly in a downward direction. This was followed, a minute or two subsequently, by the movement of the right arm (previously lying by the side) across the chest." In the same paper Barlow says: "Mr. Lawrence mentioned to me that a gentleman who died in 1832 of rapid cholera was turned after death completely on the side by a strange and forcible combination of muscular contractions."[41] These muscular phenomena after death form an interesting feature in the history of cholera, but they are by no means peculiar to that disease. They have been observed in other diseases, and especially in yellow fever--an affection in which the pathological condition is quite unlike that of cholera. In both diseases they have been manifested in robust persons and when the course of the fatal attack was both rapid and severe. Thus, Dr. Dowler of New Orleans not only found that they could be developed in such cases of yellow fever by striking the muscles, but he observed their spontaneous occurrence in several, of which the following is a remarkable example: "Not long after the cessation of the respiration the left hand was carried by a regular motion to the throat, and then to the crown of the head; the right arm followed the same route on the right side; the left arm was then carried back to the throat, and thence to the breast, reversing all its original motions, and finally the right hand and arm did exactly the same."[42] In 1860, Drasche alleged that not unusually the skin covering the contracting muscles became reddish, while the local temperature rose 1/2°, and that as soon as the contractions ceased the temperature fell below the normal and cadaveric rigidity set in. According to the same observer, analogous contractions affect the unstriped muscular fibres, in those of the skin producing a projection of the papillæ, and in the genital organs a discharge of semen. This phenomenon is said to have occurred an hour and a half after death.

[Footnote 38: Lectures, Am. ed. of 1872.]

[Footnote 39: London Med. Gaz., Nov., 1849, p. 798.]

[Footnote 40: Ibid., Jan., 1850, p. 185.]

[Footnote 41: Ibid., pp. 185, 186.]

[Footnote 42: Experimental Researches, 1846.]

{743} On opening the abdominal cavity of persons who have died in the collapse of cholera one is struck by the general pink or rose tint of the peritoneal coat of the intestines. It is produced by a repletion of the minute branches of the portal venous system. Sometimes the color is rendered very dark by the pitchy blood contained in the veins. The surface of the peritoneum, like all the tissues, is singularly dry, and often has a soapy or sticky feel, caused by a layer of albuminous matter, which forms a lather when rubbed between the fingers, and causes the intestinal folds to adhere to one another. If death takes place during the stage of reaction, these appearances are less distinct, and the intestines, which in collapse are usually retracted, are then somewhat distended.

The stomach generally contains a thin, partially transparent liquid of a greenish or grayish color, and occasionally reddish, holding in suspension portions of coagulated mucus and an unctuous substance of an albuminous nature, which adheres to the walls of the cavity. Fatty globules may be observed floating in the liquid, which under the microscope reveals epithelial débris, granular corpuscles, and fragments of gastric glands. Under heat and nitric acid coagulation of the liquid occurs, and on chemical examination it is found to contain urea. The gastric mucous membrane is of a dark violet or pale pink color, according to the stage of the disease; its follicles are enlarged, and patches of superficial abrasion may be observed on it.

The intestinal canal of those who die during the collapse of cholera is, in the majority of cases, partially filled with liquid which has the aspect of turbid serum, more or less mixed with the previous contents of the bowel if death has taken place very rapidly, but otherwise it is almost colorless. On the whole, however, it is less pale and watery than the stools. It contains, like these discharges, more or less epithelial flocculi, and generally more than were observed during life in the dejections. The mucus scraped from the lining membrane of the intestine and mixed with water renders it turbid with epithelial débris. The same mucus examined microscopically contains fragments, larger or smaller, of epithelium. These conditions are said to predominate in the large intestine. Indeed, the proportion of liquid increases from above downward. Hence in the more prolonged cases the contents of the bowel at its upper part are less liquid and are darker in color. There is, indeed, a striking contrast between the appearance of the intestine in cases which have terminated in collapse and its aspect in persons who have died during the stage of reaction. It has been clearly presented by Dr. Sutton.[43] When death took place in "the cold stage the mucous membrane was unusually pale in three cases; in two it was healthy-looking; in other two it was pale throughout, excepting that one or two of Peyer's patches were congested; and in the remaining three there was more or less congestion of the mucous membrane. When the mucous membrane was pale throughout the entire intestine, the valvulæ conniventes looked swollen and oedematous, and the color of the membrane was dead white. The solitary glands were very distinct and prominent. Those of the duodenum were remarkably so. In cases of imperfect reaction the mucous membrane of the intestine was usually found very much congested and ecchymosed. The congested portions were sometimes {744} granular, and apparently denuded of epithelium. The mucous surface had often a dark port-wine color, due to the extravasated blood and the hyperæmia, and here and there the surface was covered with a dirty gray membranous substance, likened to a diphtheritic deposit. I have, however, seen no decided false membrane, such as could be peeled off, as in diphtheria. The surface was also occasionally bile-stained, and the greenish-yellow color of the bile and the deep red color of the congested surface presented a very striking appearance. The solitary glands were very prominent, and in some cases apparently enlarged." The general paleness of the intestinal mucous membrane in the stage of collapse, and its congestive redness whenever the signs of reaction have existed before death, have a very important bearing upon the pathology of this disease, for they demonstrate conclusively that the gastro-intestinal evacuations in cholera have no relation whatever to inflammation. On the other hand, they render it altogether probable that the serous flux is in the nature of a sweat, an intestinal ephidrosis.

[Footnote 43: London Hosp. Clin. Lect. and Reports, iv. 497.]

The nature of the exfoliation found in the intestinal canal has been the subject of much discussion. As long ago as the first American epidemic of cholera (1832-35) Dr. W. E. Horner, Professor of Anatomy in the University of Pennsylvania, described an exfoliation of the epithelial lining of the alimentary canal, whereby the extremities of the venous system of the part are denuded, as being characteristic of cholera alone. In 1849, Dr. Samuel Jackson, Professor of the Institutes of Medicine, and Dr. John Neill, Demonstrator of Anatomy in the University, in conjunction with Dr. William Pepper and Dr. Paul B. Goddard, presented a report to the College of Physicians of Philadelphia, in which they, too, showed that the "epithelial layer of the intestinal mucous membrane was either entirely removed or was detached, adhering loosely." This important fact--the most important, perhaps, in the mechanism of cholera--was confirmed seventeen years later by the eminent pathologist Dr. Lionel S. Beale,[44] who, when referring to "the remarkable characters of the matter discharged from the intestinal tube, and to the fact that the small intestines almost always contain a considerable quantity of pale almost colorless gruel-, rice-, or cream-like matter," added: "This has been proved to consist almost entirely of columnar epithelium, and in very many cases large flakes can be found, consisting of several uninjured epithelial sheaths of the villi.... In bad cases it is probable that almost every villus, from the pylorus to the ilio-cæcal valve, has been stripped of its epithelial coating during life.... These important organs, the villi, are, in a very bad case, all or nearly all left bare, and a very essential part of what constitutes the absorbing apparatus is completely destroyed.... It is probable that the extent of this process of denudation determines the severity or mildness of the attack.... It seems probable also that the epithelium may become detached in consequence of the almost complete cessation of the circulation in the capillaries beneath, but the death of the cells may occur in consequence of their being exposed to the influence of certain matters in the intestine or in the blood, in which case they would simply fall off."

[Footnote 44: Med. Times and Gazette, Aug., 1866, p. 109.]

In this connection, and as complementary of the statements now made, should be considered the further description by the same author--viz.: {745} "Remarkable changes have occurred in the smaller vessels, especially in the capillaries and small veins of the villi and submucous tissue. The blood-corpuscles appear to have in a great measure been destroyed in the smaller vessels, and in their place are seen clots containing blood-coloring matter, minute granules, and small masses of germinal matter evidently undergoing active multiplication. Some of the arteries are contracted, but here and there small clots destitute of blood-corpuscles may be seen at intervals." Hence, the gastro-intestinal lesions in cholera, according to their extent and degree, they remove the natural obstacles to exhalation in the mucous membrane, and also, and in the same degree, prevent the absorption of the contents of the alimentary canal. It must not, however, be forgotten that this lesion is not altogether peculiar to the intestinal mucous membrane. Dr. Beale long ago called attention to the fact that in this disease there seems to be a tendency to the removal of epithelium from the surface of all soft, moist mucous membranes, but not from the follicles of the glands. The first statement appears to be explicable by the shrinkage of all the mucous membranes during cholera collapse, for by this merely mechanical agency the inelastic epithelium must necessarily become detached. As to the second statement, the remark may be made that the whole follicular structure furnished with columnar epithelium is an absorbing and not an eliminating apparatus, and that, since its functional activity is from the beginning of the disease diminished by an inadequate blood-supply, it can have but a small and indirect share in generating the phenomena of the disease.

In 1884, Dr. Koch, during his investigations of cholera in India, found bacilli in the bowel which he believed to be peculiar to the disease, and which presented the following characters: they were not straight, like other bacilli, but curved or comma-shaped; they proliferated rapidly and displayed very active movements. Bodies of persons who died of various other diseases did not present them, although abounding in different bacteria. The bacilli were not found, or only exceptionally, in the stomach, but abundantly in the intestine, and most so in the diarrhoeal discharges that occurred at the height of the disease. As soon as the stools began to be fecal the specific bacilli disappeared from them. After death at the height of the disease they were most abundant in the intestinal contents, and especially in the lower part of the small intestine. When death took place at a later period none of them might be detected in the liquids in the bowel, but they would still be present, in considerable numbers, in the tubular glands. They were not found at all in cases fatal from some sequela of the disease.[45]

[Footnote 45: Times and Gaz., Mar., 1884, p. 398.]

Other abdominal lesions in cholera possess a very subordinate importance. The isolated and the agminated glands are both prominent, chiefly because they are swollen by the liquid imbibed from the bowel. A whitish substance which they sometimes contain may perhaps be the albumen or fat which they have taken from the intestinal liquid. A very similar condition of the mesenteric glands is probably due to a like cause. The liver is pale and flaccid when death takes place in collapse, and it is also described as presenting a "dirty grayish-red, homogeneous appearance, and indistinctness of the lobular structure, as if some glutinous matter had been poured throughout the tissues of the organ" {746} (Sutton). This appearance would seem to be due to the total suspension of the blood-supply through the portal vein.

At all stages of the disease the gall-bladder is usually found full of bile, which is apt to be dark during the collapse and more watery after reaction has commenced.

The spleen is small, pale, and, as a rule, firm, but occasionally it is soft.

The kidneys present no marked changes when death has taken place early in the attack, or at most only exhibit a lighter color than usual of the cortical substance and a darker one of the pyramids. They show that the arteries are comparatively empty and that the veins are congested. Similarly contrasted appearances are met after death from obstructive disease of the heart and other causes that produce obstruction of the venæ cavæ. In the tubules, later on, fatty degeneration of the epithelium has been observed, and some cylindrical casts. These alterations, especially of the tubules, are most marked when death occurs in the stage of reaction, and are then apt to be accompanied by more or less hemorrhagic transudation. The urinary bladder is always contracted after death in collapse; after febrile reaction its mucous membrane may be more or less coated with false membrane.

The brain and the spinal marrow offer nothing peculiar; their venous systems are everywhere more or less engorged, and sometimes effused blood has been found in the spinal canal.

In the state of the respiratory organs the most important facts are that in algid cholera the lungs are always more or less collapsed, "shrunk and small, and lying back in the chest, toward the spine," and that, so far from being congested, they are (with the exception of a small portion of their posterior part rendered dense by hypostasis) singularly bloodless, dry, and tough. As might be inferred from these conditions, they are also lighter in weight than natural. To Dr. Parkes belongs the credit of having first described this very important fact in the morbid anatomy of cholera, as follows: "In fourteen cases the lungs were completely collapsed, appearing in some cases like the lungs of a foetus. In three cases they were considerably, in eight slightly, collapsed, and in the remaining fourteen cases the collapse was in some altogether, and in some partially, prevented by old adhesions."[46] So Dr. Sutton found that the average weight of the two lungs during collapse was about twenty ounces, and after reaction--that is, after the passage of the blood into the pulmonary artery had become completely re-established--about forty-five ounces. In the latter condition also the lungs presented the usual signs of congestion of those organs, being dark-red throughout or in portions only. Sometimes also they contained masses or nodules of apparent hepatization, and of these some may have undergone partial softening.

[Footnote 46: Med. Times, 1848, p. 378.]

In absolute conformity with the condition of the lungs that has been described is that of the heart. If the lungs are bloodless, it follows necessarily that the left side of the heart must be empty, and almost as necessarily that the right side of the heart must be distended with blood. All careful investigators of the subject agree that such is the condition of the heart when death takes place in cholera during the stage of {747} asphyxia. All report that the pulmonary artery is either empty or that it contains a small quantity of dark and usually of thick blood; that the right side of the heart and the coronary veins are distended with blood of the same description, while numerous ecchymoses exist along the course of the coronary veins; that the venæ cavæ are filled with half-coagulated blood of a tarry aspect; and that even the femoral and splenic veins contain similar blood. On the other hand, the left ventricle of the heart is usually contracted, and contains a very little semi-fluid blood, with perhaps a small and pale clot. This engorged condition of the right cavities and emptiness of the left cavities of the heart diminish very slowly during the passage from collapse to reaction, during which time the pulmonary blood-vessels are being gradually replenished. Besides the thick and tarry aspect of the blood above described, it has been observed that when the blood is withdrawn by means of a pipette, its globules rapidly subside and are surmounted by a transparent serum, and that such blood may remain for a long time uncoagulated. The red corpuscles are said to be pale and viscous, but not adhesive, and the white corpuscles abnormally numerous and easily crushed. In the free intervals are observed "very pale little objects, slightly elongated and constricted in their middle," which multiplied in blood kept for one or two days at a temperature of 38° C. (100.4° F.).[47] If death does not take place until reaction is far advanced or has merged into a febrile condition, the left ventricle is usually found not contracted, and it contains a quantity of blood. The term "usually" is employed to show that even to this rule there are some exceptions, and that, as in all other diseases, the issue does not depend absolutely and exclusively upon a definite degree of any anatomical lesion, but upon the aggregate condition of all the functions upon which life depends. The pericardium, like the pleura and the peritoneum, may be covered with a saponaceous film which is albuminous.

[Footnote 47: Rapport sur le Cholera d'Égypte en 1883, par M. le Dr. Strauss, etc.]

* * * * *

In looking now over the field that has been traversed in the foregoing pages, and searching for some link that will unite in a consistent whole the causes, symptoms, and lesions of cholera, it is evident that only one factor can possibly be so described. That factor is the gastro-intestinal flux. This it is that produces the vomiting and the purging; that prostrates the patient and wastes away in a few hours the fullest and the firmest form; that chills the limbs and afterward the trunk; that thickens the blood so that the capillary vessels can no longer convey it, and that spreads a cyanotic shadow over the whole surface of the body; that cuts off the supply of blood from the lungs and heart; that paralyzes the nervous system, ganglionic as well as cerebro-spinal; that obstructs the kidneys and arrests their secretion; and that, acting through the several links of this pathological chain, becomes the cause of death. But the question still recurs, What is the cause of the gastro-intestinal flux? To this also, in the light of observation, it is possible to give only one answer. It is a specific poison which originates in Hindostan, and, being taken into the stomach and bowels, not only produces in the individual the symptoms and lesions of cholera, but is capable of multiplying itself and rendering infectious the discharges from the stomach and bowels of the subjects of the disease, so that it may be transmitted from {748} one person to another round the whole circumference of the globe. Regarding the form and nature of that poison little or nothing is definitely established, beyond what has already been stated as the result of Koch's observations. As far as they go, they harmonize with a long-prevalent opinion that the cholera poison consists of certain microscopic germs, which, on being received into the bowels, propagate their kind and destroy the epithelium. It is believed by some that these bodies are products of the rice-plant on the banks of the Ganges, and that, having once originated the disease, the germs contained in the discharges become mixed with water or are borne upon the wind, and enter the system of new victims, who, in their turn, disseminate the plague. This theory will be further considered below.

Another view, that of B. W. Richardson, is that, "as pus undergoes changes which convert it into a septic poison, so the excreted matter from the alimentary canal is equally capable, under peculiar conditions of oxidation, of producing an alkaloidal organic poison, which, soluble in water, but admitting of deposit on desiccation," becomes the agent for disseminating the disease. In these theories a false datum and a hypothesis are offered us in place of the fact which we seek. The cryptogamous nature of the essential cause of the disease has no positive proof, but only the probability of coincidence in its favor. There is no proof, because one after another organic form has been alleged to be the essential generator of the disease, and each has been proved to be either not peculiar to cholera or has been shown to be present in other diseases than cholera.

At the present time (1884) it is the fashion to trace every disease to specific bacteria or analogous organisms. But it may be that the occurrence of cholera only furnishes the occasion for the development of these organisms, just as a certain temperature, hygrometric condition, and deficient light and air will cause mould to form on bread and other organic substances. The judgment pronounced by Dr. Beale in this question as long ago as 1866 appears now, as it did then, to approach the truth upon this point: "There is no good reason for supposing that the bacteria in such numbers in the alimentary canal in cholera have anything to do with this disease or with the falling off of epithelium from the intestinal and other mucous membranes. Bacteria are developed in organic matter which is not traversed and protected by the normal fluids of the body, and they invade the cells and textures in cholera after those cells and textures have undergone serious prior changes, just as they would invade textures removed from the body altogether. Nor would it be in accordance with known facts to infer that cholera was due to the invasion of some peculiar form or species of bacterium."[48]

[Footnote 48: Times and Gazette, Aug., 1866, p. 167.]

We repeat, then, that while nothing can be simpler than the mechanism of cholera viewed as a gastro-intestinal hyperidrosis, nothing is more mysterious than the mechanism of the primary cause which gives rise to it. That its real nature has been correctly described is rendered all the more probable by the fact, presently to be insisted upon, that sporadic cholera morbus, which is always the consequence of a direct irritation of the gastro-intestinal mucous membrane, is often with difficulty distinguishable from Asiatic cholera, which, indeed, differs from the former {749} disease chiefly by the intensity of its cause as measured by the gravity of its symptoms and by the nature of the special agent that produces it.

The above views regarding the essential cause of cholera were substantially indited before the Egyptian epidemic of 1883, but they are in accord with the more definite conclusions arrived at by the German and French commissions on the subject. Before their reports appeared, however, a communication was made by Dr. Kartulis of the Greek hospital in Alexandria, setting forth that the drinking-water and the stools and blood of the cholera patients contained, the first a mass of micro-organisms, and the others bacteria and micrococci, which, however, presented no distinctive characters.[49] The German report was prepared by Dr. Koch, the French by Dr. Strauss.[50] The former, alluding to the enormous quantity of micro-organisms found in the contents of the bowels and in the stools, did not perceive any connection between them and the phenomena of the disease. On the other hand, he did assign this relation to a species of bacterium found in the walls of the intestine, and which he compared to the bacilli of glanders. They were lodged in great quantities within the intestinal glands and behind their epithelium, as well as upon the surface of the villi and within them, and sometimes even in the muscular coat. They were most numerous at the lower end of the small intestine. Dr. Koch concluded that although these bacilli, beyond doubt, are in some manner associated with the development of cholera, they are by no means shown to be its cause, and may indeed be themselves the product of the morbid conditions belonging to cholera. All his attempts at that time to develop cholera in animals by inoculating them with the organisms gave only negative results. The conclusions of Dr. Strauss were in entire conformity with those of Dr. Koch, but involved an additional and very important statement--viz. that the shorter and the more violent were the fatal attacks of cholera the fewer were the bacteria found in the intestine. It is evident that this fact is the very opposite of what should have been found had bacteria been essential in the causation of cholera. The more recent investigations conducted in Calcutta by Dr. Koch, which have already been cited, led him, however, to attribute to bacilli of a specific form the absolute origination of the disease. He poses the question in the following manner: Either these "comma bacilli" are a product of the cholera process, or "the disease only arises when these specific organisms have found their way into the bowel." The former alternative he rejects, because, in his judgment, it assumes that the bodies in question must be pre-existent in every person who becomes affected with the disease--a hypothesis which he rejects, because they have never been found except in cholera. He therefore concludes that they are the cause of cholera. He points out that their first appearance coincides with the commencement of the disease, that they increase with it, and that they disappear with its decline.[51] The statement of Strauss quoted above does not, however, appear to harmonize with this conclusion, since the bacteria are said by him to have been fewest in the more violent and fatal attacks of the disease. Another of Dr. Koch's remarks is also open to criticism. After showing how rapidly the cholera bacteria multiply when kept moist, he states that they die after drying more quickly than almost any other form of bacteria. "As {750} a rule, even after three hours' drying every vestige of life has disappeared." It is evident that this statement is not in harmony with the numerous facts, several of which have been cited, that cholera fomites have preserved their infectious qualities after several weeks. Dr. Koch endeavored to produce in animals, artificially, with these bacteria, a disease analogous to cholera, but without success; and he adds, "If any species of animal whatever could take the cholera, it would surely have been observed in Bengal, but all inquiries directed to this point met with a negative result." Dr. Vincent Edwards, who, however, is of opinion that the cholera poison is "not an organism, but of the nature of a chemical compound of comparatively unstable nature," reports that he produced fatal cholera in pigs by giving them the dejections of cholera patients.[52] But the Times and Gazette inclines to question that the pigs employed in Dr. Edwards' experiments were affected with true cholera.

[Footnote 49: Medical News, xliii. 377.]

[Footnote 50: Archives gén., Dec., 1883, pp. 713, 722.]

[Footnote 51: Times and Gaz., Mar., 1884, p. 398.]

[Footnote 52: Notes on the Poison contained in Choleraic Atomic Discharges.]

DIAGNOSIS.--The most characteristic symptoms of Asiatic cholera have repeatedly been mentioned in the foregoing pages. They are rice-water evacuations by vomiting and purging, rapid emaciation of the whole body, a cadaverous hollowness of the cheeks and eyes, a livid color of the face, hands, and feet, a feeble, thready, and at last absent pulse, an icy coldness of the extremities, face, and even the breath, a loss of the elasticity of the skin, a thin and feeble voice, and intense thirst. But every one of these symptoms may occur in cholera morbus produced by a direct irritation of the stomach and bowels. It is rather their nature, we repeat, than their phenomena that distinguishes these two affections from each other. In attempting to separate Asiatic cholera from other forms of cholera we must endeavor to dismiss from the mind the erroneous notion that the term cholera denotes a definite disease identical in its cause, phenomena, and results. It is no more a disease than dropsy or fever is a disease. It is a complex group of symptoms which have in common the fact that they proceed directly from gastro-intestinal irritation, whose degree of severity--i.e. the presence or absence of certain grave symptoms--and, above all, its issue, depend chiefly upon the nature and intensity of the cause of the attack, and also, necessarily, upon the degree of resistance opposed to it by the subjects of the disease. Nothing has led to more error in regard to epidemic cholera than the ignorance of this pathological fact by some and the disregard of it by others.

In the first portion of this article it was shown that the Greek, Roman, and Arabian conceptions of cholera morbus included a discharge of bile, the very symptom for the absence of which Asiatic cholera is notorious; and also that the classical cholera, or cholera morbus, ended in recovery even more frequently than Asiatic cholera terminates in death. But local epidemics of cholera morbus sometimes take place which are of a severe and even of a grave type, and which also appear to originate in some peculiar atmospheric influence, for they prevail to a limited extent and in connection with vicissitudes of weather. Still more circumscribed epidemics have been traced to unwholesome food and drink, and innumerable instances of individual attacks have been caused by irritants that are ranked as poisons and others which are reckoned as food or medicines. Now, under these various circumstances, which have in common gastro-intestinal irritation, there may be produced, if the irritation is excessive, {751} a series of symptoms closely resembling, if not identical with, those of Asiatic cholera.

In illustration may be cited the comparatively familiar description of Sydenham.[53] These are his words: "There is vomiting to a great degree, and there are also foul, difficult, and straining motions from the bowels. There is intense pain in the belly, there is wind, and there are distension, heartburn, and thirst. The pulse is quick and frequent, at times small and unequal. The feeling of sickness is most distressing, and is accompanied with heat and disquiet. The perspiration sometimes amounts to absolute sweating. The legs and arms are cramped and the extremities cold. To these symptoms, and to others of a like stamp, we may add faintness." ... "As the summer came to a close the cholera morbus raged epidemically, and, being promoted by the unusual heat of the weather, it brought with it worse symptoms, in the way of cramps and spasms, than I had ever seen. Not only, as is generally the case, was the abdomen afflicted with horrible cramps, but the arms and legs, indeed the muscles in general, were afflicted also." ... At the risk of repetition an additional passage may be quoted from Sydenham's later definition of cholera morbus: "This is limited to the month of August or the first week or two of September. Violent vomiting, accompanied by the dejection of depraved humors, difficulty on passing them, vehement pain, inflation and distension of the bowels, heartburn, thirst, quick, frequent, small, and unequal pulse, heat and anxiety, nausea, sweat, cramps of the legs and arms, faintings, and coldness of the extremities, constitute the true cholera--and it kills within twenty-four hours."

[Footnote 53: Works, Sydenham Soc. ed., i. 163; ii. 8, 266.]

In spite of the general likeness between this description and the symptoms of Asiatic cholera, there are differences of considerable importance which have been italicized in the quotations. These differences are such as may be attributed to the action of a harsh irritant in the case of cholera morbus, while in the epidemic (Asiatic) disease the distinctive phenomena are the result of a sudden and profuse intestinal flux. Macpherson, who had a long and extensive experience of epidemic cholera in India, after contrasting in detail its phenomena with those of cholera nostras, sums up the discussion in these words: "Cholera indica is essentially a very fatal disease, while cholera nostras is usually a mild affection and is seldom fatal, although it was called atrocissimus et peracutus, and has undoubtedly killed in from eight to twenty-four hours."[54] In regard to the individual symptoms this very competent reporter does not recognize a single one as being absolutely peculiar to either disease. Even the ancients, already referred to, after describing bilious evacuations as being characteristic of cholera nostras, add that sometimes also they are whitish; and modern writers, both before and since the advent of Asiatic cholera in Europe, have made a similar observation. Thus, Quinquaud, in his description of cholera nostras, of which a slight epidemic occurred in 1869 at the Hospital St. Antoine in Paris, says: "The principal symptoms were vomiting and purging, sometimes of a bilious and sometimes of a rice-water liquid; a shrivelled and cyanotic skin, the latter appearance being sometimes strongly marked; anxiety, coldness, cramps, altered voice, and suppression of urine."[55] In 1875 thirty-three cases of this {752} disease occurred at Valenciennes, near Paris, and its symptoms were thus summarized by Manouvriez:[56] "Repeated vomiting, first of food, and then of a dark-green liquid; diarrhoea, which was at first fecal and then bilious, but afterward serous and like rice-water; painful tension of the epigastrium and tenderness of this part; headache, cramps in the legs, suppression of urine; pallor, coldness, and dryness of the skin, especially of the limbs; pinched features, a blue circle around the eyes, a small and scarcely perceptible pulse, and a faltering and whispering voice." Yet of the thirty-three cases only two were fatal--the one a child of four years and the other an infant of as many months. The substantial identity of nature of these two local epidemics, and the almost equally close relation of their symptoms to those of epidemic cholera, must be quite apparent.

[Footnote 54: Times and Gaz., Dec., 1870, p. 725.]

[Footnote 55: Archives gén., Mars, 1870, p. 308.]

[Footnote 56: Archives gén., Sept., 1877, p. 298.]

Yet the contrasts are neither slight nor unimportant; and the most striking and significant is the trifling mortality of the European as compared with the Asiatic disease, notwithstanding the grave symptoms present in the former. It may be regarded as certain, we think, that the reason of this difference of danger lies in a corresponding difference in the nature of the causes of the two forms of disease. The rapid recovery from cholera morbus produced by changes of weather, acid fruits, and indigestion renders it certain that no material lesion of the gastro-intestinal mucous membrane has been produced; while, on the other hand, inspection after death from epidemic cholera or by corrosive poisoning renders it equally certain that the damage to that membrane is substantial and widespread, as well as often irreparable, and that, therefore, "the powers of life that resist death" must be engaged in a very unequal and often fruitless struggle. The cramps in cholera nostras are, as a rule, less severe than in epidemic cholera, while the colicky, and in general the abdominal, pains are greater in the former than in the latter disease. The reason of this difference appears to be that muscular spasm is the natural result of depletion, whether sanguine or serous, while colic is an effect of irritation of the surface of the mucous coat of the bowel, and not of its destruction, such as occurs in epidemic cholera.

It is true only in a limited degree, and indeed only upon a superficial survey of the symptoms, that the effects of irritant poisoning are like those produced by Asiatic cholera. The analogy between the two was pointed out, among others, by Sedgwick in 1867.[57] The resemblance appeared so striking to the vulgar eye that in Paris, and perhaps elsewhere, a popular tumult followed the first violent outbreak of epidemic cholera, and it was charged that the wells had been poisoned. The cases that most resemble cholera are the following: "Acute poisoning by corrosive sublimate, by arsenic, and by mineral acids, especially nitric acid; the effects which follow the eating or drinking of poisonous animal matters, such as tainted or simply unwholesome meat or fish, and milk which has undergone some injurious but yet unknown change, decomposing vegetables and some of the poisonous fungi, and the excessive action of certain drugs, for the most part belonging to the class of drastic purgatives," as elaterium and croton oil. The effects produced by these agents constitute a cholera morbus, and therefore resemble cholera, and have been occasionally, and almost unavoidably, mistaken for it. It {753} is remarkable that suppression of urine may occur among them, as well as vomiting, purging, and collapse. As Griesinger and others have pointed out, the order in which the symptoms occur is a valuable, and generally an available, ground of diagnosis. In cholera, diarrhoea always occurs before vomiting, while in the various irritant poisonings mentioned vomiting precedes diarrhoea. In irritant poisoning also there is generally severe abdominal pain--not so much colicky and paroxysmal as constant and burning; the stools are not so copious as in cholera, and they do not possess the rice-water aspect, but are rather dark, bloody, and fetid, and are voided with tenesmus or with heat in the anus; and even when the urine is suppressed it is less persistently and completely so than in cholera, and attempts to void it are attended with vesical tenesmus and strangury. In a doubtful case it is important to ascertain whether a metallic or other unpleasant taste is perceived in the mouth, whether this cavity or the throat bears marks of corrosion, whether any unusual article of food has been used, etc. Moreover, it is of extreme importance to learn whether Asiatic cholera prevails, not merely in the immediate neighborhood, but at any place from which diseased persons or infected goods may have arrived. The instances should not be forgotten in which cholera-infected clothing from Europe has developed the disease in the valley of the Mississippi. Nor should those still more numerous cases be overlooked in which travellers affected with choleraic diarrhoea have disseminated the disease at great distances from their starting-point, although unconscious of the nature of their own ailment, whose seed they were sowing along their route.

[Footnote 57: Med.-Chir. Trans., li. 1.]

PROGNOSIS.--Like the diseases called septic, of which the eruptive fevers may be taken as examples, and also like the effects of irritant poisons, the gravity of cholera must mainly depend upon the amount and the activity of the specific poison that is received into the system. It is most probable that the cholera poison is organic, and that it has a limited power of reproduction and term of existence, a period also of intense activity and a period of exhaustion; in a word, that either by progressive dilution as an inorganic substance or by organic senescence it finally ceases to exist. By no other theory is it possible to explain the numerous degrees of severity which cholera exhibits, from a mild indisposition to a malignant and rapidly fatal disease. On the one hand, the patients, if they may so be called, are hardly prevented from attending to their customary occupations. They may even be able to travel and carry the disease to distant places, and so appear to justify the erroneous and irrational doctrine of the atmospheric or spontaneous origin of cholera. On the other hand, the entire apparent duration of an attack may not exceed two or three hours, during which all the distinctive symptoms of the disease may be crowded together in the most appalling forms. Such grave cases are always most numerous at the commencement of an epidemic. These statements are true not only in regard to individual cases in the greater number of epidemics, but they represent the distinctive character of particular epidemics, some of which are as remarkable for their benignity as others are for their extreme malignity. For such contrasts no plausible reason can be suggested, unless it be a difference either in the essential virulence of the morbid poison or in the dose of it imbibed. That they are due to the activity rather than to the quantity of the poison seems to {754} be proved by the progressive weakening in the gravity of the cases; for if the quantity of the poison remained the same some malignant cases might be expected to occur even during the decline of an epidemic.

These considerations help to explain the extreme diversities of mortality in different epidemics. The extremes may be stated at 10 and 90 per cent., and they would perhaps be still wider apart if all the mild cases, which are never reported--many of which, indeed, do not even fall under medical observation--were included in the reckoning. The general or average mortality of cholera is about 50 per cent. According to Allbu, the epidemics in Berlin from 1831 to 1873 gave a total of 28,753 cases and 18,916 deaths; that is, a mortality of 65.8 per cent. (Eichhorst). It should be noted that, as in other epidemic diseases, there is no uniform proportion between the extent and the mortality of cholera epidemics. Some of very limited extent have been proportionally the most destructive. It should also be remembered that the disease is far more fatal in infancy and old age than at any other period of life, and for a similar reason it is very dangerous to all who are weakened by any cause, such as an inherited morbid diathesis, a chronic debilitating disease, etc. There seems to be a doubt whether its male or female victims are the more numerous. In this connection it may be suggested that while males are more likely to contract the disease by drinking contaminated water, etc., more women are exposed to its contagion by their intimate relations with the sick, by their handling and washing infected fomites, by carrying away the cholera discharges, etc.

Undoubtedly, the class of society to which cholera patients belong is not without influence on its prognosis. Not only is the total mortality greater among the laboring classes, but the individual belonging to those classes has a less chance of recovery, because he is not apt to resort to treatment on the appearance of the premonitory signs of the disease, and because the treatment he receives is less intelligently and sedulously pursued by his physicians and friends.

In regard to the particular symptoms which are favorable or unfavorable, nothing need be added to what has already been stated in detail, unless it be that during the height of the attack the danger is to be measured by the degree of prostration and of the stasis of the blood, and, during reaction, by the grade of the typhoid state. Gradual reaction, as denoted by the state of the skin and the pulse and a more natural aspect of the stools, is generally indicative of improvement.

Finally, a word of caution may be given to those who are apt to attribute all the favorable changes in the conditions of an epidemic to the sanitary or medicinal measures they have instituted. Cholera epidemics are remarkable for the comparatively short period of their duration, which may be stated at less than a month in the same place. Doubtless, judicious sanitation and timely treatment save a great many lives, but the qualifying fact, already insisted upon, must not be overlooked, that the mortality occasioned by the disease in a given place is greatest during the first period of its prevalence, and that thenceforth it gradually declines. Yet it is of essential significance that the disease rarely attacks a large number of persons simultaneously; the epidemic proper is usually preceded by a few scattering cases which are apt to become foci of ignition that presently unite to form a widespread conflagration. The recognition {755} of these cases, their isolation, and the proper treatment of the localities where they occurred have frequently stamped out what might have been the commencement of a deadly epidemic.

PREVENTION.--The history of cholera demonstrates conclusively that since the disease, outside of India, never arises spontaneously, it must be more or less preventible, partly by excluding its seeds and partly by rendering the soil in which they are planted more or less unfit for their development; in other words, by quarantines and sanitary cordons and by various measures of local sanitation.

In regard to the former there would be comparatively little difference of opinion, at least theoretically, if both measures were alike efficacious. But there would seem to have prevailed a tendency in official quarters to undervalue the efficiency of both. Those who made and administered the sanitary laws relating to cholera seem to have forgotten the emphatic question, "What will not a man give for his life?" or at least to have considered that whatever value some men may set upon their own lives, the lives of other men become of no account when balanced against the needs, or even the conveniences, of commerce. The ethics which justified the introduction of opium into China by the English and the American gift of alcohol to the Indian to gratify a lust for lucre or for land is only paralleled by those contained in the official protests against cholera quarantines. At the International Medical Congress held in 1873 at Constantinople, it was almost unanimously resolved that "the practice of (land) quarantine as now carried out ought not to be maintained, because, on the one hand, it does not constitute a real protection, and, on the other hand, it is directly opposed to the interests of commerce and industry." A leading critic, in commenting upon this, remarks that if a quarantine were possible it would give no real security, because it would be evaded, just as customs laws are evaded by smuggling.[58] A logical deduction from this curious argument would be that customs laws should be abrogated. In 1880 was published the report of the German Imperial Commission on the cholera epidemic of 1873 in Germany, edited by Hirsch, from which we learn that "all the German medical experts agree in condemning the employment of quarantine, for, while largely detrimental to the interests, welfare, convenience, and happiness of a community, it is quite inert and inefficient as a safeguard against the further diffusion of cholera."[59] Whether this opinion refers only to land quarantine or not is left in doubt, but the spirit of subordinating the lives of the people to the commercial interests of a country is just the same as, and is not less worthy of condemnation than, the spirit which has more than once blinded customs officials to the disease on board of vessels from which it has afterward issued to destroy thousands of lives.

[Footnote 58: Practitioner, xii. 226.]

[Footnote 59: Ibid., xxvi. 159.]

It seems to be overlooked that in national as well as in personal affairs "honesty is the best policy," and that if, instead of concealment or false statements regarding the sanitary state of ships, their passengers, and cargoes, and equally false assertions respecting the contagiousness of cholera, and a contemptuous neglect of well-tried preventive measures,--if, instead of this delusive and disastrous policy, all nations had honestly carried out the rules prescribed by experience for the exclusion of the disease, and for its management after it had passed the frontiers of a country, {756} there can be little doubt that its ravages would ere this have been confined to the region in which it originated. As we have seen, there is urged against the enforcement of a rigid quarantine by land or sea the singular argument that it has not always excluded the disease. A more logical inference would seem to be that since it succeeded, not completely, but yet partially, its inefficiency should be charged to its imperfect execution; or, even granting that the absolute exclusion of cholera is impracticable in every instance, including cases of choleraic diarrhoea, contaminated clothing and merchandise, does it therefore follow that the transit of men and things should be unimpeded? As well might it be maintained that because one or more houses cannot escape destruction by fire, therefore no effort should be made to save the remainder of a threatened city; as well might it be argued that because some men must be killed in battle, no precautions should therefore be used to preserve the rest of the army; as well abstain from all local sanitation intended to mitigate the ravages of the disease, because, do what we may, some victims it will surely have. This is taking counsel from despair; is a stupid fatalism which one might imagine to have been imported with the disease from the East; or it may be a sign of the unconscious blindness of Mammon-worshippers, who, neither fearing God nor regarding man, have as little pity for the victims of cholera, permitted, if not invited, by them to scourge the nations, as devout Christians once felt for the negroes who were bought or kidnapped in Africa to toil and die under the lash of the slave-driver.

Probably no sanitary cordon nor any quarantine will invariably and completely exclude cholera, since it is transmissible by living men and by water and by fomites of various descriptions, and, worst of all, by men who neither exhibit its characteristic symptoms nor are conscious of the poison which they conceal and disseminate. But, as has already been urged, it is no argument against preventive measures that they are not absolutely perfect in their efficiency. If they sometimes succeed in arresting the progress of cholera, and if they always, when honestly executed, lessen the number of channels through which the infection can be conveyed, and thereby reduce to a minimum its fatal effects, they ought to be maintained and perfected, and not decried or abolished. It is difficult to characterize that state of mind which concludes against the use of a salutary measure because its efficiency is not absolute, the more so when it is admitted that its inefficiency is not intrinsic, but due to negligent, and even fraudulent, administration. The preponderance of official and personal authority is altogether on the side of the necessity of a quarantine, not in its literal, but in its technical, sense. The International Medical Congress of 1874 declared as follows: "Quarantine ought to be limited to the time requisite for the examination and disinfection of the ship, the crew, and the passengers; and if there be no disease on board the latter should be released immediately after disinfection. But if there be cholera or sickness of a doubtful nature on board, it will be necessary to isolate and disinfect the ship also." The same congress, however, wholly condemned land quarantines, apparently upon the sole ground of the extreme difficulty of rendering them efficient--an argument, as before remarked, that touches not the principle of the measure, but only the manner of its execution. In this respect the congress occupied a lower position than its predecessor of 1866, which held that the futility of {757} quarantine in "arresting the march of cholera" arose "rather from the unintelligent application of the measure than from any fallacy in its principle."[60]

[Footnote 60: Practitioner, xxviii. 393.]

It would burden this narrative even to enumerate the instances in which a strict quarantine has protected places to which cholera has been carried by sea. In the United States numerous examples might be given of seaports into which cholera was brought from foreign countries, and within whose quarantine stations it was confined by rigid sanitary regulations; but it is sufficient to cite the case of New York, through whose quarantine at Staten Island nine-tenths of all emigrants to America have passed. Writing in 1867, Dr. Peters said: "There have been fourteen epidemics of cholera at Staten Island, and only four have reached New York." A large number of illustrations has been collected by Dr. Smart, Inspector-General, R. N.,[61] who sums up the matter as follows: "Believing that cholera has frequently been excluded from islands by quarantine, and as often introduced by its non-observance, I regard it as a truly preventive measure; but, recognizing the impracticability of exacting it under many circumstances, I would insist on the most strict isolation of all the first cases or units of disease, whether introduced from without or originating from relationship to introduced cases, or persons or goods imported from infected countries."

[Footnote 61: Lancet, April, 1873, pp. 555, 659; Times and Gazette, April, 1874, p. 387. Compare also Colin, Brit. and For. Med.-Chir. Rev., July, 1874, pp. 42-44.]

While experience demonstrates the efficacy, and therefore the necessity, of quarantine against cholera in seaports, it has also shown that the same agent of prevention need not be invariably and rigidly applied. When quarantine meant literally a detention, and almost an incarceration, for forty days, it often failed through its very rigor at a time when proper methods of disinfecting ships, cargoes, crews, and passengers were either unknown or inefficiently applied. It is now certain that quarantine may be reduced to a fraction of its original duration, and yet possess a much greater degree of efficiency, its length depending upon the number and the sanitary condition of the crew, etc., the nature of the cargo, etc. It is evident that a ship carrying only cabin passengers is less open to suspicion than one crowded with filthy emigrants, although both may have sailed from the same cholera-infected port. A more liberal rule may govern the one than the other; and in the second case a rigid inspection and cleansing of luggage may be imperative which would be superfluous as well as vexatious in the first case. The importance of such a treatment of emigrants' effects has already been illustrated by cases in which they caused an outbreak of cholera after having been carried from a seaport into an interior town many hundreds of miles distant.

In regard to the time during which a vessel that has had cholera on board within a week or ten days should be detained under sanitary inspection and treatment, including a thorough cleansing of the passengers and their effects, no absolute rule can be laid down; but it would appear that if no suspicious cases arise within a week, there need be little apprehension that any will occur.

The sanitary measures which should be undertaken wherever there is reason to fear an invasion of cholera are, in the first place, such as are {758} equally appropriate in anticipation of any infectious and contagious epidemic disease, and relate especially to the removal of all sources of putrid emanations, whether in stagnant ponds, in streets, markets, shambles, sewers, privies, cellars, or inhabited rooms; for these influences, although they do not cause cholera, yet, by lowering the vitality of persons exposed to them, create an abnormal susceptibility to disease. Many instances in Europe might be cited to prove that whole cities, which in the earlier epidemics were devastated by cholera, were either spared entirely in the later ones or suffered in a far less degree. The measures which proved most efficient were an improved water-supply and a better system of sewerage; and this fact strongly corroborates the belief that contaminated water and fecal emanations are the principal agents in propagating this disease. Cleanliness is the best disinfectant, but during epidemics of cholera, as of other diseases, the popular faith is very strong in numerous articles called by that name. The real value of these preparations is commercial rather than sanitary, but, indirectly, they are useful by prompting those who use them to be more diligent in searching out and removing many sources of air-contamination that perhaps invite and intensify attacks of cholera.

The disinfectants in common use comprise chlorine gas, chlorinated soda, chloride of zinc, sulphate of iron, permanganate of potassium, carbolic acid, and the fumes of burning sulphur. Some of them--and especially the chloride of zinc, sulphate of iron, the permanganate of potassium, and carbolic acid--are supposed to be capable of destroying the infectious principle of the vomit and stools. Another method is to receive such matters in vessels containing saw-dust, which, after being dried, is consumed by fire; and still another is to mix them with dry earth and bury them. If they are thrown into water-closets or privies, they should have added to them a portion of sulphate of iron. Whatever has been used by cholera patients should be destroyed, unless of value, and in that case it should be thoroughly purified by hot air or boiling water and long exposure to the sun. The importance of having large and well-ventilated rooms for cholera patients is very great, but less, perhaps, for the patients themselves than for their medical attendants and nurses. All persons should be excluded from them who are not required by the duties of the sick chamber, and in case of death funeral assemblages ought not to be allowed; nor, during a cholera epidemic, ought crowded assemblies for any purpose to be permitted.

During epidemics of cholera, as of some other diseases, the liability to be attacked is greatest when the vital powers are depressed by mental or by physical causes. Hence it is desirable that one's courage and confidence should repose upon a consciousness of having done whatever is recognized as proper to ward off the disease--not by a minute, watchful, and anxious attention to rules at every step, but by such a general care of the health as good sense and experience enjoin. Undoubtedly, other things being equal, the weak, sickly, careless, and imprudent are more liable to suffer than the strong and cautious, and therefore it is incumbent upon all to maintain as high a degree of health as possible, avoiding not only all probable sources of contagion, direct or indirect, but excessive fatigue, catching cold, depressing emotions, sexual excesses, etc. During the first cholera epidemics in this country it was considered so dangerous {759} to eat fruit and fresh vegetables that many persons lived entirely upon meat, rice, and bread. Such a regimen intensified choleraphobia, and was also an unsuitable midsummer diet. There is no reason to believe that any intrinsically wholesome food need be prohibited during the prevalence of cholera.

The one article of diet about which the greatest and most peculiar care should be taken is water. It is the first duty of towns supplied with water from a common source to be sure that it is, and continues to be, uncontaminated. Well-water should be used as little as possible after the disease has made its appearance, and, as an additional precaution, no water should be drunken that has not previously been boiled. Where ice can be procured it may be used to restore the boiled water to an agreeable temperature for drinking. Filtered water, provided that it be properly filtered, may likewise be regarded as innocuous.

TREATMENT.--If regard be had to the various methods and particular medicines which have been used in the treatment of cholera, it will appear that in hardly any other acute disease has a greater number or variety been employed. If, on the other hand, we endeavor to learn what measures have been really and generally curative in cholera, and what are they to which, on the occurrence of an epidemic of the disease, we may turn with confidence in their power to cure, the result of the investigation is disheartening, and adds to the accumulated proofs that the power of medical art is exceedingly restricted. To this conclusion we must assent at whatever cost to a faith which is strong in proportion to the ignorance out of which it grows. Nor, if we consider the matter rationally, ought we to be surprised or humiliated on account of the comparative helplessness of medicine in this disease, since, if we reflect upon it, the case is by no means peculiar or exceptional. Every disease that may become mortal occurs more or less frequently with phenomena which place it beyond the resources of therapeutics as completely as cholera is in its most malignant forms; and yet no one lays it to the charge of medicine that the various fevers, for example, are at times utterly uninfluenced by the most rational and judicious treatment. Nor does any one bring a railing accusation against medicine when accident fatally damages a part essential to life.

One accident of frequent occurrence presents a certain analogy to cholera in its effects, and that is a burn or scald involving a very large portion of the skin. In cases of this sort experience assures us that death is almost inevitable, and that the duty of the physician is to avoid officious and meddlesome treatment, and address himself to soothe the patient's suffering and maintain his strength, if haply the powers of nature may triumph over the effects of the injury. This, too, is the lesson, substantially, which experience has taught respecting cholera. It is certain that in this disease the function of the whole gastro-intestinal mucous membrane is reversed, and that it is no longer a secreting and absorbing organ, but one almost exclusively exhaling, and that through it the liquid which is essential to carrying on the functions is rapidly running away. If the lesion on which this symptom depends is complete, if the gastro-intestinal mucous membrane has entirely lost its natural function, evidently it is quite futile to address any treatment to this organ. But if, as probably happens in a great majority of the cases, the {760} disorganization takes place gradually, it is evident that there is more to hope from remedies when the disease is gradually developed than when it reaches its acme at a single bound and leaves no time for medical intervention. The one unmistakable lesson that experience teaches respecting the treatment of cholera is, that its success depends upon its prompt and early application. Almost as distinctly does observation teach that subsequently to the first (or diarrhoeal) stage the comparative value of different methods and individual medicines is very uncertain. And, finally, it would seem that in this, as in other acute diseases, intelligent and careful nursing and regimen are quite as important as any medicinal treatment whatever. However a false notion of the power of medicine may blind us to the fact, it is none the less a fact, that if different methods of treatment are compared, that method gives the best results which is least perturbative. For example, in England, on board of a hospital ship, were 85 cases, of which 19 treated by quinine gave 12 deaths, 12 by calomel gave 2 deaths, 12 by carbolic acid gave 3 deaths, and 37 by "Nil" gave 1 death.[62] Or, again, in 1865, at the London Hospital, 159 patients were treated--48 with a mixture containing logwood, ether, aromatic sulphuric acid, camphor, and capsicum, of whom 31 died; 56 with sweetened water, of whom 28 died; 21 with castor oil, of whom 14 died; and 20 with "saline lemonade," of whom 6 died.[63] In the last example the deaths during the use of the astringent mixture were twice as great as under sugar and water, and under castor oil twice as great as under "saline lemonade."

[Footnote 62: Times and Gaz., Dec., 1866, p. 590.]

[Footnote 63: London Hosp. Reports, iii. 444.]

We shall first give an account of the management of cholera in general, and then consider some of the particular medicines used in its treatment.

The essential elements of all plans of treatment for this disease, as for so many others, are rest and abstinence. Whatever else may be done, nothing avails without them. This remark applies emphatically to the premonitory diarrhoea; if it is neglected it may readily be converted into the full-formed disease. It is therefore essential, during the prevalence of cholera, that whoever is attacked with diarrhoea should at once give up all active occupation, and confine himself to a recumbent posture and to the use of food of the blandest quality, such as mucilages and similar preparations, especially of rice, which, less than any other vegetable food, is liable to fermentation during digestion. It is prudent to drink no water that has not been boiled. If there is reason to believe that the bowels retain feces from before the attack, it is generally thought advisable to administer a laxative dose of castor oil, to procure the discharge of matters which would act as irritants. Except for this purpose purgatives are neither indicated nor expedient. In a large number of cases nothing more is necessary than the use of means to check the action of the bowels, and which should consist of absorbents or antacids, astringents, and opiates as they are contained in the officinal chalk mixture, with the addition of tincture of kino or catechu and a small proportion of laudanum. This medicine should be given in dessertspoonful doses at intervals of not more than an hour.

If, instead of a diarrhoea which differs from ordinary dyspeptic diarrhoea chiefly by its watery character, there should also be colic and profuse discharges, it is proper to add to the medicines just suggested some which are of a decidedly stimulant character, such as the essential oils of {761} cajeput, cloves, cinnamon, peppermint, etc., with which chloroform, ether, or Hoffman's anodyne may be associated. At the same time rubefacient embrocations may be applied to the abdomen, which should also be compressed slightly with a broad flannel bandage. Instead of these stimulants, and perhaps more efficiently, may be used a simple epithem made by dipping a large towel several times folded in cold or cool water, applying it so as to cover the whole abdomen, and then enveloping it and the body with a dry towel. This application is more soothing than any liniment and its action is more constant. Instead of any of these agents dry heat may be used, obtained from bags of hot salt or sand, or moist heat from thick poultices of flaxseed meal or Indian corn meal or similar substances enclosed in flannel bags and applied to the abdomen while they are as hot as can be borne. It is difficult to determine which of these applications is the most useful. But, on the whole, heat is preferable to rubefacients, and moist to dry heat. The cold-water dressing is probably best suited to young and robust persons.

It must be remembered that between choleraic diarrhoea and cholera in its complete form there are several grades, in one of the most common of which a tendency to vomit, and even a certain amount of vomiting, accompanies the diarrhoea. Anti-emetic remedies are then indicated. They may consist externally of rubefacient and aromatic applications to the epigastrium (especially the spice poultice); and it is claimed that a hypodermic injection of morphia in this part is very efficient. Internally, the best remedies are ice swallowed in small pieces and small but frequent draughts of iced carbonated water or iced champagne. Where these liquids cannot be procured, effervescing powders used in the same way form a very good substitute for them. If, notwithstanding such remedies, the diarrhoea continues or if it tends to increase, astringent and absorbent medicines may be substituted for them; for example, bismuth may be given instead of chalk, and if this also fails acetate of lead may be prescribed. The last may be used by the rectum as well as by the mouth, but with very questionable advantage. Meanwhile, especial care should be taken to avoid giving so much of any opiate as will induce sopor or excite nausea.

Whoever has had the care of cholera patients has probably, at first, felt sanguine of success in their treatment, even after the characteristic discharges and the symptoms of collapse had set in; but a little more experience has proved their hope to be deceptive, and revealed the reason of it in the absolute suspension of the sensibility and absorbent function of the digestive canal. Hence the dismal unanimity of all medical authors, who from actual observation of cholera have declared that no treatment avails to arrest the fully-developed disease. And yet there is some encouragement in the fact that recoveries sometimes occur from even the most desperate state of collapse and under the most dissimilar methods of treatment; so that the physician is warranted in not yielding to discouragement and in cheering his patients with hope even to the end of life. The popular dread of this, and indeed of all epidemics, is sure to be exaggerated, and it therefore behooves the physician to combat the fears of his patients, and by a cheerful manner as well as encouraging words administer the cordial of hope, which often proves stronger than pharmaceutic elixirs.

{762} It may be well to enumerate, as many do, the indications of treatment in the active stage of cholera, but they really need no such specification. It is evident that they consist in combating the symptoms--the vomiting, the purging, the debility, the cyanosis, the cramps, etc.; and the only means by which the carrying out of such indications can even be attempted are neither more nor less than would be used to relieve the same symptoms in other affections. If the evacuations could be controlled, evidently the cramps and the collapse would not occur; but this essential and preliminary step cannot be secured. The medicines introduced into the stomach or rectum are not absorbed, but are speedily rejected; those which are administered subcutaneously are not taken up by the stagnant blood as freely as in other diseases; the nervous system gives little or no response to the mechanical and physiological stimulants applied to the skin. Yet, in spite of these obstacles, the physician must persist in the use of rational methods, in the hope, however faint it may be, that he may succeed in restraining, and possibly in arresting, the fatal course of the attack. For this end he has hardly any means at command except those, or such as those, which were recommended in the first stage of the disease--the anti-emetic and anti-diarrhoeal medicines, which he is only too likely to see rejected as soon as administered. Yet he must not cease to allay the thirst by the repeated administration of small quantities of carbonated and cold liquids, water, or champagne wine, or morsels of ice swallowed whole. The application of pounded ice in a bladder to the epigastrium is a measure of an analogous sort, and is sometimes as efficient as generally it is soothing. In other cases the aromatic poultice seems to answer better. Of irritants little can be said that is favorable, but the combined irritant and anæsthetic action of chloroform is useful, and morphia should be applied to the epigastrium as well as given hypodermically.

If the vomiting tends to become less frequent, acetate of lead may be prescribed, in the hope that it will exert some constringing action upon the gastro-intestinal mucous membrane. The distressing symptom, hiccough, cannot with any certainty be controlled by medicine, but perhaps the inhalation of chloroform is more efficient than any other remedy, as it also is for the cramps in the limbs. For the latter purpose it is preferable to the frictions with flannel or with stimulating liniments which are generally employed. If such liniments are used, care should be taken that they do not contain ingredients that may disorganize the skin either immediately or subsequently. A dangerous compound of the latter sort introduced during the first epidemic of cholera in this country became officinal under the name of liniment of cantharides.

The loss of the water and of the salts it holds in solution in the blood is, as has now been frequently repeated, the chief pathological element of the disease, next after the conjectural cause which injures the mucous membrane of the stomach and bowels. It was rationally indicated, and therefore a method was early practised, to supply this loss by injecting into the veins a solution of sodium salts. The method was seductive as well as rational, for its primary effects were extremely encouraging; it nevertheless failed, and probably for the very reason that suggested its use. Indeed, there is no more reason, if there is as much, to suppose that a liquid artificially introduced into the blood-vessels will be retained when {763} the natural liquor sanguinis cannot be so. Necessarily, the one will escape where the other has escaped.

Certain systematic writers prescribe a method intended, on the one hand, for reviving the animal heat, and on the other for restoring the movement of the circulation. It need hardly be remarked that the two form essentially but one and the same indication. If the circulation is restored the animal heat will revive, but not otherwise. The same treatment leads to both ends, and it consists partly, as already stated, in the use of stimulants, such as alcohol, camphor, coffee, ether, etc.; but their efficacy depends upon their being taken into the blood, and with it reaching the various nervous centres upon which the renewal of functional activity depends. Little, therefore, can be expected from them at the height of the disease--that is, in the stage of collapse--but as soon as any signs of reaction are manifested they tend to promote it, and hence may enable the functions to revive. For this reason they are adapted to persons who are feeble by reason of their tender or their advanced age, or who have previously suffered from ill-health. But if they act at all, and the more they tend to act, they must be employed with circumspection, lest they outrun the purpose of their administration and produce a violent or excessive reaction. Instead of, or in conjunction with, these internal remedies the local stimulants of the skin, already enumerated, may be used with the due precautions, and, in addition, baths at a temperature of 105° F. of water alone or with the addition of salt or mustard; but all such remedies are of little avail until reaction has commenced. Before that event there is reason to believe that the cold bath is preferable, or, still better, frictions of the whole body with cold water, or even with ice, after which the patient should be wrapped in dry and warm blankets. Yet the efficacy of this powerful agency is by no means comparable to that which it produces in the algid forms of malarial fever. The two conditions, although apparently analogous, are, in reality, very different. In the cold stage of fever the mechanism is indeed paralyzed, but none of its mechanical elements are wanting; but in algid cholera there is an actual subtraction of water from the blood, that turns it from a liquid capable of circulating through the narrowest channels into one that stagnates even in the largest vessels. In the one case force is wanting to circulate the blood; in the other there is no normal blood to circulate.

The treatment of the stage of reaction when it does not exceed a moderate degree, consists simply in strictly enforcing the rules for the patient's repose; that is to say, in intelligent nursing. Mental excitement must be forbidden, and neither medicine nor food allowed that is likely to interfere with the gradual and steady progress of convalescence. Of all articles of food, cool water is not only the most urgently desired, but is the most imperatively necessary for replenishing the emptied blood-vessels and restoring the normal functions. But unless great caution is observed it will be taken too freely and provoke a renewal of the discharges. If any food besides water is allowed, it should be of the simplest sort--of whey first, and then of milk in small quantities at a time, with lime-water if it provokes nausea or retching. Afterward thin broths may be given, also in great moderation, and by degrees farinacea in milk and in animal broths. Only when the strength is much improved should even the most {764} digestible meats be permitted. In proportion as convalescence is marked or interrupted by symptoms of undue reaction is it necessary to prolong and render stringent this regimen; and if those symptoms unfortunately arise which oftener, perhaps, depend upon an over-zealous stimulant treatment than upon the natural reaction of the system, they must be combated by measures which will lessen the local congestions, especially of the brain and the lungs, and also by such as will tend to prevent the system from falling into a typhoid state. For the former dry cups applied to the back of the neck, and cold lotions and affusions upon the scalp, are to be recommended, and for the latter dry cups and warm stimulating poultices upon the chest near the affected region. It is probable that the general warm bath, with cold affusion upon the head at the same time, would prove as efficient as it does in analogous states of typhoid affections. If the urinary secretion is suspended or remains scanty, there is not usually an urgent need of using means for its restoration; for that will generally occur when the blood-vessels become replenished. It should, however, be mentioned that, according to Macnamara, if the patient does not pass any urine within thirty-six hours of reaction coming on, ten minims of the tincture of cantharides in an ounce of water should be given every half hour until six doses have been taken, and the patient encouraged to drink freely of water. If this treatment does not cause urine to pass, we must, after the sixth dose, discontinue the medicine for twelve hours, and then repeat it in precisely the same way. The dose here referred to is of the British preparation, and if the use of it were not recommended by so competent an authority its propriety might very properly be challenged.

After the cholera patient has become convalescent his restoration is very apt to be retarded by dyspeptic disorders, for which, perhaps, the best remedy is a judicious use of condiments with the food and of bitter tonics, especially quinine, colombo, quassia, etc., before meals. If there is constipation, it should be corrected by the cautious use of fruits, and, if these prove insufficient, of mild saline laxatives or small doses of castor oil or rhubarb. On the other hand, if there is a tendency to diarrhoea, it should be met by the use of a mild laxative, such as castor oil, magnesia, or rhubarb, followed by chalk or bismuth, and the use for a time of simpler food and in less than the usual quantities.

Having thus furnished a sketch of the plan of treatment of cholera which we regard as dictated by experience, it may be not without some interest to consider certain elements of the method a little more fully, and criticise, in passing, some other remedies which have from time to time been proposed. The first of these is venesection. There was a time when certain physicians, carried away by conceptions of the disease evolved from their inner consciousness, maintained that it consisted essentially of a spasm of the blood-vessels, and that the natural and legitimate cure for it was to be found in bleeding. No theory is so gratuitous or absurd but cases may be found which appear to justify it, and in this instance also examples were not wanting to illustrate at once the truth of the theory and its successful application. Longer experience, however, and a more correct conception of the disease, have long since condemned this method, which was almost as dangerous as it was irrational. If any additional argument against it were required, it would be found in the condition of the lungs after death. These organs, we have seen, are not {765} only not engorged, but they are empty of blood, and death is due not to asphyxia, but to apnoea, when it takes place in collapse.

If ever there existed any reason for the administration of an emetic--and ipecacuanha has generally been used at the commencement of an attack of cholera--it must be looked for, not in any clinical experience of its virtues, but simply in the deplorable routine that required the administration of an emetic at the commencement of nearly all acute diseases, so that, whatever else was prescribed, the lancet and an emetic seldom failed to be so. In this case also the proofs of the successful administration of ipecacuanha were not wanting, and one might be tempted to suppose, in view of the alleged facts in its favor, that it was useful by causing an evacuation of the material cause of the disease. Physicians were even to be found, of high station and character, who contended that cholera is a species of fever, and to be treated by an emeto-cathartic composed of tartar emetic and epsom salts. If the treatment had been efficient, the absurdity of the reasons for it might have been overlooked; but the one was as disastrous as the other was false. But, as usual, the facts had been misstated or misinterpreted, and emetics ceased to form a part of the systematic treatment of cholera. The idea which possessed those who advocated the use of evacuants was that there was either a poison to be eliminated from the blood or one to be expelled from the bowels. Apparently, the method was not efficacious, for the latest phase of it, the use of castor oil in acute stage of cholera, was of short duration.

When cholera first appeared in Europe the tendency naturally arose to follow in its treatment the example of the British practitioners in India. It then appeared that one of the most eminent among them, Annesley, gave a scruple of calomel, with two grains of opium, at the commencement of the attack, and repeated the dose in six or eight hours, and again upon the following day. In the decline of the disease he ordered scruple doses of calomel for the removal of a "cream-colored, thick, viscid, and tenacious matter exactly like old cream cheese, which glues the gut together and obstructs its passage." Three, four, and even five, scruples of calomel were usually taken before this effect was produced. When it is added that this practitioner held depletion to be the capital element of the treatment, and that he was equally lavish of his patient's blood and of his own drugs, we can only wonder that any subjects of his heroic method survived. It is now conceded by all enlightened physicians that mercurials in large or in ordinary doses are worse than worthless in epidemic cholera. In 1832, Dr. Ayre of Hull, Eng., proposed another method of using calomel, to which he adhered in treating this disease. It consisted in the administration of very small doses of calomel at short intervals, and with each of the first doses a few drops of laudanum. Such a method, if not carried too far, certainly has the merit of sparing the patient a great deal of the perturbative treatment against which we have, in the preceding pages, protested. But that was not at all the notion of its proposer. He claimed for it positive and active virtues. He stated, as the fundamental ground of his plan, that "the primary and leading object of the treatment must be to restore the secretion of the liver." He did not in the least doubt that he was able to do this by the administration of mercury--not, indeed, by a direct action upon the liver {766} itself, but indirectly and sympathetically through the stomach, and by the healthy and specific stimulus imparted to it, by which the due secretion of the bile is promoted. It is, indeed, difficult to conceive of any stimulus that calomel could impart to the stomach that would not be equally given by any other non-irritant and insoluble powder--subnitrate of bismuth, for example. Indeed, Ayre himself relates the case of a man who in an attack of cholera took during three days no less than five hundred and eighty grains of calomel, and recovered without any soreness of the mouth. But the plan which he finally elaborated was different. It was to give small doses of calomel repeatedly--in the premonitory stage one grain every half hour or hour for six or eight successive times, or, if this failed, every five or ten minutes--and in the stage of collapse one grain and a half every five minutes. In a few cases of extreme severity two grains of calomel were given every five minutes for an hour or two, and then the ordinary dose of one grain was resumed. But this was not all: with every dose of calomel was associated one, two, or three drops of laudanum, so that if these doses were repeated frequently the patient received a very efficient amount of the narcotic during the attack. Indeed, Ayre attributed to it the virtue of sustaining the vital powers under the depressing influence of the disease, and of removing or abating the cramps, as well as of detaining the calomel in the stomach.[64] From the preceding account it follows that the treatment of cholera by small doses of calomel with laudanum is founded on an erroneous assumption of the mode of action of calomel, and that whatever efficacy the plan of treatment may possess may with more justice be attributed to the opium, whose effects we know, than to the calomel, whose action, so far as it is known at all, has no conceivable relation to the disease for which it was given. However this may be, if the results of Ayre's treatment are compared with those of other plans, it exhibits very little if any superiority. In the report of the cholera committee of the College of Physicians, London, made in 1853, we find the statement that in 725 unequivocal cases treated on Ayre's plan the deaths were 365, or about 50 per cent., and also the following commentary: "In general, no appreciable effects followed the administration of calomel, even after a large amount in small and frequently-repeated doses had been administered. For the most part, it was quickly evacuated by vomiting or purging, or, when retained for a longer period, was passed from the bowels unchanged. Salivation but very rarely occurred, and then only in the milder cases. We conclude that calomel was inert when administered in collapse, and that the cases of recovery following its employment at this period were due to the natural course of the disease, as they did not surpass the ordinary average obtained when the treatment consisted in the use of cold water only."[65] It is of interest to compare the mortality of 50 per cent. above stated to have occurred under this sort of calomel treatment with the mortality noted at the London Hospital under various kinds of treatment, including the administration of calomel in doses varying "from five to ten and twenty grains every quarter, half, one hour, two, four, etc." Out of 509 cases, 281 were fatal, or 54.9 per cent.[66]

[Footnote 64: A Report on the Treatment of the Malignant Cholera, Lond., 1833.]

[Footnote 65: Dr. Gull's Report, p. 177.]

[Footnote 66: Lond. Hosp. Reports, iii. 437, 441.]

Every disease in which exhaustion and coldness occur is sure to be {767} treated more or less actively with alcohol, but in the collapse of cholera, as in the cold stage of fevers, it is generally useless, and sometimes hurtful. We believe that the following protest of Macnamara is sustained by almost universal experience: "I would here enter an earnest protest against the use of brandy or any alcoholic stimulant in this [the second] stage of cholera. I believe these, both theoretically and practically, to be the cause of unmitigated evil. I simply, therefore, mention brandy, champagne, and the like in order to condemn their use most emphatically in cholera; according to my ideas and experience, it is almost impossible to hit on a more detrimental plan of treatment than that usually known as 'the stimulant' in this form of disease."[67] It is true that apparent dissidents from this judgment may be found, like Playfair, a deputy inspector of hospitals in Bengal, who even circulated printed directions for the treatment of the first stage of the disease by means of brandy or strong rum, cayenne pepper, and laudanum, and had entire confidence in the efficacy of the method.[68] Dr. Macpherson, inspector-general of hospitals, also, after comparing the results of a stimulant treatment with those of other methods, reaches the conclusion that the mortality-rate of cholera is affected neither by the moderate nor by the excessive use of alcohol.[69]

[Footnote 67: Op. cit., p. 456.]

[Footnote 68: Edinburgh Med. Jour., xix. 471.]

[Footnote 69: Med. Times and Gaz., Jan., 1870, p. 62.]

Upon no other point in the treatment of cholera is the agreement of physicians more complete than upon the use of opiates in the early stage of the disease. The premonitory diarrhoea has always been treated by opiates alone or associated with astringents. Probably the best rule is to give from twenty to thirty drops of laudanum, or an equivalent dose of some other liquid preparation of opium, in a little brandy and water, and repeat the dose as often as a stool is voided. Opiates have also been generally employed to mitigate the symptoms of the fully-developed disease. But, like all other medicines introduced into the stomach or rectum, they are apt to be rejected, and even if they are not, their absorption is very doubtful, so that at the height of the attack they must be considered as nearly if not quite useless. When the vomiting and purging begin to subside and reaction is about to commence, small and repeated doses of opiates undoubtedly tend to lessen the evacuations; but great caution must be observed not to exceed the due degree of stimulation, lest a dangerous state of narcotism or collapse be induced. It might be supposed that the hypodermic use of morphia would be less open to objection than its administration by the stomach; but it is to be remembered that the suspension of gastric absorption is only a part of the similar condition affecting the whole circulatory system, and that the stagnation of the blood in the systemic veins prevents the absorption of medicines administered subcutaneously perhaps as completely as the state of the gastric blood-vessels interferes with their absorption from the stomach itself. In point of fact, the utility of opiates at any stage of cholera after the first is not easily determined, for nearly always they are associated with other medicines, and especially with astringents. In this disease, as in others that involve life, we are seldom at liberty to test the powers of individual medicines, but are bound to endeavor to save life by associating those which seem to be required for the purpose. Opiates, then, are nearly always given in conjunction with astringents or stimulants {768} during the first (or diarrhoeal) stage of the attack, but after vomiting is added to diarrhoea and a tendency to collapse is manifested they are at least useless.

The patient, it has already been said, should be disturbed as little as possible, and hence, if he becomes restless, and especially if he is rendered so by pain, he should be tranquilized by means of anæsthetics. Chloroform has generally been employed, and is best administered on the first accession of cramps. Much pain, with muscular fatigue and depression, is thus saved, and the inhalation of the medicine may be repeated as often as the pain threatens to return. No doubt other anæsthetics, and especially ether, would answer the same purpose.

Camphor has been claimed to be a valuable medicine in cholera, but there is no clinical evidence that it is so. Indeed, the only series of cases in which it was mainly depended upon gave a large mortality.

Acids have been employed in cholera, but chiefly on theoretical grounds, "in the hope of destroying the specific cholera process going on in the intestinal canal" (Macnamara). It is hardly necessary to discuss so vague a reason. What specific process is going on? What relation to it has the administration of acids? And, after all, only the hope is held out of destroying the hypothetical morbid process. The reaction of normal stools is usually acid, but sometimes it is neutral or even alkaline. In other acute bowel complaints with profuse diarrhoea they are acid, as in cholera infantum, but in epidemic cholera they are alkaline, because they consist chiefly of the water of the blood. It is far from proven that mineral acids can be useful merely by reversing the reaction of the stools. Far more probable is it that, in so far as they are of use, it is because they act as astringents upon the digestive mucous membrane. This may be inferred from the fact that, according to the advocates of these medicines, it is always difficult, and is often impossible, to acidify the stools in cholera. Moreover, it must be remembered that, like other medicines, the greater part of them are rejected by vomiting. If, then, mineral acids tend to lessen the diarrhoea of cholera, they act by their astringency and not by their acidity. Diluted or aromatic sulphuric acid may be given in the dose of from two to thirty minims, at intervals of an hour, in acid water or carbonated water, or diluted nitric acid, in doses of from twenty to fifty minims, at the same or somewhat longer intervals.

Intravenous injections were used in England during the first epidemic of cholera in 1832-33, but their results were regarded as unfavorable; subsequently, in 1849, they were tried with somewhat better success, and in 1867 the effects were still more encouraging. The liquid employed on the last-mentioned trial consisted of chloride of sodium 60 gr., chloride of potassium 6 gr., phosphate of sodium 3 gr., carbonate of sodium 20 gr., alcohol 2 drachms, and distilled water 20 ounces. The alcohol was added only when the liquid was about to be used, and the temperature of the latter was not allowed to exceed 110° F. or fall below 100° F. The liquid was contained in a zinc vessel holding about eighty ounces, with a lamp underneath, a thermometer hanging within, and a tap near the bottom, from which proceeded an india-rubber tube four feet long, with a silver nozzle at its end. The fluid was allowed to enter the vein by the force of gravity. If difficulty was experienced in introducing the nozzle, the vein was freely exposed, supported on a probe, and incised longitudinally. It was found that the success of the operation depended greatly {769} upon having an ample supply of the solution prepared, so as to repeat the injection as often as might be found necessary. Mr. Little, who practised this method in numerous cases, stated as follows: "When a patient has been long pulseless clots form in the heart, and, as I have seen, extend into the larger veins. In one case the fluid would not flow in, and only distended the veins of the arm injected. After death clots were found extending from the heart into the axillary vein."[70] Five out of twenty apparently hopeless cases recovered under this treatment. The first effect of the injection was to revive the pulse, which had ceased to be felt; the voice also was restored, the color and expression improved, the cramps were relieved, the temperature rose, and the patients became convinced that their recovery was assured. A profuse perspiration and a severe rigor accompanied these symptoms. The rigor was evidently a nervous phenomenon, and not a chill, for it occurred when the temperature was rising. Other cases might be cited which unquestionably owed their recovery to this mode of treatment. It is true, however, that much more frequently it failed of success; and probably not only because the injection could not reach the heart, but because, having permeated the blood-vessels of the whole body, it escaped, as the serum of the blood had done, from the damaged intestine. Nevertheless, it would seem that an expedient which in a certain proportion of cases has been quite successful might yet be rendered more certain in its results if the operative procedure were perfected.

[Footnote 70: London Hosp. Reports, iii. 470.]

Cramps in the limbs may be lessened by active friction and shampooing, but there is no clinical reason for believing that these measures tend to restore the circulation. Equally ineffectual are other means used for communicating heat to the algid body and thereby reviving its functions. It is true that some physicians found that warm baths, at from 90° to 104° F., gave relief to the cramps and restored the failing pulse. In most cases the calming influence of the bath was noted, but it does not seem to have been curative or to have diminished the mortality-rate.[71] It should not be forgotten that the patient has no perception of his coldness. In all analogous conditions, as has already been remarked, such as frostbite and the cold stage of periodical fevers, cold, and not heat, promotes reaction. Still more injurious, if possible, than hot applications are irritants and stimulants after the stage of collapse has set in. Not only are they absolutely futile for restoring the animal temperature, but they are liable, unless very cautiously used, to produce intractable sores upon the skin if recovery ensues. It should also be remembered that the cholera patient's exhaustion is exceptionally great, and is apt to be increased by the officiousness implied in the use of many stimulating agents.

[Footnote 71: Ibid., iii. 445; St. Bartholomew's Reports, iii. 190.]

As early as 1832 a marked advantage was ascribed to the use of cold affusions in cholera.[72] One of the physicians of the cholera hospital of Berlin said: "In these living corpses which are struck with asphyxia, lying cold and powerless, external and internal medicines cease to stimulate; no steam apparatus, no warm bathing, no friction, no irritant, avails." The condition is comparable to that in approaching death by cold, in which friction with snow is well known to be the proper remedy. Cold affusions were employed in the second stage of the disease. If the pulse revived, the affusions were continued in a tepid bath, after which the patient was {770} put to bed and gently rubbed with cold flannels. Internally, ice-water was freely administered. Labadie-Lagrave[73] refers to forty cases treated in this manner, with only seven deaths. Yet the cold-water treatment does not appear to have commended itself to physicians generally. Evidently it does not meet the prime indication, which is to restore the wasted waters of the blood and retain it in the blood-vessels.

[Footnote 72: Ainsworth, Pestilential Cholera, 1832.]

[Footnote 73: Du Froid en Thérapeutique, 1878.]

Cold water ought to be given as freely as possible to assuage the thirst that exists in every stage of cholera, and especially in collapse. Nor should it be withheld because it will presently be rejected, for not only does it produce a grateful sensation in the mouth and throat, but it renders the act of vomiting easier. Yet, to some extent at least, the thirst may be allayed by rinsing the mouth and throat with cold water. Iced water is preferable to ice used for the same purpose, for the latter, by its relatively intense coldness, irritates and dries the mouth. Fragments of ice swallowed whole allay the burning heat in the stomach.

On the hypothesis that the cholera poison consists of organic germs various antiseptics have been employed in this disease. Permanganate of potassium was fortunately excluded from the list, on account of its corrosive action, but, unfortunately, carbolic acid was conceived to possess virtues that rendered it an eminently suitable remedy, and creasote, which resembles it very closely, was presumed to possess corresponding virtues. Then sulphurous acid and the sulphites, which for a time were warranted to destroy every species of germ, were confidently appealed to to stay the progress of cholera, and it was at one time even a matter of dispute whether sulphite of sodium or sulphite of potassium was the more efficacious. In truth, all of these medicines were useless, even when they were not mischievous.

Cholera has never prevailed in any country without giving rise to extraordinary theoretical and practical divagations. One physician in the earliest American epidemic gravely proposed, as the best mode of checking the diarrhoea, to plug the anus with a soft velvet cork. Another, in England, suggested that the "blood may be kept circulating by putting the patient on his back on a board and keeping up a rocking, see-saw, to-and-fro movement from eighty to one hundred times a minute." Another had the revelation that the disease is essentially a "paralysis of the sympathetic nerve and want of performance of the organic functions, with deficient vitality of the mucous membranes," and that its proper remedies are "bleeding, turpentine, and cool drinks, without heat and stimulants;" and to this remarkable doctrine a well-known physician gives his adhesion, thus: "The cause, I firmly believe, is an union of the poison with the sympathetic."[74] Still another discovered that the disease is a spinal disorder, and is to be treated by the application of ice-bags to the spine. Were not the evidence so palpable, it would hardly be believed that such irrational ideas should have been published concerning a disease which had then been under observation by the whole medical profession in Europe and America for more than thirty years, and in Asia for a much longer period.

[Footnote 74: Times and Gazette, Aug., 1866, p. 209; ibid., Nov., 1866, p. 555.]

The most important lesson to be drawn from this history of the treatment of epidemic cholera is, that the arrest of the disease in the diarrhoeal stage is comparatively easy, and that in the stage of collapse its cure by any means whatever is altogether an exceptional occurrence.

{771}

THE PLAGUE.

BY JAMES C. WILSON, M.D.

DEFINITION.--An acute specific fever of short duration and very fatal, endemic in certain Oriental countries, and frequently epidemic; it is characterized by buboes, carbuncles, and petechiæ.

SYNONYMS.--([Greek: plêgê], plaga, a stroke); the Pest; Pestilence; the Bubonic, Glandular, Inguinal Plague; the Oriental, Levantine, Levant Plague; the Indian, Pali Plague; Máhámari; Septic or Glandular Pestilence; Pestilential Fever, Adeno-nervous Fever; Typhus Pestilentialis, Gravissimus, Bubonicus, Anthracicus, etc. Gr. [Greek: ho loimos]; Lat. Pestis; Fr. La Peste; Ger. die Pest, Beulenpest.

CLASSIFICATION.--The plague, pest, pestilence, and their equivalents in various tongues, are terms that have been used from the earliest historical times to designate every epidemic disease attended by great mortality. As knowledge of diseases becomes clearer the terms by which they are designated become more definite; those which did service for a class are restricted to particular groups, and new names are found for other maladies only allied to such groups by superficial resemblances. Hence by degrees the term plague has become more restricted in its use. To-day it is understood as designating exclusively the specific affection defined above, the bubo plague.

The student of medical history meets with insurmountable difficulties in attempting to classify the recorded epidemics which have been described under this term. Even when used in its more restricted signification, difficulties as to the propriety of its application to certain epidemics arise. Thus, nosologists are not in agreement as to whether the great plague--the black death--which swept over Europe in the fourteenth century and destroyed in three years twenty-five millions of inhabitants, was a modification of the bubo plague or an essentially different disease. A like difference of opinion exists in regard to the relationship between the Indian or Pali plague which has from time to time prevailed in North-western India during the present century and the true plague.

The black death of the fourteenth century and the Pali plague, though presenting many of the characteristics of bubo plague, differ from it, while they resemble each other, in one important particular. Among the earlier and more common symptoms of note are those dependent upon gangrenous inflammation of the lungs, a lesion, according to Hirsch,[1] extremely rare in bubo plague. This author informs us that recent observations have fully confirmed the early opinion that the Pali plague {772} differs from that of the Levant chiefly in this modification, and cites Pearson and Francis as saying of the former disease that "the collective symptoms are more like those of plague than of any other known disease.... We believe it to be in all essential particulars identical with the plague of Egypt."

[Footnote 1: Handbuch der historisch-geographischen Pathologie, Dr. August Hirsch, 1860.]

The three forms of plague--(a) the grave (or ordinary), (b) the fulminant (pestis siderans), and (c) the larval or abortive, observed in epidemics and hereafter to be described--do not represent distinct varieties of the disease, but are merely expressions of differences in the intensity of the action of the infecting principle upon different groups of individuals in given communities--differences to be explained here, as in the other infectious diseases, in part by variations in the activity of the poison itself, in part by the individual peculiarities and susceptibilities of those exposed to it.

HISTORICAL SKETCH.--Upon the authority of Rufus of Ephesus, quoted by Oribasius,[2] it is stated that the bubo plague prevailed as an endemic, and at times as an epidemic disease, in Libya, Egypt, and Syria prior to the beginning of the Christian era.

[Footnote 2: Medicinalia Collecta.]

In the year 542 A.D., according to Procopius,[3] the plague appeared in Egypt, at Pelusium; extended westward to Alexandria; eastward to Palestine, Syria, and Persia; passed from Asia Minor to Europe, where it first invaded Constantinople, whence it spread in all directions with such fury that before the close of the sixth century one-half the inhabitants of the Eastern empire had perished, either of the plague itself or of the universal destitution that followed in its train.

[Footnote 3: See Hirsch.]

With this epidemic, known in history as the Justinian plague, this disease established itself for the first time in Europe, where it maintained foothold for more than a thousand years.

About the middle of the seventeenth century the wide prevalence of the plague in Europe began to draw to an end. In Spain it was epidemic for the last time from 1677 to 1681; in Italy the last general epidemic came to a close in 1656, although local outbreaks continued to occur till the beginning of the following century. In France it still prevailed in several provinces in 1668, although it had for the most part disappeared some years before. In Switzerland we encounter it for the last time in 1667-68; in the Netherlands in 1677; from England the plague disappeared with the great outbreak of 1665. In the early part of the eighteenth century two important epidemics occurred within the boundaries of Europe. The first spread from Turkey, through Hungary and Poland, to Russia, thence to Norway and Sweden, and along the shores of the Baltic Sea to the Low Countries. This epidemic came to an end in 1714. Six years later the last great outbreak of the plague on European soil took place. It prevailed with great fury in Marseilles in 1720-21, and overran the whole of Provence. From this date till the close of the century Europe remained free from the plague, with the exception of Turkey and the contiguous countries. During the second and third decades of the present century repeated epidemics occurred in the Balkan Peninsula and the regions bordering on the Lower Danube and the Black Sea. The plague appeared also in Malta in 1813, and prevailed till 1815, and in 1816 it reached certain of the Ionian Islands. {773} Only twice has this pest shown itself during the present century in Western Europe--once, during the epidemic at Malta in 1815, at Noja, a town of the Neapolitan province of Bari; the second time, in 1820, at Majorca, whither it was carried over from the coast of Barbary.

Between 1552 and 1784 the plague prevailed twenty-six times in Tunis and Algiers. Some idea of the importance assumed by this scourge in the countries of North-western Africa may be found from the fact that many of these epidemics lasted continuously for years, that which came in 1784 not ceasing for fifteen years. Between 1816 and 1821 the plague again prevailed in Tunis and Algiers, and again in 1836-37.

During the first half of the present century a change took place in the prevalence of the disease elsewhere. Shortly before its complete disappearance from Europe it ceased to prevail in Western Africa (with the exception of the Nile countries), in Mesopotamia, and in Persia. It disappeared from Asia Minor, Syria, and Palestine in 1843, from Egypt in 1844.

For a short period the plague seemed to have disappeared altogether. Those who cherished this hope were, however, destined to disappointment. In 1853 an outbreak occurred in the Assyr country, Western Arabia; and from that time till the present unmistakable local epidemics of the bubo plague have occurred in isolated regions of Africa and Asia; thus, in 1858 at Benghazi in Tripoli; in 1857 in Mesopotamia; in 1863 in the district of Maku, Persian Kurdistan; in 1867 in the marsh district on the right bank of the Euphrates; in 1870 in Persian Kurdistan; in 1871-73 in the Yunnan province, Western China; in 1873 in the marsh district on the left bank of the Euphrates. During four years following the outbreak of 1873 the disease continued to prevail over an extensive area in the countries bordering on the northern banks of the Persian Gulf. In 1874 it reappeared also in the Assyr district, Western Arabia, and in Benghazi, Northern Africa. In 1876, whilst still infesting the regions about the Lower Euphrates, the plague appeared in South-eastern Persia, and during this and the following years it appeared at several isolated points on the borders of the Caspian Sea. Early in 1878 the disease was reported as prevailing in the district of Souj-Bulak, Persian Kurdistan, and it appeared in October of the same year at the Cossack village Vetlanka, on the Lower Volga, district of Astrakhan, Russia, after an absence from Europe of thirty-seven years. It has more recently prevailed in the Assyr district, Western Arabia, and there have been rumors of its reappearances in Persian Kurdistan.

The Indian or Pali plague (Máhámari) has prevailed in local epidemics of great severity on several occasions during the present century in the North-western provinces of India. This fever was first recognized in Kutch in May, 1815, after a season of great scarcity of food. It spread rapidly over an extensive territory, and appeared in the spring of the following year at various points in Guzerat, next in Merawi, later in Rhadenpur, spreading thence westward to Sindh. Not until the following year (1817) did the pest reach the British possessions. This epidemic continued to prevail until 1821. The disease did not reappear until July 6, 1836, when it broke out in Pali, the principal dépôt of traffic between the coast and North-western India. It spread with great rapidity to the {774} adjoining provinces. Toward the close of the year 1837 the disease broke out anew in Pali, and raged until the spring of the following year. In 1834-35, again in 1837, there were outbreaks of this pest in Gurwal, and in 1846 and 1847 in Karmoun, provinces of the southern slopes of the Himalayas. This destructive pest has raged at an altitude of 10,300 feet, and we learn from Hirsch that it has never wholly disappeared from the mountain-districts of the Himalayas since 1823, and that its ravages in these regions have been so great that certain settlements have been wholly destroyed.

The fever was remittent in type, with a great tendency to become continued; it was characterized by rapidly developing extreme prostration, and was very fatal. In most cases there were glandular swellings in the groins, armpits, and neck. Carbuncles and petechiæ are not mentioned as having been observed. Dyspnoea, cough, and bloody expectoration were frequent symptoms. Vomiting, at first of bilious matter, later of dark, coffee-colored fluid, was likewise common.

The plague has never appeared in the western hemisphere.

ETIOLOGY.--1. Predisposing Influences.--Whilst the present views as to the causation of the specific diseases compel us to assume a specific infecting principle as the real cause of every outbreak of the plague, there are certain circumstances which are recognized as so favoring the development and action of that principle that they have come to be looked upon as indirect or auxiliary causes of particular epidemics. It is more in accordance with the facts to speak of them as predisposing influences. Chief among these circumstances is that combination of physical and social wretchedness which goes hand in hand with poverty and overcrowding. The plague has been termed by a recent observer (Cabiadis) miseriæ morbus, and he has thus reproduced in 1878 a name applied to the great plague of London in 1665--the poor's plague. All observers of recent epidemics unite in ascribing to poverty the foremost rank among the predisposing influences of plague epidemics. It is only necessary to enumerate the evils which form the train of poverty, whether in cities or in villages, to complete the list.

With poverty come ignorance and neglect of all sanitary laws; overcrowding and ill ventilation; personal filthiness; improper as well as insufficient diet; indifference as to the location of dwellings and their surroundings. The condition of the villages which have been the scene of some of the recent epidemics beggars description. All observers unite in testifying to such accumulations of filth in and around the houses as requires to be seen to be believed. In these communities latrines are unknown, and no such thing as organized scavenging has ever existed.

The accumulation of unburied or imperfectly buried corpses has been looked upon as the real cause of the plague, and some of the recent epidemics have followed the prevalence of distinctive epizoötics. Whilst it is not difficult to disprove that under ordinary circumstances the effluvia from exposed and rotting carcasses can give rise to outbreaks of the plague, it is more than probable that an atmosphere charged with such emanations (together with other causes) can so unfavorably influence a community as to increase its susceptibility to the specific cause of this or any other infective disease. There can be but little doubt that the {775} dead bodies of the victims of the plague are capable of disseminating the disease, and that the reopening of graves containing such bodies, even after a long period of time, has given rise to fresh outbreaks of the disease.

The season of the year does not appear to exert any very marked influence upon the development of epidemics, if we base our deductions upon observations made in different countries. In northern countries the disease has prevailed as severely in mid-winter as in summer. The epidemics of London showed a rise during July and August, their furious prevalence in September, and a gradual decline during October and November. In Constantinople the disease has commonly remained dormant during the winter months, and become active as the weather grew hotter. In Egypt, on the contrary, the activity of the outbreaks has developed in winter, increased with the advance of spring, and suddenly abated upon the advent of the summer. Such also has been the case with the three general epidemics in Mesopotamia studied by Tholozan.[4] "Their beginning took place in winter, their development during the spring, their decline and their extinction in summer. Their recrudescences obeyed the same laws: after an incubation during the summer season ... revivification took place in winter and in spring." It is added in this writer's account that the exceptional hot weather of summer in that country, and especially that of the shores of the Persian Gulf, has always moderated or directed the course of epidemics of this pest. In Cairo the epidemics have usually ceased upon the recurrence of intense summer heat in June. Dampness, and particularly a thoroughly wet soil, are favorable to the development and spread of the disease. The marshy regions of the Lower Euphrates, the shores of the Caspian and the Black Seas, the valley of the Nile, have been the scenes of repeated visitations. On the other hand, the plague has maintained its foothold in the mountainous districts of Western Arabia, in Yunnan, on the slopes of the Himalayas at a great elevation, and upon a dry, non-alluvial soil even more firmly than in the low and humid plains of Mesopotamia.[5]

[Footnote 4: Histoire de la Peste Bubonique en Mesopotamie, 2d Mémoire, Paris, 1874.]

[Footnote 5: Tholozan, Histoire de la Peste Bubonique en Perse, 1st Mémoire, Paris, 1874.]

Individual predisposition to contract the disease seems to be increased by all depressing influences, among which may be mentioned excessive bodily or mental exertion, intense and prolonged anxiety, fear, and the like. Previous debilitating disease also increases the liability to the attack. Neither sex nor age exerts an influence in this respect, save that after the age of fifty few contract the disease. Occupation confers no immunity. Physicians, nurses, and others occupied in the care of the sick, and those who bury the dead, have especially suffered in recent[6] as well as in the older outbreaks. Oil-carriers and dealers in oils and fats, and to a less degree water-carriers and the attendants at baths, are said to enjoy a comparative immunity from attack. Those who have suffered from the disease and recovered also enjoy a relative immunity. Second attacks are usually of less intensity than the first.

[Footnote 6: See summary of a report addressed by Dr. G. Cabiadis to the Constantinople Board of Health on the outbreak in Astrakhan in Russia, 1878-79, by E. D. Dickson, M.D., Medical Times and Gazette, 1881, vol. i. pp. 4, 32, 119.]

2. The Exciting Cause.--The exciting cause of the plague must, in {776} the present state of our knowledge, be assumed to be a specific infecting principle. Upon no other hypothesis can the continued existence of a disease so specific in its characters, unchanged through the course of centuries, disappearing when the influences favorable to its presence cease, reappearing in certain regions when they again arise, be explained. Capable of being transmitted by the vehicles of commercial intercourse, of control by quarantine and cordons sanitaires, of spreading from limited foci of contagion into overwhelming epidemics, the plague is the very type of the infective diseases. The nature of this infecting principle is wholly unknown. It is probably a microphyte capable of development within the human organism--capable also of a prolonged independent existence under favorable circumstances outside of the body, and of again giving rise to the disease. The plague is properly to be classed as a contagious-miasmatic disease (Liebermeister) with cholera, dysentery, and enteric fever. It continues to exist by the continuous propagation of its cause, and it spreads by the transportation of that cause.

It is conceded on all hands that the plague has never arisen autochthonously in Europe, but has in every instance been conveyed thither. Those who regard its reappearance after long intervals of time in those countries where it still occasionally prevails as spontaneous are compelled to ignore difficulties in reasoning far greater than the supposition of an equally prolonged condition of quiescence or an inexplicable or unsuspected reintroduction of the cause.

As to the disputed question of the contagiousness of the plague, to set forth the arguments and examples adduced in favor of either view would far exceed the limits of the present article. All the facts are to be explained upon the theory that the exciting cause of the plague, like that of cholera and enteric fever, consists of a miasm that must undergo certain changes outside the body before acquiring its virulent properties, and that the time required for these changes is exceedingly brief. But what the physical properties of this miasm are, or how it finds access to the body, or how it is eliminated, are alike utterly unknown to us.

It is certain, however, that it is incapable of being freely transmitted to great distances in the air. Whether or not it is conveyed or retained by the discharges from the bowel is not known. The history of recently observed outbreaks, from which alone definite and trustworthy facts are to be obtained, goes to show that the exciting cause of the plague clings closely to the patients and their immediate belongings. The closer the relation between those sick and the healthy, the greater the risk that the latter will contract the disease. Those in the house with the patients are more liable to fall sick than those in the adjoining houses--those who are constantly in their presence than those who occasionally see them. Thus, nurses much more frequently contract the plague than doctors, though the latter have in all epidemics been largely numbered among the victims. Among 357 deaths in the outbreak in Vetlanka, already referred to, were a priest, his wife and mother, three doctors, six assistant medical officers, and two Sisters of Mercy. Dr. Cabiadis remarks that the information obtained "shows that the malady propagated itself, in the first instance, from the sick to their relatives and to those who lived with them or who assisted them during their illness. If, on the one hand, these facts showed its contagious character, on the other hand evidence is {777} still wanting to prove whether this transmission of the malady was caused by contact with the sick and their clothing, or by breathing an atmosphere impregnated with the deleterious particles emanating from their morbid bodies."

The period of incubation is from two to seven days. In the report of the commission of the French Academy of Medicine, drawn up by Prus in 1844, the statement appears that the plague has never shown itself among compromised persons after an isolation of eight days. The recent outbreaks tend to confirm this conclusion. L. Arnaud concluded from observations made at Benghazi in 1874 that the mean duration of this period was five or six days, and that the maximum did not exceed eight days. Cabiadis sets this stage down as three days as the rule, but as occasionally not exceeding twenty-four hours. He found no data, however, to show the longest period to which it could extend. Hirsch, from information collected in his investigation of the same epidemic (that of Astrakhan), concluded that the minimum period of incubation observed was from two to three days, the maximum more than eight, and that the average was five days. He states that very short or very long periods were seldom observed.

SYMPTOMATOLOGY.--Individual cases of the plague, as of other epidemic diseases, differ in their onset and progress under different circumstances and at different periods of particular outbreaks. Besides the ordinary form, to which as a type the greater number of the cases more or less closely conform, there are, on the one hand, others so severe that death takes place before the characteristic manifestations have time to appear, and, on the other hand, cases so light that such manifestations are but partly developed, and the nature of the malady is only to be recognized in the light of the prevalent epidemic influence.

Hence among the cases three forms are recognized: (a) The grave or ordinary form; (b) the fulminant form; and (c) the larval or abortive form.

(a) Grave or Ordinary Form.--The plague in typical cases is a febrile malady of the most acute kind, with localizations in the form of buboes or carbuncles.

The course of the attack may, for convenience of description, be divided into four stages: 1, the stage of invasion; 2, the stage of intense fever; 3, the stage of fully-developed localizations; and 4, the stage of convalescence.[7]

[Footnote 7: This formal division of the description is suggested in some of the older accounts. (See "Loimologia; or, An Historical Account of the Plague in London in 1665, by Nathan Hodges, M.D., and Fellow of the College of Physicians, who resided in the City all that Time, Lond., 1721.")

The appearance of the plague in France in 1720 was the occasion of a great number of curious and interesting publications on this subject.]

1. The stage of invasion is marked by a feeling of lassitude, by pains in the loins and extremities. There is extreme bodily and mental weakness, headache, fulness and throbbing of the head, dizziness. The patient's expression is dull, stupid; he replies to questions slowly or awkwardly, his face is pale, his eyes languid, his gait feeble and staggering. The appearance in this stage has been compared by several observers to that of a drunken man. Shivering occurs, but if fever be present it is slight. Nausea, vomiting, and diarrhoea are symptoms sometimes {778} observed. This stage begins suddenly. It is often imperfectly developed, and it may last only a few hours or a day or two.

2. The second stage is characterized by fever of the most intense kind. It is ushered in by a chill, sometimes slight, commonly severe. The lassitude continues, the headache increases, the dulness deepens to stupor or gives way to delirium. The temperature rises to 102°-104° F., or even to 107.6° F. The pulse quickly mounts to 120 or 130. The skin is hot and dry; the patient complains of burning inward heat and of great, sometimes unbearable, thirst. The eyes are sunken and injected; the tongue moist, pale, and thickly covered with a chalk-white or grayish pasty coating; the vomiting often continues. The delirium is commonly active or noisy, and accompanied by great restlessness; it may, however, be mild, tending to sopor or coma. The progress of the disease now rapidly advances. The patient falls into the so-called typhoid state. His tongue becomes dry, hard, and fissured; sordes collect upon the teeth and lips, bloody crusts about the nostrils. At this time the evidences of failure of the forces of the circulation become conspicuous. The pulse grows feeble, small, often irregular--sometimes it can scarcely be felt; the lips become bluish, the extremities cold. There is tendency to collapse. During the course of this stage buboes begin to make their appearance. Sometimes the enlargement of the superficial lymphatics is preceded by tenderness or pain of more or less intensity; often the glands are found to be enlarged only upon search.

The termination of this stage is marked by a sudden fall of the temperature to subnormal ranges (93.2° F. has been observed); at the same time copious strong-smelling sweat not infrequently occurs. The pulse grows feebler, and falls to 100 or below it, and the mind becomes clearer.

3. These changes lead up to the stage of fully-developed local manifestations. The enlarged lymphatics are most commonly situated in the groins or on the upper part of the thighs at a point below that commonly the seat of venereal buboes; less often they are to be found in the armpits or the region of the angle of the jaw; as a rule, they occupy only one or two of these positions in the same patient. They vary in size from a little mass or kernel, only to be discovered after careful search, to the bulk of a hen's egg or a mandarin orange. The swelling of the gland takes place at times with great rapidity. Suppuration is followed by the discharge of an ichorous pus, and not rarely by ulcerative destruction of the surrounding tissues. Suppuration occurs more frequently than resolution, but is comparatively rare in fatal cases. Hence it has come to be popularly regarded as a favorable prognostic sign, whilst the early subsidence of the swelling has been looked upon as an omen of grave import.

The time of the appearance of the buboes varies greatly. In the greater number of cases they have shown themselves on the second, third, or fourth day of the attack, occasionally within six or eight hours of the beginning of the attack, and occasionally they have been observed to precede the general manifestation of the disease; rarely they have appeared as late as the fifth day. In many cases they are absent altogether.

Carbuncles demand attention as being among the characteristic local manifestations of this stage. They are less common than buboes. Their usual position is upon the lower extremities, the buttocks, or the back of {779} the neck. In favorable cases the gangrene after a few days becomes limited and the slough separates. Boils also occasionally appear.

Petechiæ occur in the worst cases, and often at an early period in the course of the disease. Their appearance usually indicates a fatal issue. They occupy at times extensive areas of the body or the greater part of its surface; at times they appear only in the neighborhood of the buboes. They vary in size from a mere speck to spots several lines in diameter. When very numerous they give a livid hue to the skin, and that appearance to the cadaver to which, together with the high mortality, was doubtless due the term black death by which severe epidemics were known in the Middle Ages.

Vibices and extensive ecchymoses sometimes appear shortly before death.

4. The stage of convalescence sets in between the sixth and tenth days. It is often protracted by prolonged suppuration of the bubonic enlargements. Both relapses and distinct second attacks have been noted by recent as well as the older observers.

In addition to the foregoing sketch of the course of the disease in its ordinary form it is necessary to describe certain other symptoms.

The attack has sometimes begun with a convulsive tremor, at other times with a prolonged shaking, which has lasted from six hours to three days, the patient remaining free from fever and not complaining of cold. This condition has terminated in coma, followed speedily by death.

Sometimes the attack has come upon the patient with great confusion of mind, so that he appears dazed, or else a curious distraction has befallen him in the midst of his ordinary avocations. If absent from home, such patients commonly at once set out to return, either trembling and staggering as though tipsy, or else rushing wildly through the streets with frantic gestures and outcries.

The vomited matters are usually at first gastric mucus with bile, afterward dark coffee-colored fluid; in certain cases blood is vomited. Bleeding from the nose, lungs, bowels, vagina, and urethra have also been observed. Cases attended by hemorrhages have in almost all instances terminated fatally.

Constipation has been, as a rule, present during the acute stages; later in the attack diarrhoea has occasionally occurred. It has been looked upon as a favorable symptom.

The urine has been diminished and suppressed in grave cases. Trustworthy observations, both as to its quantity and its chemical composition, are wanting. It has been observed to contain blood.

As has been already pointed out, the Máhámari of North-western India has been especially characterized by lung symptoms. Other regions also have been visited by epidemics in which acute pulmonary lesions formed a prominent part of the morbid complexus.

(b) The Fulminant Form.--Chiefly in the early days or weeks of epidemics, but to some extent also later, cases occur in which the intensity of the sickness is so great that the patient dies before its usual manifestations have time to develop. The duration of the whole attack, which ends fatally, is often not more than a few hours; its symptoms, which differ but little if at all from those of similar cases of other epidemic diseases--such, for example, as epidemic cerebro-spinal fever in its fulminant {780} form--are of the most aggravated character, and the patient perishes overwhelmed by the infection as though struck by a thunderbolt. Profound disturbance of the nervous centres, convulsions, coma, the rapid formation of vibices and petechiæ, collapse, are the speedy forerunners of the fatal issue.

(c) The Larval or Abortive Form.--Toward the close of an epidemic the character of the disease usually undergoes a change. It becomes less malignant. The cases present the essential symptoms, but in diminished intensity. Some cases terminate in an early defervescence with rapid subsidence of beginning local manifestations; others present merely the evidences of a slight disturbance of the general health, without any characteristic symptoms of the prevalent disorder; others, again, are characterized by the appearance of buboes without pain or fever. These swellings undergo resolution in fourteen days or thereabout. Exceptionally they suppurate.

The duration of the plague is from six to ten days in typical cases running a favorable course; those of fatal cases from one to twenty days. Clot Bey[8] found the duration of the worst cases two or three days, of those next in point of severity five or six days, whilst in milder cases death did not occur until the second or third week. Of 534 fatal cases noted by W. H. Colvill, 126 occurred one day after the attack, 80 two days after it, 105 three days, 76 four days, 60 five days, 26 six days after the attack. After six days the number of deaths rapidly declined; on the nineteenth day 1 death, and on the twentieth day after the attack 11 deaths, occurred. It is said that death after the seventh day is commonly not in consequence of the disease itself, but of sequels. Of 16 fatal cases in the village Prischib in Astrakhan, noted in the report of Dr. Cabiadis, and of whom the names, as well as the day of their exposure, their falling sick, and their death are given, 1 died in one day, 4 in two days, 6 in three days, 3 in four days, and 2 in six days.

[Footnote 8: De la Peste observée en Égypte, Paris, 1840.]

The mortality of the plague is greater than that of any other epidemic disease. In all epidemics a large majority of those who contract the disease die. This is especially true of epidemics at their beginning, when it has often happened that for a time all the cases have perished. Of this, as of other epidemic diseases, it is true that the death-rate has varied in different outbreaks and at different periods of the same outbreak. Colvill states that in the epidemic of 1874 in Mesopotamia the mortality of stricken villages during the first half of the time was 93 to 95 per cent. of those attacked, but that afterward the majority of those attacked recovered. The same authority states that in Bagdad in 1876 the mortality was 55.7 per cent. of persons attacked. Arnauld gives the mortality at Benghazi in 1874 as 39 per cent. of attacks. The death-rate at Vetlanka was 82 per cent. of those attacked. In Toulon in 1721, of a population of about 26,000 human beings, about 20,000 were attacked, and of these 16,000 died. It has been by no means of rare occurrence that nearly half the population of towns have perished in an epidemic, or that small villages have been completely depopulated by this scourge.

COMPLICATIONS AND SEQUELS.--The appalling mortality of the plague on its approach, the rapidity of its spread, the popular commotion upon its appearance, its brief course, and the fact that its recent outbreaks have {781} taken place in regions where trained European physicians have been, with a few exceptions, beyond reach, all unite in maintaining the gloom that has since the Middle Ages enveloped the clinical facts of this disease.

Of its clinical course, beyond the brief outline already given, little is accurately known, of its complications still less. In some of the recent epidemics, and particularly in the outbreaks of plague in India, the evidences of pulmonary lesions have been so conspicuous that they deserve to be classed among the essential manifestations of the disease rather than as complications; in others pulmonary congestion, hæmoptysis, the evidences of croupous or catarrhal pneumonia, have occurred in a small proportion of the cases. Aside from this, there is nothing to be said as to the complications.

Among the known sequels are protracted ulceration of the enlarged lymphatics, boils, superficial or deep abscesses, catarrhal pneumonia, pertussis, mental troubles, and the like. Extensive and deep cicatrices are not infrequently found in the site of the ulcerating local manifestations.

MORBID ANATOMY.--The existing knowledge of the morbid anatomy of the plague is but scanty. The observers of the early outbreaks contributed nothing; the recent outbreaks have taken place under circumstances in which anatomical investigations were impracticable. The knowledge which we possess is almost wholly due to the investigations conducted by the French in Egypt at the close of the last and the beginning of the present century, and again during the years 1833 to 1838.

The descriptions of Bulant,[9] Clot Bey, and others point to gross lesions, such as are found after death in the acute stages of the infectious diseases in general. The viscera were engorged with dark fluid blood; ecchymoses were often found in the mucous and the serous membranes, in the substance of the different organs, and into the connective tissue. The spleen was in almost all cases enlarged, softened, and of a dark color. Not rarely the kidneys were deeply engorged, and extravasations of blood into their substance, their pelves, and into the surrounding connective tissues were often encountered.

[Footnote 9: De la peste oriental d'apres les matérnaux recuillés à Alexandrie, à Smyrne, etc., pendant les Années 1833 à 1838, Paris, 1839.]

The only constant and characteristic changes relate to the lymphatic system. The lymphatic glands were, as a rule, enlarged and deeply injected with blood. Where no buboes existed the glands of the various cavities of the body showed evidences of acute inflammatory processes. In some instances the affection of the glands appeared to be general; less frequently it was most conspicuous in, or apparently limited to, one or more great groups. Thus, the bronchial, the mediastinal, the mesenteric, the lumbar, etc. were severally the seat of marked changes with or without enlargement of superficial groups, or several of these groups were at the same time implicated.

In no instance were symmetrical enlargements of the inguinal regions, the axillæ, or the throat met with.

According to Runnel,[10] in 2700 cases there were inguinal buboes in 1841, axillary in 569, maxillary in 231; inguinal buboes occurred 175 times on both sides, 729 times on the right only, 589 times on the left only; the axillary buboes were double 9 times, right only 185, left only {782} 163. Buboes of the neck only occurred 130 times, and of them 67 cases were children.

[Footnote 10: A Treatise on the Plague, London, 1791.]

The connective tissue surrounding the affected glands was the seat of an infiltration sometimes serous, sometimes cellular; it also very commonly contained more or less extensive extravasations of blood. Even where no buboes appeared on the surface of the body the glands were enlarged to twice their usual size or more. The substance of the glands in the larger swellings was at times uniformly red or violet, again whitish or marbled or pulpy or denser, or of the consistence of fat. It was also sometimes soft like jelly, and rarely it contained minute collections of pus. Some observers speak of dilatation of the lymph-vessels in the neighborhood of the enlarged glands.

DIAGNOSIS.--The difficulties attending the recognition of the plague at the beginning of an outbreak speedily subside. The rapid spread of the disease, its frightful mortality, the overwhelming intensity of the symptoms, the prompt occurrence of cases characterized by buboes, carbuncles, or petechiæ, are collectively considered diagnostic of this, and of no other disease whatever. In regions subject to the repeated visitations of this pest there exists a universal unwillingness to mention even the name of a disease whose suspected presence alone is followed by consequences of the most serious nature to the freedom of personal and commercial intercourse. To this unwillingness, rather than to any real likeness between the plague and other diseases with which it has been compared, are to be traced most of the difficulties as to the differential diagnosis that have been raised, especially in the regions bordering on the Mediterranean Sea.

It is not, therefore, necessary in this place to discuss the diagnosis between the plague and malarial and other pernicious fevers, malignant typhus, epidemic dysentery, lymphadenitis, syphilitic buboes, parotitis, and so forth.

TREATMENT.--Preventive.--The efficient treatment consists in prophylaxis. The history of this disease indicates with singular clearness the measures which, properly carried out, are capable of controlling the spread of the epidemic diseases. These measures arrange themselves into two groups, of which the first has to do with the removal of the conditions familiar to the development of the disease, the predisposing influences; and the second with the restriction of the disease to the locality in which it shows itself--isolation, quarantine.

The conditions favorable to the development of the plague have already been set forth under the heading Etiology. They relate to poverty and ignorance, and their attendant evils, in communities. They are those conditions which tend to disappear under the influences of civilization, and in truth it may be said that at the present time the plague occurs only in half-civilized countries.

Preventive medicine has achieved no other work comparing in magnitude and importance with the extinction of the plague in Europe. This was, to use the words of Hirsch, "a gradual process, and kept pace in great measure with the development and perfection of the quarantine system with reference to the Orient and the different countries of Europe." This author continues: "I cannot, in fact, understand how any one criticising the facts without prejudice, and having regard to the {783} state of the plague in the East, can for a moment hesitate to attribute the chief cause of the disappearance of the plague from European soil to a well-regulated quarantine system." The European has by no means lost his susceptibility to the disease. He is liable to attack in the East. His protection at home lies in the restriction of the exciting cause of the disease to its present haunts.

Any extended notice of quarantine and quarantine laws is beyond the scope of this article. It may be said, however, that with reference to the plague measures quite unnecessary under ordinary circumstances assume the greatest importance when this disease makes its appearance in countries bordering upon Europe, and that no amount of hardship to individuals necessary to avert so great a calamity as a plague epidemic could be looked upon as excessive. Indeed, we can with difficulty realize the severity with which measures of isolation have been carried into effect at times when the devastation produced by the plague was still vividly remembered. Violation of the orders issued during an epidemic has been punished with no less a penalty than death. It is related that upon the appearance of the plague in the little town of Noja in Lower Italy in 1815, troops were despatched immediately to surround the place with a cordon. The town was encircled by two deep ditches, and opposite the gates three ditches were spanned by drawbridges, which served as a means for the introduction of provisions, but no other communication was allowed. Only letters were allowed to leave the city, and these were first dipped in vinegar. Cannons were posted at the city gates. The ditches were occupied by sentinels, who were ordered to shoot down any one who approached and failed to stand still the moment he was hailed. A plague patient who escaped while delirious and attempted to pass the lines was, in fact, shot dead. Outside this cordon two others were established. Those who disobeyed the orders were treated with the greatest severity. An inhabitant of Noja, who had thrown a pack of cards to the soldiers, together with the soldier who picked it up, was tried by court-martial and shot.[11]

[Footnote 11: Ueber die Pest zu Noja, Nürnberg, 1818, quoted by Liebermeister in Ziemssen's Encyclopedia, article "Plague."]

Lower Italy, possibly Europe also, owed its escape to the rigorous measures carried out in this instance; nor can it be doubted that the measures of isolation practised during the outbreak on the Volga 1878-79 restricted the disease to the district in which it appeared and brought it to a speedy end. On this occasion three efficient cordons were established to isolate the infected places. The first cordon was put around every place where plague prevailed, to prevent persons from entering or quitting that locality until forty-two days had elapsed after the last attack of the malady there. The second cordon was formed around the infected area, encircling all the infected localities. Its circumference extended 800 kilometres, and was guarded by pickets of soldiers stationed at intervals of five kilometres. This cordon had four quarantine stations. The third and outermost cordon was established round the whole province of Astrakhan. It served to control the functions of the inner cordons, inasmuch as all persons coming from within its area, who could not prove that they had undergone quarantine at the stations of the middle cordon, were stopped.

{784} The complete disinfection of all clothing and other articles used in the service of the sick is to be included among measures of prophylaxis. It is no uncommon thing to destroy by fire the houses in which cases have occurred, along with their contents.

No efficient means of protection are known for those who during an outbreak cannot escape from the infected neighborhood. It would be without purpose other than to amuse the reader to reproduce the quaint fancies of the older physicians in this matter, or to dwell upon the amulets and incantations, the absurd costumes, the protective power of tobacco, according to Diemerhoeck, or the disbelief in its virtues on the part of Hodges, who preferred "canary, of the best sort, of which he frequently drank while he attended the sick."

Clinical.--"The treatment of individual cases must in the present state of knowledge be expectant and symptomatic. Notwithstanding our acquaintance with the symptoms that characterize plague, we are utterly ignorant of the treatment best suited to its cases" (Cabiadis).

Physicians who have written from personal observation unite in advising a treatment of the simplest kind. Ventilation, cleanliness, a liquid diet, abundant cool drinks, are to be ordered. The initial collapse and the evidences of failure of the circulation call for the use of stimulants, and especially of alcohol. Cold or tepid sponging, in accordance with the sensations of the patient, may be resorted to. If there be high fever an energetic antipyretic treatment might be carried out. Cold effusion is said to have been of use in many instances.

Purging, bloodletting, mercurials, blistering, emetics, have proved either positively injurious or altogether without effect upon the course of the disease.

Of drugs, ammonium chloride, salicylic acid, carbolic acid, quinine, have been administered without positive effect.

It is stated that the free inunction of oil from the very beginning of the attack was affirmed to exert a favorable influence.[12]

[Footnote 12: See Griesinger, Virchow's Handbuch der Speciellen Pathologie und Therapie, ii. 2, s. 316.]

In early times the buboes were often incised, or even excised, as soon as they began to swell. More recently they have been treated with leeches or inunctions of mercurial ointment. The treatment by poultices and the evacuation of pus as soon as it can be detected is at present regarded with greater favor. Carbuncles are likewise to be treated in accordance with accepted surgical procedures.

{785}

LEPROSY.

BY JAMES C. WHITE, M.D.

DEFINITION.--Leprosy is a constitutional disease of chronic course and fatal termination, characterized by peculiar changes in the tissues of skin, mucous membrane, nerves, and most organs of the body.

SYNONYMS.--Elephantiasis of Greek writers; Lepra of Arabian authors; Anssatz (Germany); Spedalskhed (Norway). The local names in use among the numerous races in which it prevails are too numerous to be given here.

HISTORY.--Although great confusion has existed among the most ancient as well as later medical writers with regard to the definition of this disease, it having been confounded with several other affections (elephantiasis arabum, syphilis, psoriasis, morphoea, etc.), leprosy has prevailed in certain parts of the world from the time of the earliest records. The biblical accounts show that it existed among the Jews in Egypt, although it was not accurately distinguished from other diseases resembling it in some respects. It was recognized in Greece before the Christian era, and in the early centuries after Christ it had extended widely over Europe. In the seventh and eighth centuries special leper-houses were founded in Italy, France, and Germany. The disease reached its height in Europe in the twelfth and thirteenth centuries, when 19,000 lazarettos are said to have been in existence. Its spread was greatly increased by the constant intercourse kept up between Europe and the East during the Crusades. In the fifteenth century it began to diminish, and in the course of the seventeenth it had almost wholly disappeared from the most civilized states. It has lingered, however, in other parts, and exists to-day in France and Spain and Portugal, in Norway and Sweden, and in Italy, Greece, and Southern Russia. As in ancient times, it is widely spread along the coasts of Africa and prevails largely throughout Asia. It is found in many of the islands of the Indian and Pacific Oceans, in Japan, New Zealand, Madeira, the West Indies, extensively in some of the states of Central and South America and Mexico and the Hawaiian Islands.

It may be interesting to trace its history in the United States and adjacent districts more minutely. It is not known just when leprosy was introduced into North America. According to the Louisiana historian, Gayarré, the Spaniards established leper hospitals in several of their colonies on the Gulf of Mexico during the last century. One existed in New Orleans as late as 1785. In 1776 the disease was reported as existing among the blacks in Florida. It seems to have died out, and with {786} it all remembrance of its former existence amongst us, until within the last few years, when its occurrence in the Southern States has again attracted attention. In Louisiana the first case was discovered in 1866 in an old woman whose father came from the south of France; she died in 1870. In 1871 it appeared in one of her sons, in 1872 in two others, and in 1876 in a nephew. A sixth case developed in a young woman who was in constant attendance upon the first case. In addition to this group, other cases have been observed in several parishes, amounting to twenty-one in all, as collected by Salomon of New Orleans in 1878.[1] Two other cases, brother and sister, in Louisiana are known to the writer, one of whom has recently died under his care. In South Carolina the disease is reported by J. F. M. Geddings[2] to have been observed in sixteen cases since the year 1846; four were Jews, four negroes, and eight whites. In none was any hereditary taint to be traced. No new cases have developed since that report.[3]

[Footnote 1: New Orleans Med. and Surg. Journal, March, 1878.]

[Footnote 2: Trans. Intern. Med. Congress, Philadelphia, 1876.]

[Footnote 3: See article on "Contagiousness of Leprosy" by writer, in Amer. Journ. of Med. Sciences, Oct., 1882.]

In Minnesota and other North-western States leprosy has been known to exist for a considerable time among the Norwegian immigrants who have settled in them in large numbers. Holmboe in 1863 and Prof. Boeck later made visits to these colonies while in this country, and published reports concerning them after their return.[4] The latter found eighteen cases among his countrymen, most of which were leprous before emigration; in others the disease developed after arrival in America. It had not manifested itself in any person born in this country. The character and progress of the affection seem to have been little influenced by residence here. Since these observations other cases have been collected by the committee on statistics of the American Dermatological Association,[5] showing the continuance of the disease in these States. In 1879 there were fifteen cases in Minnesota. Its spread in this portion of our country is slow.

[Footnote 4: British and For. Med.-Chir. Review, Jan., 1870, and Nord. Medic. Ark., Bd. iii.]

[Footnote 5: See Transactions.]

Since 1871, 52 cases of the disease have been inmates of the hospital for lepers in San Francisco, California. Of these, all, with one exception, were Chinese, and forty-five of them had been sent back to China. It is presumed to have shown itself after arrival in this country, as "unproductive labor would not be imported by the Six Companies."[6] No case of the disease known to have been acquired in this country has yet been reported upon the Pacific Coast. One case has developed in San Francisco after residence in the Hawaiian Islands.

[Footnote 6: Trans. Am. Derm. Assoc., 1881.]

In Oregon, too, the disease has appeared among the Chinese immigrants, steps having been recently taken to re-ship five lepers from the poor-farm at Portland to China.

Since 1815, possibly earlier, leprosy has prevailed among the poor French settlements along the Miramichi River, near the Bay of Chaleurs, New Brunswick. It was first noticed in a woman whose mother came from Normandy, and has continued mainly in her descendants since. No measures were taken to control the disease until 1844, when a hospital was erected on Sheldrake Island. In 1849 the present lazaretto at {787} Tracadie was established. During the first five years (1844-49) there were admitted 32 patients; from 1849 to 1863, 67 additional patients were received; and from the latter date to 1879, 30 more, making a total number of 129 up to the last report. The greatest number present at any one time was 37. In 1878 there were 16 patients in the lazaretto--6 men and 10 women. The total number of deaths in the hospital has been, up to 1878, 123. A. C. Smith, who resides near Tracadie, states that at the latter date but three cases were known to exist outside the lazaretto. Residence is not compulsory, and no sufficient measures are taken to remove patients from their homes before they may have inoculated other members of the family. The disease is more restricted in locality than formerly.

Within the last two years two or three small groups of the disease have been discovered in the island of Cape Breton, which are described in the Canadian Journal of Med. Science, Sept., 1881.

These are all the places north of Mexico where the disease exists in an endemic form. A considerable number of cases have been reported within the past few years from other parts of the United States, where it has manifested itself in persons who have formerly resided in leprous countries or in those who have wandered from the above infected districts. A very few instances have been recorded in which it has appeared in those who have never visited any infected locality or have been in apparent contact with lepers. Such cases, if authentic, establish the possibility of a sporadic origin of the affection. The fact of so many foci already established, and the penetration of a race so prone to the disease as the Chinese into all parts of the country, give the study of leprosy in America a special importance.

ETIOLOGY.--The study of the etiology of leprosy is intimately connected with that of its history and geographical distribution. From the earliest times it was regarded in all parts of the world as a contagious affection, and efforts were made by the sternest laws of Church and State to control its spread by segregation, by interdiction of marriage, etc. No disease has ever been regarded with an equal degree of abhorrence by mankind; none has received greater attention from physicians of every age. Within the present century it has come to be regarded, almost without exception, by the profession as non-contagious. Peculiarities of climate, soil, and modes of life have been looked upon as predisposing, exciting, or even essential influences in its causation; but the widespread distribution of the disease, with the consequent diversity of diet and customs of living, its prevalence upon the coast and in interior regions, in high altitudes as well as at the sea-level, in Iceland as in the tropics, show that these conditions, however they may affect the course of the affection, have no direct relation to its causation. The theory of heredity, as the most plausible explanation, has received its strongest support in the investigations of Boeck and Danielssen in Norway, where the disease can be traced for several generations in families. The same conclusions readily present themselves where the disease is studied in restricted localities, as in Louisiana and New Brunswick at the present time, where, as we have seen, it manifests itself closely in families in different generations. But this is a narrow point of view from which to study the etiology of leprosy. It often fails to manifest itself in the descendants of lepers in {788} such communities, and affects persons in whose families it has never previously existed. Moreover, in countries where it does not prevail it not infrequently attacks individuals who have at some time visited regions where it was endemic, and in the latter places may develop in immigrants from parts of the world where it has never existed.

The same class of facts which seem to demonstrate its hereditary nature may be used in support of its infectious character. The proper field for observation in this regard would be a virgin region where its natural course could be studied independently of theories. Fortunately for science, such an opportunity is afforded in the history of the disease in the Hawaiian Islands. The exact date and mode of its introduction there are not definitely known. The islands have for years been the resort of the whaling-fleets manned by sailors coming from leprous regions. The natives also shipped as sailors, and after visiting such ports returned home. The absence of any restraint in the intercourse of crews and native women is well known. Isolated cases may have occurred as far back as 1830, but the disease made slow headway until about 1860, when it increased so rapidly that the government took stringent measures to control it, all cases discovered being sent to the leper segregation upon an island from which there is no escape. Since 1866, 2000 cases have been received there, and at last report the asylum contained 750 inmates. This by no means represents the extent of its prevalence in the islands, however. As the native population by recent census was only 44,000, it will be seen that the proportion affected is very large. This unwonted rapidity of spread cannot be accounted for on the ground of heredity. Transference from individual to individual by inoculation seems to be the only possible explanation, and all resident physicians believe that the disease is contagious in this sense. It affects almost exclusively those of native descent, and their habits of life are such as would greatly facilitate its wide dissemination in this way--viz. their great licentiousness and absence of all fear of the disease, which affords no bar to ordinary association or cohabitation; the crowding of large families in small huts and sharing the same mats and blankets; the eating of poi with the fingers from the same dish; passing a common drinking-vessel or pipe from mouth to mouth, etc.[7] Promiscuous and compulsory vaccination with impure virus, too, has been generally practised during recent epidemics of small-pox. It is evident that abundant opportunity has in many ways been presented for the inoculation of pus or blood into the circulation from infected to healthy persons. Where immunity from contraction has followed marriage with a leper, it may be assumed that the conditions of an abraded surface and the contact with pus or blood have not been fulfilled. The wide spread of syphilis among the natives, and a consequent cachexia, have no doubt contributed to these conditions and established a national lack of resistance to the ravages of the disease. Nor can we overlook the proclivity of all endemic diseases to extraordinary manifestations of virulence in insular nations not previously protected by gradual inoculation. Many reliable cases are cited by resident physicians where the evidence of direct communication of the disease seems to be reliable. Facts of the same nature may be collected in the study of the history of {789} the disease in New Brunswick and in Louisiana, where, as above stated, much better fields for investigating this question exist than in the Old-World regions where the affection has been rife for centuries.

[Footnote 7: Dr. G. W. Woods, U.S.N., in Hygienic and Med. Reports of Navy Department, vol. iv., 1879.]

If we admit the fact of transference by inoculation in a single instance, there is no reason why we should not regard this as the principal if not the only means of extension of the disease, whether we accept or not the theory of its parasitic nature. It is not inconsistent with our knowledge of its laws and history to believe that leprosy is an affection communicated with difficulty, and after a prolonged period of incubation, from one person to another by contact with certain products of the diseased tissue; that it has in past and present time in this way spread from nation to nation; and that its progress as an endemic affection has been checked only by laws based upon this theory. All the negative facts so frequently urged against this doctrine of contagion apply as strongly to that of heredity, and may be interpreted in support of the former. The latest investigations into its pathology afford tangible evidence in its favor. It may at least be claimed that the question of contagion through inoculation must be reopened.[8]

[Footnote 8: See article on the question of contagion in leprosy in the American Journal of Med. Sciences, Oct., 1882, by the writer.]

Leprosy affects both sexes in about equal degree, and may first show itself in early childhood. It is apt to produce sterility, so that marriages between lepers are rarely fruitful. This result seems to limit the extension of the disease under the law of heredity if we admit its action. There can be no doubt that cohabitation may take place for years without communication of the disease where one party alone is leprous; and such immunity may be explained by the failure of favorable conditions for sexual inoculation, just as in syphilis. The disease would naturally be most dangerous in its ulcerative tubercular form.

SYMPTOMATOLOGY.--There are two well-marked forms of leprosy--viz. the tubercular and the anæsthetic--which are characterized by certain easily recognized external manifestations, and which are accompanied by symptoms indicative of disturbances of the general economy as well as of special organs. These forms are not always sharply defined, and often occur simultaneously or in succession in individual cases. Both are generally preceded by premonitory symptoms, consisting of unaccountable languor of mind and body, tingling sensations in the skin, rise of temperature in the evening, and various disturbances of digestion, or by the occasional outbreak of single or several blebs. This prodromal stage affords no indication of the type of disease to follow, and may last for days, months, or even years, with greater or less intervals and intensity.

TUBERCULAR LEPROSY.--This form may declare itself at once by the characteristic tubercles, but frequently an earlier manifestation is the appearance of macules or dull red spots, varying in size from a pea to two or three inches in diameter. They have an indistinct margin, a glazed and smooth surface, and become paler on pressure. The patches, although not at all or but slightly elevated above the general surface, are firmer, and penetrate more or less deeply into the cutaneous tissues. They may increase in size peripherally and undergo involution in the older central portions simultaneously. During the latter process the color changes from a more or less dull red to a brown, yellow, or grayish tint, and {790} finally may become quite white. The spots also become thinner or even slightly depressed. Their seat is principally the trunk, but also the limbs, and less frequently the face. This condition of the skin may precede any other changes in its tissues for months or years, the patches appearing and disappearing or remaining as permanent stains. At last well-defined tubercular elevations show themselves, varying in size from a small shot to a filbert, flattened or semi-globular in form, generally smooth and firm to the touch, and of a dull red or brown color. They occur upon any part of the surface, but are especially abundant upon the face, where they may cause great deformity of the features. The forehead and eyebrows may become very greatly thickened by general infiltration, or thrown out into very prominent folds and protuberances by the massing of individual tubercles. The lips thicken, the nose broadens, and the ears stand out conspicuously with their increased bulk. All these changes in form, with the great darkening in tint which is often present, give at times a most repulsive expression to the face. The tubercles are sometimes to be felt imbedded in the skin, or considerable areas are found to be uniformly thickened and scarcely at all prominent. All forms are capable of involution after an existence of months, and may leave dark-colored atrophic patches to mark their seat. They are rarely painful, and occasionally slightly sensitive. They may be transformed into ulcers, especially upon prominent positions, as the knuckles, elbows, knees, as the result of pressure or injury, which are extremely indolent, although shallow, and may heal and break down repeatedly. Occasionally they give rise to serious complications--inflammation of the lymph-vessels, suppuration of the joints with loss of the attendant members, as the fingers and toes. Tubercles appear also upon the mucous membrane of the nasal cavities, the mouth, and larynx, often in great abundance, causing a very characteristic hoarseness or loss of voice. With these changes in the cutaneous tissues, which may be accompanied in their periods of greatest activity by febrile disturbances, there are developed after months or years, with gradual failure of strength, manifestations of changes in the internal organs, the lungs, intestines, and brain, which may prove fatal at any time, or the patient may die of slowly progressive marasmus. The course of the tubercular form is on the average between eight and ten years. At any period there may supervene manifestations of the anæsthetic type, which makes the so-called mixed variety, in which either form may predominate.

ANÆSTHETIC LEPROSY.--This variety is characterized by the loss of sensation in the skin over areas of varying extent, which occupy no definite positions in relation to nerve-distribution. The anæsthetic patches may appear upon the seat of old maculæ or former tubercles or of a preceding bullous efflorescence, or upon parts not previously affected in any way. They may follow a reddened and hyperæsthetic condition of the cutaneous tissues, or they may be surrounded by a serpiginous border of this character. The degree of anæsthesia in the affected parts is sometimes so complete that the skin and underlying tissues may be deeply pricked or cut or burned without the patient being aware of the injury. Such patches may possibly regain their sensibility. Their surface appears in later stages dry, wrinkled, shrunken, and of a brownish color, and atrophy, not only of the skin but of the muscles, is gradually developed, {791} in consequence of which the expression of the face undergoes a marked change. The eyelids and lips droop, the hair falls, the hands contract, and the joints of the fingers and toes are laid bare, so that the phalanges, or even the whole hands and feet, drop off. Ulceration or gangrene of the parts may develop, and whole extremities may shrivel up. With these manifestations of local derangements of nerve-action the functions of the brain fail, the patient becoming stupid and incapable of action or motion, the temperature and pulse are lowered, and death comes slowly by marasmus or the most various complications--tetanus, disease of the lungs, pyæmia, etc. The average duration of this form is from eighteen to twenty years.

PATHOLOGICAL ANATOMY.--The structural changes which take place in the tissues of parts which are the seat of the appearances above described have received the special study of many excellent observers[9] in recent times, and are now well understood. A section through the thickened skin or a tubercle shows the corium and underlying connective tissue infiltrated with round cells, as in lupus and syphilis; in other words, converted into "granulation tissue." This change first takes place along the course of the cutaneous vessels and glands, penetrating more deeply and forming a firmer cell new-growth in proportion to duration, the cells being enclosed in a coarse meshwork of fibrous tissue, and encroaching upon the various structures of the skin, so as to produce atrophy and finally destruction of all its characteristic tissues. This cell-infiltration may of itself undergo later changes, as fatty degeneration and softening (ulceration). The lymph-glands and corpuscles assume a special fatty metamorphosis. An examination of the tubercles upon the mucous membrane reveals the same small-celled new-growth. In the nerve-tissues also marked structural changes are found, both in the central and peripheral systems, in the anæsthetic form of the disease. In many cases the posterior segments of the gray cornua and the fibres of the commissure, as well as the nerves of the extremities, have been found altered by inflammation, which will account for the disordered sensibility and the subsequent disturbances of nutrition, muscular atrophy, etc. The nerve-trunks are often to be felt beneath the skin, thickened and sensitive on pressure. The chronic cell-infiltration affects the fibrous structure of the outer sheath, the neurilemma, and the septa between the nerve-bundles, producing fatty metamorphosis and atrophy of the nerve-bundles. Similar cell-infiltrations are found also in the connective tissue of all the internal organs of the body, which lead to destructive processes in their respective structures.

[Footnote 9: Boeck and Danielssen, Traité de la Spedalskhed, Paris, 1848; Virchow, Die Krankhaften Geschwülste; Kaposi in Hebra's Lehrbuch der Hautkrankheiten; Monasterski, Vierteljahressch. für Derm. u. Syph., 1879, p. 203; Hansen, Virchow's Archiv, Band 79, 1880; Neisser, Virchow's Archiv, Band 84, 1881; Cornil et Souchard, Annales de Derm. et de Syph., 1881, No. 4.]

Within the last two years repeated observations have been made which confirm the statement published by Hansen in 1873, that a peculiar bacterium occurs in leprous tissues, which, it is claimed, establishes the parasitic nature of the affection. These examinations have been carried on with leprous material derived from many parts of the world, and the results have been uniform. Within the round cells which characterize the cutaneous neoplasms, both in the distinct tubercles and the diffused {792} infiltrations, small agglomerations of minute rod- or staff-like bodies (bacilli) are found, arranged in parallel rows or placed end to end. Their length is one-half or three-fourths the diameter of a red blood-globule, and their breadth is one-fourth their length. With them minute granular particles are seen in the cells. They occur in greatest numbers in the cells of the upper layers of the true skin, which are considerably swollen by their presence. They never penetrate the epithelial layer, nor are they found in epithelial cells in any position. When the protoplasm of the cell is interfered with by the later tissue-changes of the disease, the bacillus perishes. They are found not only in the leprous cells, but also in those of the connective tissue running between the agglomerated masses of the former. Between the leprous cells and the filaments of connective tissue but few free bacilli are seen. The neoplasms of the mucous membrane and of many organs of the body have been found to contain them also. In the blood they have been detected by some observers. Their presence in the nerve-tissues is of importance as throwing light upon the question of the specific or inflammatory nature of the morbid processes above described as affecting them. If we regard the bacteria as pathognomonic of leprous tissue-changes, their occurrence, recognized in the cells penetrating between the fibres of the peripheral nerves, would seem to make all primary structural changes identical, and the anæsthetic as much as the tubercular form the direct result of their presence. Neisser draws the following conclusions from his investigations: "Leprosy is a real bacterial disease, caused by a special kind of bacterium. The bacilli appear in the tissues as such, or more probably as spores, and remain for a longer or shorter time in a state of incubation, according to circumstances, in dépôts, perhaps in the lymph-glands. This period, much longer than in other infective diseases, is in proportion to the physiological resistance of the human organism compared with the feeble developing power of the bacilli. It, as well as the course of the disease, is more rapid in tropical countries than in Europe. From these dépôts the disease extends throughout the body in those portions of the skin most exposed, the face, hands, elbows, knees, and into the peripheral nerves. The other organs are less freely invaded. The bacilli excite inflammation, and by a specific action transform the migrating cell into the leprous cell. Leprosy is probably an infectious disease, and its specific products are contagious--viz. the leprous cells of the tubercles, the tissue-fluids, and the pus containing bacilli or viable spores. On the other hand, the pus may not always be infectious, as the fluid contained in the bullæ is not."

It must be said that the bacterial nature of leprosy, if established in accordance with the above observations, furnishes a satisfactory basis of explanation of all facts, historical, clinical, and pathological, which have so long been awaiting solution. The inability of the parasite to penetrate the epithelial layer of the skin and mucous membrane explains why contagion is so difficult, and why the ulcerative tubercular form would be more favorable to such transference than the anæsthetic variety.

DIAGNOSIS.--Leprosy in some of its early appearances may be readily confounded with vitiligo, morphoea, pemphigus, lupus, and syphilis. In some cases its prodromal manifestations cannot be positively diagnosticated until other symptoms have developed, which by concurrence establish their true significance. Such are the pemphigus-like bullæ, the {793} pigment-changes, and the smaller tubercular efflorescences. In regions where the disease occurs only by importation, and in the so-called sporadic cases, it is not at all strange that it should fail of recognition, even in well-advanced forms, unless the observer is acquainted with its whole symptomatology. On the other hand, there is no disease which presents more strikingly characteristic features in its advanced stages.

PROGNOSIS.--Leprosy is almost uniformly a fatal affection, and its course toward this termination varies but slightly under the most diverse conditions of life. Its development and progress are naturally more rapid under circumstances of least individual resistance, where food is poor and scanty, where extremes of climate are most felt, where the constitution of the individual or nation is debilitated by previous disease, as that of the Hawaiians by syphilis, or where no proper professional care is employed. It has been believed that a change of residence from infected to non-leprous regions would retard its advance or avert its appearance in those supposed to be hereditarily disposed; but the former effect follows probably only so far as the general condition of the patient is affected by the change, as in other constitutional disorders, and the latter is necessarily a matter wholly of conjecture. No case of leprosy in the Norwegian colony in our North-western States has ceased to progress after arrival toward its fatal ending, even if this has been somewhat delayed in individual cases under more generous ways of living. If it could be known that a child born in Norway had escaped leprosy by removal to America, we should not, if we accept the bacterial origin of the disease, consider that climate or other mysterious influences had overcome its inherited tendencies, but that it had been taken away from the chance of direct inoculation. It is stated that very rarely cases cease to progress beyond certain stages even in countries where the disease is endemic. The course, as has been stated, varies according to the clinical form, the duration of the tubercular variety being on an average but one-half that of the purely anæsthetic type. Leprosy may be called the slow disease, its period of incubation, so far as this can be determined, extending from one to several years, its prodromal stage lasting often several more years, and its well-developed forms requiring at times more than twenty years to destroy the patient. Cases sometimes prove fatal, however, in a single year.

TREATMENT.--In a disease which affects so many of the races and such great numbers of mankind, which has been for centuries the object of special attention on the part of physicians, and of late years of government commissions and of eminent pathologists, it is evident that every remedy which the materia medica includes, as well as those of merely popular reputation in the widely-diverse geographical regions in which it prevails, must have been employed in its treatment. None of them exert any specific action upon it; it remains incurable. Every year some new article is employed with the usual claims of success which accompany the introduction of new remedies, but they merely swell the long list of failures in the therapeutics of the affection. Still, leprosy is influenced somewhat by medical care; life may be prolonged and made more comfortable. To this end we may employ remedies which are capable of improving and maintaining the constitutional powers of resistance to the disease, such as are found of service in other chronic wasting affections. {794} The patient is to be put in as healthy ways of living as possible, removed from debilitating localities, and given generous diet and tonics, as iron and quinia. Several new drugs which seem to stimulate the nutrition and produce temporary improvement in the local and general symptoms have lately been widely employed, as Gurjun balsam and chaulmoogra oil, but they have wrought no cure. Digestion is to be aided, diarrhoea to be checked, and disturbances of respiration to be alleviated. Local treatment is also of service. The tubercles may sometimes be made to disappear--partly, at least--by stimulating applications, and ulcers made to heal by cauterization and other well-known methods of dressing. These ulcers and their secretions should be regarded as possible sources of infection by attendants and members of the patient's household. For the anæsthetic alterations in the tissues but little can be done locally. If the bacterial origin and causation of the disease be eventually established, its future extinction must be based upon studies directed to the nature and mode of protection against this organism. Collectively, the disease should be treated by every nation by thorough segregation, and importation should be prevented by the most rigid quarantine laws.

{795}

EPIDEMIC CEREBRO-SPINAL MENINGITIS.

BY ALFRED STILLÉ, M.D., LL.D.

DEFINITION.--A febrile, and often malignant, but non-contagious disease of unknown origin; usually occurring as a local epidemic; confined hitherto to the North American and European continents, and to the vicinity of the latter; characterized by its rapid and irregular course, and usually by a tetanic rigidity or retraction of the neck, a tendency to disorganization of the blood, and the formation of inflammatory exudates beneath the membranes of the brain and spinal cord.

SYNONYMS.--Spotted fever; petechial fever; malignant purpuric fever; malignant purpura; pestilential purpura; black death; typhus petechialis; typhus syncopalis; febris nigra; febbre soporoso-convulsivo; tifo apoplettico tetanico; fièvre cérébro-spinale; typhus cérébro-spinale; phrenitis typhodes; epidemic meningitis; epidemic cerebro-spinal meningitis; malignant meningitis; typhoid meningitis; méningite cérébro-spinale épidémique; méningite cérébro-rachidienne; Genickkrampf; Genickstarre.

The names which have been given to this disease convey more or less distinctly one or the other of two ideas: 1st, that the disease is essentially a blood-disorder; and 2d, that it is an inflammation of the cerebro-spinal meninges. Under the first head belong the following names: Malignant purpuric fever; malignant purpura; pestilential purpura; petechial fever; spotted fever; febris nigra; black death, etc. Under the second head belong epidemic cerebro-spinal meningitis; epidemic meningitis; malignant meningitis; typhoid meningitis, etc. As partaking of the qualities of both categories may be cited the names cerebro-spinal fever and fever with cerebro-spinal meningitis. In regard to all those of the first class it is sufficient to repeat the criticism made by the early American writers who described this disease after having largely studied it. One only of them need be cited, because he expresses the opinion of all. Miner, writing in 1822, said: "It is quite unfortunate that a single symptom (petechiæ), and one, too, that is wanting in a great majority of cases, should have been seized upon to give it the odious and deceptive name of spotted fever, as that name has been applied by European writers to a very different kind of fever." Among the names given to the disease, cerebro-spinal fever is perhaps the least suitable and the least in harmony with the principles of scientific nomenclature. It is one of those terms which may be pardoned when used by the laity, but which educated physicians ought not tolerate. Parallel examples may be found in such compounds as brain-fever, lung-fever, gastric-fever, and, most unfortunate of all, enteric fever. The first three of these are {796} inflammations, pure and simple, of the brain, lung, and stomach; and, after their example, cerebro-spinal meningitis would be, what it is not, merely an inflammation of the membranes of the brain and spinal marrow. The name of the remaining disease has only to be turned into English and called intestinal fever to demonstrate its defects. It is evident that other diseases--and dysentery in particular--are equally entitled to be called enteric fever. Moreover, there are cases of enteric fever in which death takes place so early that the intestinal lesion is undeveloped, and the fatal issue must be attributed to the fever-poison in the blood or else to the changes it has wrought in that fluid. Analogous illustrations abound in the history of the eruptive fevers. The disease we are studying presents another affection in which the septic element sometimes so far overrides the inflammatory as to destroy life before the latter has developed characteristic tissue-changes. There may be no valid objection against classing it among the fevers, but there can be no excuse for denominating it cerebro-spinal fever. The very reasons that militate against its being regarded as a meningitis forbid its being considered as a meningeal fever. But if it is a meningitis, inchoate or complete, then the prefix epidemic denotes its constitutional nature and its probable blood origin, and a term is employed which is descriptive and accurate, and not misleading. Moreover, the term epidemic indicates, or at least implies, the characteristic type of the disease, which is asthenic and sometimes more or less typhoidal, just as other inflammatory diseases become so in their epidemic form--e.g. pneumonia, bronchitis (influenza), dysentery, etc.

There ought to be no doubt whether epidemic meningitis should be classed with general diseases or with inflammations. It is excluded from the latter class by the total absence of any tangible external cause from its causation, as well as by its frequent fatal termination before the characteristic signs of inflammation have had time to form, or because the peculiar type of the disease prevents their development. It belongs to the former class because it is epidemic in the largest sense, its outbreaks occurring simultaneously in remote parts of the earth and independently of all cognizable celestial or terrestrial influences. In this as in other elements of its pathology the disease stands absolutely alone. While the acute affections of the pulmonary and digestive organs, which were just now alluded to, affect large districts, and even sweep over a whole continent, epidemic meningitis breaks out in limited localities, and may for years prevail in a populous city within a hundred miles of another still more populous which during that time may altogether escape its ravages. Of this curious fact the cities of Philadelphia and New York present a striking illustration. Since, then, we are ignorant of the circumstances under which the disease arises, and since, as will more distinctly appear later on, its several forms really include quite various morbid conditions, we are compelled to consider it as occupying a peculiar and exceptional nosological position.

HISTORY.--Previous to the present century the existence of this disease can hardly be demonstrated. And yet Dr. B. W. Richardson believed that some faint traces of it could be discovered, as in the following statement:[1] "The great plague which visited Constantinople in 543, and which Procopius and Enagrius described, the plague of {797} hallucination, drowsiness, slumbering, distraction, and ardent fever, with eruption on the skin of black pimples the size of a lentil,--this plague, which usually killed in five days, and left many who recovered with withered limbs, wasted tongues, stammering speech or such utterance of sound that their words could not be distinguished,--this plague, which had passed into mythical learning under the name of cerebro-spinal meningitis, has also in our time reappeared." The concluding statement in regard to the name of the plague is quite erroneous, and there is nothing in the description which distinctively applies to the disease we are examining. On the other hand, we know that Procopius wrote a history of the Oriental plague, which invaded Europe for the first time at the very date above given. It had as a distinctive symptom the well-known inguinal bubo, and there is no mention whatever, in the descriptions of it that have survived, of the tetanoid symptoms belonging to epidemic meningitis. In 1802 an epidemic occurred at Roetlingen in Franconia which had a certain resemblance to the subject of this article, for it was characterized by lacerating pains in the back of the neck. According to Hecker, this was the sweating sickness which had ravaged various parts of Europe during the Middle Ages, and of which limited outbreaks still recur. In 1880 such a one took place at l'Ile d'Oléron in France, and many of the patients were affected with tonic or clonic spasms, both general and local, but not, apparently, opisthotonic.[2]

[Footnote 1: Diseases of Modern Life, p. 16.]

[Footnote 2: Pineau, Archives gén. de méd., tom. i., 1882, pp. 25, 169.]

If epidemic meningitis occurred before the nineteenth century, it must have been confounded with other affections, but when we consider its characteristic symptoms such an error seems improbable. The comparatively rare resort at that time to post-mortem examinations, particularly of the cranial and spinal cavities, may in part account for such a confusion of ideas; and even when dissections were made, the skill to interpret the discovered lesions was possessed by few. It has been thought that in the latter part of the last century some cases of this disease were seen and described, although their nosological value was unrecognized. Thus, Stoll[3] speaks of a young soldier who was seized with a pain in the back of the head and neck, and who was affected with opisthotonos before he died. On examination pus was found between the arachnoid and the pia mater. The first clear and unquestionable description of epidemic meningitis was published in 1805, first by Vieusseux and directly afterward by Mathey.[4] The disease appeared at Geneva in the spring of the year, in a family composed of a woman and three children, of whom two of the latter died within twenty-four hours. A fortnight later four children in a neighboring family died of it after fourteen or fifteen hours' illness, and a young man in an adjoining house, being attacked, died the same night, with his whole body of a violet color. The disease ceased during the spring, after having destroyed thirty-three lives. Its distinctive features were an abrupt attack during the night, bilious vomiting, excruciating headache, rigidity of the spine, difficult deglutition, convulsions, nocturnal paroxysms, petechiæ, and death in from twelve hours to five days. Vieusseux calls it "a malignant non-contagious fever," and Mathey gives as the lesions revealed by dissection a gelatinous {798} exudation covering the convex surface of the brain, and a yellow puriform matter upon its posterior aspect, upon the optic commissure, the inferior surface of the cerebellum, and the medulla oblongata.

[Footnote 3: Quoted by Boudin, Hist. du typhus cérébro-spinal, p. 5.]

[Footnote 4: Journ. de Méd., Chirurg. et Pharm., etc., an. xiv., tom. xi, pp. 163, 243.]

After its first appearance at Geneva the disease does not seem to have extended in any direction from that place as a centre, but we next hear of it at two points remote from it and from one another--Germany and the United States. From the former it extended to the conterminous countries, Bavaria, Holland, and the east of France, where, however, it prevailed neither extensively nor fatally, and soon died out; while in America it first appeared at Medfield, Mass., in 1806. The European epidemic was faintly felt in England the following year, and between that time and 1816 it prevailed at several places in the east of France, and slightly at Paris, while during the corresponding period it had extended through New England into Canada, New York, Pennsylvania, and several Western and South-western States. It is a noteworthy fact that on both sides of the Atlantic it ceased in the same year (1816). During the six following years we can discover no trace of its existence, but in 1822-23 it reappeared at Vesoul in France, and at Middletown, Connecticut, and does not seem to have extended beyond those places. Again, after an interval of five years, in 1828 it was heard of in Trumbull co., Ohio, two years later at Sunderland in England, and three years afterward (in 1833) at Naples.

After four years of quiescence the disease entered upon a wider and more destructive career than ever before, which was almost uninterrupted from 1837 to 1850. During the first two years of its recurrence in Europe it was confined almost wholly to France. It began in the southern departments, with Bayonne as a centre, and extended gradually westward and northward, in some places attacking only military garrisons and in others only civilians. Elsewhere the predilection was reversed, or, again, civilians and soldiers were equally affected. As Boudin has pointed out, "it located itself in certain districts; in garrison-towns it seemed to affect certain barracks only, and in them only certain rooms. In one place it broke out in a prison and spared the soldiers; in another its victims were among the soldiers and the citizens, while the prisoners were untouched." Thus the disease spread over the whole of France, and was more fatal almost everywhere else than in Paris itself. Almost at the gates of the capital, at Versailles, and among the garrison, it was very destructive in 1839, causing a mortality among those attacked of from 50 to 75 per cent. About the same time it occasioned a great mortality at other military posts, especially at Rochefort and Metz, and in 1840-41 at Strasbourg. In 1843 the disease had almost ceased to prevail in France, but in 1846 it reappeared at Lyons, and in the following years, and until 1849, affected the garrisons of Orléans, Cambrai, Saint-Étienne, Metz again, Lunéville, Dijon, Bourges, and Toulon. In some of these places the military experienced five, and even seven, successive epidemics. Meanwhile, the disease spread to Algeria (1839-47), and to Italy in the former year--not, however, on the confines of France, but at Naples and in the Romagna, whence it extended to Sicily and Gibraltar, and did not cease there until 1845. In 1839 it first showed itself in Denmark, and remained for about three years, while in 1846 it "appeared in the {799} majority of the workhouses of Ireland," and in the spring of the same year it occurred in England, at Liverpool and Rochester.

While the disease was thus spreading throughout Europe, it again, in 1842, appeared in the United States, but at places as remote as possible from Transatlantic communication and hundreds of miles distant from one another--e.g. in Louisville, Kentucky, in Rutherford co., Tennessee, and in Montgomery, Alabama. In the following year it prevailed in Arkansas, Mississippi, and Illinois. In 1848 it occurred again at Montgomery, Ala., and simultaneously, in Beaver co., Pa.; in 1849 it existed in Massachusetts and in Cayuga co., N.Y., and in 1850 at New Orleans.

Between 1850 and 1854 epidemic meningitis ceased to be heard of, but in the spring of the latter year it began to appear in the southern provinces of Sweden, whence it rapidly spread over the greater part of the kingdom, reaching an extreme degree of fatality in 1858, and not finally disappearing until 1861. It is said to have caused more than four thousand deaths. It was not until the height of the Swedish epidemic in 1858 that it invaded Norway, where it seems to have been even more malignant and extensive. Between 1850 and 1860 local outbreaks of the disease took place in Ireland, and isolated cases were observed in various parts of England, but in that country it has never prevailed as a general epidemic. This fact alone is sufficient to defeat all the attempts that have been made to trace the origin of the disease to any of the conditions associated with a crowded population. In Scotland, where such conditions exist in their greatest intensity and fulness of development, it has never occurred as an epidemic. During the decade under consideration (in 1856 and 1857) epidemic meningitis again appeared in the United States, and, as before, at points very remote from one another. In the former year it occurred for the first time in North Carolina, and in the latter year in the central portions of New York and Massachusetts.

Hardly had the disease subsided in the Scandinavian peninsula and in the United Kingdom when it reappeared in Holland during the winter of 1860-61. In the following year and at the same season it occupied a large extent of Portuguese territory, including the cities of Oporto and Lisbon, and now for the first time it spread over Germany. Beginning slightly during the summer of 1863 in Prussia, it acquired new vigor during the succeeding winter, and in the two following years it devastated almost every part of Northern Germany, and in 1864-65 extended throughout Bavaria except in its southern and western provinces. Strange to relate, the disease appears to have passed almost wholly by Austria proper, and to have prevailed, although not extensively nor fatally, in Hungary, and in the latter part of the decade in Istria, Greece, Turkey, and Asia Minor.

The American counterpart of this epidemic first appeared in Livingston co., Missouri, in the winter of 1861-62, and during the same season it invaded Indiana and Kentucky in the West and Connecticut in the East. From about the same date, and until 1864, it prevailed in Ohio, and during the last-named year in Illinois. Cases occurred at Newport, Rhode Island, in 1863, and in Vermont in 1864. In the winter and spring of the latter year it broke out at Carbondale, Pa., and in a population of 6000 caused the death of 400, principally among children and {800} very young persons.[5] In the winters of 1863-64 and of 1864-65 it prevailed in the U.S. army, and in the early part of this period in the Confederate army which at the time was stationed near Fredericksburg, Va. In North Carolina also, from 1862 to 1864, the disease assumed a very malignant type, and affected citizens and soldiers equally, and the latter in the Union and Confederate armies alike. During the winter of 1864-65 a limited but very fatal epidemic of the disease prevailed at Little Rock, Arkansas. About the same time it existed as an epidemic in Maryland, Alabama, and other Southern States, and throughout the Civil War affected both whites and negroes, but showed, as in France, an exceptional gravity among the military.

[Footnote 5: Burr, Trans. Med. Soc. State of N. York, 1865, p. 40.]

The first appearance of the disease in Philadelphia took place in 1863, and from that date until the present (1884) it has never failed to appear among the causes of death in the reports of the Health Office. A table compiled by Dr. C. F. Clark, and printed in a paper on the subject by Dr. James C. Wilson,[6] exhibits the difficulties of obtaining accurate statistics, even from official reports, on this subject. The medical profession of the city, having had but little knowledge of the disease either by reading or observation, reported deaths from it which occurred in their practice under various denominations. At first it was spotted fever, which continued to be used by many for a year or two, when it was superseded almost entirely by cerebro-spinal meningitis. There can be no doubt that both of these terms were used to designate the same disease, and therefore no error will be committed in merging the deaths charged to each of them, and in estimating by their annual totals at least the relative mortality of the disease in the successive years of the period. But in the Health Office reports there are at least three other rubrics that suggest doubt. One is typhus fever, which seems to have presented a sudden and remarkable increase of mortality during the first years, and the most fatal, of the existence of cerebro-spinal meningitis. It should also be observed that typhus fever is applied by many German physicians in this country, as in their native land, to typhoid fever. A second is malignant fever, and a third is congestive fever, neither of which has claimed many victims in the health reports of Philadelphia except while meningitis was epidemic. It seems probable, therefore, that nearly all of the deaths charged under these heads belong to the disease under consideration.

[Footnote 6: Phila. Med. Times, xiii. 88.]

Deaths in Philadelphia from Cerebro-Spinal Meningitis from 1863-82.

| Brought over 1136 1863 49 | 1873 246 1864 384 | 1874 82 1865 192 | 1875 83 1866 92 | 1876 85 1867 109 | 1877 56 1868 55 | 1878 90 1869 37 | 1879 62 1870 36 | 1880 78 1871 49 | 1881 90 1872 133 | 1882 41 to Sept. 23d. ---- ---- 1136 Total 2049

If to these deaths are added those charged to malignant fever, 111, and to {801} congestive fever, 279, we obtain a total of 2439 deaths, nearly all of which may be set to the account of epidemic meningitis. It may also be remarked that up to the date at which this computation was made (May, 1883) hardly a week passed in which the Health Office did not register several deaths from this cause. Hence it would appear that the disease continues to linger in this locality longer than has been reported of any other place from which information has been obtained.

In the city of New York it appears to have been much more limited both in extent and duration. The first recorded death from it was in 1861; in 1866 the deaths were 18; in 1867 the deaths were 32; in 1868 they were 34; in 1869, 42; in 1870, 32; in 1871, 48. In 1872 the disease became epidemic, and "from January 6 to May 31, inclusive, 632 cases were reported to the City Sanitary Inspector, and 469 deaths to the Bureau of Records of Vital Statistics" (Clymer). After this period the disease seems to have declined very rapidly, and not to have reappeared, since no notice is taken of its recurrence by the medical journals of New York.

It was mentioned above that about 1870 some traces of the disease were observed in Asia Minor, and in 1872 several cases are said to have occurred at Jerusalem,[7] but beyond that time and place it does not appear to have extended as an epidemic. In 1879, Cheevers said: "I am not aware of the existence of any report of an outbreak of the disease in India." He refers, however, to several cases occurring in Calcutta as possibly representing this affection.[8]

[Footnote 7: Berlin klin. Wochensch., May, 1872.]

[Footnote 8: Times and Gazette, Aug., 1879, p. 121.]

In 1867-68 sporadic cases occurred at Little Rock, Ark., and in the former year in Madison co., N.Y., thirty-three cases were reported.[9] In Chicago, between February and April, 1872, Dr. Davis reported forty cases observed in his own practice in seventy-two days. In the same year the disease occurred at Elizabethtown, Ky.,[10] and at Louisville, Ky., in December of the same year. It existed in Michigan between 1868 and 1874, but only in the latter year epidemically, and not to a very great extent.

[Footnote 9: Trans. Med. Soc. State of N.Y., 1868, p. 251.]

[Footnote 10: Richmond and Louisville Journ., Nov., 1872, p. 555.]

Of later occurrences of the disease the following may be mentioned: Several cases were reported in London in 1867, 1871, 1876, and 1878.[11] In 1870 four cases were observed in Providence, R.I.[12] In 1882 cases were met with in Boston, New York, Philadelphia, Pittsburg, Western Ohio, Indianapolis, Detroit, Louisville, Memphis, New Orleans, Richmond, Milwaukee, St. Louis, Salt Lake City, San Francisco, etc., but in none of these places did the disease become epidemic.

[Footnote 11: Times and Gazette, July, 1867, pp. 58, 59; Nov., 1867, p. 511; Guy's Hospital Rep., 3d Ser., xvii. 440; St. Bart's Reports, xii. 267; Times and Gaz., Aug., 1878, p. 167.]

[Footnote 12: Boston M. and S. Jour., Oct., 1870, p. 261.]

ETIOLOGY.--Epidemic meningitis has occurred in Europe and America in every portion of the temperate zone, but its greatest prevalence and mortality have undoubtedly been in the northern rather than in the southern portions of that region. One of its most interesting features consists in its appearing simultaneously at points very remote from one another and having no connection with each other save through the atmosphere. Of this statement several illustrations have already been presented. Another {802} peculiarity of the disease consists in its occurring with hardly any relation to external natural conditions or to those of its victims. It affects localities as diverse as possible in their geological, meteorological, and sanitary states, the rich and the poor, the old and the young, and both sexes, and (as it is certainly not in a strict sense contagious) its rise and spread must necessarily be attributed to some occult cause pervading the atmosphere.

It is evident that the prevalence of the disease has some relation to meteorological agencies, for not only is it greater, on the whole, in cold than in warm climates, but it is also greater in cold than in warm seasons. Thus, if we examine the epidemics in Europe and America we shall find that they almost invariably were most severe in the winter and spring. Yet the rule presents several exceptions on both continents. In France, out of 216 local epidemics, more than one-fourth took place during the warm months of the year, and in Sweden the proportion was about the same. It is evident, therefore, that cold is not an essential cause of the disease. Among the problems that remain unsolved in regard to this disease none is more obscure than the apparent immunity of Russia from its ravages, although the climate seems adapted to favor it, and the domestic habits of no people are fitter to intensify it if individual conditions entered into the etiology of the disease; but, in truth, no such causes are related to epidemic meningitis. Localities of every sort, high and low, dry and moist, those saturated with marsh miasmata and those fanned by pure mountain-breezes, have been alike visited by this disease. It has passed by large cities reeking with all the corruptions of a soil saturated with ordure and populations begrimed with filth, as Vienna, Berlin, Paris, London, and New York, to devastate clean and salubrious villages and the families of substantial farmers inhabiting isolated spots.

By far the greatest number of the subjects of epidemic meningitis are young persons. In Sweden, according to Hirsch, of 1267 fatal cases of the disease, 889 occurred in persons under fifteen years of age, 328 between sixteen and forty years, and 50 in persons of forty years and upward. In 1866, in the Kronach district (Germany), of 115 cases, 75 occurred under the seventh year, 22 between the seventh and twelfth years, and 10 between the thirteenth and twentieth years (Schweitzer). During 1865 a local outbreak of the disease in Bavaria affected 53 persons, of whom 22 were children under ten years of age, 18 between ten and twenty years, and 11 between twenty and thirty years. Under the fifth year few were attacked (Orth). Dr. J. L. Smith[13] found that, according to the reports of the Board of Health of the city of New York, out of 975 cases, 771 occurred in persons under fifteen years of age, the greatest number for any quiquennial period being 336 in children under five years. Of the 469 deaths occurring in this epidemic, 216 were of children under five years of age, and the next largest number for an equal period was 99, which represented the deaths between the ages of five and ten years. Of adults or persons beyond the age of twenty, the whole number was but 39. The peculiar liability to the disease of the young recruits in the French army has already been alluded to. The proportion of male victims to this affection is rather larger than that of females in the civil population, but in France especially the excess was greatly on the side of males, owing to the prevalence of the disease in the army. In other places, as {803} in Sweden and Germany, the number of deaths among females equalled, or even exceeded, that of males, and in Leipsic the garrison remained exempt while the disease prevailed among the citizens. In 1847 a fatal epidemic of it affected the second regiment of the Mississippi Rifles, and was entirely confined to that corps (Love). During the Civil War of the United States the disease affected particular corps or regiments in the South or in the North, yet it never became epidemic in the army, even when the disease prevailed among the adjacent civil population.

[Footnote 13: Amer. Jour. of Med. Sci., Oct., 1873, p. 320.]

Various depressing or debilitating causes, such as lowness of spirits, home-sickness, mental or bodily strain, over-eating, drinking alcohol, the action of excessive cold or heat, checking perspiration, etc., have been enumerated as causes of this disease. It is unnecessary to dwell upon such gratuitous assumptions. All of these influences are constant, but epidemic meningitis is the rarest of epidemic diseases, and the agencies referred to have no further operation than to lessen the resistance of the body to morbid influences of every description. If there be one peculiarity about this disease which is more surprising and inexplicable than another, it is that its peculiar victims are not the feeble and delicate, but the vigorous and active--not the old and decaying, but the young and stalwart.

No one of authority has claimed that this disease can be propagated by contagion. All of its early American historians are of the same opinion upon this question, and nearly all European authorities are in perfect accord with them. The apparent exceptions to this all but universal judgment are so insignificant in number and weight as not in the least to diminish its validity. A case has been published in which a pregnant woman at full term died of the disease after giving birth to an apparently healthy child. "Two hours later the infant presented symptoms of meningitis, followed rapidly by death."[14] Supposing the concluding statement to be accurate, the case only shows that the cause of the disease which destroyed the mother's life infected the system of the child also. If there is one point in the history of the disease established by the concurring testimony of American and European writers, it is the extreme rarity of its attacking either the physicians and nurses in attendance upon patients affected with it, or those laboring under other diseases and occupying beds adjacent to persons ill with epidemic meningitis. That, nevertheless, there is a material morbific principle which inheres in certain localities, so that those who occupy them successively are liable to suffer from this disease, and that also this principle may be carried from place to place so as to render certain houses (barracks) infectious, seems to be demonstrated by the history of the disease in the French army. Between 1837 and 1850, when the disease prevailed in various parts of France, it did so not indiscriminately, but it usually followed the ordinary routes of communication, and especially the movements of the military in their transfers from one post to another, and the course of navigable streams. Strangely, also, it attacked soldiers much oftener than civilians. The most curious fact of all is one already referred to--viz. that although the disease prevailed in almost every part of the provinces, and although then as ever an incessant stream from them was flowing into the capital, neither its civil nor its military population was generally affected, nor, {804} indeed, at all so, until near the close of the period mentioned. Meanwhile, however, the disease extended to several countries conterminous with France or in close and frequent intercourse with it--to Italy (1839-45), Algeria (1839-47), England, Ireland, and Denmark (1845-48). These events seem to point to a certain transmissibility of the disease until we examine the negative facts that bear upon the question. They are such as these: The epidemic did not spread at all from France into two of the adjacent countries, Belgium and Switzerland, with which the first-named country maintained an incessant intercourse by travel and traffic, but, on the other hand, it broke out at an early date within the period mentioned at places very remote and absolutely independent of all influence emanating from France or any other European source--in the south-western portions of the United States. It is by numerous facts of this description that we are compelled to remove the disease from the category of endemic and even epidemic diseases, and relegate it, along with influenza, to that of pandemic affections.

[Footnote 14: Med. Record, xxii. 547.]

There seems to be some reason for thinking that the epidemic cause of this disease may affect the lower animals as well as man. It was stated by Gallup in 1811 that during the epidemic of meningitis in Vermont "even the foxes seemed to be affected, so that they were killed in numbers near the dwellings of the inhabitants;" and of the epidemic in 1871 in New York, Dr. Smith relates that "it was common and fatal in the large stables of the city car and stage lines, while among the people the epidemic did not properly commence until January, 1872." It would be desirable to learn more precisely the characters of these vulpine and equine epidemics before associating them with the disease we are studying, the more so that we have been unable to discover a similar relation between any epizoötic and other epidemics of meningitis. In this connection may be recalled the statement of Dr. Law of Dublin, that while he was attending a lady suffering from cerebro-spinal meningitis "nine rabbits, out of eleven which her son had, died, all in the same way: their limbs seemed to fail them, they fell on their side, and then worked in convulsions, and died." On examination of the bodies of several of them congestion of the vessels of the base of the brain was found, and also "vascularity of the membranes of the spinal marrow, indicating inflammation."[15]

[Footnote 15: Dublin Quarterly Journ., May, 1866, p. 298.]

TYPES.--No disease presents a greater variety--and, indeed, dissimilarity--of symptoms than epidemic meningitis. Some of its epidemics are sthenic and even inflammatory in their type, while others have the malignant aspect of rapid blood-poisoning. These contrasts have been exhibited on a large scale, for while upon the continent of Europe the disease for the most part has presented sthenic phenomena, it has been more generally asthenic and adynamic in Ireland. One might be inclined to attribute the latter peculiarity to the permanent prevalence of typhus fever in the latter country, or rather to the special causes producing typhus, were it not that in the United States both types of the disease have been observed at different times and in different places. Such contrasts of type are, however, not unusual in other diseases that occur as epidemics, including not only the eruptive fevers, but inflammations, or affections involving inflammation, such as pneumonia, dysentery, {805} diphtheria, etc. Hence it is evident that certain epidemics, and certain cases in each epidemic, may exhibit on the one hand a predominance of inflammatory, or on the other of adynamic or ataxic, symptoms, and each of them in every conceivable degree and combination. It is this variation of type that has led to such different conceptions of the nature of epidemic meningitis, many physicians regarding it as a fever, and many others as an inflammation, while, as we believe, it is both the one and the other, and acquires from either element, according to its ascendency, the typical character of the particular epidemic under observation.

As illustrative of these statements we may mention in this place the several forms of the disease as they have been seen and interpreted by different observers. Forget classified them as follows: (A) CEREBRO-SPINAL; 1, Explosive (foudroyante); 2, Comatose-convulsive; 3, Inflammatory; 4, Typhoid; 5, Neuralgic; 6, Hectic; 7, Paralytic. (B) CEREBRAL: 1, Cephalalgic; 2, Cephalalgic-delirious; 3, Delirious; 4, Comatose. In the first of these divisions three-sevenths belong to the first and fourth varieties. But "there were slight and severe cases; violent and hectic forms; cerebral symptoms predominant in some and spinal in others, etc."

In his excellent paper on the epidemic of 1848 in New Orleans, Ames arranged his cases in two categories--the Congestive and the Inflammatory, subdividing the former into the Malignant and the Mild. Malignant congestive cases were distinguished by prostration, coma or delirium, or both; opisthotonos; and a pulse varying extremely in its degree of frequency. In mild congestive cases a good degree of strength was preserved; the pulse was below 90; there were marked pain in the head and tenderness of the spine, but no coma, delirium, or stiffness of any muscles besides those of the neck. The purely inflammatory cases were, in general, distinguished by a temperature of the skin above that of health and a full, firm pulse, but the malignant inflammatory were marked by the early occurrence of delirium or coma, great irregularity of pulse, opisthotonos, convulsive spasm, strabismus, and occasional amaurosis, with vomiting and a rapid and fatal course; the grave, by a slighter development of the same symptoms, except coma and delirium; and the mild, by a lower grade of febrile excitement, the preservation of a good degree of strength, a tendency to become chronic, and by the absence of coma, drowsiness, delirium, and a cold stage.

Wunderlich adopted the simple plan of arranging the cases in three categories: 1, the gravest and most rapidly fatal cases; 2, the less grave; and 3, the lightest. The arrangement of Hirsch had more significance, as well as a clinical foundation--viz. 1, the abortive; 2, the explosive (m. siderans, the same as m. foudroyante of Tourdes); 3, the intermittent; 4, the typhoid.

Dr. Bedford Brown,[16] who observed the epidemics in North Carolina from 1862 to 1864, arranged the cases under the following heads: 1, the inflammatory form, in which the fever is high, the pain very acute, and the delirium furious, but which is exceedingly rare; 2, the neuralgic form, which is stated to be the most frequent and protracted, with moderate fever and a pulse but slightly accelerated, and giving a favorable prognosis; 3, the ataxic form, in which great nervous depression is {806} associated with a low and busy delirium, and the temperature "is generally much reduced below the natural standard.... This is always a dangerous form;" 4, the paralytic form, in which stupor and insensibility are early and prominent features, with a very slow and feeble pulse, blanched skin, and death by syncope.

[Footnote 16: Richmond Med. Jour., ii. 1.]

Dr. Purcell of Cork[17] furnished a classification which is one of the best for practical and clinical purposes--viz. 1, the rapid variety, attended with purple blotches, embarrassed respiration and circulation, followed by sopor, insensibility, and coma; 2, the cerebro-spinal form, with retraction of the head, pain and cramps of the muscles, hyperæsthesia of the skin, delirium, etc., accompanied by fever, herpetic eruptions, etc. These two forms are apt to be more or less associated in the same case.

[Footnote 17: Dublin Quarterly Jour., Aug., 1870, p. 243.]

Of the various forms admitted by different authors, and of which we have seen examples, we would class together--(a.) The abortive, in which the characteristic phenomena are often faintly defined, and yet to the practised eye distinctive. (b.) The malignant, in which the symptoms, of whatever kind, are exaggerated, the attack sudden, the course short, and the issue fatal. (c.) The nervous, including 1, the Ataxic--viz.--1, the delirious; 2, the cephalalgic; 3, the neuralgic; 4, the convulsive; 5, the paralytic; and 6, the adynamic (comatose and typhoid). (d.) The inflammatory. (e.) The intermittent. Of these the abortive and intermittent call for a brief explanation. Abortive meningitis is observed only during the prevalence of the disease in a more characteristic form. Thus, the mother of a boy who had died of the fully-developed disease "complained of the head and back and limbs, and of chilliness, and presented a petechial eruption. After active purgative and counter-irritant treatment she was about her work on the second day."[18] The late Dr. Burns of Frankford, Philadelphia, while attending patients affected with the disease suffered from headache, severe pains along the spine and in every joint of the body, and a general languid feeling.[19] Kempf during the decline of an epidemic observed "a great number of individuals, especially adults, who complained of headache, malaise, neuralgic pains in various parts of the body, and pain in the nape of the neck or other parts of the spine."[20] In a case observed by the writer (June, 1867) most of the characteristic symptoms were present in a mitigated form, and the pulse was at 60. Within five days restoration was complete.[21] The intermittent and remittent types are apt to be quotidian or tertian, and in fatal cases the former has been taken for malignant intermittent fever, which it resembles by a periodical febrile movement, with pains, cramps, delirium, etc. This type sometimes first manifests itself during the decline of an attack.

[Footnote 18: Sargent, Amer. Jour. of Med. Sci., July, 1849, p. 35.]

[Footnote 19: Amer. Jour. of Med. Sci., April, 1865, p. 339.]

[Footnote 20: Ibid., July, 1866, p. 55.]

[Footnote 21: Epidemic Meningitis, p. 42.]

SUMMARY OF THE SYMPTOMS.--Like other fatal epidemic diseases, meningitis is sometimes sudden and sometimes gradual in its development. In the former case the patient, who has gone to bed apparently in perfect health, awakes suddenly from a sound sleep about the small hours of the night to find himself in a severe chill. In the case of young children a convulsion attends the awakening. Or the patient, while {807} pursuing his ordinary avocations, may be seized with a chill, prostration, vomiting, and headache, of which symptoms the last is often intensely distressing. In this, as in other epidemic diseases, such violent seizures are most common during the earlier periods of its prevalence, but later in its course premonitory symptoms are more frequently observed. They may last for an hour or two, or may extend to several days; and, in general, it may be stated that the longer their duration the milder will be the subsequent attack. But the symptoms in either case are essentially the same--prostration, chilliness, feverishness, and sometimes vomiting and sharp pains in the head, back, and limbs. The character of the vomiting, as well as the absence of all gastric lesions in fatal cases, proves that it is occasioned by an irritation of the central nervous system.

In the cases which are regularly developed these phenomena more or less gradually assume a graver aspect or usher in a heavy chill, which in its turn is followed by alarming symptoms, and especially by an excruciating pain in the head, a livid or pale and sunken countenance, and extreme restlessness. The pulse is as often slow as frequent, and the skin is rarely hot, and, indeed, is generally but little, if at all, warmer than natural. The vague pains that began with the attack are now concentrated, and seem to dart in every direction from the spine, which is also, at its upper part, the seat of severe aching; and in some cases hyperæsthesia of the skin is very marked. In a large proportion of cases the spinal muscles become more or less rigidly contracted, so that the head is drawn backward or the whole trunk is arched as in tetanus. Trismus is not uncommon, and clonic spasms frequently affect the limbs. Even general convulsions are occasionally observed. As these phenomena grow more decided delirium of various degrees is often manifested, from mere wanderings and hallucinations during the sleepless watches of the night to violent maniacal ravings or incoherent mutterings, or the stertor of coma. Frey and others have noted a remission of the symptoms occurring on or about the third day in cases of a regular type. The rigidity of the cervical muscles becomes relaxed, the headache subsides, and the mental condition improves. But this amelioration lasts but a short time, and then the normal course of the symptoms is resumed.

As the attack advances the pulse gradually or rapidly rises above the normal rate, and sometimes becomes very frequent, and the skin, although it grows warmer, does not often acquire the temperature observed in idiopathic fevers or sustain it as they do. In many cases eruptions appear upon the skin. During some epidemics the only one observed is herpes labialis; in others the eruption resembles roseola, measles, or the mulberry rash of typhus, or from the first it consists of petechiæ, vibices, or extensive ecchymoses. The tongue presents the characters which belong generally to the typhoid state. At first moist and coated with a whitish fur or a mucous secretion, it afterward, if life is prolonged, grows red and shining or brown and fuliginous. There is usually a complete loss of appetite, and the thirst is not commonly urgent. One or two liquid stools at the commencement are generally followed by constipation, which continues throughout the attack, although in very grave and protracted cases diarrhoea may persist, and even become colliquative. When the attack tends to a fatal issue the patient generally, but by no means always, sinks into a soporose condition, in which {808} muscular relaxation, debility, and tremulousness, such as are common in the typhoid state of fevers, are associated with paralysis of the sphincters and of other muscles. But we have seen rigid opisthotonos continue until within a few hours of death in a case of more than the average duration.

In cases that tend toward recovery the typhoid condition is rarely so grave, but patients have often survived very severe nervous symptoms. It is true that the return to health may be tedious and uncertain, and not unusually a perfect restoration of all the functions is very long delayed, or, it may be, is never attained.

INDIVIDUAL SYMPTOMS.--Pain in the head is one of the most characteristic symptoms of epidemic meningitis. It is always present, except in those malignant cases in which the morbid poison seems to spend its fatal power upon the blood. In some, however, of a less rapid but still malignant type, in which after death no exudation is found, but only an extreme venous congestion of the membranes, or it may be an effusion of blood beneath them, this symptom may be more or less marked. It is generally an excruciating pain, sometimes darting apparently through the head from the nuchæ to the forehead, extorting cries and groans, and is variously described by the sufferers as throbbing, boring, lancinating, sharp, or crushing, "as if the head were in a vice or nails or screws were being forced into the brain." Its paroxysms arouse the patient from his apathetic stupor or his coma, and cause him to become restless or violent or to shriek with agony. Even when this evidence of anguish is wanting the patient often attests his suffering by contortions or cries, or by frequently carrying his hands to his head. That it depends upon mechanical pressure upon the sensitive ganglia within the cranium and upper part of the spine is shown by the relief which revulsive and counter-irritant measures afford when applied to the occipital region and the back of the neck. Identical in cause and quality with this pain is the spinal pain proper. No better description of it has been given than that of Fiske in 1810. It is in these words: "Its bold and prominent features defy comparison.... In some a pain resembling the sensation felt from the stinging of a bee seizes the extremity of a finger or toe; from thence it darts to the foot or hand or some other part of the limbs, sometimes in the joints and sometimes in the muscles, carrying a numbness or prickling sensation in its progress. After traversing the extremities, generally of one side only, it seizes the head, and flies with the rapidity and sensation of electricity over the whole body, occasioning blindness, faintings, sickness at the stomach, with indescribable distress about the præcordia--a numbness or partial loss of motion in one or both limbs on one side, with great prostration of strength. The horrible sensation of this process no language can describe."[22] These spinal pains are always aggravated by pressure made on either side of the spinous processes of the vertebræ, and, like the cephalic pains, are more or less mitigated by revulsive applications. Accompanying the pains is a hyperæsthesia or morbid sensibility of the skin, rendering it painfully sensitive to the slightest touch; in the advanced stages of the disease, when the spinal phenomena predominate, the irritation of the nerves by the pressure of the exudation on their roots is exchanged for numbness or {809} absolute insensibility, due to the increase and continuance of that pressure. Moving the limbs or separating the closed eyelids will sometimes provoke resistance, and even extort cries; and especially is this true of attempts to straighten the rigidly bent spine or the flexed extremities. Lewis states that such outcries were so often excited by slowly introducing the thermometer into the rectum that he was forced to believe that the anal and perhaps the rectal surface was hypersensitive.

[Footnote 22: North, on Spotted Fever, p. 176.]

The physical causes that give rise to the pains which have just been described likewise occasion the spasmodic and tetanoid phenomena that are so peculiar to this disease. In general terms, they are most marked in cases attended with inflammatory exudation, and least so when, instead of this lesion, there is only vascular congestion of the meninges of the spinal cord. But the rule is, of course, not absolute, for individuals are so differently constituted that one will remain impassive under an irritation that will throw another into convulsions. There is no doubt that spinal rigidity may be produced by mere congestion of the cord, and, on the other hand, that it may be absent even when plastic exudation is abundant. This symptom is, however, more than any other one, characteristic of the disease. It existed in the original epidemic at Geneva, attracted the attention of the earliest American observers of the disease, and elsewhere has marked a greater or a smaller proportion of the cases in every epidemic. It was described by such terms as these: "a drawing-back of the head;" "a corpse-like rigidity of the limbs;" "the form of tetanus called opisthotonos;" "spastic rigidity of the muscles of the lower jaw and the posterior muscles of the neck;" "rigidity of the posterior cervical muscles, retracting the head considerably backward." The historians of the disease in Europe are, if possible, still more emphatic in their elaborate descriptions of this phenomenon, and, on the Continent at least, it seems to have been more uniformly present than it was in Ireland or in this country. Tourdes, in describing the epidemic of 1842 at Strasburg, said: "The decubitus of the sick was distinguished by a backward flexion of the head and spine; most frequently the neck alone was affected, but sometimes the whole trunk was arched." And again: "The contraction often involved all of the extensor muscles of the spine, and the trunk formed an arch opening backward and resting upon the occiput and sacrum." In Ireland, Gordon says of a patient, "Her spine presented a most wonderful uniform curve concave backward; her head was also curved backward on the spine of the neck." During an epidemic at Birmingham in 1875 in one case "the retraction was so marked that a slough formed from the occiput pressing between the scapulæ."[23] In some cases rigid flexion of the body forward or laterally has been noticed. The rigidity persists, as a rule, until death, but sometimes ceases a short time before that event. If recovery takes place, this symptom gradually subsides, and disappears within a few days; but, on the other hand, more or less stiffness of the spine may last for several weeks. In one case it continued for more than two months, and in another until death on the forty-ninth day.

[Footnote 23: Hart, St. Bart's Rep., iv. 141.]

The same physical cause that occasions rigidity, when acting less intensely or when a special susceptibility of the nervous system exists, also excites clonic convulsions. They are oftenest observed in patients of the {810} age especially liable to spasmodic affections--in children before the completion of the first dentition. They vary in degree from twitching or subsultus affecting particular muscles, as of the eyes, the face, a limb, etc., to general epileptiform convulsions with loss of consciousness. They may be associated with paralysis, as where the two halves of the body are, the one convulsed and the other paralyzed. A case occurred in Dublin which "presented the very striking phenomenon of continued and violent convulsions during the whole of the brief course of the illness."[24] These convulsions, like others occurring at the commencement of acute diseases, are by no means always fatal, even when they are general. In the case of a robust adult convulsions occurred repeatedly during the first two days, and less frequently during the two following days, but the patient ultimately recovered.[25]

[Footnote 24: Dublin Quart. Jour., xlvi. 187.]

[Footnote 25: Boston Med. and Surg. Jour., Feb., 1884, p. 121.]

Paralysis, it may be inferred from the statements already made, is an incident of this disease, for an excess of the action causing tonic or clonic spasm must induce paralysis. Paralysis of an arm or leg or of the muscles of deglutition was long ago noticed among even the initial symptoms of the attack. In Dublin (1865) it was said of a patient, "All his members seemed to be paralyzed; he could move neither arms nor legs." Wunderlich describes the case of a man who "on the second day of the disease lost both sensibility and motility in the lower limbs and over the greater part of the trunk, while his left arm also was partially paralyzed." In another case complete paralysis of the right side occurred on the third day, the left side being rigid.[26] Baxa relates the case of a soldier in whom paralysis of the left side persisted after recovery from the disease,[27] and that of a woman in whom paralysis of the left lower limb continued along with right ciliary paralysis. Ptosis, strabismus, paralysis of the bladder and rectum, of the muscles of deglutition, and even general paralysis, have been observed. Aphasia also has been recorded by Hirsch and by Hayden.[28]

[Footnote 26: Dublin Quart. Jour., 1867, p. 431.]

[Footnote 27: Wiener med. Presse, No. 29, p. 715.]

[Footnote 28: Dublin Quart. Jour., xlvi. 187.]

The condition of the eyes and of vision in this disease is directly due to pressure of the exudation at the base of the brain upon the nerves and blood-vessels that supply these organs. One of the most striking peculiarities of the countenance of a patient at the beginning of an attack is the diffused and uniform redness of the conjunctivæ. In children it has a light tint, but a darker one in adults, and in some cases the eye becomes suffused with an extravasation of blood. The conditions of the pupil are also very peculiar. Very long ago it was observed to undergo sudden changes from contraction to dilatation, or the reverse. Dilatation is, however, its ordinary condition, especially in the fully-formed attack. Very often the pupils of the two eyes are in opposite states. In cases of long duration, with great exhaustion, they are almost invariably dilated. Photophobia is not uncommon, and oscillation of the pupils and spasmodic movements of the eyeball have frequently been observed. Strabismus is a symptom of very ordinary occurrence, particularly when other paralytic or spasmodic phenomena exist. It may be convergent or divergent, but most commonly is the former, and may be either a transient or a {811} permanent symptom. Like other individual symptoms, it may be present rarely or frequently in a particular epidemic.

Blindness has been repeatedly observed. At first it seemed to be noticed as a transient symptom only. Fish (1809) states that it was sometimes the first deviation from health, and then was followed by paralytic spinal symptoms. He also observed that sight was sometimes restored in a few hours, and in no case did he know it to be permanently lost. American as well as European physicians, however, have met with many cases in which the sight was seriously and permanently impaired or altogether destroyed. In 1873 the changes affecting the eye were more fully and accurately described, especially those which tend to the structural injury of the organ. The abnormal appearances included cloudiness of the media, discoloration of the iris, irregularity of the pupils, and their obstruction with exudate. In exceptional cases the cornea ulcerated, and the globe collapsed after losing its contents. Ordinarily, however, says Lewis, "no ulceration occurs, and as the patient convalesces the oedema of the lids, the hyperæmia of the conjunctiva, the cloudiness of the cornea and of the humors gradually abate, and the exudation in the pupils is absorbed. The iris bulges forward, and the deep tissues of the eye, viewed through the vitreous humor, which had a dusky color from hyperæmia, now present a dull white color. The lens itself, at first transparent, after a while becomes cataractous, and sight is lost totally and for ever."

Impairment or loss of hearing has been occasionally observed during the successive epidemics of this disease, even from the beginning of its history, and it was early noticed that the symptom was often quite independent of any cognizable lesion of the ear itself. It was also observed that the sense of smell sometimes became impaired or was lost at the same time with that of hearing. More recently, Collins reported a case in which the patient lost the sight of one eye and became permanently deaf in both ears. Knapp states that in all of thirty-one cases examined by him the deafness was bilateral, and, with two exceptions of faint perception of sound, complete. Among twenty-nine cases of total deafness only one seemed to give some evidence of hearing afterward.[29] This surgeon holds that the deafness results from a purulent inflammation of the labyrinth, and his judgment has been confirmed by Keller and Lucas. When the impairment of hearing occurs simultaneously, or nearly so, in both ears, it is probable that the chief cause of the deafness is the pressure of the plastic exudation in which the auditory nerve is imbedded. Such deafness is rarely permanent. When the loss of hearing, whether complete or partial, does not improve, there is reason to believe that the internal ear has suffered great and incurable changes of structure. Sometimes this follows a distinct attack of suppurative inflammation of the middle ear; but as complete and permanent deafness sometimes occurs without being preceded by any such affection, it must be inferred that atrophic changes have taken place in some portion of the nervous apparatus of hearing. It is stated by Moos that of sixty-four cases of recovery from cerebro-spinal meningitis, which showed disturbance of hearing as a sequel, one-half manifested in addition a more less disordered equilibrium. Of these twenty-nine were totally deaf on both sides, two totally deaf on one and hard of hearing on the other side, and one case had merely {812} impaired hearing in both ears. The disturbance of locomotion had existed for periods varying from three weeks to five years from the inception of the disease, and was chiefly characterized by a staggering or waddling gait.[30] In the deaf-mute institutions at Bamberg and Nürnberg it is said that out of 91 pupils, 80 owed their infirmity to this disease (Ziemssen). Salamo states that some awake out of sleep totally deaf, and remain so for a long time, or, it may be, permanently (Moos).

[Footnote 29: Smith, loc. cit.]

[Footnote 30: Mening. Cerebro-spinal epid., p. 11.]

The expression of countenance in this disease is peculiar. When the pain in the head is severe and paroxysmal the features are apt to be violently distorted; when it is more persistent the face assumes a fixed or rigid expression, or is at the same time dull, particularly after a long continuance of the pain. In the apoplectic form the expression may be set and stupid, but the features have neither the dark, dull, swollen, and duskily-flushed aspect of typhus, nor the languid, sleepy expression, and circumscribed flush on the cheek which are so characteristic of typhoid fever. Except during absolute insensibility in rapidly fatal cases there is a look of greater intelligence than belongs to either of the diseases mentioned. Indeed, in the beginning of the attack in regular cases the distinctive facies presents pale and sunken features, with paleness of the skin over the whole body.

Delirium in this disease exhibits a great many degrees and varieties. It may occur among the earliest symptoms in certain rapid cases not of the congestive type, but is more apt to arise on the second or third day in those more typically developed. It may be mild, reasoning, hysterical, or maniacal, or it may change from one to another of these forms during the same attack. Fish states that it is apt to be violent if it comes on at the commencement of the illness, but that when it begins at a later period it is milder, and sometimes playful, the patient being sociable and humorous. All good observers have furnished similar descriptions of this symptom; some have added that the mental condition is often desponding and apprehensive, and others that certain patients remain sombre and silent; and it sometimes happens that the delirium comes on abruptly, as when a patient "woke suddenly in the middle of the night and began to hum tunes, to fancy that people were conversing with him," etc. (Gordon).

Coma is met with sooner or later in nearly all fatal cases, but rarely in a marked degree until the approach of death. If anything is surprising in epidemic meningitis, it is the absence of that deep and prolonged stupor that characterizes the typhoid state, notwithstanding the pressure of the exudation upon the brain in most cases, and in others such a profound alteration of the blood that it exudes through the tissues as water passes through a porous body. Another striking phenomenon of the disease is that the patient after recovery has generally a complete oblivion of all that happened to him between the beginning of the attack and convalescence. This is true even of cases in which the brain symptoms are far from being conspicuous.

Another symptom closely related to the local lesion and the blood-change in this disease is vertigo. As originally described by Miner in 1823, it occurred from the very commencement of the attack, and was even then regarded as denoting a deficient supply of the blood to the {813} brain, so that when the patient rose to an erect posture it was felt along with uneasiness in the stomach, acceleration of the pulse, dimness of sight, nausea, and fainting. Tourdes, speaking of it as it occurred in the Strasburg epidemic, says that it confused the mind and rendered walking impossible. In two cases patients were seized with a giddiness which compelled them to whirl around, when they fell and did not rise again. According to Moos (1881) unilateral affections of the labyrinth give rise to vertigo, and bilateral lesions to a staggering gait. Bilateral hemorrhage or acute suppuration of the ampullar terminations of the auditory nerve occasions paralysis and staggering. Children, and those who at the same time have the sight impaired, are apt to remain affected for a long time. Otherwise, prolonged and systematic muscular exercise may remove the tottering walk.

To the same causes must doubtless be attributed the debility which is so early and so conspicuous a symptom in this disease, and which gave it one of the names, typhus syncopalis, by which it was first known in this country. It was manifested by the vertigo already noticed, by a sense of sinking in the epigastrium, by a quick, frequent, feeble, and irregular pulse, and by a sudden and extreme loss of muscular power, so that the patient found himself unable to raise his hand before he was sensible of being ill. This state of asthenia is conspicuous throughout the whole of the disease, and is the immediate cause of the slow and irregular convalescence which is characteristic of it.

Of the symptoms peculiar to the digestive apparatus hardly any belong to it directly. They are nearly all the effect of reflex influences. The condition of the tongue is for the most part quite unlike that which belongs to the typhoid state. The fuliginous condition of the tongue, gums, cheeks, and lips which characterizes that state is seldom met with in epidemic meningitis. The older writers agreed that even when the tongue does grow dry and brown the condition is not of long continuance, and later observers have confirmed their statements. Thus, J. L. Smith (1872) says, "Occasionally, in cases attended with great prostration, the fur of the tongue is dry and brown, but only for a few days, when the moist whitish fur succeeds." We have generally found it moist, whitish in the centre and at the tip and edges.

Nausea and vomiting are very constant among the initial symptoms of the disease, and, as already pointed out, are due to irritation of the cerebro-spinal ganglia. Very often the vomiting is not preceded by nausea, and is brought on by the patient's raising himself, etc. The stomach itself undergoes no change. Both symptoms are usually accompanied by faintness or giddiness, and are more decided in the initial than in the later stages of the attack. The matters vomited, varying with the contents of the stomach and the urgency and duration of the symptom, consist of ingesta, mucus, serum, or bile, and in some grave cases of a dark grumous matter taken to be altered blood. In some epidemics, apparently, more than in others, this symptom is very distressing, as it was at Birmingham in 1875.[31] The inability of the stomach to retain food necessarily leads to a rapid wasting of the flesh, which is aggravated by the patient's suffering, restlessness, and want of sleep. Nevertheless, no sooner is the vomiting appeased than a desire for food is felt, and when {814} it is retained it generally undergoes digestion. Indeed, in no other disease is the return of a good appetite and digestion so prompt and complete. It is true that the recovery of flesh and strength is not always in proportion to the appetite. As might be expected in a disease in which fever plays so subordinate a part, there is seldom urgent thirst. But epidemics differ in this as in so many other respects. In that which we witnessed in the Philadelphia Hospital in 1866-67 the patients were clamorous for liquids. Constipation is the rule among patients with this disease, as, indeed, might naturally be expected, for no lesion affects the bowels and little or no food is retained by the stomach. Yet in a few cases diarrhoea accompanies persistent vomiting.

[Footnote 31: Hart, St. Bart's Rep., xii. 112.]

The fauces appear to have been more or less inflamed in some epidemics; swelling of the parotid glands is an occasional occurrence, and sometimes they undergo suppuration. Aphthæ have also been met with.

The secretion of urine is not affected in any uniform manner. Sometimes it is diminished and sometimes increased in quantity. The latter symptom has occasionally long survived the disease. It retains its normal acidity. In rare cases either albumen or sugar has been detected; the former may have been due to the action of blisters of cantharides used in the treatment of the disease.

One of the most curious and unintelligible phenomena occasionally met with in this disease is a peculiar affection of the joints, which first was observed in this country. Jackson (1810 and 1813) wrote: "In some cases swellings have occurred in the joints and limbs. They have been very sore to the touch, and their appearance has been compared to that of the gout. The parts so affected feel as if they had been bruised. These swellings arise on the smaller as well as on the larger joints, and are often of a purple color." So Collins[32] reports: "The joints sometimes become swollen, red, and tender; at other times red and painful without any swelling; while, again, intense pain and rapid enlargement from effusion have occurred unattended with redness. The joints most usually attacked are the knee, elbow, wrist, and the smaller articulations of the fingers and toes." In an epidemic which occurred in Greece in 1869 articular swellings similar to those of inflammatory rheumatism were observed.[33] These descriptions, which apply to some cases in most epidemics, are of more than casual interest, for they demonstrate conclusively, as we think, the truth which the whole history of the disease confirms--viz. that it is a systemic and not a local affection, and is dependent for its existence upon a specific poison which is absolutely unlike every other morbid poison known to pathology.

[Footnote 32: Dublin Quart. Jour., Aug., 1868, p. 170.]

[Footnote 33: Archives générales de med., Mai, 1883, p. 622.]

The act of respiration is variously modified in this disease, as might, indeed, be expected from the seat and nature of the cerebro-spinal lesions. It is sighing, labored, and interrupted. Burdon-Sanderson describes its differences from the so-called Cheyne-Stokes respiration; it is, he says, "marked by a slow, labored inspiration, followed by a quick expiration and a long pause." When opisthotonos is very great and persistent, it necessarily interferes with the dilatation of the lungs, and leads to oedema of those organs, and even to sanguineous effusions into them. {815} Pneumonia is not an unusual complication of the disease when it prevails in cold weather.

The distinguishing characters of the pulse are diminished force and volume, and a tone so much impaired that slight causes produce extreme variations in its rate and rhythm. If the disease be a fever, as is by some maintained, then it is the only fever in which the pulse-rate is often far below the normal, and at the same time neither full nor tense, unless transiently and in altogether exceptional cases. In no other disease attended with inflammation do the rate and quality of the pulse vary so greatly within short intervals. It may be said, in general terms, to be variable in rate and strength even in the most sthenic cases of the disease, and in those which tend to a fatal issue to be small, thready, weak, intermittent, or imperceptible for a longer or shorter time before death. It is no uncommon thing for the pulse-rate at the beginning of an attack to fall as low as 40, or even 27, and afterward rise to 120 or even more, in a minute, without necessarily indicating a fatal issue. Muscular exertion, rising from a recumbent posture, etc., will sometimes double its frequency, besides producing irregularity. Read, describing the pulse as he observed it in Boston in 1873-74, speaks of cases in which "both the rhythm and the force of the beats are entirely destroyed; ... one moment, while beating very fast, it will suddenly drop to a much lower rate.... These conditions also may outlast apparent convalescence." Some fatal cases are attended by distressing palpitations of the heart.

Nothing is more remarkable in the early histories of this affection than their unanimous statement that it is not distinguished by a febrile temperature. It is true that the observers of those days had not the advantage of using clinical thermometers, but they were too nearly agreed in their judgments and harmonious in their descriptions to permit any serious doubt of the substantial accuracy of their conclusions, which were expressed in such terms as these: "A diminution of heat may be considered as among this most striking symptoms of this disease" (Strong); or, "the temperature never exceeded the standard of health in more than three or four cases, ... and a great majority of the patients had no fever at all" (Miner); or, again, "A high febrile movement took place only in a limited number" (Gilchrist); or, "The heat of the surface was less in all cases than is usually observed in acute diseases" (Jenks). It will be observed that these statements, and very many others which agree with them, were founded upon the perception of the patients' temperature by the hand, which was of course applied to the most accessible parts of the body--the face, neck, arms, and hands--but they have more real value and significance than the more recent measurements taken in the mouth, axilla, rectum, or vagina, for we know that, however valuable the temperatures of these parts may be for comparative studies, they do not really indicate the condition of the individual who presents them. It is a familiar fact that the difference of temperature in cholera when taken in the rectum and the axilla may be 4° F., or even more than this.

Since the thermometer has been used in the study of epidemic meningitis greater accuracy of results has been attained, and yet the general statements of the earlier observers have been confirmed. Thus, Githens has shown that the temperature of the body in this disease is lower than that recorded of any other fever or inflammatory affection; the average, {816} indeed, of his cases was lower by four or five degrees than that of typhus or typhoid fever, pneumonia, etc. In 2 cases only did the thermometer in the axilla reach 105°. The highest temperature in 15 cases was between 104° and 105°; in 12, between 103° and 104°; in 7, between 102° and 103°; in 6, between 101° and 102°; and in 2 it was below 100°.[34] Tourdes, Niemeyer, and others have noted the slight rise of temperature during the first and second days of the attack, and Wunderlich found fever of very unequal degrees and with very variable maxima, but the highest temperatures were observed by him as well as others in fatal cases and immediately before death. In one instance it reached 107.5° F. Burdon-Sanderson and others have found that an increased temperature always attended exacerbations of pain. Von Ziemssen gives the average temperature as varying from 100.4° to 103° F., but with variations between higher and lower points, and particularly notes the persistence of a normal temperature while the other symptoms are undergoing a variety of changes, as well as the fact that, unlike other febrile affections, this disease has no representative temperature curve. In his clinical observations Hart found for several successive days as much as six degrees of difference between the morning and evening temperatures. A morning rise for several days was noticed in four cases, and usually there was no relation between the pulse and the temperature, nor any uniformly between the temperature and the gravity of the attack.[35] But not rarely it has been noticed that the daily exacerbations, if any, did not occur in the afternoon, but with great irregularity, so that the maxima and minima might occur on successive days and at the same hour of the day. Dr. J. L. Smith, whose thermometric observations in this disease seem to have been carefully made, used the thermometer in the rectum, and thus obtained temperatures higher that the average of other observations, such as 105.4/6° to 107.2/6° in several cases. Yet he found the fluctuations of rectal temperature remarkable, though less so than the surface temperature, of which he states that sometimes it rose above or fell below the normal standard several times in the course of the same day.

[Footnote 34: Amer. Jour. of Med. Sci., July, 1867, p. 38.]

[Footnote 35: St. Bart's Reports, xii. 112.]

Nothing can be more irregular, uncertain, or various than the eruptions and other cutaneous symptoms that have been met with in this disease. When it first appeared in New England a large proportion of the cases, and especially of the grave cases, exhibited petechial eruptions and ecchymotic spots, whence the disease presently received the name of spotted fever. Yet even then, North and the other historians of its epidemics were careful to state that spots on the skin were by no means characteristic of the disease, and very often were not present at all, especially in cases that terminated favorably. Woodward, for example, wrote (1808): "An eruption on the skin so seldom appeared that it could no longer be considered a characteristic symptom of the disease." In various American local epidemics an eruption of some kind seems to have existed in about one-half of the cases. In one that we observed in the Philadelphia Hospital no eruption whatever was observed in thirty-seven out of ninety-eight cases. In the epidemic at Chicago in 1872, N. S. Davis says:[36] "About one-third of the cases presented some red erythematous spots" between the third and the seventh day. In mild cases they were few and {817} bright red; in grave cases, darker and larger, with some swelling of the skin; and in the worst cases, purple spots one or two or more inches in diameter. In that of Louisville,[37] Larrabie states that the eruption "was generally herpetic in its character, and accompanied by sudamina; but in several instances an urticarious eruption suddenly appeared and disappeared." Nothing is said of petechiæ or ecchymoses. In the New York epidemic of 1873[38] the skin in grave cases presented dusky mottlings, especially when the animal temperature was reduced; also a punctated red eruption, bluish spots a few lines in diameter, and large patches of the same color. Herpes also was common. It is chiefly in cases of a malignant type and rapid and fatal course that ecchymoses have been observed. Of this statement illustrations will be given in the paragraph relating to the duration of the disease.

[Footnote 36: Louisville Med. Jour., June, 1872, p. 705.]

[Footnote 37: Louisville Med. Jour., Dec., 1872, p. 782.]

[Footnote 38: Amer. Jour. of Med. Sci., Oct., 1873, p. 329.]

In continental European epidemics of meningitis the proportion of cases in which a general eruption existed seems to have been smaller than it was in this country. In the Geneva epidemic of 1805 a considerable number of cases at the point of death presented purplish spots, some earlier than this, and some after death only. In the Neapolitan epidemic of 1833, and in that which occurred in Dublin in 1867-68, ecchymoses were often present, and in a very marked degree. Stokes and Banks mention that in some rare instances the spots ran together and coalesced over some portions of the body, so as to cover a large extent of the skin and render it completely black, as though it were wrapped in some dark shroud. The entire right arm and half of the right side of the chest in one case, and in the other the whole of the lower portion of one leg and foot, were thus affected.[39] In Strasburg, on the other hand, only three cases of petechiæ were observed by Tourdes; at Rochefort and Versailles, in 1839, they were rarely noticed; at Gibraltar, in 1844, they do not seem to have been observed; in 1848-49, at the Val de Grâce Hospital (Paris), they appear not to have attracted attention; and at Petit Bourg they were not noticed, although the state of the skin was fully described. In Prussia, in 1865, neither Burdon-Sanderson nor Wunderlich mentions petechiæ or vibices as occurring during life; and Hirsch, after noting their occasional presence, is obliged to draw upon American authors for an account of them.

[Footnote 39: Dublin Quart. Jour., xlvi. 199.]

Of the eruptions other than petechiæ and ecchymoses, several of which have already been mentioned, it is necessary to take some notice here. They are, chiefly, and in general terms, exanthems, including erythema, roseola, and urticaria, and in addition herpes, particularly of the lips. The last has no special relation to this affection, as it is met with in almost every febrile disease, but it has sometimes extended to the whole face in this one. The former may be connected pathologically either with the altered condition of the blood or with the irritation produced by the exudation in the spinal nervous centres. They have frequently been compared to measles and to scarlatina, but sometimes they have assumed the form of bullæ. Thus, in the case of a child four years old, described by Grimshaw,[40] an eruption of pemphigus occurred over the whole body. Jackson long before had mentioned, as one of the eruptions belonging to this disease, "large bullæ, as if produced by cantharides." Jenks {818} described "large elevated spots of a very dark color, presenting outside of the dark color a blistered appearance." In some cases gangrene of the skin has been observed when the spots have been exceptionally dark, and occasionally has been produced by pressure.

[Footnote 40: Jour. of Cutaneous Med., ii. 37.]

The cause of death in many of the more rapid cases is coma, which is often preceded by convulsions, especially in children; but in many others, even when attended with all the marks of dissolution of the blood, consciousness may be but slightly impaired until the actual imminence of death. In many other cases, which are fatal in the midst of an attack with spinal symptoms, death is due to asphyxia, partly owing to pressure on the medulla oblongata, and partly to the interference with the respiratory act due to this pressure, and occasioning excessive bronchial secretion. Again, death may occur through a gradual exhaustion of the powers of life, without marked spasm, blood-change, or complication. In these cases also the intelligence remains unimpaired almost until the moment of dissolution. Death is not very rarely due to pneumonia, and when the disease is greatly prolonged or the convalescence from it is imperfect a fatal termination by dropsy of the brain is still among its dangers.

Hirsch once declared that the duration of epidemic meningitis "is between a few hours and several months," and, however hyperbolical the phrase may seem, it is quite accurate. Such inequalities are more characteristic of acute blood diseases than of inflammations, and in this case the coexistence of elements of both kinds doubtless accounts for the extreme irregularity of the symptoms and duration of the attack. The early American writers insisted strongly on this as a characteristic feature of the disease. They record an unusually large proportion of cases that were fatal within the first day, and even after an illness of five hours, although they agree that the most usual date of death was between the fourth and seventh days--a result that has been confirmed by subsequent observation. Dr. N. S. Davis gives the duration of the disease, as seen by him, as between twenty hours and twenty-eight days. Out of 469 fatal cases in the city of New York in 1872, 334 are said to have terminated within eleven days, and of this number 270 were fatal in the first six days of the attack, including 52 who died on the first day, and 51 in from one to two days. It is perhaps worthy of note that while from the eleventh to the fourteenth day only 11 deaths occurred, 20 took place on the fourteenth and fifteenth; and while from the fifteenth to the twenty-first day only 16 died, yet from the twenty-first to the twenty-second 12 deaths were reported. This would seem to indicate a peculiar danger on the days represented by multiples of seven. Of cases that recover, the duration is even more indefinite than that of fatal cases, owing to complications that occur in many, and especially such as involve the cerebro-spinal centres. When death takes place within a few hours it usually, if not always, is attended with symptoms that denote a disorganization of the blood. In 1864 we attended a young man previously in perfect health, but who died in twenty-one hours after the first seizure. His mind was unclouded throughout his brief but fatal illness. Within seven hours of death a purpurous discoloration of the skin began, and about an hour before that event the surface everywhere assumed a dusky hue. The forearms and hands were almost uniformly purple and the face turgid; many ecchymotic spots on the trunk and lower limbs were nearly black and measured {819} one or two inches in diameter.[41] In the case of a child of five years death in convulsions took place after an illness of ten hours, the skin presenting purpurous spots, some of them very large and of a deep bluish livid hue. On post-mortem examination there was not the slightest appearance of any meningeal lesion, except a few dark spots like sanguineous effusion under the arachnoid. The heart was full of dark blood in a semi-coagulated state, and the white corpuscles were three times as numerous as the red.[42] A case is reported by Gordon[43] in which the entire duration of the illness until death was five hours. This is probably the shortest case on record. A lady aged twenty-two years died in sixteen hours, the skin covered with livid ecchymoses, some of them measuring an inch or an inch and a half in diameter.[44]

[Footnote 41: Amer. Jour. of Med. Sci., July, 1864, p. 133.]

[Footnote 42: Dublin Quart. Jour., 1867, ii. 441.]

[Footnote 43: Loc. cit.]

[Footnote 44: Med. Press and Circular, May, 1866. For other cases see ibid., pp. 296, 298-300.]

The character of the convalescence from epidemic meningitis must evidently be affected by the causes that determine its duration, the grade of the disease, the development and extent of the lesions, etc.; but it is certain that, except in those imperfect and, as it were, shadowy cases which denote a very slight action of the morbid cause, its subjects do not recover rapidly. The essential lesion of the fully-formed disease requires time for its removal, just as in typhoid fever the intestinal ulcers are often slow of healing, and hence become a cause of tardy recovery and even of unlooked-for death. The convalescence, then, from the disease we are now studying is slow and irregular, is attended often with debility and emaciation, and sometimes with persistent headache, neuralgia, convulsions, stiffness of the neck and pain in moving it, hyperæsthesia of portions of the skin, palpitation of the heart, dyspepsia, etc. Relapses are very far from being uncommon.

Among the causes of tardy convalescence in this disease are those lesions and disorders which may be embraced by the term sequelæ. Impaired vision, due to various affections of the eyes, has already been considered among the symptoms proper of the disease, but they are not infrequently developed after the acute attack has subsided. Thus, in a case reported by Larrabie:[45] "Just as convalescence seemed beginning the left eye became affected in all its parts, with entire loss of vision and also complete deafness. After a short remission hydrencephaloid symptoms appeared, followed by the same changes in the hitherto sound eye, complete blindness and deafness, general cachexia and marasmus, rigid flexion of the right limbs, and death by exhaustion at the end of sixteen weeks." The impairment of hearing, which also was described as a symptom of the acute attack, is apt to become more marked after the acute stage has passed by, and, as before stated, is very often permanent. Occurring in young children, it then involves deaf-mutism. It is in many cases associated with defective vision, weakness or loss of memory, mania, impairment of intelligence, persistent pains in the head or chronic hydrocephalus. Sometimes to one or more of these symptoms is added more or less general paresis or complete paralysis. Southhall[46] mentions the case of a child two years old whose attack was followed by incomplete paralysis, and death at the end of eight months with softening {820} of the brain. Gordon thus describes the conclusion of a case: "The man has gradually passed into a state of almost organic life; he eats, drinks, and sleeps well; he passes solid feces and urine without giving any notice, yet, evidently, not unconsciously; ... he seems to understand, but cannot answer; ... he can draw up his legs and arms, but he cannot use his hands at all." Hirsch has remarked that disorders of speech are met with, due apparently to an inability to articulate certain sounds. Von Ziemssen regards chronic hydrocephalus as not a rare consequence of epidemic meningitis, and as one not absolutely or immediately fatal. Its symptoms include severe paroxysmal pain in the head or neck or extremities, with vomiting, loss of consciousness, convulsions, and involuntary evacuation of excrements. Between the paroxysms, which sometimes occur periodically, the patient generally suffers from neuralgic pains, hyperæsthesia, and various motor and even mental disorders; but in other cases the intervals are free, or nearly so, from all morbid manifestations. Davis (1872) and many others speak of severe neuralgic pains following this disease; according to Dr. D., they are most frequent at the heads of the gastrocnemii muscles, in the abdomen, and the head; a very fretful disposition, variable appetite, and disturbed sleep are often observed. Relapses have been noticed in almost all the epidemics, and it seems probable that they are often due to the influence of accidental exciting causes, mental or physical, in renewing the inflammation around the cerebro-spinal lesions. Miner (1825) remarked that they were most apt to occur within the first week, but that when the disease had once run its course there were very few relapses during convalescence. But, he adds, there were several repeated attacks after the most perfect recovery, and several of the patients had had the disease the preceding year.

[Footnote 45: Richmond Journal of Med., Dec., 1872, p. 779.]

[Footnote 46: Ibid., Aug., 1872, p. 141.]

Like other epidemic diseases, meningitis presents itself with every possible degree of gravity between that of a slight indisposition and that of a malignant and deadly malady. The mortality in a number of epidemics compared by Hirsch varied between 20 per cent. and 75 per cent. It changes with the locality. Thus, nearly at the same time that the death-rate from this disease in Massachusetts was 61 per cent., it was but 33 per cent. in the Philadelphia Hospital. In 1872 the whole number of deaths caused by it in Philadelphia was 133, while at St. John's College, Little Rock, Ark., 21 cases out of 29 were fatal (Southhall). It differs, also, at different periods; for while ten epidemics in various places, occurring between 1838 and 1848, presented an average mortality of 70 per cent., a similar number, occurring between 1855 and 1865, gave an average mortality of only 30 per cent. It must, however, be confessed that such statistics cannot be relied upon as accurate, for in private practice many cases occur that are never reported unless they end fatally.

MORBID ANATOMY.--The lesions found after death from epidemic meningitis consist essentially of congestion or inflammation of the cerebro-spinal meninges, but they also include in many cases hemorrhage, serous effusion, plastic exudation, and tissue-changes in the brain and spinal marrow, and in many other cases an impaired constitution of the blood. As the signs of the latter, and not the former, alterations are met with in the more malignant cases, it is evident that, looking at the disease as a {821} whole, it must involve a toxic element of whose operation the various post-mortem lesions are only effects. These lesions, on the whole, vary with the type of the disease, and also with its duration, but some are chiefly met with in cases of a malignant and others in cases of an inflammatory type.

The exterior of the body after death in the early stages of this disease almost always presents the marks of transudation of the contents of the blood-vessels. The dependent parts of the body exhibit large livid patches or a uniform discoloration of the same hue. In acute cases the muscles are more deeply colored than natural, and when the attack is prolonged they are said to have their cohesion impaired by fatty degeneration. Congestion of the brain is an unfailing accompaniment of the first stage of the disease; its blood-vessels are all distended with dark blood; the sinuses of the dura mater are usually filled with coagula of the same hue, though sometimes very dense. Serum abounds in the arachnoid cavity and in the ventricles of the brain; it may be clear or milky, and sometimes it is quite purulent. It is alleged by one reporter that no less than three pints of turbid serum escaped in a case in which, however, death did not occur until the thirty-fifth day. Craig found eight and twelve ounces of a limpid fluid in two cases; and Tourdes found pus in more than one-half of his cases, either unmixed or forming a milky liquid. J. L. Smith refers to the case of an infant who had the disease at the age of five months, and two months subsequently great prominence of the anterior fontanelle, and other symptoms which indicated the presence of a considerable amount of effusion within the cranium. In a case in Dublin,[47] there was no meningeal lesion except in a "few dark spots like sanguineous effusion under the arachnoid." White[48] mentions the case of an adult that terminated fatally in thirty-six hours, in which the vessels of the pia mater were very much congested, and sanguineous effusions existed above and below the cerebellum, and a clot of blood three inches long and external to the theca extended downward from the lowest portion of the medulla oblongata. In all of these instances, then, congestion, the first stage of inflammation, existed. That such was its real nature is proved by what follows.

[Footnote 47: Dublin Jour., July, 1867, p. 441.]

[Footnote 48: Med. Record, iii. 198.]

The most characteristic lesion is a fibrinous or purulent exudation in the meshes of the pia mater. American physicians described it as early as 1806 in such terms as these: "The dura mater and pia mater in several places adhered together and to the substance of the brain; ... between the dura mater and the pia mater was a fluid resembling pus" (Danielson and Mann). In 1810, Bartlett and Wilson found "an extravasation of lymph on the surface of the brain;" and in the same year Jackson and his colleagues, after describing the congestion and serous effusion found within the cranium "in those who perished within twelve hours of the first invasion," state that the arachnoid and pia mater present an effusion between them of "coagulated lymph or semi-purulent lymph" both on the convexity and at the base of the brain. These descriptions correspond in all respects with those of Mathey relating to the epidemic at Geneva in 1805, for he says: "The meningeal blood-vessels were strongly injected. A jelly-like exudation tinged with blood covered the surface of the brain; ... on its lower surface and in the ventricles a {822} yellowish puriform matter was found." Such lesions have been described by a long line of observers--by Wilson in 1813, Gamage in 1818, Ames and Sargent in 1848; by Squire, Upham, and a host of others since 1860 in the United States, and by Tourdes, Gilchrist, Ferrus, Wilks, Gordon, Banks, Gaskoin, Niemeyer, Burdon-Sanderson, and many more in Europe.

It is evident, therefore, that in a certain number of fatal cases only sanguineous congestion of the membranes of the brain and spinal cord are found, and in certain others--constituting, it may be added, nine-tenths of the whole number--evidences exist of cerebro-spinal meningitis. Hence the natural conclusion is that the congestive lesions represent the first stage of a process which if prolonged and perfected occasions the lesions peculiar to inflammation. For the development of the latter two factors would seem to be essential--not only a fibrinous condition of the blood, but also sufficient time for exudation to occur. But when we come to study the actual results of examinations post-mortem, it is found that the duration of the attack does not determine absolutely the nature of the lesions. On the one hand, in a case which terminated fatally after a week's illness there was found reddish serum between the arachnoid and the pia mater and in the lateral ventricles, with intense injection of the pia mater of the base, medulla oblongata, and upper part of the spinal cord, but no exudation of lymph.[49] And, on the other hand, numerous cases have been published in which, although death occurred within twenty-four hours from the onset of the attack, coagulated lymph and also pus were found upon the brain and spinal marrow. For example, during the winter of 1861-62, in the army, that then lay near Washington, D.C., a soldier was attacked with a chill, severe fever, and headache, followed by opisthotonos and repeated convulsions before his death, which occurred in about twenty-four hours. No eruption or discoloration of the skin is mentioned in the history. On examination there was found beneath the arachnoid a thin layer of lymph and abundant exudation over the posterior lobes of the cerebrum, and also at the base of the brain and on the medulla oblongata.[50] In a case reported by Gordon[51] the entire duration of the illness was under five hours, and after death the cerebral arachnoid was more or less opaque, and in some spots had a layer of very thin purulent matter beneath it. And, again, not only may the symptoms belonging to blood-dissolution be consistent with a certain prolongation of life, but also with decidedly inflammatory tissue-changes. Thus, in another case of Gordon's the duration of the illness was at least six days, and the patient presented all the characteristic symptoms of the disease, including "a most wonderful and uniform curve of the spine and head backward," "spots black as ink," "bullæ which rapidly became opaque and dusky," "herpetic eruption, etc." After death the body had a very frightful appearance. It was still prominently arched forward. It was of a dusky blue color, with a copious eruption of black spots of various sizes, and one or two of them were gangrenous.... When the theca vertebralis was opened purulent matter flowed out, and a purulent effusion was found in patches on the brain. {823} The cerebral arachnoid was all opaque, the lateral ventricles were filled with serum, and the blood in all the cavities was very fluid and dark colored. From all that precedes, therefore, it must be inferred that the nature of the lesions in this disease depends not on the type alone, nor on the duration merely, of the attack--that a very brief course is compatible with marked inflammatory lesions, and a prolonged one with profound alterations in the condition of the blood. In other words, it seems that there must be something besides the appreciable lesions that influences, if it does not determine, the issue of an attack of this affection. While bringing forward prominently this proposition, and the facts on which it rests, we have no intention of under-estimating the relative significance of the two most conspicuous types of the disease, the purely inflammatory and the adynamic, or calling in question the fact that the evolution of the former is most usually comparatively slow and regular, and of the latter rapid and irregular. In the one, when death takes place early, congestive changes are found, and when later these have merged into exudative lesions; in the other or adynamic cases congestion and liquid transudation prevail, and the results of complete inflammation are seldom seen. When the disease has been very much prolonged the exudation becomes tough, adherent, and shrivelled.

[Footnote 49: Davis, Richmond Med. Jour., June, 1872, p. 709.]

[Footnote 50: Frothingham, Amer. Med. Times, Apr., 1864, p. 207.]

[Footnote 51: Dublin Quart. Jour., May, 1867, p. 409.]

The brain-tissue has generally been found softer than natural, and, although in some cases this diminished consistence might be attributed to post-mortem changes, yet on the whole it must be associated with the inflammatory lesions of the meninges. As a rule, it is greater the longer the attack has lasted, and is by no means equally diffused, but is more marked where the meningeal alterations are greatest. Ames found softening in nine out of eleven cases, and chiefly in the cortical substance, but also in the fornix and septum lucidum; and Chauffard states that in protracted cases "the interior surface of the ventricles, the fornix, and septum lucidum, were reduced to a pultaceous and creamy consistence." But it is by no means true that softening is met with in all cases of long duration.

The lesions of the spinal marrow and its membranes correspond with those of the brain. The dura mater is often very dark, its blood-vessels engorged, its arachnoid cavity distended with serum more or less bloody, turbid, or purulent. Two ounces of pus have been removed from it through a puncture. Fibrinous and purulent exudation fills the meshes of the pia mater, and is usually most abundant in the cervical and dorsal portions, and generally upon the posterior rather than upon the anterior surface of the organ; but sometimes large accumulations of lymph and pus are found at the lower end of the cord. Gordon[52] relates of a case that "when an opening was made into the lower part of the theca vertebralis purulent matter flowed out, and the entire surface of the pia mater was covered with a coating of thin purulent matter, which, like a thin layer of butter, remained adherent to it." Occasionally the cavity of the spinal arachnoid contains blood. Softening of the spinal cord has been often noticed. Chauffard states that in some cases of particularly long duration it was reduced to a mere pulp, and he adds, "in the place of portions of the spinal marrow, completely destroyed, was found only a yellowish liquid, or the empty membranes fell into contact where it was {824} wanting." Similar disorganization has been described by Ames, Klebs, and others. Fronmüller reports the case of a girl aged fourteen years in whom the central canal of the spinal cord was distended with pure pus.

[Footnote 52: Dublin Quart. Jour., xliii. 414.]

The lesions of the internal auditory apparatus consist of softening in the fourth ventricle and of the root of the auditory nerve, yet such lesions are said to have been found even when no defect of hearing had existed. In other cases in which deafness did occur the lesions consisted of inflammatory changes in the cavity of the tympanum and suppuration of the labyrinth. They probably arose from an extension of inflammation from the pia mater along the trunk of the auditory nerve (Von Ziemssen). In like manner, the inflammatory and destructive changes in the eye which have been elsewhere described arise from an analogous cause affecting the optic nerves.

It is unnecessary to dwell upon the condition in which other organs are found after death from epidemic meningitis. In cases that present a typhoid type, and even in such as are rapidly fatal with ecchymotic discoloration of the skin, the various organs present no distinctive tissue-change, but only such engorgement as is common to all diseases of a similar type. It deserves to be particularly mentioned that in this affection the spleen is not enlarged, as it always is in a greater or less degree in diseases whose primary stage involves an altered condition of the blood. This fact becomes all the more important in view of the remarkable contrast which the constitution of the blood presents in epidemic meningitis and in various typhous affections.

The state of the blood in this disease is one of peculiar interest, dominating as it does its whole pathology and determining its nosological position. It is the blood of a phlegmasia rather than of a pyrexia. This fact was early established by American physicians who observed the disease, and the opportunities for doing so were not wanting, since venesection was used by every one who treated it. In 1807-09 a rapidly fatal case or two was found in which the "blood was darker and had a larger proportion of serum than usual," but in others "it did not present any uncommon appearance, and no inflammatory buff, nor was it dissolved" (Fish). In 1811, Arnell stated that "the blood drawn in the early stage appeared like that of a person in full health; there was no unusual buffy coat, neither was the crassamentum broken down or destroyed." In the epidemic studied by Mannkopff (1866) he found that blood obtained by venesection gave a clot with a thick buffy coat. Andral, seeking to establish the law that in every acute inflammation there is an increase in the fibrin of the blood, remarks that in a case of cerebro-spinal meningitis it was very marked.[53] Ames states that "the blood taken from the arm and by cups from the back of the neck" "coagulated with great rapidity." "Its color was generally bright--in a few cases nearly approaching to that of arterial blood; it was seldom buffed; in thirty-seven cases in which its appearance was noted it was buffed in only four." Analyses were made in four cases, "the blood being taken early in the disease from the arm, and was the first bleeding in each case. They furnished the following results: {825}

Fibrin. Corpuscles. I 6.40 140.29 II 5.20 112.79 III 3.64 123.45 IV 4.56 129.50

The first was from a laboring man thirty-five years old; the second from a boy twelve years old, while comatose; and the two others from stout women between thirty and thirty-five."[54] Tourdes, whose analyses follow, states that "blood drawn from a vein was rarely buffed; if a buffy coat existed, it was thin, and generally a mere iridization upon the surface of the clot."[55]

Fibrin. Corpuscles. I 4.60 134.00 II 3.90 135.54 III 3.70 143.00 IV 5.63 137.84

Maillot gives, as the result of an analysis of six cases, an increase of fibrin to six parts and more in a thousand. This summary represents, as far as is known, all of the analyses of blood taken from living patients in this disease, and it shows that in every case the proportion of fibrin exceeded that of healthy blood, and corresponded exactly to that observed in the blood of inflammatory diseases, while the proportion of red corpuscles varied within the normal limits. How different is this condition of the blood from that of typhus fever, in which there is a marked diminution of fibrin, and a falling off in the red corpuscles as well, or from that of typhoid fever, in which neither element declines until the disease affects the body by inanition! (Murchison).

[Footnote 53: Path. Hæmatology, p. 73.]

[Footnote 54: New Orleans Med. and Surg. Jour., Nov., 1848.]

[Footnote 55: Epidemie de Strasbourg, p. 160.]

* * * * *

In regard to the condition of the blood after death the historians of the disease are not so well agreed; nevertheless, the preponderance of the testimony is in favor of the statement that the blood presents appearances resembling those belonging to the continued fevers rather than to the inflammations. It is true that even in this the agreement is neither general nor complete. Tourdes, for example, states that in an autopsy "the blood was remarkable for the abundance and toughness of the fibrinous clots," but the greater number have reported it as being dark and liquid. Such was its condition in the epidemic which we studied at the Philadelphia Hospital in 1866-67, and it has been correctly described by Dr. Githens as follows: "The blood was fluid, of the color and appearance of port-wine lees; under the microscope the corpuscles were shrivelled and crenated, and there was a space apparent between them as they were arranged in rouleaux. There were in two cases white, firm, fibrinous heart-clots extending through both ventricles and auricles and into the vessels leading to and from the heart."[56] It may be added that the red corpuscles are often crenated and shrivelled when the case has been protracted, and it has been stated--from limited observation, indeed--that "the white corpuscles are three times more numerous than the red."[57] The blood has been scrutinized to discover, if possible, some of those bodies which are judged by Koch and his disciples to differentiate {826} general diseases, but it is stated that the investigation has been without definite result.[58]

[Footnote 56: Amer. Jour. of Med. Sci., July, 1867, p. 23.]

[Footnote 57: Dublin Quart. Jour., May, 1867, p. 441.]

[Footnote 58: Jaffé, Phila. Med. Times, xii. 599.]

It does not seem difficult to reconcile the conflicting statements now given of the condition of the blood in epidemic meningitis. One of them points to an excess and the other to a loss of the spontaneously coagulable element of the blood. It is evident that venesection, which was necessary for procuring the living blood for analysis, would only be performed when the type of the disease authorized it--that is, when the type was sthenic; whereas the blood examined after death had necessarily undergone changes which tended to, if they did not actually, occasion death. Hence we find among the former cases, when fatal, the most extensive and massive exudation, and always among the latter less evidence of inflammation, but, on the other hand, a greater or less manifestation of those appearances which denote a loss of the vitality and organization of the blood. In the one case death may fairly be attributed, above all other causes, to the pressure upon, and the disorganization of, the cerebro-spinal organs essential to life; in the other, primarily, to the death of the vital elements of the blood produced by the specific cause of the disease. It is probable that the post-mortem fluidity of the blood exists under two conditions. In the one the morbid cause is powerful enough from the very commencement rapidly to destroy the life of that fluid, and in the other it acts less violently, but continuously, to exhaust the powers of life.

Our conception of the pathology of epidemic meningitis is implicitly contained in the foregoing discussion. Of its essential cause and of the conditions that call it into existence nothing whatever is known. The disease is most probably due to some atmospheric agency that is capable of acting at the same time upon widely separated localities. Its specific cause appears to enter the blood first of all, and doubtless through the lungs, and to be capable of destroying life by its action upon the blood alone. Failing this effect, its force is spent upon the cerebro-spinal pia mater, and it may become fatal by the mechanical interference of the products of inflammation with the nutrition of those parts of the central nervous system which are essential to life. An inflammatory and a septic element together constitute the fully-developed disease; either may be in excess and overshadow the other. According to the relative predominance of one or the other, the disease assumes more of a typhoid or more of an inflammatory type, and it is doubtless this diversity in its physiognomy, as well as in the lesions that attend it, which has led to the most opposite doctrines respecting its nature and its nosological affinities.

DIAGNOSIS.--The most distinctive phenomena of epidemic meningitis are suddenness of attack and rapidity of development of the following symptoms: acute pain in the head, neck, spine, and limbs; faintness, vomiting; stiffness or spasm of the cervical or spinal muscles; hyperæsthesia of the skin; delirium, alternating with intelligence and merging afterward into dulness or coma; occasional convulsive spasms; paralysis of the face or of one side of the body. The evidences of associated blood-poisoning are, the epidemic prevalence of the disease, various eruptions upon the skin (herpes, roseola, petechiæ, etc.), ecchymoses, debility out of proportion to the evidences of local disease, redness of the eyes, {827} foulness of the tongue and mouth, and more or less of the other conditions which characterize the typhoid state. To these features must be added the rate of mortality, which is greater in most epidemics of meningitis than that of any disease with which it is liable to be confounded.

It is distinguished from sporadic meningitis by the fact that the latter disease is never primary, but is always either an epiphenomenon of some other and previous malady (various fevers and chronic blood diseases) or is traumatic in its origin. The thermometer readily distinguishes it from various functional nervous affections, chiefly hysterical, in which the temperature remains normal.

From typhoid fever it differs as widely as possible by its rapid onset, the exquisite pain in the head, the neuralgic pains, the opisthotonos, and the convulsions. The alternate delirium or coma and clearness of mind in meningitis contrast with the persistent hebetude, stupor, or muttering delirium and the muscular relaxation in typhoid fever. The sordes on the tongue, the diarrhoea, the meteorism, the intestinal hemorrhage of the latter, instead of the moist or merely dry tongue and the transient vomiting and torpid bowels of the former; high or continuous fever on the one hand, slight or variable increase of temperature on the other; diffluence of blood in the one and an increase in the proportion of its fibrin in the other; in the one suppurative inflammation of the cerebro-spinal meninges, in the other specific lesions of the intestinal and mesenteric glands,--these, as well as the very different modes of origin of the two affections, draw a broad and manifest line of distinction between them.

It would scarcely be necessary to point out the contrasts between epidemic meningitis and typhus fever were it not that, notwithstanding the abundance of instruction on the subject in medical treatises and lectures, a large number of physicians confound typhus fever, typhoid fever, and the typhoid state of inflammatory diseases with one another. The confusion was intensified at one time by designating the disease we are studying as spotted fever--a term originally applied and properly belonging to typhus fever (typhus petechialis). It is true that New England physicians soon became aware of their error, which was distinctly pointed out and condemned by North, Strong, Miner, Foot, Fish, and others in the early part of this century. A similar error was at first committed both in Ireland and England, but was corrected by maturer experience. In order to contrast the two diseases as strongly as possible, we place their distinctive features side by side in the following table:

EPIDEMIC MENINGITIS. | TYPHUS FEVER. | A pandemic disease. Occurs | An endemic disease, due to local simultaneously in places remote | causes and spreading by from one another and without | intercommunication. intercommunication. | | Attacks all classes of society. | Attacks the poor, filthy, and Is never primarily developed by | crowded alone. destitution, squalor, or | defective ventilation. | | Is not contagious. | Contagious in a high degree. | Attacks more males than females.| Both sexes equally affected. | Attacks more young persons than | More adults than young persons. adults. | | Generally occurs in winter. | Epidemics irrespective of season. | Eruptions are absent in at least| Eruption rarely absent, and half of the cases; they occur | appears about the fifth day. within the first day or two. | {828} | The eruptions are various; they | Eruption always roseolous, and include erythema, roseola, | then petechial. Ecchymoses are urticaria, herpes, etc. | rare. Ecchymoses are common. | | Headache is acute, agonizing, | Headache dull and heavy. tensive. | | Delirium often absent; often | Delirium rarely absent; usually hysterical, sometimes vivacious,| muttering. Rarely begins before sometimes maniacal. Generally | the end of the first week. begins on the first or second | day. | | Pulse very often not above the | A slow pulse exceedingly rare. natural rate; often | Its rate usually between 90 and preternaturally frequent or | 120. infrequent. Is subject to sudden| and great variations. | | "The temperature is lower than | The temperature is always that recorded in any other | elevated, and does not fall until typhoid or inflammatory | the close of the attack. "The disease." It is also very | skin is hot, burning, and pungent fluctuating. | to the feel." | The body has no peculiar smell. | The mouse-like smell is | characteristic. | The tongue is generally moist | The tongue is generally dry, and soft, and if dry is not | hard, and brown, and the teeth foul. Sordes on teeth rare. | and gums fuliginous. | Vomiting is an almost constant | Vomiting is rare and not urgent. and urgent symptom, especially | in the first stage. | | Pains in the spine and limbs of | The pains, if any, are dull, and a sharp and lancinating | apparently muscular. character are usual. | | Tetanic spasms occur in a large | Tetanic spasms are unknown in proportion of cases and within | typhus. Convulsions sometimes the first two or three days. | occur, due to pyæmia. They are due to an exudation on | the medulla oblongata and | spinalis. | | Cutaneous hyperæsthesia is a | The sensibility of the skin is prominent symptom. | generally blunted. | Strabismus is common. | Strabismus is rare. | The eyes, if injected, have a | The blood in the conjunctival light red or pinkish color. | vessels is dark. | The pupils are often variable | The pupils are equal and and unequal. | contracted. | Deafness and blindness are often| Deafness almost always ceases complete and permanent. | with convalescence. Blindness | never follows typhus. | Duration very indefinite, but | Duration from twelve to fourteen generally from four to seven | days. days. | | Relapses are common. | Relapses are rare. | The blood is often fibrinous. | The blood is never fibrinous. | The lesions, except in the most | In typhus no inflammatory lesions rapid cases, consist of a | exist. plastic or purulent exudation in| the meshes of the cerebro-spinal| pia mater. | | Mortality from 20 to 75 per | Mortality from 8 to 40 per cent. cent. |

PROGNOSIS.--In the section relating to the mortality of epidemic meningitis it has been seen that its death-rate varies at different times and places between widely remote extremes. This fact must be borne in mind in estimating the influence of various circumstances in controlling the issue of the disease. The relative as well as the aggregate mortality is far greater in childhood than in adult life. After the age of thirty or thirty-five it decreases rapidly until old age, when recovery from the disease is quite exceptional. A sudden or rapidly developed attack is generally unfavorable, especially when the symptoms are adynamic and there is a purplish discoloration of the skin. Indeed, even apart from evidences {829} of blood-change, cerebral are, on the whole, of graver importance than spinal phenomena, and the more so the more typhoidal their type. Of still more serious significance is a want of perception of the gravity of the situation or unconcern about its issue. A preternaturally slow and compressible pulse implies danger, and so does coolness of the skin, especially if it grows purplish from a diffusion of blood beneath it or even from venous stasis. The various eruptions that have been described including petechiæ, are not necessarily dangerous signs. Profuse sweats during a soporose state, bullæ and gangrenous spots, obstruction of the bronchia with mucus or serum, pneumonia or pericarditis,--these are all grave indications. So, too, are a dry, fissured, shrivelled, and pale tongue or a fuliginous state of the mouth, swelling of the parotids, obstinate vomiting, and profuse diarrhoea at an advanced stage of the disease. Among the most unfavorable nervous symptoms are great restlessness, rigid retraction of the head, spasms of other than the spinal muscles, general convulsions, extensive hyperæsthesia, deep coma, dilatation and insensibility of the pupils or their rapid change from a dilated to a contracted state, retention or incontinence of urine, and all cerebral paralyses, including that of the muscles of deglutition. The favorable indications comprise a general mildness of the symptoms, a moderate loss of strength, a slight degree of pain and muscular stiffness, the absence of petechiæ or vibices (although in many grave epidemics they are of rare occurrence), a desire for food and the ability to digest it. Yet it is imprudent to make an absolute prognosis in any grave case of this disease. Recovery has sometimes occurred when it appeared impossible, and some have died when the period of danger seemed to have passed on the sudden accession of cerebral or spinal nervous symptoms.

TREATMENT.--The difficulties that attend the solution of therapeutical questions regarding diseases which are comparatively regular in their evolution, and are produced by definite causes acting in an intelligible manner, are very numerous and often insuperable. They become multiplied in relation to a disease which, like this one, stands alone in many respects; whose causes, phenomena, and lesions--in a word, whose laws--are specific; and whose varieties of type are as numerous as can be formed by the combination, in a constantly varying proportion, of a special (hypothetical) alteration of the blood, deranging the molecular actions of the economy, and at the same time of an inflammation of the cerebro-spinal meninges, and even of the substance of the great nervous centres. These reasons are sufficient to account for the diverse and often opposite methods of treatment that have been applied to the disease. As in almost all other cases, the methods have consisted in using remedies to counteract certain symptoms--now a stimulant or tonic regimen to combat the debility which conferred the name of "sinking typhus" on the disease; now an antiphlogistic course to allay the inflammation of the brain and spinal marrow denoted by the neuralgic pain and the tetanoid phenomena; and, again, large doses of narcotics to blunt the pain and subdue the spasm. Still other medications have been used with a similar purpose, and some, as we shall see, with more or less theoretical views. It may be said, with Von Ziemssen, "that we are far from having it in our power to decide whether a rational treatment of the symptoms has cured the disease or lessened its mortality;" but a review of the methods {830} that have been employed and their results leads to no doubtful conclusion that some are mischievous and others more or less salutary.

Emetics were among the first medicines used in the treatment of this affection, and were probably suggested by the vomiting which is one of its most constant initial symptoms. But we can readily understand why they failed to afford relief. The vomiting and retching are not gastric symptoms at all, but, as already stated, are due to the irritation of the congestive or inflammatory process at the base of the brain. These medicines may therefore be omitted. The employment of purgatives is even less rational; they debilitate without affording any relief.

Venesection was probably employed as a part of a routine treatment which neither sound reason nor clinical experience justified. It was generally found to fail of its curative purpose, and often induced, especially in young persons, dangerous exhaustion. No better illustration is needed to show that the disease we have been studying is far more than a local inflammation of the cerebro-spinal meninges. On the other hand, local depletion is often of marked utility. Our own experience would lead us to conclude that in the more sthenic cases scarified cups, applied to the nape of the neck and along the cervical vertebræ, are of essential service in mitigating--and generally, indeed, in wholly removing--the neuralgic pains which form so prominent and severe a symptom in many cases of this disease. When any abstraction of blood appears to be contraindicated by the patient's debility, even dry cups will afford him signal relief. Leeches have been applied to the parts mentioned, and over the mastoid processes have sometimes been used with advantage, but their depletory surpasses their revulsive action, and is, so far, injurious. Cold to the head and spine is among the most efficient means of relieving certain symptoms. In the Massachusetts Medical Society's Report of 1810 we read: "Cold water, snow, and ice have been applied to the head when there was violent pain in that part with heat and flushed face, and when there was violent delirium. They afforded great comfort to the patient, and mitigated or removed those important symptoms." It is probable, however, that the value of the remedy is almost entirely restricted to the forming--or at least the early--stage of the attack, when the pain in the head is most intense. Its soothing influence is then very marked, as well as its indirect action in promoting sleep. Heat of head is not an essential condition for its use, for even in the most violent cases it is rarely extreme, and is often entirely wanting. Pain calls more distinctly for the application, and when that symptom has subsided cold is apt to be more annoying than grateful to the patient. Cold is best applied to the head in the form of pounded ice enclosed in a bladder or rubber bag; but cold affusions are also very valuable, especially for children. For the application of cold to the spine the most efficient apparatus is the long, flat rubber bag, either single or double.

From the earliest history of epidemic meningitis in this country blisters formed a conspicuous element in the treatment. They were used, as they had been in other forms of meningitis, to relieve the pain and diminish the congestion in the cerebro-spinal centres. The results of their use were by no means uniform, for not only were they employed in many of the cases which must almost necessarily have been fatal before inflammation could be established, but even in the inflammatory cases {831} they were often applied when time enough had elapsed to allow the exudation to be fully formed, and when, therefore, they were too late to be useful. Again, they were sometimes used so as to vesicate too deeply, and thus by the pain they caused at first, and by the exhaustion that resulted from the excessive discharges they maintained, the patient was more injured than benefited. Our own experience proves that in the early stage of the inflammatory form of the disease blisters applied below the occipital ridge and upon the back of the neck, and only allowed to vesicate superficially, not only remove the pain in the head, but diminish the delirium, spasms, and coma, and therefore contribute as directly as other remedies, if not more so, to the favorable issue of the attack. But such salutary effects are not to be looked for when the disease assumes a malignant type nor after its constitution has become definitely fixed. The application of stimulant and even vesicating agents to the spine below the neck has not been generally practised because, probably, the seat of the spinal lesions was known to be chiefly at the upper part of the organ. Still, the neuralgic pains felt in the spinal nerves may be mitigated by stimulant and anodyne liniments applied with friction to the spinal column.

American physicians early recognized coolness of the skin among the most striking phenomena of the disease; and this probably suggested their use of diaphoretic remedies, among which were the external application of moist heat in baths and warm wrappings, as well as "bottles of hot water or billets of wood heated in boiling water and wrapped in flannel," or the patient "was wrapped in flannel wrung out of boiling water, sinapisms were applied to the feet, while hot infusions were administered, made from the leaves of mint, pennyroyal, and other similar plants, and also wine-whey, wine and water, wine, brandy, and other ardent spirits more or less diluted, camphor, sulphuric ether, and opium. It was not generally thought useful to excite profuse sweating, but important to maintain the activity of the skin from twenty to forty hours, and even longer in some instances. Soup and cordials were at the same time administered. Under this treatment most commonly the violent symptoms, and not very rarely all the appearances of disease, have subsided" (Jackson). Beyond all doubt, this method was a rational one, for it tended to promote an elimination of the morbid poison, while it depleted the blood-vessels and acted revulsively upon the local inflammation of the cerebro-spinal meninges. Yet it seems not to have been revived during the more recent epidemics of the disease, unless, partially, by Gordon (1867), who says: "What I have seen most useful in the stage of collapse is external warmth applied to the entire surface by means of flannel bags containing roasted salt, applied along the spine, along the chest, inside the arms, and to the feet and legs and between them."

Except typhus fever, there is no disease in which a due administration of alcoholic stimulants may become more important. In cases of the inflammatory type they are rarely needful, and are frequently hurtful, but in those which exhibit signs of blood disorder with nervous exhaustion they are often indispensable. Nothing demonstrates their necessity more clearly than the extraordinary tolerance of alcohol exhibited in some cases of the disease. Among the earlier American authorities may be found many illustrations of this statement. Woodward (1808) {832} observed that very large quantities of wine or ardent spirits may be given without injury. Arnell said: "In some cases I have given a quart of brandy in six or eight hours with the happiest effect." Haskell maintained that "the bold and liberal use of diffusible stimuli is the only safe and efficacious mode of treatment." In Ireland the habitual use of alcohol in the treatment of typhus fever no doubt suggested its liberal employment in this disease, but such stimulants have never been in vogue among the physicians of France or Germany. This difference may in part be accounted for by the generally asthenic type of the disease in the first-named country and its more inflammatory character in the others. Similar contrasts of type mark different epidemics, and individual cases during the same epidemic. We have no doubt that while these agents are indispensable in the treatment of cases of the former type, they must even then be exhibited discreetly, for their too lavish exhibition entails the gravest peril by intoxicating the patients and oppressing instead of arousing their vital energies. In 1866, on taking charge of the medical wards in the Philadelphia Hospital, we found that the patients were using as large quantities of alcohol as are given in typhus fever, but a very short period of observation showed that this use of the stimulant was excessive; consequently the dose of it was first reduced, and finally it was omitted altogether unless special indications for it arose. This change was followed by a manifest improvement in the general aspect of the sick and the subsidence of symptoms which, it then became evident, were due to a lavish use of stimulants rather than to the gravity of the disease. Alcohol is no more essential to the treatment of epidemic meningitis than of any other acute affection; it is a cordial to be held in reserve to meet those signs of failure of the heart and nervous system which may arise in all acute diseases attended with changes in the condition of the blood.

The use of opium in the treatment of this disease was strongly advocated by nearly all of the early American writers upon the subject, and by many of them enormous doses were given. It was observed not to produce narcotic effects in ordinary doses. In one case, marked by excruciating pain in the head and maniacal delirium, sixty drops of laudanum were given every hour until nearly half an ounce had been taken within eight hours (Strong). Haskell states: "We have been obliged frequently to exhibit ten grains of opium for a dose in some of the violent cases attended with strong spasms, and have never known it to produce stupor in a single instance." Miner relates that "a few cases imperiously required half an ounce of the tincture of opium in an hour, or half a drachm [of opium] in substance in the course of twelve hours, before the urgent symptoms could be controlled, and even some cases required a drachm in the same time. All these patients recovered." In Europe, Chauffard administered opium in doses of from three to fifteen grains, and Boudin frequently prescribed from seven to fifteen grains at a single dose at the commencement of the attack, and subsequently one or two grains every half hour, until the patient grew sleepy or his symptoms subsided. This tolerance of the drug is remarkable, and so is the fact that it does not cause constipation. These and many similar statements agree entirely with our personal experience. We were in the habit, during the epidemic above referred to, of prescribing one grain {833} of opium every hour in very severe and every two hours in moderately severe cases, and in no instance was narcotism induced, or even an approach to that condition. Under the influence of the medicine the pain and spasm subsided, the skin grew warmer and the pulse fuller, and the entire condition of the patient more hopeful. It seemed probable, however, that the benefit of the opium treatment was most decided in the early stages of the attack, and hence in those in which the inflammatory and spasmodic elements predominated. The hypodermic injection of morphia is to be preferred before the internal administration of other preparations of opium, not only on account of its prompter action, but because it avoids the rejection of the medicine by vomiting. On the whole, Von Ziemssen is within the bounds of truth when he says, "Beyond all doubt morphia may be considered the most indispensable medicine in the treatment of epidemic meningitis."

There is no evidence sufficient to show that epidemic meningitis has ever been cured by quinia alone. In the early prevalence of the disease it was treated by large doses of cinchona, but unavailingly, and subsequently smaller doses were given during the convalescence, as it was in that of other acute diseases. In some parts of this country where miasmatic diseases prevail, and epidemic meningitis, like all other acute, and especially febrile, disorders, displayed more or less of a periodical or paroxysmal type, quinia was used in large doses, but the expected result was not realized. Upham states that in some instances it was given to the extent of sixty, or even eighty, grains within twelve hours from the beginning of the attack, but without effect. In Europe it was extensively tried and unanimously condemned. It may very properly be left out of the list of medicines suitable for this disease, particularly since it is no longer probable that any physician would be rash enough to employ it in the so-called antipyretic doses with or without their usual associates, cold baths. According to Karl Jaffé, the medicinal antipyretics (quinia, salicylic acid, and also sodium benzoate) may be entirely discarded, because they ruin the already weakened digestion.[59]

[Footnote 59: Phila. Med. Times, xii. 600.]

Common sense has also proved stronger than theory in excluding mercurials from the treatment of epidemic meningitis. At one time they were extensively used, especially when it was learned that the disease in its full development included a paramount inflammatory element. But it was soon found that the results of their use were far from uniform, and farther still from being demonstrably beneficial. In this, as in many other similar cases, it is quite impossible to reach a definite judgment unless it were known what was the type of the cases in which the medicine was given, whether they were asthenic or inflammatory, and again whether it was used during the active or during the declining stage and toward convalescence. In the absence of any trustworthy testimony upon the subject it is only possible at present to state that in the treatment of this disease mercurials should not be used. This conclusion is all the more imperative because the medicine is not an indifferent one. If it is not necessary--and it certainly is not--it is too dangerous in its immediate and ultimate effects for its employment to be warranted.

Since belladonna and ergot were shown to diminish vascular action in the cerebro-spinal axis by contracting its capillary blood-vessels, they have {834} been put forward as having a specific virtue in this disease. If the fact be so, how is that other fact--a clinical one, moreover--to be disposed of, which is that opium, the physiological antagonist of belladonna and ergot, is more efficient than they are in curing the disease? It is possible, indeed, that they may have that curative power, and that opium possesses it also, and that the explanation given of the action of all of these agents is erroneous. Upham states that, in 1863, Haddock recommended ergot upon theoretical grounds, and that during an epidemic at Newbern, N.C., several cases treated by it recovered. Three cases recovered in which it was prescribed by Borland. Read used it in 1873-74 at Boston, Mass., and out of 19 cases 16 recovered and 3 died.[60] This mortality of about 15 per cent. is not more than half of that which has generally been met with, and if it can be attributed to the treatment would go far to prove the efficacy of the latter. One grain of ergotine, with one-tenth of a grain of extract of belladonna, was administered every three hours. Considering the exiguity of the dose of belladonna, it is not surprising that, except in one case, it did not dilate the pupil; and the dose of ergotine is likewise far smaller than the average medicinal dose of that preparation. Moreover, all of the cases except the fatal ones appear to have presented the disease in a subacute, and certainly not in an aggravated, form.

[Footnote 60: Philadelphia Med. and Surg. Reporter, Jan., 1875, p. 68.]

In 1872, Dr. S. N. Davis,[61] moved by the success of Calabar bean in tetanus, employed it in this disease. A mixture of one ounce of tincture of Calabar bean with one and a half ounces of fluid extract of ergot was administered in doses of half a teaspoonful every two hours, and with better results than had followed other remedies. Here, again, it is to be noticed that the analogy suggesting the use of physostigma is not a logical one. That drug indeed relieves the spinal spasms of tetanus--a disease in which there is an irritation of the spinal axis, but no exudation from its meningeal vessels, as in the affection we are studying. Moreover, it is a disease of extraordinary power, as shown not only by the spasms, but by the exceptionally high temperature, and thus again is in direct contrast to epidemic meningitis. If, therefore, Calabar bean benefits that disease, it cannot do so in the manner suggested by the author.

[Footnote 61: Richmond and Louisville Med. Jour., xiii. 711.]

Bromide of potassium and hydrate of chloral have also been employed to allay the spasmodic symptoms; but the former is too feeble for the purpose, and the depressing action of the latter upon the heart renders it dangerous. Bromide of potassium has been given to children of two and five years in doses of four and six grains every two hours; but these doses appear to be quite too small even for the purpose in view--viz. to prevent convulsive attacks. Whatever remedies may be suggested hereafter, none should be employed that tend to reduce the power of the heart, which, as we have seen, is dangerously depressed by the disease.

During the decline and convalescence of the affection it is probable that iodide of potassium may be advantageously used to promote the removal of the exudation-matter on the brain and spinal marrow, and probably to prevent the hydrocephalus which sometimes follows the attack, and is attributable to the pressure of effused lymph upon the cerebral veins.

DIET.--The mildly febrile character of epidemic meningitis, and the {835} remarkable debility which characterizes so many cases of the disease, and which, as was before pointed out, conferred upon it the name typhus syncopalis, plainly justify what experience has taught, that appropriate food for the subjects of this affection is at once the most digestible and nutritious that can be taken. It is true that this regimen is interfered with by the vomiting, but, as that symptom is of cerebral and not of gastric origin, it is more apt to be allayed by suitable food than by abstinence. It has been our custom to observe in this disease the same rules respecting diet that are recognized as the most suitable in typhus fever. In doing so, indeed, we did, without at the time knowing it, follow the example of the early American physicians. Strong, who wrote in 1811, advised "soup made from chicken, veal, mutton, and beef, richly seasoned with pepper and savory herbs." These articles were prescribed by him during the height of the disease. Later on he says: "The stomach soon begins to crave something more solid than soup; oysters, beefsteak, cold ham, or neat's tongue are received with peculiar relish. Often I have seen convalescents, when they had hardly strength enough to raise themselves in bed, make a hearty meal of the above-mentioned articles, which were received with great satisfaction, sat well upon the stomach, and were well digested and assimilated." This method is substantially the same that was found successful in the earlier, as it has been in the later, epidemics in this country, and we have no hesitation in attributing to it and the appropriate use of opium and blisters the degree of success we enjoyed in the treatment of the disease in the Philadelphia Hospital and elsewhere.

During convalescence from epidemic meningitis the patient should carefully abstain from physical exertion and mental excitement, and before this state is fully established he should even very cautiously change his position from a recumbent to an erect posture. And, finally, he should return to his ordinary occupations, mental or physical, as late as possible, on account of the danger of a relapse, which has already been described.

{836}

PERTUSSIS.

BY JOHN M. KEATING, M.D.

HISTORY.--A careful study of this disease from the various writings since the time of Hippocrates leaves little doubt in the mind of the reader as to its antiquity, so little indeed has it changed in its various characteristics. Whether the affection passed to continental Europe from Africa, or whether its starting-point was India, are questions difficult to solve, and, except for the medical historian, of little import. Desruelles probably truthfully asserts that the many differences which mark the descriptions of the disease, especially by the early Grecian writers, may be due, not to the non-existence of the disease as we know it, but to the influence which climate exerted then as now, and to the unrecognized fact that it is only fatal in its complications. The writings of Hippocrates, Galen, and Avicenna, though undoubtedly referring to the many affections in which paroxysmal cough is a prominent symptom, contain many expressions that would point clearly to the existence of a specific disease. Dr. Watt believed that the disease was not known to the Greeks, and other writers claim that it came from the north and spread southward over Europe about the sixth century; nevertheless, it first appears on record as a distinct affection, disentangled from the confused mass with which it was involved for centuries, about the middle of the seventeenth century. Steffen mentions the first well-established accounts as coming from Baillou in the year 1600, and Schenck in 1650, and Ettmüller in 1685. Sydenham casually mentions it in 1670. Since the time of Willis the definition of the disease has remained unaltered, and so accurate was the description then given of it that we can but naturally conclude that for many centuries at least it has varied but little.

In studying affections of this kind, occurring in epidemic form especially, and which are increased in intensity by whatever means the contagious element, whether gaseous or parasitic, is made more virulent, much allowance is to be made for the climate, customs, and habits of the people whence our data are derived. Thus, most of the diseases of antiquity, the descriptions of which have reached us, have been drawn from types modified by mild climates where the people have led an out-door life, and though the disease we see at the present day is one and the same so far as its causation is concerned, the indoor life and close confinement, the bad ventilation, and the artificial existence in our large cities must weaken the individual, intensify the poison, and exert an influence on the disease.

DEFINITION AND DESCRIPTION.--Whooping cough has been {837} characterized as an acute contagious affection, occurring usually in childhood, though it may occur at any age, and lasting several weeks. It is manifested usually by malaise, catarrh of the respiratory tract, and subsequently by a convulsive cough occurring in paroxysms, the peculiarity of which consists of a series of forcible expirations, followed by a sonorous inspiration or whoop, which may be repeated several times.

At the beginning of these paroxysms of coughing, there are evidences of slight laryngeal irritation, attended by an effort at suppressing the cough; then follow gradually increasing and more audible inspirations, which become more and more difficult. The child is agitated, the face becomes pale, and the countenance has a mingled expression of supplication and fear. If it is old enough it will seize the nearest object for support. As the spell advances, the eyes become suffused and prominent and the loose tissue surrounding the orbits appears puffy and congested. Finally, the paroxysm reaches its height; the child, with a livid countenance, with veins standing out like cords, gives a succession of violent expiratory efforts, followed by a long inspiratory whoop. The same is repeated several times, until finally almost complete cyanosis takes place; the spasm relaxes, a glairy, tenacious mucus runs from the mouth, the contents of the stomach are vomited, and the child falls back exhausted. The lividity of the countenance is succeeded by a deathly pallor; the face still appears swollen and puffy beneath the eyes; the tears course down the cheeks, and frequently hemorrhage occurs from the eyes, nose, ears, or throat, owing to the terrific strain upon the circulation. As soon as the child has recovered from the fatigue of the paroxysm all is apparently over, and were it not for the characteristic expression of the eye, which is pathognomonic in a well-advanced case, nothing would be noticed to even suggest the disease when uncomplicated. The voice is clear; there is little or no elevation of temperature.

The paroxysms which have given the name to this disease can only be likened to an epileptic convulsion, which by gradually increasing cyanosis is self-curable, the carbonized blood finally bringing about an anæsthetic effect. The severity of the paroxysms is by no means in proportion to the local catarrh, which latter may be superficial and slight, not to be detected during life by the most careful laryngeal examinations, and only after death by the aid of the microscope. The frequency and intensity of the paroxysms are dependent in a measure upon the degree of excitability of the nervous system, which of course differs in individuals. It is evident that the success of treatment must be powerfully influenced by this circumstance, and it is partly owing to it that there are so many opinions as to the value of remedies in this disease.

The complications are usually dependent upon outside causes, and have nothing to do with the poison proper of whooping cough, as far as we can tell. There are some which depend on an inflammation of the mucous membrane, which may be limited to any portion of the respiratory tract or may extend throughout it. Complications may arise from mechanical obstruction to inspiration by the swollen mucous membrane or from plugs of tenacious mucus, which may cause pulmonary collapse and favor the development of catarrhal pneumonia, and later even of phthisis; or from impediments to free and easy expiration, whether from spasm of the bronchioles, from forcible compression of the thorax through reflex {838} nervous irritation, or from other obstructions, all of which tend to produce emphysema. Disturbances of the circulation, in the brain or elsewhere, may proceed from thrombi or emboli and give rise to complications which will render fatal an otherwise mild form of the disease. The invariable disturbance of nutrition which accompanies every disease affecting the nervous system is apt to show itself in the breaking down of products which are simply inflammatory. Vomiting may be a most serious complication, both from its immediate and remote effects. It may be due to gastric catarrh, or more frequently to irritation of the pneumogastric nerve.

ETIOLOGY.--Very numerous theories have been advanced as to the nature of this interesting disease. Hufeland, Lebenstein, Pinel, Jahn, Todd, Cullen and a host of others have regarded it as essentially a neurosis. By many others it has been supposed to be due to a lesion of the brain or of its membranes, but careful investigation has established the fact that there is no lesion in whooping cough at all constant or characteristic. By still others, and especially by Gueneau de Mussy, it has been regarded as essentially an affection of the tracheo-bronchial glands, a bronchial adenopathy, causing irritation of the pneumogastrics and of their bronchial branches by pressure of the enlarged glands. We have, however, seen many post-mortem examinations of the bodies of children who have died of measles, where marked enlargement of these glands was constantly found, but where no symptoms of whooping cough had been present. There are indeed many features of the disease which seem inexplicable on any other theory than that the essential cause of whooping cough is a specific poison, and such is the view now generally adopted. This poison is capable of being carried by fomites, though as it is highly infectious it is often communicated through the atmosphere, and is most frequently conveyed from individual to individual. Dolan,[1] who has recently published a very interesting and valuable monograph on this affection, quotes Linnæus, who ascribed it to the irritation of insects, as the author of the modern view that whooping cough is due to the presence of a peculiar microbe, though it must be conceded that as yet it has not been discovered. Most observers hold that the contagium is not in the blood, but that it resides in the secretions of the respiratory passages, and is most virulent during that stage of the disease when the secretion is abundant. Letzerich states that he has {839} succeeded in producing whooping cough in rabbits by inoculating the trachea with the sputa of the human subject. Dolan obtained similar results by injecting the nasal secretions, and also by compelling rabbits to inhale air impregnated with decomposing sputa and vomit of patients suffering with the disease.

[Footnote 1: Dolan, Thos. M., Whooping Cough, London, 1882.

The following brief statement of his conclusions may be quoted as presenting the most important facts concerning the pathology of the disease:

1st. Pertussis depends on a specific poison or contagion; this is universally admitted.

2d. This contagion is active and highly infectious; this is also granted.

3d. The contagion is analogous to the contagia which produce splenic fever, measles, scarlatina, variola, etc.

4th. It has a peculiar determination to the lungs.

5th. Like all other contagia, it has its period of activity and decline.

6th. The period of greatest activity is in the first and second stages.

7th. Pertussis runs a regular course like measles, scarlatina, variola, etc., and rarely attacks a person but once.

8th. It may thus be classed among zymotic diseases.

9th. The fact that there is no primary pathognomonic morbid change supports this view.

10th. There are various secondary lesions which are characteristic, as ulcerations of the frænum linguæ.

11th. The mode of death harmonizes with this view.]

I do not, however, feel entirely satisfied in adopting the view that the contagium of whooping cough resides alone in the mucous membranes of the air-passages.[2] Children have been known to be born with the disease, the mother having suffered from it some time previous to confinement. The following case occurred under my own observation: Mrs. F----, the mother of two children, was in her eighth month of pregnancy; the two children had at the time a very severe attack of whooping cough, which required the constant attendance of the mother. She, though an extremely intelligent woman, belonged to the poorer classes, and had no one to assist her at this trying time. One day she complained that the movements of her child in utero had entirely changed. Suddenly, without any previous motion, the child would become very active; the force of its movements was such as to make hazardous any attempt on her part to walk in the street. The suddenness with which the movement would come on would oblige her to seize the nearest object for support. This continued until the child was born. Shortly after labor my attention was called to the infant, which had a curious attack, it became deeply cyanosed, seemed asphyxiated, as it were, for a moment, had no convulsions, and within a few seconds resumed its normal breathing and the circulation seemed once more established. I saw the child in several of these attacks; its health did not seem to be impaired, and without treatment, within a few weeks they disappeared altogether. The mother insisted upon the fact that the child had whooping cough, and the absence of the characteristic whoop was the only thing that prevented the diagnosis from being positive. This would show--and there are enough cases on record to warrant our basing an opinion upon them--that the contagium of whooping cough is found not alone in the matters expectorated, notwithstanding the statement of Dolan and others that their experiments failed to show its existence in the blood.

[Footnote 2: Colson, Lancet, July 2d.]

It must not be forgotten, in reference to cases which seem to have arisen without any exposure to the specific poison, that the characteristic whoop is not always present, and that consequently the true nature of mild cases of the disease which may infect other individuals may have been overlooked. Childhood probably acts as a predisposing cause, though the disease occurs at all periods of life, and as it usually occurs but once in the same individual, it is clear that the apparent diminution of susceptibility in later years may be largely due to the fact that most persons have had the disease in childhood. More children are attacked from one to five years, and the disease is more prevalent in summer and fall months. Causes which, like exposure to inclement weather, give rise to irritation of the bronchial mucous membrane, or diseases which, as measles, are accompanied with catarrhal symptoms and susceptibility of the bronchial mucous membrane, also may serve as predisposing causes. Sex appears to exert some positive influence. Of 360 cases of pertussis by Dessau,[3] the total number of males were 154, that of females 206. Girls are more {840} frequently attacked than boys, in proportion of 2 to 1.50; this seems true at all ages; this statement is substantiated by Unruh of Dresden, based on an analysis of 1952 cases.

[Footnote 3: N.Y. Jour. of Obst., 1881, xiv. 490-503.]

SYMPTOMS.--The disease begins usually with an ordinary catarrh, preceded by malaise and slight laryngeal irritation, which may be overlooked; in fact, during the first stage there is nothing to attract special attention, unless a direct history of exposure be known and suspicion be aroused on that account. Meigs and Pepper state that the earliest period at which they have known the distinctive whoop of the disease was three days, though in a great many instances it was delayed as late as three weeks. The same authors state that the ordinary duration of a paroxysm or kink is from one-fourth to three-fourths of a minute. They mention a case where the paroxysm lasted fifty-five minutes. Ordinarily they number about thirty-five or forty during the twenty-four hours at the height of the disease, differing greatly in individuals. Their number is most frequent in the course of the third or fourth week, after which they remain stationary, and then gradually decline. The paroxysms may occur spontaneously, or they may follow some irritation, either direct or reflex, or they may be induced by nervous excitement. Toward the end of the attack, after the catarrhal irritation has greatly subsided, or in fact has entirely disappeared, the paroxysmal kinks may be provoked by irritation of the fauces, and also by nervous excitement; and there is no question but that at this time they can be controlled by will-power. In many cases a distinct relapse occurs after the disease has been apparently cured.

Dolan believes the phenomena of the cough or kinks to be due, as suggested by Laennec, to a "spasmodic condition of the muscular or contractile fibres of the bronchi and their branches." He remarks that the lungs are supplied from the anterior and posterior pulmonary plexuses, formed chiefly of branches from the sympathetic and pneumogastrics. The filaments from these accompany the bronchial tubes upon which they are lost. Irritation of these nerves is said to have the effect of producing contractions of the bronchial canals sufficient to expel a certain quantity of air. If this theory is true, it helps us in explaining why the large, mediate, and smaller bronchi are closed during the expiratory stage of the paroxysmal cough of pertussis. The general opinion seems to be that the pneumogastric nerve is not inflamed, as has been asserted by some.

The highly sensitive condition of the nervous system, which is probably in a great measure intensified by the anæmia, and by the interference with nutrition due to the disturbance of the circulation by the cough, will show itself in many ways, and even when no secondary nervous affections complicate the attack or follow it. Some time will elapse after the disease has passed away before the child will recover its self-control, or its nutrition will show the influence of a healthy nervous system. The total duration of the affection is said to vary from six weeks to three months in ordinary cases; though probably, if active treatment could be instituted early enough and kept up with thoroughness, there is no specific disease more capable of being shortened in its course than the one under consideration; this remains, however, for future statistics to decide.

During the second stage of the disease the symptoms are sufficiently {841} marked to attract attention and render a diagnosis easy to make. Frequently the catarrh seems to extend to the bronchioles, and gives rise to symptoms that are alarming; and the intensity of the paroxysm will cause the engorgement of the blood-vessels to get relief in profuse hemorrhage; this is the period for caution. Complications may arise, the strength may fail, the secretions may become too abundant, and asphyxia may ensue; emphysema may show itself, or catarrhal pneumonia may gradually supervene.

The period of decline is very gradual; the secretions become less in quantity and more viscid, the paroxysmal cough is less frequent, but may at times be equally severe, the child's strength is usually exhausted, and its nutrition is greatly impaired. The expected paroxysm throws it into a state of intense nervous excitement; it is sleepless--in fact, worn out. Probably at this period of the disease treatment will show the most marked results, and the long lists of sedatives, tonics, etc. which are presented to us by their zealous advocates owe much of their popularity to their value at this stage of the disease. The catarrhal symptoms are the first to subside; the nervous disturbances remain for some time, and gradually fade, and the constitutional symptoms, or those from exhaustion, are the last to leave the patient.

Strange as it may seem, the heart appears to suffer but little in the long run from the great strain upon it; the palpitation and irregularity of its actions are not followed by structural changes as a rule, though we may state that feebleness of the circulation has remained in most of our bad cases for some months after recovery.

As regards the ulceration of the frænum linguæ, which has given rise to so much discussion as to its exact value as a symptom of this disease, our own experience leads us to believe that though it is nearly always present in the severe cases, its almost invariable absence before dentition and in milder cases shows it to be of traumatic origin. Roger's exhaustive report before the French Academy supported this view, and showed how clearly it is caused by the violent rubbing of the frænum on the free border of the incisors. On the other hand, Delthil of Paris and Blake of England believe that it is a pathological feature of the disease. The former reported cases in which it occurred before dentition. The ulcer is not always found on the frænum linguæ, but is found on either side of it. Bouffier noted severe cases of ulceration in children who had no teeth, but he attributed it to the injury produced by the mother in detaching the mucus with the finger.

Examinations of the urine have been carefully made by many observers. The appearance of sugar, about which so much has been said, does not seem to be constant, or even very frequent. Out of 50 cases, Dolan found traces of it in but 13. This coincides with our experience also, for we have frequently tested the urine in seven cases with negative results. Since, as is well known, irritation of the pneumogastric centre may cause glycosuria, it was at one time attempted to show that the paroxysms in whooping cough were due to congestion of the pneumogastric nerves, a condition which is said to have been occasionally found in this disease. Dolan says he has never seen hemorrhage from the kidneys during the course of whooping cough, nor blood in the urine.

MORTALITY.--It is an extremely difficult matter to reach, with any {842} degree of certainty, the true mortality of this affection. Meigs and Pepper say: "Of the 208 cases observed by ourselves, 143 were simple, all of which recovered;" and, again, "Some form of complication occurred in the 65 of the 208 cases observed by ourselves; of these 65, 12 died." The mortality seems greater under five years; thus: Of the 9008 deaths attributed to it in the United States during the census year ending June 1, 1870, the number of persons under one year of age was 4424, and 8396 were under five years. There were 1784 deaths from it recorded in Philadelphia from 1860 to 1876; of this number, 1724 were under five years of age. The census of the United States for 1880 gives a return of 11,102 deaths from this disease.

Females seem more liable to die of it than males; of the 1784 deaths in this city, 766 were males and 1018 females. As we have already seen, females are more liable to the disease than males.

Robt. J. Lee, M.D.,[4] says that from the Registrar-General's report of 1876 it is seen that in a total mortality in England of 510,315, whooping cough was returned as the cause of death in 10,554 cases, or nearly 2 per cent.

[Footnote 4: In a paper in the British Med. Jour., 1879, vol. i. p. 307.]

As for the time of year, we quote the following: "Thus, according to the census statistics, most deaths occur in the spring, there being a rise up to the middle of May. From the middle of May the number lessens largely until August, when a rise occurs and continues until October, when a decline sets in and continues until December, when a rise begins and goes on increasing until the middle of May. This rise in mortality from August to October is attributed to the wear and tear of a hot summer and the intestinal troubles then so prevalent."

The mortality statistics of this disease are uncertain. It is fatal in its complications or by inducing a debilitated condition which invites degenerative processes. The severity of the symptoms is no guide for prognosis as far as uncomplicated cases are concerned, and there is no doubt but that at present we are able to greatly reduce the mortality-rate by care and medical treatment, as well as to shorten the attack. Sporadic cases are apt to be neglected until they become complicated. When the disease occurs in epidemic form, measles is often prevalent simultaneously, and in consequence children who become affected by both diseases have a greater tendency, from debility, to become the victims of those affections of the respiratory organs which are such frequent and fatal complications of both maladies.

Instead of surprise at the mortality of this affection, the marvel is that so large a percentage of recoveries take place, when we consider that we are dealing with a disease whose lesion is a catarrh of the air-passages which seldom lasts less than two months, with a tendency to involve the lungs in one way or another, and then witness the carelessness with which, among the lower classes, the child is often treated--exposed to all weathers, under-clothed, under-fed, and probably allowed to pass through the whole attack without medical treatment. Taking this into consideration, the probability is that the mortality of this disease could be reduced to a very small figure by careful management, even if the investigations of those now seeking the microbe of pertussis do not lead to any plan, in accordance with Pasteur's teachings, which will still further lessen the gravity of the disease. Until {843} then, we can but insist upon a rigid quarantine of schools, a registration of all cases, and the seclusion of them, as we have done to-day in the case of variola and scarlatina.

MORBID ANATOMY.--Although whooping cough is a serious disease, the cause of death is generally found to be dependent upon its complications, and there is no lesion at all characteristic of it. The chief complications and sequelæ are--bronchitis, which may become capillary; lobular collapse, which, according to Alderson,[5] is frequently found; emphysema, usually marginal, probably due, as suggested by Jenner, to violent expiratory exertions; rupture of air-vesicles, with subcutaneous emphysema; catarrhal pneumonia, pleurisy, phthisis, acute tuberculosis, croup, cerebral apoplexy, meningitis, etc. As any of these complications, and others which may arise from debility, may be the cause of death, independent of the action of the specific poison itself, it is usual to divide the post-mortem appearances into those that are the result of the extension of the catarrh itself and those produced by the interference with the circulation and with nutrition from mechanical violence. Of the former, the usual causes of death are pneumonia, gastritis and enteritis. Of the latter, we have thrombosis of the cerebral sinuses, hemorrhages, emphysema, and exhaustion following constant vomiting.

[Footnote 5: Medico-Chir. Trans., pp. 90, 91, 1830.]

Tubercular disease of the lungs or of the brain is apt to be a cause of death. Convulsions carried off 5 of the 12 fatal cases reported out of 208 by Meigs and Pepper. This may be due to congestion of the brain, especially in teething children. Spasm of the glottis with sudden death is occasionally found. In such cases there is found intense congestion of the brain, also of the liver and kidneys, and at times of the mucous membrane of the stomach and intestines, as well as of that of the respiratory tract.

In all cases, especially at the teething age, sudden death may occur because effusion into the ventricles of the brain or the formation of heart-clot has taken place. It is important to know this, that active treatment applied early enough may save the patient.

PROPHYLAXIS.--Should the interesting and seemingly conclusive statements of Dolan and the microscopic investigations of Carl Bruger[6] receive the endorsement of future workers, the subject of prophylaxis will assume a degree of importance which hitherto it has only maintained with the medical profession. No one has doubted that the disease was contagious, and yet there is no affection which has attached to it a corresponding fatality that is so carelessly dealt with as pertussis.

[Footnote 6: Bruger of Bonn, in the Berliner klinische Wochen., describes at length the special micro-organisms of pertussis. They appear as small elongated elliptical bodies of unequal length, the smallest being double as long as broad. High powers show subdivisions in the largest specimens. They are generally isolated, but may appear in groups. They bear some resemblance to Leptothrix buccalis, the spores of which are often found in whooping-cough sputa. Occasionally the bacillus is seen inside the mucous corpuscle in the sputum. They stain in the usual way, fuschin and methyl violet. This bacillus is not found in any other kind of sputum, is very abundant in pertussis, and increases in direct proportion to the severity of the disease.]

Within the past few days we have heard on two occasions in crowded railway-cars the characteristic paroxysm of the third stage of the disease, and yet people will endeavor to convince themselves that unless contact with the child takes place the danger is little.

{844} The atmosphere in school-rooms, railway-cars, and places of amusement which are badly ventilated, is an excellent medium for the propagation of the contagious matter, and many extraordinary cases are on record of momentary exposure being sufficient to contract the disease. Believing that the contagium or virus resides in the mucus and air thrown off by the child, and also in the vomited matters, which contain a large amount of ropy mucus, and also that it gains entrance by means of the respiratory organs, protection from contagion divides itself as follows: thorough disinfection of the exhaled air, of the mucus remaining within the bronchial tubes and air-passages, and of the clothing, together with exposure to fresh air and thorough cleansing of all furniture and household utensils, including cups, silverware, and toys, used by the child. Oxygen is said to have this effect, and thorough, constant ventilation, with the breathing of fresh air by the child, the thorough washing of its surface, and disinfection of its clothing, are the first indications; while the impregnation of the atmosphere with the spray of well-known germicides by means of the steam or other atomizer and the frequent inhalation of such materials by the patient are no less important. Every case of whooping cough should be compelled to use two or three times daily the spray impregnated with a substance of this sort, either carbolic acid, the oil of eucalyptus, a solution of quinia, or thymol. Chlorine (from chloride of lime) used thus has of late been followed by excellent results, and the spray of a solution of corrosive sublimate or of ammonium chloride has been found very useful. The protective treatment should be applied to those exposed to contagion. Such children should be guarded from exposure to colds; their diet should be simple and nourishing, their clothing warm; they should be kept as much as possible in the open air. The breathing of air impregnated with such substances as above mentioned will no doubt act upon the virus before it comes in contact with the mucous membranes so as to be absorbed, and probably the severity of the attack might be mitigated by modifying the germ of the disease.

TREATMENT.--As can be readily imagined, a disease which is so universal, so distressing, and at the same time so obscure in its pathology, as the one under consideration, would have in its literature a mass of recommendations for treatment from zealous advocates, based upon theory or experience, as numerous as the authors themselves. It would be impossible for us to dwell at length upon all of these, but we will confine ourselves especially to the consideration of a few of the most important. It will be convenient to consider first those remedies which have been used with the view of relieving the congestion and irritability of the respiratory mucous membrane and of promoting more free secretion. It will also be observed that many of these remedies may now be regarded as of value for destroying the special germ which is thought to be the essential cause and real virus of pertussis. Allusion has been made above to the importance of inhalations as a prophylactic for those who have been exposed to the contagion, as well as for the purpose of rendering the secretions less contagious; and so too we find that the inhalation of various substances has received favor with many as a method of treatment. Thus, hyoscyamus, belladonna, ammonium bromide have been used. Helenke and Serbaud say that bromide of {845} potassium is best for inhalation. Letzerich recommended the insufflation of quinia twice daily, using the quinia muriate with potassium bicarbonate and gum-arabic. Forchheimer[7] reports 97 cases of whooping cough treated by the insufflation of the quinia muriate; of the 97 cases, 52 were females, 45 males--the youngest three weeks, the oldest nine years old. Five cases gave no results, while in the others benefit was shown by a shortening or amelioration of the disease. The vapor of benzole has been used with good results. The vapor of carbolic acid has of late been highly recommended, either administered with the atomizer several times daily, or used by saturating flannels in carbolic acid solution and placed around the child's bed at night. It is said that the inhalation of the vapor of a few drops of carbolic acid on some hot coals will ensure a night of freedom from violent coughing. Probably in this way we may account for the belief that proximity to gas-works is beneficial to a child with this disease. As is well known, Niemeyer and others in the north of Germany believed in the value of the inhalation of oxygen, and the experience of every one who has had much to do with this disease favors an out-door life. We may here also mention the value of a small quantity of chloroform or ether, by inhalation, in allaying the severity of the paroxysms of cough. We have also tried the nitrate of amyl, but without marked result.

[Footnote 7: New York Jour. Obstet., 1882.]

Others have recommended the use of solutions of various substances, applied directly by a brush to the interior of the larynx. Quinia has been used in this way also by Hagenbach; but the most satisfactory results have been obtained by the application of very weak solutions of nitrate of silver, as first recommended by Watson in 1849.

After the secretions have been fully established and the characteristic whoop has appeared, the indications in the treatment are to relieve the respiratory tract of its burden by occasional emesis with alum or ipecacuanha, to give freely antispasmodics and sedatives, as belladonna, chloral, the bromides, hydrobromic acid, or, as recommended by some, digitalis; to give quinia freely, and to use counter-irritants to the neck and chest with liniments composed of oil of amber, croton oil, or turpentine.

The value of emetics has been long recognized in this affection, although we are told by Vogel that the continuous use of emetics in the early stage for several days causes harm. Copeland ordered an emetic every third day in ordinary cases. All writers agree that the milder emetics should be used by preference; that tartar emetic should be avoided, except as an external application where a counter-irritant is desired; and that ipecacuanha is the safest, though alum is also safe and as an astringent useful. Trousseau preferred the sulphate of copper. In the earlier stages of the disease emetics are not, as a rule, indicated; it is only when the secretion has become extremely tenacious, and the paroxysms so frequent and severe as to greatly strain the patient and endanger his lungs, that they are of value. There seems to be a close connection between the amount and tenacity of the secretion and the severity of the paroxysm. The potassium carbonate has been recommended as an active agent in the amelioration of this affection; it is probably valuable in rendering the secretion less tenacious. Alum has been used with success, as has tannin, probably owing to their local action on the mucous membrane. Macartan[8] says that in the East {846} Indies the disease is treated in the first stages by astringent and tonic gargles.

[Footnote 8: Dictionnaire des Sciences Méd., 1813, vol. vi.]

Belladonna certainly receives the endorsement of the greatest number of writers. Vogel considers it superior to all other drugs, and regards dilatation of the pupil as the only sure guide in its administration. He says it does not cut short the attack, but mitigates the paroxysm. Trousseau was also an advocate of this form of treatment. When combined with alum[9] it is considered by Meigs and Pepper to be one of the most valuable drugs recommended. They also advise the use of potassium carbonate. Seiner trusted belladonna more than any other remedy; so also Rilliet and Barthez. William Lee, in an interesting paper in the New York Medical Journal, 1883, advocates the use of atropia hypodermically; he believes that atropia chiefly acts in these cases on the laryngeal branches of the pneumogastric nerves, and that it is probable that it has a decided effect also on the medulla oblongata itself, and renders it less capable of exciting reflex action. Kroon's experiments led him to conclude that the valerianate of atropia was the most useful. Evans[10] gave the 1/120 of a grain of atropia to a child aged three years until the pupils were dilated, then reduced the dose; this stopped the paroxysm in twenty-one days. At the commencement of the treatment the child had twenty-three paroxysms in the day, and twenty-seven at night. Case No. 2 under same circumstances recovered in fourteen days. In case No. 3 the paroxysms were reduced from twenty-six to two or three a day. Arthur Wiglesworth[11] used a solution of sulphate of atropia, administered in the morning fasting; the dose he advises for children from one to four years is gr. 1/120, given only once a day except in some cases. The results are as follows: There is a steady diminution in the number of paroxysms; a change in the character of the whoop as if the vocal cords were not so closely approximated. If atropia is withheld, the beneficent effect derived from it subsides.

[Footnote 9: Golding Bird, Guy's Hosp. Rep., April, 1845.]

[Footnote 10: Glasgow Med. Jour., 1880.]

[Footnote 11: Lancet, April 12, 1879.]

West advises dilute hydrocyanic acid, and many writers agree with him, ranking it next to belladonna.

Harley and others are strong advocates for the bromide of ammonium; it is supposed to have a local anæsthetic action on the pharyngeal and laryngeal mucous membrane. Fordyce Grinnell[12] during four months treated 223 cases with this remedy, and highly recommends it. The doses were in accordance with those of Dr. Kormann--3/4 to 4 grains, as indicated by age, three or four times a day and at night when the paroxysms were severe. No other treatment was used in these 223 cases, except camphorated oil to the throat and chest in some cases. Potassium bromide has been recommended by Helenke, Beaufort, Erlenmeyer, and others. Henry Field[13] recommends sodium bromide.

[Footnote 12: Med. News, 1882.]

[Footnote 13: Brit. Med. Jour.]

Probably next to belladonna in the treatment of this disease we should place chloral hydrate.

Hebner, after an elaborate study of the relative value of potassium bromide, quinia, salicylic acid, chloral, and belladonna, says: "Salicylic acid and chloral tend to relieve the paroxysms--belladonna and quinia to shorten the disease." Kennedy[14] writes: "I cannot doubt {847} its specific effects on the cough. Chloral seems to me to yield the best and most constant results. The advantage of chloral hydrate seems to exist in producing sleep; it should be given in from 2- to 5-gr. doses, at night." If there is much irritability or fretfulness, or any premonition of eclampsia, it should be associated with potassium bromide.

[Footnote 14: Dublin Jour. M. S., 1881.]

Croton chloral has received much praise from those who have used it; we have had no experience with it.

We have already alluded to the value of quinia, which has been used largely in this disease, both internally and as a local application. Originally recommended in the latter manner on account of its power of controlling the development of low organisms, it has not proved so satisfactory or valuable as when given internally. Binz in 1870 was perhaps the first to recommend quinia given frequently and in solution, and Dawson in 1873[15] reports excellent results from the sulphate or muriate of quinia given in full and frequent doses, and in such solutions as will not prevent its acting on the mucous membrane in its passage through the pharynx. Breidenbach[16] gives the quinia muriate in larger doses--one and a half to fifteen and a half grains per diem. The effects were surprising as soon as the proper dose for each person had been determined; this, he says, is the keynote of success. To prevent complications he continued it for a long time in small doses.

[Footnote 15: Am. Jour. Obstetrics.]

[Footnote 16: Practitioner, Feb., 1871.]

Our own experience favors the view that quinia, when given in solution or suspended in mixture, is valuable in many cases of this disease; it can be ordered in powder, and given in a spoonful of simple syrup or of the preparation known as the syrup of yerba santa, which makes an excellent vehicle. Liquorice also disguises the taste of quinia admirably for children.

Albrecht[17] has found from an experience of ten cases of whooping cough in children between the ages of one and a half and nine years, all of a marked scrofulous type, much benefit from the muriate of pilocarpine, given in small doses after every fit of coughing. To prevent collapse, he advises that it should be given in a mixture containing a little brandy. After twenty-four hours of its administration an obvious change for the better takes place in the appearance of the mucous membrane of the throat, velum palati, and uvula, which becomes paler, less swollen, and more moist; laryngoscopic examination shows a similar improvement. During the catarrhal period cold compresses to the neck and sweetened milk containing potassium chlorate are used instead of the pilocarpine, which is to be resumed as soon as a whoop recurs.

[Footnote 17: London Med. Rec., March 15, 1882, p. 110.]

Dr. Tordeus, of the Hospice des Enfants Assistés, Brussels, states that he has found the sodium benzoate useful in whooping cough, diminishing the frequency and violence of the paroxysms, and by its action on the pulmonary mucous membrane preventing those pulmonary complications which so frequently supervene and constitute the danger of the disease.

Sulphur has been largely used by the Germans in two- or three-grain doses, and is said to be greatly esteemed by them. Cantharides has been recommended, and it is stated that when strangury is produced the whoop will cease; we should consider this rather severe treatment. The {848} fluid extract of castanea is used by many with undoubtedly good results, though this also has been somewhat of a disappointment in the way of treatment, as at one time it was looked upon almost as a specific. Many claim that an infusion of the fresh leaves gives a better result. Dewar[18] regards ergot with great favor in the treatment of pertussis. Certainly in those cases where, from violent straining, hemorrhages have taken place we have found it to be highly valuable. We have had no experience with it in the treatment of ordinary cases, though Dewar claims that it shortens the attack. The ammonium picrate, and recently resorcine, have been used with success.

[Footnote 18: The Practitioner, London, May, 1882.]

Counter-irritation to the neck and chest has always been found useful in the treatment of this disease. Autenreith[19] recommends tartar emetic to the epigastrium till vesicles appear and even ulcerate. Milder forms of counter-irritation over the chest seem equally efficacious if continued for some time. The oil of amber, when used in liniment with camphor or turpentine, is by some considered almost a specific. Great care should also be observed in the dress of children with whooping cough. Warmth about the chest is always indicated, while there should be nothing close or tight about the throat allowed.

[Footnote 19: Dict. des Sciences Med., 1813.]

In the third stage, when there is the nervous element remaining, tonics, such as cod-liver oil, iron, the phosphates and hypophosphites, are required.

The diet should be nutritious, easy of digestion, and abundant, and the bowels should be kept regular by fruits or laxatives. Over-feeding should of course always be avoided, and the attempt at weaning a babe with this disease would certainly meet with unfavorable results.

Bicarbonate of soda or lime-water should be given freely with the milk taken by children with this disease. Milk certainly should form the basis of the diet of children with pertussis, and reliable meat-extracts are to be recommended in this disease even for older children, who from the severity of the attack would vomit more solid food. If the vomiting be so severe as to affect nutrition, the child should be sustained by peptonized milk, soup, or gruel, given by the bowel.

The importance of a proper regulation of the temperature of the air which the patient breathes is especially recognized in France. If the attack occurs in mid-winter and the seashore be inaccessible or inexpedient, the child should be restricted to a well-ventilated nursery or suite of rooms, the temperature of which should be kept uniform.

Salt air is recognized to be of great value in advanced cases of this disease; this has been attributed partly to the effects of stimulation of the mucous membrane in rendering less viscid and more copious the bronchial secretions, and also to the balmy softness and great purity of the atmosphere at the sea-shore. But probably there is another element in the local action of the chloride of sodium, either in establishing a resistance on the part of the patient or in modifying the germ of the disease.

The most serious complication of whooping cough is pneumonia. It occasionally happens that an attack of croupous pneumonia may develop during the course of whooping cough, but in the vast majority of cases the disease is of the catarrhal type. When, indeed, it is remembered that a bronchial catarrh, which is the invariable precursor or accompaniment {849} of catarrhal pneumonia, is a constant factor in whooping cough, and, further, that all conditions of debility, and especially of enfeebled or embarrassed respiration, dispose to this form of pneumonia, it is not surprising that this complication should be of such frequent occurrence. It is not impossible that in aiming at securing sufficient fresh air and out-door exercise to maintain the general health, an injudicious degree of exposure may be permitted which will aggravate the existing bronchitis and induce an extension of inflammation to the alveoli. But usually the catarrhal pneumonia develops in a subacute and more or less insidious manner, and without being traceable to any such exposure. It may happen occasionally that in the violent inspiratory efforts at the close of the paroxysms irritating secretions may be sucked from the bronchioles into the alveoli, and there excite inflammation. Or, again, it doubtless happens frequently that, with the existence of swelling of the bronchial mucous membrane and of viscid secretions in the bronchial tubes, collapse of portions of lung tissue is developed by the forcible expulsion of air during the paroxysms of cough, which cannot be replaced owing to the relative weakness of inspiration and to the ball-valve action of the plugs of mucus in the obstructed bronchioles. The intimate relation between pulmonary collapse and catarrhal pneumonia is familiarly known. It is not to be considered that the mere occurrence of collapse will induce pneumonia in the areas affected, but certainly it will aid in rendering effective the other irritating causes. As a consequence, it usually happens that when catarrhal pneumonia occurs in whooping cough it is associated with more or less collapse. When, then, especially in children of debilitated or rachitic constitution, or in those who are subjected to unfavorable hygienic influences, such as overcrowding, bad air, and the like, there is a rather gradual development of dyspnoea, with increasing debility, emaciation, and evidences of impaired oxygenation of the blood, it is to be feared that this serious complication has developed. The physical signs are often difficult of interpretation, but if careful examination of the chest be conducted, together with thermometric observations, the approach of this danger or its actual presence may be detected. The result is fatal in a large proportion of cases, so that suitable treatment--for the details of which reference is made to the appropriate section--must be instituted without delay.

* * * * *

Our investigations of this disease have led us to the conclusion that we have to deal with an affection caused by a specific germ, which is usually, after a period of incubation, made manifest by a catarrh of a portion of the air-passages; that this catarrh, existing for an indefinite period, is capable of being influenced by medication, applied either by means of inhalation or by acting on the mucous membrane after absorption by the stomach. In this way we have known the administration of quinia and of alum diminish the number of paroxysms, to all appearance checking the excessive secretion to a marvellous extent. The other element of the disease, the neurosis, which soon follows the initial catarrh, and seems to last for an indefinite time after the mucous membrane has regained its normal appearance, is also capable of being controlled by the use of drugs, especially belladonna, chloral, the bromides, and hydrocyanic acid, not to speak of the other antispasmodics and sedatives, and by the {850} analgesic effect of carbonic acid gas, or by the spray of bromide of ammonium, carbolic acid, and other substances upon the larynx.

Vogel tells us in his classical work on children, "If now, as a résumé, I would give an explanation of my views, it would go to show that there never has been, and most probably never will be, a remedy by which whooping cough may be abridged, any more than we are able to cut short the acute exanthemata or typhus fever or pneumonia." And yet the experience of many whom we have quoted in this article tends to support the view that by a form of treatment calculated to act on the two elements of the disease which we have just noted, the affection can be greatly modified in its intensity, and probably the attack be somewhat shortened. Certain it is that the recent studies of this disease give us hope that the day is not far distant when the cause, whatever it is, will be definitely known, and if it is found to reside in the secretions from the larynx, that treatment by inhalation or atomization will modify or destroy it, and prevent its dissemination.

{851}

INFLUENZA.

BY JAMES C. WILSON, M.D.

DEFINITION.--A continued fever, occurring in widely-extended epidemics, and due to a specific cause; it is characterized by early catarrh of the mucous membrane of the respiratory tract, and in many cases also of the digestive tract; by quickly oncoming debility out of proportion to the intensity of the fever and the catarrhal processes; and by nervous symptoms. There is a strong tendency to inflammatory complications, especially of the lungs. Uncomplicated cases are rarely fatal except in feeble and aged persons. An attack does not confer immunity from the disease in future epidemics.

SYNONYMS.--Febris catarrhalis; Defluxio catarrhalis epidemicus; Catarrhus a contagio; Rheuma epidemicum; Cephalalgia contagiosa; Epidemic catarrhal fever; Tac; Horion; Quinte; Coqueluche; Ladendo, also written La Dando; Baraquette; Générale; Coquette; Cocotte; Allure; Follette; Petite poste; Petit courier; Grenade; La Grippe; Ziep; Schaffhusten and Schaffkrankheit; Huhner-Weh; Blitz-Katarrh; Mödefieber; Mal del Castrone. There are also several names indicating its supposed origin; thus it has been called in Russia, Chinese catarrh; in Germany and Italy, the Russian disease; in France, Italian fever, Spanish catarrh, and so forth.

It is a remarkable fact that in two instances at least the popular name for the disease under consideration has found its way widely into medicine and medical literature, almost to the exclusion of the studied terms by which science has sought to designate it; these are influenza and la grippe.

Such obsolete and now meaningless terms as Peripneumonia notha (Sydenham, Boerhaave), Peripneumonia catarrhalis (Huxham), Pleuritis humida (Stoll), have been omitted from this list of synonyms as being of interest rather to the student of medical history than to the student of medicine.

Febris catarrhalis, Defluxio catarrhalis epidemicus, Rheuma epidemicus are terms which no longer retain the place given them in the literature of influenza by the older medical authorities.

Catarrhis a contagio (Cullen) and Cephalalgia contagiosa are derived from a view of the nature of the disease, which has been the cause of no little controversy.

Epidemic catarrhal fever is, with its Latin equivalent, the most satisfactory of the so-called scientific names by which the disease is at present known.

In the popular names for the affection there is to be noted an {852} indication of the national character of some of the peoples who have suffered from its frequent visitations.

Among the English it is known as cold or epidemic cold, or, in deference to medical authority, as catarrh or epidemic catarrh; and at present, both among the folk and the doctors, as influenza. Englishmen are neither quick to see in the disease a resemblance to some common circumstance or thing, nor are they disposed to make a joke about it.

The Germans find obvious resemblances. In the labored respiration and the character of the cough they find a suggestion of a common epizoötic affecting the sheep, hence Schaffhusten and Shaffkrankheit; or, because the cough is like the crowing of a cock and the disturbance of respiration and rapid prostration suggest some resemblance to a common disease of the domestic fowl, it has been called Huhner-Weh (chicken disease, whooping cough), and Ziep, which is about equivalent to pip. They call it also, from its rapid invasion, Blitz-Katarrh, and from its diffusion, Mödefieber.

The French are disposed to make a jest of everything, and the more serious the subject the better the joke. Hence they have found a new name for almost every great epidemic, and each more trivial than the last. Thus, tac (rot); horion (in jest, a blow); quinte, because the spells occur at intervals of five hours (sic); coqueluche (a hood or cowl), from the cap worn by those suffering from the malady; and so on through the long list given above.

La grippe is said to be derived from the Polish Chrypka (Raucedo); it may, however, be derived from agripper (to seize).

Influenza is of Italian derivation. It is said that the disease received this name because it was attributed to the influence of the stars, or from a secondary signification of the word indicating something fluid, transient, or fashionable.

HISTORICAL SKETCH.[1]--Epidemics of influenza have been clearly recorded only since the beginning of the sixteenth century. There are numerous accounts of earlier epidemic diseases resembling it, but they are not sufficiently particular to warrant us in inferring its undoubted existence. It is supposed to be referred to in the writings of Hippocrates, who, however, gives no exact description.[2] An outbreak in the Athenian army in Sicily (415 B.C.), recorded by Diodorus Siculus, has been supposed to have been influenza. Despite these statements, and those of others to the effect that it is a disease known from a remote antiquity, it may be said that no accounts can be confidently established, as referring to the disease now known as influenza, in the writings of classical antiquity.[3]

[Footnote 1: See also The Continued Fevers, by the author of this paper, New York, 1881.]

[Footnote 2: Parkes, Reynolds's System of Medicine, vol. i., 1868.]

[Footnote 3: Zuelzer, Ziemssen's Cyclopædia of Medicine, vol. ii., 1875.]

As early as the ninth century several epidemics of catarrhal fever, Italian fever, and the like, which were probably influenza, were made matter of history. In the year A.D. 827 a cough which spread like the plague was recorded. In 876 there appeared in Italy a similar epidemic, which spread with great rapidity over all Europe. It is related that dogs and birds suffered with symptoms not unlike those characterizing the affection in man. In 976, Germany and all France suffered from a fever of which the chief {853} symptom was cough. No further epidemic is noted until two centuries later, when, in 1173, a widespread malady, of which the symptoms were chiefly catarrhal, raged throughout Europe; while less important epidemics of a like character are recorded as having occurred during the following century (1239-99).

In the medical writings of the fourteenth century there are to be found records of six epidemics, and in the fifteenth seven great visitations of influenza are described (Parkes).

Aitken[4] speaks of a very fatal prevalence of influenza throughout France in 1311, and of an epidemic in 1403 in which the mortality was so great that the courts of law in Paris were closed in consequence of the deaths.

[Footnote 4: Aitken's Practice of Medicine, vol. i., 1872.]

Influenza is mentioned in the Annals of the Four Masters as having prevailed in Ireland in the fourteenth century, and a disease characterized by similar symptoms is alluded to in early Gaelic manuscripts under the name of Creatan (creat, the chest). The disease is described also in an Irish manuscript of the fifteenth century under the terms Fuacht and Slaodan.[5]

[Footnote 5: Theophilus Thompson, Annals of Influenza, 1852.]

The earliest epidemic that prevailed in the British Isles of which any accurate description remains is that of the year 1510. The disease came from Malta, and invaded first Sicily, then Italy and Spain and Portugal, whence it crossed the Alps into Hungary and Germany as far as the Baltic Sea, extending westward into France and Britain. Its track widened over the whole of Europe from the south-east to the extreme north-west, and it is said that not a single family and scarce a person escaped it. It was attended by a "grievous pain in the head, heaviness, difficulty of breathing, hoarseness, loss of strength and appetite, restlessness, retchings from a terrible tearing cough. Presently succeeded a chilliness, and so violent a cough that many were in danger of suffocation. The first day it was without spitting, but about the seventh or eighth day much viscid phlegm was spit up. Others (though fewer) spat only water and froth. When they began to spit, cough and shortness of breath were easier. None died except some children. In some it went off with a looseness, in others by sweating. Bleeding and purging did hurt."[6] Blisters were commonly employed--two each upon the arms and legs, and one to the back of the head. The description is sufficiently clear to place the nature of this epidemic beyond all doubt.

[Footnote 6: Thomas Short, A General Chronological History of the Air, Weather, Meteors, etc., London, 1749; quoted in the Annals of Influenza.]

The epidemic of 1557, starting westward from Asia, spread over Europe, and then crossed the Atlantic to America. The malady broke out in England, after a season of unusual rain and great scarcity of corn, in the month of September. "Presently after were many catarrhs, quickly followed by a more severe cough, pain of the side, difficulty of breathing, and a fever. The pain was neither violent nor pricking, but mild. The third day they expectorated freely. The sixth, seventh, or at the farthest the eighth day, all who had that pain of the side died, but such as were blooded on the first or second day recovered on the fourth or fifth; but bleeding on the last two days did no service." "Some, but very few, had continual fevers along with it; many had {854} double tertians; others simply slight intermittent. All were worse by night than by day; such as recovered were long valetudinary, had a weak stomach, and hypped." Gravid women either aborted or died. This epidemic spread with frightful rapidity. Thousands were attacked at the same time. The entire population of Nismes, with scarcely an exception, fell ill of it upon the same day. It was extremely fatal. In Mantua Carpentaria, a small town near Madrid, it broke out in August, and so fatal were the bloodletting and purging which constituted the treatment at first, that, of the two thousand persons who were bled, all died. The disease raged in some parts till the middle of the following year (1558), and carried off, in Delft alone, five thousand of the poor. In all cases mild treatment was called for, with warm broths and speedy immersals, "to recall the appetite and keep the vessels of the throat open."

In 1580 a great epidemic of influenza spread from the south-east toward the north-west over Asia, Africa, and Europe. From Constantinople and Venice it overran Hungary and Germany, and reached the farthest regions of Norway, Sweden, and Russia. It spread into England, and has been described by Dr. Short. In Italy it prevailed during August and September, in England from the middle of August to the end of September, and in Spain during the whole summer. In most places its duration was about six weeks. As a rule, the termination was favorable, although the disease ran a somewhat protracted course. In the account of Dr. Short it is stated that "few died except those that were let blood of or had unsound viscera." In some places, on the contrary, the course of the disease was very severe. In Rome two thousand died of it, according to the author just cited, but Zuelzer informs us that the victims of this epidemic in the Eternal City were not less than nine thousand, and adds that Madrid must have been almost depopulated by it. This high mortality has been attributed to the bloodletting practised in the treatment of the disease. The symptoms were similar to those of the previous epidemics, with a greater shortness of breath, which continued in many cases for some time after the disappearance of the catarrhal trouble. There was great sweating at the end of the attack. The plague, measles, and small-pox prevailed also, and with considerable violence, during the year 1580.

Influenza, unfelt for several years, reappeared in Germany in 1591; an epidemic extending from Holland through France and into Italy occurred in 1593. In 1610 catarrh is said to have prevailed throughout Europe. In 1626-27 epidemic catarrhal fever made its appearance in Italy and France; in 1642-43 in Holland; in 1647 in Spain and in the colonies of the Western World; and again, in 1655 in North America. According to Webster,[7] this epidemic of 1647 was the first catarrh mentioned in American annals.

[Footnote 7: Noah Webster, A Brief History of Epidemic and Pestilential Diseases, London, 1800.]

In 1658 and 1675 it again visited Austria, Germany, England, etc. The first of these two epidemics is described by Willis,[8] and the second by Sydenham,[9] as they occurred in England, and the accounts are to be {855} found in the Annals of Influenza. It is about this period that the disease began to be known as influenza, and it is not without interest to observe that the influence of the stars suggested itself, in connection with its sudden appearance and wide prevalence, to the minds of the physicians of this date. Willis writes that "about the end of April (1658), suddenly a distemper arose, as if sent by some blast of the stars, which laid hold on very many together; that in some towns in the space of a week above a thousand people fell sick together."

[Footnote 8: Dr. Willis, The Description of a Catarrhal Fever Epidemical in the Middle of the Spring in the Year 1658: Practice of Physick, 1684.]

[Footnote 9: The Epidemic Coughs of the Year 1675, with the Pleurisy and Peripneumony that supervened: from the Works of Thomas Sydenham, M.D.]

Epidemics are recorded as having occurred in Great Britain and Europe in 1688, 1693, and in 1709. The disease raged in 1712 widely over Europe from Denmark to Italy.

In 1729-30 a widespread epidemic swept over Europe. In five months it extended over Russia, Poland, Germany, Sweden, and Denmark. In Vienna sixty thousand persons fell ill of it. In the autumn it spread to England, and reached France and Switzerland; from there it extended to Italy, and by February it had reached Rome and Naples. Spain did not escape its ravages, and it is said to have found its way to Mexico. The symptoms did not differ in any important respect from those already described as characterizing previous epidemics. Pains in the limbs and fever marked the onset of the attack; catarrh, oppression, hoarseness, cough followed. In some cases delirium, drowsiness, and faintings occurred. A petechial eruption was observed, in some instances, between the fourth and seventh days. This renders it probable that typhus or cerebro-spinal fever prevailed at the same time. Turbid urine, copious sweats, bilious stools, and nose-bleeding were often noted. In Switzerland only children and old persons died. The disease was not very fatal.

Two years later (1732-33) an epidemic, starting from Saxony and Poland, overran Germany, Switzerland, and Holland, and invaded Great Britain in the month of December. Toward the end of January it spread in a south-easterly direction to France, Italy, Spain, and westward to North America, thence southward to the islands of the West Indies, and on to South America. The course of the disease in this epidemic was favorable. The attack terminated in from three to fourteen days, with sweating, bleeding from the nose, or an abundant discharge from the nasal passages. The aged and those suffering from chronic pulmonary diseases mostly perished. In Scotland three forms of the affection were described--namely, the cephalic, the thoracic, and the abdominal. The epidemic slowly spread over Eastern Europe and in a south-easterly direction, and may be said to have lasted till 1737.

Concerning this epidemic John Huxham of Plymouth wrote as follows:[10] "About this time a disease invaded these parts which was the most completely epidemic of any I remember to have met with; not a house was free from it; the beggar's hut and the nobleman's palace were alike subject to its attacks, scarce a person escaping either in town or country; old and young, strong and infirm, shared the same fate." The malady had raged in Cornwall and the western parts of Devonshire from the beginning of February; it reached Plymouth on the 10th, which was on a Saturday, and that day numbers were suddenly seized. The next day multitudes were taken ill, and by the 18th or 20th of March scarcely {856} any one had escaped it. "The disorder began at first with a slight shivering; this was presently followed by a transient erratic heat and headache and a violent and troublesome sneezing; then the back and lungs were seized with flying pains, which sometimes attacked the heart likewise, and though they did not long remain there, yet were very troublesome, being greatly irritated by the violent cough which accompanied the disorder, in the fits of which a great quantity of a thin, sharp mucus was thrown out from the nose and mouth. These complaints were like those arising from what is called catching cold, but presently a slight fever came on, which afterward grew more violent; the pulse was now very quick, but not in the least hard and tense like that in a pleurisy; nor was the urine remarkably red, but very thick, and inclining to a whitish color; the tongue, instead of being dry, was thickly covered with a whitish mucus or slime; there was an universal complaint of want of rest and a great giddiness. Several likewise were seized with a most racking pain in the head, often accompanied by a slight delirium. Many were troubled with a tinnitus aurium, or singing in the ears; and numbers suffered from violent earaches or pains in the meatus auditorius, which in some turned to an abscess. Exulcerations and swellings of the fauces were likwise very common. The sick were in general very much given to sweat, which, when it broke out of its own accord, was very plentiful and continued without striking in again, and did often in the space of two or three days wholly carry off the fever. You have here a description of this epidemic disease such as it prevailed hereabouts, attacking every one more or less; but still, considering the great multitude that were seized by it, it was fatal to but few, and that chiefly infants and consumptive old people. It generally went off about the fourth day, leaving behind a troublesome cough, which was very often of long duration, and such a dejection of strength as one would hardly have suspected from the shortness of the time.

"On the whole, this disorder was rarely mortal, unless by some very great error arising in the treatment of it; however, this very circumstance proved fatal to some, who, making too slight of it, either on account of its being so common or not thinking it very dangerous, often found asthmas, hectics, or even consumptions themselves, the forfeitures of their inconsiderate rashness."

[Footnote 10: Observations on the Air and Epidemical Diseases, translated from the Latin, London, 1758.]

Arbuthnot also described this visitation of the disease.[11] He regarded the uniformity of the symptoms in every place as most remarkable, and tells us that during the whole season in which it prevailed there was "a great run of hysterical, hypochondriacal, and nervous distempers; in short, all the symptoms of relaxation."

[Footnote 11: An Essay concerning the Effects of Air on Human Bodies, London, 1751.]

During the years 1737-38 influenza again swept over England, North America, the islands of the West Indies, and France; in 1742-43 it prevailed in Western Europe and the British Isles; in 1757-58 in North America, the West Indies, France, and Scotland. In 1761 it overran the North American colonies and the West Indies.

The epidemic of 1762 extended very generally over Europe and Great Britain. In Germany nine-tenths of the population were attacked by the disease.

Widely extended epidemics prevailed in Europe and America in 1767 {857} and 1775; in 1772 it raged in North America; in 1778-80, in France, Germany and Russia. Noah Webster found influenza prevalent in North America in 1781; the next year one of the most remarkable epidemics of this disease (described as the epidemic of 1782) appeared in Europe. It came from the East, from Asia into Russia. From St. Petersburg it spread during the winter and spring over Sweden, Germany, Holland, and France. In the autumn it was in Italy, Spain, and Portugal. The crews of Dutch and English ships were taken ill with the disease upon the high seas.

In Vienna three-fourths of the population fell ill of it with such suddenness that it got here for the first time its name of "Blitz Katarrh" (lightning catarrh). It was characterized by great pain in the back, breast, and throat, and by extraordinary enfeeblement. Relapses occurred, and inflammation of the lungs and bowels was common. Children remained relatively exempt from its seizure. This epidemic broke out in England about the end of April and raged until the end of June. "The duration of the malady in some was not above a day or two, but it usually lasted near a week or longer. In a few the symptoms seemed to abate in two or three days, but some returned and raged with more violence than at first."[12] The disease was not regarded as in itself fatal, and few could be said to have died of it "but those who were old, asthmatic, or who had been debilitated by some previous indisposition."

[Footnote 12: An Account of the Epidemic Disease called the Influenza of the Year 1782. Collected from the Observations of several Physicians in London and in the Country, by a Committee of the Fellows of the Royal College of Physicians in London. Read at the College, June 25, 1783.]

Numerous recurring outbreaks took place in Europe and America during the years 1788-90. One of these, as it occurred in America, is well described by Dr. John Warren[13] of Boston in a letter to Lettsom. This letter is dated May 30, 1790, and among other matters of great interest respecting the disease it is stated that "Our beloved President Washington is but now on the recovery from a very severe and dangerous attack of it in that city" (New York).

[Footnote 13: Memoirs of the Life and Writings of J. Coakley Lettsom, Thomas Joseph Pettigrew, 1817.]

Webster mentions an epidemic in America in 1790, one in Europe in 1795, and another in Europe in 1797, but there seems to have been no general epidemic of sufficient importance to attract the attention of other writers upon the subject until 1798, when the malady again broke out in Russia and spread over the greater part of Europe, continuing to prevail in various regions till 1803, when it again appeared in England, and is described by several writers of that country.

From 1805 to 1827 influenza prevailed (according to Zuelzer, who tells us that few years during this interval were free from it) in frequently-recurring epidemics in Europe and America. Thompson mentions no visitation in England between 1803 and 1831.

In the year 1830 began a series of epidemics remarkable for their wide diffusion and the rapid succession with which they followed one upon another. The disease began in China; in September it reached the Indian Archipelago; it swept into Russia, and invaded Moscow in November; in January, 1831, it was raging in St. Petersburg; March found it in Warsaw; April in Eastern Prussia and Silesia; in May it prevailed in Denmark, Finland, and a great part of Germany, and in {858} the same month it fell upon Paris; in June it affected England and Sweden; it was still creeping about Middle Europe and lingering in Great Britain at the end of July; in the early winter it swept southward into Italy, and westward across the Atlantic to North America, and was still harassing the inhabitants of certain regions of the United States in January and February, 1832. Meanwhile it continued in the East, spreading to Java, Farther India, and the Indian Archipelago. It continued in Hindostan after it had died out in Europe. But in January, 1833, it again visited Russia, and rolled thence southward and eastward over the most of Europe. It is recorded that by February it had reached Galicia and Eastern Prussia; in March it was in Prussia, Bohemia, and Warsaw, and had extended to Syria and Egypt; in April to many parts of Germany and Austria and to France and Great Britain. Midsummer found the disease yet prevailing in some districts of Germany and Northern Italy, and in the early autumn it was in Switzerland and Eastern France; in November it visited Naples.

Epidemics so frequent, so widespread, and so unsparing of individuals wherever the disease appeared could not fail to excite a deep and general interest. From this period the literature of the subject has been voluminous.

A brief period of repose ensued. For three years no epidemic occurred which was of sufficient importance to attract the attention of medical historians.

In December, 1837, influenza reappeared, and first, as so often before, in Russia; Sweden and Denmark were almost simultaneously affected; in January, 1837, it broke out in London, and rapidly swept over all England and into France and Germany. In January it appeared in Berlin, and shortly afterward in Dresden, Munich, and Vienna. The disease spread by February into Switzerland, and into Spain as far as Madrid by the end of March. In London almost the whole population was attacked, and the mortality was enormous. It is stated that the deaths were quadrupled during the prevalence of the disease. Large populations suffered most. This epidemic spread into the southern hemisphere, and prevailed at the same time, and consequently at exactly the opposite season that it prevailed north of the equator, in Sydney and at the Cape of Good Hope.

From 1837 to 1850-51 numerous epidemics of influenza occurred. Few years were exempt from them. The epidemic of 1847-48 has been described by many writers, and more particularly, as it occurred in London, by Peacock[14] with great exactitude. It is estimated that one-fourth of the entire population of that city were more or less affected by the disease. The epidemic prevailed in London for six months, and, although the deaths registered for the entire period as from influenza amounted to only 1739, it is stated in the report of the registrar-general that during the six weeks the epidemic was at its height not less than five thousand persons died, in the metropolitan districts, in excess of the average mortality of the period, the excess showing itself in nearly every class of disease, the local maladies which had been the predominant affections being doubtless in many cases assigned as the cause of death. This {859} epidemic affected between one-fourth and one-half of the population of Paris, and in Geneva the proportion of those attacked was not less than one-third of the entire population.

[Footnote 14: On the Influenza, or Epidemic Catarrhal Fever of 1847-48, Thomas Berill Peacock. M.D., 1848.]

More or less widespread epidemics of influenza are recorded as having occurred in 1857-58 and 1860; in 1864 in Switzerland; in 1867 in Paris in the spring; and at various times in the United States and Canada.

A mild epidemic occurred in 1874 in Berlin.

Influenza prevailed over a wide area in the United States during the early months of 1879. The characteristics of this visitation have been well described by Da Costa.[15]

[Footnote 15: "The Prevailing Epidemic of Influenza--Its Characteristic Phenomena--Pulmonary, Gastro-intestinal, Cerebral, and Nervous--Its Wide Distribution, Mortality, and Treatment," Medical and Surgical Reporter, Philadelphia, March 8, 1879.]

The disease, since the great epidemic of 1847-48, has affected a smaller proportion of the inhabitants of the localities visited, and has run a less dangerous course, than in the earlier epidemics. It has for this reason occupied a less conspicuous place in the medical literature of recent years. It is nevertheless true that even in the mildest epidemics, when a relatively small number of persons are seized and the symptoms are in most cases almost insignificant, cases do here and there occur which are of a serious or even fatal character, and that the death-rate from other diseases is for the time considerably increased.

Catarrhal affections have often prevailed among the domestic animals when influenza has been epidemic. Horses, dogs, and cats are subject to these disorders; neat cattle, goats, and sheep have been less commonly affected; chickens and pheasants have suffered, and it is stated by some of the older writers that birds, and particularly the sparrow, have deserted localities in which influenza was prevailing, and that migratory birds have taken flight earlier than usual.

These epizoötics have sometimes preceded the appearance of influenza among men by a period of some weeks or days; in other instances they have appeared at the same time; and in a widespread outbreak among horses in the United States in 1872, in which the symptoms and morbid anatomy, accurately observed, were undoubtedly those of influenza, the disease did not affect man except to a very limited extent. A want of fulness of description, and the inaccuracy of diagnosis too common in the consideration of the general diseases of the lower animals, leave the precise nature of most of the epizoötics described by the earlier writers doubtful.

An extensive influenza of moderate intensity prevailed as an epizoötic, chiefly affecting horses, during the latter part of the summer and the autumn of 1880 in Canada and the United States east of the Mississippi River. Dogs were also affected, but less generally, and human beings to a still slighter extent. In several localities where this invasion was observed by the writer the horses were first affected, the dogs next, and after the lapse of some weeks, as the animals were recovering, the disease became epidemic; but those persons who took care of horses and were much in contact with them neither suffered earlier nor more severely than others not so exposed.

ETIOLOGY.--1. Predisposing Influences.--There are no {860} well-established facts pointing to the existence of individual peculiarities that can be regarded as predisposing influences. When the disease appears a large proportion of the population is attacked without distinction of age, sex, social condition, or occupation. Previous illness, whether acute or chronic, local or constitutional, affords no protection. Aged and infirm persons and those of nervous temperament are peculiarly liable to attack, but the robust possess no immunity. All races and dwellers in every climate are the victims of influenza. In a community invaded by the disease females are apt to be the first attacked, adult males next, and children last. It has been observed that in some epidemics children are but little liable to contract the disease.

An attack confers no exemption from the disease in another epidemic, and independently of relapses, which are not infrequent, persons have been known to experience a second attack during the prevalence of the same epidemic.

Persons dwelling in overcrowded and ill-ventilated habitations and in low, damp and unhealthy situations have, in certain epidemics, especially suffered, and the increase of deaths by influenza is proportionately much greater in districts in which there is ordinarily a high mortality than in healthier places.

Influenza appears at all seasons of the year and affects the inhabitants of every latitude. It has no connection with known atmospheric conditions. Many of the earlier writers sought to establish a relation between low temperatures and sudden variations of temperature and influenza, and by reason of the confusion among the people between these diseases and common "colds" there has always existed an opinion that such a relation obtains. There is, however, no evidence to sustain this view; neither low temperature nor abrupt changes give rise to the affection. It has prevailed in hot and dry seasons, in the West Indies, on the coast of Java, in India, in Egypt, at the Cape of Good Hope, on the Riviera in summer.

The condition of the air as regards moisture, or dryness, does not influence the spread of the disease. It has occurred at sea, on low sea-coasts, and in the dryest climates, as, for example, in Upper Egypt.

Its spread is not much influenced by local winds. It does not travel with the same velocity, and even sometimes advances against them. In several well-authenticated instances a dense and foul fog has preceded and attended the local outbreak of epidemics. The much greater number of epidemics that have occurred altogether without such manifestations make it in a high degree probable that this has been a coincidence. Ozone in large quantities artificially produced may give rise to the symptoms of ordinary catarrh, but it is not a cause of influenza. The disease is not in any way connected with the condition of the soil, elevation, volcanic eruption, or any other local cause. The history of every epidemic may be adduced in proof of this statement.

Before taking up the consideration of the exciting causes of influenza, it is important to review the known facts concerning the march of epidemics and the spread of the disease in affected localities. It has prevailed with greater or less frequency in almost every region of the globe. Epidemics recur at irregular periods. It was at one time supposed that the course of the disease was cyclical, with a return at intervals of about one hundred years. This view was long ago proved to be unfounded. About every {861} twenty-five or thirty-five years great epidemics have swept over vast areas of the globe, and influenza may be said to be, at such times, pandemic. Less-widely extended epidemics have taken place with greater or less frequency in the intervals between the great outbreaks. But it is not possible to establish anything like a regular periodicity in the returns of the disease.

It has been supposed in some instances to prevail within restricted localities, as, for example, in a single city. Such local epidemics are without doubt due to local causes, and are of the nature of simple ordinary catarrhal fever, rather than true influenza.

The epidemics have extended over great areas, usually in a direction from the east or north-east toward the west and south. At other times they take the opposite course, and in some years they have appeared to radiate in various directions from several centres. It is in consequence of these facts that two views have arisen concerning the origin of the affection. The first of these is, that each epidemic starts out from some single unknown source, and spreads thence from point to point, invading more distant localities successfully as it advances, until at length it dies out in regions remote from the starting-point. This opinion is in accord with the popular belief. Thus, the Italians have called it the German disease; the Germans, the Russian pest; the Russians, the Chinese catarrh. The geographical relation of these nations indicates the usual track of the great epidemics, as shown in the foregoing historical sketch. The other opinion is, that it arises not from some single particular place, but that it may start anywhere, and that widespread epidemics are due to the successive outbreaks of the disease at many distinct points of origin.

The evidence that the great epidemics of influenza are due to some general and pandemic influence is conclusive. The point of origin of the great epidemics has not yet been indicated with precision, and must remain beyond conjecture until further facts bearing upon the question of their source are brought to light. When it has prevailed over a large portion of the earth's surface its progress from place to place has usually been rapid. In this respect, however, the epidemics show a great diversity. It sometimes travels exceedingly slowly. It is said to have overrun Europe in six weeks, and it has again taken six months to do so. It sometimes attacks places widely remote from each other within short intervals of time, and it has appeared at the same time in different quarters of the globe. It does not follow the great lines of travel and commercial intercourse.

When influenza enters a city it continues to prevail, as a rule, from four weeks to two months, but exceptionally it remains a longer time; for example, the epidemic of 1831 was prevalent in Paris for the greater part of the year. It in all instances finally disappears, and sporadic cases do not occur in the intervals between the epidemics.

In rare instances the epidemics are heralded by scattered cases. But as a rule this disease attacks simultaneously great numbers of the inhabitants of affected districts, so that, when the epidemic is severe, the sick are in a short time to be counted by thousands and business is paralyzed as by a blow. Epidemics rapidly reach their height, and subside almost as suddenly as they began. In a large city the disease frequently, perhaps always, makes its appearance nearly at the same time in several {862} different localities, affecting certain streets and quarters solely or more generally than others for a time, and spreading thus from several centres through the entire community. Large towns and cities are generally affected earlier than the villages around them, and the latter, though closely adjacent, sometimes escape for weeks. The crews of ships upon the high seas, not sailing from an infected port, are said to have suffered from the seizure, and epidemics have many times crossed the Atlantic from the Old World to the New, and more than once in the opposite direction.

2. The Exciting Cause.--Large as has been the place in medical literature occupied by the histories of epidemics of influenza, the nature of the "epidemic influence" which gives rise to the disease is still unknown.

The question of the contagiousness of influenza is one of grave interest, and has been the subject of much controversy. The great rapidity of the spread of epidemics, the vast area they overrun, the fact that they do not follow the lines of human intercourse, the suddenness with which great numbers of the inhabitants of an invaded district or city are seized, the fact that the most complete seclusion from intercourse with affected persons, or even the shutting up of houses, affords in most instances no protection whatever,--all go to show that the disease spreads, in the main, independently of direct contact. This opinion has been almost universally entertained. There is evidence, however, to show that the disease is to some extent contagious; and so convincing have the facts bearing upon this point appeared to some that they have believed it to be propagated entirely by human intercourse. Haygarth[16] declares, as the result of his observations during the epidemics of 1775 and 1782, that the influenza spreads "by the contagion of patients in the distemper;" and Falconer,[17] writing of the epidemic of 1803, says, "I have no doubt that it is contagious in the strictest sense of the word." Watson[18] regards the instances in which the complaint has first broken out in those particular houses of a town at which travellers have arrived from infected places as too numerous to be attributed to mere chance. Very often those dwelling near the invalids are attacked next in the order of time, and when the disease affects a household all do not usually manifest the symptoms at the same time, but one member after another is stricken down with it.

[Footnote 16: John Haygarth, M.D., F.R.S., On the Manner in which the Influenza of 1775 and 1782 spread by Contagion in Chester and its Neighborhood.]

[Footnote 17: William Falconer, M.D., F.R.S., An Account of the Epidemic Catarrhal Fever, commonly called the Influenza, as it appeared at Bath in the Winter and Spring of the Year 1803, Bath, 1803.]

[Footnote 18: Principles and Practice of Medicine.]

In a few rare cases the isolation or seclusion of a community has appeared to give protection, as in cloisters, prisons, garrisons, and the like; at all events, there are instances on record where segregated communities of this kind have escaped attack.

The following observation, conducted under unusual circumstances, establishes the fact that influenza may be brought from an infected city in such a way as to give rise to a localized outbreak in a remote community. Drs. Guitéras and White[19] narrate that, influenza prevailing in Europe, and particularly in Paris and London, an American gentleman in bad health contracted the disease in London, improved, suffered a relapse {863} shortly afterward in Paris, and died there at the end of December, 1879. His body was embalmed and sent home. Following the exposure of the remains of this person to the view of his family in Philadelphia there was an outbreak of influenza with characteristic symptoms, which affected, in the first place, members of that family; afterward, friends living in close intercourse with them; next, the medical attendant of some of them; and finally, the housekeeper and a patient or two of one of the physicians who wrote the paper, the whole number affected in Philadelphia being eighteen at the time of the publication of the account. Subsequently two or three other cases were developed, but the disease did not extend beyond the immediate circle of those in direct communication with the invalids.

[Footnote 19: John Guitéras, M.D., and J. W. White, M.D., "A Contribution to the History of Influenza, being a Study of a Series of Cases," Philadelphia Medical Times, April 10, 1880.]

It was at one time thought that influenza developed at once, without a period of incubation, persons in perfect health being struck down with it as by lightning-stroke. It is, however, now known that a period of incubation, varying from a few hours to several days, and usually without subjective symptoms, exists. Many instances are recorded in which persons coming into an infected city have remained well for one, two, or three days, but have eventually shared the sufferings of those into whose midst they have come. There are cases also in which the period of incubation could not have been less than two or three weeks.

There is no sufficient evidence of a causal relation between influenza and any other epidemic disease. The statement that other prevalent diseases abate in frequency and intensity upon its outbreak is not sustained by well-observed facts. Graves[20] holds that those suffering with acute diseases are less liable during the febrile stage, but that they are attacked as convalescence sets in.

[Footnote 20: Clinical Medicine.]

The facts in reference to the spread of epidemics of influenza and the course of the disease in infected localities are comprehensible upon no other theory than that of a specific infecting principle as its exciting cause. What this principle may be is not yet known; where it originates is equally unknown; and our knowledge of the influences that from time to time call it into activity and send it forth in definite directions over the earth is no less negative.

So general a disease can only be disseminated by the most general medium, the atmosphere, and its exciting cause must be capable of reproducing itself in that medium, otherwise it would be lost by dispersion in traversing distances measured by the boundaries of continents and oceans. The rapid diffusion of influenza, sweeping over continents in a few weeks at one time, its slow migration, creeping about a city and its environs for months, at another, are to be most easily explained upon the theory of a living miasm capable of being transmitted by the air, and possessing at the same time an independent existence. Such an entity would find certain localities more favorable to its growth, reproduction, and prolonged existence than others. From this point of view influenza is a miasmatic disease. The infecting principle of this disease is also, to a slight extent, capable of being reproduced in or about the human body and transmitted by personal intercourse, as well as conveyed from place to place by the persons or clothing of those affected or those travelling from localities in which the disease prevails. We are thus led to the conclusion that it is also contagious, though feebly so.

{864} CLINICAL HISTORY.--Influenza, in individual cases, presents the greatest variation as regards intensity, from the most trifling indisposition to an illness of the gravest kind, terminating in death. These variations are dependent upon--1st, the previous health of the individual, his age, and the power of resisting depressing influences which he possesses; 2d, the energy and the amount of the specific cause of the disease to which he has been exposed--in other words, the dose of the fever-producing poison; and 3d, the character of the prevailing epidemic.

It is important to observe that cases of very great severity are occasionally encountered during the prevalence of mild epidemics. In every epidemic, on the contrary, a considerable part of the community suffers from influenza in the mildest, or what has been called the rudimentary, form. This is characterized by general malaise, an easily oncoming weariness upon bodily and mental effort, a disinclination for business, some inability to fix the attention, and slight mental confusion; to these nervous disturbances are added catarrhal symptoms, as coryza, sore throat, a tickling cough, and the like; but the indisposition is subfebrile--it does not amount to a fully-developed fever. Other cases present the symptoms of an ordinary attack of acute coryza, laryngitis, bronchitis, pharyngitis, with unusual constitutional disturbance, distressing headache, and pains in the back and limbs. The fever in this class of cases does not range high, yet the patients are ill enough to betake themselves to bed.

In severe cases the onset is usually abrupt. The attack begins with shivering or a chill, or with fits of chilliness alternating with heat. Fever is rapidly established. It is usually moderate; sometimes it reaches a high grade. It shows a tendency to morning remissions. Sensations of chilliness occur; they are called forth by slight changes in the external temperature. They are often followed by flushes of heat, and are, in many cases, attended by annoying sweats. The febrile outbreak is sometimes preceded by intense frontal headache, with pain in the orbits and at the root of the nose. In other cases these pains quickly follow the chill. Sneezing, redness of the eyes and edges of the nostrils, a more or less abundant thin discharge from the nose, and lachrymation, now occur. In some instances there is bleeding from the nose. The throat becomes sore; there is a tickling sensation in the upper air-passages; a dry cough sets in, attended by more or less hoarseness and shortness of breath. The cough is paroxysmal, hard, distressing. It sometimes causes vomiting, like that which occurs in the paroxysms of whooping cough. Chest-pains, stitches in the side, frequent sneezing, loss of the sense of smell and of taste, attend the development of the general catarrhal manifestations.

The fever is attended by great depression, pains in the limbs, loss of appetite, thirst, constipation, and diminished secretion of urine. The pulse is full, but, as a rule, only moderately increased in frequency. There is in many cases slight, or even decided, blueness of the lips and finger-tips. The patient is distressed by restlessness and want of sleep. At the end of four or five days the febrile symptoms decline, at times gradually, oftener rapidly, with copious sweats or spontaneous flux from the bowels. The fever continues, however, when severe complications have taken place, ten or twelve days. The defervescence is marked by {865} an increased flow of sedimentary urine and considerable amelioration of the subjective symptoms. The catarrhal symptoms outlast the fever two or three days, but cough and expectoration may not disappear for some time.

With these symptoms are associated the evidences of functional disturbance of the nervous system. There is remarkable nervous depression; loss of strength and lowness of spirits are combined with mental weakness, or even stupor and delirium. In some cases slight convulsions take place. Cutaneous hyperæsthesia occasionally occurs, and areas of burning pain in the skin are to be met with. Neuralgia, muscle-pain, and aching referred to the bones are very common and often severe.

In other cases abdominal symptoms are prominent, while those referable to the head and chest are less urgent. The disease assumes the guise of a more or less severe catarrh of the gastro-enteric mucous membrane, with disturbance of the functions of the liver. The fever and the peculiar nervous depression are, however, the same. Cases likewise present themselves in which but little of the usual tendency to localization of the catarrhal processes is to be observed; there is fever of varying intensity, with great depression, and simultaneous and equal implication of the head and the organs of the chest and abdomen.

Many writers have sought to arrange the foregoing different forms of influenza in definite categories. It would be a useless task to reproduce their views upon the subject, or even to enumerate the varieties that have been described. In practice, the various described types merge so gradually into each other, and are so modified by the individual peculiarities of the sick, and by the complications which arise in the course of the attack in consequence of such peculiarities or of previously existing diseases or tendencies to special forms of disease, that, in point of fact, particular cases cannot usually be referred to theoretical categories. Hysterical persons and those of a nervous constitution are prone to suffer especially from the peculiar nervous symptoms of influenza. The disease is also modified by the age of the subject of the attack; children manifest in a high degree the signs of cerebral congestion, while old persons are subject in a peculiar manner to dangerous pulmonary complications, and those of a gouty or rheumatic constitution suffer more than others from muscular pains.

The duration of the mildest form of influenza is from two to three days; in well-developed cases without complications convalescence sets in between the fourth and tenth days; while severe cases with complications last much longer, several weeks often elapsing before recovery is complete.

SYMPTOMATOLOGY.--ANALYSIS OF THE SYMPTOMS.--For the purpose of separate consideration it is convenient to take up the symptoms belonging to the fever first, then those of the special catarrh, and finally those more particularly referable to the nervous system; but we encounter in the present state of our knowledge of the pathology of influenza--or our ignorance of its pathology--no little difficulty in deciding under which of these headings particular symptoms are properly to be classed, by reason of the close interdependence of the chief processes of the disease and the anomalies of its phenomena viewed as a whole.

The Fever.--The fever is of the sub-continuous or remittent type, {866} but its range is very irregular. Irregularity of temperature is characteristic of influenza and may assume diagnostic importance.

The intensity of the fever is variable. As a rule, it is moderate or slight; occasionally it is severe. I observed in several cases during the epidemic of 1879 in Philadelphia an evening temperature of only 39° C. (102.2° F.). Da Costa in the same outbreak found the febrile movement not high; the highest temperature he observed was 40° C. (104° F.). Biermer found a temperature of over 39° C. in moderate cases of catarrhal fever, and does not doubt that under certain transient conditions the temperature may reach the height of that of pneumonia or typhus. In weakly persons and the aged the fever is adynamic.

The pulse has no constant characters. Its frequency is moderately increased; it is apt to be less forcible than in health, is generally compressible, sometimes full, often irregular, changing in character in the course of a few hours.

The urine is usually diminished; sometimes its secretion is temporarily suppressed; as a rule, it shows little change, and is rarely, as in other fevers, concentrated and high-colored. It deposits on cooling a sediment of urates, which toward the close of the fever is often very abundant. The defervescence is in many instances attended by a copious secretion of urine. Albumen is not present except as a result of some complication.

At first the skin is hot and dry; later, frequent sweats occur; sweating generally attends the febrile remissions and the defervescence not rarely sets in with copious, acid, ill-smelling sweats. In some cases a tendency to sweat shows itself early and continuous throughout the attack. Sudamina occur in great numbers.

The face is often flushed, and irregular mottlings of the skin, especially upon the neck and chest, have been frequent in some of the epidemics. An outbreak of herpes about the lips is occasionally seen.

Disturbances of the digestive tract are more or less prominent in almost all cases. Only in a rudimentary and sub-febrile form are they absent. In many cases they are such as are usually seen in febrile disorders--namely, loss of appetite, thirst, impaired taste, pasty tongue, tenderness in the epigastrium, and constipation. Nausea and vomiting sometimes usher in the attack. In other cases (the so-called abdominal form) all the above symptoms are more severe, and diarrhoea, colicky pains, and vomiting are superadded. In certain epidemics the intestinal catarrh has shown a tendency to run into dysentery.

The expression of the countenance is changed, in part by the appearance characterizing an ordinary attack of coryza of considerable or great severity, and in part by anxiety and depression. It is pale. Where the pulmonary catarrh is excessive and dyspnoea great the lips become bluish. The facies sometimes suggests that of typhoid fever.

The Catarrh.--A more or less extensive hyperæmia of the mucous membrane of the respiratory tract is invariably present, and may be said to characterize the disease.

There is cold in the head, more severe in most cases than ordinary simple coryza. The eyelids are swollen and reddened, there is lachrymation, sneezing is frequent, and the discharge from the nose is abundant. Epistaxis is not rare. Sore throat, with tickling sensations and difficulty {867} in swallowing, is due to inflammation of the pharynx and neighboring parts. In many instances the catarrhal symptoms are due to a pharyngitis and tonsillitis only, the lower air-passages escaping. Hoarseness is common.

Cough is a prominent symptom. It is apt to be frequent and distressing--sometimes paroxysmal from the beginning of the sickness, almost always so at some period of its course. Its spasmodic character in some of the older epidemics led to the confounding of epidemic catarrhal fever with whooping cough. It is apt to be worse toward evening and at night, but the sick are often tormented day and night by the loud racking cough. It often leads to vomiting, and by its violence and persistence gives rise to pain and soreness in the muscles of respiration (myalgia), and occasionally to hernia. It is at first dry or attended with a scanty muco-serous expectoration; later on the sputa become opaque and muco-purulent, and in consumptive or full-blooded persons or those having mitral disease they are sometimes streaked or mingled with blood. Toward the close of the attack the cough becomes less urgent and loses its spasmodic character. In some epidemics cough is not a prominent symptom, and a few cases are encountered in most epidemics in which well-developed influenza runs its course without unusual, peculiar, or excessive cough. If the cough be due to bronchitis, we find on auscultation the physical signs of that affection. They are of course wanting when it is due simply to laryngo-tracheal irritation. Hence we frequently detect sonorous and sibillant or mucous and subcrepitant râles upon both sides of the chest in the course of the attack, as in non-epidemic acute bronchitis; and, on the other hand, cases occur where the auscultatory signs are but little or not at all altered from those of health. It is scarcely necessary to add that there are no special physical signs that can be regarded as diagnostic of influenza.

Many patients suffer from dyspnoea. Although due in some instances to complications, it occurs with remarkable frequency in those in whom none of the objective signs of any pulmonary lesion can be discovered. It is here of nervous origin. Graves assumes a direct disturbance in the function of the vagus as its cause. This view is sustained by the observation that the dyspnoea is now and then intermittent, or shows rhythmically recurring remissions, which are unattended by alteration of the physical signs. To Biermer it appears more probable that the congestions so common in influenza, not attended by marked physical signs until they lead to oedema, are to be regarded as the cause of the dyspnoea. It varies greatly in intensity. In many patients it goes on to marked oppression, great shortness of breath, precordial pain, and the like. In certain epidemics orthopnoea and suffocative attacks were very common. Stitches in the side and pain under the sternum are observed without appreciable physical signs.

Symptoms Referable to the Nervous System.--Great prostration of muscular strength is a very early symptom, and constitutes, in most epidemics, one of the remarkable features of the disease. Patients from the onset feel extremely weak, and are exhausted by the slightest bodily effort. The ordinary strength is not regained until convalescence is far advanced.

Headache is a constant symptom. Severe frontal pains are scarcely {868} ever absent. They extend across the brow and deeply about the orbits and at the root of the nose, having their seat in the Schneiderian mucous membrane and its prolongations lining the frontal sinuses and the nasal ducts. Sometimes the pain is referred also to the region of the antrum of Highmore and to the Eustachian tube and the middle ear. It occasionally extends over the whole head. Cutaneous hyperæsthesia of the head and neck and stiffness of the neck-muscles are also met with. The headache is often most intense; it lasts commonly till the end of the attack, and may even outlast it. It increases in severity with the fever and mental agitation toward evening. The occurrence of epistaxis affords some relief.

Among the more constant symptoms of influenza are very severe pains in the limbs. Patients experience sensations of soreness and bruising, such as follow the most severe and unaccustomed muscular effort. Dull, tearing, and burning pains are felt sometimes in particular muscles or tendons; sometimes they are diffused over the whole body. Distressing pains of a dragging or boring character in the loins and calves of the legs are complained of. These pains are neither relieved nor aggravated by gentle movement or by moderate pressure. A sense of contraction of the chest and precordial distress also occurs, and stitches in the side (pleurodynia), substernal pain, and pains in the throat and nape of the neck are common. When the attack is severe the patient is usually restless, sleepless, and anxious. Dizziness and a tendency to faint occur on rising, particularly in women. Mild delirium is not uncommon, but the more intense forms are occasionally observed. Active delirium was thought to be a mortal symptom in some of the older epidemics.

The inability to sleep bears no direct relation to the intensity of the fever. It is seen in some cases where fever is slight or even absent.

Somnolent states also occur. Great hebetude and torpor have marked some epidemics. That of 1712 was called the sleepy sickness, by reason of the prevalence of these symptoms.

In grave cases painful muscle-cramps, subsultus tendinum, twitchings of particular muscles, and tremblings of the hands occur.

The mental power is enfeebled, and the acuteness of the special senses is diminished.

COMPLICATIONS AND SEQUELS.--The most important complications of influenza are inflammatory diseases of the lungs. The hyperæmia and intense bronchitis already described as occurring in the severer cases cannot properly be looked upon as complications. They constitute rather essential processes of particular forms of the disease. But capillary bronchitis, catarrhal pneumonia, and less frequently croupous pneumonia, arise as complications in the course of the disease. Satisfactory statistics are wanting, but Biermer estimates that from 5 to 10 per cent. of the whole number of patients suffer from inflammatory lung-complications, and holds that the bloodletting so frequently practised by the older physicians was due to a desire to combat inflammation. The comparative frequency of chest complications in different epidemics varies greatly, but the estimate of Biermer may be accepted as an approximate average.

Owing to the masking of the physical signs in the early stages and the pre-existing pulmonary oedema, it is not always easy to recognize at once {869} the occurrence of capillary bronchitis. This complication is attended with increasing dyspnoea, decided lividity of the face and extremities, and great prostration. Crepitant and subcrepitant râles at the lower portions of the posterior dorsal regions, rapidly spreading to all parts of the chest, without dulness at first and with increased resonance later, instead of the signs of consolidation which are met with in pneumonia, are the signs which attend its appearance.

Catarrhal pneumonia occurs insidiously, with gradual intensification of the bronchitic symptoms about the fourth or fifth day, but it may set in as early as the second day, or much later, during convalescence. It is, as a rule, developed without chill or great increase in the fever.

Old persons and those of feeble constitutions are most liable to the foregoing complications.

Lobar pneumonia is less common. It is a late complication, occurring toward the close of the attack or even when the patient is beginning to get about. It is easily recognized, and differs in no wise from acute lobar pneumonia occurring under other circumstances.

In October, 1880, influenza being prevalent in Philadelphia, both epizoötic and epidemic, but very mild both among horses and men, I attended a medical student who, having had what he regarded as a cold for about a week, had kept at his work without treatment, until, upon the occurrence of a chill followed by grave thoracic symptoms, he was obliged to betake himself to bed. I first saw him the following day in the hospital of the Jefferson College. There were the symptoms of acute lobar pneumonia, with the signs of extensive consolidation of the left lung and pleurisy of the right side. Moreover, there were delirium and jaundice. The urine was non-albuminous. The next evening he died. At the same time many members of the class suffered from influenza, and a careful inquiry into the history of the case of this young gentleman satisfied me that the pneumonia had arisen as a complication in a neglected and moderate severe catarrhal fever. Until the eighth day before his death he was in excellent health. No examination of the body was permitted.

Graves[21] thought that a kind of paralysis of the lungs, with great oedema, takes place in some cases, and attributed it to an affection of the vagus. It was his conviction "that the poison which produced influenza acted on the nervous system in general, and on the pulmonary nerves in particular, in such a way as to produce symptoms of bronchial irritation and dyspnoea, to which bronchial congestion and inflammation were often superadded."

[Footnote 21: Annals of Influenza.]

It is certain that localized collapse of the lung often occurs. White and Guitéras attributed the consolidations of the lung to congestive collapse due to enlargement of the tracheal and bronchial glands and "disturbance of the great nervous tract about the root of the lung." They were enabled to satisfy themselves of the existence of glandular enlargement--adenopathie bronchique--in nine of their eighteen cases by percussion practised in the method of M. Geneau de Mussy,[22] who was the first to call attention to the importance of percussing the spinous processes of the vertebræ over the course of the trachea. Following this line in the healthy subject, a distinct tubular (high-pitched and slightly {870} tympanitic) sound is elicited by percussion down to the point of bifurcation of the trachea on the level of the fourth dorsal vertebra. Opposite the fifth and downward we get the lower-pitched pulmonary resonance. When the tracheal and bronchial glands are enlarged, the tubular sound over the upper dorsal vertebræ is replaced by dulness, which may contrast sharply, above with the tracheal, and below with the vesicular resonance.

[Footnote 22: Chirurgie médicale, Paris, 1874.]

Some well-recognized peculiarities of the so-called pneumonias of influenza give weight to the view that the consolidations are not, in the beginning, pneumonic at all. Thus, we have at first weakness of the vesicular murmur, then its absence; the respiration soon becomes bronchial, without being preceded by dulness or the crepitant râle; the extension of those consolidations from one part of the lung to another is very irregular; the process is more apt to involve both sides than one; the disappearance of the consolidation is frequently very rapid.

The relations of cause and effect between collapse and catarrhal pneumonia are so close that it is not difficult to see how the condition spoken of may lead to secondary lobular or catarrhal pneumonia. In truth, this is a frequent result of collapse from any cause.

White and Guitéras do not adduce any post-mortem facts in support of their theory. Peacock, however, observed in the epidemic of 1847 softening and enlargement of the bronchial glands in several cases, and in one instance where there was no antecedent disease of the lungs, and where the physical signs corresponded to some extent with those of the cases upon which White and Guitéras base their views.

Gangrene of the lungs must be named as one of the less common complications.

These complications are the chief cause of the danger of influenza in the aged, the debilitated, and those suffering from previous disease of the thoracic organs.

Pleurisy is rare except where there is coexisting inflammation of the lungs. It may be associated with pericarditis. In old persons serous effusions into the pleural sac are now and then encountered.

Troublesome laryngitis and chronic bronchitis may follow the attack. In consequence of the extension of the catarrhal processes along the Eustachian tube an actual inflammation of the middle ear is, in rare instances, set up. Parotitis with salivation sometimes occurs, likewise aphthous inflammations of the mouth.

Herpes labialis occasionally occurs toward the end of the attack; it is then a favorable indication.

Phthisis may be developed in consequence of an attack of influenza, and if phthisis be already established it is apt to run a more rapid course. Emphysematous affections are aggravated; diseases of the heart are unfavorably influenced; chronic nervous affections are made worse, and, in particular, neuralgias are aggravated. Old neuralgias, that have long ceased to give trouble, occasionally reappear during the convalescence.

Persons subject to latent or chronic Bright's disease are especially liable to the more serious manifestations of influenza. The fatal termination of such cases not unfrequently occurs in consequence of an attack.

Many of the older observers speak of the intermittent character of {871} influenza in certain epidemics, and its tendency to run into intermittents, particularly of a certain type, during convalescence. This has not been observed in the outbreaks of later years, and it is probable that in such instances an endemic malaria has modified the epidemic catarrhal fever, or the former has broken out as the latter passed away.

Pregnant women are in danger of aborting.

PATHOLOGY.--Our knowledge of the pathology of influenza is as yet very imperfect. Biermer has described it as the sum of a series of catarrhal manifestations developed under a common epidemic influence. The close association of the various local affections arises from their almost simultaneous occurrence as results of primary pathological processes common to them all. Each of the three groups of symptoms which make up the clinical picture of the disease--namely, the fever, the catarrh, and the symptoms referable to the nervous system--constitutes a distinct factor of influenza, and is a direct outcome of the action of the infecting principle. There is no constant interdependence among these groups, either in the order of their succession or in their intensity. Thus, while all three groups are commonly present from the beginning of the attack, any one of them may be the first to appear or have an intensity out of all proportion to each of the others. The fever is not a result of the catarrhal inflammation, nor are the nervous symptoms the result of both the others. They all spring directly from the action of the same cause.

This view is at variance with the opinion--based upon the fact that ordinary acute local inflammatory diseases, tonsillitis, bronchitis, and the like, sometimes run their course in a similar way to influenza, with fever, nervous depression, and a serious sense of illness--that influenza is a simple epidemic catarrhal inflammation.

The sudden onset of influenza, its not infrequent abrupt termination, which suggests crisis, its unsparing seizure of great numbers of the population, the severity of the nervous symptoms, and the amount of laryngo-bronchial irritation, often out of measure with the lesions of the mucous membranes,--all point to the action of a morbid agent affecting the body at large. The severity of the symptoms also, in many cases, is much greater than in similar acute non-specific local affections, while the complications, and in particular the recrudescence of fading neuralgias and the tendency to abortion, and the sequels, as cough, weakness, headaches, flying pains, which often remain long after convalescence, are evidences of its belonging to the group of infectious diseases rather than to that of simple acute inflammatory diseases.

In conclusion, it must be urged that the similarity of the symptoms in many epidemics, occurring during the course of several centuries and under different social conditions, and even different degrees of civilization, forcibly demonstrates the specific and definite character of the causes which give rise to influenza.

Very little light is thrown upon the pathology of the disease by the anatomical changes found after death. Uncomplicated influenza is rarely fatal. As a rule, the unfavorable termination is due to lung complications. The essential lesions are congestion and catarrhal swelling of the mucous membrane of the upper air-passages and the bronchial tubes. These changes may be restricted, in the lungs, to the trachea and larger {872} bronchi, or they may extend to the finest twigs. They may amount to great thickening and deep capillary injections of the mucous lining of the tubes, which contain clear, frothy mucus or thick, viscid masses of muco-purulent secretion unmixed with air.

More or less congestion of the gastric mucous membrane, and more rarely of that of the intestine, is also met with. The solitary and agminate glands of the intestine are not affected, save as the result of special complications. A few observations relate to the finding of enlarged and softened bronchial glands. More extended researches are needed, not only upon this point, but also in the whole domain of the pathological anatomy of the disease.

Hyperæmia, oedema, hypostatic congestions, splenization, catarrhal pneumonia, and hepatization affect the lung-tissue in cases fatal by the complications which are associated with such changes. The tissue-changes of diseases existing prior to the attack of influenza, such as old consolidations, tubercle, brown induration, emphysema, and so forth, are of course frequently discovered.

DIAGNOSIS.--The discrimination of influenza from other affections having some points of resemblance to it is, under ordinary circumstances, unattended with difficulty. The march of the epidemic, the number of persons attacked, the prominence of the nervous symptoms, the rapidly developed debility, and the character of the cough, usually severe out of proportion to the physical signs, distinguish it from all other epidemic diseases.

It is to be differentiated from non-specific catarrhal affections attended by fever, malaise, weakness, severe headache, and pain in the extremities by a due regard to the causative relations of the two affections. Simple catarrhs not rarely present the group of symptoms which characterize epidemic catarrhal fever, but they occur almost constantly as the result of great and sudden changes in the weather, and are therefore met with in greatest frequency in bad seasons, and are particularly common at the end of winter and in the spring. Influenza is not in any way dependent upon the vicissitudes of the seasons, and may occur, as has been shown, at all times of the year, in wet or dry, mild or cold seasons equally, and in every variety of climate. It is of course diagnosticated without difficulty from the sporadic catarrhal fevers, which lack the characteristic depression, neuralgic and rheumatoid pains, the irritative cough, dyspnoea, and so on.

Cases of influenza are met with that bear a strong resemblance to beginning enteric fever. The malaise, headache, obtunded hearing, mental depression, high fever, coated tongue, tender belly, diarrhoea, are symptoms to be observed in both affections. But influenza lacks the temperature curve, the splenic enlargement, and the eruption of enteric fever, and the progress of the disease will in a few days clear up the most doubtful case.

PROGNOSIS AND MORTALITY.--Death is rare in uncomplicated cases. The very young bear influenza badly; the old bear it more badly still. Nevertheless, children have in some epidemics enjoyed a considerable proportionate immunity. Healthy persons in the middle periods of life bear it well. Certain pre-existing diseases modify its course unfavorably; among these are chronic bronchitis, emphysema, fatty heart, and Bright's disease. {873} The debility of advanced phthisis and other exhausting diseases renders influenza dangerous. Death takes place, in by far the greater number of cases, as the result of the complication of the attack, either by some pre-existing affection or by an acute disease arising in its course. The commonest of the latter are inflammations of the parenchyma of the lungs.

Patients presenting very severe symptoms generally recover if they be not the subjects of complicating maladies or very young or very old.

Relapses are not uncommon; independently of relapses, second attacks have been known to occur during the continuance of an epidemic; it is often the case that an individual in the course of his life passes through several epidemics of influenza, and is the subject of the disease in each of them.

The prognosis is greatly modified by the character of the prevailing epidemic. In some epidemics the deaths are few, and the mortality from other diseases does not appear to be greatly augmented. In others many die of the epidemic disease, and the death-rate of certain endemic affections is much increased. In some of the older epidemics the high mortality was doubtless due to injudicious measures of treatment, among which bloodletting and other depressing agencies were conspicuous. Some of the older accounts also warrant the suspicion that a coexisting typhus had to do with the high death-rate. It is estimated that in the epidemic of 1837, which was a very severe one, 2 per cent. of those attacked died. The proportion of fatal cases in particular epidemics varies in different countries, and even in different quarters of the same city.

TREATMENT.--Efficient measures of prophylaxis are as yet unknown. Unfavorable hygienic surroundings, overcrowding, a damp, unhealthy locality, appear to increase the prevalence and severity of influenza. The opposite conditions of living do not, however, secure immunity from the attack. During an epidemic aged persons, those enfeebled by chronic diseases, and in particular those subject to chronic bronchitis, consumption, emphysema, fatty heart, and Bright's disease should be cared for with unusual diligence and solicitude, since they constitute the classes most prone to the graver complications of the disease, and from which its fatal cases are almost wholly derived. Such individuals should be warmly clad; they should shun, so far as possible, the vicissitudes of the weather, even, if practicable, keeping within warmed and well-ventilated apartments; they should exercise unusual prudence in diet and lead a carefully regulated life, with long hours of sleep. It is true that these measures are not preventive of the attack. Families not quitting the house, living in the greatest seclusion, even the bedridden, do not always, or even as a rule, escape. Yet it has frequently been observed that those whose occupations are carried on in the open air are attacked earliest and in greatest numbers. On the other hand, in rare instances, persons isolated from the community with strictness--in prisons, cloisters, hospitals--have remained free from the disease prevailing around them. It therefore appears probable that, under certain favorable circumstances not as yet perfectly understood, the avoidance of the open air and of the direct influences of the weather may confer some degree of immunity from the attack, and it is desirable that the class of persons most liable to the graver consequences of the disease should avail themselves of even the most uncertain precautions.

{874} The treatment of influenza is expectant and supporting. Not only is the epidemic self-limiting, tending to exhaust the susceptibility of a community, in most instances, in the space of a few weeks, but the attack is also of definite duration, and the perturbations set up by the action of the influenza-poison upon the individual subside spontaneously in three or four, or at most ten or twelve, days. The susceptibility of the individual is also, for the time being, exhausted, for second attacks in the same epidemic are not very common. In cases where the duration of the attack is prolonged beyond the period indicated, it is kept up by complications, and we have to do not so much with the pathological processes of influenza as with secondary diseases that the influenza has excited either by the intensity of its action or by reason of some peculiarity of the subject of the attack.

By far the greatest number of cases are light and unattended by danger. The treatment is therefore, for the most part, an extremely simple one. These lighter cases seldom require medical measures. The patients are uncomfortable and anxious, easily fatigued, and unfitted for business. It is best that they keep the house, and, if willing, the bed or sofa, for the space of two or three days. The diet should be restricted to a few simple and easily-digested dishes. Meat should be avoided. The common custom of taking hot beef-tea is an extremely bad one; it often increases the headache and languor. Moderate quantities of cold drinks may be taken. The fruit-syrups, lemonade, raspberry vinegar, a weak solution of citrate of potash or of cream of tartar, and barley-water with lemon, are useful. Very weak wine-whey is often liked. The effervescing mineral waters or Apollinaris are preferred by many persons. The best of such drinks is a mixture of equal parts of Seltzer-water and milk, iced. If the stomach be irritable, koumiss will be found an excellent beverage and food. In the mild cases stimulants are not necessary. Sound claret, with or without Seltzer-water, is not contraindicated. In all cases the amount of fluid taken should be moderate.

Quinine in moderate doses should be taken from the onset. The head-pains are not increased by it. Dover's powder, if well borne, should be administered at night. Some form of opiate may be required, even in mild cases, to counteract wakefulness. A compressed pill, containing extract of opium 0.030 gramme (gr. 1/2), camphor 0.15 (gr. ij), and ammonium carbonate 0.15 (gr. ij), will be found useful when Dover's powder cannot be employed. During convalescence iron and barks are often requisite.

The coryza, tonsillitis, laryngitis, bronchitis are to be treated according to general principles, if they require treatment at all. In most mild cases the catarrhal symptoms call for no special measures of treatment.

Free inunctions of fatty substances about the brow and over the bridge of the nose are of use as regards the coryza. For this purpose animal fats, washed lard, simple cerate, cold cream, and the like are to be preferred to cosmoline and vaseline.

Morphine dissolved in cherry-laurel water, one part in fifty or sixty, is useful for the relief of the head-pains associated with the coryza. A few drops may be snuffed up from time to time. These pains are mitigated to some degree by wearing a flannel cap or wrapping the head in a silk handkerchief. Warm applications sometimes give comfort, while cold almost invariably add to the distress.

{875} Distress in the upper air-passages and the tickling cough call for steam inhalations, and the air of the apartment may be rendered moist by the evaporation of water kept boiling in a broad, shallow vessel. Gargles of potassium chlorate, or potassium chlorate with sumac, exert a soothing influence upon the congested tonsils.

Severe cases call for more energetic measures of treatment. The most prominent indications are the control of the fever; the diminution of the hyperæmic fluxion to the mucous tracts; measures of support; the mitigation of pain and the induction of sleep; and, finally, the prevention of the pulmonary congestion, to which the depression leads by enfeeblement of the circulation. The last indication is especially urgent in infants, the very old, and those previously debilitated from any cause.

Inflammatory complications require special treatment or modifications of treatment.

The febrile movement is not, as a rule, high; grave nervous symptoms and serious catarrh may be associated with moderate fever.

An anti-febrile regimen is to be observed. The moderate duration of this fever, as compared with enteric fever, renders it less important that large amounts of fever-food should be given, while the tendency to depression makes it of the utmost importance that the administration of food be systematic and carefully looked after by the medical attendant. The disinclination to take food is so great that it is often with difficulty that a sufficient quantity can be given in the early days of the attack, and it is to be doubted whether benefit follows anything in excess of the most moderate amount. It is necessary to observe regular hours, as in the management of all the low fevers. As soon as convalescence begins the patient should be urged to eat; the quantity of food taken at one time is to be augmented, and the intervals between the meals may be longer.

A favorable action upon the excretory function of the skin and kidneys will result from the moderate drinking of water or of the beverages already spoken of. At least enough fluid should be taken to relieve thirst.

Diaphoretics have been much used, upon the theory that by determination to the skin they correspondingly diminish the tendency to hyperæmia of the affected mucous tracts. Dover's powder, solution of the acetate of ammonia, and other mild diaphoretics are to be selected. Jaborandi should be employed with caution. The wet pack and other hydrotherapeutic measures have been employed to act upon the skin and to effect a direct reduction of temperature in influenza. For old and feeble persons warm packs are employed. A profuse sweating at the onset of the attack is said to occasionally cut it short. Early diaphoresis often brings about a rapid and lasting amelioration of the symptoms. It is to be borne in mind that the fever is rarely excessive, and that sweating is not infrequently a troublesome symptom. In some epidemics it has been a very troublesome one.

General bloodletting is not to be resorted to in influenza. Its danger was apparent to some of the early writers. As has been pointed out, the high mortality of some of the older epidemics is to be explained by the venesections practised at the beginning, and even during the course, of the attack. It has no favorable effect upon the catarrhal processes, and but little upon the subjective symptoms. The fever is not relieved by it; the {876} nervous depression is increased and the risk of lung-congestion is augmented. Bleeding is not likely to be practised in epidemic catarrhal fever while the present views of its place in therapeutics continue to influence practice. Cautious local bloodletting for the relief of local inflammatory trouble is spoken of in most of the modern books. The occasions for its employment are so rare in the treatment of this disease that even this statement should be henceforth omitted. In influenza, as it is known to medical men of the present from the descriptions of the old and personal experience of the few recent and milder epidemics, bloodletting, either general or local, is clearly uncalled for.

Emetics hold a high historical place. It was of old customary to begin the treatment with a vomit. As late as the epidemic of 1837, Lombard of Geneva believed that they shortened the attack and lessened the intensity of the symptoms when administered at the beginning. In cases attended by early gastric disturbance and nausea they are said to be especially of use. They sometimes set up great irritability of the stomach, with vomiting that it is difficult to control. On the whole, the cases in which an emetic would do good are extremely rare.

Purgatives were formerly regarded as important in the treatment. This view no longer prevails. In case of constipation gentle purgation, ex indicatione symptomaticâ, is a necessary part of the proper management of the case. For this purpose the laxative mineral waters, as Friederichshalle, Hunyadi, Pullna, are excellent. Castor oil may be given, and calomel is in some cases, and particularly in childhood, of great service. Simple enemata of warm water or soap and water will often suffice. The tendency in some cases to exhausting and troublesome diarrhoea, and the fact that diarrhoea occurs spontaneously some time in the course of most cases, should inspire caution in the use of purgatives. Repeated purgation during the progress of the attack is not only useless--it is also positively injurious.

In the severe cases quinine is to be given early and in full doses. It exerts at the same time a powerful influence upon the temperature, upon the tendency to local hyperæmias, and upon the nervous symptoms, and in particular the headache. Rawlins,[23] as early as 1833, found that excellent results followed its administration, the effect being the better the earlier it was given. It has even been lauded as a specific for influenza.

[Footnote 23: London Medical Gazette, May, 1833.]

The mineral acids may be given with a view to realizing their tonic effects.

For the most part, the foregoing measures, directed against the fever, will exert a favorable influence upon the catarrhal processes. Expectorants are of advantage; ipecac is useful. The preparations of antimony are inadmissible by reason of their tendency to depress. Ammonium chloride is indicated in the earlier stages of the bronchitis. Among recent drugs, yerba santa (Eryodiction glutinosum) and the oil of eucalyptus are of use in mitigating the symptoms in epidemic catarrh, as they do in certain forms of simple sporadic catarrh.

The peculiar dry, racking cough so often present in the early days of the attack should be relieved. It is not useful in removing bronchial accumulations, being, as has been shown, in most instances out of proportion to the lesions of the bronchial mucous membrane; on the other {877} hand, it tends to increase the hyperæmia of the upper air-passages by the mechanical violence of the cough-paroxysms. Further, it is distressing and exhausting, and contributes to the muscular and nervous prostration. Benefit will be derived from keeping the air of the apartment moist, and from the occasional inhalation of the steam from hot water, either used alone or poured upon the compound tincture of benzoin, a pint to the teaspoonful, or upon paregoric, a pint to the tablespoonful, in a proper vessel or inhaler.

No drugs are more potent to this end than opium and its derivatives, and in particular morphia and codeia. The hypodermic use of the morphia salts, judiciously resorted to, constitutes our most valuable therapeutic resource in fulfilling the threefold indication of relieving cough, alleviating both the head-pain and the pains in the extremities, and in procuring sleep. The old-time dread of opium in influenza was not well founded. The administration of this drug in moderate doses is attended with advantages that far outweigh any danger of increasing the tightness across the chest and retarding expectoration. It is necessary to observe the same caution in giving it to infants and aged persons in influenza that is necessary under other circumstances. The influence of carbolic acid in restraining cough makes it a useful addition to soothing draughts in this disease.

The substernal and other chest-pains may be combated with sinapisms, turpentine stupes, repeated inunctions of fatty substances containing extract of belladonna, and the like. Pleurodynic stitches call for similar measures; a long strip of machine-spread belladonna plaster, about five centimetres (two inches) in width, applied very firmly to the side of the chest from the spine in a direction downward and forward parallel with the ribs, and reaching to the median line in front, affords great relief to the lateral chest-pains.

The control of the debility must be regarded as the most important indication in old and feeble persons. Wine, spirits, milk-punch, ammonia, spirits of chloroform, are to be used, not in accordance with fixed rules, but as occasion may require. In many cases wine or whiskey will be indicated from the beginning, the quantity being determined rather by the effect upon the circulation and the general condition of the case than by rule. Women and others unaccustomed to the use of alcoholic drinks often take wine and brandy in considerable quantities, with striking benefit and without flushing or other evidences of its disagreeing.

Chloral is inadmissible as a hypnotic by reason of its depressing effect upon the heart. Paraldehyde may be used, or the bromides in connection with opium if the latter alone is not well borne.

Diarrhoea must be managed in accordance with general principles. If slight, it does not require special treatment. It is apt to occur at one period or another in the course of most cases, and not infrequently marks the beginning of convalescence. Colic may be treated with warm fomentations and carminatives; if it be due to constipation, mild laxatives are to be combined with them.

Severe cases of influenza demand the careful attention of the physician, who must be on the alert to detect the inflammatory lung complications which so often lead up to the fatal issue as early as possible. Their treatment must be regulated by the circumstances of the case, the nature {878} of the particular complication, the age of the patient, and so on, in accordance with general therapeutical indications.

Finally, all measures, of whatever kind, that tend to depress the general nervous system or the functional activity of the respiration, and especially the heart-power, are to be sedulously avoided in the management of influenza. During the convalescence unfavorable influences of the weather are to be guarded against. It is important to warn the patient that a severe attack of influenza renders him liable for some time afterward to pulmonary disorders. The sequels, and in particular those implicating the respiratory tract, are to be appropriately treated. After severe cases a course of tonics is commonly of advantage, and a change of climate often necessary to re-establish the health.

As bearing on what is stated in the foregoing pages on the causation of influenza, reference may be made to the investigations of Seifert,[24] who claims to have found in the mucus expectorated by patients with influenza numbers of a peculiar micrococcus. It is evident, however, that no conclusions can be based upon these observations until the results have been subjected to careful examination in other epidemics.

[Footnote 24: Volkmann's klinische Vorträge, No. 240, June 20, 1884.]

{879}

DENGUE.

BY H. D. SCHMIDT, M.D.

SYNONYMS.--Break-bone fever, Dandy fever.

HISTORY.--The history of this disease dates only from the second half of the last century, though it appears very probable that previous to this time dengue existed in the tropical regions of Africa and Asia, whence it was carried to Europe and America.

In Spain the disease has been known since 1764, when, up to 1768, it prevailed in Cadiz and Seville under the name of la piadosa or la pantomina.[1] In 1780 it appeared in the form of an epidemic in Philadelphia, where it was first noticed and described by Rush under the name of bilious remitting fever, commonly called break-bone fever on account of the violent pains attending it. Next it prevailed in Calcutta in 1824, and two years afterward it made its first appearance on the southern coast of the United States, in Charleston and Savannah, where it prevailed to 1827. Toward the close of 1827 another dengue epidemic broke out in the West Indies, whence the disease proceeded to the American continent, reaching New Orleans in the spring, and visiting Charleston and Savannah in the summer and autumn of 1828.[2] In 1844 it showed itself in Mobile, and in 1848 in Natchez, whilst in 1850 it reappeared along the Southern seacoast, particularly in Charleston, from which it proceeded even to inland towns, such as Augusta, Ga.[3] In 1865 dengue appeared in Teneriffe and other Canary Islands, whilst at the same time and through the years 1866 and 1867 it prevailed in Andalusia and in some other Spanish provinces.[4]

[Footnote 1: R. H. Poggio, La calentura roja observada in sus apariciones epidemicas de los anos 1865 y 1867, Madrid (reported in Virchow und Hirsch's Jahresbericht für das Jahr 1871, vol. ii. p. 200).]

[Footnote 2: G. B. Wood, Practice of Medicine, 4th ed., vol. i. p. 444.]

[Footnote 3: S. H. Dickson, Elements of Medicine, 2d. ed., p. 747.]

[Footnote 4: R. H. Poggio, Virchow und Hirsch's Jahresbericht für das Jahr 1871, vol. ii. p. 200.]

One of the most extensive epidemics of dengue prevailed from July, 1870, to January, 1871, in Zanzibar,[5] on the East Coast of Africa, whence it extended to Aden in Arabia and Port Said in Egypt. In December, 1871, the disease appeared simultaneously at Bombay and Calcutta,[6] to which place it had been carried by transport-ships from Aden. Proceeding from Bombay in a northern direction along the railroad, it spread {880} over the central regions of the North-western Provinces, the Rajputana states, Cashmir, and the Punjaub. From Calcutta it passed over Assam and Bhotan to Thibet, and thence downward into Burmah and to all the large cities along the coast; while it also extended along the coast of Malabar over Visigapatam to Madras and Pondichery, finally arriving at Mysore. Thus the disease had actually spread over the whole Peninsula from Cape Tutikorin to the foot of the Himalayas, attacking equally all races or nationalities without regard to age, occupation, or position. Forty years previously, however, an epidemic of dengue had prevailed in Burmah. In 1873 it appeared on the island of Mauritius, to which it had been carried from India by an emigrant ship. In the same year a considerable number of cases of dengue were observed in New Orleans. In 1877 it appeared again in Egypt, where it prevailed in Ismailia.

[Footnote 5: J. Christie, "Remarks on Kidniga Pepo, a peculiar form of exanthematous disease epidemic in Zanzibar, East Coast of Africa, from July, 1870, to January, 1871," Brit. Med. Journal, July 1, 1872, p. 577 (reported in Virchow und Hirsch's Jahresbericht für das Jahr 1872, vol. ii. p. 203).]

[Footnote 6: Virchow und Hirsch's Jahresbericht für das Jahr 1873, vol. ii. p. 208.]

Finally, in 1880, dengue, in the form of a very extensive epidemic, prevailed once more along the Southern coast, visiting equally Charleston, Savannah, and New Orleans. A number of valuable observations concerning the nature and symptoms of the disease were made during this epidemic by Drs. D. C. Holliday of New Orleans, J. G. Thomas of Savannah, and F. T. Porcher and J. Forrest of Charleston.[7] At the same time it prevailed at Alexandria[8] (Egypt) to such an extent as to affect nearly the whole population.

[Footnote 7: The papers of Drs. Holliday, Thomas, and Porcher were read before the American Public Health Association at its annual meeting, December, 1880, and published in the Proceedings of the Association. Dr. Forrest's paper was published in the American Journal of Med. Science, April, 1881.]

[Footnote 8: A. Vernoni, "Le Dengue à Alexandrie d'Égypte en 1880," Gaz. hebd. de méd. et de chir., 41, 42 (reported in Virchow und Hirsch's Jahresbericht für das Jahr 1880, vol. ii. p. 5).]

Dengue has been known under various popular names which it received from the people of the particular localities where it appeared in epidemic form. Even the designation, dengue, itself, by which the disease is at present generally known to the medical profession of the leading civilized nations, is of popular origin,[9] for it is supposed to be a Spanish corruption of the word dandy, the name of dandy-fever having been jocosely conferred on the disease by the negroes of St. Thomas from the stiff carriage of those affected with it. At Zanzibar it received the popular name of kidniga pepo, signifying spasmodic pains.

[Footnote 9: G. B. Wood, Practice of Medicine, 4th edit., vol. i. p. 444.]

DEFINITION.--Dengue is a peculiar febrile disease, generally appearing epidemically in tropical or semi-tropical regions, and characterized by a single paroxysm with or without remissions, severe pains, and stiffness in the joints and muscles, a peculiar exanthematous eruption, and almost never terminating fatally.

SYMPTOMS, COURSE, AND DURATION.[10]--Dengue never commences with a decided chill, though in many cases the attack of the disease is preceded by a feeling of general uneasiness and depression, vertigo, and headache, or even by a slight chilliness--a condition which may last from a few to twelve or even eighteen hours. In the majority of cases, however, the disease appears suddenly, very frequently at night, and announces itself at once by pains and a feeling of stiffness in the muscles, joints, back, and loins; in severe cases the pain may even extend to the {881} bones.[11] The larger and smaller joints are equally affected, either simultaneously or successively, and frequently swollen, those of the hands and feet generally before the others. The pain in the joints is increased by motion, and is therefore justly regarded by most authors as rheumatic in nature. The same may be said of the muscles. Sheriff even observed redness of the skin covering the joints. According to the degree of severity of the case these pains may be more or less intense. In some cases hyperæsthesia of the skin of the palms of the hands and of the soles of the feet has been observed.

[Footnote 10: Judging from the various accounts rendered by a considerable number of observers, it appears that the clinical symptoms of dengue had been the same in all the different localities on the globe where it has hitherto prevailed epidemically.]

[Footnote 11: M. Sheriff, "History of the Epidemic of Dengue in Madras in 1872," Med. Times and Gazette, Nov. 15, p. 543 (reported in Virchow und Hirsch's Jahresbericht für das Jahr 1873).]

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