A system of practical medicine. By American authors. Vol. 1 (part 5 of 8)

A system of practical medicine. By American authors. Vol. 1 (part 5 of 8)

The cold pack is also effectual for reducing the temperature. The patient is placed upon a mattrass protected by oil-cloth, and is covered by a sheet wrung out of water at a temperature of 70°. This is covered by one or two blankets. In half an hour he is returned to bed, and will be found to have a temperature two or three degrees less than that before the bath. Another method is to apply the sheet wrung out of water at 90°, and then reduce the temperature by adding water at a lower degree from a sprinkler. In most cases, however, I prefer to reduce the temperature by the constant application to the head of an india-rubber bag containing ice. The bag should be about one-third filled, so that it should fit over the head like a cap. At the same time, as a potent means of abstracting heat, at least when the temperature is at or above 104°, a similar application should be made by an elongated rubber bag lying over the neck and extending from ear to ear. Cold applied over the great vessels of the neck promptly abstracts heat from the blood, while it diminishes the pharyngitis, adenitis, and cellulitis; which is an important gain. At the same time, it is proper to sponge frequently the hands and arms with cool water. If the temperature with this treatment be not sufficiently reduced, one or two thicknesses of muslin frequently wrung out of ice-water should be placed along the arms and upon either side of the face. By such local measures, which are agreeable to the patient and without any shock or perturbing effect on the system, we can reduce the temperature two or three degrees. By adding alcohol or one of the alcoholic compounds to the water the popular objection to the use of cold is overcome.

Trousseau, in the treatment of sthenic cases attended by a high temperature, was in the habit of placing the patient naked in a bath-tub and directing three or four pailsful of water to be thrown over him in a space of time varying from one quarter of a minute to one minute, after which he was returned to bed and covered by the bed-clothes without being dried. Reaction immediately occurred, often with more or less perspiration. This treatment was repeated once or twice daily, according to the gravity of the symptoms. Trousseau, alluding to this treatment, says: "I have never administered it without deriving some benefit." But the application of cold water in a manner that does not excite or frighten the patient seems preferable. Henoch, having a large experience, gives the following advice in reference to the water treatment: "If the fever continue high and the apparently malignant {543} symptoms described above develop, the head should be covered with an ice-bag, ... and the child placed in a lukewarm bath, not under 25° R. (88.25° F.). I decidedly oppose cooler baths, because in scarlatina, which presents a tendency to heart-failure, cold may produce an unexpected rapid collapse more than in any other affection. But I strongly recommend washing the entire body every three hours with a sponge dipped in cool water and vinegar."[9] In grave cases with a high temperature the application of cold should be sufficient to produce a decided reduction of heat, otherwise the full benefit from its use is not obtained. With proper stimulation and proper precautions prostration does not occur from the ice-bags to the head and neck and cool sponging of other parts, so long as the temperature does not fall below 102° or 103°. The danger alluded to by Henoch can only occur from the use of the pack or general bath, and the water treatment can be efficiently carried out and the temperature sufficiently reduced without resorting to these. Even Currie of Edinburgh, who first drew attention to the benefit from the cold-water treatment of scarlet fever in an age when the sweating treatment, and even the exclusion of cool and fresh air from the apartment, were deemed necessary, recommended cold affusion only in sthenic cases with full and strong pulse, and he mentions as a warning two cases with quick and feeble pulse and cool extremities in which death occurred immediately after the use of the water.

[Footnote 9: Diseases of Children.]

Sodium salicylate is in some instances a useful remedy for the reduction of heat in the infectious diseases. It seems to be more decidedly antipyretic than quinine in the febrile and inflammatory diseases, though somewhat depressing to the heart's action. James Couldrey writes to the London Lancet (Dec., 1882, p. 1064) that he has derived great benefit from its use in seven cases of scarlet fever. He administered it every two hours till ringing in the ears was produced, and afterward every four hours, prescribing one grain for each year in the age of the patient. It is, in my opinion, a proper remedy when the pulse is full and strong and the temperature is not sufficiently reduced by the cold-water treatment.

Aconite and veratrum viride reduce fever, but they are too depressing to be safely employed in grave scarlet fever, and their antipyretic effect is less than that of water. The use of digitalis might be suggested by the quick and feeble pulse in certain cases that are attended by high temperature, but the judgment of the profession is for the most part against its use in such cases. What Stillé and Maisch state of its employment in typhoid fever appears equally applicable to scarlet fever: "Even its advocates have not shown that it abridges the disease or lessens its mortality, while it is abundantly demonstrated to impair the digestion, reduce the strength, and even to occasion sudden death. The use of digitalis in other forms of fever is equally unsatisfactory, and justifies the judgment of Traube, that the true field of action for digitalis is not fever."

Quinine is the medicine which above all others has been heretofore most used, by almost common consent of the profession, to reduce the temperature in malignant scarlet fever, but its use for this purpose is, according to my observations, far from satisfactory. To obtain its {544} antipyretic action it must be administered in large doses, and if any of the quinine salts in ordinary use be administered by the mouth in sufficient quantity, they are apt to be vomited. To a child of five years five grains should be administered twice daily by the mouth, or ten grains of a soluble salt, as the bisulphate, may be given per rectum, dissolved in a little warm water. Administered per rectum, it is frequently not retained unless held for a time by a napkin. A considerable proportion of the malignant cases are attended by not only irritability of the stomach, already alluded to, but by diarrhoea, so that quinine, if administered at all, should be employed hypodermically. The double salt of quinia and urea answers for this purpose, as it is very soluble in water and does not produce inflammation of the connective tissue. When the antipyretic doses of quinine are discontinued, this agent may be prescribed as a tonic in the doses recommended for the treatment of mild scarlet fever.

In severe cases with frequent and rapid pulse, in which ante-mortem heart-clots are apt to occur, the ammonium carbonate is often useful. It should be dissolved in water and given in milk, in as large doses as five grains every hour or second hour to a child of five years. It aids in producing stronger contraction of the cardiac muscular fibres, and thus diminishes the danger of the formation of thrombi. Ten-drop doses of the aromatic spirits of ammonia may be employed instead of the carbonate, given in sweetened water. It is especially useful if the stomach be irritable.

In severe cases attended by considerable angina and foul and offensive secretions upon the faucial surface an antiseptic, as boracic acid in small quantity, should be added to the potash and iron mixture recommended above. If no drink be allowed for a few minutes after the dose, so as not to wash it too soon from the fauces, the antiseptic effect is more certainly produced. Those old enough should be directed to hold the medicine for a moment like a gargle in the throat before swallowing it. I employ boracic acid by preference, as in the following formula:

Rx. Acid. Boracic. drachm ss; Potass. Chlorat. drachm ii; Tr. Ferri Chloridi fl. drachm ii; Glycerinæ, Syrupi aa. fl. oz. i; Aquæ fl. oz. ii. M.

S. Give one tablespoonful every two hours to a child of five years.

More minute directions will presently be given for the treatment of the pharyngitis when we speak of the complications.

Alcohol, whether administered in one of the stronger wines, as sherry, or in whisky or brandy, is a most useful remedy in scarlet fever, and is indeed indispensable in all grave cases which are attended by feeble capillary circulation and evidences of prostration. Milk is also the best vehicle for this agent. The wine-whey or milk-punch should be given every hour or second hour. In scarlet fever, as well as diphtheria, comparatively large doses are required, as a teaspoonful of the stimulant every hour or second hour for a child of five years.

During convalescence the hygienic treatment already described is important. Nutritious diet and a moderate amount of alcoholic {545} stimulants are required, while the patient is kept indoors and protected from currents of air as long as desquamation is occurring. More or less anæmia is present in most convalescent patients, so that a mild tonic containing iron will aid in restoring the health. Elixir of calisaya-bark and iron; preparations of beef, iron, and wine, or the following prescription, will be found useful under such circumstances:

Rx. Ferri et Ammon. Citrat., Ammon. Carbonat. aa. gr. xxiv; Syrupi fl. oz. i; Aquæ fl. oz. ii. M.

S. Dose, one or two teaspoonfuls, according to the age, every third hour.

ANTISEPTIC TREATMENT.--It is still to be determined whether or to what extent antiseptics, administered internally, antagonize and control the scarlatinous poison, and are therefore curative of scarlet fever. The most important agent of this class, carbolic acid, can only be employed in small doses, for a dose much exceeding a drop for a child, or even exceeding a fractional part of a drop for a young child, might produce poisonous symptoms. Carbolic acid is a cardiac and arterial sedative, and it appears to reduce temperature. Intra-uterine injections of carbolized water in the treatment of puerperal fever are known to reduce temperature, even when there is no septic matter in the uterus to be disinfected and washed away, as in a case related to me in which the fever proved to be due to measles. It is not improbable that the antipyretic action in patients of this class who have no septic substance within the uterus is due largely, if not mainly, to the absorption of carbolic acid from the uterine surface and its sedative action on the vascular system. Whether this agent, so highly extolled by Declat, and to which I have alluded in a preceding page, can be safely employed in doses large enough to be efficient and curative will be determined by future observations. The same remark is applicable to the sulphocarbolate of sodium, whose antiseptic action is supposed to be due, as already stated, to the liberation of carbolic acid in the system. Since boracic acid does not seem to have any deleterious action, this agent has been administered to most of my scarlatinous patients during the last year, in addition to the older and better known remedies, and with a very small percentage of deaths. What may be the result in a more severe type of the disease remains to be seen.

TREATMENT OF COMPLICATIONS AND SEQUELÆ.--Local measures designed to diminish or cure the pharyngitis are important in all but the mildest cases. They are more especially required in the anginose variety and in those not infrequent cases in which diphtheria complicates scarlatina. Formerly it was necessary, in making applications to the fauces, to employ the brush or probang for those too young to use the gargle, but hand-atomizers, as Richardson's or Delano's, which are now in common use, afford a quick and easy method for making such applications. Six or eight compressions of the bulb of a good atomizer are sufficient to cover the fauces with the spray. Those hand-atomizers in the shops which have slender metallic points are apt to prick the buccal surface and cause bleeding if the child resist and toss the head. To prevent this, I am in the habit of directing india-rubber tubing to be drawn over the point in such a way as not to obstruct its action. The following will be found useful mixtures for the atomizer: For ordinary cases, {546}

Rx. Acidi Carbolici drachm ss, vel. Acid. Boracic. drachm ii; Potass. Chlorat. drachm ii; Glycerinæ fl. oz. ii; Aquæ fl. oz. vi. M.

If the surface of the throat be covered by foul secretions,

Rx. Acidi Carbolici drachm ss; Potass. Chlorat. drachm ii; Glycerinæ fl. oz. j; Aquæ Calcis fl. oz. vii. M.

Or else,

Rx. Tinc. Ferri Chloridi fl. oz. ss; Acidi Sulphurosi fl. drachm ii; Potass. Chlorat. drachm ii; Glycerinæ fl. oz. i; Aquæ q. s. ad. fl. oz. vi. M.

If diphtheritic exudation complicate the scarlatinous angina, or the surface of the throat in consequence of ulceration or necrosis present an appearance like that in diphtheria when the exudation begins to soften, being foul, jagged, of a dirty brown appearance from dead matter and fetid secretions, the following should be prescribed for use in the atomizer:

Rx. Acidi Carbolici drachm i, vel. Acidi Boraci drachm iii; Liq. Potassæ fl. drachm i; Potass. Chlorat. drachm ii; Glycerinæ fl. oz. ii; Aquæ Calcis fl. oz. viii. M.

Liquor potassæ, although a very efficient solvent of pseudo-membranes, is too irritating for use in the atomizer unless largely diluted. One part to eighty, as in the above mixture, will not be found too concentrated. The following powder, used every third hour through the insufflator, is also useful in cases of diphtheritic exudation:

Rx. Acidi Salicylici drachm ii; Bismuth. Subnitrat. oz. ii. M.

To be used every third hour. It is the favorite remedy of some of the prominent New York physicians in the local treatment of diphtheria.

The following mixture is also beneficial for local treatment when the faucial surface is foul and offensive from the exudations and secretions. It should be applied by a large camel's-hair pencil every three to six hours:

Rx. Acidi Carbolici gtt. x; Liq. Ferri Subsulphatis fl. drachm ii; Glycerinæ fl. oz. i. M.

In all cases of scarlatinous pharyngitis sufficiently severe to require special treatment, cool applications should be made over the neck from ear to ear, as by two thicknesses of muslin frequently squeezed out of cold water, or by the elongated india-rubber bag already recommended in our remarks relating to methods to reduce temperature.

In the first days of scarlet fever the coryza is slight, and no discharge from the nostrils occurs, so that no local treatment is required; but before the termination of the malady, in cases of ordinary gravity, a nasal discharge usually supervenes, producing more or less redness and {547} excoriating the upper lip. Moreover, in localities where diphtheria occurs, if this malady complicate scarlet fever, it is apt to affect the nostrils at the same time that the fauces are invaded. These conditions require local treatment of the nares. It should be remembered that the Schneiderian membrane is midway in sensitiveness, as it is in location, between the conjunctival and buccal surfaces, and is readily irritated by strong applications. Medicinal applications made to it must be much milder than those which the fauces tolerate. They should always be applied warm, and a teaspoonful of any mixture properly employed is sufficient for each nostril at one sitting. The applications should usually be made every two or four hours, according to the gravity of the case and the amount of discharge. The best instrument for this purpose is a small syringe of glass or brass with curved neck and bulbous tip. The child's head should be thrown back and the piston depressed rapidly, so as to thoroughly wash out the nasal cavity. The application can also be made through an atomizer with a rounded tip or a tip covered by rubber tubing. The following is a useful prescription:

Rx. Acidi Carbolici drachm ss; Sodii Chloridi drachm ii; Aquæ Oj.

The substitution of 2 or 3 drachms of boracic acid in place of the carbolic acid makes a nicer preparation. If the diphtheritic pseudo-membrane appear in the nares, the officinal lime-water, injected every hour or second hour, is beneficial in consequence of its solvent action on pseudo-membranes.

It is evident, from what has been stated above, that the condition of the ear should be closely observed in and after scarlet fever. If the patient have earache, considerable relief may be obtained in the commencement by dropping a few drops of laudanum and sweet oil into the ear and covering it by some hot application, either dry or moist, which will retain the heat. A light bag containing common table-salt, heated, or dry and hot chamomile flowers will also answer the purpose. Water as hot as can be well tolerated dropped into the ear or allowed to trickle from a fountain syringe, so as to fill the ear, is also very beneficial in allaying the pain. If a few drops of laudanum be added it is more useful. If the pain be not quickly relieved, a leech should be applied at the base of the tragus. O. D. Pomeroy, an experienced aurist of New York, says: "Leeching employed at the right time rarely fails to subdue the pain and inflammation. The posterior face of the tragus is ordinarily the best place for applying the leech, but it may be applied in front of the ear or behind, wherever the tenderness on pressure is greatest. In my opinion, paracentesis may frequently be rendered unnecessary by the timely use of one or two leeches applied to the meatus."

If the otitis continue, as shown by pain in the ear, of which children old enough to speak bitterly complain, and which causes those too young to speak to press their fingers into or against their ears, this inflammation should not be neglected, as it may involve serious consequences. Multitudes of children have had permanent impairment or even loss of hearing, with caries or necrosis of the walls of the middle ear and of the mastoid cells, which might have been prevented by prompt and skilful {548} management of the ear in the early stage of the inflammation. If, therefore, the otitis continue without mitigation of pain after the above measures have been employed, paracentesis of the drumhead is probably required. The following directions for performing this operation, which will be useful to country practitioners who may not be able to obtain the assistance of a specialist, are from the pen of Pomeroy: "The forehead mirror should be worn, in order to leave the hands free to operate by either artificial or day light. A good-sized speculum is introduced into the meatus. Then an ordinary broad needle, about one line in diameter, with a shank of about two inches, such as oculists use for puncturing the cornea, should be held between the thumb and fingers, lightly pressed, so as not to dull delicate tactile sensibility. The part being well under light, the most bulging portion of the membrane should be lightly and quickly punctured with a very slight amount of force. The posterior and superior portion of the membrane is most likely to bulge. The chordæ tympani nerve ordinarily lies too high up to be wounded. The ossicles are avoided by selecting a posterior portion of the membrane. After puncture the ear should be inflated by an ear-bag whose nozzle is inserted into a nostril, both nostrils being closed, so as to force the fluid from the tympanum. The puncture may need to be repeated at intervals of a day or two, provided that the pain and bulging return."

Albert H. Buck of New York, in a highly instructive paper read before the International Medical Congress in 1876, writes as follows of paracentesis of the membrana tympani in scarlatinous otitis: "In this one slight operation, which in itself is neither dangerous nor very painful, lies the power to prevent the whole train of disagreeable and dangerous symptoms." Buck relates an instructive example: The age of the patient was three years, and the earache had been complained of only about twenty-four hours. "Toward morning," says he, "I was sent for, as the pain had become constant.... An examination with the speculum and reflected light showed an oedematous and bulging membrana tympani (posterior half), the neighboring parts being very red, though as yet but little swollen. In the most prominent portion of the membrane I made an incision scarcely three millimetres (one-tenth inch) in length, and involving simply the different layers of the membrana tympani. This was almost immediately followed by a watery discharge (without the aid of inflation), which ran down over the child's cheek. At the end of three or four minutes the child had ceased crying, and in less than a quarter of an hour she was fast asleep. At first, the discharge was very abundant and mainly watery in character, but it steadily diminished in quantity and became thicker, till finally, on the fourth day, it ceased altogether. On the tenth day the most careful examination of the ear could not detect any trace of either the inflammation or the artificial opening." The ear had probably been saved from ulceration of the drum membrane, long-continued suppurative otitis, and perhaps from permanent impairment of hearing.

When an opening has been made in the membrana tympani either by incision or ulceration, it is advisable in some instances to inflate the tympanum by Politzer's method, which has been alluded to above. The nozzle of an india-rubber bag, with a flexible tube attached, is introduced into the nostril on the affected side, and both nostrils are compressed {549} against it. The patient fills his mouth with water, which he swallows at a given signal, as after the words one, two, three, spoken by the operator. During the act of swallowing, which opens the Eustachian tube, the rubber bag is forcibly compressed, which forces the air along the tube into the middle ear and facilitates the escape of the pent-up secretions in the tympanic cavity.

If the otitis have continued unchecked by treatment until the secretions within it, after days and nights of suffering, have escaped by ulceration through the drumhead, the opportunity for prompt and certain cure is passed. Still, the patient under these circumstances may quickly recover, or there may be the other alternative described above, in which the ear is badly damaged and chronic inflammation established in the walls of the tympanum, giving rise to an offensive otorrhoea. In this state of the ear internal remedies are indicated, such as surgeons employ in suppurative inflammations of bone occurring in other parts of the system. Cod-liver oil and iodide of iron are required, especially by patients of strumous diathesis, the object being to promote a more healthy state of system, so as to prevent extension of the inflammation and facilitate the healing process. Carbolized solutions, as the following, syringed warm into the ear in which otorrhoea is occurring, are useful in promoting cleanliness and increasing the comfort of the patient:

Rx. Acidi Carbolici drachm ss; Glycerinæ fl. oz. ii; Aquæ fl. oz. iv. M.

But recently a much more effectual curative agent for local treatment has been discovered in boracic acid, by the use of which the discharge more quickly diminishes and the condition of the ear more certainly and rapidly improves than by the use of the carbolized mixtures. When the inflammation is recent and the ear sensitive and painful, the following prescription should be used:

Rx. Acidi Boracici drachm iiss; Morphiæ Sulphat. gr. i; Glycerinæ, Aquæ aa. fl. oz. i. M.

S. Drop one to three drops into the ear three times daily.

If the acute stage of the otitis have passed, with fever and pain, and no tenderness be present on pressure, the following prescription, which causes too much pain in the acute stage, will be found useful to check the inflammation and otorrhoea and restore a healthy state to the granulating surface:

Rx. Acidi Boracici drachm iiss; Alcohol. Aquæ aa. fl. oz. i.

S. Drop one to three drops into the ear three times daily.

The beneficial effects observed from the use of boracic acid in aural surgery have given it nearly the same position as a curative agent to diseases of the ear which atropine holds to diseases of the eye. Recently, aurists are employing finely-triturated powder of boracic acid dusted into the ear. The patient lies upon the side with the affected ear uppermost. The ear is thoroughly cleaned by syringing with tepid water, and by means of a little scoop made of stiff paper or pasteboard or the segment {550} of quill as much of the powder is introduced into the ear as would cover a five-cent silver piece. By working the ear it descends to the drumhead. I can bear witness to its efficacy in the otorrhoea of children when it is used in this manner three times daily.

The following astringent has also been employed with good results for the otorrhoea resulting from scarlet fever as well as from other causes:

Rx. Zinci Sulphatis, Aluminis aa. gr. v; Aquæ fl. oz. i. M.

A few drops of this should be dropped into the ear, or, if the ear be sensitive and painful, five drops should be added to a teaspoonful of warm water and dropped or syringed into the ear.

But in recent times aurists have discovered a remedy superior to the above in iodoform, the action of which is safe and efficient for protracted otorrhoea with granulations, and it is superseding to a great extent the agents heretofore used in the treatment of this disease. The ear should first be thoroughly cleaned by syringing with warm water and dried, and iodoform, to which a little balsam of Peru is added to cover the disagreeable odor, should be pressed down to the bottom of the auditory canal by any convenient instrument. It is anodyne, astringent, and disinfectant, and should be employed in a dry state in considerable quantity.

The sequelæ of otitis media, such as granulations sprouting out from the drumhead, some of which may be of large size and are known as polypi, may require treatment by the aurist. A polypus may sometimes be removal by the forceps or better by the snare. Polypi not large and favorably located can sometimes be cured by an astringent powder, as iodoform, sulphate of zinc, or alum, or by applying the liquid subsulphate of iron. The otitis externa produced by the irritating discharge which flows from the middle ear soon disappears when the flow ceases.

The renal affection, which, as we have seen, so often commences in the declining period of scarlet fever or during convalescence in mild as well as severe cases, is frequently more dangerous than the primary disease. It largely increases the percentage of deaths. A clear appreciation of its therapeutic requirements is important, since by judicious treatment many recover who would inevitably be sacrificed by improper measures. The family should be informed that the danger from scarlet fever does not cease with the decline of the eruption, and that the kidneys may become seriously affected by too early exposure of the patient to currents of air or sudden changes of temperature, by which cutaneous transpiration is checked. He should therefore be kept indoors in a comfortable and uniform temperature three or four weeks after the termination of the fever, until desquamation has entirely ceased and the new epiderm is sufficiently thick and firm to protect the surface. During the changeable temperature of the autumnal, winter, and spring months even longer confinement at home may be advisable.

The nephritis and consequent albuminuria antedate by some days the occurrence of dropsy, and a physician should never discharge a scarlatinous patient without one or more examinations of his urine. When his visits cease the nurse should be instructed to make the examinations by heat and nitric acid during the ensuing month, and if any evidence, however slight, appear that the kidneys are involved, he should be notified, {551} in order that appropriate treatment may be immediately commenced. Early and correct treatment of the nephritis is attended by much better results than delayed treatment, and many more patients are doubtless now saved than in former times, when little attention was given to the state of the kidneys until dropsy or other prominent symptoms appeared. I have found no mother or nurse so ignorant that she could not properly employ the test of nitric acid and heat, and, if she be solicitous for the welfare of the child, she will not hesitate to carry out the directions and immediately notify the physician if the tests employed produce the least cloudiness or turbidity of the urine.

The patient as soon as nephritis commences, as shown by the state of the urine, should be put to bed in a room of warm and equable temperature (72° to 75° F.). His diet should be liquid, consisting of milk, farinaceous food, and a moderate quantity of animal broths. He may drink liquids freely, especially water not too cool, to which spiritus ætheris nitrosi is added. If he be prostrated by the primary disease, alcoholic stimulants should be allowed.

The indications are to relieve the hyperæmic kidneys by diaphoresis and purgation. To produce the former the patient should be immersed in a warm bath at about the temperature of the body (98° to 100°), in which, if he be quiet and comfortable, he should remain from fifteen to twenty minutes, but if restless and frightened by the water a less time, after which he should be placed in a warm bed and well covered by blankets. If perspiration result, the bath has been useful, and it may be employed in grave cases two or three times daily. If perspiration do not result, it may be produced by surrounding the body either by hot dry or moist air. Hot dry air may be produced by burning alcohol in a thin layer upon a plate under a chair upon which the patient sits while he is surrounded by a blanket, or he may be covered in bed and the hot air introduced under the bed-clothes. In New York a convenient apparatus is used for this purpose, consisting of a small sheet-iron pipe enclosed in a small box of the same material. The box is in the form of a trunk, with a handle for convenience in carrying, and the lower end of the pipe, which extends nearly to the floor, contains an alcohol lamp. Hot moist air may be produced by placing against the patient bottles of hot water surrounded by towels wrung out of water. The steam arising from them and enveloping the body and limbs produces a prompt sudorific effect. There is in use in this city, in the treatment of these and similar cases requiring diaphoresis, a convenient apparatus for generating steam. It consists of a cylinder pierced with holes for the admission of air and containing a spirit lamp, over which is a pan or pail holding a little water. The patient, nearly naked, is placed in a chair with the apparatus underneath, and is covered by a blanket, so that the steam surrounds the body. This gives rise to free perspiration, which continues after the patient is placed in bed. This treatment should be repeated one or more times daily, according to the gravity of the case.

The sudorific effect of the treatment by external warmth described above should be aided by employing diaphoretics. Those which have been most used are the acetates of ammonium and potassium, the bitartrate and citrate of potassium, and spiritus ætheris nitrosi. If employed when the surface is cool, they act rather as diuretics than diaphoretics. {552} These agents, being simple in their action and without deleterious effects, may be given frequently and in large proportionate doses for the age.

But lately a diaphoretic which far surpasses these in efficiency has been discovered in pilocarpine, the active principle of jaborandi. Being soluble in water and tasteless, it is easily administered, and is retained when, on account of the uræmic poisoning present in scarlatinous nephritis, the stomach is irritable and other medicines, as digitalis, are rejected. Ether may be employed with it, or the amount of alcoholic stimulant may be increased at the time of its exhibition in order to guard against any depressing effect. To a child of two years one-fortieth to one-twentieth of a grain may be given every six hours by the mouth. It may also be employed hypodermically, as one-twentieth of a grain to a child of five years. It has both a diaphoretic and diuretic action, while it stimulates both the salivary and mucous secretions. According to one observer, an adult when fully under the influence of pilocarpine secretes from one pint to one quart of saliva within two hours, and Leyden reports a case of diphtheritic nephritis in which the quantity of urine rose from half a pint to five pints daily. But its most prompt and certain action is upon the sweat-glands. Hirschfelder speaks of its beneficial action in relieving various forms of dropsy, and adds: "In one morbid condition of the kidney, however, jaborandi is the remedy par excellence, and that is the acute parenchymatous nephritis which frequently follows scarlatina.... This disease heals spontaneously if the danger that threatens life from reduction of the urine and from the effusions of fluid into the cavities of the body be averted. In this disease jaborandi works wonders." I have also found it an invaluable agent when the older remedies failed and death seemed imminent. The following cases, in which the beneficial action of this agent was apparent, occurred in my practice:

Case 8.--G----, male, aged five years and six months, sickened with scarlet fever on June 2, 1882. It began with vomiting, and was attended by a degree of febrile movement which indicated an attack of rather more than the average gravity. The fauces at one time exhibited a slight exudation like that of diphtheria. In the declining stage of the malady rheumatic pain and tenderness occurred in the wrist and finger-joints, but not in those of the lower extremities. The case, however, progressed favorably, and during the convalescence my attendance ceased. On June 24th my attention was again called to the child, when the urine was found to be scanty and very albuminous. External measures, such as are described in the foregoing pages, were employed, and the infusion of digitalis with potassium acetate ordered to be given every three hours, but this medicine was for the most part vomited. The bowels were kept open by jalap and the potassium bitartrate. The urine, however, continued scanty, and on June 28th severe convulsions occurred. At this time the quantity of urine was only fl. oz. ij in twenty-four hours. The pulse in the convulsions was quick and feeble, the skin very hot, and the axillary temperature 103°. The eclampsia continued one hour, and were controlled by large and repeated doses of bromide of potassium, aided by clysters of five grains of hydrate of chloral in water. Muriate of pilocarpine was now directed to be given in doses of one-thirty-second of a grain every three hours, dissolved in cold water. This agent was not vomited, and it must have been given by the parents in their fright and {553} anxiety in larger or more frequent doses than were directed, for on July 1st the bottle containing one grain was empty. Free diaphoresis resulted from the pilocarpine, and the quantity of urine was increased. The mother stated that the child had taken only two doses, or one-sixteenth of a grain, of pilocarpine when the diuretic effect was apparent and free diaphoresis also occurred. She also stated subsequently that the quantity of urine was larger when the pilocarpine was administered every third hour than when given at a longer interval. A flaxseed poultice on which mustard was dusted was also applied over the kidneys. On June 29th the pulse was 96, temperature 100.5°; occasional convulsive attacks occurred, which were readily controlled by enemata of hydrate of chloral. On June 30th the symptoms were all better; no more attacks of eclampsia had occurred, and the urine was more abundant and less albuminous. The mother remarked that the new medicine (pilocarpine) had settled the stomach and increased the urine. The patient continued to improve, and on July 4th the record states: "Now takes the pilocarpine, gr. 1/32, every six hours; passes urine freely since yesterday; has not vomited since he began to take the pilocarpine; pulse 106, axillary temperature 99°; is playful and takes milk freely, nearly three quarts in twenty-four hours, with some farinaceous food. Digitalis with potassium acetate is also given in occasional doses." July 6th, pulse 92, temperature 99°; perspires much, and urine nearly normal in quantity and character.

Case 9.--Mary S----, aged five years, on Dec. 22, 1882, presented the symptoms of severe nephritis. Her brother had scarlet fever two weeks previously, and she had sore throat at about the same time, but without efflorescence; pulse 98, temperature 98.5°; her urine highly albuminous, and reduced to fl. oz. iv in twenty-four hours; bowels constipated. Ordered a single dose of

Rx. Hydrarg. Chlor. Mitis gr. iii; Resin. Podophylli gr. 1/6. M.

The muriate of pilocarpine was also ordered, gr. 1/20, but the patient vomited soon after taking it. Another dose was retained, and was followed by considerable perspiration. Dec. 23d, had one stool from the powder of yesterday. Has taken five doses of pilocarpine, but vomited after three of them. The last dose was administered at 10 P.M., and the mother says she "sweat fearfully" during the night. The patient was kept warm in bed; stimulating poultices of mustard and flaxseed, one to sixteen, were constantly in use over the kidneys, and the pilocarpine was administered three or four times a day. The record for Dec. 26 states: "Took the pilocarpine four times since yesterday morning, and each dose is followed by perspiration lasting from one to one and a half hours; quantity of urine, from fl. oz. vj to fl. oz. viij daily; vomited twice yesterday, not to-day; pulse 104, temperature 97.75°; complains of frontal headache; bowels regular; has considerable salivation. The patient is warm in bed, and the flaxseed and mustard poultice over the kidneys is continued." Dec. 28th, specific gravity of urine 1019; urine still quite albuminous, and containing blood-corpuscles and granular casts, also crystals of oxalate of lime. Dec. 30th, takes gr. 1/20 pilocarpine twice daily, and occasional doses of infusion of digitalis; urine more abundant; its specific gravity 1014, slightly albuminous, and containing {554} very few granular casts and blood-corpuscles; has lost its smoky appearance; reaction alkaline; perspiration slight; patient convalescent.

In another instance, a child of five years, from three to four weeks after scarlet fever was noticed to have anasarca of the face and extremities, with scanty and albuminous urine. One-thirty-second of a grain of muriate of pilocarpine was administered every six hours without the desired sudorific effect. It was then administered every four hours, with an increase of perspiration and urination, so that the nephritic symptoms were relieved and the patient apparently out of danger within three or four days.

In a fourth patient, a girl of three years, having scarlatinous nephritis, with symptoms very similar to those in the last case, the administration of one-twentieth grain doses of pilocarpine in conjunction with the hot-air bath, was followed by increased perspiration and urination, and progressive and rather rapid convalescence. This child had been taking bichloride of mercury in one-fiftieth grain doses, prescribed by a homoeopathic physician, without appreciable benefit. It had been for the most part vomited.

Given, as in the above cases, in moderate doses and with sufficient interval, pilocarpine has never in my practice had any deleterious effect, and I regard it as a very important addition to the remedies for the relief of scarlatinous nephritis. It is apparently the most useful and important diaphoretic for this disease which we possess.

Cathartics, especially those of a hydragogue nature, are also very beneficial. Their action is more certain than that of most diaphoretics and diuretics, and their employment is imperatively required in severe or dangerous cases in which it is necessary to remove as soon as possible the serum or urea which endangers life. Young children or those with delicate stomach, and those much enfeebled by the primary disease, may take magnesia, either the citrate or the calcined. A good cathartic for ordinary cases is a mixture of jalap and potassium bitartrate, the pulvis jalapæ compositus, consisting of one part of jalap and two of cream of tartar. Ten grains of the mixture may be given to a child of five years, and repeated according to circumstances. Its effect is increased by dissolving a teaspoonful of potassium bitartrate in a gobletful of water, and allowing the patient to drink from it. The following is a good cathartic in some instances, especially if the stomach be irritable, so that the more bulky and nauseating cathartics are rejected. Care should be taken to obtain a good article, as some of the podophyllin of the shops is not reliable:

Rx. Resinæ Podophylli gr. j; Sacchari scruple j. M. Ft. in chart. No. v.-x.

S. Give one powder, and repeat according to circumstances.

In the treatment of one of the cases reported above it will be recollected that the mild chloride of mercury mite was given with the podophyllin, with a good result.

After the use of laxative agents the kidneys, being less congested on account of the diversion that has occurred, often begin to excrete urine more freely. But if the patient be anæmic or enfeebled and the symptoms are not urgent, it is frequently better to avoid active catharsis, which {555} more or less reduces the strength, and employ remedies of a sustaining character, as in the following case, which occurred in my practice: A little boy, pallid and scrofulous, began to have anasarca after scarlet fever, chiefly in the scrotum, accompanied by a moderate degree of ascites. The urine, which was passed in nearly the normal quantity, contained albumen, but not in large amount. This patient gradually and fully recovered, with no treatment except the use of an oil-silk jacket over the kidneys and abdomen to promote diaphoresis, and the use of iron. Such a patient, treated by the powerful eliminatives which we employ for the more urgent and robust cases, would probably have been injured rather than benefited. No treatment can therefore be recommended in a treatise on scarlatinous nephritis which will be strictly applicable for all cases. Variations are demanded according to the state of the patient and the form and gravity of the disease.

Diuretics which do not stimulate the kidneys are proper at an early as well as late period of the renal malady, and digitalis is the one usually prescribed. I do not hesitate to order it from the first day in combination with the acetate of potassium. One teaspoonful of the infusion may be given every third hour to a child of five years. The following formula is for one of this age in good general condition:

Rx. Potass. Acetatis oz. ss; Infus. Digitalis fl. oz. vi. M.

The following formulæ are recommended by Meigs and Pepper:

Rx. Potass. Bitart. drachm i; Spt. Junip. Comp. fl. drachm ii; Spt. Æther. Nitros. fl. drachm i; Tr. Digitalis, minim xv; Syrupi fl. drachm v; Aquæ fl oz. ii. M.

Dose one teaspoonful every two hours to a child of two to four years.

Rx. Potass. Acetat. drachm i; Tr. Digitalis fl. drachm ss; Syr. Scillæ, fl. drachm i-ii; Syr. Zingib. fl. drachm v; Aquæ q. s. ad fl. oz. iii. M.

Dose, a teaspoonful every two or three hours to children two or three years old.

Local treatment is important. L. Thomas, Romberg, and others recommend the application of leeches, three or more, over the kidneys. Thomas says: "In many cases the abstraction of blood causes immediate and permanent relief; the fever and the pain in the region of the kidneys cease, the secretion of urine becomes augmented, the albuminuria lessens from day to day, and the moderate degree of dropsy that has been developed disappears." It is only in the more robust children, who have been but little reduced by the primary disease, that leeching is, in my opinion, admissible. In the majority of cases instead of depletion a poultice slightly irritating, so as to cause redness of the skin, should be applied over the kidneys, or for older children, not likely to be frightened by the process, the dry cups may be applied daily. In subacute cases, not attended by any alarming symptoms, sufficient redness may be produced by one of the irritating plasters which the shops contain, constantly worn.

{556} Eclampsia, described in the preceding pages, is produced, as we have seen, during the course of scarlet fever by the irritating effect of the scarlatinous poison upon the nervous centres, but, occurring after the decline of scarlet fever, it is ordinarily produced by the retained urea. The same remedies are required to control the convulsive movements as when they occur under other circumstances. The bromide of potassium should be immediately administered in large and frequent doses whenever eclamptic symptoms arise. During eclampsia a child of three years should take five grains of this agent every five to ten minutes till the attack ceases, and then at longer intervals. The hydrate of chloral is a more powerful agent, and if the eclampsia be not quickly controlled, I commonly employ it per rectum, dissolved in one or two teaspoonfuls of water. For a child of three to five years five grains should be thrown into the rectum by a small glass or gutta-percha syringe, and retained by pressure. Properly administered and retained, it rarely fails to control the eclampsia within ten or fifteen minutes. Subsequently, occasional doses of the bromide should be given to prevent the occurrence of eclampsia while the measures described above are being employed to relieve the uræmic condition.

Rheumatism, endocarditis, and pericarditis, arising as complications or sequelæ, require the treatment which is appropriate when they occur under other circumstances, but the remedies should not be depressing, as the system is already enfeebled by the primary disease. The rheumatism, if mild, usually abates in a few days without medication, and the affected joints require only some soothing lotion and support by a bandage. The following liniment may be applied upon muslin and covered by cotton wadding:

Rx. Acid. Carbolici fl. drachm i; Tinc. Belladonna fl. oz. i; Ol. Camphorati fl. oz. ii;

If the rheumatism be severe and affect several joints, the sodium salicylate should be prescribed, as in the idiopathic disease, with an occasional opiate to procure rest.

Endocarditis and pericarditis require rest in the horizontal position, avoidance of all excitement, the use of the tincture or infusion of digitalis or of the fluid extract of convalaria to procure a slow and steady action of the heart. Three drops of the tincture of digitalis or five minims of the fluid extract of convalaria may be given every four hours to a child of five years. The same external measures should be employed as in acute pleuritis. I prefer the application of a thin poultice of flaxseed containing one-sixteenth part of mustard and covered with oiled silk. The cardiac inflammations, as well as rheumatism, require opiates in sufficient doses to procure rest and sleep.

Pleuritis, which we have stated is apt to be suppurative, demands the same treatment as the idiopathic disease when it occurs in cachectic patients.

{557}

RUBEOLA.[1]

BY W. A. HARDAWAY, M.D.

[Footnote 1: In the preparation of this article the writer has consulted the following works: Thomas, in Ziemssen's Cyclop. Pract. Med., vol. ii., N.Y., 1875, Am. edit.; Bohn, in Gerhardt's Handbuch der Kinderkrankh., Zweiter Band, Tübingen, 1877; Squire, in Quain's Dict. Med., N.Y., 1883; Ringer, in Reynolds's System Med., vol. i., Phila., 1879; Meigs and Pepper, Dis. of Children, Phila., 1882; J. Lewis Smith, Dis. of Children, Phila., 1882; Hebra, Dis. of Skin, London. 1866; Vogel, Dis. of Children, N.Y., 1871; Niemeyer, Handbook of Pract. Med., N.Y., 1869; Trousseau, Clinical Med., Phila., 1871. Other references will be found in the foot-notes to the text.]

SYNONYMS.--Rubeola, Morbilli, Measles, Masern, Flecken, Rougeole.

DEFINITION.--Measles is an acute infectious disease involving the skin and mucous membranes, characterized by successive stages and a maculo-papular eruption, which terminates in a fine branny desquamation. In normal cases it runs a definite course, which from the date of invasion to the end of desquamation occupies about fourteen days. It is highly contagious, and occurs, as a rule, but once in the same person.

HISTORY.--The word rubeola is probably of Spanish origin and was formerly written rubiola or rubiolo. The designation morbilli is the diminutive of the Italian il morbo, the plague. Although it is doubtful, as claimed by Willan, that the Greek and Roman physicians were acquainted with measles, there is no question that Rhazes was one of the first to describe the affection correctly. Rubeola is said to have been distinguished from variola by the Arabians in the twelfth century; but, nevertheless, as late as the middle of the seventeenth century we find Sennertus discussing the question "why the disease in some constitutions assumed the form of small-pox, and in others that of measles;" and in a posthumous work of Diemerbroeck, published in 1687, it is asserted that small-pox and measles are only different degrees of the same affection.[2] According to Mayr, the merit of having shown measles to be a distinct malady from scarlatina must be ascribed to Forestus and Sydenham. It is not clear, however, that the two diseases were accurately differentiated till the close of the last century, and notably by Withering in 1792.

[Footnote 2: Cyclop. Pract. Med., London, 1834, p. 625.]

ETIOLOGY.--The exact nature of the measles contagium has never been satisfactorily established, although we are in possession of numerous researches in that direction, which, however, are to a great extent contradictory. A brief examination of these various observations will not prove uninteresting. Hallier found in the blood and sputa numbers of free cocci, which fructified upon various substrata, but was invariably the same fungus--mucor mucedo verus, Fres. In 1862, Salisbury[3] published {558} his observations on the relation of the straw fungus to measles. He recorded instances of inoculation with this organism that resulted, according to him, in the production of a modified form of rubeola, and, moreover, was protective against further attacks of the same disease. In an exhaustive paper bearing on this question H. C. Wood[4] quotes certain experimental inoculations made by William Pepper, which showed conclusively that measles was not propagated in this way, and that where any symptoms were developed they were not those of true measles, nor did they protect the subjects from unquestioned measles. Salisbury also claimed that measles had occurred in camps where damp and mouldy straw had been employed for bedding. J. J. Woodward in his work on Camp Diseases points out that camp measles prevailed almost exclusively in regiments from the rural districts, while men enlisted in towns and cities were more or less completely exempt. The explanation was, that those from the country had hitherto escaped the disease, while townspeople had suffered from it at some previous time--a condition of affairs inconsistent with the theory of the straw fungus. Coxe and Felz found numerous bacteria in the blood of measles patients, especially in regions where the eruption was most pronounced. The nasal mucus also contained similar germs. Inoculation of the blood from the subjects of measles upon rabbits did not produce an analogous affection (Thomas). Klebs[5] obtained micrococci from the trachea and from blood taken from the hearts of infant cadavers. "In the latter, collected in flattened capillary tubes, there developed balls of micrococci; in the trachea both micrococci and bacteria were present in large quantities. Under observation, pale, finely-granular micrococcus balls developed and changed very quickly to bacteria, which moved about very actively. These sought the periphery, about 1/2 mm. distant from the centre of development, and formed a zone, comparable with a hedge or fence that is composed of rods. From this were formed new masses of micrococci, but further no regular process of arrangement or development could be observed."

[Footnote 3: Am. Jour. Med. Sci., July and Oct., 1862.]

[Footnote 4: Ibid., Oct., 1868, p. 333.]

[Footnote 5: Würzbr. Verh., N. F., v., 1874, quoted by Forchheimer in Supplement to Ziemssen's Cyclopedia, W. T., 1881, p. 102.]

Braidwood and Vacher,[6] as the result of a number of experiments, believed that they had sufficient evidence for concluding that the most active mode of the transmission of measles was through the breath, and accordingly instituted a series of experiments by carefully examining the breath of children in the acute stage of the disease.[7] With this object in view they coated over with glycerine the inside of several clean glass tubes of a diameter of a half to three-quarters of an inch. As soon as the nature of the eruption was manifest the patient was required to breathe through one or more of the tubes, and so on each day till the eruption had faded. Upon examination of the glycerine with an one-eighth objective every specimen showed numerous sparkling bodies, something like those found in vaccine, but larger. Some were spherical; others were elongated, with sharpened ends. They were most abundant during the first and second days of the eruption. Healthy children and patients suffering from typhoid and scarlet fevers were made to imitate these {559} experiments, but no such bodies were to be seen in their specimens. They conclude from these observations that the small spherical elements discovered in the breath are perhaps the active agents in the propagation of measles. Upon post-mortem of patients who had died of rubeola these germs were found in the lungs and liver, and, particularly, close to the walls of the capillaries. They believe that the "lungs are the favorite breeding-ground of the contagium."

[Footnote 6: Brit. Med. Jour., Jan. 21, 1882.]

[Footnote 7: Several years ago Ransome of Manchester obtained particles from the breath of two persons suffering from measles (Squire).]

That inoculation of morbillous blood may convey the disease was first demonstrated by Home in 1757, which experiments were verified by Speranza in 1822 and by Katona in 1842. The inoculations of the latter are especially noteworthy, as they numbered more than a thousand. No person inoculated by him died, and only 7 per cent. of the inoculations failed. On the other hand, inoculations made by Mayr gave negative results. It is stated that Monro and Locke communicated measles by inoculating with the tears and saliva. Attempts of the same kind were fruitlessly made in Philadelphia in 1801, although the blood, the tears, the nasal and bronchial mucus, and the exfoliated lamellæ of the epidermis were successively employed in the trials.[8]

[Footnote 8: Rayer, Diseases of the Skin, Phila., 1845.]

Mayr has shown that the nasal mucus is capable upon inoculation of propagating the disease. He performed the experiment upon two healthy children living at a distance from each other, at a time when the disease had ceased to be epidemic. Some nasal mucus taken from the patient during the stadium flavitionis, and kept fluid in a glass tube, was the same day placed upon the mucous membrane of each of these children. In one of them the first symptom of sneezing occurred after eight days, in the other at the expiration of nine days. Febrile symptoms set in two days later. In each child the rash appeared on the thirteenth day after infection. The inoculated disease was mild and regular in its course.

While it is perhaps true that the contagion of measles is not so tenacious as that of small-pox and scarlatina, it is a matter of observation that susceptible persons are liable to contract the disease, even if not directly exposed to its influence. There is incontestable evidence that it is conveyed by fomites--a fact well worth bearing in mind.

It is but just to say that so excellent an observer as Mayr taught that measles could not be conveyed by clothes, linen, etc. unless transferred immediately from one individual to another. Panum, however, showed that contagion could be carried many miles by an unaffected third person without losing its activity. Aitken[9] has also pointed out the fact that children's clothes sent home in boxes from schools where the disease has raged communicated the disease, and that susceptible children who had slept in the same beds, in the same rooms, after they had been occupied by persons suffering from measles, have taken the malady. Squire observes that the contagium of measles, except in the catarrhal stage, is not far diffusible in the air, but clings to surfaces, and may be thus carried from place to place; on the other hand, children have been brought, while in full eruption, into a house among others, and nursed in a room apart, without any extension of the disease to the most susceptible.

[Footnote 9: Science and Pract. of Med., Phila., 1868.]

{560} Various circumstances render it probable that measles is most readily propagated during the stage of efflorescence; but that it is also highly infectious during the prodromal period is now universally acknowledged.

According to Niemeyer, the probability of infection during the prodromal stage is supported by the wonderful spread of measles through schools; for, while the strictest surveillance is established over children with any suspicious eruptions, and those known to have had the disease are not allowed to return till long past the stage of desquamation, no heed is paid to those exhibiting the premonitory cough and coryza. There is no reason for believing that measles can be propagated during the period of incubation; on the other hand, there is no satisfactory argument for the denial of its infectiousness in the desquamative stage. Although Panum is inclined to doubt its contagiousness at this time--and his observations are worthy of the greatest confidence--other good authorities differ from him materially, and extend the stage of personal infection to a period of from three weeks (Squire) to forty days (Hillairet).

Reasoning from analogy, we would naturally expect that the period of incubation in measles suffered a certain amount of variation; the result of numerous observations confirms this expectation. It is manifestly a difficult matter in densely populated communities to establish with accuracy the date of a given infection, but from a study of more or less carefully noted cases it will be found that the period of incubation may vary from three to thirty days. For the vast majority of cases the average time between the reception of the measles poison and the appearance of the characteristic eruption will be about from thirteen to fourteen days. Panum, under exceptionally favorable surroundings, found it more frequently fourteen than thirteen days. Therefore, deducting the three or four days occupied by the invasion stage, we shall find that the real incubation period is from nine to ten days from the date of exposure. Mayr's two cases of inoculation with nasal mucus showed no departure from this rule, but in the inoculations made by Katona with blood the prodromic symptoms made their appearance in seven days, the cutaneous lesions developing two, and at the most three, days afterward.

Minor epidemics of measles are said to occur every three to five years, more extensive and severe ones every seven or eight years. In the centres of population measles may be said to be endemic; in isolated regions the visitations of the disease may be widely separated. Measles is a less severe disease in warm than in cold climates, and, as a rule, we also find the affection more common and more intense in the fall, winter, and spring than in the summer months.[10] Epidemics of measles are usually short, and it is thought that there is a definite relation between the severity of their onset and their duration, this being in general short in proportion as the given epidemic was at first severe (Mayr). Intestinal complications are more frequent in summer, and involvements of the respiratory organs more common in winter. The varying aspects of different {561} epidemics--sthenic, asthenic, etc.--depend on changes in the weather, season of the year, the presence of complications, and other agencies not very clearly understood. Epidemics of whooping cough may precede, accompany, or follow in the wake of measles, and it has therefore been suggested that it stands in some peculiarly close connection with the latter; but, aside from this often-observed coincidence, we are not justified in our present state of knowledge in assuming any definite relation of cause and effect between the two diseases.

[Footnote 10: Aitken (op. cit., p. 295) declares that the mortality returns from England and Wales show that the influence of season is most trifling. Occasionally it has been found that the deaths in summer exceeded those in winter, but we believe that the statement made above is, in the main, correct. For instance, Parson's figures for Berlin for the years 1863-67, inclusive, are: spring, 11.9 per cent.; summer, 13.3; autumn, 33.4; winter, 41.4. Voit's statistics in an average of thirty years at the Children's Clinic at Würzburg establish the same general principles (Thomas).]

There would seem to be neither geographical nor racial bar to the propagation of measles, for it has been observed in all countries and among all peoples. As in the case of other zymotic diseases, a tolerance is established for measles in countries where the disease is more or less constantly prevalent; but where the affection becomes epidemic for the first time, or reappears after many years, it rages with terrific violence. This fact was particularly exemplified in the epidemic in the Faroe Islands, and more especially in the recent (1877) visitation of the Fiji Islands, where one-fourth of the population succumbed in a comparatively short time.

It is quite probable, as asserted by Mayr, that children affected with scrofulous complaints, as well as those who are the subjects of diseases of the respiratory organs--pertussis, bronchitis, or tuberculosis--are eminently susceptible of measles; but his statement that sufferers from epilepsy, chorea, and paralysis exhibit an unusual power of resistance cannot be accepted without reservation. Acute diseases often appear to delay the outbreak of measles, so that the latter does not appear till convalescence from the former (Thomas). The development of vaccinia is occasionally interfered with by an attack of rubeola; on the other hand, the two diseases may be seen running their courses together.[11] The emphatic statement made by Hebra, that measles is never seen to occupy a patient simultaneously with another acute exanthem, has not been confirmed by other observers. My own experience furnishes several examples. Measles may also occur during the course of other acute or chronic maladies. From a study of the literature of measles complicating pregnancy and parturition Underhill[12] finds it to be quite uncommon, due probably to the fact that most adults are insusceptible of further attacks; but when it does occur in pregnancy he regards it as a very serious and frequently fatal complication. Underhill believes measles to be most fatal when it supervenes soon after delivery, while those who are confined during the course of the malady stand a better chance of recovering from it. That puerperal women are not always unfavorably affected by measles is well shown in two remarkable cases reported by Nelson[13] of St. Louis and Chantier[14] of Geneva, in which the mothers were safely delivered, though suffering from measles contracted at the end of their pregnancies.

[Footnote 11: Hardaway, Essentials of Vaccination, p. 60.]

[Footnote 12: Obstet. Jour. Great Britain and Ireland, July, 1880.]

[Footnote 13: St. Louis Courier of Med., Sept., 1879.]

[Footnote 14: Annales de Gynécologie, May, 1879.]

All ages are susceptible to the measles poison, and the apparent exemption enjoyed by adults is due to the fact that most grown-up people have already suffered the disease in childhood; but in Panum's epidemic, mentioned above, it was discovered that nearly all who had not had measles {562} elsewhere, or were not old enough to have been exposed at the last visitation, sixty-five years before, acquired the affection regardless of age. It is quite probable, however, that the law of decrease of susceptibility with age holds good for measles as well as for variola, etc., but to a less degree. It will therefore be seen that measles is not essentially a disease of childhood. Although there is no special limit to the susceptibility of rubeola at one extreme of life, it would seem to be quite well established that it is much modified at the other--namely, that infants under six months are rarely attacked. This latter fact is conceded by individual experience, by the records of epidemics, and by the testimony of most observers.[15]

[Footnote 15: On the other hand, as quoted by Forchheimer (loc. cit.), H. C. Fox publishes some tables which show that for England and London a much larger number of young children are attacked by measles than other statistics would lead us to believe.]

+-------------+-------------+ | England. | London. | +------+------+------+------+ | | Fem- | | Fem- | |Males.| ales.|Males.| ales.| ---------------------------------------+------+------+------+------+ Under one year | 3022 | 2530 | 3571 | 2987 | One and under two years | 6086 | 5825 | 8630 | 8050 | Two " " three " | 3178 | 3255 | 4683 | 4757 | Three " " four " | 1730 | 1851 | 2594 | 2620 | Four " " five " | 980 | 1028 | 1358 | 1466 | |------+------+------+------| |------+------+------+------| Five and under ten years | 255 | 278 | 301 | 316 | Ten " " fifteen " | 29 | 38 | 24 | 32 | Fifteen " " twenty " | 9 | 13 | 9 | 11 | Twenty " " twenty-five " | 7 | 9 | 5 | 7 | Twenty-five " " thirty-five " | 5 | 8 | 5 | 7 | Thirty-five " " forty-five " | 3 | 5 | 2 | 3 | ---------------------------------------+------+------+------+------+

Even sucklings do not enjoy a complete immunity from measles. Steiner[16] states that he has met with it in children only four or five weeks old. Monti has recorded ten cases of rubeola in children under two months of age. A case is reported by Kunze where a mother in the stage of efflorescence gave birth to a child, which contracted the disease five days afterward. Quite a number of cases of congenital measles have been put on record from time to time; but Thomas, after a careful investigation, says that he has been able to discover but six authentic accounts of such occurrences.[17] That children born to mothers suffering at the time of parturition from measles may yet escape it themselves is proven by the cases of Nelson and Gautier mentioned above. Whether a pregnant woman attacked by measles transmits the disease to the foetus in utero, thereby securing immunity from it in after life, is a question difficult of decision, especially as we have not yet been able to decide this same inquiry, with infinitely better opportunities, for vaccinia.[18]

[Footnote 16: Compendium of Children's Diseases, N.Y., 1875, p. 396.]

[Footnote 17: I believe that, under certain circumstances, the erythema papulatum of the new-born is often mistaken for measles.]

[Footnote 18: See experiments of Burckhardt, Rickett, Gart, and others, quoted in Hardaway's Essentials of Vaccination, p. 38.]

There is no good reason to believe that sex is of much importance in establishing a predisposition to measles, although the statement has been repeatedly made that males are more frequently attacked than females. {563} Fox's statistics show a slight preponderance in favor of the male sex; but a careful examination of accessible statistics proves, as would be expected, that this degree of susceptibility varies at different times in obedience to circumstances not readily understood.

By the older writers (Willan, Rosenstein, Fuchs) it was very dogmatically asserted that one attack of measles completely extinguished all future susceptibility to the disease. Of late years this dogma has met with much opposition, and numerous observations have been recorded which, if entirely trustworthy, would lead us to believe that rubeola may occur not only twice, but several times, in the same individual. While from analogy and actual experience we are quite sure that the recurrence of measles is not so uncommon an event as it was once held to be, a closer examination of the question in all its bearings clearly confirms us in the belief that subsequent attacks are much more infrequent than is now thought to be the case by many, and that other diseases, more or less resembling true measles, are largely responsible for errors of diagnosis in this regard. Panum found that all the old people who had measles during the epidemic on the Faroe Islands in 1781 escaped it in 1846. Both Rosenstein and Willan declared that they had never witnessed an instance of the true recurrence of measles. Among other facts, it may be stated in this connection that Woodward (loc. cit.) has shown that during our late war, while members of regiments recruited from the rural districts, who had never before had measles, largely took it when exposed to its influence, regiments from the cities, who had presumably acquired the disease in childhood, remained almost entirely exempt.[19] Other arguments of a similar sort could be readily adduced. There is no question that mistakes in diagnosis have occurred from confounding rötheln, roseola, etc., which closely simulate measles, with that disease. Those particularly engaged in the treatment of cutaneous affections could multiply instances of such errors. It is quite significant that for certain analogous infectious diseases--e.g. variola and scarlatina--the same frequency of recurrence is not claimed, although as a matter of fact they do occur. The explanation would seem to lie in the fact that neither small-pox nor scarlet fever is so closely counterfeited by other skin affections, notably by rötheln, as is measles. But it would be entirely contrary to analogy and indubitable experience to go to the extreme of the older writers and absolutely deny the possibility of second, and even third, attacks of rubeola. The frequency of such cases is, however, as Henoch[20] truly states, much overestimated.

[Footnote 19: These observations of Woodward were made without any reference to the question at issue.]

[Footnote 20: Lectures on Diseases of Children, N.Y., 1882, p. 282.]

Occupying quite a different position from the measles induced by reinfection from without are the so-called relapses of rubeola. These relapses, which may occur in from two to four weeks after the original invasion, are analogous to the similar occurrences in scarlatina and typhoid fever. I am cognizant of but a single case of this sort, but Steiner and other accurate observers record a number of such instances.

SYMPTOMS AND COURSE.--It is generally stated that the stage of incubation exhibits no symptoms whatever; but it is undoubtedly true that the patient will sometimes appear dull and listless, and, on occasion, even give evidence of some slight and ephemeral elevations of temperature. {564} As a rule, however, this period is devoid of any marked indication of the presence of the measles poison in the system.[21]

[Footnote 21: Some writers describe a much more marked train of symptoms as prevailing at this time than seems warranted by general experience, and Rehn has gone so far as to declare that the prodromal period, as usually understood, properly commences in the stage of incubation. Bohn is inclined to a similar view. The prodromic stage of authors is, then, to be looked upon as the "period of the mucous membrane exanthem."]

The prodromal stage is usually ushered in by symptoms of general malaise, fretfulness, more or less frontal headache, shiverings, nausea, loss of appetite, excited sleep, and sometimes delirium. Vomiting is not so common in measles as in scarlatina, and may occur at any time previous to the appearance of the rash. The tongue is apt to be coated, although it may remain clean; the taste is bad, and pressure over the stomach and bowels occasionally elicits considerable pain; an aching pain over the sternum is also noted. As a general thing, at this time patients are drowsy and inclined to sleep much. Meigs and Pepper found this a very constant symptom, which they state is in no way alarming unless associated with other more serious symptoms of local or general disturbance. Constipation is present in some cases, or the bowels may be relaxed or remain in their natural state.

The prodromal fever of measles follows a peculiar course. It is remarkably remittent in character, and is rarely of such intensity as to threaten life, as is often the case in scarlet fever. The temperature will rise on the first day to 102°-104° F., and the height of the fever at this time will measurably foreshadow the character of the subsequent course. On the second day of the prodromal stage the fever suffers a marked remission, or may even entirely disappear, to again rise in the evening. Smith has observed two exacerbations in the day. Again, in some instances, after the high initiatory fever, the temperature may remain normal till just before the rash comes out (Bohn). It is this peculiar behavior of the fever, together with the fact that the child may regain its usual vivacity in the fever-free intervals, which so often misleads the physician into the diagnosis of malarial poisoning.

The most pronounced feature of this stage of the disease is, beyond all others, the catarrhal affection of the mucous membranes. The mucous membranes of the eyes, nose, mouth, and air-passages are all more or less involved, and the patient suffers in varying degrees from photophobia, coryza, hoarseness, cough, and pain in swallowing. Sneezing is frequent and annoying, and slight epistaxis is not uncommon. The cough usually appears on the first day, simultaneously with the fever. It is not very troublesome at first, but by the fourth day it becomes more frequent, assuming a hoarse, barking, paroxysmal character. Expectoration is scanty, and auscultation reveals a harsh vesicular murmur or else sibilant râles. Alarming but not dangerous attacks of false croup may come on during the night. Many observers have called attention to the red spots (papules) in the oral cavity, which make their appearance during the period of invasion. According to Bohn, usually on the second or third day from the beginning of the fever there appear upon the slightly hyperæmic mucous membrane of the soft palate, palatal arch, and uvula small or large, dark, red spots that spread to the mucous membrane of the cheeks, and sometimes to the hard palate, lips, and gums. Soon they become more defined, and are to be distinguished by shape and coloring {565} from the membrane upon which they are situated. According to the same authority, they also afford an index to the intensity and extent of the coming cutaneous eruption. It is also stated that if the latter partakes of a hemorrhagic character, the spots on the mucous membrane may also become livid. This same punctate reddening has been demonstrated in the epiglottis, larynx, and trachea (Gerhardt), and upon the bronchi and small intestines of children who had died during this stage of the eruption. It is also to be noted on the conjunctivæ. It has been assumed that this period of this disease is not to be looked upon as the stadium prodromorum, but as the period of the "exanthem of the mucous membrane." This view of the pathology of measles seems to me most reasonable; but in whatever way we may look upon the question, the practical importance of this precutaneous eruptive stage is to be insisted upon for diagnostic purposes, just as is the analogous eruption upon the mucous membrane in small-pox.

In ordinary cases of measles we do not find such profound reaction of the nervous system as in scarlatina. I believe that convulsions in the prodromal stage are much more common than available statistics would have us believe; at least, this is my own experience. Meigs and Pepper met with convulsions but five times in 314 cases at the beginning of the eruption, while Rilliet and Barthez observed but one convulsion in 167 cases. Thomas says that convulsions are almost always absent. On the other hand, Trousseau and Bohn expressly declare that they are very common, the former stating that they occur with greater frequency than in scarlatina. I consider that convulsive seizures occurring in connection with marked catarrhal affection of the mucous membranes are very important aids in forecasting a probable attack of rubeola. Fortunately, convulsions at this stage are not very serious unless repeated or injudiciously treated.

The duration of the period of invasion in regular cases is from three to five days, with an average of about four, but in perfectly uncomplicated attacks this period may be extended to six or eight days, or even longer. But that the duration of this stage may be much shorter than the average is not sufficiently insisted upon by writers. Ringer,[22] for instance, says that he had an opportunity of testing the earliest appearance of the rash in an epidemic of measles in a large public school for boys under twelve. In every case during the epidemic the rash appeared on the first day, the cases being severe, though of short duration, the temperature rising to 103° and to 104° F. In some instances the rash preceded (?) the fever. Thus, several of the boys feeling poorly, their temperature was carefully taken night and morning under the tongue, and in several cases the rash appeared in the morning about the face and collar-bone, while the temperature remained normal, and did not rise till the evening, when it ran up to 101°-103° F., and even higher. These cases certainly resemble rötheln more than measles. In two cases, which I observed under very favorable conditions, the eruption commenced to appear on the morning of the second day, and more or less similar experiences are recorded by others.

[Footnote 22: Handbook of Therapeutics, 6th ed., London, 1868--note to p. 26.]

The skin eruption, which appears, as a rule, on the third, fourth, or fifth day of the attack, is ushered in with an increase in the general and {566} local symptoms of the disease. It is particularly to be remarked that the fever does not subside at this time, as is the case in variola. The eruption appears first upon the face, about the cheeks and forehead, then on the chin and neck, and thence gradually overspreads the trunk, and finally reaches the extremities. When the eruption is intense no part of the body is free from it, the rash being found upon the palms and soles and upon the hairy scalp. The cutaneous lesions proper consist at first of hyperæmic spots of about a line in diameter, which gradually increase in size, until at their full development they may attain a diameter of from one-twentieth to a quarter of an inch. In the beginning they bear a very close resemblance to the sub-papular lesions of small-pox. The maculo-papules, when fully developed, are slightly elevated above the level of the skin, the elevation, however, being more appreciable to touch than sight, have a smooth velvety feel, and are so arranged as to enclose areas of healthy skin. In the individual spots we may frequently observe one or several minute, darker-colored papules, due to follicular congestion, which when more intense constitutes the morbilli papulari presently to be described. The maculæ are, as a rule, roundish, or they may be moon-shaped, or their borders may present an indented or notched appearance. Where the capillary circulation is active--on the cheeks, for example--or upon parts subjected to pressure, the eruption may become confluent; that is to say, the usually pale intervening skin becomes injected or the papules coalesce, and in this way produce a uniform redness over large single tracts of skin. This scarlatinoid rash, however, never occupies the whole surface of the body, but only limited regions, and in other situations may be detected the characteristic discrete papules of rubeola; the color is not uniform, but is broken here and there by the darker streaks and spots of the measly eruption. The rash, which disappears upon pressure to return when the pressure is removed, is of a more or less rosy red, with a tendency in some to deep red, and has occasionally a purplish hue. According to Mayr and Hebra, it is of the precise color which is obtained by adding a little yellow or brown to a red pigment.

According to the researches of Thomas, Squire, and Wunderlich, as abstracted by Seguin, the fever of the eruptive period is divided into a moderately febrile stage and the fastigium or acme. The moderately febrile stage averages thirty-six to thirty-eight hours, and is made up of one or two exacerbations of 100.4° to 102.2° F., but not quite so high as the initial fever. If there are two exacerbations, the second one is the higher; the intervening remissions are not so low as those of the prodromal stage, yet even now the norm may be noted on a single occasion. The fastigium commences early in the day or in the evening; if the rise should occur in the morning, the evening temperature rises still higher, with or without a slight remission the following morning, and the next evening attains the maximum. If the acme begins in the evening, the remission on the next morning is either absent or very slight. The greatest height of the fever in normal cases corresponds to the greatest intensity and development of the eruption. This rule is not invariable, however, for sometimes the fever is higher soon after the eruption appears, and has fallen when the exanthem has reached its highest point. The whole fastigium lasts from one and a half to two {567} and a half days, so that the complete eruptive fever occupies from three to four and one-half days.[23] The pulse in general preserves a proportionate correspondence to the temperature, and never attains the great frequency to be observed in scarlatina.

[Footnote 23: According to Ringer, the highest temperature reached in normal cases is 103° F. Thomas places it as high as 104° F., but states that it may go up to 105° F. without the intervention of any complication.]

The general symptoms, with the exception of the fever, do not greatly differ from those common to the prodromal stage. The skin is hot and more or less swollen, particularly about the face; there are anorexia, photophobia, lachrymation, and sometimes epistaxis; the cough continues, and is generally frequent and harassing, and attended with little or no expectoration; the voice is hoarse. The tongue is coated, principally in the middle, through which the swollen papillæ protrude, while the tip and sides are red. The blotchy redness of the oral cavity is visible for some days, and finally becomes indistinguishable from the surrounding congestion. The tonsils sometimes become considerably enlarged, though suppuration must be rare. Enlargement of the glands behind the jaw and in the neck and groin are to be observed. At the outset of the eruption a profuse diarrhoea supervenes in most cases--a symptom which Trousseau rightly insists to be an essential feature of measles. This occurrence is interpreted by some writers as an evidence of the implication of the mucous membranes in the specific exanthem of the disease. This flux, which is sometimes accompanied by a little blood and tenesmus, rarely continues long, and may be succeeded by a degree of constipation. The respiration is generally somewhat accelerated, mostly in correspondence to the amount of fever present. Some degree of deafness is not uncommon, owing to the extension of inflammation along the Eustachian tubes. The urine is scanty and high colored; there is sometimes scalding in urination and vesical tenesmus, and at the acme of the fever traces of albumen may be detected.

The eruption, in fact, generally occupies the skin an average of four days, and, although this period may be shortened materially, it is less apt to be lengthened. The duration of the eruption at its maximum of development over the whole surface is about half a day, more or less, and, as a rule, corresponds with the greatest elevation of the temperature. The retrocession of the rash takes place in the order of its appearance--viz. first from the face, then from the trunk and upper parts of the extremities, and last from about the feet and hands, where, indeed, it may remain vivid, or even progress for a short time longer, after the eruption has begun to subside in other situations. Sometimes the almost faded spots will be temporarily renewed by an abnormal rise in the temperature.

With the decline of the eruption the other symptoms begin to subside. The cough loses its hacking, paroxysmal character, and becomes less and less frequent, and gradually disappears. The voice regains its normal tone, the tongue loses its fur, cleaning up in patches, and expectoration, which was absent or scanty and viscid in the beginning, increases and is free, the masses coughed up being coin-shaped and floating in a clear watery mucus--a symptom much dwelt upon by the older writers. The behavior of the temperature at this period--the stage of decline--is quite {568} characteristic. The fall usually begins at night, and generally the next morning it has reached the norm or else fallen below it. On the other hand, the descent may be less precipitate, and the fall continues less rapidly all through the day; or there may be a slight rise again in the evening, the norm being reached the following morning. The termination by lysis--that is, slight elevations in the evening for several days--is much rarer, and while it may occur in perfectly regular cases, it should put the medical attendant on his guard against complications.

The comparatively normal course of measles portrayed in the preceding paragraphs does not always occur, but, on the contrary, the disease may depart from the more usual type in one or more particulars, either in especial stages of its progress or in the greater or less intensity of the malady as a whole.

In addition to those cases of measles where the eruptive and catarrhal symptoms are so slight as to almost escape observation, except for the existence of other cases in the same house or family, there are to be recognized two other trivial varieties of the disease--namely, measles without the catarrh, and measles without the rash.

That the eruption of measles should occur upon the skin without implication of the mucous membranes seems to be much more doubtful than that the catarrh should appear without the eruption. It is quite probable, at any rate, that many so-called cases of rubeola sine catarrho are merely instances of rötheln, which we know may occur without any reference to an existing epidemic of measles. But that this form of measles does exist is admitted by trustworthy observers, although its diagnosis under any circumstances must be a matter of great difficulty. Measles without the eruption (rubeola sine eruptione) is more readily recognized, especially and only, however, when a susceptible person is exposed, and as a result acquires the characteristic catarrhal symptoms. Since in recent years more attention has been paid to the eruption on the mucous membranes, it may be that its discovery in these situations may lend positive assistance to the diagnosis in such cases. It is hard to understand how this variety of measles, which presents no inflammatory changes in the skin, should be followed by desquamation; yet this observation has been made. The assertion that these anomalous forms of the affection afford no protection against subsequent attacks seems to be founded in error, and is undoubtedly due to the confusion existing between measles and rötheln or other exanthems.

Continental writers, especially, describe a form of measles called by them inflammatory or synochal. It is simply an exaggeration of the symptoms, particularly those appertaining to the mucous membranes, found in ordinary measles (morbilli vulgaris). The prodromal stage is much more violent, the nervous symptoms more threatening, the implication of the mucous membranes more pronounced and persistent, the febrile movement is of a higher inflammatory character, and the eruption, which instantly covers the whole body (Vogel), is made up of dark-red or purplish spots which fade slowly. It is this form of measles, according to Niemeyer, which is chiefly attended by croupous instead of catarrhal laryngitis, in which the inflammation of the air-passages often extends to the alveoli of the lungs, and in which the gastric and intestinal coats are often affected with catarrh.

{569} Let the contagion of measles be a grade more virulent, or perhaps the resisting power of the patient more feeble, and the case will assume the features of the septic, typhous, or hemorrhagic variety (rubeola nigra). It is said that the hemorrhagic measles is most apt to occur in epidemics; certain it is that the dreaded black measles of former times is very infrequent now-a-days, due, no doubt, to a more rational treatment and a better hygiene. Isolated cases, however, are occasionally encountered. As a rule, from the beginning all the symptoms evidence an overwhelming of the system by the virulence of the poison--a condition of things much more common in scarlatina. The pulse becomes weak, thready, and frequent; the temperature lacks the typical remittent character of normal measles; there is unusual prostration; and the nervous centres are profoundly concerned, as shown by delirium, convulsions, and coma. The eruption lags, and finally makes its appearance in an imperfect or irregular manner. The spots are of a livid hue, interspersed with larger or smaller ecchymoses. Hemorrhages from the mucous cavities take place, and the patient dies in convulsions or sinks into fatal coma. It has been said that the grave constitutional symptoms do not generally make their appearance till the eruptive stage, but I know from experience that the patient may be overwhelmed quite early, as in purpura variolosa.

Too much stress should not be laid on these different types of the disease, whether mild or grave, since they depend upon a common cause, however much modified in one way or another; but they may be allowed to stand for the sake of clinical convenience.

Measles may also present certain irregularities in its various stages without necessarily departing from the otherwise benign character of the disease.

As stated elsewhere, it is believed by some writers that a greater part of the period of incubation is occupied by symptoms which already indicate the activity of the measles poison in the system, and that, therefore, this stadium in reality lasts but a few days. This opinion does not seem to be generally accepted; at any rate, I think we are quite safe in saying that in the majority of cases no departure from the usual latency is observed. The deviations in the stage of invasion have been considered above, and mostly concern its duration and the character of the temperature. Evanescent rashes, which have nothing in common with the specific exanthem, are sometimes observed at this period. The eruption of measles may present certain peculiarities. First, as to localization. Instead of coming out on the face first, it may primarily develop on other parts of the body, provoked into existence, as it were, by local exciting causes; thus, where ointments or plasters have been applied or upon a part subjected to constant pressure. It may affect only one-half of the body, or entirely spare paralyzed extremities (Mayr). In some instances the papules are so sparse, indistinct, and short-lived as to be scarcely appreciable.

Second, as to the physical characters of the eruption. Hebra and Mayr recognize the following modifications:

Morbilli lævis. The efflorescence is smooth and flat, and the individual lesions are separated from each other by normal integument. This is the common form of measles.

{570} Morbilli papulosi. The papules are dark red and more elevated, are about the size of hempseeds, and situated at the mouths of the hair-follicles.

Morbilli vesiculosi. In this variety the mouths of the hair-follicles are filled with fluid and produce delicate transparent vesicles.

Morbilli confluentes. The maculæ are here so crowded together that no healthy skin intervenes.

Morbilli hæmorrhagici. The efflorescence consists of maculæ or papulæ of a dark-red color, due to extravasations of blood, and do not fade on pressure. It is well to mention in this connection the fact, particularly noted by Meigs and Pepper in this country, that hemorrhages into the skin may occur in cases which otherwise run a benign course. They are best seen after the eruption has faded. In some cases the efflorescence of measles may remain visible for a week or ten days.

As heretofore observed, there may be a relapse of the measles eruption after some weeks, accompanied by fever. It is said that the spots appear on parts of the skin hitherto normal (Thomas). So far as I know, Hebra was one of the first to point out the fact that the so-called striking-in of the eruption was the result, and not the cause, of some complication in the disease; for, as this author states, before the rash fades or disappears the internal disease is always present. It is well known, for instance, that syphilitic eruptions will sometimes disappear upon the supervention of some acute intercurrent affection, such as pneumonia, acute rheumatism, etc.; but no one will suppose for a moment that the retrocession of the syphilides was the cause of these affections.[24] The pathological explanation seems obvious.

[Footnote 24: See Bumstead and Taylor on Venereal Diseases, 4th edit., p. 513.]

COMPLICATIONS.--The complications of measles consist, as a rule, in the exaggerated morbid action of organs or parts that are essentially implicated in the disease; therefore we are most apt to encounter such affections as laryngitis, bronchitis, pneumonia, etc. Inflammation of serous membranes, on the other hand, are rare; thus, pleurisy is infrequent unless in connection with a lobar pneumonia.

The exact causes of the complications are not always obvious, but in many instances can be traced to the previous bad health of the patient, to the influence of insanitation, or, finally, to certain ill-understood features attendant upon some epidemics.

Simple bleeding from the nose, not associated with the hemorrhagic diathesis, is not an uncommon accompaniment of the prodromal stage, and is rarely a dangerous symptom--rather the contrary. It may also arise after the development of the rash, and occasionally proves a complication of serious import.

The aural complications, unlike those in scarlatina, are generally not sufficiently prominent at first to attract attention. The symptoms, particularly pain and deafness, are apt to be masked. Purulent processes and consequent perforation may occur during the eruption, but are more frequent at the stage of desquamation (Spencer).[25]

[Footnote 25: Oral communication.]

Various disorders of the skin have been observed during the course of measles--viz. miliary vesicles, and even pustules, as already described; herpes facialis, zoster femoralis (Thomas), and erythematous rashes, which {571} may precede, accompany, or, it is said, follow the eruption. Of considerably more importance is the pemphigoid eruption mentioned by several observers. In Henoch's[26] case, a girl of four years, the usual remission of the fever on the evening of the second day was absent, and from the third day there appeared over nearly the whole surface blebs filled with a limpid fluid, which varied in size from a hazel-nut to a thaler, and even larger. The cheeks and the backs of the hands were each covered with a single bleb. The exanthem was of a hemorrhagic character, and the intervening skin was red and the face swollen. The bullæ appeared not only where the eruption existed, but also on parts of the body free from it. The fever remained at the same height till the fifth day, when, upon the cessation of the bullous eruption, it fell to 100° F. A.M., and 101° F. P.M. The child died on the eighth day of a pneumonia which developed between the sixth and seventh days. Other cases have been reported by Steiner, Klüppel, and Löschner. Henoch rejects the theory that the bullæ are the result of the morbillous dermatitis, but thinks that they are merely instances of the coincidence of a contagious pemphigus.

[Footnote 26: Berl. klin. Woch., No. 13, 1882.]

The severe affections of the eye described by continental writers--blennorrhoea, keratitis, iritis, etc.--are certainly very rare in this country as complications of measles. Various so-called strumous disorders of this organ, as will be seen hereafter, not uncommonly, however, come under the care of the ophthalmologist as sequelæ of the disease.

The tonsils and the mucous membrane of the pharynx may become severely inflamed. The tonsils are sometimes very much enlarged, but suppuration, if it occur, is certainly rare. Slight ulceration of the gums close to the teeth is occasionally noted, also aphthous ulcerations on the lips, tongue, and gums (Ringer).

Some degree of laryngitis is an accompaniment of all cases of measles. It has already been stated that catarrhal or false croup is frequently observed during the stage of invasion. Inflammation of the larynx may be present in all grades of severity. Rilliet and Barthez found ulcerations and erosions, especially of the vocal cords, upon post-mortem examination of a large proportion of measles subjects; and Gerhardt, both during life and by autopsy, has verified these observations. Loeri[27] states that inflammatory changes are more marked in the larynx and trachea than in the pharynx. According to his examinations, hemorrhages or ecchymoses seldom occur, but more frequently superficial or even deep catarrhal ulcers, especially on the anterior aspect of the posterior wall of the larynx at the apices of the cartilages of Santorini, or on the posterior portion of the vocal cords. The physical condition of these parts readily accounts for the frequent and harassing cough and attacks of spasmodic laryngitis which are such frequent complications of the invasion and eruptive stages of measles.

[Footnote 27: Jahrb. f. Kinderheilk., xix. B., 1 H.]

There may be an extension of the tracheo-bronchitis to the finer bronchial tubes, thus producing capillary bronchitis (suffocative catarrh). It is apt to prove fatal to very young children. It occurs more generally during or after the eruption.

Pneumonia is one of the most frequent and, directly and indirectly, most dangerous complications of measles. Catarrhal pneumonia (broncho-pneumonia) is, for obvious reasons, more common than the lobar or {572} croupous variety. Pneumonia may develop at almost any stage of measles, but experience does not confirm the statement occasionally made that it is most frequent in the initial stage. Most observers will agree as to its greater frequency just at the end of the eruption or during the desquamative period. The occurrence of epileptoid convulsions, or an untoward increase of the fever, or an unexplained continuance of the same, should direct the attention of the attendant to the chest, if his anxiety have not already been aroused by a change in the character of the respiration or other symptoms. It may be mistaken for meningitis (Squire). In estimating the prognosis it should be remembered that croupous and catarrhal pneumonias run quite different courses. The influence of inflammation of the lungs upon the rash is quite decided. If an intense pneumonia should develop in the initial stage, the eruption will be pale and sparse, or else absent; if the eruption is already out at the time of the attack, it may become temporarily more vivid, to rapidly fade later.[28]

[Footnote 28: A scanty rash by no means indicates an unfavorable course of the disease; this symptom is only serious when evidently due to some complication.]

Chadbourne[29] has the merit of calling attention to the occurrence of heart-clot and subsequent pulmonary oedema as a fatal complication of measles. In a number of autopsies he found that in each case the heart contained clear gelatinous clots of a very firm consistence, which in most instances extended to the pulmonary arteries, and in some to the extent of one and one-fourth inches. In the series of cases observed by him pneumonic consolidation was mostly absent, and there was very little evidence of collapse, but the lungs were exceedingly oedematous. But Keating has also found heart-clot to be the cause of death in some cases, and believes, as the result of his investigations, that the presence of large numbers of micrococci in the blood and in the white blood-corpuscles is responsible for this condition.[30]

[Footnote 29: Am. Jour. Obstet., Oct., 1880.]

[Footnote 30: Phila. Med. Times, Aug. 12, 1882.]

There is a strong tendency in measles to intestinal catarrh. As already stated, a quite sharp diarrhoea is not uncommon at the beginning of the eruptive stage; but, unless it should prove very profuse and long-continued, it is not to be looked upon as of very serious import, especially if the other general symptoms of the disease are following a normal course. In other instances the bowel affection may be much more severe, giving rise to tenesmus, bloody stools, and the other phenomena of colitis. In weakly children the early diarrhoea may persist in spite of treatment for many days; indeed, under the influence of high temperatures it may take on a true choleraic character. Diarrhoea is a very frequent and grave complication of the broncho-pneumonia of measles.

Acute miliary tuberculosis as an immediate concomitant of measles is rare. According to Thomas, the disease at times immediately follows the exanthem, and reaches a fatal issue in a few days or weeks. The tubercles are more particularly to be found in the lungs and in the membranes of the brain.

Among the more common disturbances of the nervous system convulsions play an important rôle. The epileptoid seizures of the prodromal stage generally terminate favorably, but in some cases of a malignant character the onset of the disease may be ushered in with fatal {573} convulsions. Convulsions in the later stages are apt to have a lethal termination, as they usually occur in connection with some grave complication, particularly of the thoracic organs.

Diphtheria is an exceedingly grave complication of measles, although not necessarily a fatal one. It is of less frequent occurrence than in scarlatina. It may attack any of the usual oral, nasal, or laryngeal regions, sometimes extending into the bronchi, but suffers no modifications in its symptoms and course from the primary disease. It may also rarely involve other parts--e.g. genitals, eyelids, etc. There is reason to believe that it is most prone to attack those cases in which the mucous membranes have undergone the greatest inflammatory alterations.[31]

[Footnote 31: Loeri (loc. cit.) says that diphtheria may appear at any stage of measles, and commences generally in the larynx, and sometimes in the trachea simultaneously; seldom in the pharynx, as in primary diphtheria or in that complicating other diseases than measles.]

Many other complications of measles have been recorded in literature (see Thomas, op. cit.); but it is no doubt true, as observed by Bohn, that very few of them have a real essential connection with that affection, and might as readily be associated with any other malady, especially in already vitiated constitutions. In the above sketch the endeavor has been made to indicate those disorders which from the nature of measles would seem to have a more or less close and definite relationship to it. It is certain that the more serious complications and sequelæ of measles are comparatively infrequent in private practice in America, although common enough in continental Europe, and to a certain extent in the children's asylums and foundling hospitals in this country.

SEQUELÆ.--It is a difficult matter to dissociate the complications and sequelæ of measles. Properly speaking, the sequelæ are to be looked upon as the complications which have continued in existence after the subsidence of the exanthem; but it is also customary to include under this head certain affections that are the result of the derangement of the system by the morbillous process.

As would be expected, among the most frequent sequelæ of measles are those diseases which have their seat in the mucous membranes. Thus, we may observe various grades of inflammation and ulceration of the larynx, trachea, and bronchial tubes. According to Loeri, follicular ulcers of the larynx always give a bad prognosis, for these cases usually succumb to tuberculosis. It is not uncommon to observe a bronchial catarrh, apparently simple in nature, which persists with frequent exacerbations for many months. The very frequent broncho-pneumonia, which occurs as a complication, always remains as a sequel, or it may develop after the morbillous process has come to an end. In favorable cases recovery may take place in two or three weeks, or, preceded by hectic and progressive emaciation, the disease may prove fatal after a number of months. But even here it is not impossible for affected persons to recover.

Chronic pulmonary tuberculosis is one of the most formidable and frequent sequelæ of measles. It is a not uncommon occurrence that, with the exception of some trivial bronchitis, a patient may apparently recover his health completely, and only after a lapse of time slight daily elevations of temperature, accompanied by loss of appetite and emaciation, {574} first give warning of the impending danger. This form of phthisis may follow either croupous or catarrhal pneumonia. Granular meningitis or general miliary tuberculosis also frequently follows in the wake of measles, connected in many cases with foci of caseous degeneration in the involved lymphatic glands or unabsorbed pneumonic exudation.

Various gangrenous affections, particularly of the oral cavity (noma) and genitals, but also of the skin, subcutaneous connective tissue, cartilages of the nose, ear, etc., are often to be observed after an attack of measles. Cancrum oris is to be especially noted.

Albuminuria is not an essential sequel of measles, although it may occasionally occur as the result of great exposure and neglect.

A large group of chronic affections may follow in the track of measles, either in the form of sequelæ to the complications which arise during the course of the disease or in the nature of secondary accidents. Some few, perhaps, are more common after measles than after any other complaint, but the majority are such as might arise in weakly children subsequent to any specific disturbance of the health. In addition to those already mentioned we may especially designate chronic intestinal disease, together with ulcerations and strictures of the bowel; chronic coryza, in varying degrees of obstinacy and severity; chronic ophthalmia, under which title may be included ciliary blepharitis, granulations, trachoma, phlyctenular conjunctivitis, ulcers of the cornea, etc. (Michel[32]); aural affections in the form of chronic suppurative inflammation, and, more rarely, chronic catarrh of the middle ear (Spencer); certain cutaneous diseases, more especially in my experience furunculosis and pustular eczema; chronic bone and joint disorders (strumous), which, according to Gibney,[33] may not only be evoked in the already hereditarily predisposed, but also induced when the diathesis has not heretofore existed; and, lastly, various derangements of the nervous system.

[Footnote 32: Oral communication.]

[Footnote 33: See valuable statistical article in N.Y. Med. Record, June 3, 1882.]

In Thomas's valuable and freely-quoted monograph on measles (op. cit.) it is stated that secondary measles can exert various influences upon the primary disturbance. In most instances when measles attacks a person already the subject of some other disease, particularly when the latter belongs to the common complications of the former, it usually is aggravated. This is a matter of common experience; but this author further declares--and supports his assertion with numerous references--that, on the other hand, should measles appear during the existence of a disease to which it does not usually give rise, it may favorably influence the course of the latter. In spite of the cases quoted in support of this view, such results would appear to be contrary to pathological laws.[34]

[Footnote 34: Thus, while Thomas seems to be without personal experience in the matter, he quotes without dissent a number of observations in support of his assertion--viz.: Behrend saw a chronic eczema of the scalp permanently disappear after measles; Rilliet found that a chronic coxitis improved noticeably after measles; various chronic skin symptoms, and also chorea, epilepsy, incontinence of urine, mania, worms, dropsy, joint diseases, ophthalmia, gonorrhoea, etc., have been known to recover under the same influence. Gibney (loc. cit.) in his valuable paper states that he can readily believe that, occasionally, any acute disease, occurring in the course of a chronic one, will prove beneficial to the other, but that he is far from considering this to be anything more than an exception to a very general rule to the contrary. Chronic joint disease, he continues, is especially a disease of exacerbations, and any one not familiar with their natural history may interpret the post hoc as a propter hoc. Gibney has collected 24 cases of chronic bone disease in {575} children, 21 of whom were under ten years of age and all under thirteen. On analysis he found that 12 of these came out of the intercurrent disease in a worse condition, 11 were unaffected, and 1 only seemed a little better. In my personal experience I have invariably seen the eczemas of children made worse by measles. I have no wish to dispute the trustworthiness of the statistics quoted by Thomas; indeed, I regard them as mostly thoroughly reliable instances of exceptions to a general pathological law; but I wish it to be clearly understood that they are such, and that measles is not a disease to be slightly regarded as to its effects upon the system.]

MORBID ANATOMY.--The normal rash of measles is not to be observed on the dead body, and the only lesions of the skin to be noted are those resulting from extravasation of blood into that tissue. Examination of the skin removed during life from a patient with measles reveals the following anatomical changes, according to Morris.[35] In the earliest stages are found usually slight hyperæmia around the orifice of a sebaceous follicle, with slight swelling from effusion of plasma. Occasionally swelling alone is present, and more rarely hyperæmia only. Round the small hyperæmic papule thus developed--often pierced by a hair--a roseolar patch, due to congestion of the papillary body, soon makes its appearance. Slight exudation of plasma, with a few corpuscles, usually follows, and produces elevation of the papule itself. As most of the deaths in measles are due to the presence of some complication, the post-mortem changes will be found to correspond to the lesions produced by these diseases, principally affections of the respiratory organs and intestinal tract.

[Footnote 35: Skin Diseases, Phila., 1880, p. 57.]

DIAGNOSIS.--As a rule, the diagnosis of measles offers no great difficulties, especially if a correct clinical picture of the disease has been thoroughly impressed upon the mind. The salient points may be thus summarized: A period of incubation of about fourteen days--i.e. from the date of infection to the commencement of the eruption; a prodromic stage of about four days, ushered in with fever and marked implication of the mucous tract, notably cough, coryza, epistaxis, and photophobia; in this stage may also be noted the punctated redness of the conjunctivæ and of the palatal mucous membrane, which is to be regarded as a diagnostic sign of great value and importance; finally, there appears at the conclusion of the stage of invasion, simultaneously with increase of the febrile movement, a characteristic eruption upon the cutaneous surface, this eruption coming out first upon the face, and composed of large maculo-papules of brownish-red color, arranged in a crescentic form with tracts of normal integument intervening. Of all the symptoms of measles, the catarrh of the mucous membranes is undoubtedly the most pathognomonic. In the colored races, where the recognition of the skin lesion is often a matter of difficulty, this combination of symptoms should be borne in mind.[36]

[Footnote 36: Corre (La Mère et l'Enfant dans les races humaines, Paris, 1882) states that measles and scarlatina exist in all climates and among all races; however, they are less frequent in warm than in cold climates. This relative rarity may be only apparent, and has only been established by reason of the difficulty of recognizing exanthems among dark-skinned peoples. In the negro the eruption (of measles) often escapes observation, but the general symptoms, the angina, coryza, and bronchitis, and the special coloration of the bucco-pharyngeal membranes, permit the establishment of the diagnosis. The skin appears more tense, and the face especially is puffed and glossy; in passing the hand over the different regions of the body slight elevations are felt--a difference in the level of the skin exists in the affected and unaffected portions. On examining the surface of the body obliquely at a well-pronounced angle of incidence, these elevations can be perceived by the eye. Desquamation, which is very manifest in the negro, also confirms the diagnosis; this desquamation is formed of epidermic débris; it gives rise to a {576} white dust, which is well defined against the black skin. The skin itself seems to have lost its gloss; it is completely dry, and no longer gives the abundant and odoriferous secretion characteristic of the subjects of that race.]

In the way of conjectural diagnosis, the presence of an epidemic of measles in the community should be taken into account. Although measles possesses features so characteristic and pronounced, there are a number of other diseases with which it may be confounded, especially in its earlier stages.

There is no other disease which presents so close a resemblance to measles as does rötheln, and it must be confessed that under certain circumstances the question of diagnosis is a perplexing one. In rötheln the appearance of the eruption is often the first symptom of the affection, whereas in measles there is a prodromic period, having a peculiar remittent type of fever, which continues for three or four days. According to Liveing, the short duration of the febrile attack before the eruption appears is one of the most constant and distinctive features wherein rötheln differs from ordinary measles. In some instances, in rötheln the premonitory fever is not at all appreciable. The catarrhal involvement of the mucous membranes is not nearly so marked as in measles, while the very frequent sore throat bears more resemblance to the angina of scarlet fever. In many instances, although by no means constantly, the eruption of rötheln first appears on the chest, and not on the face, as is the rule in measles. It is quite evident that the eruptive spots of rötheln have presented different physical features in different epidemics; but, as a general thing, it may be said that they are smaller than those in measles, of a paler color, and, according to Thomas, not so angular, less indented, and not so often provided with processes, therefore less apt to assume the crescentic arrangement so often seen in measles.[37] The incubation period is longer in rötheln than in measles.

[Footnote 37: According to Curtman (St. Louis Courier Med., June, 1882), the eruption of rötheln consists, when not confluent, of single papules, each separated by a distinct small red areola. Not infrequently the papules are large, and sometimes a few pass into vesicles or pustules. In measles the papules are very small, mostly confluent, from four to six landing on a single areola, which is larger than that of rötheln.]

In scarlet fever the incubation stage is shorter than in measles, and the constitutional symptoms are apt to be more pronounced; the temperature is higher, the pulse more rapid, and vomiting more frequent. The stage of invasion in scarlatina is but twenty-four hours; in measles, seventy-two. There is absence of the characteristic catarrh of measles, and the presence of severe sore throat, strawberry tongue, and swelling of the lymphatics at the angle of the jaws. In measles the rash begins on the face; in scarlatina, on the neck and chest. In measles the eruption consists of large papules arranged somewhat crescentically, with intervening normal skin, followed by bran-like desquamation; in scarlatina the rash is made up of large patches formed of minute red spots on a bright red, hyperæmic base, and is followed by desquamation in large lamellæ. In measles the rash is brightest on exposed parts; in scarlatina, most vivid on covered regions. The sequelæ of the two diseases are quite different.

There is no great difference in the duration of the invasion stages of variola and rubeola; but in the former disease we have the marked lumbar and sacral pains and vomiting, while in the latter the catarrhal symptoms and photophobia are pathognomonic. When the eruption of {577} small-pox appears there is subsidence of fever; in measles, an exacerbation. A point of great importance in the diagnosis of variola is found in an examination of the mouth and pharynx, for in these situations on the fourth day we will often find the vesicles fully developed, while on the skin they are still in the stage of papulation. When measles assumes the papular form (morbilli papulosi, rougeole bouttoneuse), it is often confounded with the papular stage of small-pox. I have seen a number of such mistakes made. Attention to the general symptoms of the two diseases, however, and particularly an examination of the mucous membranes, will generally clear up any doubt. At any rate, the question will generally settle itself in the next twenty-four hours, for if it be variola the papules will have undergone their specific development and the rubeolous elevations will have become more decidedly macular.

Typhus sometimes offers a certain resemblance to measles. According to Buchanan,[38] the eruption of typhus is occasionally, though not commonly, a good deal like that of measles, and appears about the same time after invasion. Coryza, when present and distinct, points to measles. The eruption of typhus is of a smaller pattern, discrete, and not raised; that of measles, often coalescent, crescentic, and elevated. Subcuticular mottling is present in typhus, and absent in measles. The palatal mucous membrane should always be examined in suspected measles.

[Footnote 38: Art. "Typhus" in Reynolds's System Med., Am. ed., p. 262.]

As I have never been able to convince myself of the existence of an independent disease called roseola, I am at a loss to give the points of differential diagnosis; on the other hand, the various forms of symptomatic erythema, occurring either as the result of numerous slight derangements of the system, or in connection with grave constitutional disease, should be carefully considered. In the first group of cases the absence of premonitory symptoms, catarrh, etc., and the presence of the smooth, rose-colored macules, mostly on the trunk, and in the latter the existence of symptoms belonging to the primary disease, should prove of assistance. The erythema papulatum of new-born children I have seen mistaken for measles, but the fact that rubeola is exceedingly rare in sucklings, and the absence of fever and catarrhal disturbances, are sufficient grounds for a differential diagnosis.

The erythematous syphilide (roseola syphilitica), particularly when accompanied by fever, may bear some resemblance to the rash of measles; but the history of the case, the circumscribed, indolent character of the syphilide, in many instances sparing the face, the absence of pathognomonic catarrhal symptoms of measles, and the coexistence of other features of syphilis, are quite distinctive.

PROGNOSIS.--The prognosis of normal uncomplicated measles is very favorable. Thus, of 257 cases observed by Meigs and Pepper (op. cit.), all terminated favorably. But in coming to any conclusion in regard to prognosis a number of different factors must be taken into consideration. Among the more important are--the hygienic surroundings of the patient, the age, the nature of the complications, whether the measles be primary or secondary, and the character of the epidemic. In the first place, rubeola in foundling hospitals and among the poorer classes in large cities gives a larger ratio of deaths than among the well-to-do members of the community. For instance, Bartels has shown that catarrhal pneumonia, one {578} of the most frequent causes of mortality in this disease, is particularly prone to occur among those dwelling in crowded, poorly-ventilated houses. Then, again, the asylums and hospitals for children are peopled in many instances with the victims of depraved constitutions, who readily succumb to intercurrent maladies.

Leaving out of consideration sucklings under six months of age, in whom measles is rare and said to be slight, most deaths from the disease occur among very young children, from their greater liability to complications. According to Beddoes,[39] the mortality from measles is, beyond all comparison, greatest in the second year of life, and by the tenth has become quite trifling. An examination of the statistics bearing on this question coincides with this general statement; but Fox's tables, already quoted, would show that more infants under one year of age die of measles than has hitherto been supposed. The susceptibility to measles decreases with years, perhaps on account of the fact that most adults have already contracted the disease; but when it does attack the unprotected adult it may prove fatal. This statement is borne out by the large death-rate in the so-called camp measles of our late war.[40] The ravages of measles in virgin communities have been referred to in preceding pages. The general temper of the epidemic must also be considered, since it is well recognized that the essential character of epidemics differs much as to severity.

[Footnote 39: Art. "Mortality" in Quain's Dictionary Med., p. 1002.]

[Footnote 40: In the general field hospital at Chattanooga the death-rate was 22.4 in 100 cases. In General Hospital No. 1, at Nashville, it was 19.6 in 100, or nearly 1 in 5. Many died or became permanently disabled from the sequelæ (Bartholow).]

Such complications as diphtheria, catarrhal pneumonia, diarrhoea, convulsions, etc. necessarily affect the prognosis of measles most seriously. More patients die of measles in the second than in the first week of the disease. The careful studies of temperature made by Thomas, Bohn, and others show that an unusually high and increasing fever in the prodromal stage is of ill omen, particularly on the second and third days, and a fever heat measuring over 105° F. at any stage should be considered as very unfavorable.[41] Particularly to be feared is continuation of the fever after the subsidence of the eruption, or a sudden elevation after the normal curve has been reached. In fact, it is a safe rule to look upon all anomalies of the curve with suspicion. Secondary measles, or measles grafted upon some serious existing affection, is particularly fatal.

[Footnote 41: In adolescence a body heat of 107° F. has been safely passed during the decline of measles with no marked complication (Squire).]

TREATMENT.--There is no remedy which will destroy the susceptibility to measles. The future may develop some form of vaccination against rubeola, for, certainly, the hopes held out by the inoculation of measles upon the healthy subject have not been realized, as this procedure merely reproduces the original complaint, without any diminution in its intensity, and does not lessen the probability of complications (Mayr). The matter of carrying out a practical and efficient quarantine in measles is one of unusual difficulty, for the reason that the disease is capable of active propagation at a time--the prodromal stage--when it is not yet sufficiently characteristic for positive diagnosis. But, as measles is by no means as trivial a disease as would seem to be the common impression, I hold it as a well-established principle of preventive medicine that a {579} strict isolation should be enforced whenever, from the nature of the case, it is at all possible; certainly, very young children and those suffering from or showing a tendency to other diseases should be jealously shielded from exposure.

The usual precautions as to disinfection and purification of the room, bedding, and utensils used by patients should be observed, as in other infectious diseases. Squire is of opinion that there is danger of personal infection for perhaps a month, and Hillairet that isolation for forty days should be enjoined. It is quite certain that inunction lessens the danger of infection, and Kaposi[42] is authority for the statement that a warm bath administered after the completion of desquamation, or about fourteen days from the beginning of the attack, will effectually prevent contagiousness.

[Footnote 42: Pathologie u. Therapie der Hautkrankh., Wien, 1880.]

The apartment occupied by a patient suffering from measles should be kept at a uniform temperature of from 66° to 70° F., and free ventilation, at the same time avoiding draughts, should be enforced. The room should be kept moderately dark. The bed-clothing should be light, yet sufficiently warm, and the old notion of keeping the patient in a profuse sweat the better to bring out the eruption should be discouraged. The diet should be bland and nutritious, and may preferably consist of milk, gruel, tapioca, and such like substances. As convalescence progresses there may be a gradual return to more substantial food. The patient may be allowed cool water in moderation, as it is cruel and useless, and even harmful, to restrict one suffering with fever to warm or sweetened drink. The patient should be confined to his room until convalescence has been fully established, and should not be allowed to leave the house, both on his own account and that of others, until the usual health has been regained. Any of the lingering results of the disease, such as bronchitis, otorrhoea, conjunctivitis, etc., should receive prompt attention; iron and cod-liver oil should be prescribed for the weakly and strumous, and regular hours of sleep, careful diet, and appropriate bathing and exercise should be advised. It may be said, without exaggeration, that neglect of the after-care of measles patients is, in some instances, more to be deprecated than a similar neglect in the actual treatment of the disease itself.

Since we are powerless to cut short an attack of measles by any remedial agents at present known to therapeutics, the intervention of the physician is limited to assisting the cases through to a safe termination. Quite a number of cases, as seen in private practice, require no special medicinal treatment, or at most one that is merely symptomatic. The value of the so-called specific treatment, such as by carbonate of ammonium, etc., has not been verified by experience.

In ordinary uncomplicated attacks, if the temperature should run high, in addition to the general rules as to diet and hygiene referred to before it will usually be found advisable to put the patient on some diaphoretic mixture, to which may be added a mild opiate. I know of nothing better than the formula found in the work of Meigs and Pepper on the Diseases of Children:

Rx. Potass. Citrat. drachm i; Spt. Ætheris Nit. fl. drachm ii; {580} Tr. Opii Deodorat. minim xii vel xxiv; Syrupi fl. drachm ii; Aquæ fl. oz. ii. M.

S. A teaspoonful every two or three hours for a child of five years of age.

Aconite in small doses has been well spoken of in this connection, but I have no personal experience in its use. Bromide of potassium, together with a few drops of syrup of ipecac., dissolved in syrup of wild cherry, acts pleasantly both on the cough and the nervous system.

The inunction of fatty substances, as originally proposed by Schonemann, and recently urged by Milton,[43] is an excellent routine practice, and in addition to adding very much to the patient's comfort, has, perhaps, the merit of lessening somewhat the danger of infection to others. For this purpose one may use leaf lard, cold cream, or vaseline, to each ounce of which it is well to add a few minims of carbolic acid.

[Footnote 43: Archives of Dermatology.]

Stimulants are rarely needed in uncomplicated measles, but Squire very wisely calls attention to the great value of wine in the depression following upon the crisis.

In spite of some excellent authority to the contrary, I cannot see that any benefit is to be derived from using severe measures to bring out an eruption that has undergone retrocession. As stated in another part of this article, the so-called striking-in of the rash is the result of the supervention of some complication, and not the cause of it; therefore, a rational course of action would be to ascertain the nature of the complicating trouble, and to endeavor to correct it, which, at the same time, would be the very best means of restoring the normal course of the disease.

Quinia is of great value in controlling the excessively high temperature which is sometimes observed either in connection with, or independent of, complications. If the quinia should prove ineffectual or else be rejected by the patient, the physician should not hesitate to abstract heat by cold water in the shape of the wet pack or the general bath. I think the latter method is to be preferred. It is but to employ the gradually cooled bath of Ziemssen, perhaps, commencing at 90° F. and going to 80° or 70° F. The condition of the patient, as ascertained by the thermometer and also the state of the pulse, must be the guide as to the duration and repetition of the baths. In Germany excellent results are claimed for the treatment of hyperpyrexia in measles by the cold pack, even when the excessive temperature is due to such a complication as broncho-pneumonia.

There is little hope from therapeutical interference in malignant forms of measles, but the medical attendant should endeavor to reduce temperature and support the strength by free stimulation and nourishing food.

It will now be advisable, at the risk of some repetition, to call attention to the treatment of some of the more prominent disturbances and complications of measles.

Epistaxis, if severe, should be checked by cold applications and astringents. Plugging will rarely be found necessary. Trousseau recommends the injection of water as hot as can be borne. Ergotine by the mouth or hypodermically will sometimes prove highly valuable.

The lids should be anointed with vaseline or cold cream to prevent their sticking together, and it is well to occasionally evert them to see that no {581} serious mischief has happened to the eye. If the conjunctivitis is intense, the discharges should be removed and cold compresses applied.

Since aural complications are due to extension of inflammation from the oral and nasal cavities, Spencer urges the importance of early and systematic treatment of these parts. He advises astringent applications (Monsell's solution 1 to 4 of glycerine) to the pharyngeal mucous membrane. Ointments of boracic acid, zinc, or iodoform are likewise useful when introduced through the nostril. Earache will require warm opiated poultices and inflation. Otorrhoea is best treated after the dry method.

For sickness of the stomach a spice poultice may be applied and small bits of ice given to suck. If constipation exist, a little oil or syrup of rhubarb or some stewed prunes, or an enema, may be ordered. Active purgation should be withheld.

The early diarrhoea need give little concern, as it usually soon ceases; but if it should persist, recourse must be had to more energetic measures, such as the use of opium by mouth or enema, given cautiously in the case of children, vegetable and metallic astringents, and the application of hot poultices to the abdomen. The diet should be carefully guarded.

The cough, even in mild cases, generally requires some slight palliative, such as syrup of ipecac., and an occasional small dose of Dover's powder. Loeri very properly advises against the use of irritating expectorants. I think it advisable to keep the chest well smeared with camphorated oil, over which should be worn an oil-silk jacket. These simple measures, perhaps, diminish the tendency to thoracic complications. The sometimes violent paroxysms of false croup are very satisfactorily managed, after the manner of Graves, by gently pressing a sponge, soaked in very hot water, under the chin and over the front of the neck. When the dyspnoea is alarming, emetics, and the general warm bath should be brought into requisition.

Convulsions in the early stage require little treatment other than the warm bath and appropriate doses of the bromide of potassium; occurring later, they are very fatal under any treatment, as they generally supervene in connection with some of the grave complications of the disease. Chloral, preferably by enema, and chloroform may be tried. The management of the severe bronchitis and pneumonia of measles requires great care and circumspection on the part of the physician. The application of a well-made flaxseed poultice, which should be neither too heavy nor too hot, is to be regarded as invaluable. To the flaxseed may be added a small quantity of mustard. Over the whole is to be placed an oil-silk jacket. Alcoholic stimulants, nourishing, easily-digested food, and expectorants containing carbonate of ammonium are to be recommended.

For the treatment of the other complications and sequelæ of measles the reader is referred to the appropriate sections of this work.

{582}

RÖTHELN.[1]

BY W. A. HARDAWAY, M.D.

[Footnote 1: In the preparation of this article the author has consulted the following authorities: Emminghaus, in Gerhardt's Handb. der Kinderkrankh., Zweiter Band, 1877; Thomas, in Ziemssen's Cyclop. Pract. Med., vol. iii., Am. ed., 1875; Squire, in Quain's Dict. Med., 1883. References to current literature will be found in foot-notes to the text.]

SYNONYMS.--Rubeola, Rubella, Roseola, Epidemic Roseola, German Measles, French Measles, Hybrid Measles, False Measles, Rubeola Morbillosæ et Scarlatinosæ.

DEFINITION.--Rötheln is an acute infectious disease, presenting an eruption of reddish macules upon the skin, accompanied by mild catarrhal symptoms, and usually producing but slight disturbance of the general system. It is self-protective, and occurs but once in the same individual. It has no relationship to measles or scarlatina.

HISTORY.--A rapid glance at the interesting historical evolution of rötheln to a specific position among the acute infectious diseases is all that our space will allow. Some writers have attempted to show that this affection was known to the Arabian physicians; but since it is only in comparatively recent times that the contagious epidemic exanthemata in general have been thoroughly differentiated, it is quite likely that the modern conception of it was not held by them nor by other medical men till many centuries later. Indeed, in our day, physicians are yet to be found, though the number is rapidly diminishing, who refuse to recognize in rötheln a distinctive specific malady. Certain German observers in the middle of the last century (De Bergen, 1752; Orlow, 1758) favored the idea of specificity, but these views were soon disputed. In the years following a number of other physicians announced their belief in the specific nature of rötheln, while, on the other hand, various noted authorities still insisted upon its connection with scarlet fever or measles. In 1815, Maton, an English physician, most unequivocally declared that he had observed cases of an eruptive disorder which resembled neither measles, scarlatina, nor roseola, and which was worthy of a new designation.[2] In the second and third decades of this century Hildebrand, and afterward the celebrated Schönlein, taught that rötheln was a hybrid of measles and scarlatina, although at this time Wagner (1834) advocated the essential independence of rötheln. There is no doubt that under the name of rubeola sine catarrho Willan, Bateman, and later writers described what we now call rötheln, for they stated that this variety of measles was not self-protective. Space will not allow of a detailed mention of the various writers who, during the first half of this century, {583} have contended for or against the autonomy of rötheln. It will be well to state, however, that Hebra, from the standpoint of the dermatologist, very properly regards the manifold roseolæ of Willan as in many instances merely symptomatic erythemata, or else as irregular forms of measles or scarlatina; but he also fails to recognize the distinctive features of rötheln. Even so recent a writer as Niemeyer declares that roseola arising from infection consists in a modification of measles or scarlet fever. It is only in the last twenty years that our present exact ideas of rötheln have obtained. For example, while Trousseau[3] asserts that rubeola (rötheln) is a perfectly distinct nosological species, he speaks of the rash as appearing and disappearing alternately for some days, of its frequent recurrence in the same individual, etc. American physicians were almost entirely ignorant of rötheln till within the last ten years, when they were made acquainted with it through the medium of a careful paper on the subject from the pen of J. Lewis Smith of New York.[4] Before this time, however, cases had been described by Homans, Sr., of Boston (1845), and in 1853 and 1871 by Cotting. Very few authorities now dispute the distinctive specific nature of rötheln; which statement is borne out by the fact that at the last meeting of the International Medical Congress, held at London in 1881, there were but two dissentients to this view in the section before which it was discussed.[5]

[Footnote 2: Squire, Trans. Internat. Med. Congress, London, 1881.]

[Footnote 3: Clinical Medicine, vol. ii.]

[Footnote 4: Archives of Dermatology, Oct., 1874.]

[Footnote 5: See especially Kassowitz's paper, "Die Wirkliche Stellung der sogenannten Rubeola," etc., Trans. Internat. Med. Cong., 1881.]

ETIOLOGY.--The contagium of rötheln is unknown, but that the disease is contagious has been fully demonstrated by numerous observations of epidemics and sporadic cases. From my own experience I should judge that unprotected persons are not so susceptible of it as is known to be the case under similar conditions in measles;[6] yet cases are recorded which would prove that the contagion may be conveyed through a third person and for some distance. It is probable that the vehicles of contagion are the same as in measles. At what period of its course the disease is most capable of transmission has not been satisfactorily determined. Squire is of the opinion, however, that the disease is contagious before the appearance of the rash, and may continue so for some days or for two or three weeks. Rötheln may be called a disease of childhood for the same reason that the other contagious exanthemata are--namely, that the majority of adults have already been attacked. From an examination of available statistics I am inclined to regard the ages between five and fifteen--the years of school attendance--as the period of life most susceptible of the influence of rötheln, although, of course, no time of life is entirely exempt. The non-susceptibility of sucklings, as in measles, holds true as a rule, although I am in a position to supply exceptions to this from my own experience, as well as from that of others. Sex seems to be without influence in determining liability to the disease.

[Footnote 6: In this regard it resembles scarlatina more than measles, for I have a number of times seen the disease introduced into families, where it would attack one or two of a number equally exposed. J. L. Smith regards it as feebly contagious, and quotes Chadbourne's experience to the same effect. Liveing declares that rötheln is more distinctly epidemic in Great Britain than either measles or scarlet fever, although probably less contagious.]

The period of incubation is not very definitely settled, and, indeed, {584} owing to the generally trivial character of the affection, evidence on this point is difficult to obtain. Taken as a whole, it is probably longer than is observed in measles. According to J. Lewis Smith, in the epidemic observed by him the incubation period varied from seven, or less than seven, to twenty-one days; Emminghaus places it at from two to three weeks; Thomas, from two and a half to three weeks; Squire, mostly a fortnight, the extreme being twenty-one days; Cheadle, from eleven to twelve days.

There is nowhere recorded a trustworthy instance of a second attack of rötheln, although from analogy such an event is to be expected. As in measles, true recurrences of rötheln--that is, the result of a fresh infection--are not to be confounded with relapses. I have never witnessed a relapse, but cases of such a nature have been recorded by other observers (Lindwurm, Emminghaus, Körtlin, Kingsley).

Rötheln is a disease sui generis, and is in no way related to either measles or scarlatina; that is to say, it is not an irregular form of either of these nor a hybrid of them, nor has it ever been observed to propagate anything but itself. That it is not connected with any of the symptomatic skin eruptions--the so-called roseolæ--is proved by its contagiousness and epidemic character. I quite agree with other observers in declaring that rötheln has very little clinical resemblance to scarlatina, and that, on the other hand, in the greatest number of cases the points of likeness are with measles. In the section on diagnosis the differential points between rötheln, measles, and scarlatina will be considered; therefore in this place it will only be necessary to call attention to certain general facts. Thus, aside from the marked divergence in clinical symptoms--incubation, invasion, fever, eruption, complications, and sequelæ--we are at once met by the positive fact that epidemics of rötheln, while always presenting identical features, prevail without regard to the existence of similar epidemics of measles and scarlatina--following or preceding them--and that attacks of rötheln offer no bar to the reception of their contagions, or vice versâ. Literature is so full of examples of this statement that it need scarcely be dwelt upon. By way of illustration, however, the accurate observations of J. Lewis Smith may be quoted in this connection. Of 48 cases recorded by him prior to May 1st in the New York epidemic of 1874, 19 had had measles. Rötheln in the N.Y. Foundling Hospital in 1873-74 followed an epidemic of measles. During the epidemic of 1880-81 the same fact was observed--namely, that a previous attack of measles, as well as scarlatina, afforded no protection from rötheln. I could multiply such examples from my own experience. A single interesting instance may be noted here. A physician asked the writer to examine his child, suffering, as he thought, from measles. A careful investigation revealed a typical rötheln. A number of weeks later an older child got measles, from which the rötheln patient acquired a characteristic attack of the same. In the following year both children were taken with scarlet fever.

The only escape for those who would deny the autonomy of rötheln is in the bold assertion that both measles and scarlatina more frequently recur in the same individual than universal experience and observation will allow; and this leaves them in the dilemma of determining to which group rötheln must be relegated. The hypothesis of the hybrid nature {585} of rötheln cannot be accepted by the pathologist nor the clinician, if for no other reason than that no one has ever seen rötheln generate anything but rötheln, and in no case give rise to either scarlatina or measles.

SYMPTOMS AND COURSE.--As already stated, the probable average duration of the incubation period in rötheln is about fourteen days, varying, however, within the limits of from six to twenty-one days. In this respect rötheln resembles scarlatina more than measles, the period of latency in the latter observing considerable uniformity. No deviations from the general health are to be noted in the incubation stage.

In most cases prodromal symptoms are entirely absent, the presence of the eruption being the first thing to show the existence of rötheln in the system. On the other hand, in a certain proportion of cases there will be present for a half day, or even longer, the general symptoms of malaise, such as slight nausea, some sore throat, pain in the limbs, stiffness of the neck, etc. Vomiting is generally absent. J. L. Smith records one case of convulsions in the stage of invasion, and I have notes of a single case in which the prodromal stage was initiated by mild delirium and fever, the latter anticipating the eruption for two days and a half, and disappearing when the rash came out. As Thomas well observes, however, such cases are anomalous, and indicate either abnormal sensibility on the part of the patient or are due to a secondary rötheln.

Most observers (Emminghaus, Thomas, Smith, Squire) describe the rash as coming out in the order usual in measles--namely, first upon the face, scalp, and neck, then the trunk and arms, and finally the legs. Others (Liveing, Morris) have stated that the rash first appears upon the back and chest. In many cases in my own experience this has seemed to be true. It is quite probable that the situation of the exanthem in rötheln, as in measles and scarlatina, may present various irregularities; but I am inclined to believe that a careful investigation will in most instances show that the normal course of the eruption is as first stated. Now, a marked characteristic of the rash of rötheln is that, unlike that of measles, there is no period, however short, in which its maximum is simultaneous over the whole body; on the contrary, the eruption will have reached its full development upon the face, and will be almost or quite faded again, before the exanthem, for example, will have blossomed upon the trunk, and especially upon the lower extremities. The duration of the eruption upon individual parts of the body is probably from a few hours to half a day at most (Thomas). A consideration of these facts explains, according to Emminghaus, how different observers have described the eruption as having its seat upon this or that region of the body; in other words, it is probable that in a certain proportion of the cases in which the rash was supposed to have begun on the chest it had already run its course upon the face. The eruption usually continues altogether about four days, sometimes disappearing sooner, and sometimes being visible, especially as a fine mottling, for some days longer. So far as the individual lesions of the eruption are concerned, there is no question that they present, within a certain range, varying aspects; and this clinical fact has been taken advantage of by the opponents of the idea of specificity in order to make it appear that the disease is not sui generis, inasmuch as it lacks uniformity of expression. Such an argument wants force when we consider that in making up a given diagnosis we lay stress {586} not upon special, but upon the ensemble of, symptoms. For example, no one would deny to measles an independent position because the eruption, as is well known, may assume this or that form (morbilli lævis, m. papulosi, etc.); on the contrary, we recognize a particular case or series of cases to be measles from a due appreciation of all the symptoms present. So it is to be expected that while the cutaneous lesions will present a certain similarity of feature, as they do, there will also exist minor differences in detail.

In the greatest number of cases in my own experience the exanthem is composed of ill-defined, roundish, punctate macules, without special grouping. These are usually discrete, but in certain situations they may coalesce. The color is of a pale rosy red, quite difficult to describe, but less purplish than in measles, and not so livid a red as in scarlatina. I have occasionally observed large irregular spots not unlike those of measles.[7]

[Footnote 7: According to Emminghaus (op. cit., p. 345), the eruption generally forms roseolæ of pin-head, lentil, or small bean size. They are mostly round, sometimes oval, and bordered by well-defined or by blurred edges. The intervening skin is not always unchanged, for here and there we find upon it small dilated blood-vessels, and from the spots processes extend with a certain regularity to other spots in such a way as to give the skin a marbled appearance.]

Thomas distinguishes three types of eruption--one with large spots, which is rare; one with medium-sized spots; and one with small spots. Emminghaus describes a discrete and a more confluent variety. I have observed one case where the maculæ on the back had undergone a vesicular transformation. Others have mentioned this occurrence. Itching of the skin is marked in some cases, and a fine desquamation is observed after the rash, but by no means invariably.

The mucous membranes are implicated to a slight degree in rötheln, but the amount of involvement varies considerably. In some cases that I have observed the catarrh of the mucous membranes has been barely appreciable. As a rule, however, the eyes are somewhat suffused, and there is slight lachrymation and photophobia. Sneezing may be noted, but there is little discharge from the nose. Sore throat is not uncommon, perhaps the most constant feature, and, according to Liveing, is apt to persist after the subsidence of the rash. The fauces are injected, and the tonsils are red and swollen, but with no evidence of ulceration. J. Lewis Smith and others state that the buccal mucous membrane shows a more or less diffuse patchy and spotted redness. The tongue may be, and usually is, covered by a white fur, through which protrude a few enlarged red papillæ. There may be slight cough. Loeri[8] describes the mucous membranes of the pharynx, larynx, and trachea as presenting a spotted or uniform hyperæmia. There is no marked participation of the intestines in the catarrh. Some few writers have noted a transient albuminuria, but it is safe to say that such cases are entirely anomalous, if not, indeed, in some instances, examples of mistaken diagnosis.

[Footnote 8: Jahrb. f. Kinderk., xix. Bd., 1 Heft.]

A very constant feature is the swelling of the lymphatic glands of the neck, especially those back of the sterno-mastoid; the swellings may come on before the rash appears. In all the cases that have fallen under my notice this symptom has not been absent in a single instance. Less constantly, and it would seem in proportion to the development of the rash, engorgement of the glands may be noted elsewhere.

{587} There is but slight disturbance of the temperature in rötheln, and when it does occur it is usually limited to the first few hours of the eruption. This has been the rule in my observation, and certainly holds good for the majority of cases. In a minority, varying degrees of fever may be present; thus, the temperature may reach 102° F. or 103° F., and then rapidly sink by the second day of the disease, or, having fallen a degree, it may continue at this point till the subsidence of the rash, or, it is said, may retain its initial height till the end of the disease. During the following week Squire states that the temperature may be readily disturbed--either elevated by exertion or depressed by fatigue or chill. A relapse or recrudescence of the rash may be looked for at this time.[9]

[Footnote 9: Cheadle (Trans. Internat. Med. Congress, London, 1881) has reported an epidemic of rötheln of a very severe type, all the symptoms of the disease as ordinarily recognized being very much exaggerated.]

COMPLICATIONS AND SEQUELÆ.--In the vast majority of cases neither complications nor sequelæ have been observed in connection with rötheln. J. Lewis Smith has recorded instances of diphtheritic inflammation as a complication, which, however, as he justly remarks, may, when prevalent, attack any inflamed surface. Pneumonia and bronchitis have been occasionally reported as complicating or following rötheln. Liveing and Duckworth mention albuminuria, but, so far as I know, they are alone in this experience. I have known otorrhoea and ciliary blepharitis to occur as sequelæ. It would not be a matter of surprise that in weakly children various chronic ailments should be set up by rötheln, as by any other disturbance of the general health.

DIAGNOSIS.--There is no other disease which so much resembles rötheln as measles. Especially is this true of atypical cases occurring sporadically. In rötheln the whole course of the disease is much milder than in measles, the incubation is longer as a rule, and the fact of a previous attack of rubeola is of much importance, since we know that recurrences are very rare. In measles there is a prodromic period, having a characteristic temperature curve, and presenting pathognomonic catarrhal symptoms, which precedes the eruption for three or four days; in rötheln the appearance of the rash is often the first sign of the affection. The sore throat of rötheln resembles that seen in scarlatina more than the angina of measles, and the general catarrhal implication of the mucous membranes, so marked a feature of measles, is either absent in rötheln or exists to a very trivial extent. Measles is essentially a febrile disease, having a peculiar type of fever; rötheln may run its whole course without appreciable rise of temperature. As will be seen in the preceding pages, the development and progress of the exanthem of measles differs materially from that witnessed in rötheln. In measles the lesions are larger, more vivid, more angular and indented, more frequently provided with processes, and therefore more apt to assume the crescentic arrangement, than in rötheln. Finally, it must be urged that the tout ensemble of the case should be taken into consideration, and not some special feature of the skin eruption.

The incubation period of scarlet fever is much shorter than in rötheln, and all of the constitutional symptoms are, as a rule, infinitely graver. In scarlatina there is a febrile invasion stage of twenty-four hours; in rötheln, if fever is present at all, it is most generally simultaneous with {588} the rash, and rapidly disappears, while in the former it persists for a number of days longer. Vomiting is common in scarlet fever, rare in rötheln. In scarlet fever the lymphatic glands are notably involved at the angles of the jaw, in rötheln at the sides and back of the neck. Sore throat is a feature common to both scarlet fever and rötheln, but it is very much less marked in the latter. Thomas[10] says that in scarlatina only the posterior parts, the uvula, the arches of the palate and their vicinity are affected, while in rötheln the anterior parts are also affected, and both in much the same degree. In scarlet fever the rash, which mostly begins on the neck and chest, is made up of large patches formed of minute red spots on a bright-red hyperæmic base; in rötheln the eruption is composed of roundish pea-sized macules, with normal integument intervening. In cases of doubt--for example, when the rash of rötheln consists of very small spots which have become confluent--the further development and persistence of the scarlatinal efflorescence, the temperature, the pulse, the angina, and the character of the desquamation must be taken into consideration. The complications and sequelæ are very different in the two diseases.

[Footnote 10: Article "Scarlatina," op. cit.]

The symptomatic eruptions of the skin which pass under the name of roseola bear no resemblance to rötheln. They usually occur as the result of some trivial derangement of the system or in the course of some primary affection. They are not contagious, the lymphatic glands and the mucous membranes are not involved, and the rash is quite different in character.

PROGNOSIS.--The prognosis of simple uncomplicated rötheln is invariably good. Complications arising in delicate children necessarily affect the prognosis, as would any other disturbance of the general health.

TREATMENT.--Simple cases of rötheln require no treatment, as the patients are rarely sick enough to be confined to bed. Graver forms of the disease must be met by such measures as are indicated by the symptoms present. The after-management must be conducted on general principles having reference to the previous and present condition of the person attacked.

{589}

MALARIAL FEVERS.

BY SAMUEL M. BEMISS, M.D.

In the medical nomenclature of this country the term malaria is synonymous with swamp or ague poison.

Malarial affections, therefore, comprise all those diseases or morbid manifestations which the swamp poison produces in the human organism.

This article is not designed to notice in a systematic manner any of these disorders which are not properly classifiable under the head of malarial fevers. It will, however, be necessary to make such references to the pathology of chronic malarial toxæmia as may serve to explain the influence this condition exerts in occasioning departures from type in the febrile attacks.

When a poison generated outside the human system obtains admission to it, and produces deleterious effects, three questions naturally arise: What is the essential character and natural history of this noxious agent? How does it obtain access to the human system? What is its mode of action when received?

In reference to the first of these questions, it must be admitted that the substantive essentiality of the malarial poison remains as yet undemonstrated. It is true, however, that the attempts at an objective study of this poison by means of the microscope and the cultivating retort point to the conclusion that it is an organism.

Its subjective or analogical study affords quite incontestable evidence in support of this conclusion. The leading features in the natural history of malaria are closely coincident with those of certain known organisms. It requires for its production suitable conditions of moisture, temperature, and a properly circumstanced breeding-place. Within certain bounds these conditions are requisite to the life and perpetuity of all organisms.

Again, when all the above-enumerated conditions correspond apparently in the most favorable degree, their continuous concurrence for a lapse of time is necessary before the poison manifests its presence. It is not improbable that this period of development may differ in different climates, but in this country we assume it to be about thirty days. If these facts related to some noxious organism visible to the eye, no doubt would be entertained that the presence of its germs in the places where it appeared was the indispensable condition. It would then follow that the concurrence of suitable meteorologic and telluric conditions with sufficient time for its growth and maturity were merely accessories to its perfect development. According to this theory, the coincidence of five circumstances is necessary before malaria can be fully matured--viz.: Its own {590} specific germ; suitable soil or pabulum; suitable moisture; suitable temperature; sufficient time for its growth and development.

Certain physical qualities which pertain to the malarial poison can also be profitably made points of subjective study. These are very closely connected with the answer to the second question, or "How the malarial poison obtains access to the human system." They will therefore be briefly noticed in relation to the instrumentality of each in conveying malaria into the system.

The first to be mentioned is ponderability, which the following facts prove that malaria possesses:

Those different atmospheric states which affect the range of diffusion of known air-borne yet ponderable substances exert similar influences upon the malarial poison.

Altitude illustrates the ponderability of malaria by powerfully retarding its diffusion.

High readings of the barometer favor its aërial dissemination.

Fogs, smoke, dust, or floating particles presumably more buoyant than this poison may exert greater or less influence in overcoming the obstacle which ponderability attaches to malaria as an air-borne agent.

Currents of air passing continuously and steadily in one direction over the breeding-places of malaria increase the limits and intensity of toxic range.

The atmosphere is undoubtedly the medium by means of which malarial poison is most frequently brought into the human system. Liability to intoxication is increased in direct ratio to the proximity of points of exposure to places of development; to similarity of level; to situation in the line of prevailing winds which have traversed the breeding-ground; and, lastly, to the extent and fertility of the locality of production.

Whether malaria passes through the respiratory apparatus directly into the circulation, or is lodged upon the fauces and absorbed through some other surface, is not clearly ascertainable. It is certainly not deprived of its noxious qualities by stomach digestion, and therefore, sometimes at least, may reach the blood through the alimentary canal.

Malaria is miscible with water. It is capable of being carried by currents of water through distances and periods of time altogether undetermined, without losing either its toxic effects or, perhaps, the faculty of reproduction. It is more than likely that this means of conveyance has effected its distribution to continents and islands too widely separated to justify a belief that it was wind-wafted. No observations need be adduced to establish the water-borne habit of the malarial poison, or the positive liability to its toxic effects when received into the stomach through this medium. These facts have been well understood from the time of Hippocrates.

The matter of communicability of malaria by means of drinking water should not be dismissed without some allusion to the great probability that other fluids or solids are open to a similar charge. There is a widespread popular prejudice, especially notable in the southern part of the United States, that drinking milk occasions attacks of the endemic fevers. It is the usual custom to pour the evening supply of milk into broad uncovered pans, and allow it to remain exposed in the open air for {591} consumption at the morning meal. This viscid fluid, so tenacious of ordinary air-borne particles, may well be suspected of entangling sufficient quantities of swamp poison to produce sickness if exposed where it is rife during a whole night.

A similar popular prejudice exists in regard to the muscadine grape, which flourishes best in swampy localities. The rough skin of this fruit, frequently covered with its own juice, offers favorable conditions for the adhesion of air-borne particles.

The malarial poison is not reproduced within the human system. This proposition is undeniable, since no intensification of the poison is produced by any degree of crowding of the sick which can be practised; neither do any conditions of contact with the sick ever impart malarial affections.

Malarial poison is specific. This allegation is sufficiently established by its specific effects on the human economy. There is no other agent known which is capable of originating morbid phenomena characterized by such marked diurnal periodicity.

It is not interchangeable with other specific poisons. This statement may be rested upon all fairly collected clinical observations.

There are no facts which justify the belief that malaria is capable of becoming mixed in the atmosphere, or outside the system, with any other specific morbific germ, so as to produce a third something which may give rise to compound forms of disease.

The answer to the second question which is best supported is, that the malarial poison is brought into the system principally by breathing an atmosphere impregnated with this miasm.

It is also ingested by being held in suspension in fluids used as drink or food; perhaps also by eating certain fruits or vegetables in their natural state whose external surfaces afford favorable conditions for its lodgment.

MORBID EFFECTS AND PHENOMENA WHICH FOLLOW ITS INTRODUCTION INTO THE HUMAN SYSTEM.--The discussion of the morbid process established by the malarial poison involves some difficult problems. A period of incubation must be admitted to follow the inception of the ague germs. But this period has no definitely marked limits. Perhaps it is a shifting one, according to the quantity or quality of the poison received, or the sudden or gradual manner in which it is received, or the state of receptivity of the system.

Certain facts seem to indicate very clearly that malarial poison is very slowly removed from a system which has been brought under its influence. These evidences of long systemic residence of the poison are principally displayed in those attacks which occur after long periods of removal from any surrounding where intoxication was possible. Vernal attacks may be classed in the same connection. In many instances the subjects of these long-delayed attacks have never suffered a paroxysmal seizure, and yet when some accidental derangement of health occurs, as from a fit of indigestion or a sudden wetting, they fall sick with one or another form of malarial fever.

It does not appear to me that we are justified in assuming that such attacks as I refer to are to be ascribed to secondary changes produced in either the fluids or solids of the system by the malarial poison. In so {592} far as the clinical phenomena are worth anything in demonstrating the presence and agency of the specific malarial poison in these deferred attacks, they are precisely similar to those observed in paroxysms arising after a few hours' or a few days' exposure to marsh miasm.

But we find further proofs of the long-continued and silent manner in which malaria exerts its pathological influences in those enlargements of the spleen which occur without specific attacks of sickness. The alterations of nutrition in this organ are so characteristic of malaria that they can scarcely be supposed to depend upon those chances which determine the nature of secondary blood-impurities.

Intermittent Fever--Simple Forms.

The clinical phenomena of intermittent fevers afford strong support to the opinion that this type of malarial attacks illustrates more strongly than any other the primary influence of the poison upon the human system. Fits of ague often occur very shortly after exposure in infected localities, and the persons thus suddenly attacked may present little or no evidence of cachexia before or after the paroxysm. Indeed, they frequently resume their ordinary avocations after the paroxysms, apparently as well as if they had not occurred.

It is therefore my opinion that the pathology of an intermittent fever does not necessarily involve an hypothesis that the attacks are the results of certain changes which the poison undergoes after its inception, nor, on the other hand, that certain perversions of systemic chemistry are required to inaugurate the paroxysms.

In accordance with these conclusions, it seems likely that the phenomena of intermittent malarial fever result from the primary effects of its specific poison exerted directly upon the fluids and solids of the system, and disturbing their functions, and especially the nerve-function.

Those malarial attacks which ensue almost immediately after exposure are principally manifested in persons exposed at points of unusually abundant evolution. The rule of malarial attacks in temperate latitudes is, that they require repeated exposure to infection for their production. The long residence of the poison in the system may render additional doses possible, until a point of saturation is reached which occasions paroxysmal explosions. In these cases the period of incubation is reckoned from the first date of exposure, thus forming the most striking contrast with the incubative periods of the cases occurring almost immediately after exposure.

Whether the quiescent period after exposure to malaria be long or short, attacks are seldom abrupt in their announcement. The symptoms which usually precede pronounced attacks consist, for the most part, in some derangement of the functions presided over by the organic nervous system. Derangement of digestion, vitiated taste, coating of the tongue, loaded urine, and sallow skin are ordinarily found among the prodromic symptoms. Next in succession come feelings of malaise, hot and cold flushes, and those neuralgias which precede and attend malarial paroxysms.

The symptoms of an ordinary or typical malarial paroxysm are so characteristic, as to be generally readily interpreted. Creeping, chilly, {593} sensations over the surface, especially along the spine, yawning, livid coloration beneath the finger-nails, retreat of blood from superficial capillaries, and that consequent papillary elevation which is commonly called goose-skin, comprise the earliest symptoms. Then decided shiverings with chattering of the teeth come on, and the patient asks for blankets to be heaped upon him and hot applications to be made, even though the atmospheric temperature may be decidedly elevated.

Nausea and vomiting are frequent symptoms, no doubt due to the fact that the portal system of blood-vessels is so often the seat of congestion during a chill. No intelligent practitioner can watch a patient during the cold stage of a malarial paroxysm without realizing how important the attendant congestion is as a pathological state. It should first be considered that every chill necessarily implies a condition of congestion in some part of the system. The blood driven from the surface and extremities must be accounted for elsewhere; and the amount of blood which is lost from one part of the circulatory tree must correspond with that accumulated elsewhere. But in treating of the pernicious forms of malarial fevers this question will again receive notice.

In our present state of knowledge we are no more able to explain those perversions of the normal action of the physical forces of the system which occasion the phenomena of a chill than we are to explain how the altered circulation in the first steps of an inflammation is brought about. The theory which Cullen adopted is quite as explanatory and consistent as any which has been promulgated since his time. According to this, a state of spasm of the arterioles and capillaries causes the chill, while the fever is merely the rebound of functions held in abeyance during the chill.

After a variable length of time there occurs a change in these symptoms: the patient begins to remove the blankets which covered him; the face shows signs of returning circulation; the veins of the whole surface gradually fill again, apparently beyond their normal state. But the reaction goes far beyond any normal physiological state. The face becomes flushed and the eyes injected, and the patient complains of headache, thirst, dryness and heat of the surface; he will not permit any covering, and constantly shifts his place in the bed in the hope that some new position may afford him more comfort. Nausea and vomiting are commonly present. If the fever runs high, delirium is apt to occur. The thermometer seldom shows a temperature above 105°, but I have seen 106.5° recorded in the axilla in the hot stage of a paroxysm of simple intermittent fever.

The duration of the hot stage is different in different cases. According to Aitken, the mean duration is three to eight hours.

There is a very old and quite well-supported opinion, that the cold stage is shorter in the quotidian than in the tertian type, and also that the hot stage is longer in the former than in the latter. It may certainly be affirmed that in individual cases of either type there is no fixed relation between the duration of the chill and that of the hot stage.

The decline of the hot stage begins by the appearance of a gentle perspiration, limited at first to the forehead, face, and neck. This gradually extends itself over the surface and increases in quantity until the whole body is bathed in a profuse sweat. During this period the {594} patient's symptoms, both subjective and objective, undergo wonderful mitigation, and, although this stage is usually short, it often happens that by the time it is concluded a restoration to ordinary health seems to have occurred.

The sweating stage terminates a malarial paroxysm. The intermission now begins, and lasts until the inauguration of another paroxysm. The intermission is longer or shorter accordingly, first, as the paroxysm occupies less or more time; and, second, as the interval may affect it. The interval is that period of time which reaches from the beginning of one paroxysm to the beginning of another. It therefore furnishes the basis of classification of simple intermittents into the following forms: quotidian, tertian, and quartan.

Statistics gathered from a great many sources and relating to many countries and climates indicate that quotidian intermittents are more common than tertian. It may then be assumed that the natural type of intermittents is that form characterized by diurnal paroxysms. It must be remarked, however, that if any natural law does exist establishing the quotidian as the typical form of intermittent fevers, it is very often set aside by unknown influences. In certain epidemics the tertian cases preponderate, and under all circumstances convertibility may be witnessed between the various forms.

It is probable that the statistics gathered by the medical staff of the United States Army during the late Civil War afford the most valuable data which we possess touching these points, in so far as they relate to this country. During three years of the war 724,284 cases of intermittent fever were recorded, tabulated as follows:

Quotidian, 370,401 cases, 388 deaths--equivalent to 1047 + deaths per 1,000,000 cases.

Tertian, 318,704 cases, 324 deaths--equivalent to 1007 + deaths per 1,000,000 cases.

Quartan, 35,179 cases, 79 deaths--equivalent to 2245 + deaths per 1,000,000 cases.

It has been remarked by several writers that quartan attacks have a smaller ratio in the Southern States than in other parts of the Union. My observations on this point have not been sufficiently well recorded to make them especially authoritative, but they support such a conclusion.

The morbid anatomy of malarial fevers is more properly discussed in treating of the graver forms, since the paroxysms of simple intermittent do not often occasion death.

TREATMENT.--This must necessarily vary with the stage of the paroxysm and condition of the patient at the time of the first visit.

Let us suppose this to be the incipiency of the paroxysm, or the early part of the cold stage. However little the danger to life from the paroxysm of a simple intermittent attack, the practitioner should not forget that whatever danger does exist is to be ascribed to damages suffered during or in consequence of the chill. There are few exceptions to this rule, and those will be noticed presently. With this fact in view the practitioner's duties are much simplified. He should first endeavor to remove any complications present which tend to aggravate the cold stage. If the chill has come on after a full meal or after eating indigestible food, the stomach should be promptly emptied; otherwise the cold stage will {595} be prolonged and rendered more violent. Large draughts of warm water will frequently produce sufficient emesis. If this should fail, ipecacuanha may be added. The warm infusion of eupatorium perfoliatum answers well as an emetic, producing also a laxative effect. But it is disgusting to the palate, and sometimes prolongs its action beyond desired results. The effect of an emetic in abridging a chill by revulsive action are uncertain, and I avoid resorting to them for this purpose alone in simple intermittents.

The patient's subjective complaints of suffering should receive a due degree of attention. Additional blankets and warm applications should be allowed when solicited. I always discourage hot or heating drinks, except for the purpose just mentioned. I especially oppose alcoholic stimulants, because they seldom do any good in mitigating the chill, oftener aggravating the patient's symptoms during the hot stage, particularly the headache and vomiting, and sometimes directly occasioning perplexing perturbations. For example, I have seen convulsions speedily follow a strong brandy toddy given to shorten a chill.

While the removal of complications is imperatively indicated, it is also important to use promptly those means which are designed to modify and shorten the chill. It is a remarkable fact that all the agents found to be useful for this purpose are such as directly influence nervous function. Opium in some form enters into all prescriptions which I have found efficient in modifying a chill. It is quite efficacious when given alone, but I think its therapeutic energy and certainty are increased by the addition of other agents of the same class. I have often exhibited twenty to thirty drops of chloroform with an equal quantity of laudanum with excellent results. The tincture of opium may be combined with aromatic spirit of ammonia, or with bromide of potassium, or with chloral hydrate. In combination with either of the latter medicines it may be given by rectal injection. If the stomach is intolerant, or by preference because of facility of dosage and quickness of effect, the opiate may be given hypodermically. For this purpose one-sixth to one-quarter of a grain of morphia may be given, together with one-sixtieth to one-fortieth of a grain of atropia. It is rarely necessary to repeat the dose whichever form may be adopted.

After much experience in these methods of mitigating and abridging the chills of intermittent fever, I feel entitled to say that, whether the objects be achieved or not, no injurious consequences ensue.

The conditions of the circulatory and digestive organs are not favorable for the introduction of quinia or of any preliminary purgative which may be supposed to be necessary, and I therefore delay their exhibition. It may be excepted, however, that sometimes a very obstinately irritable stomach or exceedingly vitiated state of the fluids can be appropriately met by gr. x to xx of calomel.

The hot stage of a simple intermittent seldom calls for medical interference on account of excessive temperature. If the headache is very violent or the vomiting troublesome, a subcutaneous dose of morphia will bring speedy relief. The existence of high temperature does not contra-indicate its use.

I am in the habit of giving opium in the following combinations:

Rx. Morphiæ Acet. gr. ss; Liq. Ammon. Acet. fl. oz. iv. M.

S. Two tablespoonfuls every second hour.

{596} Or, occasionally, the following:

Rx. Sodii Bicarb. gr. xx. Morphiæ Sulph. gr. i; Aquæ Lauro-Cerasi, Aquæ Menth. Pip. aa. fl. drachm iv. M.

S. Teaspoonful pro re nata.

I do not limit the use of opiates in the hot stage to old and infirm subjects, as Dickson suggests, but give them in all cases where vomiting, headache, or other neuralgias are excessive, or where unusual restlessness and jactitation are present.

The propriety of giving purgatives as a preliminary measure of treatment during the hot stage must be determined by symptoms connected with individual cases. In the majority of cases falling under my care purgatives are avoided. When regarded necessary, gentle purgation is solicited by administering bitartrate of potassium in lemonade or by combining mild mercurial doses with antiperiodics when these latter are resorted to during the fever. In some cases a very furred tongue, sallow skin, and costive bowels indicate more active purgatives, which may be exhibited during the febrile stage.

The most important question which relates to medication during the hot stage is in respect to the administration of antiperiodics. It may be safely stated that practitioners of this country were the first to adopt this method of procedure in malarial fevers. Here it has been well demonstrated that a competent dose of quinia, given during any part of the hot stage, is so often followed by the defervescence of the fever that it would be illogical to attribute the change to any other cause. Sometimes the remedy fails in producing this result; then excessive physiological disturbances may follow, and perhaps some general aggravation of the patient's symptoms.

There are four different circumstances, each of which, in my opinion, calls for the exhibition of quinia during the hot stage, whether the fever has reached its maximum point or not:

First. If the period which has elapsed since the beginning of the paroxysm is so considerable that further delay might prevent sufficient cinchonism to intercept the next accession.

Second. When the fever is so excessive that quinia should be given as an antipyretic.

Third. When apprehensions exist that the fever will occasion some complication or accident.

Fourth. When the tongue is clean and the state of the system is favorable to absorption.

The hot stage is not usually favorable to absorption, and consequently the economical use of quinia must not be attempted. It should be given in doses varying from ten to twenty grains, preferably in solution. I may remark that I have seldom failed in getting good results from the powder or pills if lemonade or some fluid facile of absorption be given at the same time. The mixtures previously formulated answer this purpose very well, and at the same time mitigate the disagreeable physiological effects of the quinia.

Allusion has been made to certain symptoms occasionally connected {597} with the hot stage which involve danger. Convulsions are among the most important of these. They occur most often among children, but occasionally with adults. They should be met by chloroform, cold to the head, hypodermic injection of morphia, and cupping or leeching if the face is flushed, the eyes injected, and the carotids pulsating forcibly.

The sweating stage may be classed with the intermission in respect to medication. No time should be lost in securing cinchonism. From the moment the sweating stage announces itself the fluids of the system begin to resume their normal physiological functions. Absorption from the intestinal surfaces is again restored, and remedies may be administered with confidence in their effects.

The question is now no longer whether antiperiodics should be administered, but how they shall be given. Many practitioners prefer exhibiting them in one large dose; others think it better to give them in repeated small doses. I have usually adopted the latter method. Beginning with the sweating stage, I give three grains of quinia every hour or two hours, until eighteen grains have been taken. This would occupy periods of five to ten hours to complete the doses, ordinarily quite a sufficient length of time to obtain cinchonism before the advent of another paroxysm. If the physician elects to give his antiperiodic in one or two large doses, he should not trust to so small an amount as eighteen grains. Allowance must be made for the loss incident to the probable over-taxation of the power to dissolve and receive a large amount into the circulation.

Purgation should not be induced to a sufficient degree to hurry the quinia off before absorption takes place. Some practitioners favor the employment of adjuvants to the quinia. Very few of these have appeared to me to be of service except opium. A very convenient formula is a solution of quinia in peppermint-water by addition of dilute sulphuric acid, in such proportions that fl. drachm j of the solution shall represent five grains of quinia and seven and a half drops of laudanum.

But, however we may boast of the efficacy of cinchona as the anceps remedium for malarial diseases, we are forced to admit that it is not certainly an immediate cure, and very commonly fails in producing a permanent curative effect. If we could in all cases discern and remove the impediments to its immediate or temporarily curative action, its claims to be regarded as a practical specific would be undeniable. It is probable that these impediments generally rest upon the fact that either the remedy does not gain admission to the circulation or that some complication exists not within the range of its therapeutic action.

The failure of cinchona to cure a malarial attack in such a permanent manner that it shall not be liable to return is probably owing to the incompetent action of the drug because of its transitory stay in the system as compared with that of the malarial poison. Some objections apply to this theory, because when the succession of intermittent attacks is broken by quinia and it is continuously administered afterward, the paroxysms occasionally recur in spite of its presence in the system. These objections may be answered by pleading that under these circumstances secondary blood-poisons precipitate the attacks, and cinchona should not be expected to cure these conditions.

The best methods of practice I know of to prevent a recurrence of {598} intermittent fever after having interrupted the succession of attacks are, first, to continue the cinchona for at least forty-eight hours, giving at least three three-grain doses a day. After this no medicine need be given except such as may be required to correct chronic toxæmic states of the system or to act as blood-restoratives until such time as prodromes of another paroxysm may exhibit themselves. At the instant when these manifest themselves ten to fifteen grains of quinia in solution should be taken. In order that no loss of time should occur in applying this method, I always advise patients to keep a solution of quinia within immediate reach. The following prescription has sometimes appeared to effect a permanent exemption from recurrence of paroxysms:

Rx. Ferri Redacti gr. xl; Acid. Arseniosi gr. j; Quiniæ Sulph. gr. xl; Ol. Pip. Nigr. gtt. x. M. Ft. pil. No. xx.

S. One pill three times daily.

It seems sometimes to occur that intermittent attacks so impress the nervous system that they become, like epilepsy, more liable to recur because of an established habit. I have known chills to occur when the ears were ringing with quinia. Strychnia fails to arrest them; arsenic has more value, but frequently fails. Pure nitric acid, properly diluted, in doses of six to ten drops, given every four to six hours without regard to the stage of the paroxysm, succeeds more often than any medication I have ever resorted to.

Before dismissing the subject of the treatment of simple intermittent fever it may be proper to mention that I have made trials of cure by carbolic acid, administered by mouth and subcutaneously, and also of the sulphites, with no results worthy of recommendation.

Remittent Fever.

The difference in definition between the words remittent and intermittent expresses the clinical distinction between these two forms of fever in a very satisfactory manner.

Remittent fever exhibits oscillations of temperature regulated as to hours of recurrence by laws similar to those which govern the periodic returns of intermittent fever; but there is no complete defervescence of the fever. While the lowest angles of the fever curve approximate the normal body heat more or less closely, they never decline to a standard of apyrexia.

That remittent fever is a malarial disease, produced by a cause identical with that which produces intermittent fever, is well proven by the following facts:

First. Cases occur in close relation with cases of intermittent fever in populations similarly exposed to malaria, and at the same periods of the year.

Second. The two forms of disease are readily convertible, the one with the other.

In non-tropical countries remittent fever cannot be regarded as the {599} natural type of malarial fevers. At least, it may be affirmed that the proportion of cases which begin as remittent attacks is so small that we are warranted in looking upon them as departures from type. In the United States army during the years 1861-66, inclusive, there occurred 286,490 cases of remittent fever. The fatal cases were 3853, being a mortality-rate of 13,450 per 1,000,000 cases. By comparing these statistics with those of intermittent fever recorded in a previous section it will be found that remittent fever is more than twelve times as fatal to life as the simple intermittent forms.

If we accept this view of the pathology of remittent fever, it is of interest to the sanitarian or practitioner to endeavor to arrive at the causes which occasion these departures from type. Some of these are undoubtedly extraneous to the system, and relate wholly to circumstances affecting the malarial poison as a disease-producing agent. Increased quantity of malaria is well understood to enlarge the ratio of remittent cases. There is also strong presumptive evidence supporting the hypothesis that different annual crops of malaria vary in respect to the noxious qualities of this agent. The same presumption relates to all crops produced in certain localities as contrasted with others. Other causes which determine remittent rather than intermittent attacks are personal to patients. They may be classed as follows:

First. Unusual personal receptivity or impressibility to malaria may exist, either because of some constitutional idiosyncrasy or of some state the system at the time of exposure.

Second. Want of timely medical treatment or of proper medical treatment may convert intermittents into remittents.

Third. The rapid occurrence of secondary blood infections, extraordinary in character or amount, may cause the fever to be continuous.

Fourth. The existence of complications, inflammatory in their nature, may change intermittent into remittent attacks.

However various or complex the causes may be which operate to convert intermittent attacks into remittent forms of fever, each one must be supposed to act by disturbing the functions of those centres which preside over the normal physiological and chemical changes of the system.

SYMPTOMS AND DIAGNOSIS.--Attacks of remittent fever are, as a rule, more abrupt in their advent than intermittents. When prodromic symptoms exist, they are similar to those which precede ordinary cases of ague.

The chill is seldom attended by such violent symptoms as the cold stage of intermittents. The duration of the cold stage is also more brief. In a small proportion of cases severe vomiting with large bilious ejections complicate the cold stage. The chill is quickly followed by the hot stage.

The mildest cases of remittent fever are not readily distinguishable from the intermittent forms. In these cases the temperature curves are marked by sharp angles and long tracings between the lowest and highest records. As cases become more decided in diagnosis, and consequently represent higher degrees of departure from the intermittent type, the angles of temperature curves become more obtuse and exhibit a more or less high average range. The accompanying temperature diagram (Fig. 23) shows the thermometric record of an unusually protracted and grave case. The patient was a near relative of my colleague, Prof. Logan, a leading practitioner of New Orleans, and the clinical records may be {601} accepted as altogether accurate. It is somewhat to be regretted that the records of temperature were not begun at an earlier period, but the gravity of the case was not manifest until the continued type of fever was found to exist. The latter part of the diagram illustrates the lapse of the remittent fever into an intermittent. This is so commonly a mode of cure that the practitioner watches with solicitude for increasing oscillations of temperature to announce mitigations of severity in his gravest cases.

{600} [Illustration: FIG. 23. Temperature chart showing the lapse of a remittent fever into an intermittent. NOTE.--From the third to the fifteenth day after attack a half drachm of quinia was given daily. Observing no good result, it was omitted until the twenty-ninth day, on which date two doses of eight grains each were administered. On the morning of the thirty-fourth day eight grains were again given; on the thirty-fifth day one scruple was given.]

The differential diagnosis of intermittent and remittent fevers may be looked upon as practically unimportant. All cases so near the borderline as to make differential diagnosis a question should receive identical treatment.

There are, however, two other very grave forms of fever which are liable to give trouble in differentiation from remittent fever. These are typhoid and yellow fevers. The sanitary protection of communities exposed to cases of the latter, and also the practical treatment of the sick, call for early and correct differentiation.

But it is only in the early stages of the pathological processes of these affections that difficulties of diagnosis are liable to obtain. The facial expression of patients suffering with remittent is sufficiently characteristic to afford some diagnostic inferences. During the pyrexia the face is flushed and the eyes injected, but the redness is more vivid and the countenance more animated than in either typhoid or yellow fever. It would not be inaccurate to say that, however great may be the flushing or other alterations of the countenance in remittent fever, the natural facial expression is better preserved than in either of the fevers under comparison with it. Sallowness of the skin is an early and almost constant event in remittent fever. It comes on as a secondary manifestation, and appears in a large ratio of cases to bear some relation to the high temperature preceding its occurrence. The icteric hue is seldom intense, indeed very infrequently equalling the orange-yellow of jaundice resulting from obstruction. There is an exception to this statement in those cases in which remittent fever attacks a person already jaundiced. I have seen many cases in which the jaundice preceded the remittent fever, and became more strongly marked after its incursion, particularly in those persons who had remained for some time in a malarial region and suffered repeated attacks. In all cases of remittent fever it seems reasonable to ascribe the more or less jaundiced state to one or both of two factors, viz.--the accumulation of excrementitious material and bile constituents in the blood from primary derangement of its chemistry; and that excessive activity of the liver which the malarial poison appears to induce. Whether the latter mentioned factor results from some action of malaria directly affecting the nutritive processes of the liver, as it does those of the spleen, or whether the altered blood-currents during the paroxysms cause this supposed hypersecretion of bile, we certainly know that to malaria only can we ascribe those fevers which are marked by such peculiar symptoms of biliousness or superabundance of bile as to justify the prefix bilious fever or bilious remittent fever.

The state of the alimentary tract may properly receive notice after these remarks. In the early stages of remittent fever the tongue may be moist and large, and covered with a white or lead-colored or yellowish coat. The edges may be indented with imprints of the teeth. This is {602} Osborne's malarial tongue, and its appearance is worth something in diagnosis.

Later in the progress of remittent fever the tongue may become dry, brown, cracked, and difficult of protrusion, but seldom showing the tremulousness of a typhoid-fever tongue, and differing also from the yellow-fever tongue in the fact that in this disease the appearance of the tongue is usually indifferent as a symptom, except that in advanced stages it is liable to be smeared with blood.

The stomach is irritable from the very beginning of an attack, and the acts of emesis are generally in striking contrast with those of typhoid or yellow fever, both in respect to their violence and to the relative amount of bile they eject.

The bowels are ordinarily costive, and when moved by purgatives the stools contrast strongly with those of typhoid or yellow fever by presenting evidences of the bile-coloring principles which attend all excretions in malarial fever, and are found in the urine, the perspiration, and occasionally the sputa.

Some unusually violent cases of malarial fever, which may become remittent, are inaugurated with convulsions, profuse diarrhoea, and coma.

Before closing the remarks concerning the digestive organs in remittent fever I should mention that in the long array of cases I have treated I cannot recall one solitary instance of black vomit. It is, however, true that I have observed hemorrhage from the bowels in quite a number of cases. These occurred late in protracted cases, and were sometimes the cause of death. Whether it be merely a coincidence I am unable to say, but it is true that the majority of these cases have been in young females just after the establishment of the catamenia.

Hemorrhage from the nose is frequent in remittent fever, but I have never seen a case with general tendency to hemorrhage.

The pulse in remittent fever differs from that of the typhoid or yellow fevers by being more synochal in character, firmer, and more resisting to pressure. The longer the duration of the case the less is this characteristic discernible.

The nervous system shows less ataxia. Delirium may occur in any stage of the disease, but differs from the delirium of typhoid and yellow fevers in showing a lessened degree of perversion of the reasoning faculties. The neuralgias have nothing special.

The urine is acid, high-colored, and scanty. I have never found much albumen in the urine of a case of remittent fever, unless there was some other cause to account for its presence. A small amount may be detected during excessive fever. Blood is a rare constituent.

Mild cases of remittent fever should terminate in recovery in from five to seven days. Fatal attacks usually end from the fifth to the tenth day. Many cases pursue a course which lasts from twenty to forty days. Under proper treatment the usual termination is in recovery, either directly or by conversion into the intermittent type.

POST-MORTEM APPEARANCES.--When death occurs in remittent fever the post-mortem changes generally consist of those which are principally due to chronic malarial toxæmia and those ascribable to the acute attack.

Under the former division are permanent enlargements of the spleen and liver, and pigmentary matter in the blood and deposited in various {603} organs. Under the latter are to be classed hyperæmic or even inflammatory states of the stomach and intestines, and those degenerative changes which are the consequence of continuous hyperpyrexia. The post-mortem changes which are so uniformly found as to be most often appealed to in the establishment of diagnoses are enlargements of the liver and spleen. These may be due in part to hyperplasia and in part to blood-engorgement. The brown or slate color of an enlarged liver is strongly diagnostic of malarial affections. It contrasts strongly with the yellow and natural-sized liver of yellow fever and with the negative liver of typhoid fever.

The skin is generally yellow, sometimes quite intensely icteric, but seldom showing the ecchymotic extravasations of yellow fever. In remittent fever we never find the cadaver oozing blood from the nose and the mouth, nor are the stomach or intestines ever found to contain black vomit.

TREATMENT.--The indications of treatment in remittent fevers differ from those of intermittents in two leading essentials.

First. It is a far graver form of fever, and calls for more promptitude and energy in treatment for its successful management.

Second. The important pathological condition to be combated is the hyperpyrexia, and not the cold stage, as in intermittents.

But even with a clear realization of the practical importance of these facts in governing the treatment of remittents, the practitioner must still exercise care and self-control, lest he shall unconsciously adopt the doctrine that inflammatory lesions must be present to occasion such violent pyrexia as often exists. The physician who comes directly from a case of pneumonia or rheumatic fever and finds a patient suffering from remittent fever, with temperature higher and pulse more bounding than those of the patient he has just left, is pardonable for finding it difficult to realize that these furious symptoms are not also associated with inflammation.

Attempts to cure remittent fevers by an exclusively antiphlogistic treatment either result fatally or induce long periods of confinement and suffering before recovery is reached. The great indication is to secure cinchonism as promptly and completely as possible. Nothing should divert our attention from this object. The condition of the patient as it respects fever, delirium, or state of the tongue, should form no bar to the administration of quinia. There are no practitioners who have had much experience in treating these grave forms of malarial fever after this method who are not able to recall the numerous instances of most astonishing and gratifying amelioration of symptoms as soon as saturation with quinia was brought about. The dry tongue becomes moist, the skin is bathed in gentle perspiration, the delirium ceases, and the patient sinks into a quiet sleep.

The amount of quinia necessary to produce cinchonism must be estimated for each particular case according to the measure of its severity or to states of the system more or less favorable to its absorption. It must be borne in mind, however, that questions concerning the patient's safety are paramount to those of economy. In the mildest cases I never trust to a smaller amount than from twenty to thirty grains. In violent attacks I have administered scruple doses every fourth hour until a {604} sufficient test had been made of its capability to arrest or modify the febrile paroxysm. I have never met with any of those exaggerated physiological effects which some observers teach us to fear from the exhibition of cinchona preparations during fever. Certainly, I can declare that no permanent deafness or other lasting lesion of nerve-function has ever occurred under my observation. I must also add that I know of no reasons why remissions afford more favorable conditions for the administration of quinia, beyond the fact that the system is in a better state for its absorption and assimilation. The quinia is preferably given in solution, but may be exhibited in the form of pills, or in powder suspended in black coffee, or in the thick mucilage of the slippery elm.

The considerations of treatment which are naturally connected with those just advocated relate to measures which it may be proper to associate with the quinia. The answers to the two following questions comprise all that is necessary to be said on this point--viz.:

Are conditions of the system present which may interfere with the specific treatment by quinia, and which are not, in themselves, curable by it?

Are any medicines to be given as succedanea to the specific remedy for the purpose of rendering its action more sure or prompt?

In regard to the first inquiry, it must be admitted that in quite a large proportion of cases of remittent fever specific treatment fails to cure. I suppose that may be a reasonable proposition which holds that in the majority of these cases the presence of secondary blood-impurities annuls the ordinary specific effects of cinchona. These must be gotten rid of by depurative medicines. The intestinal canal, the skin, and the kidneys are the emunctories through which elimination must be effected. It is therefore proper for the physician to endeavor to recognize cases where such impurities exist, and to so modify his treatment as to remove them. The indications for depurative treatment are jaundiced skin and eyes, furred tongue, costive bowels, and scanty, loaded urine. These are more or less positively expressed symptoms in a large majority of cases. It is therefore proper that in this large majority of cases of remittent fever depurative treatment should be conjoined with the specific treatment. In my opinion, no drugs meet this indication so well as mercurials and saline purges and diuretics. Calomel or blue mass may be given either simultaneously with the quinia or in alternate doses.

There are three very important rules to be observed in regard to cathartics: They should never be carried to such an extent that absorption of the quinine is interrupted. They should not be given in such large or repeated doses as to produce prolonged irritation, or it may be even inflammation, of the alimentary canal. Purgatives should be used for their depurative effects, and never as antiphologistics.

Opium exercises excellent effects in preventing local irritation or hypercatharsis, and in relieving derangements of nerve-function and insomnia. It is preferably given in small doses, combined either with purgatives or with the quinia.

I have found bitartrate of potassium the most grateful and efficient saline for depurative action. I have generally given it in lemonade in such amounts as to secure a gentle aperient and diuretic effect. I hold strongly to a conviction that all drugs as soluble as this facilitate the absorption of those less soluble--as, for example, of quinia.

{605} If the first efforts to break the febrile paroxysms fail, it is better to discontinue the quinia and place the patient under symptomatic treatment, and await conditions of the system more favorable for its repetition. Of course the high temperature is generally the symptom requiring most care and attention.

Vomiting is one of the troublesome symptoms of remittent fever. As internal medication minute doses of morphia, dry upon the tongue or in solution in cherry-laurel water, or in combination with eight or ten drops of chloroform, are generally efficacious. Swallowing pellets of ice or frequently taking iced effervescing mixtures are good measures of treatment. Occasionally, a mild emetic, such as warm chamomile infusion, or warm water alone, will arrest the vomiting temporarily. It is doubtful, however, whether this relief is secured by the ejection of any offending matter from the stomach. It is more than probable that the forced dilatation of the stomach has arrested the spasms, for filling this viscus with cold drinks to repletion will often effect the same result.

Of all applications to the epigastrium, a cold wet towel occasionally sprinkled with chloroform is the best.

A tympanitic or tender abdomen requires stupes wrung from warm water. They may be dashed with turpentine at first, and afterward consist of warm water with whiskey. I have occasionally given two or three doses of turpentine emulsion with benefit, but from much observation I am forced to protest against the turpentine treatment, as it is called, which is to give twenty drops of turpentine every two to four hours as a curative agent.

Hemorrhage from the bowels must be met by hæmostatic treatment--preferably, in my experience, by the use of five grains of gallic acid in half an ounce of camphor-water every two hours, of morphia subcutaneously, and of cold cloths over the bowels. As in all diseases liable to cause death from exhaustion, careful attention must be paid to the nutriment, and stimulants must be administered as required.

Pernicious Malarial Fever.

Certain departures from the ordinary types of malarial fever are termed pernicious, because of their great tendency to inflict more than usual systemic damage and danger to life upon those who suffer such attacks. The word pernicious is used in its common English sense of being hurtful or injurious.

It is entirely unnecessary to enter upon a discussion respecting the propriety of employing this adjective to designate a class of cases of disease which are primarily due to the same poison which produces simple intermittent attacks. The extreme hurtfulness and danger of the attacks to be described in this section, and the awful suddenness with which they often occasion death, form striking contrasts with the more typical forms of malarial fever, and appear fully to justify the use of the qualifying adjective pernicious.

While all these various departures from type to be grouped under the term pernicious possess the quality ascribed to them, they nevertheless differ so widely in their modes of inflicting injury that it seems desirable to arrange them under distinct sub-classifications.

{606} Some cases of pernicious malarial fever preserve the periodicity of simple attacks sufficiently well to enable one to classify them as intermittent or remittent in form. But more commonly it is impossible to determine this classification, and for practical purposes it is unimportant to attempt to make any such distinction.

The classification which appears to me most true to nature is the following:

First. The algid or congestive form; Second. The comatose form; Third. The hemorrhagic form.

The algid or congestive form occurs more frequently than either of the others. Its perniciousness is due to an aggravation or sheer exaggeration of the cold stage of an intermittent attack.

The following brief clinical histories of two cases will serve to illustrate the symptomatic phenomena of this form of pernicious malarial fever:

M. S., aged fourteen, had accompanied his father to a malarious locality in the country, and had remained with him during September and a portion of October. Shortly after his return I was asked to visit him because of some unusual symptoms attending a chill. I found him in a stupor, from which he was with difficulty aroused sufficiently to be able to swallow a dose of quinia combined with laudanum. His face was pallid and inexpressive; the skin cool and moist; extremities shrunken and cold; pulse small, easily obliterated by pressure, and irregular; tongue large and moist; and pupils rather dilated.

My second visit was at 12 M., one hour and a half later than the first. Patient was found in a deep stupor; surface cold; extremities and face shrunken and blue; pulse barely perceptible; large liquid and offensive stools occasionally escaped from the bowels without the consciousness of the patient. Death at 3 o'clock P.M.

Miss H., living in a malarious situation, complained about noon of September 19th of great cerebral fulness and unaccountable sleepiness and debility. She retired to her room, and after a few hours' sleep resumed her household occupations. On the 20th similar symptoms manifested themselves, but earlier in the day. She again slept for some hours, but complained of great prostration after the sleep. On the 21st, about 10 A.M., she complained of a return of the stupor, and while retiring to her room requested that I should be called if she did not awake in a better condition. At 1 P.M. she was found profoundly comatose, with cold extremities and surface and bathed in perspiration. When I reached her residence at 3 P.M. she had expired.

There is a common belief among non-professional people that the third congestive chill is necessarily fatal. There is no foundation for this opinion, except in the fact that when congestive chills are waxing in their perniciousness the subject is seldom able to survive the third recurrence if the second or first should not prove fatal.

It is difficult to account for the pathological dissimilarity between the simple and congestive types of malarial fevers. If we say that congestive chills are produced by an intensification of those causes which produce and govern an ordinary chill, we make an explanation which, however unsatisfactory, represents very nearly the full extent of our knowledge on this point.

{607} It cannot be admitted that alterations of quantity or quality of the malarial poison exercise the sole influence in determining the occurrence of congestive cases. All experienced practitioners understand that certain constitutional conditions may pervert simple chills into congestive forms by producing prolongation or aggravation of the states of congestion always present in ordinary chills. Weakened cardiac function, from whatever cause, may be reckoned among these conditions. In these cases the feeble vis a tergo yields readily to those perturbations of vaso-motor influence which occasion passive blood-accumulations in the small veins and capillaries. I may say further, in speaking of the influence of the vaso-motor nerves in governing the phenomena of a chill, that we know that in congestive chills the cerebro-spinal system is much less the seat of symptomatic phenomena than in simple attacks. On the other hand, the organic system is far more profoundly affected.

However we may account for the perversions of normal circulation underlying and producing congestive chills, the great degree of injury they are liable to inflict is so well understood as to awaken the most serious apprehensions whenever we are called upon to treat them. Congestion, however occasioned, may destroy life through abolishment of function by the sheer physical change of infarction, or, again, through those inevitable consequences which arrested circulation entails upon the blood. Blood-stasis is followed by separation of its constituents, and its disqualification as a circulatory fluid in a degree proportionate to the duration of the stoppage, and probably also to the actual extent of the passive engorgement. Thence result the formation of coagula in the congested vessels and deposits of pigmentary matter. If partial reaction should occur, portions of this blood-débris may be floated to various parts of the circulatory system, and give rise to greater or less important alterations of function.

Among the white soldiers of the United States army from May 1, 1861, to June 20, 1866, 13,673 cases were diagnosed as congestive intermittent fever. Of this number, 3370 died, being a mortality-rate of 23.91 per cent. The aggregate number of malarial cases returned was 1,255,623. It would therefore appear that 1 case in not quite 372 was congestive in its type, or 1.08 per cent. The late Dr. Cook of Washington, La., estimated 2 per cent. of his malarial cases to be of the congestive type. It can scarcely be doubted that the ratio of congestive attacks is greater in the more southern belts of latitude than in the middle or northern parts of the United States. Chronic malarial toxæmia and the enervating effects of long-continued heat upon the circulation must occasion an increased proportion of such attacks, but my own observations show slightly more than 1 per cent. of the cases treated in the Charity Hospital to have been of the congestive form.

The cure of a congestive chill is one of the most difficult problems the physician can possibly encounter. It is nothing less than the proposition to remove a perverted state of the blood-vessels which is dependent upon some influence exerted through a nervous apparatus whose therapeutics and experimental physiology are imperfectly understood. While a satisfactory solution of this problem will probably be a remote achievement in medicine, it was long ago empirically ascertained that certain {608} agents exercised some degree of control over the cold stage of febrile attacks. For the most part, these agents are addressed to those perversions of nerve-function which constitute so important a part of the pathology of a chill. They are identically the same remedies whose aid we invoke to allay many other forms of perturbed nervous action. Opium, chloroform, belladonna, chloral hydrate, and bromide of potassium have proved more or less valuable, according to the idiosyncrasy of the patient or the circumstances under which they have been used. I consider opium the most valuable of these remedies. It should be given in moderate doses, and preferably combined with chloroform or ammonia, or, if more expedient to administer per rectum, combined with solutions of chloral hydrate or bromide of potassium. One-sixth of a grain of morphia, combined with one-fortieth or one-fiftieth of a grain of atropia, is an available and useful prescription when given hypodermically. Rubbing the extremities or the spine, or indeed the whole surface, with ice, is a mode of practice well worthy of attention. In the event of inability to procure ice, douches of cold water, followed by frictions with coarse towels, may be substituted. I have used nitrite of amyl by inhalation, but its effects are too transitory to prove serviceable.

Some practitioners speak highly of alcoholic stimulants. My own experience has not been favorable to their use. Perhaps their benefits are altogether restricted to those cases in which previously weakened heart-function existed. But it is important that alcohol be added in all those cases of pernicious malarial fever, whatever the type may be, where cardiac stimulation and improvement of nutrition are leading indications.

I am sure I have often derived benefit from enemas consisting of four ounces of well-prepared beef essence with a half ounce of whiskey or brandy and a half ounce of strong infusion of coffee.

The value of the hypodermic syringe in treating congestive chills must never be lost sight of. The suspension, or even reversal, of normal systemic currents is made evident by the serous vomiting and purging attending congestion of the abdominal cavity. Medicine placed in the stomach under these circumstances is virtually thrown away.

The term comatose is applied to certain cases of pernicious malarial fever because they present coma as a marked symptom. To appreciate the propriety of this classification, it must be well understood that the coma present is not due to cerebral congestion. Further than this one restriction upon the application of the word there is in its employment no declaration of any pathological views respecting the cases it is intended to define. While, therefore, the term is unquestionably liable to criticism, I suppose its use may still be admitted, provided it is accompanied by a satisfactorily explicit account of the symptoms and probable pathological conditions of the cases included under its caption.

There is a sharp line of distinction between the symptoms and conjectural pathology of comatose cases and of those of the congestive form of pernicious fever. The following notes of cases will sufficiently establish this statement:

C. L., fisherman, aged forty-four, brought into Ward 20, Charity Hospital, in an insensible condition, November 18, 1875. Temperature at time of admission 104.8°, pulse 120, respiration 40; able to swallow liquids placed far back in his mouth. Ordered scruple ij of quinia in {609} solution, ten grains to be given every fourth hour. Nov. 19th, patient has taken and retained all the quinia ordered; is perspiring profusely; temperature 97.8°, pulse 88; more conscious; takes food and water when offered him. Ordered blue mass, comp. extr. colocynth., aa gr. v, to be taken at once. To drink through the day bitartrate potass. oz. j, dissolved in lemonade, until bowels are moved. Evening temperature 99.3°. Nov. 20th, temperature 98°; patient placed under convalescent treatment; discharged from hospital Nov. 29th.

Another comatose patient was admitted to Ward 19 on the 29th of October, entirely insensible. He was treated by large doses of quinia in solution per rectum, and by calomel gr. xx, sodii bicarb. gr. v, placed upon base of tongue, and caused to be swallowed by a tablespoonful of water trickled over the powder. As the patient began to recover it was noticed that his right arm was paralyzed. A history subsequently obtained showed that the patient was an engineer, and had been engaged in making some land surveys in a swampy portion of the State of Louisiana, and had been often obliged to wade or swim across the bayous and to sleep at night in the open air, sometimes without any protection from the weather. He had previously enjoyed good health, and was altogether unable to account for the paralysis of his arm. During convalescence he was treated with iron, strychnia, and preparations of cinchona, and by cold douches and frictions to the paralyzed arm. Convalescence was slow, but he was discharged, completely recovered, on November 20th.

In typical cases the differential diagnosis between the congestive form and the comatose is made without difficulty. In a congestive chill the surface is cold, blue, or livid, the pupils dilated, and the pulse generally slower than natural and irregular. In the comatose form the surface is preternaturally warm, of a muddy, semi-jaundiced hue, and the pulse and temperature both indicate the feverish rather than the algid state.

The subjects of attacks of the comatose form of malarial fever are for the most part persons who, having contracted attacks of fever in malarial regions, continue to reside in the same localities and yet use no proper medication, either for cure or for prophylaxis. We have in these cases accumulations of secondary blood-poisons quite sufficient to greatly impede brain-function, and the additional doses of the primary toxic agent must exercise more or less influence in determining the phenomena of the attacks.

Very little need be said of treatment, beyond a recommendation of the courses pursued in the cases cited. Hypodermic medication must be resorted to when necessary. Efforts to nourish the patient must never be relaxed. One must see many of these cases before he can realize how often they recover, from conditions apparently utterly hopeless, when promptly treated and properly nourished.

The hemorrhagic form of pernicious malarial fever can scarcely be regarded as an original type. Malaria is not a hemorrhage-inducing poison. Indeed, it may be positively stated that malaria never establishes the hemorrhagic diathesis as a primary effect; and it is only by changes effected in the human economy by its prolonged influence that it appears to become capable of doing so. The most experienced and accurate observers of malarial affections concur in the opinion that this rule is almost without exception.

{610} The morbid conditions whose concurrence entails upon malarial fevers a tendency to hemorrhages may be classed together as follows: First. The blood-changes of chronic malarial toxæmia so alter the consistency of that fluid as to favor the occurrence of hemorrhage. Second. The long persistent states of malnutrition in chronic malarial cachexias produce textural weakening of the vascular walls and increased liability to their rupture. Third. There should be added to these one other factor, which is mainly operative during a malarial paroxysm--namely, the increased blood-pressure put upon the vascular walls by passive congestions.

Two of these factors, as above enumerated, are more or less general to the system, being the consequence of general cachectic states. The third factor acts in a purely dynamical manner in causing hemorrhages, and must necessarily have its area of influence confined to some certain portion or portions of the vascular tree, since the congestions of malarial paroxysms cannot by any possibility be general. It is an interesting fact that the influence of this last-mentioned factor is so frequently paramount in producing malarial hemorrhages. These hemorrhages occur in such immediate relation to chills that we are forced to the conclusion that while altered blood and weakened blood-vessels were previously present, yet some increase of pressure beyond the normal was required to precipitate the hemorrhage.

More than once in the presence of medical classes I have illustrated the influence of these various factors, respectively, by showing the arm of a patient suffering with chronic malarial cachexia, with no extravasation of blood, but upon which the slightest suction with the lips would produce exaggerated ecchymoses. This explains the fact that hemorrhages in malarial fevers are never general, but only manifest themselves upon those surfaces or into those structures which are the seats of congestion during the cold stage of an intermittent.

I do most earnestly assert that during a practice of almost half a century, nearly all of which has been passed in malarious localities, I have never once seen a malarial-fever patient with a general hemorrhagic tendency, if yellow fever and other hemorrhage-inducing diseases could be authoritatively excluded. The medical profession cannot be too watchful in guarding itself against erroneous entries upon mortuary records to account for deaths from fevers accompanied by hemorrhages from multiple surfaces of the body. Such aliases as hemorrhagic malarial fever, climatic fever, rice fever, hæmatemesic paludal fever, and many more of the same character, should receive the severest examination before approval and adoption.

When hemorrhage does attend malarial fevers, it may occur from one or another of a variety of surfaces or into shut cavities or in parenchymatous structures. Some years ago I visited a gentleman who was suffering from an attack of malarial fever, with hæmaturia. He made a rapid and, apparently, a complete recovery. Disobeying my injunctions, he returned to the intensely malarious locality where he had formerly resided. After a few weeks he was seized with a chill, followed by apoplectic symptoms, hemorrhage, and death on third day. It is hardly to be doubted that his death was caused by cerebral hemorrhage. But, however much in consonance with ascertained facts the foregoing remarks may appear to be, there are certain points of pathology connected with {611} malarial hemorrhagic fevers not easy of explanation. Within the last score of years hæmaturia has been a far more common form of hemorrhage in malarial fevers than formerly. In many localities and during certain seasons it has been very prevalent.

In the present state of our knowledge it is not at all possible to explain why it is that different epidemics of malarial diseases should give rise to such a diversity of phenomena, so that one epidemic will be characterized by a peculiar train of symptoms which shall be absent in another, being there replaced by different symptoms equally distinctive of the second epidemic. Whatever may be the cause of these epidemical peculiarities, it must rest in a something which is capable of acting as a force upon the human system. We must think of that unknown agency which exercises this force and gives it some peculiar direction as possessing at least a conventional essentiality. It is not satisfactory to say that the renal blood-vessels are the first to give way, because they are accidentally more weakened than other parts of the vascular system, or accidentally more often the seat of congestion. When accidents become as numerous as these cases sometimes are, they acquire the authority of laws.

The following notes of two cases of malarial hemorrhagic fever may be found of interest:

C. E., aged twenty-six years, was admitted to Ward 19, Charity Hospital, Nov. 18, 1872. Had been in America more than a year, and for several months had been working in an intensely malarial district preparing the bed of a railroad; has had malarial diseases for several months, and suffered a severe chill the day before admission. A few hours after admission temp. 103°, pulse 120, respiration 29; effusion in both thoracic cavities, and very marked in abdominal cavity; lower lobe of right lung oedematous, legs anasarcous, pitting greatly on pressure, with several ulcers of long standing. Urine loaded with albumen and showing under the microscope abundant blood-corpuscles; considerable jaundice present, which the patient states to have occurred suddenly. Ordered five grains each of calomel and bicarbonate of sodium, to be followed after catharsis with ten grains of quinia in solution every two hours. Nov. 22d, patient has taken and retained one hundred and eight grains of quinia; secretion of urine abundant; no blood present, and only a trace of albumen; ordered twenty drops of tincture of chloride of iron three times daily. Discharged cured December 12th. The above comprises the whole treatment in this case, except one important measure, which consisted in determined and persistent efforts at forced nutrition. Meat essences, milk, eggs, and milk-punch were given as methodically as drugs.

H. K., fifteen years of age, was admitted to Charity Hospital Sept. 15, 1872; has a history of malarial poisoning for several months; was considerably jaundiced at time of admission, with anasarcous legs. Under the administration of a mercurial, followed by quinia and iron, he improved so greatly that he was discharged from my wards and placed upon some duty in the hospital. Dec. 19th, at 11 A.M., had a chill which lasted several hours; this was followed by violent fever, with rapid but compressible pulse; much jactitation; incessant vomiting of a greenish-black fluid; urine loaded with blood; and sudden supervention of intense jaundice. Ordered quinia gr. xij by hypodermic injection; {612} small doses of calomel and soda to be placed upon the base of the tongue and washed down with ice-water. Secretion of urine ceased on the morning of the 20th, followed by death at 11 P.M. Autopsy showed both kidneys dark-colored and swollen from complete blood-engorgement.

The treatment of hemorrhagic malarial fevers may be included under the following indications:

First, to secure cinchonism as early as possible;

Second, to arrest the extravasation of blood;

Third, to sustain the patient's strength, and to preserve the systemic fluids at as near a healthy standard as may be possible.

The first-mentioned indication is certainly the first in importance. If the hemorrhage originates during a chill, or exhibits degrees of aggravation in such close relation to the cold stage of malarial paroxysms as to point to a relation of cause and effect, then that course of treatment which breaks the recurrence of paroxysms will at the same time mitigate the hemorrhage, if, in truth, it should fail to stop it entirely. Quinia should be given in large doses by the mouth or rectum, or both, or subcutaneously if demanded by the urgency of the symptoms. I have generally used carefully prepared solutions of the sulphate for hypodermic injections, but many practitioners prefer solutions of the hydrobromate for this mode of exhibition. I have never witnessed any symptoms following the administration of cinchona salts which justified a belief that they increased the hemorrhage. My rule of practice has invariably been to endeavor to prevent the occurrence of another paroxysm, without regard to this very questionable charge.

In regard to the second indication, it may be stated that patients are not likely to die from actual loss of blood in any form of hemorrhagic malarial fever. The blood which is poured out on free surfaces and escapes by some outlet is seldom so much as to endanger life, but the hemorrhagic process is likely to involve deeper-seated vessels. This is especially true in malarial hæmaturia. Hemorrhages into the stroma of the kidneys, the Malpighian tufts, and the uriniferous tubules arrest urinary secretion, and thus entail death. In order to prevent these results hæmostatics should be resorted to as often as attendant circumstances will permit. Generally these are such as to admit of the use of hæmostatics without prejudicing the effects of other remedies. In my experience ergot in combination with gallic acid and dilute sulphuric acid has been very efficient. The following prescription has been usually given:

Rx. Ext. Ergot. Fluid. fl. drachm iv; Acid. Gallic. gr. xl; Acid. Sulphuric. dil. fl. drachm j; Syr. Zingiber. fl. drachm iij; Aquæ q. s ad fl. oz. ij. M.

S. Dessertspoonful every four hours, diluted with water.

Some practitioners place a very high estimate upon the hæmostatic effects of turpentine. This is undoubtedly a most valuable and accessible remedy. Dr. Schnell of Plaquemine Parish, La., has found the tincture of chloride of iron the best hæmostatic. He places fl. drachm ij in fl. oz. iv of water, and directs a dessertspoonful every hour as long as the hemorrhage continues. In a great majority of cases of malarial hæmaturia occurring under my observation solutions of bitartrate of potassium have {613} been given with great apparent benefit. Its action is certainly not that of a direct hæmostatic, but by setting up currents through the kidneys, and perhaps by some solvent power over exudations in the uriniferous tubules, it has acted as a renal deobstructive.

In the arrest of renal secretion diuretics, cupping over the lumbar region, and large injections of warm water into the bowels may be resorted to. Some practitioners state that they have found buchu beneficial.

The third indication involves a twofold duty. One relates to judicious and vigilant attention to the patient's nutrition; the other relates to such measures for depuration as may be called for in each particular case.

It must be admitted that there is a degree of antagonism in the measures of practice proper to effect these two purposes, which renders their coincident exercise a difficult practical question. In many cases of hemorrhagic malarial fever a competent supply of properly prepared foods is sufficient. In other cases--and this is especially true of malarial hæmaturia--depurative medication becomes paramount. A person suffering under the effects of chronic malarial poisoning is seized with a chill; this is followed by bloody urine, and in the course of four or five hours intense jaundice appears. Incessant vomiting, delirium, and jactitation also occur. The experienced physician is at once brought to the conclusion that he has to deal with a case of blood-poisoning bearing a close resemblance in symptoms to uræmia. To render this conclusion still more absolute, he has only to recall the suddenness of the occurrence of the jaundice and to inquire what has occasioned it. Its appearance is too rapid to permit us to ascribe it to obstruction. It is altogether improbable that it is due to sudden hypersecretion in such pathological states of the system as are present. If, however, we account for it by saying that the addition of a new toxic constituent, urea and its congeners, to an already profoundly poisoned fluid suddenly arrests those processes which dispose of bile in physiological conditions of the system, it seems to me that we adopt the most rational theory. It is then jaundice from lack of consumption. The mere probability of truth in this theory will impress the practitioner with the great importance of eliminant practice in these conditions.

Calomel has been the medicine to which I have principally trusted. I give it merely as a depurative, and not as an alterative. Doses of from two to ten grains may be repeated at suitable intervals until catharsis has been produced. Bitartrate of potassium, Seidlitz powders, or solutions of citrate of magnesia may be also administered if indicated. After purgation the vomiting is mitigated, if not altogether relieved. On this account, and because of bettered states of the system for absorption and assimilation, the way is now clear to the physician. He can ply his antiperiodics, his properly prepared sustenance, and his alcoholic stimulants according to the exigencies of each particular case.

The following propositions may seem not inappropriate in closing this section:

1st. Attacks of pernicious malarial fever are attended by more danger to life or subsequent health than simple attacks; therefore more prompt and energetic efforts should be made to cut them short by cinchonism.

2d. The blood depravations of pernicious malarial fevers far exceed those of simple cases; and therefore it becomes a leading indication of treatment to correct faulty conditions of this fluid as early as possible. {614} In endeavoring to secure this end assimilable foods, stimulants, and depurants must have a shifting scale of value according to the exigencies of each particular case.

3d. The complications of attacks of pernicious fever are far more important than those of simple forms; and therefore symptomatic treatment is often urgently required.

4th. Attacks of pernicious fever may be greatly diminished in number by properly directed treatment of chronic malarial toxæmia, and especially also by the removal of persons suffering under this cachexia to non-malarious localities.

Typho-Malarial Fever.

The prefix typho- is properly applicable to a class of malarial fevers which are complicated by the specific poison which produces typhoid fever.

This term was introduced into medical nomenclature by Surgeon J. J. Woodward of the United States Army. His classical paper on this subject has been published in the Transactions of the International Medical Congress at Philadelphia in 1876. The following extract from the proceedings of this congress will show the interpretation of this term by Woodward:

"On motion of Dr. Woodward, seconded by Dr. Pepper, the following was adopted as expressing the opinion of the section: Typho-malarial fever is not a specific or distinct type of disease, but the term may be conveniently applied to the compound forms of fever which result from the combined influence of the causes of the malarious fevers and of typhoid fever."

It follows, therefore, that the term should be so restricted as to define a disease compounded of the two pathological factors which when acting separately produce either typhoid or malarial fever.

When understood in this sense, and carefully employed, the term appears to me unobjectionable. Perhaps, indeed, it may be a convenient addition to medical nomenclature. If such a name had not been introduced, we would be forced to speak of these cases of compound disease as complications. As it is customary to regard the minor or less important affection as the complicating disorder, we would often have confusion in determining whether the case should be typhoid fever complicated by malaria or malarial fever complicated by typhoid. This term leaves all questions of precedence or predominance in abeyance.

There are no facts, however, which support a conclusion that the malarial poison is capable of forming combinations with the particular poisons of other specific fevers and give birth to a new special poison, which may be perpetuated by successive generations, and thus produce epidemics of a new but compound disease.

The importance of a proper use of the term typho-malarial implies co-ordinate care in diagnosing the true nature of the malady it should define.

It may be said, in brief, that the diagnosis of typho-malarial fever must rest upon the blending of the symptomatic phenomena peculiar {615} to each one of the two fevers which enter into combination. In other words, if the differential diagnosis between the two diseases when they are distinct is made by contrasting the symptoms peculiar to each, the compound disease is to be recognized by more or less positive combinations of these symptoms.

These blended symptoms should not be expected to exhibit the results of a copartnership in which each member exerts equal influence. It is well understood that when two diseases coincide, that one which is more violent or excessive in its morbid process holds so much sway as in some cases almost to extinguish the symptoms of the weaker member of the combination. Consequently, in typho-malarial fever, the typhoid, being the graver of the two forms of disease, ordinarily rules the pathology.

The following notes, accompanied by a temperature chart, will illustrate the clinical course of a case of typho-malarial fever:

J. L., aged thirty years, of French nativity, but a resident of New Orleans for three years, was admitted to Ward 21, Bed 311, Charity Hospital, on the night of December 10, 1881. Had been ill some days with ague. The house-surgeon administered gr. x. of quinia in solution and gtt. xv. of tincture of opium.

The records and temperature date from the 12th of December. During the 11th he took drachm ij sulph. cinch. in solution.

{617} [Illustration: FIG. 24. PART I., showing the temperature-curve from December 12th to 31st, inclusive, during which time the more characteristic typhoid symptoms predominated. PART II., showing the temperature-curve in same case from January 1st to 20th, inclusive, during which the influence of the associated malarial poison was prominent.]

Dec. 13th, tenderness and gurgling in ileo-cæcal region; epistaxis; rose spots on abdomen; deafness and ataxia; no stools since 11th. Ordered

Rx. Acid. Sulphuric. dil., Syr. Aurantii Cort. aa. fl. drachm ij; Tinct. Cinchonæ Co. fl. oz. j. M.

S. Teaspoonful in water every four hours.

Also ordered beef-essence, milk-punch, and milk.

Dec. 13th, two very offensive liquid stools; ataxia greater; skin yellow and countenance dull and listless. Dec. 14th, fresh rose spots; tongue brown and dry; three stools; much jactitation. Dec. 15th, more ataxia; some delirium; pulse 100, weak. Gave gr. iiss quinia in solution, with tincture opium gtt. iii, every two hours. Dec. 16th, pulse 128, weak; delirious. Dec. 17, new rose spots; belly tympanitic; tongue brown, dry; sordes on teeth and lips; eyes injected; very delirious. Treatment continued; nutrition and stimulants given methodically. From 17th to 22d but little change in condition or treatment. Diet and stimulants administered regularly. Dec. 22d, coma vigil; completely delirious. Ordered

Rx. Liq. Morphiæ Sulph., Tinct. Digitalis aa. fl. drachm iij; Spts. Æther. Nitrosi fl. drachm ij; Liq. Potass. Citrat. fl. oz. iij. M.

S. Tablespoonful every three hours.

As the oscillations of temperature became more marked, quinia was resorted to, apparently with good effect. The patient was discharged from the hospital Feb. 8, 1882.

It should be observed that after the 14th of December the patient's bowels were rather costive, and the stools occasionally moulded and very {616} dark in color. On the forty-fifth day after admission the patient had a severe chill, followed by a rise of temperature to 104°. This yielded to competent doses of sulphate of cinchonidia.

This was a typical case of typho-malarial fever. The blended symptoms, as well as those special to each disease, are sufficiently exhibited in the clinical account. The presence of typhoid fever was established by the rose spots and the marked nervous symptoms. The typhoid process seems to have been unusually mild in so far as evidence of bowel lesions were made manifest.

The history of the patient before admission, the color of his skin and stools, and the temperature curves gave abundant proofs of the malarial element in the pathology of the case.

Perhaps nothing need be added on the subject of diagnosis. I may, however, remark that I am very cautious in asserting the diagnosis of typho-malarial cases unless the nervous symptoms, positively-marked bowel symptoms, or rose spots are present to vindicate such a decision. The presence of malarial poison may be determined with less difficulty from the previous history of the case and its special symptoms in the early stages of an attack. But if the morbid processes of the typhoid poison are violent, there are likely to be stages of the disease when it is not possible to detect symptoms which indicate the presence of malaria. On the other hand, it is unquestionably true that the typhoid condition, as it is termed, which so often complicates malarial fevers, can very generally be differentiated from true typhoid fever. While certain cases, or even epidemics, of malarial fevers are attended by remarkable adynamia, often manifesting itself from the very incipiency of attacks, it differs widely from that utter nervous ataxia which characterizes typhoid fever. Again, the adynamia of malarial attacks is generally ascribable to some cause not essential to those affections. Imperfect reaction from a chill, long persistent hyperpyrexia, diarrhoea or vomiting, or chronic paludal cachexia, or, it may be, some epidemic influence, may produce it. The ataxia of typhoid fever is part of its morbid process.

Woodward's statistics show that 49,871 cases of fever diagnosed as typho-malarial occurred among the white forces of the United States during the late Civil War. Of this number, 4059 proved fatal, a mortality-rate of 8.13 + per cent. Among the colored troops 7529 cases occurred, with 1301 deaths, a mortality-rate of 17.27. Statistics borrowed from the same excellent authority give the number of cases of unmixed typhoid fever (or fever classed as typhoid without reference to any complication) as 75,368 among the white troops, with 27,056 deaths, a mortality-rate of 35.89. Among the colored troops 4094 cases occurred, and 2280 died, a mortality-rate of 55.68. These figures show very singular comparative results. They prove that typhoid fever as an uncomplicated malady, was four and a half times as fatal among the whites as the same disease when in combination with malarial poison. Among the colored troops typhoid fever was three and a half times more fatal than typho-malarial fever.

It is highly probable that inaccuracies exist in statistics gathered in the confusion of a great civil war, but I am not prepared to say that the conclusions they point to are incorrect. When an acute inflammation is complicated by malaria, its prognosis is rendered more grave. This, no doubt, {618} is due in part to degradations of the fluids of the system by the malarial poison, and in part to the revulsions of circulation during paroxysms. But it does not follow from this fact that the presence of malaria in the blood, or its effects upon that fluid, exercise an unhappy influence upon diseases due to other specific poisons. It may, on the contrary, be ascertained in the future that it modifies the typhoid process, so as to deprive it of some of its most dangerous features.

Further investigations are required to determine the facts in regard to these questions. But it may be premised that if such a conclusion shall ever be reached, it will influence our expectations of cure rather than our practice. If the malarial poison is capable of modifying the toxic effects of the typhoid poison, it must do so in the very formative stages of that affection, if not in its incubative period, so that, having accomplished all the good it is capable of effecting, we may proceed at once to rid ourselves of its presence.

In entering upon the treatment of two diseases compounded in the same patient, if one should ordinarily be amenable to specific treatment, it must certainly be wise practice to endeavor to simplify the case by subtracting that one from its composition. This is more especially true if the treatment does not affect the course of the other disease in any injurious manner. It is therefore proper to begin the treatment of a case of typho-malarial fever by administering large doses of quinia. A scruple may be given every fourth hour, until its effects in eliminating symptoms ascribable to malaria, and also as an antipyretic, have been sufficiently tested. In the early stages of typho-malarial attacks the febrile exacerbations conform to those laws of periodicity which govern uncomplicated malarial fevers. After the first week, or when the typhoid process has become well established, periodic returns of the fever are less plainly observable. It is possible that in some cases in which the typhoid process manifests itself with great severity the temperature curves may be very characteristic of that disease. I am satisfied that the indications for giving quinia to eliminate the malarial element must be based upon the fever curves which mark the case. Perhaps a more frequent application of the thermometer would often exhibit malarial periodicity where it may otherwise remain unsuspected. I know this to be very often the case in pneumonia complicated by a malarial fever.

Whether thorough cinchonism in the early progress of the attack rids the case of symptoms due to malaria or not, only a very few days are likely to elapse before oscillations of temperature call for its repetition.

The typhoid processes require very much the same measures which are applicable in uncomplicated cases of that disease. The stools of the early stages of attacks should not be checked unless excessive, and mercurials and laxatives should be more freely used than in simple typhoid fever. The effects of the malarial fever and of the hyperpyrexia of typhoid fever, when combined, must almost necessarily entail more accumulation of excrementitious material in the blood than would occur either disease existing separately. On this account eliminating treatment is an important indication. When it becomes necessary to check the diarrhoea because excessive or on account of failing strength, diuretics subsequently prove serviceable. Effervescing solutions of potassium or ammonium, lemonade, Apollinaris water, iced tea, strawberry, mulberry, or raspberry juice, are {619} grateful beverages and increase renal activity. The mineral acids may be given during the ulcerative periods of the disease. Insomnia must be relieved by opiates, chloral hydrate, or other hypnotics.

Tympanites should be met by warm stupes, large enemas of warm water with fl. drachm j tincture of asafoetida or fl. oz. j of whiskey. Small doses of turpentine in emulsion are often beneficial.

In the early progress of cases the diet should consist of farinaceous foods, with milk and the pulps or juices of fresh fruits, given either cooked or in their natural state as the physician may determine for each patient. Methodical and forced nutrition becomes necessary at more or less early periods in different cases.

The stools and all ejecta of the sick should be disinfected and disposed of with the same care and for the same purpose as those of unmixed typhoid fever.

{620}

PAROTITIS.

BY JOHN M. KEATING, M.D.

The term parotitis is applied to a condition of painful enlargement of one or both parotid glands, inflammatory in nature, acute in its course, and usually subsiding by resolution, but sometimes ending in suppuration. The different methods of termination, together with certain etiological distinctions, form the basis of a division of the affection into two sub-classes--namely, 1, idiopathic parotitis; and 2, symptomatic or metastatic parotitis. These demand separate consideration.

I. Idiopathic Parotitis.

Idiopathic parotitis, parotitis epidemica, or mumps, as it is variously named, is an acute contagious inflammation of one or both parotid glands, which usually appears but once in a lifetime, and which, although by no means limited to children, is commonly met with between the second year and the age of puberty. In certain exceptional cases the disease affects the submaxillary glands alone.

NATURE.--The undoubted contagiousness of mumps, with the fact of its frequently occurring in extended epidemics, entitles it to a place among the zymotic diseases, from which it differs, however, in the marked disproportion between the local and constitutional symptoms, the former being well developed, the latter but slight or altogether absent.

ETIOLOGY.--While it is more than probable that, like the other diseases of the zymotic class, mumps is due to a contagium that finds its way into the body in the inspired air or with the food or drink, nothing is known of the nature of this infecting principle.

The predisposing agencies are better understood. Age is one of these, the greater number of cases occurring, as already stated, between the second and the fifteenth year. Infants at the breast are almost entirely exempt, and so, too, are individuals advanced in years. In extended epidemics it is not unusual to meet with cases in adults, but it will generally be found on careful examination that these patients have escaped the disease during childhood. Sex exerts some influence, a much larger percentage of males being attacked than females. Epidemics appear more frequently in the spring and fall than at the other seasons of the year, so that cold and dampness of the atmosphere must be looked upon as predisposing causes. Mumps bears a peculiar relation to measles, scarlet fever, and diphtheria, epidemics being apt to occur directly before, during, or immediately after the prevalence of either of these affections, especially {621} the first. The popular idea of mutual protection is entirely without foundation.

Certain peculiarities are presented by the disease in its mode of occurrence and in the duration and intensity of its epidemics. Thus, some localities are visited annually, others only at intervals of thirty years or more; again, one epidemic may last but a few weeks and affect a small number of individuals, while another extends over months and attacks all the children and many of the adults in the affected region.

ANATOMICAL APPEARANCES.--The exact pathological lesion in mumps is obscure, since the trifling nature of the disease and the almost invariable termination in recovery afford no opportunity for post-mortem investigation. According to Foerster, who seems to have made examinations in cases where mumps occurred as one of the accidental complications of other and fatal diseases, the affected gland at first becomes hyperæmic, and is then the seat of serous exudation. It is reddened, swollen, and on section presents a uniform flesh-like, moist appearance, in place of the ordinary granular aspect. The tumor is often greatly increased in size by a simultaneous serous infiltration of the periglandular connective tissue, and occasionally this tissue alone is involved, the gland itself being entirely free from lesion. The great point in favor of this view of the pathology is the rapid and complete subsidence of the parotid swelling by resolution--a termination to be expected only when the inflammatory process stops short of suppuration or fibrinous exudation.

Virchow regards all cases of parotitis as the result of an extension of a more or less malignant catarrh originally affecting the gland-ducts. This is undoubtedly true in some cases, but that it is far from being the rule is proved by the infrequency of parotitis as a secondary complication of catarrhal affections of the mucous membrane of the mouth.

COURSE AND SYMPTOMS.--The course of the disease is susceptible of a division into three stages--a period of incubation, of invasion, and of actual attack.

The stage of incubation extends over a period variously estimated as from seven to fourteen days. It is marked by no symptoms, though sometimes a history of impaired appetite and digestion, irregular bowels, and languor during the last two or three days may be obtained.

The period of invasion is short, lasting only twelve, or at the most twenty-four, hours. The patient is pale and languid, has slight rigors, pains in the breast and head, and loss of appetite; later, local pain in the parotid region on moving the jaws or on taking acid liquids into the mouth. The surface temperature increases from hour to hour, and just before the glandular swelling appears it reaches 100° or 101° F. In some cases the invasion is characterized by the same train of symptoms that ushers in the acute exanthemata, such as repeated vomiting, diarrhoea, restlessness and anxiety, a disposition to syncope, and, in very irritable children, convulsions. Contrasted with this violent invasion other cases are met with, in which there are no prodromes whatever except a gradual rise in temperature, imperceptible without the use of the thermometer.

The first symptom of actual attack is a peculiar slight stitch-like pain in one parotid region, usually the left. This radiates toward the ear of the affected side, and is increased by movements of the jaw, as in {622} chewing or talking, and by external pressure. The pain rapidly grows more intense, and soon becomes associated with swelling. The tumor first appears in the depression between the mastoid process and the ramus of the jaw, which it fills up, and at the same time thrusts outward the lobe of the ear. As the gland alone is swollen at first, the tumor has the outline of a triangle, with the apex directed downward and forward; soon, however, the connective tissue becomes oedematous and the swelling is greatly extended, involving the cheeks and neck, in the latter region, in severe cases, running forward as far as the median line, downward nearly to the shoulder and backward toward the spine. The most prominent point is directly in front of the ear. The oedema also extends internally, involving the pharynx, the tonsils, and sometimes even the larynx. The skin covering the tumor is either perfectly natural in color or slightly reddened. The central portion is firm and elastic to the touch, the periphery doughy, and pressure here often produces pitting. There is but moderate tenderness. The swelling reaches its height in three days, remains stationary for two days longer, and then rapidly declines, the oedema first disappearing and afterward the glandular swelling, the process of resolution occupying four or five days and being attended with a slight desquamation of the cuticle.

While mumps almost uniformly begins on one side, both glands are, as a rule, affected during the attack. The second tumor begins to develop twenty-four to forty-eight hours after the first, though its appearance may be delayed much longer, even until resolution has begun on the side primarily affected. As the course of the inflammation is similar in both parotids, the whole duration of the attack will depend on the time of involvement of the second gland.

Among the other symptoms an alteration of expression is prominent. At first, the head is inclined toward the affected side; later, when both glands are involved, it is held perfectly erect, and, as the slightest movement increases the pain, it is maintained stiffly in this position. The swelling of the cheeks prevents all play of the features, and this, combined with widely-open, staring eyes and increased thickness of the neck, gives the patient a stupid, almost idiotic, expression. The swelling of the neck is sometimes so great that its diameter exceeds that of the head, and the shoulders, neck, and head, viewed together, have the outline of a truncated pyramid.

As any movement of the lower jaw greatly augments the suffering, the mouth is kept closed, often so tightly that it is impossible to see more than the tip of the tongue. All efforts at mastication are suspended, and deglutition is so painful, especially when the tonsils become enlarged, that the sufferer bears the pangs of hunger and thirst rather than endure the agony entailed in satisfying his wants. The act of speaking even augments the pain; the voice, when heard, has a nasal tone. The acuteness of hearing is impaired, there are singing noises and shooting pains in the ears, headache, and sometimes, in extreme cases, symptoms of cerebral hyperæmia due to pressure upon the cervical veins.

The tongue is heavily coated, the mouth is either dry or there is an increased flow of saliva, and the fluid dribbling from the mouth adds another element to the idiotic expression already referred to. There is loss of appetite, increased thirst, occasionally vomiting, and commonly {623} constipation. The temperature is elevated and the pulse increased in frequency, both to a moderate degree. The respiration is unaffected, except when the oedema has invaded the submucous connective tissue of the larynx; then the movements are increased in frequency and difficult.

Throughout the attack the pain, unless intensified by some extraneous influence, as pressure or the act of speaking or swallowing, is only moderately severe. In ordinary cases the patient rests quietly and sleep is undisturbed, unless the tonsils are enlarged, when it is liable to interruption from loud snoring. When the attack is severe and in nervous, excitable children there is restlessness, sleeplessness, and slight delirium at night.

The general symptoms keep pace with the local in their increase, but they commence to subside before, beginning to disappear while the swelling remains stationary. As soon as resolution sets in the general and local improvement are both rapid, and by the end of the week nothing is left but a trifling weakness and pallor, which disappear in a few days more, leaving the patient perfectly well.

Besides the ordinary symptoms, mumps in certain instances shows a peculiar tendency to metastasis, or secondary involvement, of the testicle and scrotum in males, and the mammæ, vulva, and ovaries in females. This metastasis occurs much more frequently in males than in females, and is usually met with in pubescents and adults, being very rare either in childhood or old age. It generally begins six or eight days after the appearance of the parotid tumor. The latter, as a rule, subsides on the occurrence of any of these metastatic affections, though occasionally the two run a simultaneous course. This occurrence, together with the fact of the secondary inflammation appearing at the date on which the parotitis naturally begins to disappear, tends to support Niemeyer's view, that the two affections are in reality due to the same cause, and that no true transference of inflammation takes place from one point to the other. Occasionally, the parotitis disappears a variable time before the onset of the metastatic affection; then the interval is marked by grave symptoms of depression and cerebral disturbance, but there are no proofs of actual meningeal involvement. In these cases there is, at times, an excessive elevation of temperature, which may account for the brain symptoms.

The most constant secondary manifestation is swelling of the testicle proper, or true orchitis; less frequently there is epididymitis, and with it acute hydrocele and oedema of the scrotum. The orchitis in most cases is unilateral, the right testicle being affected, just the opposite to the parotids, of which the left is the one first involved. When the orchitis is double, both testicles do not become swollen at once, the one preceding the other by an interval of several days.

The course of the orchitis is very similar to that of the mumps, the inflammation increasing gradually for from three to six days, then undergoing rapid resolution, the gland returning to its normal condition by the end of two weeks.

The local symptoms are swelling, the testicle being enlarged to two or three times its natural size, dull pain, and moderate tenderness, while in very severe cases there is burning on micturition and a purulent discharge from the urethra. The spermatic cord does not sympathize in the {624} inflammation, and neither the swelling, pain, nor tenderness is so great as in specific orchitis.

The general symptoms are confined to a moderate elevation of temperature and increase in the frequency of the pulse, thirst, and loss of appetite. This fever is separated from that of the parotitis by an interval of two or three days.

The course of bilateral orchitis is longer by forty-eight hours than that of the unilateral form, and the attending fever is more intense.

The rapid return of the testicle to its natural size and shape shows that, as in the parotid glands, the inflammation does not extend beyond the stage of serous exudation.

THE DIAGNOSIS of mumps is easy after the disease is sufficiently developed to produce the characteristic alterations in the facial expression. In the earlier stages the position of the swelling, immediately beneath and in front of the ear, its triangular shape, and the elevation and outward displacement of the lobe of the ear of the affected side, distinguish it from the enlargement of the cervical lymph-glands so liable to occur in strumous subjects. The acute onset and course of mumps are the points of distinction between it and morbid growths, or the very rare condition of chronic hypertrophy of the parotid gland. The metastatic orchitis cannot be mistaken for gonorrhoeal orchitis if the least care is taken to investigate the history in either case.

THE PROGNOSIS is extremely favorable, there being no record of a fatal case of uncomplicated mumps. Suppuration may occur, but it is an exceedingly rare event. In scrofulous children the course may be protracted for several weeks, and in them resolution is occasionally imperfect, a degree of enlargement and induration of one or both parotids remaining for some time.

Metastatic orchitis, as a rule, leaves the testicle in a normal condition, but, according to Vogel, in some epidemics complete atrophy results.

Dogmy reports an epidemic which raged in a garrison of Mount Louis in January, 1828. Of sixty-nine bilateral and eighteen unilateral cases of parotitis, metastasis to both testicles occurred in four cases, all of which resulted in atrophy of the affected testicle.

THE TREATMENT is simple. The patient should be kept in a uniform temperature, confined to one room, or, better still, to bed, until resolution is well established. While the difficulty in swallowing and fever continue the food should consist of milk and beef-tea; later, other nutritious articles of diet may be added as the appetite demands. Water, iced carbonic acid water, or lemonade may be allowed as freely as the patient will take them, to allay the thirst. A daily evacuation of the bowels must be secured by the use of saline laxatives. During the early stage, if the fever be high, tincture of aconite-root should be cautiously administered; afterward liquor potassii citratis will sufficiently fill the indications for a febrifuge. Tonics are required during the decline of the disease; of this class of remedies, syrup of the iodide of iron, bitter wine of iron, and ferrated elixir of cinchona are most useful.

Special symptoms may demand attention. For example, headache and delirium should be relieved by hot mustard foot-baths and moist cold to the forehead; difficult deglutition from enlargement of the tonsils, by the frequent swallowing of bits of ice, or, if possible, by the application of {625} astringent lotions, as tannic acid and glycerine (one drachm to the ounce); sleeplessness, by the administration of bromide of potassium, with or without small doses of hydrate of chloral in children and of some preparation of opium in adults.

In the way of local treatment the best results and greatest relief to suffering will be obtained by gently rubbing the swollen glands with a mixture of tincture of opium and sweet oil (one drachm to the ounce), three times daily, and in the mean while keeping the parts enveloped with a moderately thick layer of cotton wadding covered by oiled silk. Water dressings or light poultices may be used with advantage. When resolution begins a more stimulating lotion will hasten the disappearance of the swelling.

In the exceptional instances in which the skin covering the tumor becomes tense and red, and suppuration is threatened, two or three leeches may be applied behind the ear of the affected side. When suppuration has actually taken place the abscess should be immediately opened to prevent further destruction of the gland-tissue and perforation into the external auditory meatus.

If, particularly in strumous subjects, resolution be incomplete and glandular enlargement and induration remain after the cessation of the acute symptoms, cod-liver oil and iodide of iron are demanded for internal administration and the compound ointment of iodine for external application. It is well to dilute the latter sufficiently to prevent its causing irritation of the skin, and to apply it twice daily.

When metastasis occurs, the return of fever calls for the same general treatment as in the early stage of parotitis. In addition, an emetic should be given, as this often cuts short the fever or causes it to disappear more rapidly. The patient must be kept at perfect rest in bed, with the scrotum elevated by a cushion and covered with warm anodyne lotions. Salines must be administered sufficiently often to secure regular and free action of the bowels.

When the mammæ or ovaries are secondarily attacked, the seat for local treatment is of course different, but in all other respects the management must be the same.

For the uncommon cases in which the transference of the inflammation is attended with depression stimulants are required, and for those in which meningitis is threatened cutting off the hair and the application of cold to the head, hot mustard foot-baths, local and general venesection, drastics, and irritants to the cutaneous surface, are necessary.

II. Symptomatic or Metastatic Parotitis.

Symptomatic, metastatic, malignant, or suppurative parotitis, as the condition is variously designated, is an inflammation of the parotid gland which occurs during the course of different grave acute diseases, is usually unilateral, and terminates in suppuration, or much more rarely in gangrene, of the gland involved.

ETIOLOGY.--It may occur in association with typhus, typhoid, relapsing, puerperal, and scarlet fevers, or with the plague, measles, dysentery, cholera, and pyæmia, springing into notice at different periods of the {626} course of these affections, which may be regarded as predisposing causes. The exciting cause is perhaps mechanical in nature--namely, the excessive dryness of the mucous membrane of the mouth so common in the severe fevers. This dryness may lead to an occlusion of the orifice of the parotid duct, with retention of the saliva, which fluid, undergoing decomposition, may act as an irritant, producing inflammation, and finally suppuration, of the glandular tissue. This is a likely enough explanation of the causation in some cases, but dryness of the mouth is such a uniform symptom in fever, and suppurative parotitis such a comparatively rare complication, that it cannot be a very active or common cause. Nevertheless, it is impossible to fix upon any other direct cause, though the altered condition of the blood in the conditions mentioned must not be lost sight of as an important etiological factor.

ANATOMICAL APPEARANCES.--The character of the pathological lesions have been well established, owing to the frequent opportunities that arise of examining the diseased gland at different stages of the inflammatory process. When the inflammation has lasted a short time, a day or two, the tubes and acini of the gland are seen on section to be swollen and reddened, and the connective tissue infiltrated with serum and yellowish-red in color; a fluid, either viscid, ropy, grayish in color, or more purulent in character, fills the duct, and may be forced out into the mouth by stroking it in the direction of the orifice. If of several days' longer duration, purulent softening will be noticed in the centre of the acini; this gradually extends until each acinus is converted into a little sac of pus. Then the inter-acinous connective tissue breaks down, and the multiple, minute, purulent collections become converted into a single large abscess or into two or more smaller ones. Next, the pus seeks an outlet. The position of pointing may be on the cheek or in the external auditory meatus--a very common location; again, the abscess may break into the mouth, the pharynx, the oesophagus, or into the anterior mediastinum, the pus burrowing its way along the sheath of the sterno-cleido-mastoid muscle.

While the parotid abscess is forming, suppurative inflammation is apt to be set up in the masseter, pterygoid, and temporal muscles, and from these positions the pus forces its way upward to the temporal or zygomatic fossæ. The periosteum of the neighboring bones, and even the bones themselves, may become involved, and sometimes the cranial bones are partially destroyed, and there is an extension of the inflammation to the brain or its membranes. The middle ear may participate in the general destruction, and the patient is left permanently deaf, if indeed he escape with his life.

The lymphatics, veins, and nerves traversing the parotid are affected by the suppuration in the gland. Irritation of the lymph-vessels results in swelling, tenderness, and suppuration of the lymph-glands. Thrombi form in the jugular vein and its branches, and by breaking down lead to septicæmia and ichorization of the sinuses of the dura mater. The nerves resist for a long time, but seem to act as paths of conduction of the inflammation, the facial nerve leading it to the ear, and the branches of the trifacial to the brain. When gangrene of the gland takes place, the traversing nerves as well as the gland elements are rapidly destroyed.

SYMPTOMS.--Symptomatic parotitis, occurring during the course of {627} any of the diseases already named, produces no change in the general symptoms; if, on the other hand, it occurs during convalescence, the onset is marked by a moderate elevation of temperature and increase in the frequency of the pulse, by thirst, loss of appetite, and sluggish bowels. The tumor, which occupies the same position and thrusts outward the ear-lobe as in mumps, is hard, dense, well defined, and the seat of considerable pain until suppuration takes place, when the latter subsides greatly. The skin over it is red, hot, and tense, and there is much tenderness and little or no pitting on pressure. After the abscess has formed there is well-defined fluctuation on palpation, and at the position of pointing the skin becomes very thin and assumes a bluish-red hue. Gangrene of the gland is manifested by the cadaverous odor, blackening of the skin, the formation of a cavity, and the discharge of ichor and shreds of tissue. The alteration in the expression, the pain in the ear, the difficulty in moving the jaw and in swallowing, are as constantly present here as in idiopathic mumps. It must not be forgotten, though, that when the disease arises during the course of any of the severe infectious diseases, the brain may be so overcome that the subjective symptoms are frequently not complained of.

The course is usually rapid, the abscess pointing on the fourth or fifth day after the appearance of the parotid tumor; occasionally, however, the inflammatory process is much slower, extending over a period of several weeks. The course is also much protracted when secondary abscesses form in other parts of the gland or in the surrounding tissues, when the abscess is transformed into an ichorous cavity, and when gangrene sets in. Ordinarily, where the pus is evacuated by spontaneous rupture or by incision the abscess heals quickly by granulation, leaving the gland enlarged and indurated for some time.

THE PROGNOSIS depends upon the gravity of the original disease, the period of the disease at which the complication occurs, and whether or no mortification sets in. When the vital processes are greatly impaired by the primary disease, the onset of the parotitis, trifling in itself, may prove sufficient to determine a fatal result. The danger of such a result is much increased, too, if the inflammation begins in the earlier stages or during the height of the disease which it complicates, while if it commences during convalescence by far the most frequent result is recovery. Gangrene of the gland involves great risk of life--a risk which increases in proportion to the early date of its onset in the course of the original disease. Even when the gangrenous process ends in recovery, the face is much distorted, the hearing is lost in the ear, and the facial muscles are paralyzed on the affected side. Bilateral symptomatic parotitis has naturally a graver prognosis than the unilateral form.

DIAGNOSIS.--The disease is readily distinguished from idiopathic mumps by the history, the less marked degree of the enlargement and surrounding oedema, the greater degree of pain and tenderness, the hardness of the tumor, the red discoloration of the skin covering it, and the termination in suppuration. Further, it never displays an epidemic tendency.

TREATMENT.--The general treatment of this form does not differ from that of the disease it complicates, though the employment of stimulants in increased quantities may be indicated.

{628} Before the first appearance of tumefaction of the parotid the introduction of a probe or canula into the duct of Steno, associated with pressure on the gland from the outside, may, by forcing from the duct a collection of mucus or muco-pus, abort the inflammation. If this is unsuccessful, a poultice should be applied over the gland to encourage suppuration and pointing externally. As soon as the abscess points the pus must be evacuated by an incision, and, as this has a tendency to close again, a piece of lint must be kept between the lips of the wound.

The enlargement and induration left after the healing of the abscess require the application of tincture of iodine or of compound iodine ointment to the surface.

When gangrene occurs it demands the same treatment, both local and general, as when it is seated elsewhere.

{629}

ERYSIPELAS.

BY JAMES NEVINS HYDE, M.D.

DEFINITION.--Erysipelas is an acute disorder, characterized by the systemic symptoms common to the febrile state, and by an involvement of the integument and deeper parts, the affected surface being tumid, hot, reddened, painful, and often the seat of well-defined bullæ, the process terminating either in complete resolution after cutaneous desquamation or in a fatal result commonly due to complications of the malady.

SYNONYMS.--Eng. St. Anthony's Fire; Fr. Érysipèle; Germ. Rothlauf; Ital. Risipolo.

CLASSIFICATION.--Erysipelas is properly recognized as one of the acute infectious diseases. Though by its symptoms and career it would seem to be properly assigned to the category of the exanthemata, it is yet by most authors set apart from the latter--first, because its career is less specifically defined; second, because its contagiousness is less demonstrable in every case; third, because one attack is not known to confer upon its victims immunity against a second; fourth, because the occasional prevalence of the disease in apparently epidemic form is evidently due to extrinsic causes, and does not depend exclusively upon its sudden appearance among the unprotected; fifth, because no definite period of incubation precedes its earliest manifestations; and, sixth, because at times it appears in local manifestations apparently unaccompanied by systemic phenomena.

HISTORY.--The earliest writers on medicine bear witness to the fact that the disease was recognized at the date when men first made record of human ailments. It has occurred in all parts of the world and at all seasons of the year, sparing neither age nor sex in its development. Zuelzer[1] refers to epidemic occurrences of the disorder, described by Rayer, as visiting the Paris hospitals in 1828; by Schönlein, as existing in Zürich in 1836; by Gintrac, as spreading in Bordeaux in 1844-45; and by Trousseau, as prevailing in the Maternité in Paris in 1858.

[Footnote 1: Cyclop, of the Prac. of Med., Ziemssen, vol. iv. p. 424.]

ETIOLOGY.--Authors have in general assigned different causes to the forms of erysipelas hitherto regarded as either idiopathic (or medical) or traumatic (or surgical). The modern view, however, is that which regards all cases as alike produced by the absorption of the toxic agent capable of exciting this peculiar inflammation of the skin. The peculiarly well-characterized symptoms of the disease--for example, when it affects the head and face--were long regarded as etiologically distinct from the affection which complicates surgical injuries and wounds. But {630} a closer study of many of the cases first named has again and again disclosed the fact that they originated in such traumatism, for example, as the piercing of the lobule of the ear for the insertion of an ear-ring, a carious tooth, an alveolar abscess, or a pathological product in the antrum of Highmore.

The disease is equally common--apart from the puerperal state--in both sexes and at all ages, and occurs under favorable circumstances in all seasons of the year. It is unquestionably at times spread by direct contagion, either from the living or dead body affected with the disease. Such contagion may occur mediately or immediately. It is, however, not readily shown to be producible by the media of clothing and other articles which have been in contact with a diseased surface. The contents of the bullous lesions which appear upon the erysipelatous surface are inoculable; and the disease has in this way been transferred not only to men, but also, by Orth and others, to the lower animals, and even from one of the latter to another of the same species.

Certain it is, however, that the disease does occur, characterized by symptoms indistinguishable from those to be recognized in the contagious type of the malady, where the most careful investigation wholly fails to reveal the cause, and where the disorder rapidly spreads if the conditions for its extension are favorable. Under these circumstances it is wisest at present to admit that the exact etiology of erysipelas is unknown. Its relative frequency in the puerperal state is unquestionably to be explained by the favorable local conditions which at such times exist in the female for the development of all septic disorders.

As regards the circumstances which might be supposed to specially favor its development, these the capriciousness of the disease, which is its striking characteristic, often quite disregards. Thus, on the one hand, it may and often does prevail, year after year, in certain hospitals, and even in certain wards of a single hospital, especially where these are crowded with patients. But it may also repeatedly spare masses of men affected with disease of a different type when the latter are gathered together in prisons or camps, and indeed even may appear among such individuals and fail to spread to others who are in close proximity to them.

With respect to the propagation of erysipelas from infected to sound individuals, a contrast is exhibited when the transmission of variola, for example, is compared with it. Thus, it is well known that the mildest cases of varioloid may be sources of malignant forms of variola to the unprotected, while those who are partially protected and exposed to the virus of confluent forms of the disease may exhibit the mildest symptoms of varioloid. In erysipelas, however, it is tolerably certain that there are different degrees of virulence to be recognized in different cases, and that the disease at times is transmitted in its different types. Thus, traumatic erysipelas is much more closely related to childbed fever than the varieties of the disease appearing upon the head and face, which cannot be attributed to traumatism, surgical accidents, dental abscesses, or local injuries of the antrum of Highmore. Parturient women frequently escape infection when the erysipelatous disorder is of the so-called medical type. Per contra, it is to be noted that women who are prone to the relapsing and so-called chronic forms of erysipelas are {631} particularly apt to suffer from that involvement of the genital organs, peritoneum, spleen, and febrile movement whose sudden occurrence after confinement is so portentous.

SYMPTOMATOLOGY.--The disease is usually announced by the occurrence of a chill, which may precede by a day or but a few hours the appearance of the cutaneous disorder. The rigor may be severe or mild in grade, so that it may even be forgotten by the patient till his attention reverts to it in connection with the resulting symptoms. There may be simultaneously some gastric distress, rarely of severe character. These symptoms are commonly followed by a febrile reaction. In other cases the first recognized symptoms of the malady occur in the skin, the patient scarcely recalling the fact of a slight preceding malaise.

The cutaneous lesions appear in the form of a circumscribed oedema and redness of the surface, often preceded and usually accompanied by a sensation of tension, heat, and burning pain. This macule, plaque, or patch of diseased integument is in its typical features characteristic. It is distinctly or irregularly circumscribed; its oedematous condition elevates its level decidedly above that of the adjacent integument, so that there is a somewhat sudden descent from the former to the latter for a space of from one to two or more lines. The redness is also of a bright crimson hue, and the reddened surface has a sheen or glossy appearance uniformly displayed over its area. It disappears under the pressure of the finger, leaving a yellowish-white color in the region of impact, the erysipelatous blush rapidly returning when the circulation at the surface is restored. This smooth and shining condition of the reddened patch is so characteristic of erysipelas that it arrests the attention of the diagnostician as soon as he observes it. According to Zuelzer, it is caused simply by the tension of the epidermis. When first observed it may occur in the form of circular, small or large coin-sized patches, or in streaks, striæ, and radiations, or as very irregularly disposed, rosy, and shining marblings or mottlings of an oedematous surface.

The skin thus affected is hot to the touch, tender, firm, and smooth. It is occasionally the seat of pruritic sensations, more commonly of a peculiar sensation of heat and burning.

In the course of two or three days the involved area spreads uniformly or irregularly and centrifugally from the point first involved, after which time, in mild cases, the disease persists without apparent change for a few days more, prior to its decadence by resolution. This final stage of the malady is characterized by a progressively diminishing fever, moderate desquamation, gradual disappearance of the oedema, and a color-change to the darker shades of bluish-red or to a light brown. In this form of the disease the erysipelatous patch, after being fully developed, does not tend to spread from the affected to the unaffected surfaces; and, as a consequence, the affection may complete its entire career in less than a fortnight.

In other cases, however, a remarkable tendency is developed to the progressive spreading of the inflammation from one point or surface of the body to another, the parts first affected paling as the disease passes on to involve those in the vicinity, or being yet deeply involved while the process of peripheral extension is in progress. In yet other cases the red blush sweeps away from its first position in tongue-like projections over a {632} tumid and painful skin, while the region first invaded becomes paler, though still preserving its oedematous features. In still another class of cases the advancing ribbon or band of elevated and reddened integument passes over to a new area, leaving the regions it has traversed tumid, painful, and here and there streaked with rosy lines, patches, or irregular gyrations.

In yet severer types of the malady the intensity of the inflammatory process is such that the epidermis is raised from the tissues below by the free exudation of the serum of the blood. In this way vesicles, or, more commonly, bullæ, develop upon the surface. Bullæ thus formed may be typically perfect, but are often exceedingly irregular in contour, having an appearance which is suggestive of the blistering of a surface by boiling water. The bullæ may be well distended and filled with a perfectly limpid serum. This fluid may, however, in the course of a few days become purulent, the contents in such case drying into crusts. In the severest types of the disease gangrene results from the intensity of the dermatitis, and the loss of tissue which thus occurs is repaired by the processes of granulation and cicatrization.

The migration of erysipelas from one part to another of the surface is sometimes so extensive as to invade from time to time the larger part of the superficies of the body. Erysipelas of this ambulant character may also, after invading the entire surface of the body, be relighted at the point where it first appeared. In other cases this phenomenon of recurrence or reawakening on patches of skin traversed by the disease may be noticed only after moderate extension from a given point. Reddish or rosy-colored islets then appear as new centres of a fresh extension-process upon an integument whose swollen tissues still exhibit the evidences of the prior invasion. In still other cases similar islands of fresh disease are recognized in advance of the elevated edge and tongue-like prolongations which mark the onward progress of the erysipelatous inflammation over areas previously unaffected.

The swelling of the involved tissues is one of the most characteristic features of erysipelas. By this is meant not the tumefaction simply of the superficial portions of the integument, nor the tumefaction which may be measured by the height of the affected above the level of the unaffected skin at the edge of the involved area, but a swelling much more than this, involving the entire skin, and often indeed the subcutaneous tissues, differing, of course, in the extent to which it advances in different cases. In those of severe grade the swelling is enormous, an affected limb assuming the elephantiasic aspect, while the deformity thus induced in the head is fully as great as that seen in the height of confluent variola. In such cases the neighboring ganglia are, as a rule, enlarged and often painful.

It is indeed this swelling which gives to erysipelas of the head and face its peculiar physiognomy. The disorder is apt to find its starting-point in the ear, the side or point of the nose, or one cheek. At this moment it may be possible to recognize the fact that the adjacent mucous membrane is also involved. Thence the disease progresses over the face, and possibly over the scalp also, the resulting tumefaction being occasionally, as already stated, enormous. Thus the eyes are usually closed and sealed by the swollen lids and the orbital depressions are effaced. The lips, enormously pouting and reddened, project from the swollen visage to as {633} great an extent as the tumid ears, which, for similar reasons, depart from the usual plane. The mouth, nares, and eyes alike are covered with mucous secretions, possibly commingled with the contents of bullæ which have formed and broken. Crusts may thus collect near the mucous outlets. The tongue is dry, parched, and cracked, and exhibits a reddish-brown hue. In less severe cases it may be seen to be covered uniformly with a thick yellowish or yellowish-white paste. The fauces and buccal membrane are reddish in color, glazed, and dry.

The patient having this serious form of the malady is indeed in a critical condition. There is usually a coincident coma or delirium. The pulse is either greatly accelerated and full, or thready, fluttering, and destitute of rhythm. The temperature rises to 105° F., and even higher. In this condition a fatal issue may be heralded by collapse, with decadence of the external evidences of the disease, or by the occurrence of blood-filled blebs, or indeed by larger or smaller areas of the surface falling into gangrene. This latter accident may also involve the mucous surfaces, large patches of the buccal membrane, the gums, and even the palate, losing their vitality and showing as greenish-black, insensitive tracts, quite firmly attached to the healthy tissue. These accidents may be of very rapid occurrence, more particularly in the case of individuals prone to exhibit the severest forms of the malady, such as very young infants and those enfeebled by advanced age, by alcoholism, or by any of the cachexiæ.

Other types of erysipelas, chiefly noticeable by reason of their location, are those spreading from the umbilicus, the genital region, the sites of vaccination, of varices of the lower extremities, and the surfaces near the seat of surgical accidents and operations.

The various names which have been, especially by older writers, given to the several expressions of this disorder relate almost exclusively to their external characteristics. Among these may be mentioned--E. ambulans, e. erythematosum, e. bullosum, e. glabrum, e. levigatum, e. miliare, e. oedematosum, e. pemphigoides, e. phlyctenulosum, e. puerperale, e. vaccinale, e. variegatum, e. verrucosum, and e. vesiculosum.

The resolution of erysipelas in favorably terminating cases is accomplished by very gradual amelioration of symptoms. The swelling begins to subside, usually between the third and sixth days. The blebs that have formed then disappear by absorption, bursting, desiccation, or crusting, and subsequent exfoliation. Desquamation of the involved surface may be a prominent or a very insignificant feature. When the patient with erysipelas capitis enjoys a favorable crisis in his disease, there is occasionally noted a very rapid amelioration of the symptoms. The tumefaction speedily subsides, the features become recognizable, and defervescence is complete. Throughout the course of all attacks the febrile process and the erysipelatous blush proceed pari passu with but little deviation of the severity of the one from the intensity of the other.

The complications and sequelæ of the disease are less numerous than they are grave. In erysipelas of the head there is usually a rapid shedding of the hair, though in convalescence the growth of the hair may be restored. An obstinate seborrhoea sicca may, as after variola, linger long afterward upon the scalp; here also, as in other {634} portions of the body, one or many abscesses may form in the subcutaneous tissue after the resolution of the dermatitis; while in phlegmonous erysipelas these abscesses may accompany the disease at its height.

Lymphangitis and adenopathy are common complications of erysipelas, the former betrayed in thickened and often knotted cords, which may be felt radiating from involved areas to neighboring glands. A singular modification is often undergone by the integument affected with erysipelas which has also been the seat of other cutaneous disorders. In this way lupus, psoriasis, chronic eczema, and some of the syphilodermata have been relieved.

Besides the surfaces of the nasal, pharyngeal, and buccal mucous membranes which have been indicated as at times involved by the disease, the inflammatory redness and swelling may extend to the epiglottis, the larynx, and the trachea. Croupous and other forms of pneumonia, pulmonary oedema, and pleuritis have been not rarely noted. In erysipelas of the head the membranes of the brain may inflame and serous effusions distend the ventricles.

The joints may be inflamed either by sympathy or by direct extension of the erysipelatous inflammation to the periarticular tissues, or yet by the occurrence, in or about them, of metastatic abscesses in septicæmic conditions.

The peritoneum may be also acutely or subacutely inflamed in erysipelas, though it is doubtful whether the accident occurs in consequence of the extension of the disease to this membrane from the skin of the abdominal wall. The same may be said of the endocarditis and pericarditis noted by several authors. Of all other complications, it may be said that they can usually be assigned to the occurrence of either septicæmia, or pyæmia, or to the development of metastatic abscesses.

With respect to the eyes, a distinction should be drawn between those attacks originating in deep or superficial affections of the globes and those in which the visual organs are merely involved as by accident in the extension of the disease. In the former case deep orbital abscesses or inflammatory affections of the iris and retina may be followed by erysipelas of the lids or neighboring parts, while in the latter event the issue is more commonly a transitory conjunctivitis, lachrymation, and photophobia, which soon disappear when the disease has declined. The cornea, being unmacerated with pus as in severe variola, commonly escapes perforation.

Erysipelas is a disorder which, without question, produces in a certain proportion of patients a susceptibility to recurrent attacks. This susceptibility, however, is less a systemic tendency to the development of the disease than a peculiar liability to recrudescence originated by chronic local ailments. Thus catarrhal, ulcerative, and other affections of the nasal mucous membrane are particularly apt to originate repeated erysipelatous attacks in the integument covering the nose, and the same is true of the skin in the vicinity of the orifices of fistulous sinuses and varicose veins.

The forms of disease which are often described as instances of chronic erysipelas belong to several classes. There are, first, those in which are observed recurrent attacks of true erysipelas. Second, those in which a chronic eczema or dermatitis produces a circumscribed patch of infiltration {635} in a skin having a lurid reddish hue, which is also the seat of marked subjective sensations, chiefly itching. The well-known forms of chronic eczema erythematosum of the face in middle years or advanced life are commonly, and erroneously, regarded as erysipelatous in character. Third, there is a peculiar dermatitis, of the cheeks chiefly, with regard to whose identity as an erysipelatous affection there is much doubt. The skin is infiltrated in a circumscribed patch, and has a peculiarly glossy red hue. It is essentially a chronic disorder, the affected patch remaining unchanged for months at a time, and then exhibiting aggravation in consequence of accidental exposure to heat or traumatism. These patches may be relics of relapsing forms of erysipelas; and in my experience are more commonly encountered in the subjects of chronic alcoholism.

PATHOLOGY AND MORBID ANATOMY.--The pathological changes exhibited in the erysipelatous skin are those of an exudative process involving the cutaneous and subcutaneous tissues. Nothing specially different from the phenomena observed in a simple dermatitis can be recognized by the microscope alone. Biesiadecki's careful investigations[2] certainly do not disclose any such specificity. The epithelia are swollen with serous fluid, and the exudate, though largely serous, contains also the corpuscles recognized in plastic lymph. It is this serum, rapidly invited to the surface by the acuity of the exudative process, which raises the epidermis into the bullæ described above. The nuclei of the bodies recognized in the exudate are evidently in a state of division and consequent multiplication. The epithelia of the rete mucosum are swollen and stretched. The connective-tissue elements in the derma are also swollen, and exhibit reversion to the embryonal state. There is within each a relative increase of protoplasm, as a consequence of which they undergo a species of liquefaction. The blood- and lymph-vessels enlarge and are crowded with corpuscles. The subcutaneous tissue participates in this process, its elements being filled with finely granular cells disseminated or in aggregated masses. The chief peculiarity of this exudation, and of these changes in the tissue-elements where it recurs, is the rapidity with which, when involution is in progress, the fluid is absorbed and the inflammatory elements disappear. When abscess or gangrene complicates the erysipelatous inflammation the changes are not different from those recognized in dermatitis calorica.

[Footnote 2: Sitzungsber. d. k. Acad. der Wissen., Wien, ii., 1867.]

The changes noted in the viscera are also of a congestive and inflammatory type. According to Ponfick,[3] there is at times a parenchymatous degeneration of the muscular tissues of the large vessels, and of the extremities, as well as of the kidneys, liver, and spleen, the latter organ occasionally undergoing softening. The mucous surfaces of the mouth, larynx, lungs, and alimentary canal have also been found affected with oedema, congestion, and infiltration, rarely terminating in ulcerative changes.

[Footnote 3: Deutsch. klin., No. 20, 1868.]

DIAGNOSIS.--The diagnosis of a typical case of erysipelas is so simple that the nature of the malady is often recognized by those unskilled in such matters. It is difficult to mistake for any other affection the circumscribed, swollen, shining, and rosy-reddish patch of skin, accompanied by fever or marked malaise, with adenopathy of near glands, and often with a history of traumatism to which the origin of the disorder may be readily referred.

{636} It is to be distinguished from dermatitis in its various forms (venenata, medicamentosa, phlegmonosa, suppurativa) by its characteristic features, and by the frequent absence in these inflammations of a febrile reaction and of a shining, rosy-red hue of the skin, and by the peculiarities described above of the elevated margin of the erysipelatous area.

Eczema, especially in its chronic erythematous forms, exhibited in the face of adults in middle and later life, is of much slower development, is productive of itching, is ill-defined in contour, and is not accompanied by fever.

Erythema in all its varieties is a purely hyperæmic affection and unaccompanied by fever. In erythema multiforme there is an exudative process by reason of which various papules, nodosities, and at times even bullæ, appear upon the surface. None of them, however, are accompanied by a diffused area of redness spreading at the periphery. All of its lesions are circumscribed, and rarely affect the face.

Pemphigus could only be mistaken for the form of erysipelas bullæ, but its lesions do not rise from a broadly inflamed area; they rather have attended with each a distinct individual halo when the integument from which they spring is at all congested. They are also rarely accompanied by a febrile process.

Scarlatina, though a febrile affection, is readily distinguished from erysipelas by the appearance of its exanthem, symmetrically and generally developed over the entire surface of the body, or progressively and symmetrically from the upper to the lower segment of it. The exanthem has also a dull scarlet color or the boiled lobster hue, differing thus from the rosy-red and shining patch of erysipelas.

Urticaria also is often of symmetrical development, is rarely accompanied by fever, and is characterized by typical wheals, which, however closely packed together, never have the smoothness of the surface affected with erysipelas.

PROGNOSIS.--The prognosis of a simple case of uncomplicated erysipelas occurring in an individual in fair health and possessed of a reasonable degree of vigor may be regarded as favorable. Even in the weakness of infancy a large area may be involved in the disease and a high degree of fever be aroused without alarming results.

Erysipelas should, however, always be regarded as a serious disease or a serious complication of any existing malady. It is often a grave feature in surgical injuries. Erysipelas involving the entire surface of the face and head is always a formidable affection. In the puerperal state it is dreaded by every accoucheur.

All these circumstances are rendered more portentous by the existence of the disorder as a complication of any other grave malady, or by its occurrence among the subjects of alcoholism, struma, phthisis, or various other cachexias, and among the aged. Occurring in epidemic form among the inmates of prisons, camps, and hospitals, the mortality of the disease may be increased tenfold.

TREATMENT.--The prophylaxis of erysipelas is that of all contagious diseases. It involves isolation of the affected individual, disinfection of body- and bed-clothing before the latter are again employed upon the persons of others, and destruction by fire of all dressings which have been in contact with the integument.

{637} The hygienic management of the patient is not to be neglected. The complete ventilation of the sick chamber is to be secured, and its temperature uniformly sustained at a point between 65° and 70° F.

The general treatment of the sufferer need not greatly differ from that commonly pursued in the febrile state by modern therapeutists. There is but little confidence to-day in the methods by venesection and purgation, upon which at one time reliance was placed. Cool or cold water may be freely employed when there is hyperpyrexia, either by general bathing or by wrapping the patient in sheets dipped in and wrung out of the same fluid. The results are favorable as regards the bodily temperature, and are not productive of danger, though water thus applied has no effect upon the local disorder of the skin. Iced or cool water, by the ice-bag or compresses, is specially indicated as a topical application for the head when there is delirium or other indication of disturbance of the cephalic centres, irrespective of the invasion of the scalp and face by the erysipelatous inflammation. The sulphate of quinia in full doses is indicated especially when there is any tendency to remittence in the febrile accessions, but is not known to possess any power to cut short the disease. In many cases of erysipelas the febrile condition is readily managed by the administration of the simpler remedies found grateful to the palate of the sufferer, such as iced, acidulated, and effervescing draughts, with perhaps the employment of the spiritus Mindereri or the spirit of nitrous ether. In other cases the mineral acids can be substituted with advantage for the latter. With many American physicians it is customary to add to these remedies the tincture of the root of aconite, with a view to its effect upon the pulse.

Few internal remedies, however, have in this country enjoyed as much popularity with the profession in the treatment of erysipelas as the muriated tincture of iron in full doses. Its use, first suggested for this purpose by Bell in 1851, has here steadily gained in favor since its general adoption. It is well to give it in doses of not less than 20 or 30 drops, repeated every two or three hours, diluted with water. When there is high fever, and especially if the secretion of urine is scanty, the following formula will be found valuable:

Rx. Tr. Ferri Chloridi; Sp. Ætheris Nitrosi; Glycerinæ aa. fl. drachm i. M.

S. A teaspoonful in water every three hours.

This preparation of iron certainly seems, in many cases, to shorten the disease, but, per contra, it is to be remembered--first, that in many other cases it has been found to exercise no control whatever over the severest manifestations of the disease; second, that in other countries, especially in Germany, where it is rarely employed, the mortality from the disease is no greater than elsewhere.

The widest difference in practice has obtained relative to the local treatment of the affection. They who have had the fortitude to content themselves with watching the evolution of the specific dermatitis, merely protecting the skin by dusting over it a simple powder or leaving it covered with a cold compress, have certainly no worse results to tabulate than those who entertain a belief in the efficacy of the abortive treatment of the local disorder.

{638} No remedies, locally applied, can be recognized as certainly possessing the power to cut short the inflammation. Those which enjoy the highest reputation for topical employment are saturated solutions, hot and cold, of the hyposulphite of sodium, of boracic acid, and of the bicarbonate of sodium; salicylic acid; iodoform in powder; and, quite lately, resorcin. Hot fomentations of the erysipelatous patch are in general most grateful to the patient, and with these an opiate and astringent effect can be obtained, as by a hot lead and opium wash or by solutions of the sulphate of iron or of alum and tannin. Useful methods of applying these are by the medium of borated cotton, oakum, tow, or spongiopiline, covered with oiled silk or the Lister protective material.

Other medicaments which have enjoyed favor in the topical treatment of the disease are lime-water and linseed oil (carron oil), sulphur in powder, carbolic acid, camphor, the oil of turpentine, collodium, cataplasms and ointments containing mercury, lead, zinc, tar, and tannin.

Respecting the measures adopted with a view to checking the extension of the disease at the periphery of the patch, the belief in such a possibility has been wellnigh abandoned. For this purpose the nitrate of silver, caustic potash, tincture of iodine, and similar substances have been boldly and broadly applied, alike over the sound and affected integument, with the production of an artificial dermatitis intended to supplant that which was previously in progress. Again and again has the local inflammation transgressed these artificial limits; and when they have been by it apparently respected there has been little ground for believing that the result was due to the treatment pursued. Inasmuch as the disease is often self-limited and distinctly limited in its progression over the surface, it is manifestly difficult to determine that its limitation in any given case is the result of topical agencies. These agencies have, moreover, the marked disadvantage of adding their irritative effects to those incidental to the dermatitis.

The surgical treatment of erysipelas invading special regions of the body or the deeper tissues is a matter of importance. Free incisions are requisite for the liberation of pus, and all abscess cavities should be treated antiseptically and stuffed with iodoform or resorcin. Great tension of the lids demands free incisions in the long diameter of either, and the same surgical procedures are often demanded in erysipelas of the scrotum or of the labia in the female. Gangrene and sloughing are to be treated in accordance with the principles recognized as important in the management of these accidents in general.

The mouth when involved may be benefited by gargles containing the chlorate of potassium, alum, tannin, the compound tincture of cinchona, or by the use of the spray with a saturated solution of boracic acid in rosewater. Kaposi lays stress, in all cases of erysipelas of the face, upon the importance of searching for and evacuating all dental abscesses and pustules seated upon the Schneiderian membrane. Crusts in the nasal cavity are to be soaked with vaseline and removed by washing, their re-formation being prevented by the insertion of small tampons smeared with a bland ointment or oily fluid. Abscesses in other portions of the body, not suspected as being etiologically significant, are to be carefully searched for and emptied, whether occurring about the anus, the genitals, or the legs.

{639} Subcutaneous injections of carbolic acid and other antiseptic solutions have not been rewarded by such results as to establish in any degree their special efficacy.

In all ordinary cases the expectant treatment recommended by Zuelzer is abundantly to be commended. The inflamed tissue is to be dusted with finely-powdered starch, and protected by a layer of soft cotton-wool which exercises a moderate degree of pressure upon it. Antiseptically, the highest ends are thus reached.

The diet of the patient should consist of animal broths, soups, milk, and eggs, with a view to the reparation of the waste incidental to the febrile process. Stimulants are to be freely used in all asthenic conditions. In convalescence the warm water and soap bath is to be employed, followed by dusting of the surface with starch powder or by inunction with vaseline.

{640}

YELLOW FEVER.

BY S. M. BEMISS, M.D.

Yellow fever is a specific, infectious, and communicable disease of one febrile paroxysm.

This definition includes some of the most prominent characteristics of the disease. The malady, however, derives its name from a symptom not mentioned in the definition. The yellow color of the skin and scleroticæ which appears in advanced stages of grave cases of yellow fever, and which becomes especially marked in the cadaver, has ruled its nomenclature. Whatever objections may be urged against the term "yellow fever" as being founded upon a symptom of the disease not always present, it is too strongly fixed in both medical literature and popular usage to justify efforts to change it.

Neither is it liable to beget confusion as long as it is understood that it is to be restricted in its application to a specific fever induced by a specific poison, and that as an incident of its morbid process it produces yellow coloration of the surface so frequently as to suggest the prefix yellow to its title.

ETIOLOGY AND SYMPTOMATOLOGY.--In this day of almost general belief in the theory which holds that each specific disease has its own specific poison or morbific germ, it is scarcely expedient to occupy much space in discussing the propriety of classing yellow fever among the specific maladies.

Whether we rest the decision of this question upon the uniformity of those circumstances and conditions which originate and develop epidemics of yellow fever, or upon the sameness of its symptomatic phenomena wherever observed, we find very nearly as substantial claims to a specific individualization of the disease as any one of the eruptive fevers possesses. Not only are its morbid phenomena so characteristic that even non-professional observers designate it by such epithets as Bronze John, Yellow Jack, Vomito Prieto, etc., but it is inconvertible with other specific affections. This inconvertibility of yellow fever with other diseases is absolute, and affords irrefrangible evidence of the specificity of that germ or poisonous principle which produces it.

The study of yellow-fever poison after the objective method has hitherto been unproductive of definite results. When such experienced and truthful observers as Sternberg, Woodward, and Schmidt, working with the most approved microscopes, have failed to identify any organism or object peculiar to the products from the bodies of yellow-fever subjects or to the circumfusa of the sick, this declaration is sufficiently supported.

{641} But when we turn to a subjective method of investigating that toxic agent which causes yellow fever, it is found to possess sufficiently well-marked characteristics to justify practically valuable conclusions. Some of these characteristics or modes of behavior merit notice.

1st. The human system is a field of reproduction and multiplication of yellow-fever poison. This is sufficiently established by two facts:

(a) A person in the incubative stage of yellow-fever intoxication may be divested of all fomites and yet originate other cases after a developed attack.

(b) The infection is intensified by aggregation of the sick.

These propositions are indisputably true.

2d. The poison or infection undergoes some change after leaving the human system. This appears to be susceptible of proof, because communication of the disease from person to person is not a common event. When this does apparently occur, there is often very strong reason for a belief that the contagion was resident in some fomites connected with the patient's bed or clothing.

3d. There are no sustained observations which prove that yellow-fever poison is ever created de novo.

The autochthonous birthplace of the poison is unknown. The suggestion of Niebuhr, that yellow fever may have been one of the causes of death during the plagues of Athens, can not be authoritatively denied. It may have been called into existence at the moment when all things else were created which were to perpetuate each its kind.

4th. Some of those conditions and circumstances which favor or retard the development or maturation of yellow-fever poison outside the human body are quite well understood. Warm, damp weather is most prominent among those climatic conditions which are favorable to the growth of yellow-fever epidemics.

5th. A freezing temperature ordinarily destroys the contagium of yellow fever. A high degree of artificial heat produces a similar result. It is highly probable that certain chemical agents would also effect its destruction if brought in contact with it.

6th. If yellow-fever fomites are hermetically enclosed in situations protected from cold or other agents which are destructive to their infection, its vitality may be preserved for an undetermined length of time, and its toxic qualities again made manifest when unacclimated persons are exposed to it.

7th. Yellow-fever poison possesses ponderability. This characteristic is so distinctly marked that it has been frequently termed a "low-lying poison."

8th. It is incapable of being air-borne through any great distance, at least without being deprived of its toxic effects.

9th. It is transportable in fomites through great distances, either on sea or land, and as often as its toxic effects are manifested after these portations they are so uniform as to be promptly recognizable.

A great number of different materials in common use may act as fomites, such as loose wool, cotton, or hair, or textile fabrics of various descriptions.

The following facts, which illustrate how yellow-fever infection may be conveyed in the most unsuspecting and innocent manner, are well {642} authenticated. There can be no ground for accusation of error except in the hypothesis that the infection was encountered simultaneously in some unexplained manner. The facts are furnished by Dr. Shannon of Ocean Springs, Mississippi: "On the 14th of October, 1883, Maj. J. B. B. died of yellow fever in Ocean Springs, Miss. I moved the family at once to the healthy locality where you saw Miss B., not allowing them to take any article from the room where the husband and father had died. The children applied to me for a lock of their father's hair, which I refused, but the oldest daughter, now dead, prevailed upon the nurse to give it her. She placed it in an old envelope that had been torn open at the end and carefully folded the torn end down, thus practically sealing it, and laid it away among other old letters. On Sunday, the 4th of November, at 12.30 P.M., she brought this envelope out upon the open gallery, and opened it for the first time to examine the lock of hair and show it to her aunt, Miss S., who was visiting her, and upon inhaling the concentrated poison confined in the envelope and emanating from the hair, exclaimed, 'Oh, what a peculiar smell!' She then handed the envelope to her aunt, Miss S., who, unconscious of danger, also inhaled the 'messenger of death' with a similar exclamation, when Mrs. B., who was standing near, reached out her hand for the envelope, but was prevented from getting it by the entreaties of a fretful child to be taken up in her arms. This gave time for sufficient reflection, and she admonished the young ladies of the possible danger. The envelope was then carefully folded, and with its fatal contents replaced in the drawer where it had been since the 14th of October. This drawer had been almost daily opened. On the following Saturday night, Nov. 10th, at 9 P.M., Miss S. was taken sick with a chill, and Miss B. at about 2 A.M., some five hours later, the period of incubation being less than seven days in both cases. No other person handled the fatal envelope or in any way came in contact with it, and there is, after the most careful inquiry, no suspicion of any other source of infection in these two cases. Miss S. died on Oct. 14th, Miss B. on Oct. 16th."

10th. These qualities of yellow-fever infection, and especially its faculty of reproduction (which only organisms possess), furnish almost conclusive evidence that yellow fever is a germ disease produced by a specific contagium vivum.

Many facts are patent which sustain the generally accepted opinion that yellow-fever poison gains admission to the system through the medium of atmospheric air. On the other hand, I know of no observations which prove that the disease is ever communicated by food or drinks, or through any other vehicle than atmospheric air.

In respect to atmospheric infection by yellow fever, localizations of aërial impregnation are often observable, not common in other air-infecting diseases. A certain district of a large and populous city may become the seat of a sweeping and fatal epidemic, and yet no case occur outside of this area of prevalence. It is customary to speak of these points of epidemic prevalence as infected localities. If unprotected persons visit such infected places, even for a short period of time, they are liable to attacks of yellow fever, although they may take neither food nor drink within the limits of infection and bring no fomites away with them. Under these circumstances atmospheric impregnation is conclusive.

{643} But it is difficult to determine how this infection of a locality has been produced in the first place, and how, in the second place, it is maintained sometimes for periods of from one to three months, with so little apparent diminution or change in the liability to communicate yellow fever to unprotected visitors within the limits of infection.

It seems highly probable that yellow-fever poison, after its exit from the human body, attaches itself to various solid surfaces in proximity to the sick, where, under suitable climatic conditions, it undergoes more or less speedy processes of maturation in toxic qualities. The poison thus matured is capable of being preserved with but little change for the periods indicated above, and is communicable through the atmosphere for short distances. It is also capable, by virtue of some unexplained process or quality, of spontaneously extending its area of infection. But this is at all times slow, and is readily interrupted by streams of water, high walls, or even by much-travelled thoroughfares.

There are no instances in which the water-supply of cities has been shown to have distributed yellow fever.

The periods of time which may intervene between exposure to yellow-fever poison and attacks of the disease are extremely variable. The shortest period of incubation which has come under my observation was about twenty hours. In three cases in which I was able to fix the hours of first exposure with precision attacks followed in 72 hours, 83 hours, and 101 hours, respectively. Of 55 unacclimated physicians who exposed themselves at Memphis during the epidemic of 1878, 54 suffered attacks of yellow fever. In these cases the periods of incubation varied from one to twenty-five days, the average duration being ten days. These physicians all remained steadfastly at their posts of duty; consequently, the attack which occurred on the twenty-fifth day was postponed for that length of time during constant exposure in a locality most intensely infected.

It must be true that many cases of individual resistance to the effects of yellow-fever infection depend upon states of the system or idiosyncrasies which diminish liability to the action of the poison. In other words, their personal receptivity to it is lessened by certain constitutional states.

That this position is correctly taken is proved by the fact that many circumstances which violently disturb the system determine attacks in persons who may have for a long time enjoyed immunity from them. Anxiety, grief, fright, fatigue, or exposure to sudden wettings or cold may precipitate attacks, either by disturbing vital processes by which the system is ridding itself of the poison--so far, at least, as to prevent an accumulation great enough to occasion attacks--or by lowering powers of resistance through enfeeblement of nerve-force.

But it can be affirmed in regard to yellow-fever poison that it is not more capricious or eccentric in its behavior as an infection than that of scarlet fever. Each of these diseases may appear in a large family of unprotected persons with a degree of violence which results in death in every instance, and suddenly cease, leaving a greater or less number of the household without attacks, though equally exposed with those who have died.

One attack of yellow fever confers immunity from the disease during after life. A person who has suffered an attack is said to be acclimated {644} or protected. Neither of these terms should be applied to those who have not suffered attacks, however long they may have withstood exposure during epidemics. It often occurs that persons who have escaped attacks through many years of renewed exposure at last succumb to the disease. On the other hand, I know of three well-authenticated instances of immunity in a sweeping epidemic of persons whose mothers had suffered attacks during the gestations which respectively resulted in their births.

While negroes are susceptible to yellow-fever infection, attacks are far less fatal than among whites.

SYMPTOMS IN MILD OR SIMPLE CASES.--Yellow fever is usually sudden in its onset. Persons are liable to be seized while pursuing their ordinary avocations, or, as often occurs, the attack may begin during the night. The initial symptoms are chilliness or cold sensations, seldom amounting to a decided rigor. Reaction is usually prompt and decided, the temperature reaching within a few hours 102° to 105° F. Yellow fever is not a disease in which it is very common to observe excessive body heat.

As the fever is established, the countenance becomes flushed and the eyes injected and glistening. Frontal headache and lumbar pain are experienced very early in the attack, and are liable to become more intense during the progress of the fever. Muscular neuralgias, especially in the lower extremities, are not uncommon.

During the early period of the attack the tongue is indifferent as a symptom. It is generally moist and free from any coating. In cases attended by much furring of the tongue careful investigation is pretty sure to disclose the fact that it has been brought about by some pre-existing state of disease.

The bowels are generally inactive, though naturally impressible to cathartic drugs. The stomach is querulous from the inception of the attack to its conclusion. Vomiting may not occur spontaneously, but it is easily provoked by repletion of the stomach with any description of ingesta or by harsh or disgusting medicines. The acts of emesis are sudden and short in duration. Bile is a very uncommon constituent of the matters ejected. Whether vomiting has occurred or not, patients nearly always express repugnance to the weight of the physician's hand over the epigastrium. In the very mildest cases it seems to excite gastric distress and a tendency to emesis. The stomach and bowels are liable to distension by flatus, sometimes to the extent of producing colicky pains. Gaseous eructations are common.

During and shortly succeeding the cold stage the urine may be somewhat increased in amount, but after the fever is established both the quantity and the specific gravity are notably lessened. Albumen seldom appears in the urine during the first twenty-four hours of an attack. In very mild cases it is altogether absent throughout.

Delirium is not unusual during the fever. Among children attacks are often ushered in by convulsions. In such cases delirium may be persistent and alarming in violence.

The pulse in the early stage of yellow fever is slower in proportion to the temperature than in most other acute diseases. This is more especially true in respect to mild cases. Another characteristic feature of the pulse in {645} yellow fever is that it declines in frequency before the fever has reached its maximum. In the mildest forms of the disease the temperature will attain its highest record within twelve hours. It then rapidly defervesces, never to return again. But in some cases of a moderately mild form the body heat does not reach its acme of intensity until the second day, occasionally not until the third or fourth day. In these cases also the pulse is apt to decline in frequency before the fever has culminated. There are therefore no fixed laws which govern the duration of the hot stage of yellow fever. Those which relate to the pulse are more uniform.

The following clinical reports of two cases support this statement. The detailed account of the symptoms establishing their diagnosis as mild cases of yellow fever is omitted.

Susie W----, white, aged seventeen years, was admitted to Charity Hospital on August 28, 1878. First observation, nine hours after the beginning of the attack, pulse 100, temperature 104.6°. Morning of 29th, pulse 94, temperature 102.8°; evening, pulse 80, temperature 101.5°. Sanguineous discharge from vagina began on 29th; patient supposed it to be her proper period. Aug. 30th, pulse 80, temperature 99.2°; convalescent and dismissed from further observations. In this case the urine presented a trace of albumen early on the second day, but as the menses appeared shortly after the urine was obtained, the presence of albumen may be in that manner accounted for.

Bessie L----, white, age twenty-seven years, admitted to Charity Hospital on August 28, 1878. First observation, twelve hours after beginning of attack, pulse 100, temperature 100.6°. 29th, pulse 76, temperature 102.3°. 30th, pulse 64, temperature 101.5°. Sanguineous discharge from vagina began on 30th and continued until Sept. 4th; this was two weeks before the patient's regular period. The urine showed traces of albumen at date of admission. Discharged, cured, Aug. 31st.

It may also be stated of the pulse of yellow fever that it is easily compressible and often gaseous in character.

Perspiration is probably an incident in the natural clinical history of a case of yellow fever. It occurs spontaneously if the patient's surface is protected from those influences which conflict with its appearance. It is not critical in any sense of the word, and may coexist with high temperature.

Yellow fever is considered to have two clinical stages. The first is the paroxysm. This is made to include the cold stage and succeeding fever. The cold stage is often almost or quite inappreciable, and when this is not the fact it is in simple cases a very unimportant event. It is therefore quite convenient to include it with the fever under the term paroxysm. The paroxysm of a simple case is terminated by a subsidence of the fever to nearly or quite a normal temperature. Sometimes the temperature falls below the normal standard.

The neuralgias and subjective sufferings are greatly mitigated or cease altogether. Thirst and restlessness are relieved, and the patient sees before him a delicious, but too often treacherous, mirage of restoration to perfect health. This is termed the stage of calm, perhaps because it often precedes a tempest of fatal symptoms.

In mild cases convalescence begins at the termination of the paroxysm, and may proceed without interruption until complete re-establishment of {646} health has been accomplished. But in the very mildest cases the process of recovery is easily interrupted.

In these simple forms the tendency to hemorrhage first manifests itself in the calm stage. The gums become red, tumid, and spongy, the tongue pointed and red at the tip. Epistaxis is liable to occur. The eyes and skin may be slightly yellow, and the urine may show traces of albumen. However mild the other symptoms may appear, the tendency to hemorrhage, to albuminous urine, and to jaundice in the calm stage bears a direct relation in frequency of occurrence and in degree to the blood-stasis, or sluggish capillary circulation, of the first stage.

The foregoing is a recital of the clinical phenomena of typical and simple forms of yellow fever. The departures from type have been divided by different writers into a variety of forms. The most important of these will be referred to in connection with suggestions as to treatment.

PROGNOSIS.--Prognosis is variable in different epidemics, this observation being understood to apply to the same localities. Some of those circumstances which affect epidemic force, so as to increase the mortality-rate, are appreciable. If an epidemic invades a population after an interval of exemption sufficiently long to allow a large number of unprotected persons to have accumulated in its midst, the crowding of the sick will increase the death-rate. We may naturally assume that this is attributable, first, to sheer multiplication of the infection; second, to lack of proper attention to the sick, and to fright, grief, exhaustion, etc.

Tabulated Abstract of Practice in Yellow-Fever Epidemic of 1878, New Orleans Charity Hospital.

---------+---------+-----------+-----------+---------+-----------+----- AGES. | July. | August. | September.| October.| Total. | ---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------ | N | N | N | N | N | N | N | N | N | N | P | o | o | o | o | o | o | o | o | o | o | e | . | . | . | . | . | . | . | . | . | . | r | | | | | | | | | | | | t | f | t | f | t | f | t | f | t | f | c | r | a | r | a | r | a | r | a | r | a | e | e | t | e | t | e | t | e | t | e | t | n | a | a | a | a | a | a | a | a | a | a | t | t | l | t | l | t | l | t | l | t | l | . | e | . | e | . | e | . | e | . | e | . | White. | d | | d | | d | | d | | d | | | . | | . | | . | | . | | . | | ---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------ Under 5 | .. | .. | 7 | 3 | 3 | 1 | .. | .. | 10 | 4 | 40.0 5 to 10 | .. | .. | 2 | 1 | 1 | 1 | .. | .. | 3 | 2 | 66.66 10 to 20 | 8 | 3 | 26 | 7 | 25 | 6 | 7 | .. | 66 | 16 | 24.2 20 to 40 | 18 | 9 | 246 | 141 | 175 | 91 | 61 | 24 | 500 | 265 | 53.0 40 to 60 | 9 | 6 | 75 | 45 | 83 | 45 | 18 | 10 | 185 | 106 | 57.3 60 to 80 | 2 | 2 | 7 | 6 | 5 | 1 | 1 | 1 | 15 | 10 | 66.66 ---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------ Total. | 37 | 20 | 363 | 203 | 292 | 145 | 87 | 35 | 779 | 403 | 51.7 ---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------ Black. | | | | | | | | | | | ---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------ 10 to 20 | .. | .. | 2 | ... | 5 | ... | 1 | .. | 8 | ... | ... 20 to 40 | .. | .. | 11 | 3 | 8 | 1 | 5 | 1 | 24 | 5 | 20.8 40 to 60 | .. | .. | 2 | 1 | 1 | 1 | 3 | 1 | 6 | 3 | 50.0 ---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------ Total. | .. | .. | 15 | 4 | 14 | 2 | 9 | 2 | 38 | 8 | 21.0 ---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------ Grand total. | 817 | 411 | 50.3 -----------------------------------------------------+-----+-----+------

{647} Prognosis is especially bad in hospital practice. The foregoing statistics of cases admitted to the Charity Hospital of New Orleans during the greater part of the epidemic of 1878 illustrate the usual results of hospital practice.

Many of these patients were conveyed to the hospital in extreme conditions; occasionally they were moribund on admission. It is hazardous to the life of a yellow-fever patient to transfer him over the rough streets of a city, often for two or three miles, unless this is done in the very earliest hours of the attack.

Prognosis is seriously influenced by the condition of the patient at the moment of attack. If pregnancy exists or delivery has just occurred, it is, under most circumstances, extremely unfavorable. Fatigue, anxiety, despair, or grief, all render prognosis more gloomy.

The march of temperature is also important in determining fatal results.

The following statistics show the influence of temperature in relation to mortality from yellow fever:

|First| |Second| |Third| |Fourth| |Fifth| | day.|Died.| day. |Died.| day.|Died.| day. |Died.| day.|Died. -----+-----+-----+------+-----+-----+-----+------+-----+-----+----- 106° | ... | ... | 3 | 2 | 1 | 1 | 2 | 2 | ... | ... 105° | 9 | 3 | 5 | 4 | 2 | 5 | 2 | 2 | 2 | 2 104° | 18 | 10 | 23 | 13 | 8 | 3 | 2 | 2 | 3 | 2 103° | 14 | 4 | 11 | 8 | 2 | 2 | 3 | 1 | 2 | ... -----+-----+-----+------+-----+-----+-----+------+-----+-----+-----

It will be seen from this table that the danger line of temperature in yellow fever descends as the case progresses.

It may again be stated that yellow fever, like scarlet fever, exhibits such striking contrasts in its mortality-rate that it is hardly possible to assert any average standard. It is true that in this disease, as in all others, statistical accumulations tend to correct their own errors in exact proportion to the magnitude of the collections.

In 1878 some 36,000 cases occurred in Louisiana, of which number not less than 6000 were fatal, a percentage of 16.66. The results of private practice in New Orleans are exhibited in the following statistics: Four of the principal practitioners in the city treated in private practice 975 patients--909 white and 66 colored. Of the former, 92, or 10.11 per cent., died; of the colored only 2 died. The cases and deaths among the whites, classified by age, were as follows:

AGE. | Cases. | Deaths. | Per Cent. ---------------------------+---------+----------|---------- Under 5 years of age | 206 | 26 | 12.67 From 5 to 10 years of age | 233 | 20 | 8.61 " 10 to 20 " " " | 183 | 9 | 4.9 " 20 to 40 " " " | 232 | 39 | 16.7 " 40 to 60 " " " | 47 | 6 | 12.7 " 60 to 80 " " " | 4 | 2 | 50 ---------------------------+---------+----------+----------

The physicians above quoted lived in different parts of the city. All of them extended their visits and professional services to the sick to the {648} very limits of physical endurance, and consequently included in the above lists some patients who were not able to procure the comforts and attention necessary to the sick. Some cases also were included to which the physician was only brought that he might sign the death-certificate and so avoid the coroner's inquest. After making allowance for increase of mortality on these scores, I think it safe to assert that the best results obtained in private practice varied from 7 to 10 per cent. of mortality-rate.

DIAGNOSIS.--While there is no one symptom pathognomonic of yellow fever in every stage of the disease, its differential diagnosis is nearly always possible. The morbid action of its special poison produces phenomena sufficiently characteristic to prove its presence. The sudden attack, the slight cold stage, the frontal and lumbar pain, and the capillary congestion are important diagnostic symptoms.

Even in mild attacks this capillary blood-stasis is usually sufficient to alter the patient's countenance to such a degree as to attract attention. A great many different adjectives are used in description of the countenances of yellow-fever patients. While no one among them is constantly applicable, the presence of a changed facial expression should enlist the physician's attention and incite investigation. If this altered countenance be associated with watery or glistening injected eyes, the probability of yellow fever is increased.

The slow pulse which coexists with elevated temperature is a point of much diagnostic value. But it must be remembered that this symptom is not peculiar to yellow fever. I have noted this lack of correlation of pulse and temperature in several cases of dengue. It is also not infrequently found in ordinary cases of jaundice. The slow pulse of yellow fever must be attributable to the special action of the poison upon the nervous system. The heart's action may be slowed by influences exerted directly or through the retrograde effects of the delay of blood-currents in the capillary distribution.

Albuminous urine is a symptom of much diagnostic importance.

A tendency to hemorrhage may be safely stated to exist in all cases of yellow fever. In the mildest cases hemorrhage may not actually take place unless the patients be non-gravid females within the ovulating limits of life. These patients seldom pass through yellow-fever attacks without sanguineous vaginal discharges. But even in the mildest cases yellow fever establishes the hemorrhagic diathesis to an extent sufficient to render the occurrence of hemorrhage an imminent event. This fact is shown first, by the congested and tumid gums, from which blood can be readily pressed, and also by the still more important circumstance that medical or hygienic mismanagement is so quickly and certainly followed by black vomit or by hemorrhages from other parts of the system. Capillary congestion is undoubtedly an important factor in the production of hemorrhages in yellow fever, since we cannot otherwise account for the liability to hemorrhage which is so general in this disease.

The yellow color of the skin and eyes during life, and of the tissues and serum of the cadaver, is probably due to the coincident influence of two causes: first, to the coloring matter of the red corpuscles diffused in the serum of the blood; second, to an accumulation of secondary blood-poisons. The occurrence of the yellow color and its intensity bear a {649} direct relation to the sluggishness of capillary circulation during the paroxysm. It appears likely, therefore, that the yellowness is principally ascribable to coloring principles derived from dissolution of the blood, to which capillary obstruction would so strongly predispose this fluid.

Schmidt has made a very careful résumé of the pathological changes found after death from yellow fever. The most important and uniform of these affected the nervous system, liver, and kidneys. They consisted for the most part of hyperæmic conditions, not infrequently attended by points of extravasation and of degenerative changes. The latter are principally found in the liver, and bear some relation to the duration of the case, and it may be also to the degree and persistence of the pyrexia. When the liver is the seat of fatty degeneration, it is yellowish in color in whole or in parts. It is then sometimes spoken of as the café au lait or the box-wood liver.

In cases which run a very rapid course these changes are not observed, but only those which indicate congestion are found, and often hemorrhagic puncta. In these instances the depending portions of the body have dark or livid ecchymoses.

TREATMENT.--There are two propositions to which due attention should be given before formulating rules for the treatment of yellow fever. The first of these is, that yellow fever is strictly a self-limited disease, and therefore is insusceptible of jugulation. Both clauses of this proposition are indisputably true. Cases have been observed in which mitigation of symptoms and abridgment in duration appeared to follow spontaneous diarrhoea. Such events must be extremely uncommon, since in my large experience I know of but one such instance supported by good testimony.

Efforts to abort the disease by purgatives, bleedings, cold baths, quinia, etc. have all signally failed. Among the possibilities of the future is the discovery that some drug or combination of drugs is capable of meeting yellow-fever poison in the field of the circulation and antagonizing it sufficiently to rescue the victim from its fatal toxic effects.

The second proposition is, that the formative stages of the disease--that is, the early hours of the paroxysm--afford the most precious moments for instituting such medication as may be considered proper. This proposition applies no doubt to a number of other acute affections, but in no one among them all is it so important to be regarded as in yellow fever. The primary effects of the poison are so boldly outlined that it appears highly probable that the damage it exerts upon the economy is chiefly inflicted during the paroxysm. This affords an additional reason why efforts at medication should be principally restricted to the paroxysm and to the earliest periods of that stage.

It is probable that during an attack of yellow fever the patient's hold upon life is more or less secure in direct ratio to the number of functions which retain their physiological integrity fairly well. The suggestion of such a fact should exclude all scholastic or routine rules of treatment.

In simple forms of yellow fever the first desideratum of the practitioner is to become acquainted with the patient's condition at the moment of attack. If this has occurred after eating indigestible food or after a hearty meal of any description, the stomach should be emptied. Ipecacuanha may be given in warm water or chamomile infusion until this result {650} has been accomplished. After emesis, provided this should have been considered necessary or as a first step of treatment under other circumstances, a purgative is usually given. The benefits of purgation are, in my opinion, limited to the act of ridding the bowels of any fecal accumulations present. For this purpose those purgatives which combine a due degree of efficiency with inoffensiveness in operation have appeared to me to be the best. Castor oil is at the head of this class. An ounce may be given to an adult in some acceptable vehicle. This may be followed by an enema of tepid water when required. Salines are more agreeable to the palate, but far too unmanageable in their cathartic effects to be adopted generally.

Some very good practitioners believe that a mercurial purge at the onset of the attack impresses the subsequent career of the case in some favorable manner. I do not share in this opinion, but I do select calomel as the preliminary purgative in cases where much gastric irritability attends the early periods of the attack. I exhibit it also in those cases in which previous indisposition had occasioned coating of the tongue, or in which other conditions of systemic derangement existed for which calomel is usually prescribed.

In many cases it is desirable to avoid the disgust at taking a purgative or the perturbation it may occasion by its action. Enemas of tepid infusion of linseed or of milk and water may be substituted, with the addition of castor oil when necessary.

In the early hours of the attack warm pediluvia are always grateful and proper. They are to be given by placing a basin of warm water near the foot of the bed, beneath the covering of a light blanket or sheet, and allowing the patient's feet to remain immersed for ten or fifteen minutes. If the feet are cold, mustard should be added. During the foot-bath the patient usually falls into a perspiration which is sometimes profuse and general.

Perspiration is a desirable event during the paroxysm, although it is not, like the sweatings of the malarial fevers, critical, in the sense of being accompanied by a marked decline in temperature. The idea that sweating is beneficial is so strongly and generally prevalent as to give countenance to the erroneous practice of resting the cure of the disease upon its production and maintenance. I have seen valuable lives sacrificed by obstinate persistence in measures to promote diaphoresis, more especially in the later hours of the paroxysm or in the succeeding or calm stage. It is quite sufficient to encourage the perspiration by the pediluvia and by a moderate allowance of cool, palatable drinks. Much value is attached by non-professional persons to a warm infusion of orange-leaves or some other warm and grateful beverage. When agreeable to patients I permit them in moderate amounts, but do not regard them as especially valuable.

Jaborandi has been used in yellow fever. Strong hopes were quite naturally based upon the action of this drug in exciting excretory functions, especially diaphoresis, but the observations of my friend Dr. Thomas Layton and of others show that it possesses no special value, while it frequently increases the vomiting and has to be discontinued.

After the bowels have been relieved of fecal accumulations it is good practice to exhibit a scruple of quinia in solution with ten to thirty {651} drops of tincture of opium, by rectal injection. Infusion of linseed or mucilage of elm-bark or gum-arabic are the best vehicles.

The combined action of the quinia and opium mitigates the patient's headache and lumbar pains. But the influence of these drugs is not limited to their effect on the nerves of sensation. In quite a proportion of cases reaction is not so prompt or complete as usual; or reaction may be quite pronounced, and still the surface may alternate between a dry and a perspiring state. These oscillations of function of the organic nerves are also often corrected by this prescription. In the great majority of simple cases no other medication than this is requisite or proper, for no medication is proper in yellow fever unless it is requisite.

When the neuralgias are excessively violent, opium may be again administered, preferably by enema, and in combination with bromide of potassium or chloral hydrate. But the effects of opium in limiting excretory function must always be borne in mind and carefully avoided.

External applications are very efficacious in relieving the neuralgias. In the southern part of this country the "eau sedative" of Raspail is greatly used. This is a mixture of ammonia, camphor, and common salt in solution, and may be prepared extemporaneously. The applications may be made hot or cold, but if used cold they must be continuously kept up. It is therefore better to use them warm if sufficiently effective. Stimulating embrocations of turpentine or mustard, or dry or wet cups, are sometimes resorted to for relief of pain.

Excessive temperature demands attention and antagonistic treatment in direct measure with its persistence, its degree, and its occurrence in advanced periods of an attack.

In the epidemic of 1867, I used gelsemium as an antipyretic in fifty cases or more, but the results were so unsatisfactory that I have quite abandoned its exhibition. I have given quinia as an antipyretic, but never in doses of more than a scruple. In these doses it has failed to accomplish the desired result in the great majority of the cases. Perhaps its antipyretic effects are limited to those cases in which malaria is a known or an unknown complication.

I have exhibited small doses of digitalis with apparent benefit, but aconite and veratrum viride I have long since discarded. The physician cannot afford to sacrifice gastric quietude and competency of function to the use of remedies whose value as antipyretics is, to say the most, quite doubtful.

Cold has for a long period of time been brought into use as an antipyretic in yellow fever. Its positive value and instantaneous action should be constantly borne in mind, and in the hyperpyrexia of yellow fever it constitutes by far the most reliable remedy, though its mode of application must be carefully adapted to the degree of fever present and to the susceptibilities of the patient. Cold drinks in limited quantities, but frequently repeated; cold spongings of the surface, or the use of the cold pack, especially in very high degrees of body heat; large injections of cold water per rectum, which may be passed off and repeated once in two to four hours,--form safe and effective modes of treatment.

Hemorrhages are a constant source of anxiety in yellow fever. It is very true that persons do not often die from actual loss of blood. I do not know that I have ever witnessed such an event except when the {652} blood was poured out from a recently-emptied uterus. But the chances of recovery are lessened, because the hemorrhagic state indicates a degree of spoliation of both the fluids and solids of the system incompatible with maintenance of life. When this condition of constitution is once established, the stomach rarely escapes, and in a majority of instances it is the first, and sometimes the only, bleeding surface. The treatment should be directed, first, to the great indication of correcting the hemorrhagic diathesis; secondly, to quiet gastric irritability, in order that vomiting shall not cause rupture of capillaries. To meet the first indication I regard nutrition and stimulants as the most important measures of treatment. The mode of administration will be specially referred to under the head of alimentation.

Hæmostatic remedies, given as specific treatment, generally fail in accomplishing the purpose for which they are administered. It has always appeared to me that those therapeutic agents which are capable of controlling hemorrhage where yellow fever is not present are completely neutralized by the effects of its toxic agent upon the vaso-motor nerves. Consequently, while ergot, turpentine, gallic acid, and other like remedies may be resorted to, too much hope should not be entertained as to their good effects.

Some excellent practitioners rely greatly on preparations of iron. The tincture of the chloride is undoubtedly the best. This may be given in water or upon shaved ice in doses of five or ten drops every half hour. To allay the gastric irritability pellets of ice should be swallowed. Effervescing drinks may be given with benefit.

I have often used with good results the following prescription:

Rx. Sodii Bicarb. gr. xx; Morphiæ Sulph. gr. ss. Aquæ Lauro-Cerasi, Aquæ Menth. Pip. aa. fl. drachm iv. M.

S. Teaspoonful after every act of emesis.

Occasionally I have given the following prescription:

Rx. Creasoti gtt. viij; Tinct. Opii Deodorat. gtt. xl. Aquæ Menth. Pip., Muc. Acaciæ aa. fl. drachm iv. M.

S. Teaspoonful after every act of emesis in iced Seltzer or Apollinaris water, or in champagne.

Sometimes a few drops of chloroform in a spoonful of iced mucilage of acacia act favorably.

In cases which appear utterly hopeless the physician, acting desperately, is sometimes able to save life by treatment which could scarcely be safely recommended. I once administered a fourth of a grain of morphia to a child of seven years, who, after a sleep of ten hours, ceased to throw up black vomit and recovered.

External applications to the epigastrium usually afford some relief to nausea at any stage of yellow fever. Mustard or aromatic cataplasms may at all times be used with hopes of favorable effects. Towels wrung from cold water are very efficacious. Sometimes a drachm or two of chloroform dashed over them increases their anti-emetic action.

Suppression of urine is generally a symptom of fatal import. {653} Attempts may be made to establish the secretion by dry or wet cups in the lumbar region, by warm applications around the loins, or by mustard cataplasms or blisters. If the condition of the patient's stomach is such as to permit this practice, copious diluent drinks and diuretics should be given. Lemonade holding bitartrate of potassium in solution is generally the most acceptable, and probably the most efficient. Some physicians think they oftener obtain good results from small and frequently repeated doses of turpentine. I can bear testimony to the good results which sometimes follow large rectal injections of warm or cold water, the latter being preferable when there is high fever.

In certain cases of yellow fever reaction from the cold stage is feeble and imperfect, or perhaps may not occur at all. This departure from type is very fatal. The patients are stupid, sometimes semi-comatose and incoherent, from the earliest hours of the attack. The face is listless, drunken, or idiotic in expression. The color of the skin is dark olive and almost livid. The print of a hand on the chest is very slowly effaced. Sometimes the surface is covered with a peculiarly unctuous perspiration. The pulse is feeble and compressible; the temperature seldom more than one or two degrees above the normal standard. Albuminous urine is found during the first day. Death, attended by convulsive rigors, generally closes the scene within seventy-two hours from the moment of seizure.

Hot mustard-baths should be resorted to. Blood may be drawn by cups or leeches from the back of the neck or temples, and this may be followed by the application of a blister. Morphia and atropia may be exhibited subcutaneously in small doses, to be repeated as often as proper. Quinia may be administered per rectum or by the hypodermic method. Lastly, pilocarpine may be thrown into the tissues in sufficient doses to procure its vigorous physiological action.

Almost in precise symptomatic contrast with these cases of failure in reaction is another form of attack, in which violent disturbances of nerve-function occurs; such cases often being characterized as congestive in type. The most typical of these attacks are among children or adolescents. If attended by noticeable chill, it is ordinarily slight. Reaction is quick and excessively violent. The face is flushed, the eyes injected, and convulsions with delirium are liable to occur as early symptoms. I have watched with much interest the alternate flushings and pallor of the countenance occurring in these cases, such as are often observed in basilar meningitis.

The treatment in this type of attacks should include chloroform by inhalation in sufficient amount to control convulsions. Chloral hydrate may be administered by enema, or morphia hypodermically. Cathartic doses of calomel often exert a beneficial effect. Leeches or cups, to be followed by cold applications or by blisters, may be applied about the head or neck. But cupping and leeching should only be resorted to in the treatment of grave symptoms, since obstinate hemorrhage is liable to occur from any and every point from which the cuticle has been removed.

Yellow fever is often masked during the paroxysm by some pre-existing disease. Malarial fevers, the febrile states of pulmonary consumption or of the recently-delivered female, may all mask the early clinical {654} phenomena to such a degree that the most experienced and vigilant practitioners are sometimes astonished to find black vomit, suppression of urine, and all those symptoms which mark the last stages of the disease, suddenly developed.

Walking cases should be classed in the same category as masked forms. In these instances the early symptoms are so slight as to be overlooked or neglected by their subjects. They continue to prosecute their usual pursuits until, by sheer exhaustion, they are driven to beds from which they seldom arise.

The hygienic and dietetic management of yellow-fever patients is extremely important, and the strictest attention must be paid to the condition and discipline of the sick chamber. In this disease those occurrences and circumstances which in other affections would be reckoned as unimportant and trivial become matters of serious magnitude.

The physician, by a composed and cheerful demeanor, often decides which end of the balance shall go down. But an intelligent, experienced, and faithful nurse is equally as important as the excellent physician.

The patient should be confined in strictly recumbent positions, and all drinks and foods must be given through tubes or from pap-cups. It frequently occurs that patients are unable to void the bladder in such positions. In these cases the catheter should be used, rather than suffer any violation of the rule which demands a maintenance of unbroken decubitus.

The sick room should be kept freely ventilated, and the patient's bedding should be changed, when requisite, by removing him to one side of the bed while the other is renovated. If the patient's night-shirt becomes soiled and disagreeable, it may be cut so as to remove it, and another, cut in the same manner, may be substituted and stitched together. The room must be kept quiet, and useless visiting entirely forbidden.

Cool and grateful drinks may be given in any stage or state of yellow fever if demanded by patients. The quantity allowed at one time should be small, since over-distension of the stomach almost certainly causes vomiting. Effervescing drinks are nearly always grateful, and are better tolerated than others. Seltzer-water and lemonade, or Seltzer or Apollinaris on shaved ice, are to be recommended. Sometimes patients call for sparkling wines or beers. I never refuse them or any other alcoholic drink asked for in any stage of the disease. Wine surely possesses valuable therapeutic effects in yellow fever.

Alimentation must be severely controlled by the physician, and the tolerance and effects constantly watched. Even to the most experienced physician the kind of food to be selected, and the time and manner of administration, constitute difficult problems. In simple forms of the disease food had better be strictly withheld during the continuance of the paroxysm. Even after the stage of calm has been reached, sufficient time should be allowed to elapse to enable the physician to form some estimate of the degree of damage his patient has suffered and his competency to retain foods and be nourished by them. This question can seldom be answered in a decided manner, except through a cautious trial of some bland and inoffensive food.

{655} On the third or fourth day of sickness a single tablespoonful of iced milk may be given, and the immediate consequences closely watched. If no retching or gastric uneasiness should ensue, it may be repeated at the end of thirty minutes. Some physicians prefer to begin with spoonful doses of equal parts of sweet milk and thin barley-water. In my own experience chicken-water has proved to be the most universally acceptable, as well as the most beneficial, of all the various forms of nutriment to be chosen as a first venture. I have frequently combined this with barley-water when first given. In this cautious and tentative manner even the most experienced physician prefers to proceed, rather than to attempt to prescribe rules of diet in an abstract and arbitrary manner.

If these light articles of diet are well borne, they are to be gradually and watchfully exchanged for beef-essences, the blood of a rare beefsteak, and the more substantial broths. Solid articles of food should not be allowed during the first ten days after an attack, and for still longer periods patients should be admonished against excesses in eating, and especially in respect to indigestible articles. Those lesions of the blood and of the stomach, and those grave disorders of nerve-function which occasion hæmatemesis in yellow fever, are slowly repaired. Instances are reported in which black vomit and death have followed excessive eating and drinking ten or twenty days after dismissal from treatment.

There are, however, certain conditions which are liable to complicate yellow fever which demand a course of dietetic procedure different from that which I have recommended. Thus, children cannot bear privation of food until the paroxysm is over if its duration is long. In like manner, a more supporting course is required in most of those cases in which yellow fever occurs as an intercurrent affection, in all those cases which are termed typhoid or adynamic per se, and, more emphatically still, in every case in which hemorrhages are occurring. A failing pulse should in all instances admonish us to resort to nourishment and stimulants.

It is a fortunate circumstance that in yellow fever the lower bowel is generally in a state favorable for the retention of nutritious enemas. In the most trying and critical hours of desperate cases I have seen patients tided through by the use of skilfully prepared and skilfully administered injections of some suitable meat-essence. When insomnia exists, chloral hydrate or bromide of potassium may be conveniently given in these vehicles.

It is evident that the discussion of the vastly important sanitary questions pertaining to the prevention of yellow fever cannot be appropriately discussed in the present article.

{656}

DIPHTHERIA.

BY A. JACOBI, M.D.

DEFINITION; SYNONYMS; HISTORY.--Diphtheria is a specific, infectious, and contagious disease, characterized principally by epithelial changes in, and the exudation of fibrin on and into mucous membranes, the surface of wounds, and the rete Malpighii, thereby constituting the so-called pseudo-membrane. Under the names ulcus syriacum, ulcus ægyptiacum, garotillo, morbus suffocans, morbus suffocatorius, affectus suffocatorius, pestilentis gutturis affectio, pedancho maligna, angina maligna, angina passio, mal de gorge gangréneux, ulcère gangréneux, angina polyposa, angine couenneuse, cynanche, croup, diphtheritis, and diphtheria, the disease has been known and described at different periods by the writers of different nations. The Hippocratic writings and some remarks in the Talmud allow of some doubt in regard to their explanation. Whether their authors observed or recognized diphtheria cannot be proven. There is less doubt in regard to Archigenes, quoted by Oribasius. Aretæus of Cappadocia is notably the first, if we except Asclepiades only, who is said to have performed laryngotomy. The description of the pharyngeal and laryngeal manifestations furnished by the former, however, can leave no doubt in our minds that he knew diphtheria and recognized it. Galen, in his remarks on the Chironian ulcer, tells us that the pseudo-membrane was gotten rid of by coughing when the respiratory passages were affected by the disease, and by hawking when the disease was in the pharynx. Cælius Aurelianus recognized diphtheria of the pharynx and larynx, as well as the diphtheritic paralysis of the soft palate; it is to him we are indebted for the information that Asclepiades resorted to scarification of the tonsils, and even to laryngotomy. Aëtius in the fifth century distinguished white and grayish patches and gangrenous degeneration, observed paralysis of the soft palate, and advised against energetic local treatment and the forcible removal of the deposits before they were in a condition to fall off spontaneously. The Arabs and Arabists contain no allusions to the subject, but early chronicles tell of an epidemic raging in St. Denis in 580, subsequent to a great inundation. There appear to have been memorable epidemics in Rome in 856 and 1005, in Byzantium in 1004. The former are mentioned by Baronius, the latter by Cedrenus.[1]

[Footnote 1: Haeser, Lehrb. a. Gesch. du Med. u. d. Epidem. Krankh., 3d ed., vol. iii., p. 434.]

According to Morejon, Gutierrez wrote his Tradado del enfermedad del garrotillo in the second half of the fifteenth century. A malignant form of angina raged in 1517 in Switzerland, along the Rhine, and in the Netherlands; in 1544 and 1545 in Northern Germany and on the Rhine; {657} in 1557 in France, Germany, and Holland; to the latter refer the reports of Tetrus Fosterus. Antonio Soglia, quoted by Chomel, describes an epidemic in Naples and Sicily (1563), which spread in the following year as far as Constantinople; Joannes Wierus, epidemics in Dantzic, Cologne, and Augsburg (1565); Ballonius (Baillon), in Paris (1576). At the same time this disease was frequent in Denmark. From Spain there are reports on severe epidemics between the years 1583 and 1618; the year 1613 was long known as the year of diphtheria (anno de los garrotillos).

Mercado (1608) speaks of a child that had communicated the disease to his father by biting his finger. Casealez advised gargles containing alum and sulphate of copper. Herrera described diphtheria of the skin and of wounds, and looked upon the pseudo-membrane as the essential characteristic of the disease. Heredia, in 1690, recognized the suffocative and asthenic forms, as well as the paralysis of the soft palate, the pharynx, and the limbs; he also called attention to the occurrence of relapses, which he attributed to the absorption of the morbid products, and endeavored to prevent by cauterization.

Naples had diphtheria 1610-45, in its worse form 1618-20, together with erysipelas, and diphtheritic affection amongst cattle. About those times tracheotomy was often performed by Severino, the same who found pseudo-membrane in the larynx at a post-mortem examination made in 1642. In 1620 the disease was in Portugal, Sicily, and Malta; in 1630 in Spain, according to Fontechu, Villa Real, and Herrera. It was remarked that in some instances no membranes were perceived in the throat, but the cases were liable to terminate fatally with large glandular swellings round the neck and general symptoms of adynamia. Sicily was again invaded in 1632, Rome in 1634, Italy from 1642 to 1650, Spain in 1666. The Italian reports emphasize the marked contagiousness of the disease and its tendency to depress the vital powers, also the weakness of the mental faculties left behind. In Germany the disease was described by Wedel in 1718. The epidemics observed by him were not very instructive, yet they sufficed to teach the importance of isolating the sick.

In the New England States diphtheria appeared in the seventeenth century. Samuel Danforth lost the four youngest of his twelve children by the "malady of bladders in the windpipe" within a fortnight in December, 1659, in Roxbury, Mass. John Josselyn mentions an epidemic in New England, mainly in Maine, which lasted at least until the year 1671. Mr. Douglass reports another, which commenced on the 20th of March, 1735, in Kingston township, about fifty miles east of Boston, and extended all over, and also to Boston, where it was mild at first. But in 1738 it was very severe, and remained so for some time. Indeed, it did not abate for a long time, to judge from a letter of Cadwalader Colden written in 1753 to Dr. Fothergill, and the two letters of Dr. Jacob Ogden, written in 1769 and 1774 to Mr. Hugh Gaine of New York; as also from John Archer's "Inaugural Dissertation on Cynanche Trachealis, commonly called Croup or Hives," published in 1798.[2] In 1809 there was a severe epidemic in Philadelphia;[3] in 1816 in Crete.

[Footnote 2: For extensive quotations from these and other writers on diphtheria at a very interesting period of our medical literature, see A. Jacobi, A Treatise on Diphtheria, New York, 1880.]

[Footnote 3: Caldwell, in ed. of Cullen's First Lines of the Practice of Physic, Philadelphia, 1816, 1, p. 260.]

{658} The reports of Le Cât concerning epidemics in Rouen in 1736 and 1737 being doubtful, the first great epidemic must be set down, in France, for 1745. It commenced in Paris, and invaded the provinces afterward. Chomel gave an accurate description of the diphtheritic paralysis of the soft palate, and reports a case of strabismus. Epidemics are reported from the Netherlands in 1745, 1746, 1769, 1770, 1778-86; from Spain in 1764-71; from England in 1744-48 (by Starr), from Plymouth, England, in 1751-53 (Thurham) and 1776. Dropsy and glandular swellings were frequent; emetics and pure air were the sheet-anchors of treatment. The Netherlands, France, and the West Indies were invaded from 1770-80 by the disease, which was found often complicated with scarlatina; Portugal in 1786 and 1787; France again in 1787 and 1788; Northern Germany in 1790. At that time, particularly in France, the main reliance was had on the internal administration of cinchona and the insufflation into the throat of alum.

Epidemics have been described since from different localities in different years: in Glasgow, 1812 and 1819; Switzerland, 1823-26; Norway and St. Helena, 1824; New York and Kentucky, 1826 and 1828; French provinces, 1834; Paris, 1841; several parts of Europe and North America, 1845-56; Paris, 1853-55; England, 1854 and 1859, when 95 per cent. of all the cases of nasal diphtheria proved fatal; Netherlands and Sweden, 1855; all Western Europe, 1855-65, up to the present time, and all Europe since; California, 1856 and 1857; Portugal and France, 1856; Eastern Prussia, 1850, 1852, 1856, 1857; and all the countries with a cold or moderate climate to this very day.

During the second half of the eighteenth century but two writers are worthy of especial notice--Home, a Scotchman, 1765, and Samuel Bard, an American, 1771.

Home deserves credit for having distinctly drawn the line between the pseudo-membranous and the gangrenous affections. He also endeavored to prove that croup and angina maligna were two distinct diseases, notwithstanding all that had been said since the time of Aretæus in favor of their identity. The false membrane of croup he looked upon as an aggregation of mucus. He sought for it exclusively in the respiratory tract, and disregarded any connection between it and the false membrane found in the pharynx.

Bard's experience was very extensive; he saw membranous pharyngitis, laryngitis, and pharyngo-laryngitis; he speaks of the membrane as met upon the skin, of paralysis of the muscles of deglutition and of the larynx, and likewise of paralysis of the lower extremities, as sequelæ. He looked upon the morbific process as the same whichever were the mucous membranes attacked, and made a distinction only according to the localization of the disease. The influence which he might have exercised in shaping the professional opinion on the nature of the disease did not make itself felt, partly because of his classical modesty, and partly because of his remoteness from the centres of European learning. Not before 1810 was his book translated into French (by Ruette). While his style is classical in its simplicity, his observation is astonishingly correct, and his conclusions as to the actual identity of all the diphtheritic processes in the most various clinical symptoms unimpeachable this very day. His description of the various forms of pharyngeal diphtheria is painfully {659} good, his observations on cutaneous diphtheria very accurate, his few dissections well recorded, particularly when he speaks of tracheal and tracheo-laryngeal diphtheria, and his historical reviews very judicious indeed. "Upon the whole, I am led to conclude that the morbus strangulatorius of the Italians, the croup of Home, the malignant ulcerous sore throat of Huxham and Fothergill, and the disease I have described and that first described by Douglas of Boston, however they may differ in symptoms, do all bear an essential affinity and relation to each other, or are apt to run into each other, and, in fact, arise from the same leaven. The disease I have described appeared evidently to be of an infectious nature, and, being drawn in by the breath of a healthy child, irritated the glands of the throat and windpipe. The infection did not seem to depend so much on any prevailing disposition of the air as upon effluvia received from the breath of infected persons. This will account why the disorder sometimes went through a whole family, and yet did not affect the next-door neighbors. Here we learn a useful lesson--viz. to remove young children as soon as any one of them is taken with the disease, by which many lives have been saved and may again be preserved."

Jurine, in his prize essay of 1807, denies the gangrenous nature of angina maligna and emphasizes the frequent complication of membranous croup with membranous pharyngitis. It was reserved for Bretonneau to enforce attention to the ideas of Bard by asserting (though he did not mention either his monograph or its French translation of 1810) the identity of angina maligna, or by whatever other title it may be known, with membranous laryngitis, and by inaugurating his theory with a new name for the disease to perpetuate the views expressed therein. First and foremost, he called attention to the continuity of the membrane (according to him, composed of coagulated mucus and fibrin) of the nose, pharynx, and respiratory tract, its identity with certain morbid conditions of the skin, and promulgated the theory that "diphtherite"--the name dates from that time--is a specific disease, an affection sui generis, and differs both from a catarrhal and a scarlatinous inflammation.

The modern history of diphtheria may be dated from June 26, 1821, when Bretonneau read his first essay on that subject before the French Academy of Medicine, and gave to the disease the name it now bears. His second and third (Nov. 25th) papers belong to the same year; his fourth was read in March, 1826; his fifth appeared in the Archives gén. of January and September, 1855. It was only in 1826 that the material, previously gathered, was summed up in his celebrated monograph.[4] Before this time, however, the separate essays had received prominence from the reports and commentaries of Guersant, who laid particular stress on the statement that diphtheria was a non-gangrenous affection, identical, and even synchronous, with croup in the majority of epidemics. Since that epoch the literature on the subject has assumed enormous proportions. It is a matter of regret that the limited space allotted to this subject should exclude much historical detail of the etiology, pathology, and therapeutics of diphtheria. If the history of any disease is interesting, and the neglect of its study has ever punished itself, it is diphtheria. {660} Particularly would the treatment have been more successful if the knowledge of former times had been available and more heeded. As long ago as in the seventeenth century depletion in diphtheria was condemned, and in the seventeenth and eighteenth centuries the local treatment with muriatic acid and the internal administration of cinchona, camphor, and roborant diet were held to be the only admissible ones. Bretonneau urged the same principles, and still in our own times, for want of historical knowledge, we had to learn the old lesson over again.[5]

[Footnote 4: P. Bretonneau, Des Inflammations spéciales du tissu muqueux, et en particulier de la Diphthérite, etc., Paris, 1826.]

[Footnote 5: See history and bibliography of diphtheria in Chatto; Sanné, Traité de la Diphthérie, Paris, 1874; Jacobi, in Gerhardt's Handb. d. Kinderk., vol. ii., 1877; Seitz, Diphtheric und Croup gesch. u. Klin. dargest, Berlin, 1879; Index-Catalogue of the Library of the Surgeon-General's Office, U.S.A., vol. iii., Washington, 1882.]

The following is a brief review of the main points of discussion upon subjects connected with the symptomatology and pathology of diphtheria since Bretonneau's first paper:

Bourquoise and Brunet express their belief (1823) in the contagious character of this disease. Desruelles (1824) sees a diagnostic difference between the sporadic and the epidemic forms in the participation of the brain in the latter. Louis referred a number of cases of croup in adults to pharyngeal diphtheria as their source. Mackenzie considers that croup has its origin in the fauces, and urges the employment of lunar caustic. Billard (1826) denies the specific character of diphtheritic inflammation. Hamilton describes cases that terminated in suppuration, and which he therefore distinguishes from Bretonneau's cases. He describes two modes of termination of the disease--one in croup, the other in a state of debility arising from the effect of the absorbed secretion on the respiratory nerves. Pretty looks upon those cases of croup that have their original seat in the tonsils as contagious. Bland (1827) explains the difference between croup and diphtheria. Deslandes declares them to be identical. Bretonneau publishes a work in which he compares diphtheria with scarlatina anginosa, and recommends the use of alum. Emmangard is the first one of the physiological school who, likening diphtheria to typhoid and claiming its origin in a malarial infection, calls it angina gastro-enterica. Abercrombie is in favor of distinguishing diphtheria from croup, but reports a number of cases of diphtheria of the pharynx that terminated fatally by stenosis of the larynx. Ribes, who encountered the disease in nine members of a single family, asserts that croup rarely occurred without a preceding diphtheria in his experience; he advises an examination of the throats of apparently healthy individuals. Fuchs relates the history of epidemics of angina maligna, and declares croup to be a genuine angina maligna trachealis, which only does not run through all the stages. Broussais opposes the identity of croup and diphtheria (1829), and gives a report of cures by means of antiphlogistic regimen and laryngotomy. Diphtheria and gangrenous angina are synonymous with him. Gendron expresses a belief in the identity of diphtheria and gangrenous angina. Roche considers the membrane rather of hemorrhagic than of inflammatory origin, and consisting of discolored fibrin. About the same time Trousseau is endeavoring to clearly establish the diagnosis between diphtheria and scarlatinous angina. Shortly after (1830), he reports cases of diphtheria which originated in blistering wounds, and of diphtheria of the skin giving rise to throat affections, and {661} diphtheria of the throat followed by skin disease. T. F. Hoffmann cites a severe case, that ultimately recovered, with consecutive paralysis of certain cranial nerves. Cheyne (1833) makes a stand against the "confounding of croup and cynanche maligna under the name of diphtheritis." Bourgeois witnessed an epidemic succeeding mumps.

Fricout and Burley (1836) declare their belief in the contagiousness of the disease. Bouillaud attacks the theory of its specific character on the ground that abstraction of blood produced favorable results. Stokes makes a distinction between primary and secondary croup according to the original seat of the affection (1837). Kessler advocates (1841) the view of its contagious nature, and Rilliet and Barthez adduce evidence of the occurrence of ulceration and gangrene in the course of the disease. Taupin, like Ribes, enjoins a methodical examination of the throat of every patient during the prevalence of an epidemic of diphtheria, whatsoever be the disease from which the child suffers. Boudet (1842) opposes Bretonneau's hypothesis that croup is a descending diphtheria, and holds to the identity of diphtheria and gangrenous angina. In this contest Durand (1843) also takes sides against Bretonneau, and lays particular stress on the point that the diphtheritic patient succumbs rather from the severity of the constitutional symptoms than from suffocation. Rilliet and Barthez, on the other hand, rally to the support of the attacked master, asserting that the usual form of croup and that resulting from a descending diphtheritis are one and the same, while they claim that diphtheritis and gangrenous angina are distinct affections.

Meanwhile, the strife regarding the nature of the disease continued. Guersant and Blache (1844) describe the stomatite couenneuse (noma, stomacace, according to them, the rarest kind of gangrenous angina) as a form of Bretonneau's diphtheritis, and Landsberg raises the question whether a nerve-inflammation, present in a certain case, was to be looked upon as an accidental or an essential feature of the disease, and finally comes to the conclusion, with Schönlein, that it was a neurophlogosis dependent on the disease. Bouisson (1847) reports a case of diphtheritic conjunctivitis resulting in loss of the eye. Robert publishes his observations on diphtheria of the skin and of wounds, which he attributes to an atmospheric contamination in crowded wards of hospitals, and looks upon it, with Delpech and Eisenmann, as a form of hospital gangrene. Virchow, in the same year, distinguished the catarrhal, croupous, and diphtheritic varieties of the disease. Meanwhile, reports of paralysis of the soft palate after diphtheria came from Morisseau, from Trousseau and Lasegue, and lastly (1854-59) from Maingault. The subject of diphtheritic conjunctivitis was studied by A. v. Graefe (1854), who encountered the disease as a complication of diphtheria of the pharynx, nose, and skin, and hence considered it a part of the general disease rather than an independent local affection. Diphtheria, in its effects on the system, had at the same time been investigated by Trousseau, who sums up with the statement that the principal source of danger lies in the invasion of the larynx, and that the large majority of cases of croup began as a diphtheria of the pharynx, but that, even without the occurrence of a laryngeal localization, many cases terminate fatally owing to adynamia.

Outside of France, too, the subject had attracted attention. West, who had never seen the disease occur primarily, describes diphtheria as a {662} complication of measles. Bamberger (1855) divides the inflammations of the mouth and pharynx into the catarrhal and croupous forms, and considers croup and diphtheria to be subdivisions of the latter form, differing only in degree. The paralysis of the muscles of deglutition is discussed by Dehænne (1857) who had contracted the disease, and the paralysis of other muscles by Faure. A case of diphtheria of the tonsils, nipples, and vagina in a woman recently confined, followed by infection of the new-born and the death of both, is reported by Mathieux; and cases of diphtheritic conjunctivitis by Grichard, Warlomont, and Testelin. The same year Isambert published a work in which he divided the diphtheritic affections into three forms--viz. angine couenneuse, scarlatinous angina, and diphtheritic angina. The last-mentioned is further subdivided into a croupous-diphtheritic angina, in which croup of the larynx plays an important part, and into that form in which death results from adynamia; in the latter form there is a marked swelling of the lymphatic glands. Apparently, at this time the epidemic in Paris underwent a considerable change, for the croupous form does not occur by far so frequently as Bretonneau had asserted, and croup of the larynx without a preceding diphtheria of the pharynx was observed more frequently than he would lead us to believe.

The various changes in the symptoms of the epidemics of diphtheria which were observed in different places and countries, and at different times, explain many of the differences of opinions in regard to the nature of the disease. The literature of that subject is in the last twenty-five years simply stupendous, and a few more notes must suffice for the elucidation of the drift of theories and observations. Beale was the first to look for organic beings as the cause of the disease, without finding any. Laycock sees it in the bacilli and spores of oidium albicans; Wilks, however, found the same parasite in other affections. Cammack declares the diphtheritic membrane to be herpetic. Feron also calls Bretonneau's mild form of the disease a herpetic angina with pseudo-membrane; so does Gubler. Bouchut writes against the identity of diphtheria, croup, and gangrene. Condie describes the disease as occurring with scarlatina. Litchfield claims that it is a concealed scarlatina, and Hillier that it has some connection with it. Millard cites one case in the course of which gangrene occurred, and another in which skin, mouth, pharynx, respiratory passages, oesophagus, and vulva were affected at the same time. Harley vainly endeavored to inoculate the disease in animals. Stephens declares the disease to be infectious. Sanderson looks upon it as identical with the angina maligna of the aged. Farr considered the exhalations from sewers an important etiological factor. Sellerier, Kingsford, and Harley (1859) report paralyses as sequelæ. Maugin speaks of a specific eruption; Ward, of an accompanying purpura. Bouchut and Empis remarked the frequent presence of and danger from albuminuria; so did Wade. Maugin calls attention to the fact that, when present in diphtheria, it occurs early, whereas in scarlatina it is seen during the period of desquamation, and is not of frequent occurrence even then. Gull gives an account of cases in which death resulted from asthenia, and speaks of a nerve-lesion which he attributes to the severity of the local inflammation. Hildige describes diphtheritic conjunctivitis as seen in Graefe's practice, and looks upon it as contagious. Magne denies its contagious or {663} infectious character. Mackenzie, while probably having seen false membrane appear on the conjunctiva when in a state of inflammation, yet refuses to recognize diphtheritic conjunctivitis as a distinct disease.

In the same degree that observations of cases and epidemics increased in number, the nature of the disease and its cause commenced to be studied. The assumption that the latter was a chemical poison was soon doubted, and the parasitic nature of diphtheria considered by many as proven.

After Henle had (1840) expressed his belief in the existence of a contagium animatum, and morbid processes had for some time been compared with the phenomena of fermentation, Schwann demonstrated the presence of lower organisms in fermentation and putrefaction. The discovery of the cause of the silk-worm disease by Bassis, of the achorion by Schönlein, of the acarus by Simon, of bacteria in malignant pustule by Pollender, Brauell, and, above all, by Davaine, in relapsing fever by Obermeier, the teachings of Pasteur concerning the conditions under which putrefaction occurs,--all tended to explain the various infectious and contagious diseases by analogy also, and to stimulate the search for a vegetable organism in diphtheria. Buhl was the first to discover schizomycetæ in diphtheritic membrane, but expressed no opinion as to the part they played in the process. Hüter found them in the gray diphtheritic covering of wounds, in the surrounding apparently healthy tissues, and in the blood. Hüter and Tomasi found them in the diphtheritic membranes of the pharynx and larynx, inoculated them on the mucous membranes of animals, and described them as small, round or oval, dark-colored, active little bodies. The latter observers look upon these organisms as a part of the infectious element. Oertel found them in diphtheritic membrane and in inflamed mucous membranes in the lymphatic vessels, lymphatic glands, kidneys, and other organs; he considers them as the contagious element of diphtheria. Nassiloff, too, after inoculations in the cornea resulted in an enormous multiplication of the microscopic organisms and their appearance with pus-cells in the lacteals and in the lymphatics of the palate, and even in the bones and cartilages, asserts that the development of organisms is the primary step in the diphtheritic process. Eberth made successful inoculations in living tissues; the micro-organisms, introduced into the cornea, proliferated actively and caused an inflammation of irritative character in the surrounding tissue. He asserts, with the positiveness of an evangelist, that diphtheria cannot occur without bacteria. Klebs inoculated the micrococci in pigeons and dogs, and found them in the blood of the animals after death. Orth found them in the pleura, lungs, kidneys, and urinary bladder. But what their action is, whether they are directly pernicious, or deprive the body of certain elements (as of oxygen in malignant pustule, according to Bollinger), or injure mechanically by acting on the coats of the blood-vessels (either directly or by means of altering the blood), thus depriving whole territories of their blood-vessels, is a question upon which the principal advocates of the parasitic theory have not yet agreed. Even Oertel acknowledges the impossibility of explaining the manner in which bacteria act (Ziemssen, Handbuch, ii., 1, p. 581, 2d ed.). This much is positive, at any rate: that no one has yet proven that the vegetable organisms alone, and not other, free or fixed, parts of the {664} diphtheritic membrane, are the vehicles of the infecting elements (Steudener); and even now the question has not been decided whether the bacteria met with in diphtheria constitute the cause of the disease, or are a part of the process, or co-effects of the poisonous action--whether they are the carriers of the poison or entirely indifferent entities.

The most important observations made by those who deny a direct etiological connection between micro-organisms and septic diseases in general, and diphtheria in particular, are those of Hiller and Billroth. The latter has proven the morphological identity of the various kinds of bacteria, although it cannot be denied that the apparent similarity may mask a yet unknown difference. Hiller calls attention to the fact that large numbers of micrococci have been found in the cadaver where death has not been the result of septic disease, and also that septic infection is not always severest where the bacteria most abound, but where an extensive chemical decomposition or a mass of putrefying tissue is found. This would indicate that the septic process is rather dependent on chemical decomposition than on the presence of bacteria.

Panum, Bergmann, and Schmiedeberg have isolated poisons that contained no bacteria. Rawitsch and many others prove that septic infection is not dependent on the existence of bacteria. Davaine has shown that an infinitely small amount of a chemical poison, free from bacteria, can kill quickly.

The presence of cocco-bacteria (Billroth) in the blood during life has not once been proven, not even in pyæmia or septicæmia. Yet their being swept into the lungs with the atmospheric air is indisputable. It would therefore seem as though living blood had a greater tendency to destroy bacteria than to allow itself to be decomposed by them. Not only, however, would it seem so, but P. Grawitz (Virch. Arch., vol. lxx., p. 546) proves that sporules do not grow in the (tissue and) blood, but that they are in part dissolved, in part eliminated through the kidneys, and that this result is accomplished through the combination of the following four factors--viz. the elasticity of the blood, its constant motion, the absence of oxygen in sufficient quantity in the circulating blood, and the presence of living animal cells. All of these factors appear to be of great importance. Thus it is that, where the constant motion of the blood and the animal living cells are not present (as in the anterior chamber of the eye or in the humor vitreous) a rapid proliferation and accumulation of bacteria can take place. They are also known to increase rapidly and emigrate into the liver when deposited in the abdominal cavity.

The destruction of bacteria in the circulating blood, into which they may have penetrated, accounts for some microscopical facts in connection with (actually or apparently morbid) blood. Their remnants are probably the pale and dark particles which are discovered in the blood alongside the red and white blood-corpuscles. They could not be identified as micrococci, while in the tissue they are more recognizable. In autopsies they have been found in the urinary tubules, pressing forward and piercing the walls, not occupying a nidus of inflammation, however, and probably are even here a post-mortem phenomenon. A direct necrosis or inflammation by the inoculation of diphtheritic elements can only be produced in the cornea, as was shown by Recklinghausen, and particularly Eberth. Besides, there is nothing characteristic in the cocco-bacteria of {665} diphtheria, with the exception, perhaps, of their browner color, to justify their being looked upon as a distinct variety, certainly not as another species. It is more likely that a difference of action is not so much to be sought for in a different parasite as in the peculiarity of the corneal tissue. When fluid containing cocco-bacteria was injected into the eye of a rabbit, in twenty-four hours the eye was destroyed. If injected into the eye of a dog or guinea-pig, only a slight inflammation resulted (Billroth and Ehrlich). If these experiments were continued on a larger scale, we might eventually, by analogy, infer, and even prove, that the immunity against certain diseases enjoyed by some animals is owing to peculiarities in the very structure of their own tissues. In a similar manner I shall prove hereafter that even peculiarities and variations in the tissue and epithelium of the human body give rise to different shades and variable clinical symptoms in the diphtheritic processes.

The views of Curtis, Satterthwaite, and Charlton Bastian fully agree with those of the above observers. The latter is rather inclined to look upon bacteria as an effect of the disease than as a cause. Similar views were expressed by Burdon Sanderson.

Nor are the researches of Weissgerber and Terls, Lukomsky, Weigert, Lücke, any more conclusive; and, finally, Fürbringer, in his most recent and careful studies of diphtheritic nephritis, insists upon this, that it is not caused by immigration of fungi into the kidneys, that the very best methods employed for the finding of parasites result in the absence of micrococci from the inflamed organ, and that the renal inflammation following diphtheria is the result of a chemical process.

H. C. Wood and Henry F. Formad, in Supplement 7 of the National Board of Health Bulletin (1880), declare it altogether improbable that bacteria have any direct function in diphtheria--i.e. that they enter the system as bacteria and develop as such in the system, and cause the symptoms. It is, however, possible that they may act upon the exudations of the trachea as the yeast-plant acts upon sugar, and cause the production of a septic poison which differs from that of ordinary putrefaction, and bears such relations to the system as to, when absorbed, cause the systemic symptoms of diphtheria. Now, these bacteria may be always in the air, but not in sufficient quantities to cause tracheitis, but enough when lodged in the membrane to set up the peculiar fermentation; whilst during an epidemic they may be sufficiently numerous to incite an inflammation in a previously healthy throat.

The same authors publish a number of other experiments and conclusions in Suppl. 17 (Jan., 1882): "There is no proof as yet that the micrococci are the cause of the disease. Their presence in the exposed dead tissue is no evidence, for the membrane represents but the necrotic mucous lining.... Indeed, when the healthy mucous membrane of the mouth or trachea is destroyed by caustics--for instance, ammonia--the eschar into which it is converted--really a pseudo-membrane--contains the same micrococci as are found in true diphtheria, as Wood and Formad have learned. Moreover, in the scrapings of the healthy tongue the same micrococci can be seen. Of more significance is the detection of the same or similar micrococci in the blood of the living patients during severe attacks. But since these parasites were found only in the more severe cases, and not in all instances of the disease, were seen also {666} in the blood of other septic disorders, and since no cultures have been made with the fresh blood, there is not yet enough evidence for any decision. In the internal organs bacteria are not found with any regularity in diphtheria."[6]

[Footnote 6: H. Gradle, Bacteria and the Germ Theory of Disease, Chicago, 1883, p. 186.]

O. Heubner, while studying both the local affection and the general infection of diphtheria, availed himself of the methods of Cohnheim and Litten, who produced diphtheritic deposits by cutting off the circulation of the blood. He ligated the neck of the bladder in rabbits for two hours. On the first day he noticed a hemorrhagic oedema of the mucous membrane, with loosened and tumefied epithelium; on the second a firm and coagulated exudation took the place of the normal tissue; on the third there were genuine diphtheritic spots in the mucous membrane. The newly-formed pseudo-membrane exhibited all the morphological elements of human diphtheria (genuine or scarlatinous) and epidemic dysentery.[7] Thus Heubner's results agree with the definition of diphtheria as the compound of severe inflammation and necrosis. The inoculation of his diphtheritic artefacts he found sterile. Animals, however, which were inoculated with diphtheritic masses taken from the diseased human patient fell sick with tumor of the spleen, hemorrhages, and general sepsis, besides a local diphtheritic affection. Scarlatinal diphtheria used for the same purpose had the same effect. Bacilli were developed, but they were not found in the blood-vessels (differing in that respect from the bacilli of anthrax), in spite of continued examination. Thus, Heubner refuses to accept the bacilli as the diphtheritic poison; they are, in his opinion, the result of the morbid process, and not its cause. Thus, though he believes the diphtheria poison to be organic, he concludes that its nature is not yet explained; contrary to the assertions of many prolific prophets of the bacteria literature, who now and then claim for this year's microscopic revelations the same infallibility which was claimed for last year's opposite views.[8]

[Footnote 7: Die Experimentelle Diphtherie, Leipzig, 1883.]

[Footnote 8: L. Letzerich recognized in former years the specific parasites of diphtheria, whooping cough, and typhoid fever as if they were labelled. Then, again (Arch. f. Experim. Pathol. u. Pharmacol.), he admitted the great difficulty in discriminating the specific schizomycetæ of diphtheria, croupous pneumonia, epidemic influenza, and typhoid fever.]

E. Rindfleisch[9] expresses himself as follows: "The microphytes of diphtheria, septicæmia, and pyæmia have not been isolated and cultivated as yet. But experimenters are convinced that there are a great many species of microphytes underlying genuine putrefaction. In producing septicæmic conditions in animals their efficacy differs. Not every animal is influenced by the same microphyte. Thus it becomes probable that the human organism is endangered by a certain number of the putrefaction microphytes. Some one may have a particular predilection for granulating wounds and mucous membranes, and thereby produce a diphtheritic inflammation. Another may enter the blood from a recent wound and give rise to a septicæmic fever with rapidly fatal termination. The third may invade the body by means of a phlegmonous inflammation, purulent infiltration, thrombosis, embolism, and metastatic abscesses, accompanied with a pyæmic fever of a remittent type."

[Footnote 9: Die Elemente der Pathologie, Leipzig, 1883, p. 301.]

After all, it does not appear to me that the bacteria question has come {667} any nearer its solution in the last few years, in spite of the most eager researches and the fact that some of the best medical names in the world of medicine take the parasitic nature of diphtheria for granted. For instance, in the second Congress for Internal Medicine (Wiesbaden, 1883) C. Gerhardt rises in its favor. He makes the statement, or rather admits, that several parasites have been found by different men, that every one considers his the genuine one, that several writers assume that there are several diphtheria parasites, and suggests that, in his opinion, the disease may be produced by different varieties of bacteria. At the same time, he contends that the essence of the disease consists in the erosion (and change) of the epithelium and the emigration of leucocytes. If that be the case, I understand less than ever why diphtheria is, or is to be called, a parasitic disease.

Panum's words seem still to be the soundest expression of all our knowledge on the subject when he says: "It is a matter of rejoicing that physicians have come to the conclusion that certain microscopic organisms, be they considered vegetable or animal, and designated as bacteria, fungi, monads, micrococci, or vibriones, do not exist merely in the minds of theorists as causes of disease, but are in reality enemies that must be combated with all the known efficient weapons in our possession. But, while thus rejoicing, it must be borne in mind that we have but a feeble insight into the relation between these organisms and diseases, and in order to effect that much-desired advance in scientific knowledge--a matter of considerable importance in the practice of medicine--it is necessary not only to grasp at isolated data, but carefully and deliberately to observe and study all the facts before us, and even to devote some attention to those which would tend to prove that there are bacteria and fungi which, under certain circumstances, are perfectly harmless, and that even some of the malignant ones among them do not commit all those outrages with which they are charged, directly and personally."

SYMPTOMS.--In the majority of cases the disease has a prodromal stage, which usually lasts a day or two, and may run a similar course to that of a catarrhal pharyngitis. The patient feels somewhat indisposed, has slight fever, is dejected, complains of painful deglutition, more marked when swallowing fluids than solids or semi-solids, has headache and occasionally vomiting. The occurrence of the latter, however, is very much less frequent than in the outbreak of scarlatina. In very severe cases convulsions have been observed, chills very rarely; elevations of temperature of from 102.5° to 104° F. are frequent; higher ones, from 105° to 107°, rare. At this time it is often difficult or impossible to distinguish a catarrhal angina from a diphtheritic by the subjective symptoms. Slight glandular swellings under the jaw may occur in either. The characteristic objective symptom of the latter disease is the presence of membrane on the reddened mucous membrane of the fauces, which, usually, is markedly injected over all or part of the surface. The arches of the palate and the tonsils, less frequently the posterior wall of the pharynx, are so affected. A distinctly localized redness cannot be but either traumatic or diphtheritic. Larger or smaller deposits are found thereon, lying loose on the surface or deeply imbedded according to the locality. At times the first examination reveals their presence in large numbers; at other times but a single one can be {668} detected, which is soon followed by others, however. Within a certain period of time, as a rule twenty to twenty-four hours, the single deposits coalesce and form a membrane of greater or less extent. Mostly in the same proportion to its increase in size it increases in thickness. On the uvula, soft palate, and the posterior wall of the pharynx the membrane is located superficially, and at times can be easily removed; on the tonsils it has a firmer hold, and is usually amalgamated with their uppermost tissues. On the other hand, there are cases in which no actual membranous formation is observed; in such cases the tissues are more or less swollen, the surrounding portions more or less reddened, and the grayish-white discoloration is the result of an infiltration of the tissues themselves, and cannot be removed.

There are still other cases in which deposits of membrane and tissue infiltration are found at the same time, and where both history and evidence indicate that these two phenomena are the result of one and the same process. When the uvula takes part in the process the swelling is, as a rule, more marked than when the remaining parts of the fauces only are implicated. Its circumference is very considerable, and amounts sometimes to the treble or quadruple of the normal, in consequence of the oedematous condition of the entire tissue.

We have to deal, then, with three different manifestations of the diphtheritic process: first, with a membrane lying on the mucous membrane, and removable without causing much injury to the epithelium or any to the basement membrane; such membranes were given by some the name of croupous deposits; secondly, with a membrane implicating the epithelium and upper layers of the mucous membrane; to this the title of diphtheritic membrane has been given by preference; thirdly, with a whitish or grayish infiltration of the surface and the deeper tissue, which, if abundant, may give rise to a necrotic destruction of the tissue.

The severity of the disease does not always depend on the predominance of one of these three forms, for any of them may accompany a mild or a severe attack. By a severe attack we understand one attended with chills, temperatures as high as 105° and 107° F., and marked nervous symptoms, such as vomiting and convulsions. It is characteristic of such cases that when the membrane is accidentally or forcibly removed it is speedily reproduced; the lymphatic system, in addition, takes an active part in the process. The neighboring glands become swollen; the periglandular tissue does likewise, so that the circumference of the neck becomes enormous, and the space between the lower jaw and the clavicle appears one immense tumefaction. These are the cases in which, as a rule, loss of strength and general debility speedily ensue, and death occurs from exhaustion. The membrane in cases of this description frequently undergoes changes in appearance; under the influence of the atmosphere and of foreign substances, and by admixture of blood, its color becomes yellowish or brownish. The odor of the membrane and surrounding parts becomes sweetish and musty, and occasionally so fetid that it contaminates the atmosphere of the room, and the air in its transit through the nose and over the pharynx becomes by inhalation dangerous to the patient. His throat becomes more swollen, his respiration loud; he keeps his mouth open constantly, has an indifferent expression; the saliva dribbles continually, the color of the skin is sallow and livid, the {669} appetite very poor, and pulse both frequent and small. When the symptoms are of long duration, and a deep infiltration of the affected parts occurs, hemorrhages not infrequently make their appearance. These may be slight although frequent; occasionally, however, larger blood-vessels are encroached upon in the process of destruction, and dangerous, nay even fatal, hemorrhages may be the result. The septic forms which I have here described are more dangerous than the mild ones previously mentioned. Still, even in the latter bad results may ensue from a direct absorption into the blood of putrid substances and by the penetration of fetid gases to the lungs.

Occasionally, where the infiltration has been extensive, we meet with a condition that can only be considered as gangrene. In such cases we see collections of a grayish pulpy mass, which on falling off leaves a considerable loss of tissue, the further course of the disease being either favorable, or dangerous through absorption of septic material, or accompanied by local hemorrhages. When, after a time, health is completely restored, marked cicatrices are left behind. Such loss of tissue is generally seen in the tonsils only, but it may also be encountered in the soft palate. Its cicatrices on the soft palate are always a source of inconvenience, partly in swallowing, partly in speaking. Actual local perforation of the soft palate I have seen but five times in twenty-five years, sloughing without perforation very often.

The diphtheritic membrane not infrequently spreads from the pharynx to the neighboring organs. From the posterior aspect of the soft palate or pharynx the disease gradually ascends to the nasal cavities; this is particularly apt to occur when the uvula is the seat of extensive deposits, and by forced inspiration and deglutition its posterior surface becomes affected. In such cases the membrane which extends thence to the nasal cavities is very dense, and capable of narrowing the capacity of the nasal cavities anteriorly, and occasionally even to close them entirely; as a rule, however, several days elapse before the membrane assumes such a condition. Usually, when this form of nasal diphtheria is in its incipient stage, it is impossible to diagnosticate it; the most important sign thereof, besides a more nasal articulation and sometimes greater difficulty in deglutition, and the result of close ocular examination while the uvula is turned sideways or drawn forward, is a swelling of the deep facial glands at the angle of the lower jaw; when these swell rapidly it can be asserted positively that the nasal cavities have been invaded. There is little or no discharge from the nostrils under these circumstances.

The picture is a very different one, however, when the nose becomes primarily affected. This usually occurs only where an acute catarrh with but little secretion, not so often where a chronic catarrh, has preceded infection. When the secretion is thin and serous, the diphtheritic infection renders it no thicker, but makes it slightly flocculent, and it may become very profuse. This form is frequently attended with a disagreeable odor, equally unpleasant to the patient and to those around him. During the prevalence of an epidemic one must always be prepared to see an acute nasal catarrh or an influenza, or even a chronic nasal catarrh, become complicated with diphtheria or pass into it. Schuller reports the case of a five-weeks-old male child who, having had a nasal catarrh since birth, became affected with diphtheria of the nose. The glandular {670} swelling of which I spoke above is a very important diagnostic, and likewise a decidedly unpleasant symptom, which becomes very marked inside of twenty-four hours; frequently a partial swelling remains long after the disappearance of the diphtheritic membrane. Such glands rarely suppurate or undergo a necrotic degeneration; sometimes they become permanently indurated. This induration and a chronic pharyngeal and nasal catarrh are very serious matters in many instances. Both of these conditions are starting-points for a number of acute or subacute attacks of diphtheria in the same person. It is they which constitute the liability of persons once affected to be taken sick again. Not only are they liable to be affected themselves, but they are a constant danger to all around them. Diphtheria, in a large family of children living in one of the best houses of the city, after having returned half a dozen times in the course of a year, disappeared instantaneously, not to return, when a seamstress living in an infected neighborhood and suffering from occasional sore throats was relieved of her daily work in the house. Oedematous swelling of the mucous membrane and submucous tissue is often observed for a long period to come; elongated uvulæ, enlarged tonsils, often date back to such an acute attack. Thus it is with the upper portion of the larynx about the posterior insertion of the vocal cords (see below); its large amount of loose submucous tissue is liable to swell considerably in acute attacks. Frequent spells of croupy cough and a certain degree of dyspnoea are often observed for years afterward. Though the cases of genuine cicatrization between the arytenoid cartilages, as described by Michael,[10] be rare, with their result of permanent paresis of the thyroarytenoid interni muscles, when they do occur they are either obstinate or altogether incurable.

[Footnote 10: Deutsch. Arch. f. klin. Med., 1879, xxiv. p. 618.]

Diphtheritic conjunctivitis occurs either primarily or as a complication of pharyngeal or nasal diphtheria. Fortunately, it is not of frequent occurrence; the cornea may become destroyed either by pressure through the considerable swelling of the eyelid or by diphtheritic keratitis. Usually the upper eyelid is the first to suffer; it is red, rigid, swollen. In the beginning the conjunctiva palpebræ is smooth, dry and pale, while that of the eye is chemosed; afterward diphtheritic deposits take place either in floccules or in solid masses. Knapp distinguishes between croup and diphtheria of the eyelid according to the facility or impossibility of removing the deposit. In favorable cases the membranes begin to macerate and the eyelids to soften after a few days. In those less favorable perforation of the cornea, prolapse of the iris, or total destruction of the eye take place.

The ear is but rarely the primary seat of diphtheria. A girl of three years died of laryngeal diphtheria on Sept. 6, 1882, after an illness of four days. A girl of seven years was removed from the house on Sept. 6th and returned on Sept. 8th. On the afternoon of the 10th an earring taken from the corpse was attached to the left ear of the sister, after having been washed with soap and water only. About noon on the 11th the lobe of the left ear reddened, on the 12th it exhibited a membrane and became swollen, and some glands enlarged in the neighborhood. On the right mastoid process the skin was not quite healthy, a vesicatory having been applied three weeks previously. This surface became {671} diphtheritic on the 12th, without consecutive glandular swelling. On the 13th the membranes grew thicker; on the 14th the pharynx was also affected, and the physician called in.

Most diphtheritic affections of the ear, however, are secondary. In pharyngeal and nasal diphtheria the narrow orifice of the Eustachian tube is easily obstructed by either catarrhal swelling or diphtheritic deposit. The disease may invade the middle ear and the drum membrane with perforation, caries, and deafness following.

The descent of the diphtheritic process into the respiratory organs may give rise to various conditions. The membrane is not always found to pass uninterruptedly from the mucous membrane of the fauces into the larynx; not infrequently isolated diphtheritic spots are found in the pouches on either side of the attached extremity of the epiglottis, or on the epiglottis, or in the larynx. At such times the epiglottis is moderately swollen, its margins hard and reddened. Occasionally the redness is interrupted by small diphtheritic deposits, which may remain isolated for a considerable time, but generally coalesce so as to coat the edges of the epiglottis with a continuous membrane. As a rule, the upper surface of the epiglottis is not completely covered by membrane, while only now and then diphtheritic deposits are found on its under surface.

The subjective symptoms accompanying the affection of the epiglottis are not always in direct proportion to the extent of the membranes. Dyspnoea and hoarseness occasionally occur where the only abnormal condition is a marked oedema at the entrance of the larynx, particularly of the posterior wall near the arytenoid cartilages and the attachment of the vocal cords. The oedematous condition causes a functional paralysis of the vocal cords, together with marked dyspnoea on inspiration. The difficulty of breathing may become so excessive that the clinical diagnosis of croup is unquestionable, and tracheotomy resorted to, while expiration is comparatively free and the voice not markedly affected. Furthermore, cases occur in which there is no marked oedema, but merely a general catarrh of the epiglottis and larynx; here, too, the subjective symptoms of hoarseness and dyspnoea may become severe and necessitate the performance of tracheotomy. Still, bearing this in mind, I have on several occasions refrained from performing this operation where I judged that, aside from the diphtheria of the pharynx, I had to deal with a moderate oedema of the glottis or a laryngeal catarrh.

Frequently, however, membranes form in the larynx in the same way as in the pharynx or nose; then inspiration and expiration are equally interfered with, and hoarseness is a more constant symptom than in the above-mentioned cases. Fever and pain are not necessarily prominent symptoms; in fact, they are frequently unimportant, but in proportion as the degree of narrowing of the larynx increases the respiration becomes more difficult, long-drawn, and loud.

It may happen that the trachea and bronchi may become affected, although diphtheria of the fauces does not exist. This does not occur as rarely as Henoch and Oertel seem to believe. They think that diphtheritic tracheo-bronchitis is mistaken for the primary condition, because the throat is not examined early enough.

Oertel is of the opinion that the membrane in the fauces is {672} overlooked in such cases. Steiner,[11] too, asserts that "the tendency of the times is to question, nay, rather to deny, the existence of croup extending from below upward." Now, on the contrary, repeated experience enables me to assert with positiveness that diphtheritic tracheo-bronchitis may occur without an affection of the pharynx at the same time. I do not deny that it may last for days without giving rise to dangerous symptoms. I know it does. But when the process reaches the larynx, the symptoms of suffocation become so urgent that tracheotomy may be absolutely required at once, and, in spite of the operation, death soon after occurs.

[Footnote 11: Ziemssen's Handb., iv., 1, 126.]

Of course these cases are exceptions; as a rule, laryngeal and tracheal diphtheria result from a descent of the disease from the fauces. More or less uncomplicated cases of primary laryngeal diphtheria, or so-called sporadic membranous croup, were, however, observed before the end of the sixth decade of this century. They were then almost the only cases of diphtheria, and linked former epidemics and the present one together.

Inflammatory affections of the lungs may occur at various times and in various forms during an attack of diphtheria. That which appears after tracheotomy is usually a broncho-pneumonia, and results from rarefaction of the air in the respiratory passages during the period of impeded respiration, with consequent collapse of pulmonary tissue and dilatation of the blood-vessels, and hence a disturbance of the circulation. It may not fully develop until after tracheotomy, and is a frequent cause of death on the second or third day after the operation. Now and then a case of lobular pneumonia will result from the aspiration of pieces of membranes into the smallest bronchi. It can be easily recognized when the trachea is opened, but previous to the operation the auscultatory signs are of little or no value, being masked by the laryngeal râles. Percussion is equally useless, for a dulness may just as well indicate collapse of the lung as infiltration. The second form of pneumonia associated with diphtheria is from the beginning fibrinous in character. Here, too, auscultation and percussion are of little assistance in establishing a diagnosis when there is a laryngeal diphtheria at the same time, for the above reasons. Where, however, the dulness on percussion is accompanied by high fever, and the long-drawn inspiration is replaced by rapid respiratory movements, the diagnosis of pneumonic complication is justified.

Diphtheria of the mouth, as a primary affection, is not of very frequent occurrence; not rarely, however, is it associated with diphtheria of the fauces and nose, mainly when they have assumed a septic or gangrenous character; it appears on cheeks, tongue, angles of the mouth and gums, and, after the fetid discharges have excoriated the skin, on the lips also. In all of these localities it appears less in the form of an extensive, thick membrane than an infiltration of the tissues. It is most apt to occur where, from the start, the mucous membrane of the mouth was eroded or ulcerated. The ulcerated base of a follicular stomatitis is very frequently the starting-point of a general diphtheria of the mouth. It is always a disagreeable symptom, points to a long duration of the whole process, and threatens septic absorption.

The oesophagus and the cardiac portion of the stomach are the seat {673} sometimes of very massive and extensive, mostly fibrinous exudations, in typhoid fever, dysentery, cholera, measles, and scarlatina, or after injuries following contact with mineral acids, alkalies, corrosive sublimate, or antimony. When the normal tissue was not injured I never saw any that were not superjacent and could not easily be peeled off (croupous). In cases of extensive pharyngeal and laryngeal diphtheria the upper part of the oesophagus is often covered to a distance of half an inch or an inch with membrane, the lower part of which is thinning out into a mere film. A case of local diphtheritic deposit near the cardiac portions of the oesophagus, upon the seat of a stricture, I have described in my Treatise, p. 83. Actual diphtheria of the stomach is rare. So is that of the intestine, which is much more liable to be affected in animals than in man. In the cow intestinal diphtheria is frequent (Bollinger). In the gall-bladder, resulting from the irritation produced by calculus, it was seen by Weisserfels. The diphtheritic form of inflammation of the human colon and rectum--dysentery--is frequent enough, but will be the subject of discussion in another place. But, besides this, in the lower portion of the small intestines and in the colon long, tough, coherent membranes are sometimes found in the male and female (not in the hysterical female only). As a rule they are not diphtheritic, but consist mostly of nothing but mucus hardened and flattened down by protracted compression. The few cases of intestinal diphtheria I have met with gave rise to the usual symptoms of enteritis, and were diagnosticated as such.

Wounds of all kinds are easily and rapidly infected by diphtheria; for instance, vaginal abrasions and erosions of the external ear, tongue, and corners of the mouth. Scarification or removal of part of the tonsils is followed in half a day or a day by a deposit of diphtheritic membrane on the wound. The wound caused by tracheotomy becomes liable to be infected with diphtheria within twenty-four hours. Leech-bites, skin denuded by vesicatories, removal of the cuticle by scratching during cutaneous eruptions, all furnish a resting-place for diphtheria in a short time. What Billroth has described under the name of muco-salivary diphtheritis, as it occurs after the extirpation of a large portion of the tongue and resection of the lower jaw, belongs to this class.

At times immediately at the beginning of an invasion of diphtheria, at other times only on the second or third day, an erythematous eruption, more or less general, appears on the skin. Now and then it appears on the chest, shoulders, and back; at other times it covers the body, and has not infrequently led to its being confounded with scarlatina. It is not always accompanied by much fever, and cannot therefore be mistaken for that form of erythema which frequently appears in children with delicate skins during high fever from any source. I cannot say that I have found this complication to give a more malignant character to the disease, but true erysipelas does. I am not prepared to prove that the two processes, erysipelas and diphtheria, are identical under some circumstances, but the complication of the two, and the ferocity with which they combine, renders a close relationship probable. I have seen an infant dying from an erysipelas added to a post-auricular diphtheria, this being due to a slight abrasion of the surface. Erysipelas originating in the tracheotomy wound, though ever so carefully disinfected and secured, is {674} frequently observed after two or three days, and is a very ominous symptom. Erysipelatous surfaces, denuded of their epidermis by spontaneous vesication or injured by ever so slight a trauma, are very liable to be covered with diphtheritic membranes.

An eruption resembling urticaria in the beginning is as innocent as erythema, but purpura in the latter stage is a symptom of mostly ominous nature.

On the vulva and vagina of little girls diphtheria is sometimes met with; probably in every case it is due, under the epidemic influence, to a local catarrh or erosion. In but few cases, comparatively, the inguinal glands are swollen. There are not many cases of vaginal diphtheria which are followed by the pharyngeal affection. Diphtheria of the vagina in puerperal women is liable to become the cause of general sepsis, and is a dangerous disease; it is seldom complicated, but uterus, Fallopian tubes, and peritoneum may become the seat of inflammatory and septic disturbances. In the bladder it may occur when the urine is alkaline, in chronic cystitis, after lithotomy, urethotomy, the operation for vesico-vaginal fistula, and in ectopia vesicæ. This form has a marked tendency toward localization, but by extension of the phlegmon, when of putrid character, to the retro-peritoneal cellular tissue, peritonitis may ensue and terminate fatally. Sepsis from absorption is also frequent. Vesical diphtheria is sometimes quite unsuspected. A man of sixty had urinary trouble a long time; his urine was frequently very offensive, containing blood and pus. About five days before his death he suddenly collapsed. I found the bladder well filled, and introduced a catheter, but succeeded in removing but a few drops of fetid liquid. Assuming the presence of a malignant tumor at the neck of the bladder, I attempted to draw off the urine by puncturing above the symphisis pubis; again without success. At the post-mortem examination a thick membranous lining of the bladder was found detached in the form of a sac containing about a quart of urine. During life the beak of the catheter evidently passed into the space between the bladder and the membranous sac, which accounts for the unsuccessful attempts at catheterization.

Diphtheria of the placenta was observed by Schüller. The membrane was between uterus and placenta, and attached to the latter. It resulted from puerperal sepsis. Balano-posthitis is liable to result in local and general diphtheria; so are circumcision wounds. They are apt to become affected either primarily, without apparent cause, or when other members of the family are suffering from the disease.

The kidneys may become affected in various ways. Albuminuria is not always of significance, as it occurs in severe and mild cases alike, both before and after tracheotomy, and therefore is not connected always either with the height of the fever or the degree of dyspnoea; at times it disappears in a few days, in other cases it is of longer duration. It is not invariably complicated with changes in the kidney, neither do we always discover casts or degenerated epithelial cells in the urine. In other respects also it does not behave like albuminuria in scarlatina. In the latter it appears seldom before the second week of the process, and frequently later, while in diphtheria it is often seen early. It sometimes lasts but a few days, particularly in many cases which set in with a high fever, which rapidly diminishes, and terminates in speedy recovery. In {675} these occurrences the presence of albumen appears to attend the rapid elimination of the poison.

Albuminuria seldom lasts longer than a week, and is not often complicated with oedema, but sometimes it is but a symptom of a local or general nephritis, and then hyaline, epithelial, and fibrin casts and granular cells are found in the urine. Nephritis then assumes as serious a character as it possesses in scarlatina. Cases of nephritis, fortunately rare in a very early period of diphtheria, are liable to run a rapid and often fatal course.

The heart and blood are affected in various ways by the diphtheritic process. Where the disease runs a slow course, accompanied by high fever, a granular degeneration occurs, similar to that appearing in other acute infectious disorders--typhoid, for example. In diphtheria, however, it would seem that this condition may arise even without marked elevation of temperature. The pathological changes in the heart produced by diphtheria are not always the same. Ecchymoses, cellular hypertrophy, and granular degeneration have frequently been noticed after death where the symptoms had been severe. The result, of course, is considerable weakness of its muscular tissue, evidenced by the formation of local (Beverly Robinson) thrombi, general sluggishness of the circulation, dyspnoea, muffled heart-sounds, a cool and pale skin, and sudden death, preceded by a very feeble and frequent, sometimes, however, by a very slow, pulse. Aside from this, there is actual endocarditis during the course of diphtheria or convalescence therefrom. It affects especially the valves, and among them particularly the mitral. It is characterized by high fever, precordial pain, attacks of syncope, and a systolic murmur.

The rapid decrease of red blood-cells and a moderate increase of leucocytes were demonstrated by Bouchut and Dubrisay, but the disproportion was not such as to necessitate the diagnosis of leucocythæmia. Wunderlich reports two cases of Hodgkin's disease, the pseudo-leukæmia developing during diphtheria. And the slowness of final recovery in many cases, even of but short duration and not complicated with nervous disorders, appears to point to a serious disintegration of the elements of the blood. The dark color and defective coagulation of the blood in autopsies of diphtheria cases have often been remarked.

The direct and rapid introduction into the blood of a foreign substance has amongst its earliest symptoms fever. This reaction of a nervous system depends both on the quantity and quality of the substance or poison introduced, and on the susceptibility of the patient. High temperatures are, however, not the only, nor are they the most dangerous, nervous symptoms. To the latter belong the different shades of paralysis met with during or subsequent to diphtheria.

Sudden and unexpected collapse is sometimes observed, not infrequently in the earlier part of the disease. The changes found in autopsies, such as a dark color of the blood, deficient coagulability, extravasations into and friability and granular degenerations of the tissues, accumulations of degenerated cells, and granules between the fibres, degeneration mainly of the heart-muscle, the presence of heart-clots, thrombi in remote veins,--they all show to what extent the disease can destroy life in the shortest time possible. In the heart either the pneumogastric or the ganglionic {676} nerves may be affected, and the symptoms will vary accordingly. Paralysis of the former will accelerate the pulse, degeneration of the sympathetic will diminish its frequency, yet death may ensue in either.

The usual form of diphtheritic paralysis makes its appearance during the period of convalescence, at a time when all danger seems to have passed by. As a rule, the soft palate and the muscles of deglutition are the first to be attacked, while the condition of these organs is apparently normal (and no longer oedematous, and thereby inactive, as in the first period of the disease). While they are recovering, or before, the accommodation muscles of the eyes become paralyzed. Sometimes, however, these are the first to be affected. This paralysis does not, as a rule, follow severe cases; on the contrary, it is not uncommon to observe it after apparently mild attacks of the disease. In consequence of the former paralysis, deglutition becomes difficult; fluids are expelled through the nose or enter the larynx and bronchi, thereby giving rise to pneumonia; in the latter there is strabismus. The upper and lower extremities become paralyzed afterward. As a rule, a number of muscles are affected at the same time, and improvement will take place in about the same order in which the individual muscles became affected. After paralysis has become affected, circulation begins to suffer. The extremities now and then become bluish, cool, emaciated; rarely atrophy and fatty degeneration have been observed. The muscles of the neck also become paralyzed; the head cannot be carried, or with difficulty only. The fingers are but seldom affected. The same holds good of the bladder and intestines. The respiratory muscles are not frequently attacked. Their paralysis is very ominous, and may prove fatal in a short time from apnoea.

Not only motory but sensory paralyses may occur. Anaesthesia, amaurosis, deafness have been observed; a number of cases of locomotor ataxia are on record, and but lately Hadthagen[12] publishes a case which he claims as disseminated sclerosis.

[Footnote 12: Arch. f. Kinderheilk., vol. v., 1883.]

Sometimes the nervous affection in diphtheria is localized in a peculiar manner; it seems as if there is a predisposition on the part of a certain nerve to become diseased. The case of a boy, active and healthy, in the practice of H. Guleke, is very interesting. In the course of three years he had three attacks of diphtheria. In the very beginning of the disease he always became soporous with an almost normal temperature and a slow but regular pulse. Probably the heart's ganglia are the first to submit to the influence of the poison and exhibit symptoms of flagging function. In most of the cases of diphtheritic paralysis the prognosis is good; the large majority will run a favorable course in from six to ten weeks.

INVASION.--Is diphtheria, primarily, a local or a constitutional disease? Mercado's well-known case of diphtheria, engendered by the biting of a finger, has been alluded to. I know of one case in which the vagina became first affected, and later the pharynx. Bayles saw denuded portions of skin assume a membranous character, and general diphtheria develop afterward. Fresh wounds become diphtheritic, and the general disease arises from this source. Even paralysis will follow. I had a death from diphtheria when a long incision into a phlegmon of the thigh had become diphtheritic. A little girl, who had a considerable amount {677} of discharge from a catarrhal vagina, and sore thighs in consequence, exhibited first, during the epidemic of 1877, membranes on the denuded cutis, and afterward general diphtheria. Brehm reports the case of a woman on whom he performed colotomy. The wound became thoroughly diphtheritic and gangrenous, but the pharynx and respiratory organs remained intact. A few days after, her daughter, who attended her in her sickness, was infected. In her the pharynx was the seat of disorder. Besides, the tonsils are very frequently coated with a membrane without any general symptoms in the beginning, fever and general illness occurring only later on. Now, all of these facts tend to show that there are cases in which the origin of the disease is purely local.

It must, however, not be forgotten that during the prevalence of an epidemic every one is more or less under its influence, and but little is wanting to call forth the disease. Some years ago a well-known physician, with whom I was intimately acquainted, died from facial erysipelas and meningitis which had originated in a slight abrasion of the upper lip. During an epidemic of typhoid we daily see persons with fever, headache, and lassitude. Diarrhoeas are frequent during an epidemic of cholera. An epidemic of diphtheria is accompanied by a great number of cases of pharyngitis. When, in the year 1860,[13] I reported two hundred cases of bonâ fide diphtheria, I at the same time observed one hundred and eighty-five cases of non-membranous inflammations of the throat. Such occurrences may be considered as possible or incipient cases of pharyngeal diphtheria. Therefore, contrary to the view of a local origin of diphtheria, it may be claimed that the individual taking the disease was already saturated with the poison, and the local membrane represented perhaps nothing but a symptom, or at the utmost the causa proxima. Accordingly, then, there are undoubtedly cases in which the pharyngeal membrane is the first cause and symptom of the final affection, and others in which the poisoning of the blood through inhalation is the first step in the development of the disease, amongst the symptoms of which the pharyngeal or nasal membrane counts as one.

[Footnote 13: Amer. Med. Times., Aug.]

In these cases the first complaints of the patients relate to their general condition. Sometimes they are ignorant of any local trouble when they consult a physician. When it is perceptible, however, it is usually found on the visible pharyngeal and respiratory mucous membranes. This would seem to indicate that the infectious elements while being inhaled are there deposited. Thus there is a possibility of simultaneous affections of both the throat and the blood in the lungs, in either equal or variable proportions. We are easily led to defend at least a partial admission of the poison by the respiratory act, when we reflect that the membranes which are swallowed are rendered innocuous by the action of the gastric fluids, and, therefore, the alimentary canal, from the oesophagus downward, cannot be made responsible for the admission of the poison into the system. Thus it is that the general symptoms--as fever, lassitude, etc.--precede the local phenomena in very many cases, while there are exceptional cases in which the membrane appears first and the fever later. This is especially the case when the tonsils are very large and occupy a prominent position in the throat.

Those cases which begin with high fever and moderate or no local {678} symptoms must be looked upon as constitutional diseases. If a person, in the course of several hours or a day, be taken with high fever and a moderate membrane-formation, these symptoms subsiding in one or two days, leaving the patient weak and exhausted, but fully restored to health at the end of a week, we would be justified in assuming (cæteris paribus) that there was a rapid absorption of a large amount of poison, and an equally rapid elimination thereof. They are, moreover, the same cases in which the second or third day of the disease furnishes albuminuria, with rapid elimination and speedy recovery. When, however, the process is slow in developing, accompanied by moderate fever, and the course is indolent, we have reason to infer that moderate amounts of the poison are being continually taken into the system and making their influence felt to a moderate degree, but for a longer period. Such are the cases which, without any violent symptoms, are accompanied by frequent local relapses, or run, when the absorption is constant as well as copious, a septic course, or terminate in paralysis.

Thus there are cases in which a local infection of the skin or of a wound may be one of the causes, or the only cause, of the disease, and there are cases in which the poison, in passing through and caught in the pharynx, gives rise to local phenomena before the system at large gives evidence of infection. But, as a general thing, diphtheria must be looked upon as a constitutional disease, giving rise to local phenomena, in the same way as scarlatina does on the skin, on the mucous membrane of the alimentary canal, and in the uriniferous tubules; measles on the skin and respiratory mucous membrane; or typhoid in the lymph-follicles and on the mucous membrane of the intestine; or, in other words, the diphtheritic poison may enter the system locally through a defective, or sore, or wounded integument or through the lungs.

Is diphtheria contagious? Undoubtedly it is. The contagious element is liable to be directly communicated by the patient; it also clings to solid and semi-solid bodies, and in this way is transmitted even after a long time. There is hardly any disease which can cling so tenaciously to dwellings and furniture; it can be transported by the air, though probably not to a great distance, and hence in houses artificially heated, while the windows and doors are mostly closed, rises from the lower to the upper stories; and it is for this reason advisable to keep the sick on the top floor. It is certainly transmitted by spoons, glasses, handkerchiefs, and towels used by the patient. The contagious character increases directly in proportion to the neglect of proper ventilation. That it is spread by the feces is not clearly established in my mind. I can give personally no examples of its being carried by visitors or by the attending physician; this is said to have occurred, however. The character of the disease communicated, and the local manifestation, do not depend on that of the original sufferer; thus mild cases may produce severe ones, and vice versâ, and convalescents can convey the disease in its full force. Naturally, the softer character of the tissues in children renders them more susceptible to infection, and the activity of their lymphatic system more liable to severe forms of the disease.

Many tragic cases are recorded in literature of infection by direct contact from pharynx to pharynx, or from the opening in the trachea to the mouth of the surgeon; and one of the saddest cases, perhaps, is that of {679} the much-lamented Carl Otto Weber. Myself and others have contracted diphtheria from sucking tracheotomy wounds.

In regard to the length of the incubation periods, there can be no better authenticated facts than those contained in a report of Elisha Harris to the National Board of Health, an abstract of which is found in No. 1, National Board of Health Bulletin, June 28, 1879. The report says that in the fourth school district of the township of Newark (Northern Vermont), amidst the steep hills where reside a quiet people in comfortable dwellings, the summer term of school opened on the 12th of May. Among the twenty-two little children who assembled in the school-room in the glen were two who had suffered from a mild attack of diphtheria in April, and one of them was, at the time school opened, suffering badly from what appeared to have been a relapse in the form of diphtheritic ophthalmia. Besides, it is proved that these recently sick pupils had not been well cleansed, one of them having on an unwashed garment that she had worn in all her sickness three weeks previously. At the end of the third day of school several of the children were complaining of sore throat, headache, and dizziness, and on the fourth day and evening so many were sick in the same way that the teacher and officers announced the school temporarily closed. By the end of the sixth day from school opening, sixteen of the twenty-two previously healthy children became seriously sick with symptoms of malignant diphtheria, and some were already dying. The teacher and six of the pupils were not attacked, nor have they since suffered from the disease.

A case[14] is reported of a surgeon who, while attending a diphtheritic child, had some secretion thrown into his face. Twelve hours after his right eye was inflamed and painful. The affection proved diphtheritic, and recovery was completed after several weeks only. In a case seen by me, with Dr. L. Bopp, a child removed from a house infected with diphtheria was attacked after fourteen days and eight hours.

[Footnote 14: Würt. Med. Corresp. Bl., 1878, No. 2.]

It would then appear that, in the direct communication of the disease to healthy or nearly healthy mucous membranes--as healthy as the prevailing epidemic will allow--the period of incubation is from one or two to fourteen days. In only a small number of cases the disease has an even shorter period of incubation than this, as when tonsillotomy or a similar operation is undertaken during the prevalence of an epidemic. One may rest assured that any operation on the tonsils while an epidemic of diphtheria is at its height will be followed within twenty-four hours by diphtheritic deposits on the wounded part. To what extent we are justified in considering this a bonâ-fide incubation of the disease in a previously healthy body is, of course, another question. It seems to me that these cases positively prove that the operation is only the causâ proxima of a diphtheritic affection, and that we may take it for granted that during an epidemic every individual is more or less under its influence and affected by it, so that it needs but a wound or an accidental abrasion of the surface of the mucous membrane to call the disease into action. In a similar way, fresh wounds or morbid conditions of the mouth may call forth the disease. The ruptured vesicles of a follicular stomatitis are liable to serve as resting-places for diphtheritic membranes, and thus I have seen the complication of a follicular stomatitis with oral diphtheria; and any {680} lacerations of the vagina during labor may become diphtheritic within twenty-four hours. If now, on the one hand, incubation depends on the condition of the affected surface, it is probable, on the other hand, that the intensity of the poison at the time plays an important part in determining the period that is to elapse between infection and the invasion of the disease.

ETIOLOGY.--Diphtheria is pre-eminently a disease of early life; in this respect it is said to differ from the genuine fibrinous bronchitis, which by some is held an absolutely different disease, and stated to occur but rarely in children. But even this statement is probably incorrect. In the spring of 1879 I met with four cases of fibrinous bronchitis in children under three years of age. The number of cases of diphtheria in adult life is not very large, while in old age it is very small. Of 501 deaths in Vienna in 1868, only 1 had reached the age of sixty-two; of more than 300 cases in which I performed tracheotomy but 2 were over thirteen years old.

I do not know that sex exerts any predisposing influence over diphtheria, yet of the six hundred cases or thereabouts of laryngeal diphtheria in which I either personally performed tracheotomy or observed the progress of the disease in the practice of others, I found the majority in males, and the recoveries in inverse proportion to the number thereof, the mortality being greater among boys. As far as age is concerned, nearly all the zymotic diseases are seen most frequently in children. They exhibit a greater disposition to submit to diphtheria than adults, if we except those under ten months. Where, however, the disease has occurred previous to the seventh or eighth month, the greater number of cases has been found under three months. Tigri reports the disease in a child of fourteen days. A child of fifteen days was seen with diphtheritic laryngitis and oesophagitis by Bretonneau, one of seventeen days by Bednar, one of eight by Bouchut, one of seven days by Weikert; Parrot mentions several cases, and Sirédey[15] reports eighteen cases of diphtheria in the newly-born. They occurred in the Hospital Lariboisière in the spring of 1877, and were probably infected by the nurses of a neighboring children's asylum. Membranes were found on the soft palate, tonsils, or larynx, and also on both pharynx and larynx. One case occurred where the posterior nares alone were affected. I have met with four cases of diphtheria of the pharynx and larynx in the newly-born myself. One of these became sick on the ninth day after birth, and died on the thirteenth day; the other died on the sixteenth day after birth; the third was taken when seven days old, and died on the ninth day. The predisposition to diphtheria during childhood[16] seems to be explainable by several circumstances. The mucous membrane of the mouth and pharynx in the child is more succulent and softer, and frequently the seat of a congestive and inflammatory process. The nasal cavities are small and frequently affected by catarrhs, the buccal cavity often the seat of catarrh and of stomatitis, and insufficient cleanliness leads here to irritation of the mucous membrane. Any abnormal state of the mucous membrane, with {681} the exception of an atrophic condition and cicatricial changes, affords an excellent abode for diphtheria. The tonsils are proportionally large; in fact, we rarely see the tonsils in children completely sheltered by the arches of the palate. On the other hand, the pharynx is anything but spacious, and while the protuberant condition of the tonsils affords a resting-place for the invading disease, the remaining space is so small that it becomes a source of uneasiness to the well in many instances, and very much more than that to the child during diphtheritic tumefaction. Furthermore, we must take into consideration the large number and size of the lymphatics, which can be more easily injected in the child than in the adult, according to Sappey, and the fact of greater intercommunication amongst the lymphatics and between them and the system; for S. L. Schenck has found that the network of lymphatics in the skin of the newly-born, at least, are endowed with stomata, loopholes through which the lymph-ducts can communicate with the neighborhood, and vice versâ.[17] These circumstances, although they may have no influence in calling the disease into existence, yet assist in its development and in adding to the severity of the symptoms.

[Footnote 15: Thèse, Paris, 1877.]

[Footnote 16: W. N. Thursfield (London Lancet, Aug. 3d, 10th, 17th, 1878) collects 10,000 cases of diphtheria in England between the years 1855 and 1877. Of these 90 per 1000 were under a year, 450 per 1000 from 1-5 years, 260 from 6-10, 90 from 11-15, 50 from 16-25, 35 from 26-45; 25 per 1000 were 45 years and over.]

[Footnote 17: Mittheil. aus d. Embryol. Instit., i., 1877.]

On the other hand, while the above reasons go to prove that diphtheria attacks children by preference, there is again an anatomical and physiological condition--to wit, the free slightly acid secretion of the mouth, beginning with the third month--that acts as a hindrance to the frequent occurrence of diphtheria after the third month. A poison or poisonous product of whatever nature can less readily find a hiding-place so long as it can be readily--we might always say must surely be--washed away. During these months of eruptive secretion from the mouth diphtheria, therefore, is not very frequent; thus teething, in the case of diphtheria, cannot be held responsible by mothers fond of diagnosticating dental diseases. In this connection the remark of Krieger ought not to be overlooked, who explains the relative scarcity of the disease in the first year of life by the fact that cumulative influences will produce a great number of cases, and cumulation requires time. Undoubtedly, however, an important etiological consideration is the fact of having had the disease previously. We can cite a host of zymotic diseases the occurrence of which once serves as a protection against future attacks. Not only can no such security be expected after one attack of diphtheria, but, cæteris paribus, the disease shows a preference for those who have survived a previous attack. The statement that only the mild cases, with but slight elevation of temperature and freedom from severe constitutional symptoms, are likely to suffer a relapse is founded on error. True, I have more frequently seen relapses after mild cases--which, fortunately, are in the majority--but the disease has also recurred where originally high fever and an extensive lymphadenitis proved it to be a severe case. Besides, second attacks of membranous croup are also recorded (Guersant, N. F. Gill, Quincke).

As there are individuals, so there are families, which have a predisposition to diseases, as there are others in whom, notwithstanding ample exposure, infection does not easily take place. Yet in the families in which diphtheria is of frequent occurrence it cannot always be attributed to enlarged tonsils and a tendency to pharyngeal or nasal catarrh.

{682} Still, catarrh and the vulnerability of mucous membranes must be considered as a frequent source of diphtheria; children will get numerous relapses often after a nasal or pharyngeal catarrh. Sudden changes in the temperature of the atmosphere or of the surface of the body are therefore dangerous in predisposed persons. And thus it is that while severe epidemics have spared no climate or land known to us, the majority of cases have occurred in winter and spring; in other words, at a time when catarrhal disorders are of most frequent occurrence. In my experience at New York, the first quarter of the year yielded more cases than any other. Still, they are frequent enough in warm seasons. Krieger insists upon the injurious influence of hot summers and dry hot rooms. I do not doubt the correctness of his views, which cannot but be strengthened by the damaging results of our furnace-heating. But the influence of season on the invasion and course of diphtheria is but indirect and conditional, and may be, perhaps, after all, compared with that exerted by filth--a term which is lately used to express all sorts and forms of nastiness, from filthy bodies of men to their clothes, their habits, their food, and the air they breathe, whether polluted by carbonic acid, by excrementitious gases, or by exhalations of sewers.

Cases of diphtheria which are traced to exhalations from sewers (or even to filthy habits of life) are very frequent. Yet typhoid is attributed to the same causes. So is dysentery. Can, then, foul exhalations produce alike diphtheria, typhoid, and dysentery? Do these diseases arise from a common poison? Or is the poison of a treble character, so that a part may give origin to diphtheria, another part to typhoid, a third to dysentery?[18] Have we to deal, in such occurrences, with specific influences, or only with a lowering of the standard of health, thereby affording other morbid influences an opportunity to exercise their power? These questions are still involved in darkness, and constitute problems the solution of which still engages the minds of both individual writers and authorities. A report of the Board of Health of Massachusetts, closely adhering to the results of exact observations,[19] leaves them doubtful, and the affirmative reports of some modern writers do not bear scrutiny.[20]

[Footnote 18: In regard to the causal connection of the two latter diseases with sewer exhalations we can be more positive than in regard to the former.]

[Footnote 19: Author's Treatise on Diphth., p. 35.]

[Footnote 20: M. A. Avery, Med. Jour. and Obst. Rev., Feb., 1882.]

Air polluted by bad drainage or leaky sewers has been considered responsible for diphtheria as well as for typhoid fever and dysentery. Not only the impairment of general health, but the direct and unmistakable disease, has been attributed to it. Thus Bayley refers, in the endemic of Bromley,[21] the first cases to unventilated sewers and cesspools. School-children multiplied the disease. Thursfield attributes the diphtheria at Ellesmere[22] to the accumulation of excrements under the school-room, and to deficient supply of water, which, moreover, was of bad quality. Tripe (like Railton, Bailey, Russell, Bell) accuses sewer gas;[23] others polluted waters or bad drainage.[24] I have not been convinced, however, that diphtheria can be considered a sewer-gas disease, in the same way as typhoid fever. The deterioration of the general health resulting from the inhalation of foul air is sufficient to explain the outbreak of the individual attack during a prevailing epidemic.

[Footnote 21: Sanit. Record, Aug. 10, 1877.]

[Footnote 22: San. Rec., 158, 1877.]

[Footnote 23: Ibid., June 14, 1878.]

[Footnote 24: Ibid., April 18, May 2, 1879.]

{683} In regard to polluted water, I do not think that pathologists who attribute infectious diseases to bacteria only are justified in condemning it. It may not be so guilty, after all, for the admixtures, inorganic and organic, minerals, admixtures of wood and plants, also lower fungi and their products--algæ, infusoria--would render water rather disagreeable, but not exactly unhealthy. The latter effect can be accomplished--always assuming the bacteria theory correct, for the sake of argument--by bacteria only. But when they arrive in the stomach, their doom is sealed; they are decomposed. The only places where, possibly, they could take root would be diseased or ulcerated places in either the oral cavity or the upper portion of the oesophagus.

Not only water, but the milk of animals also, has been accused of being the direct cause of diphtheria. Powers concludes, though a connection between diphtheria and the consumption of milk have not been proven as yet, that it is very probable indeed. His careful investigations into the causes of some local epidemics in North London exclude any other source from which the people could have been affected. Perhaps one of the forms of garget, cow mammitis, is of an infectious character. His reasoning, however, is not accepted by A. Dowrus,[25] who still believes that the milk which gave rise to diphtheria at a distance may have been soiled and infected. For though the connection between milk and scarlatina and typhoid fever had been known for years and variously studied, no observation of the kind had yet been made in regard to diphtheria. Besides, where the young, in England, drink much milk--viz. in the cities--diphtheria was very much less frequent than where little or no milk was taken--viz. in the country. Even in the country the well-to-do classes, who drink milk, had but little diphtheria, while the children of the poor, who obtained none, suffered a great deal from it.

[Footnote 25: "Diphtheria and Milk-Supply," Brit. Med. Journ., Feb. 1, 1879.]

In regard to this transmission of diphtheria by means of milk O. Bollinger[26] hesitates to express any opinion, except that the matter is very doubtful indeed. Probably the possibility of contracting diphtheria directly from animals is very much greater than the danger from water or milk. On a Pomeranian farm, during the winter 1875-76, every newly-born calf died of diphtheria. The superintendent of the farm and the woman who attended to the calves were taken with diphtheritic angina.[27] Similar occurrences have been recorded. Bollinger reports a mycotic disease of the trachea and lungs in birds.

[Footnote 26: D. Z. f. Thiermed. u. vergleich. Pathol., vi., 1879, p. 7.]

[Footnote 27: Damman, in D. Zeitsch. f. Thiermed., 1876, p. 1.]

Friedberger's report,[28] presented to the Veterinary Society of Munich, on croup and diphtheria of domestic fowls, leaves no doubt as to its frequency, particularly amongst the nobler varieties.

[Footnote 28: D. Zeitsch. f. Thiermed., v., 1879, p. 16.]

Nicati[29] studied an epidemic diphtheria amongst hens which had similar symptoms and a course very much like that in man; it could be inoculated into other animals, and was contemporaneous with the outbreak of the epidemic amongst the human population of Marseilles. Trasbot[30] succeeded in inoculating a healthy hen from a diphtheritic one, but the {684} attempts at transmission to dog, pig, and man were unsuccessful. The Med. and Surg. Journal[31] contains the following: In a house at Ogdensburg, N.Y., five children were ill with diphtheria. Three kittens who had been playing with them from time to time took the disease and died. Post-mortem examination showed diphtheritic membranes in their throats.[32]

[Footnote 29: Revue d'Hygiène et de Police sanitaire, 1879, p. 3.]

[Footnote 30: "De la transmission de la Diphth. des Animaux à l'Homme," Gaz. hebdom., 1879 Avril 25.]

[Footnote 31: Med. Rec., Nov. 8, 1879.]

[Footnote 32: An elaborate description of the croupo-diphtheritic inflammations of mucous membranes in hens, turkeys, pheasants, and pigeons may be found in Zürn. Krankh. d. Hausgeflügels, 1882, p. 104.]

Gerhardt[33] reports the following: 2600 hens were imported from Verona, Italy, into a village, Messelhausen, in Baden. Some of these hens were affected with diphtheria when they arrived. Within six weeks 600 of their number died of diphtheria, and 800 more soon after. In the following summer 1000 chickens were raised by artificial breeding, all of which died of diphtheria within six weeks. Five cats kept in the place also died of diphtheria; a parrot fell sick with it, but recovered. An Italian cook, suffering from diphtheria, in the month of November, 1881, while being subjected to local treatment with carbolic acid, bit the head-nurse's left foot and hand. Both these wounds became diphtheritic, the man falling sick with high fever, and requiring three weeks for his gradual recovery. Besides, four of the six workingmen employed in taking care of the hens of the establishment were taken with diphtheria. Not a single case, however, occurred in the neighboring village. Thus, it is safe to assume that the diphtheritic disease of hens can be transmitted to man.

[Footnote 33: Verhandlungen des (ii.) Congresses für Innere Medicin, Wiesbaden, 1883, p. 129.]

Diphtheria may be also produced by outside influences. In this regard the attempts at generating pseudo-membranes by artificial means are very interesting indeed. As early as 1826, Bretonneau, by the introduction of tincture of cantharides and olive oil into the trachea, succeeded in producing a "dense, elastic, reed-like membranous concretion." Delafond called croup into existence by the use of ammonia, oxygen, chlorine, corrosive sublimate, arsenic, and sulphuric acid. On the other hand, H. Mayer asserts that it is impossible, by means of ammonia, to produce a croup in the windpipes of animals which in the slightest degree resembles that occurring in human beings. Trendelenburg, however, after producing membranes in the trachea by the use of a solution of corrosive sublimate (1:120), succeeded in hardening the entire mass with bichromate of potassium, which it was impossible to do with the most tenacious mucus.

Rey observed croup in horses that inhaled smoke in a burning stable.[34] In the collection of the veterinary school of Zurich there is a croup membrane from a heifer which had been exposed to a fire; at Munich, one from the trachea of a horse, produced by forcibly injecting medicines into the nose. Hahn made an observation on cows, W. Ammon on horses, of long croup membranes after the animals had been exposed to smoke and fire; and Oertel constantly insists on there being "no actual difference between croup as it ordinarily occurs and that excited in the windpipe of a rabbit by means of ammonia. The color and texture, the physical, chemical, and histological characteristics, are identical."

[Footnote 34: Journ. de méd. vét. de Lyon, 1850, p. 249.]

{685} MORBID ANATOMY.--Either the membrane or the granular infiltration is characteristic of diphtheria. The statement that the former occurs only when atmospheric air can gain access thereto, as A. d'Espine and C. Picot still hold,[35] is plainly contradicted by its appearance on the mucous membrane of the lower intestines. The condition of the membrane is not unalterable, any more than the clinical symptoms of the disease, for, according to different circumstances, epithelium, mucus, blood, and vegetable parasites are added thereto. The membrane can either be lifted from the mucous membrane on which it lies or is imbedded into and underneath it. In the first instance, it consists to a great extent of fibrin, the result either of epithelial changes or derived directly from the exuded blood-serum. E. Wagner, who makes no anatomical distinction between croup and diphtheria, considers epithelial changes the principal source. The pavement epithelium becomes altered in a peculiar manner. It becomes turbid, larger, dentated, and dissolves into a network; it is at first uninhabited, but serves later as the vehicle of newly-formed cells; there also occurs a considerable infiltration of the mucous membrane pus-cells and granules; besides, the cellular tissue is studded with granules, the granular degeneration resulting sometimes in necrotic destruction, which is looked upon by Virchow as the most important element in severe forms of diphtheria. The several conditions or degrees may occur independent of each other, associated or in succession. Classen shares Wagner's views, but, according to Boldygrew, the pseudo-membrane consists of successive coagulations of a fibrinous fluid which exudes from the diseased surface. Steudener also opposes the views of Wagner. He does not believe in the probability of an exclusively endogenous origin of the cellular elements of croup membrane; in fact, he doubts the occurrence of an endogenous formation of pus-globules in epithelium. Croupous membrane, according to him, is formed by the migration of numerous white blood-globules through the walls of the vessels in the mucous membrane, and by a direct formation of fibrin from the transuded plasma. In addition to this, the mucous membrane is stripped of its epithelium (except at the mouths of the acinous glands) and infiltrated with migrating cells. Fresh croupous membrane consists of a delicate network of homogeneous structure and shining appearance, in which numerous cells and the epithelium of the various layers of the trachea are imbedded. In old membranes the cells are destroyed by granular degeneration and general maceration. Tenacious mucus with pus-cells and detritus are then found. C. Weigert looks upon the deposits as analogous to those on serous membranes. Every inflammation yields an exudation which may coagulate when the coagulating ferment is added. This latter is probably produced by the white blood-cells when in disintegration. But he does not say why it is that there is no such coagulation in suppurative processes, where the leucocytes are more numerous. He believes himself justified in establishing pathological differences of croup, pseudo-diphtheria, and diphtheria. A croupous inflammation means destruction of epithelium, which gives rise to a fibrinous exudation upon the surface, while the cellular tissue remains intact. The only difference between it and the pseudo-diphtheritic inflammation is looked for in the larger number of emigrated white {686} blood-cells. The superficial deposit consists, to a great part, of them and the fibrinous exudation. When there are but few leucocytes the deposit is a network of fibrillæ (croup). When there are many, the masses are more solid and voluminous (pseudo-diphtheritis). When, however, the tissue is changed into a hard substance resembling coagulated fibrin, when the exudation does not exist on the surface, but takes place into the mucous membrane, the process is diphtheria. Zahn also establishes three varieties--viz. 1st, such as result from a peculiar degeneration of pavement epithelium; 2d, such as originate in the solidification of a muco-fibrinous, and, 3d, of a fibrino-purulent, exudation. Each of these varieties may contain colonies of micrococci, but these organisms are neither essential nor are they constantly found.

[Footnote 35: Man. prat. des mal. de l'enfance, 1877, p. 81.]

The diphtheritic process does not merely consist of the membranous changes in the pharynx and air-passages. Its fatal cases have afforded marked evidence of the implication of most of the organs. Reimer's 17 cases give the following post-mortem results: the lungs were hyperæmic in 8 cases, twice the seat of pneumonia, and three times of embolic infarctions; in addition, emphysema in 12, oedema in 6, atelectasis in 7, subpleural ecchymoses in 7, pericardial ones in 4. The heart-muscle had undergone fatty degeneration in 6, and was the seat of ecchymoses of the size of a pin's head in 3. In addition to frequent hyperæmic conditions of the abdominal viscera, emboli of the liver in 3 (with capillary hemorrhages of the peritoneal covering in 1), emboli of the spleen in 5, desquamative nephritis in 7 (in 6 of which there were colonies of micrococci in the uriniferous tubules), cellular hyperplasia of the cervical and mediastinal glands in 14 (complicated in 6 with capillary hemorrhages in the glandular tissue). The blood was frequently normal, very often watery and dark, at times leucocythæmic. Thus the disease exerts its influence everywhere.

Rindfleisch defines diphtheritic inflammation as that form of inflammation which produces a coagulating necrosis in the tissues by the immigration of schizomycetæ. The coagulating necrosis differs from the usual form of necrosis in this, that the change from life to death is accompanied with the coagulation of fluid albuminoids. This process takes place mainly in the interior of cells and other parts of tissues, and therein differs from the coagulation of fibrin. In the cells there is taking place a peculiar homogenization of protoplasm; at the same time the nuclei disappear, and are changed into irregular masses liable to cohere and form membranous conglomerates, which owe their peculiar wax color to the invasion of a solid albuminoid endowed with a strong tendency to refract the light. Coagulating necrosis is found in circumscribed localities, and gives rise, in the neighborhood, to a marked amount of inflammation and suppuration, which leads to the expulsion of the necrotic part, with more or less loss of substance--either mild or phagedenic ulceration.

Leyden describes a gray degeneration of the muscular tissue which he believes to be truly inflammatory, and Unruh has lately published an account of some cases in which myocarditis occurred. In Leyden's cases, the muscular nuclei were increased, became atrophied, and underwent fatty degeneration, giving rise thereby to extravasations, softening, dilatation and debility of the heart, with general debility, collapse, {687} and--probably by reflex action on other branches of the pneumogastric--vomiting. Micrococci he found neither in the heart nor in the kidneys.

In the heart, particularly on the right side, numerous thrombi are frequently found in various stages of development; its muscular tissue is often in a state of fatty degeneration or the seat of parenchymatous inflammation and hemorrhages. Bridges first called attention to the occurrence of endocarditis in diphtheria.[36] This complication, which, however, occurs more frequently with rheumatism, puerperal fever, diphtheria of wounds, pyæmia, and old valvular affections than in the course of an acute diphtheria, does not, as found in the latter affection, consist simply of a fatty degeneration and subsequent ulceration, but is considered a genuine diphtheritic process (Virchow), affecting the mitral valve more frequently than the tricuspid or pulmonary valves. It begins with hyperæmia and the exudation of plasma in the cellular elements, so that they appear larger and darker. The granulations which form are frail and easily destroyed, so that ulcers form on which fibrin is deposited, and whence it is conveyed as emboli into the terminal arteries (Cohnheim) of the spleen, nerves, brain, and eye. Infarctions may also occur in the valveless veins of these organs, giving rise rather to small multiple abscesses than to large purulent collections. Suppuration but rarely takes place in the heart; the granular mass found there resists the action of æther and alcohol, and spreads throughout the cardiac parenchyma, so that perforation of the septum and of the right auricle and aorta has been observed.

[Footnote 36: Med. Times and Gaz., ii. p. 204.]

Bouchut and Labadie-Lagrave, out of 15 cases of diphtheria, met in 14 with a plastic endocarditis, which became the source of emboli. Thus, there were infarctions of the lungs, at times in their centre colorless, at other times in a state of purulent degeneration; superficial thrombi of the small veins of the heart, subcutaneous connective tissue, pia mater, brain, and liver; and in addition, moderate leucocytosis.

The lungs exhibit (post-mortem) all sorts of inflammatory and congestive conditions, with their consequences, as oedema, catarrh, broncho-pneumonia, atelectasis, emphysema, ecchymoses, and large infarctions.

The spleen (and occasionally the liver) is frequently large, congested, and friable, and studded with infarctions to a greater or less extent.

The kidneys are either simply congested or the seat of nephritis or infarctions. The same forms of inflammation which accompany scarlatina--to wit, the desquamative and the diffuse--are here observed. The diffuse form is not of so frequent occurrence as in scarlatina, but is sometimes extensive and dangerous.

The muscles occasionally exhibit ecchymoses, and are at times the seat of parenchymatous inflammation, gray degeneration, and atrophy.

The lymphatic glands are frequently inflamed and swollen, either hard or doughy, oedematous or congested. Large abscesses are rare. It is more especially the gland tissue, and less the connective tissue of the glands, which takes part in the pathological process. The periglandular tissue very soon becomes involved, however. Necrotic foci have been described by Bizzozero. When the entire surface of the mucous membrane of the mouth and of the air-passages, from the nose to the trachea, is the seat of the disease, there is an impregnation of the mucous membrane, from the epithelial surface to the submucous tissue, of the entire {688} tongue, borders of the lips, and frequently of the lips and cheeks, as well as of the tonsils, the lower portion of the nasal cavities and the upper, and especially the anterior, portion of the larynx. The fossæ Morgagni and the posterior aspect of the soft palate are more frequently affected in the same way than the anterior aspect. Small isolated spots are found on the tonsils and occasionally on the posterior wall of the pharynx. The so-called croupous form--that is to say, the one in which the membranes deposited may either be removed in large patches or lie macerated in the profuse secretion of subjacent mucous glands--is found partly in the nasal cavities, on the posterior surface of the soft palate, and also in the trachea and its subdivisions.

The character of the mucous membrane varies with the locality. Its different elements, as the epithelium, the basement membrane, the connective tissue mingled with elastic fibres, the blood-vessels, the nerves from the cerebro-spinal and sympathetic systems, and the papillæ and ducts of numberless glands, all influence the pathological process going on upon the surface. Their distribution in the oral cavity and the respiratory organs is a very interesting study, and in a table already published,[37] I have exhibited it in a condensed tabular form.

[Footnote 37: Treatise on Diphtheria, p. 126.]

Where elastic tissue predominates, diphtheritic impregnation is slow to take place, and recovery is also slow when the tissue has finally submitted. Pavement epithelium yields the easiest foothold to diphtheritic membrane. Thus it is that the tonsils, not from their prominent situation alone, favor the reception and development of the infection. But the elastic and connective fibres when once affected are apt to harbor the disease a long time. Still, there is another reason why the diphtheritic process should favor the tonsils. For Th. Höhr has demonstrated that their epithelium exhibits interruptions in its continuity. Through them round cells may emigrate. Wherever the epithelial covering of the integuments (skin or mucous membrane) is intact and unbroken, diphtheria takes hold with difficulty. But where a defect is established, large or small, diphtheritic formations will be apt to take place according to the size of the abrasion. This is one of the modes of the formation of small diphtheritic deposits on the tonsils, which it has been the tendency of many, both practitioners and authors, to honor with special names.

Ciliated epithelium is not so liable to be affected. It occupies a higher rank in the scale of animal formations, has a more complex function and a greater power of resistance. The presence of a large number of mucous glands impedes, as a rule, by the presence of the normal secretion, an extensive destructive action upon the tissues. The secreted mucus assists in removing epithelial masses, and even fibrinous exudations, from the surface. Thus it is that the deposits in the respiratory portion of the nasal cavities are frequently cast off through the nostrils, and in a similar manner the membranes that have formed in the trachea are ejected in a semi-solid condition through the opening made by tracheotomy. The large number of mucous glands in the larynx and trachea is unquestionably the reason why the lymphatic vessels of the mucous membrane are not influenced by the overlying loosened masses, and will not absorb; hence laryngeal and tracheal diphtheria, when not complicated, have decidedly a local character, and are usually devoid of constitutional symptoms. For the {689} same reason the usual form of tonsillar diphtheria is a mild disease. On the other hand, the large number and size of the lymphatic ducts of the Schneiderian mucous membrane, as well as their direct communication with the lymphatic glands of the neck, accounts for the dangerous character of nasal diphtheria.

Diphtheria of the intestinal canal is characterized by fibrinous deposits on the surface and in the tissues of the intestine, with subsequent granular degeneration. It is mostly preceded by a catarrhal process. The same condition is found in the urinary organs.

There are but few autopsies of cases which have died of, or during, diphtheritic paralysis. In some instances there was considerable thickening of the spinal nerves at the junction of the posterior and anterior roots, with hemorrhages. The superficial connective tissue in these places exhibited a diphtheritic exudation (Buhl). There was in the sheath of the nerves of the cerebral and spinal meninges and in the gray substance of the cord voluminous nuclear infiltration; in one case there were extensive hemorrhages in the spinal meninges, with nuclear proliferation in the gray substance of the cord (Oertel). Disseminated meningitis with perineuritis of the neighboring roots, characterized by infiltration of nuclei between the nerve-fibrillæ was found by Pierret; and degeneration of the palatine nerves and fatty degeneration of the palatine muscles by Charcot and Vulpian. Dejerine, in five autopsies, records an atrophy of the anterior roots secondary to a myelitic degeneration of the ganglia of the anterior horns. E. Gaucher found the same in the case of a boy who died with paralysis of the muscles of deglutition, of the extremities, and of the trunk. In a child of two years with paralysis of the palate and extremities the autopsy was negative. In two cases Dejerine reports finding changes in the intramuscular nerves, such as liquefaction of myelin and loss of axis cylinders.

Thus, Buhl, Charcot, Vulpian, and Dejerine are unanimous about an affection of the peripheric nerves and muscles. Oertel, Dejerine, and Gaucher believe in a disease of the spinal cord. It is true that a disease of the gray substance would fully explain the symptoms of the bad cases, but what we know of poliomyelitis anterior, with which this affection would be identical, precludes the idea of the rapid and almost certain complete recovery. Therefore, in most cases, diphtheritic paralysis consists of a trophic affection of the motor system, almost always seated peripherally in the nerves and muscles, seldom, if ever, in the centres. This affection must be compared, in most of its relations, with the degenerative processes taking place in the muscular tissue after typhoid fever, or in the renal epithelium after infectious diseases, both of which give rise to serious results, with usually a favorable termination.

DIAGNOSIS.--The characteristic sign of diphtheria is either the membrane or the gray infiltration, with more or less injection of the surrounding parts. In regard to this greater or less injection, I will say that pharyngeal congestion, when it is uniform, may or may not point to imminent diphtheria. When it is local, confined to one side mainly, it is either traumatic or diphtheritic. White spots which are easily washed away, or which can be removed with a brush, or squeezed out of the follicles of the tonsils, into which a probe can be introduced sometimes to the depth of one-half inch, soon announce their true character--viz. either a {690} simple catarrhal secretion or suppuration. Even though the superficial deposit contain oidium or leptothrix in considerable numbers, it can easily be removed; I have only known the totally inexperienced to mistake muguet (thrush) for diphtheria. In the larynx muguet is, moreover, very rare indeed, and always circumscribed. It is sometimes seen on the true vocal cords. The gray discoloration of superficial follicular ulcerations, as observed in the ordinary form of stomatitis follicularis, can hardly fail to be recognized. Such patches are very numerous in the fauces and on the lips and cheeks--never on the gums, except in ulcerous stomatitis (which is not follicular). They are accompanied, too, by vesicles containing more or less serum which have not yet ruptured. It must be remembered, however, that the mucous membrane, when deprived of its superficial covering, is liable during an epidemic of diphtheria to become infected, like every other wound. I have seen cases in which stomatitis and diphtheria existed side by side, the latter having invaded the surfaces exposed by the former. The examination of the entire throat is not always easy. Very young children vomit frequently and persistently before the whole surface is exposed to view, and not infrequently repeated examination with the spatula is absolutely necessary. In general, however, the slight attempts at vomiting suffice to cause a great part of the swollen posterior portion of the tonsils to become visible. I have heard that the pale surface of old hyperplastic tonsils has been mistaken for diphtheria; I merely mention the fact. When a discoloration happens to be the result of a deposited flake of mucus, a drink of water will remove it.

Fever is not always a prominent symptom; as a rule, simple diphtheria of the tonsils is accompanied by very little fever. Still, there are plenty of exceptions. But the differences of temperature are not more striking than in most other infectious diseases, whose either mild or severe invasion may offer an obstacle to immediate diagnosis. As the height of the fever does not absolutely determine, or even indicate, the character of the subsequent course of the disease, but little importance is to be attached to the temperature unless there be a very marked elevation. A sudden rise frequently occurs with lymphadenitis. High fever in the beginning may render the diagnosis difficult or may postpone it.

The absence of glandular swelling does not exclude the diagnosis of diphtheria, for when the tonsils are affected by the disease there is usually little or no swelling of the neighboring glands. Swelling of the glands enables us to locate the affection in a mucous membrane richly endowed with lymphatic vessels. It is very marked when the nose is affected. A few hours' duration of nasal diphtheria suffices for the development of a severe lymphadenitis, especially at the angles of the jaw. When the latter condition is found to exist, the throat should be examined with the idea of finding a membrane extending upward; nasal diphtheria is very liable to complicate an affection of the uvula and arches of the palate. The membrane cannot well be seen by looking through the nostrils; highly serviceable for this purpose is a very short, broad rhinoscope reaching upward to the bony structure of the nose. However, nasal diphtheria may frequently be diagnosticated some days before the membrane becomes visible, by the rapid development of lymphadenitis; this may be done even where the sweetish, musty odor of certain forms {691} of diphtheria is absent. Still, nasal diphtheria may occur without much lymphadenitis; as, for instance, when the blood-vessels are very numerous and superficial, and thereby give rise to slight hemorrhages at the very beginning of the sickness. In such cases the lymphatic vessels are little, if at all, required to transmit the poison, the open blood-vessels replacing them in the function of absorbing. Naturally, there are cases in which an ocular examination cannot be satisfactorily made. In the journals we read of brilliant results of rhinoscopic and laryngoscopic examination; in practice we see but few. This holds good especially for the cases of dyspnoea accompanying laryngeal diphtheria, where the diagnosis may be doubtful when no membrane can be detected in the fauces; even if membrane be observed there, symptoms of suffocation may still arise from a laryngeal stenosis independent of membranous deposits in the larynx. If aphonia and difficulty of both inspiration and expiration be present at the same time, there is certainly membranous occlusion. If aphonia appear late, or even toward the very last, and only inspiration be impeded while expiration is comparatively free, there is an oedematous saturation of the ary-epiglottidean folds and of their copious submucous tissue, and consequently of the posterior attachment of the vocal cords. Although a general oedema glottidis in connection with diphtheria is of exceedingly rare occurrence, the above condition is not at all uncommon, and has forced me to tracheotomize many times; but, again, a comprehension of the true condition, where it occurred in not very severe cases, has on several occasions enabled me to avoid an operation. This local oedema may sometimes be detected by palpation in the region of the swollen posterior wall of the pharynx.

One of the diagnostic symptoms of membranous laryngitis, believed in and referred to by Krönlein, does not exist--viz. the swelling of the lymphatic glands, which in his opinion is pathognomonic. Not only is that not the case, but the absence or scarcity of lymphatics on the vocal cords and in their neighborhood renders the absence of glandular swellings a necessity, provided the latter do not depend on complicating diphtheria in other localities. In uncomplicated diphtheritic laryngitis I expect no lymphadenitis. The character of the laryngeal pseudo-membrane does not depend at all on the condition of the pharynx. The latter may have membranes of any description or consistency without permitting the diagnosis of the condition of the larynx. I lay stress on this fact because no less a writer than Krönlein believes that where there is but little or no membrane in the pharynx, that in the larynx is rather loose and movable.

One of the diagnostic symptoms of diphtheritic laryngitis, or membranous croup, is the relative absence of fever. Catarrhal laryngitis, or pseudo-croup, is a feverish disease. A sudden attack of croup with high temperature, provided there is no pharyngeal or other diphtheria present, yields a good prognosis; without much fever, a very doubtful one.

The diagnosis of diphtheritic paralysis offers very little difficulty in most cases. Its occurrence after an attack of diphtheria, its beginning in the fauces or in the muscles controlled by the ciliary nerves, the immunity of the sphincters, the gradual development, the irregularity of its progress, are good diagnostic points. Examination by the interrupted or continuous current is not conclusive. Very frequently in the {692} beginning the response to the interrupted current is normal, sometimes deficient; to the continuous current, exaggerated. After some time the power of both to excite contraction is diminished. When we reflect on the numerous causes which may underlie diphtheritic paralysis, and that we have not to deal with one and the same anatomical change in all cases, it becomes apparent that no reliable conclusions can be based upon electrical examination.

PROGNOSIS.--In general, the prognosis in diphtheria is favorable when the affected surface is of small extent and where such parts are the seat of disease as have little communication with the lymphatic system. To the latter class belongs simple diphtheria of the tonsils. Marked glandular swelling, particularly if arising suddenly, is always an unfavorable sign, and calls for the utmost caution in prognosis, especially if the region of the angles of the jaw be speedily and markedly infiltrated. This, as we have seen, is particularly apt to occur with nasal diphtheria, whether developed primarily, (and then accompanied by a thin fetid discharge), or, as is more commonly the case, secondarily from an affection of the pharynx and palate which ascends into the posterior nares. With the appropriate local disinfection this form of the disease is neither so alarmingly dangerous as Oertel depicts it, nor so assuredly fatal as Roger but a few years ago taught in his clinique, or as Kohts appears to believe,[38] yet it is ever grave. With energetic treatment many cases will, however, get well. Diphtheria of wounds, complicating diphtheria of the pharynx, is always an unfavorable sign; that of the mouth and angles of the mouth, associating itself with a previously existing diphtheria, having an indolent course, and producing more frequently a deep impregnation of the tissues than a thick deposit, causes a painful and serious condition. Diphtheria of the larynx, whether it be of primary origin or the result of extension from the fauces, is nearly always fatal. In severe epidemics the mortality is 95 per cent. Tracheotomy, too, saves but few of those who take the disease at such a time. In fifty consecutive tracheotomies from 1872 to 1874 I did not see one recovery. In the last few years I have seen few good results. In average epidemics tracheotomy will save 20 per cent. A pulse of 140 to 160, and high fever immediately after the operation, render the prognosis bad; so does absence of complete relief after the operation. An almost normal temperature the day after the operation is an agreeable symptom, but does not exclude a downward extension of the diphtheritic process, and hence cannot be looked upon as assuring a favorable prognosis. A marked elevation of temperature is apt to indicate a renewed attack of diphtheria or a rapidly-appearing pneumonia, and is an unfavorable symptom. A dry character of the respiratory murmur some time after tracheotomy indicates the approach of death within from twelve to twenty-four hours from descent of the membrane; so does cyanosis, whatever be its degree of intensity. Diphtheria of the trachea, which ascends to the larynx, is positively fatal. It has a rapid course, and tracheotomy only postpones the end for a little while, if at all. The general health and strength of the little sufferer have no influence whatever.

[Footnote 38: Gerhardt, Handb. d. Kinderkr., iii., 2, p. 20, 1878.]

Thick, solid deposits need not of themselves render the prognosis so unfavorable as do septic and gangrenous forms. Even in the nose they {693} are not of as serious import as the thin, putrid discharge. I have seen recovery ensue in cases where I was obliged to bore through the occluded nasal cavities with probes and scoops. Fetid, putrid discharges are unfavorable, but in no wise fatal; conscientious disinfection accomplishes a great deal. Slight epistaxis indicates the possibility of rapid absorption through the blood-vessels; but here, too, the final result depends on whether the disinfection be equally rapid and thorough. The same holds true for the sweetish, fetid odor of the breath, whether of the nose or mouth, which, on the one hand, demonstrates the significance of the disease, while, on the other hand, it indicates the possibility of infection by inhalation.

The height of the fever is not in proportion to the danger in any individual case; some have a favorable, some an unfavorable termination, without fever of any account. Simple catarrh of the pharynx and larynx frequently begins with a sudden and marked rise of temperature; diphtheria in the same parts but rarely. There are cases, however, in which the height of the fever and the deposited membranes are in inverse proportion to each other. In these cases the fever may subside rapidly, owing to a speedy elimination of the poison. Young children only are in danger of death from convulsions or a rapid tissue-degeneration due to hyperpyrexia. If the temperature rise suddenly after some days of sickness, either a complication or a fatal termination is to be apprehended. Yet, there are as many deaths in cases with comparatively low as with very high temperatures. Whether collapse has resulted rapidly or slowly, the patient dies often with low temperature. Thus, a rapid elevation is hardly a more unfavorable sign than a rapid fall. The pulse, too, may be very variable. True, a small, rapid, and irregular pulse is always unfavorable, because it indicates a weakening of the cardiac function; yet as long as it retains an approximately normal relation to the frequency of respiration a rapid pulse gives no cause for alarm. Moreover, the pulse is not always rapid when the strength gives way. It occasionally becomes slower, and sometimes very slow, and may then become a dangerous symptom.

Every complication adds to the danger. Bronchitis and pneumonia are not infrequent, yet I have seen cases of laryngeal diphtheria recover in which I had suspected pneumonia before performing tracheotomy, and was enabled to diagnosticate it after operating. Albuminuria in the early part of a diphtheritic attack with high fever is of little significance; nephritis, later in the course of the disease, partakes of the character of scarlatinous nephritis; cases of acute diffuse renal disease are fortunately infrequent, and the remainder are very submissive to treatment. The cases of diphtheria complicated with endocarditis in my practice have ended fatally. An early affection of the sensorium, not dependent on pressure upon the jugulars by greatly swollen glands, is an unfavorable symptom. Purpura, with profuse hemorrhages and a livid hue of the skin, is ominous; icteric discoloration, together with marked glandular and periglandular tumefaction, is absolutely fatal.

Most cases of diphtheria of the pharynx and of the tonsils have a favorable termination, yet a positive prognosis can in no case be given with certainty. Still, even in malignant epidemics the mortality is not very great, for even though there be a large number of severe cases in {694} any one epidemic, yet it is greatly overbalanced by the number of moderately severe and mild ones. True, not a few cases end fatally in several days, owing to the high fever, or to septic absorption, or nephritis, or croup, but the majority of cases end in recovery in one or two weeks. Yet diphtheria does not always take so regular a course; not infrequently, after the pulse has become stronger, the appetite improved, and the pharynx cleared, and the patient is apparently on the high road to recovery, another attack occurs accompanied by fever, as before, and a rapid formation of membrane. Occasionally two or three such relapses may occur in the course of three, four, or five weeks; not to speak of the fact that those who have once suffered from diphtheria are more susceptible to the action of the poison than those who never suffered before.

TREATMENT.--Every case should be treated on general principles; thus, it is not possible to lay down a routine treatment for every individual case. High fever should be reduced by sponging and bathing, quinia, and sodium salicylate; collapse speedily treated, and severe reflex symptoms, as vomiting, etc., checked at once. Whether to employ for this purpose ether, wine, cognac, champagne, or coffee must be decided by the physician in individual cases. The administration of the remedy, whether by mouth, by injection into the bowels, or subcutaneously, as I have employed cognac, ether, alcohol, and camphor dissolved in ether or alcohol, in some cases with decided and rapid success, must depend on the condition of the organs and on the urgency of the case. However, all the above remedies are frequently of no service, because administered too late and in too small doses. If I have ever had cause to feel contented with the results of treatment in diphtheria, it is owing to the fact that I lost no time. No medicines, however, must be resorted to which are apt to derange the digestion of the patient; alcoholic stimulants must be given in fair dilution only, for that reason. The nourishment of the patient is a matter of very great importance. On general principles it is true that care must be taken in regard to food administered to febrile patients, but we must bear in mind that, when the lymphatic vessels are kept empty and no new and proper material is introduced into them, the absorption of locally-existing poisonous substances is proportionately increased. Hungry lymph-vessels are the organism's fiercest enemies.

I dwell particularly on the foregoing remarks for the reason that in diphtheria, unlike certain diseases having a typical course and those of a simple inflammatory character, expectant treatment should not be indulged in. Oertel's advice, that when neither high fever nor complications are present we should quietly wait, and "act only when new and most alarming symptoms present themselves," is decidedly perilous. A mild invasion does not assure a mild course. Never has a "possibly superfluous" tonic or stimulant done harm in diphtheria, but many a case has a sad termination because of a sudden change in the character of the disease, putting the bright hopes of the physician to shame. Only the philosopher may be a passive spectator; the physician must be a guardian. When I again read, in the work of the same meritorious author, "that when in exceptional cases, in children and young people, death is imminent, not from suffocating symptoms in the larynx and trachea, but from septic disease and blood-poisoning, it is necessary to resort to {695} powerful stimulants," it strikes me that he is frequently too dilatory with his remedies, and, furthermore, that his experience concerning the terrible septic form of diphtheria which is so frequently met with in some epidemics must have been very limited at the time he was writing. In New York, during the past twenty-five years, for every death from diphtheritic laryngeal stenosis (membranous croup) there have been three from diphtheritic sepsis or from exhaustion.[39]

[Footnote 39: We have to improve somewhat on the plan of Thomas Wilson, though his general instructions be good (as laid down in his Tentamen medicum inaugurale de cynanche maliqna, Edinb., 1790, p. 24): "Cum hactenus nullum inventum est remedium quod contagionem in corpus receptam suffocare possit; cum medicamenta pleraque quæ putredinem corrigere dicuntur, corpus ejusque functiones manifesto roborant; et denique cum hunc morbum comitantur virium prostratio, et, etiam ab initio, summa functionum debilitas, qualis evacuantia omnigena prohibet, indicationem curandi unicam, scil. debilitatis effectibus obviam ire, proponam. Hinc corporis conditioni obviam itur præcipue tonica et stimulantia administrando." (As no remedy has yet been found which can extinguish the contagion after it has been received into the body; as most medicines which have the reputation of correcting putrefaction are roborants for the body and its functions; and, lastly, as this disease is attended with great prostration and such debility of functions as to preclude the use of all sorts of evacuants,--I propose but this one indication for treatment--viz. to meet the effects of debility. This is fulfilled by the administration mainly of tonics and stimulants.)]

In regard to the dose of stimulants, it is a fact that there is more danger in diphtheria from giving too little than too much. When the pulse barely begins to be small and frequent they must be administered at once. A three-year-old child can comfortably take thirty to one hundred and fifty grammes (fl. oz. j-v) of cognac, or one to five grammes of carbonate of ammonium, or a gramme of musk or camphor (gr. xv) and more, in twenty-four hours. In the septic form especially the intoxicating action of alcohol is out of the question; the pulse becomes stronger and slower, and the patient enjoys rest. In those cases in which the pulse is slow, together with a weak heart's action, the dose can hardly be too large. The fear of a bold administration of stimulants will vanish, as does that of the use of large doses of opium in peritonitis, of quinia in pneumonia, or of iodide of potassium in meningitis or syphilis. I know that cases of young children with general sepsis commenced immediately to improve when their one hundred grammes (fl. oz. iij) of brandy were increased to four times that amount in a day.

The remarks I have made in reference to the general treatment of diphtheria naturally render superfluous a discussion of the value of abstraction of blood. To be sure, it could only be a question of local bleeding. For nobody would dare to resort to jugular venesection, as our predecessors did in the last century. It may be safely asserted of the latter that it has no influence on the process, but frequently increases the local swelling and makes the patient more anæmic. There is no case in which a resort to it would not be criminal. I can distinctly recall the time when bleeding and calomel formed the groundwork of the treatment. Until the year 1862 the death-rate in Rupert, Vermont, from diphtheria was 90 per cent., according to the reports of the local physicians, and particularly of my pupil, Dr. Guild, who at that time finished his studies in New York and commenced practising. When, in the same epidemic, bleeding and calomel were replaced by stimulants and iron, with the chlorate of potassium, 90 per cent. recovered.

That attention must be paid to the general condition mainly during a {696} retarded convalescence from previous sickness is self-evident. Any complications, too, must be subjected to early treatment. Diarrhoea must be mentioned among these; it reduces the patient's strength very quickly; likewise, the early appearing nephritis, which may suddenly end life.

In this connection I must allude to the great danger of self-infection, which may occur in every variety of cases, severe or mild. The poison is diffused by expiration and expectoration. Though care may have been taken to disinfect the linen, towels, handkerchiefs, the bedstead and bedding, chairs and wall-papers, and carpets and curtains, even the clothing of the attendants will be infected. While the patient is getting well he will be infected again, and have a more serious relapse; and a third one, and succumb. I have met with such cases often, and with some which went from one attack into another, and would certainly have perished but for their removal to a distant part of the town. Where there are vacant rooms the indication is to change rooms every few days and to thoroughly disinfect (with sulphurous acid) that which has been used and infected.

One important axiom must be borne in mind--namely, that prevention is easier than cure. I do not refer simply to the removal of the healthy members of the family beyond the danger of infection or to the isolation of the patient. If the latter becomes necessary, the first indication is his removal to the top floor of the house. There are, in addition, however, certain prophylactic measures which will prove valuable in the hands of every good physician. It is necessary under all circumstances that the mouth and pharynx of every child be constantly kept in a healthy condition. Eruptions of the scalp must be treated at once, and glandular swellings of the neck caused to disappear. Some cases of laryngeal diphtheria have been traced directly to the presence of suppurating bronchial glands, with or without perforation.[40] The same rule applies to nasal and pharyngeal catarrhs, the treatment of which should be commenced in warm seasons, when general or local remedies yield better results. Enlarged tonsils should be resected, or, where that can not be done, scraped out with Simon's spoon, at a time when no diphtheritic epidemic is raging. It is important that this take place at a time when, even though sporadic cases of diphtheria occur, the danger of infection is not great; for during the height of an epidemic every wound will give rise to general or local infection. This holds good for any part of the body as well as of the mouth. I avoid, therefore, an operation at such a time, provided it can be postponed.

[Footnote 40: Weigert, in Virch. Arch., vol. lxxvii., p. 294, 1879.]

Prevention, after all, is not the business of the physician only, but just as much that of the individual or the complex of individuals--viz. the town, the state, and the nation. Those sick with diphtheria must be isolated, though the case appear ever so mild, and, if possible, the other children must be sent out of the house altogether. If that be impossible, let them remain outside the house, in the open air, as long as feasible, with open bedroom windows during the night, in the most distant part of the house, and let their throats, and those of their nurses, be examined every day. The watching eye of a father or mother will discover deviations from the norm, so that the physician can be notified. Let the temperatures {697} of the well children be taken once a day, toward evening. Ten minutes of a mother's time are well paid by the discovery of a slight anomaly which may require the attention of the physician. Happily, there are now many mothers who keep and value a self-registering thermometer as an important addition to their household articles. The attendant upon a case of diphtheria must not get in contact with the rest of the family, particularly the children, after his visiting and handling the patient, for the poison may be carried, though the carrier remain well or apparently well. Unnecessary petting of the patient on the part of the well ought to be avoided, and kissing must be forbidden; the bed-clothing and linen should be changed often and disinfected, the air of the sick-chamber should be cool and often changed, and if possible the chamber itself should be changed every few days.

The well or apparently well children of a family that has diphtheria at home must not go to school nor to church. The former necessity is beginning to be recognized by the authorities and teachers, and also, in consequence of partially enforced habit, by parents; the latter will be resisted longer. Schools ought to be closed entirely when a number of cases have occurred. Even when the school-children have not been affected to a great extent, but an epidemic of diphtheria has commenced in earnest, it will be better to close the schools for a time. If that be not advisable, the teacher ought to be taught to examine throats, and directed to examine every child's throat each morning, and to send home every one with even suspicious appearances.

In times of an epidemic every public place, theatre, ball-room, dining-hall, or tavern ought to be subjected to supervision. Where there is a large conflux of people there are certainly many who carry the disease with them. Disinfection must be enforced by the authorities at regular intervals. Public vehicles must be treated in the same manner. That it should be so when a case of small-pox has happened to be carried in them appears quite natural. Hardly a livery-stable keeper would be found who would not be anxious to destroy the possibility of infection in any of his coaches. He must learn that diphtheria is, or may be, as dangerous a passenger as variola. And what is valid in the case of a poor hack is more so in that of railroad-cars, whether emigrant or Pullman. They ought to be thoroughly disinfected in times of an epidemic, at regular intervals, for the highroads of travel have always been those of epidemic diseases, and railroad officers and their families have often been the first victims of the imported scourge. Can that be accomplished? Will not railroad companies resist a plan of regular disinfection because of its expensiveness? Will there not be an outcry against this as despotic and as a violation of the rights of the citizen? Certainly there will be. But so there was also when municipal authorities began to compel parents to keep their children at home when they had contagious diseases in the family, and when a small-pox patient was arrested because of endangering the passengers in a public vehicle. In such cases it is not society that tyrannizes the individual; it is the individual that endangers society. And society begins at last, even in America, to believe in the rights of the commonwealth, and not in the rights of the democratic person only. The establishment of State and National Boards of Health proves that the narrow-hearted theories of the strict constructionists {698} have not only disappeared from our politics, but also from the conscience and intellect of society.

The sick room must be kept cool, the windows kept open--more or less--by night as well as by day, the floor frequently washed, the linen soaked at once, the excrements removed. Dead bodies ought to be kept moist, for infectious material, chemical or otherwise, will spread more easily when dry. Attendants must not talk unnecessarily over the mouth or diphtheritic wounds of the patient, and will do well to carry a little dry loose cotton--to be changed often--in each of the nostrils, for it aids in protecting those who are necessarily exposed to infection.[41]

[Footnote 41: Wernich, in F. Cohn's Beitr., iii., 1859, p. 115.]

A very important mode of prevention consists in disinfection. The experiments of Schotte and Gaertner, and of Sternberg, prove the inefficiency of small doses of most of the disinfectants in common use. The popular idea, sometimes even shared by physicians, that the faint odor of chloride of lime or of carbolic acid in a sick room or in a foul privy is evidence that the place is disinfected, is entirely erroneous. Particularly in regard to the latter agent, it may be stated at once that its employment for disinfecting purposes on a large scale is impracticable, both on account of the expensiveness of the pure acid and the enormous quantities required to produce the desired effect. For in regard to its efficiency it does not rank very high in comparison with a great many other articles, as may be seen from a table of the disinfectant properties of different chemicals published by Miquel in the Semaine Médicale.

For practical purposes I know of no better or simpler rules for disinfection than those published by the National Board of Health. In its Bulletin No. 10, of September 6, 1879, the following instructions for disinfection were published: Deodorizers, or substances which destroy smells, are not necessarily disinfectants, and disinfectants do not necessarily have an odor.

"Disinfection cannot compensate for want of cleanliness nor of ventilation.

"I. Disinfectants to be employed:

"1. Roll-sulphur (brimstone) for fumigation.

"2. Sulphate of iron (copperas) dissolved in water in the proportion of one and a half pounds to the gallon; for soil, sewers, etc.

"3. Sulphate of zinc and common salt, dissolved together in water in the proportion of four ounces sulphate and two ounces salt to the gallon; for clothing, bed-linen, etc."

Carbolic acid is not included in the above list, for the following reasons: It is very difficult to determine the quality of the commercial article, and the purchaser can never be certain of securing it of proper strength; it is expensive when of good quality, and experience has shown that it must be employed in comparatively large quantities to be of any use; it is liable by its strong odor to give a false sense of security.

"II. How to use disinfectants:

"1. In the sick-room.--The most available agents are fresh air and cleanliness. The clothing, towels, bed-linen, etc. should, on removal from the patient and before they are taken from the room, be placed in a pail or tub of the zinc solution, boiling hot if possible.

"All discharges should either be received in vessels containing copperas {699} solution, or, when this is impracticable, should be immediately covered with copperas solution. All vessels used about the patient should be cleansed with the same solution.

"Unnecessary furniture--especially that which is stuffed--carpets and hangings, should, when possible, be removed from the room at the outset; otherwise they should remain for subsequent fumigation and treatment.

"2. Fumigation with sulphur is the only practical method for disinfecting the house. For this purpose the rooms to be disinfected must be vacated. Heavy clothing, blankets, bedding, and other articles which cannot be treated with zinc solution should be opened and exposed during fumigation, as directed below. Close the rooms as tightly as possible, place the sulphur in iron pans supported upon bricks placed in wash-tubs containing a little water, set it on fire by hot coals or with the aid of a spoonful of alcohol, and allow the room to remain closed for twenty-four hours. For a room about ten feet square at least two pounds of sulphur should be used; for larger rooms proportionately increased quantities.

"3. Premises.--Cellars, yards, stables, gutters, privies, cesspools, water-closets, drains, sewers, etc. should be frequently and liberally treated with copperas solution. The copperas solution is easily prepared by hanging a basket containing about sixty pounds of copperas in a barrel of water.

"4. Body- and bed-clothing, etc.--It is best to burn all articles which have been in contact with persons sick with contagious or infectious diseases. Articles too valuable to be destroyed should be treated as follows:

"A. Cotton, linen, flannel, blankets, etc. should be treated with the boiling-hot zinc solution; introduce piece by piece; secure thorough wetting, and boil for at least half an hour.

"B. Heavy woollen clothing, silks, furs, stuffed bed-covers, beds, and other articles which cannot be treated with the zinc solution, should be hung in the room during fumigation, their surfaces thoroughly exposed and pockets turned inside out. Afterward, they should be hung in the open air, beaten, and shaken. Pillows, beds, stuffed mattresses, upholstered furniture, etc. should be cut open, the contents spread out, and thoroughly fumigated. Carpets are best fumigated on the floor, but should afterward be removed to the open air and thoroughly beaten.

"5. Corpses should be thoroughly washed with a zinc solution of double strength; should then be wrapped in a sheet wet with the zinc solution, and buried at once. Metallic, metal-lined, or air-tight coffins should be used when possible; certainly when the body is to be transported for any considerable distance.

"It might have been added here that no public funeral must be permitted."

In this connection I have to speak of a remedy which I class among the prophylactic agents--namely, the chlorate of potassium or the chlorate of sodium. I cannot say that I rely on either of these remedies as curative agents in diphtheria, and yet I employ them in almost every case. The reason lies in the fact that the chlorate is useful in most cases of stomatitis, and thereby acts as a preventive.

There are very few cases of diphtheria which do not exhibit larger surfaces of either pharyngitis or stomatitis than of diphtheritic membrane. There are also a number of cases of stomatitis and pharyngitis, {700} during every epidemic of diphtheria, which must be referred to the epidemic, sometimes as kindred diseases, and sometimes as introductory stages only, which, however, do not, or do not in the beginning, show the characteristic symptoms of the disease.

When, in 1860,[42] I wrote my first paper on diphtheria, I based it upon two hundred genuine cases, and at the same time enumerated one hundred and eighty-five cases of pharyngitis, which I considered to be brought on by epidemic influences, but which, the membrane being absent, could not be classified as bonâ fide cases of diphtheria.

[Footnote 42: Amer. Med. Times, Aug. 11th and 18th.]

Such cases of pharyngitis and stomatitis, no matter whether influenced by an epidemic or not, furnish the indication for the use of chlorate of potassium. They will usually get well with this treatment alone. The cases of genuine diphtheria, complicated with a great deal of stomatitis and pharyngitis, also indicate the use of chlorate of potassium; not, however, as a remedy for the diphtheria, but as a remedy for the accompanying catarrhal condition in the neighborhood of the diphtheritic exudation. For it is a fact that, as long as the parts in the neighborhood of the diphtheritic exudation are in a healthy condition, there is but little danger of the disease spreading over the surface. Whenever the neighboring surface is affected with catarrh or inflammation, or injured so that the epithelium gets loose or thrown off, the diphtheritic exudation will spread within a very short time. Thus chlorate of potassium or sodium, the latter of which is more soluble and more easily digested than the former, will act as a preventive rather than as a curative remedy. Therefore it is that common cases of pharyngeal diphtheria will recover under this treatment alone; and these are the cases which have given its reputation to chlorate of potassium as a remedy for diphtheria.

The dose of chlorate of potassium for a child two or three years old should not be larger than half a drachm (2 grammes) in twenty-four hours. A baby of one year or less should not take more than one scruple (1.25 grammes) a day. The dose for an adult should not be more than a drachm and a half, or at most two drachms (6 or 8 grammes), in the course of twenty-four hours.

The effect of the chlorate of potassium is partly a general and partly a local one. The general effect may be obtained by the use of occasional larger doses, but it is better not to strain the eliminating powers of the system. The local effect, however, cannot be obtained with occasional doses, but only by doses so frequently repeated that the remedy is in almost constant contact with the diseased surface. Thus, the doses, to produce the local effect, should be very small, but frequently administered. It is better that the daily quantity of twenty grains should be given in fifty or sixty doses than in eight or ten; that is, the solution should be weak, and a drachm or half a drachm of such solution can be given every hour or every half hour or every fifteen or twenty minutes, care being taken that no water or other drink is given soon after the remedy has been administered, for obvious reasons.

I have referred to these facts with so much emphasis because of late an attempt has been made to introduce chlorate of potassium as the main remedy in bad cases of diphtheria, and, what is worse, in large doses (Seeligmüller, Sachse, L. Weigert, C. Küster, Edlefsen.)

{701} Large doses of chlorate of potassium (2 drachms daily to an adult I claim to be a large dose, particularly when its use is persisted in for many days in succession) are dangerous. In several of my writings I have given instances of its fatal effects.[43] I have seen fatal cases since, and scores have been published in different journals. The first effects of a moderately large dose are gastric and, more especially, renal irritation; the latter it was which I experienced when I took half an ounce twenty-five years ago. Fountain of Davenport, Iowa, experienced the same before more serious symptoms developed, of which he died.[44] The symptoms are those of acute diffuse nephritis, with suppression of urine, or scanty secretion of a little black blood, and uræmia deepening toward death in fatal cases. My earlier cases I considered as primary diffuse nephritis, and I have even been inclined to attribute the frequent appearance of chronic nephritis, amongst all classes and ages, in part to the influence of the chlorates, which have become a popular domestic remedy and are found in every household. But the experimental researches of Marchand[45] and others prove that, at least in many instances, the extensive destruction of blood-cells is the first and immediate result of the introduction into the circulation of the chlorate, and that the visceral changes are due to embolic processes.

[Footnote 43: C. Gerhardt's Handbuch der Kinderkrankheiten, vol. ii., 1876; Med. Record, March, 1879; Treatise on Diphtheria, 1880.]

[Footnote 44: Stillé, Therap. and Mat. Med., 2d ed., 1874, p. 922.]

[Footnote 45: Sitzungsber. d. Naturforsch. Ges. h. u. Halle, Feb. 8, 1879, and Virch. Arch., vol. lxxvii.]

Special Treatment.--The first axiom in the treatment of diphtheria is that there is no specific; the second, that in no other disease the individualizing powers of the physician are tested more severely.

The treatment is both internal and external. The local remedies are either such as dissolve the mucous membrane, or such as thoroughly modify the mucous membrane from which the pseudo-membrane has been removed, or real antiseptics, with the power of destroying either chemical or parasitic poisons.

The number of remedies recommended in diphtheria is immense. No other proof of its dangerous nature is needed. In the following I shall review those which I consider it worth while either to reject or to recommend.

Steam is used partly to soften the membranes, but principally to increase the secretion from the mucous membrane, and thereby throw off the superjacent membrane. This can be done to advantage only where there is a natural tendency to it; that is, where there are a great many muciparous follicles under a cylindrical or fimbriated epithelium. This is the condition on part of the pharynx, but not on the tonsils; and in a small portion of the larynx, in the trachea and bronchi, but not on the vocal cords. Wherever there is pavement epithelium on the normal surface, and where the membrane is imbedded into the tissue, steam can hardly be expected to do good. In the other cases it will. Thus, the locality of the diphtheritic process determines to a great extent whether steam is indicated or not. If it be used, the necessity of a full supply of atmospheric air must not be disregarded. Steam, with an overheated room and without pure air, is liable to be as injurious as steam in pure air is beneficial in a number of cases.

{702} There can be no better proof for the necessity of individualizing, and the impossibility of treating all cases alike, than the fact that many will do well under steam treatment, and others are certainly injured by it. I have repeatedly had the joy of seeing children with croup become less cyanotic after their removal from an atmosphere of vapor, and I can readily see that pure atmospheric air would be more agreeable and wholesome to a child with stenosis of the larynx than an atmosphere laden with steam. Of course this remark does not apply to cases of pseudo-croup and bronchitis, which are generally benefited by a warm, moist atmosphere. Those, however, who deem it judicious to employ steam as a vehicle for carbolic acid, salicylic acid, chloride of sodium, chlorate of potassium, or lime, had best resort to the atomizer for applying these remedies. It can be used without trouble; most children are sufficiently intelligent to allow the spray to be directed upon the fauces and larynx every ten or fifteen minutes in case of necessity. When it is deemed advisable to administer steam, I warn against the use of gas stoves. They require a great deal more oxygen than an alcohol lamp, which ought to be preferred when a stove or slaking lime or hot iron or bricks immersed in water are not available.

Water may be made serviceable in different ways. Its effect on the skin, when taken in large quantities, under normal or abnormal circumstances, is a matter of daily experience. Copious perspiration is its immediate result. The very same effect is produced on the mucous membranes. In diphtheria, besides professional hydropathists, I know of but one[46] who favors the plentiful use of water, 100-200 grammes (3-6 ounces) every hour or oftener, either by itself or mixed with an alcoholic beverage.

[Footnote 46: C. Rauchfuss, in C. Gerhardt's Handb. d. Kinderkr., iii. 2, 1878.]

Severe inflammatory symptoms, such as redness of the throat, great pain, swelling of the glands, require cold applications, either an ice-bag or ice-cold cloths well pressed out and frequently changed. They must, however, be placed where they can do most good--in laryngeal diphtheria around the neck, in pharyngeal diphtheria with glandular swelling over the affected part. In the latter, therefore, the flannel cloth which covers the whole of the application must be tied over the head, and not behind. When ice-bags are used, care is to be taken lest they should be too large; if so, they will not affect the desired spot at all. Small pieces of ice frequently swallowed are greatly relished by the patient; water-ices in small quantities will render the same service; ice-cream, in half-teaspoon or teaspoon doses every five or ten minutes, adds to the necessary nutriment. When the fever is high and the surface hot, sponging with tepid or cold water, or water and alcohol, will mitigate both. For the cold bath or the cold partial pack (trunk and upper part of the thighs) the general indications hold good. As a rule, I favor the latter, for many cases have such a tendency to debility and collapse that sometimes the circulation of the surface of the body is badly interfered with by cold bathing. Therefore, a contraindication to cold bathing must be found at once in cold feet, either before or after a bath. When, unfortunately, the feet do not recover their normal temperature in a very short time, they ought to be warmed artificially, and the cold bath not repeated. In such cases the cold pack, however, is still indicated. A linen or cotton cloth, {703} large enough to cover the trunk and half of the thighs, is dipped in cold water, well pressed out, and the body of the patient wrapped tightly in it. The arms remain outside; the whole body is then wrapped up in a blanket; the feet may be warmed meanwhile when necessary, and the cold pack repeated as often as required to reduce the temperature--viz. once every five minutes, every half hour, every hour.

The contraindications to the use of cold have in part been alluded to. Very young infants bear it but to a limited extent. The beginning of recovery contraindicates it, unless for some local cause; for instance, an inflamed gland. The extensive use of cold water or ice is also forbidden when there is no fever, where there is perhaps an abnormally low temperature, where we have to deal with the septic or gangrenous form of diphtheria, where the vitality is low and the mucous membranes pale or even cyanotic. In such cases, on the contrary, while unlimited internal stimulation is required, the hot bath, or hot pack and hot injections into the bowel, will be found beneficial.

Lime-water, glycerine, lactic acid, pepsin, neurin, papayotin, chinolin, and pilocarpine are all solvents of pseudo-membrane, but whether there is sufficient time and opportunity to produce a curative effect by every one of them is a question open for discussion. Of lime-water and glycerine I have employed a mixture of equal parts in considerably more than a hundred cases after the completion of tracheotomy, directing the remedy through an atomizer into and below the canula, but cannot say that the descent of the membrane into the trachea or bronchi was prevented by it. Lime-water may be used in the nose and throat as an injection, spray, or gargle, but its solvent effect is greatly diminished by the action of the carbonic acid of the breath on the lime. I have no doubt that if water alone was used with the same persistence as lime-water, its effects would be nearly the same. Still, what little effect the minute dose of lime (1:800) in the lime-water may have may just as well be utilized. What I object to is the omission of more powerful agents. If lime is to be used, slaking lime frequently in the presence of the patient is attended with vastly more benefit, inasmuch as by that proceeding a large amount of powdered lime is projected into the air of the room and the mouth and respiratory organs.

Lactic acid also, in from ten to twenty-five parts of water, has yielded no better results in my hands. Those cases of tracheotomy which I afterward treated with lactic acid spray terminated no better than such as were treated with lime-water and glycerine. Of the solvent effect of pepsin I have not been able to convince myself so as to recommend it. The accounts of neurin have not encouraged me to try it at all. Chinolin (tartrate) has been used locally by O. Seifert,[47] Müller, and others. It is said to remove the membranes and relieve the fever. For a gargle it is dissolved in five hundred parts of water, or it is mixed with ten parts of water and alcohol each, and applied by means of a sponge. To relieve the burning sensation ice is swallowed afterward. The local applications of alcohol have the same drawback. There are but few patients who do not suffer intensely from its local contact.

[Footnote 47: Berl. klin. Woch., Nos. 36, 37, 1883.]

Papayotin has been recommended by Rossbach for the purpose of dissolving membranes in a one-half per cent. solution. It peptonizes {704} albuminoids, and macerates meat, intestinal worms, and croup membranes in both neutral and feebly alkaline solution. In concentrated solutions it has a caustic effect. It is recommended, not as an anti-diphtheritic, but merely as a solvent remedy.[48] Whatever reliance may have been placed upon it has, however, been jeopardized by Rossbach's remarks[49] on the variability of the preparations in the market. Not only are the specimens very unequal, but each of them is variable, easily spoiled, and particularly affected by moisture.

[Footnote 48: Berl. klin. Woch., March 10, 1881.]

[Footnote 49: Transactions of the Congress for Int. Medicine, 1883, p. 162.]

Muriate of pilocarpine was recommended for this purpose three years ago. It was praised by Juttmann as a specific, and has failed. The quackish recommendations of the drug have, indeed, earned for it a certain amount of distrust which it does not deserve in all cases. It is expected to increase the secretion of the mucous membranes to such an extent as to float the pseudo-membranes. It sometimes succeeds in so doing, but only in those cases in which the membrane is deposited upon the mucous membranes. When the tissue is impregnated the drug fails. It also fails in septic cases, and mostly for the reason that it diminishes and paralyzes the heart's action. It ought, therefore, never to be given unaccompanied with large amounts of stimulants. Where the patient is strong, and the heart healthy, it may be tried; I know that a few cases of moderate laryngeal diphtheria improved with pilocarpine, steam, and turpentine inhalations. The dose is 1/30 grain, dissolved in water, every hour.

Turpentine inhalations were recommended by C. Edel.[50] Fifteen drops of oil of turpentine are inhaled from a common inhalation apparatus, which is placed at a distance of three inches from the mouth of the patient, for a period of ten minutes every hour. He claims recoveries in from twelve to forty-eight hours. I allow the patient to remain in his bed, and keep water boiling constantly on an alcohol lamp, on the stove, or over the gas. A tablespoonful of turpentine, more or less, is poured on the water, care being taken that nothing is spilled in the fire. Thus the room is constantly filled with a penetrating odor of turpentine, which is not at all disagreeable, even when in great concentration. The effects are very satisfactory indeed. Where circumstances allowed or required it I have raised a tent over the bed, large enough not to give inconvenience to the patient and to admit either the whole apparatus or the tube containing the mixed vapor of water and turpentine.

[Footnote 50: Med. Rev., Jan. 19, 1878.]

Ammonium chloride may sometimes be used to advantage for its softening and liquefying effects. Its internal administration in bronchial and tracheo-laryngeal catarrh is so old that it has several times been obsolete. Of late, more stimulant effects have been attributed to it than it actually possesses. But its liquefying action, in cases where the secretion of mucus is defective and expectoration scanty and viscid, is undoubted. Thus it proves valuable in many cases of simple catarrh, both when administered internally and inhaled. The latter mode I have often resorted to, and believe that its macerating influence has been of service to me in cases of laryngeal diphtheria. Half a teaspoonful of the pure salt is spread on the stove or burned over alcohol {705} or gas. It evaporates immediately, and fills the room or the tent with a white cloud, which, when dense, excites coughing. But it does not irritate to any uncomfortable degree, and the process may be repeated in an interval of an hour or more.

Not all cases of diphtheria are septic or gangrenous, nor are all the cases occurring during an epidemic of the same type. Some have the well-pronounced character of a local disease, either on the tonsils or in the larynx. The cases of sporadic croup met with in the intervals between epidemics present few constitutional symptoms, and assume more the nature of an active inflammatory disease--very much like the sporadic cases of fibrinous tracheo-bronchitis. These are the cases in which mercury deserves to have friends, apologists, and even eulogists. Calomel, 0.5-0.75 gramme (gr. viij-xij), divided into thirty or forty doses, of which one is taken every half hour, is apt to produce a constitutional effect very soon. Such doses, with minute doses, a milligramme or more (gr. 1/60), of tartar emetic, or ten or twenty times that amount of oxysulphuret of antimony, have served me well in fibrinous tracheo-bronchitis. But the mucous membrane of the trachea and bronchi is more apt to submit to such liquefying and macerating treatment than the vocal cords. The latter have no muciparous glands like the former, in which they are very copious. And while the tracheal membrane, even though recent, is apt to be thrown out of a tracheal incision at once, the pseudo-membrane of the vocal cords takes from six days to sixteen or more for complete removal. Still, a certain effect may even here be accomplished, for maceration does not depend only on the local secretion of the muciparous glands, but on the total secretion of the surface, which will be in constant contact with the whole respiratory tract. Thus, either on theoretical principles or on the ground of actual experience, men of learning and judgment have used mercury in such cases as I detailed above, with a certain confidence.

If ever mercury is expected to do any good in cases of suffocation by membrane, it must be made to act promptly. That is what the blue ointment does not. In its place I recommend the oleate, of which ten or twelve drops may be rubbed into the skin along the inside of the forearms or thighs (or anywhere when their surface becomes irritated) every hour or two hours. Or broken doses will be useful, such as given above, or hypodermic injections of corrosive sublimate in 1/2 or 1 per cent. solution in distilled water, four or five drops from four to six times a day, or more, either by itself or in combination with the extensive use of the oleate, or with calomel internally. Lately, the cyanide of mercury has been recommended very strongly. I hardly believe that it will work more wonders than any other equally soluble preparation. Within the past few years the internal administration of bichloride of mercury has been resorted to more frequently and with greater success than ever before. My own recent experience with it has been encouraging, and so has that of some of my friends. Wm. Pepper[51] gave 1/32 grain of corrosive sublimate every two hours in a bad form of diphtheritic croup, with favorable result. But in this very bad case, desperate though it was--child of five years, resp. 70, pulse 160--large membranes, "evidently from the larynx," had been expelled before the treatment was commenced on the {706} seventh day of the disease. The remedy ought to be given in solution of 1:5000, and in good doses. A baby a year old may take one-half grain every day for many days in succession, with very little if any intestinal disorder and with no stomatitis.[52] A solution of the corrosive chloride of mercury in water is frequently employed of late as a disinfectant. It acts as such in a dilution of 1:20,000. As healthy mucous membranes bear quite well a proportion of 1:2000-3000, any strength between these extremes maybe utilized. A grain of the sublimate in a pint or more of water, with a drachm of table-salt, will be found both mild and efficient. As a gargle or nasal injection it will be found equally good. But it has appeared to me that frequent applications give rise to a copious mucous discharge; hourly injections into a diphtheritic vagina became quite obnoxious by such over-secretion, which ceased at once when the injections were discontinued. Thus, when it is desirable not only to disinfect but also to cleanse the diseased surface, the injections with corrosive sublimate appear to yield a result inferior to less irritating applications.

[Footnote 51: Trans. Am. Med. Ass., 1881.]

[Footnote 52: Med. Record, May 24, 1884.]

Chloride of iron is undoubtedly a valuable remedy in diphtheria, but in its administration it must by no means be forgotten that small doses at long intervals are out of the question. I have not the least doubt but that the failure of the remedy may be attributed in most cases to the fact that the doses were too small and administered too seldom. A dose of from five to fifteen drops, properly diluted, every fifteen minutes, half hour, or hour is indispensable for a proper estimation of its effects. Gargles are not of much service, for the simple reason that they do not come into sufficient contact with the affected parts, and reach at the utmost to the anterior pillars of the soft palate. A direct application of the remedy to the mucous membrane of the pharynx may also be desisted from, thereby avoiding any irritation, the internal administration at short intervals causing the pharynx to be sufficiently influenced by local contact with the remedy. It must, of course, not be expected that the chloride will remove the membrane, but it can frequently be seen to reduce the hyperæmia and swelling and prevent the reproduction of exuded material. The chloride of iron exerts a decided influence on the vital contractility of the blood-vessels. This increased contractility certainly assists in diminishing the rapidity of absorption of putrid fluids through the blood-vessels, which constitutes the principal source of danger from the disease.

It cannot yet be positively asserted that the chloride of iron exerts a direct effect on the lymphatic vessels. Naturally, this was claimed when the remedy was recommended, in the treatment of diphtheria, on account of its therapeutic effects in erysipelas, with the accompanying inflammation of the lymphatic vessels of the skin. Although we know of no direct compression of the lymphatic vessels due to the action of the chloride, yet it may be assumed that perhaps the compression of the blood-vessels exerts a similar influence upon the neighboring lymphatics. In consequence of this there would be an impediment to the absorption and further development of poisonous substances in the lymph. The chloride, like the sulphate of iron, is a tolerably powerful disinfecting agent. If this observation be correct, it may go very far toward explaining the action {707} of the chloride of iron in septic diseases, which are accompanied by an exalted activity of the lymphatic vessels and an increase of the white blood-corpuscles. Furthermore, Saase has endeavored to show that the ferrous salts possess the power of converting oxygen into ozone. They share this power with the blood-globules exclusively, and could hence, to a certain degree, supply a deficiency of the latter. Pokrowsky, too, has shown that iron increases the process of oxidation in the body by demonstrating that in health there is an elevation of temperature and an increase of the percentage of urea in the urine during its administration. In anæmic persons, to whom iron has been given for the purpose of increasing the amount of blood, the above phenomena may be observed before this object is accomplished. Thus iron appears to replace the blood-corpuscles to a certain extent. Now, in infectious disorders of the blood, where the red globules are perpetually menaced with destruction, it seems plausible that the preparations of iron should exert an antiseptic action.

Finally, it has been found that of all the preparations of iron the chloride possesses the greatest power of stimulating the nervous system. Possibly this effect may be traced to an increase of the arterial pressure in the nerve-centres. It has been said that this effect has been vividly illustrated in certain forms of chlorosis. If this be true, iron would be all the more indicated in diphtheria, since it would act as a prophylactic against a series of nervous phenomena that so frequently present themselves, both during and subsequently to the diphtheritic process. Thus it is that for many years the muriate of iron has constituted the main element, with me, of internal medication in most cases of diphtheria, both of the mild and the most dangerous septic type. A common formula is, for a child of two years,

Rx. Tinct. Ferri Chloridi fl. drachm ij; Potass. Chlorat. gr. xx; Aquæ fl. oz. v; Glycerin. Pur. fl. oz. j. M.

S. A teaspoonful every fifteen, twenty, or thirty minutes.

Carbolic acid exerts a powerful influence on the vitality of all living elements, and hence also on rapidly proliferating epithelium, which constitutes a part of the diphtheritic membrane. It is of great advantage for local use. Its local effect, undiluted or diluted with equal or larger parts of glycerine or alcohol, in shrinking and removing membranes, is sometimes very useful; in mild solutions in water (1/2, 1, or 2 per cent.) it is very efficient in nasal injections or for external applications or mouth-washes. Rothe's prescription for external use is carbolic acid and alcohol each 2 parts, water 10, tincture of iodine 1. Its internal administration to the extent of five to twenty grains daily, given largely diluted, in small and frequent doses, is of less positive value.

Salicylic acid, in a solution of 1:30-50, is caustic. A milder solution, 1:200-300 relieves or removes foul odor from the nose or throat, but it does not detach membranes or shorten the duration of the disease, apparently. Internally, it acts no longer as a disinfectant, but is changed into a salicylate and is an antipyretic. It is then better to replace it by the sodium salicylate. With its administration (for a child of 2 years 3 grains every hour until 20 or 25 grains are taken) it ought not to be {708} forgotten that serious brain troubles, collapse, and irregular and paralytic breathing, as well as gastric and intestinal disturbances, may follow its use. It ought not to be given without careful watching and the simultaneous free use of alcoholic stimulants.

Binz found, as the result of experiments with solutions of pure quinia varying from one part in a hundred to one in a thousand, that the latter sufficed to prevent the development of bacteria in fluids capable of undergoing putrefaction; but even estimated thus, a patient with eighteen pounds of blood would require one hundred and thirty-eight grains of quinia circulating therein in order to satisfy the conditions of Binz's experiment. If Binz considers two grammes (half a drachm) of quinia per day sufficient for an individual weighing one hundred and twenty pounds, his calculation is founded on experiments with dogs, in which septicæmia was avoided by the injection of quinia. It is also necessary to bear in mind that Binz makes a distinction with regard to the preparations of quinia employed. He warns against the use of the bisulphate as being the most inactive. No matter which preparations are used--I prefer the muriate--I have come to look upon quinia as of no great service in reducing the temperature in infectious fevers. The main indication for its use can only be found in inflammatory fevers. When it is given, however, salicylate of sodium may be added for a short time to obtain a speedier effect.

On the part of bromine Wm. H. Thompson claims the following advantages: 1. When applied locally, it promptly arrests fetor by arresting directly the gangrenous process, and thus lessens risk from absorption. 2. It acts as an anti-putrefactive likewise in the fluids of the body generally--i.e. blood, interstitial circulation, and secretions--owing to its high rate of diffusibility, equal to that of sodium chloride itself. 3. It locally destroys the communicable property of the discharges, shown by the immunity of attendants from any sore throat when it is used, and from its checking the spread of the disease in the locality. He orders two solutions to be used: the first of equal parts of Lawrence Smith's solutio bromini and of glycerine, applied with a hair pencil to the membrane, as gently as possible. Sometimes he uses the solution full strength. The brush should be washed at once in water, and does not last more than one day, owing to the action of the bromine on the hair. If, however, the membrane be very extensive and the parts much swollen or difficult to reach, he resorts instead to douching with a Davidson syringe, using half a drachm to one drachm of the solution to a pint of warm water. By beginning gently with the stream directed against the buccal mucous membrane, the child soon becomes accustomed to the current and allows it then to play against the deeper parts.

Internally he orders from six to twelve drops of the solution in a half ounce of sweetened water, every hour, two, or three hours, according to the urgency of the case, and continuously.

The most convenient way of making Smith's solution is: Take two ounces of a saturated solution of potassium bromide in water; add to this, very slowly, in a bottle and with constant shaking, one ounce of bromine. It is better to add a part, and then let it stand a while before adding the rest; then fill up gradually, and with constant shaking with water, until it measures four ounces.

{709} Ozone has been used as an anti-fermentative in inhalation during three or five minutes every hour or two, by Jochheim.

Boric (boracic) acid, in saturated (1:25) or milder solutions, has some antiseptic effect. It is mild, and not very injurious when swallowed by necessity or mistake. In diphtheritic conjunctivitis it is valued highly, and in nasal injections I have found it very useful. It is less repugnant than most other substances administered in that way.

Sodium benzoate cannot be relied on either as an anti-diphtheritic nor as an anti-febrile. The doses which were recommended were two scruples or a drachm daily for a child a year old.

Sulphur has been used locally. It gives rise to coughing and vomiting.

Cubebs have been given in incredible doses, two drachms of the powder to a child a year old. The drug disorders the stomach and kidneys.

Local Treatment.--The mechanical removal of the membranes is not permissible unless they are almost detached. It is best to avoid their being cast off, unless partly loosened membranes in the larynx or trachea afford an indication for an emetic. Scratching and eroding the mucous membrane of the neighborhood give rise to new deposits. Even after spontaneous elimination of a membrane a new one may be formed within a few hours.

To cauterize a diphtheritic membrane or infiltration I consider wrong, unless I shall be able to do so thoroughly and to limit the action of the caustic to the diseased surface. Therefore potassa or chromic acid cannot be utilized, because of the impossibility of limiting their effect. Nitrate of silver and mineral acids can be restricted in their effects, but these are not sufficiently thorough, particularly as but few patients will consent to have the remedy applied properly. When I do cauterize, I prefer a mixture of equal parts of carbolic acid and glycerine or the undiluted acid. The membrane crumbles and falls off in pieces. Force must never be used. Where it would be required in the case of obstinate children mild washes must be employed instead of the caustic. Besides, the internal medication detailed above meets every indication. When there is a slight swelling of the lymphatic glands, cold water or ice applications are usually all that is needed. The latter should be made according to general indications. The glandular and peri-glandular swellings are less the result of an actual filling up with foreign matter than of secondary irritation. Ice has a happy effect in such cases, both on internal administration, in the form of frequent small quantities of ice-water, ice-pills, ice cream, and iced medicaments, and also externally by ice-cold cloths or india-rubber bags filled with ice.

In general, the treatment of the swelled glands must be both based on its causes and adapted to the present condition. The adenitis and peri-adenitis is of secondary nature, the irritation being in the mouth, pharynx, and nares. In these localities is where the main treatment is required. The sooner the primary affection is removed or relieved or rendered innocuous, the better it is for the secondary complaint. Frequent doses of chlorate of potassium or sodium, or biborate of sodium in mild doses frequently repeated, according to the principles laid down in another part of this article, mouth-washes, gargles, nasal injections with water, salt water, or solutions of disinfecting substances, are not only {710} indicated, but highly successful. When the case is recent, cold applications are required, but no washes. When it is of older date, stimulant embrocations are in order. Iodine ointments are absorbed but slowly; mercurial plasters do good in some cases; iodide of potassium dissolved in glycerine (1:3-4), frequently applied, iodine in oleic acid (1:8-12), iodoform in collodion or flexible collodion (1:12-15) applied twice daily, the latter frequently with very good result, are beneficial. Copious suppuration is very rare. Cases in which a free incision meets with an abscess ready to heal are very uncommon. But numerous small abscesses with gangrenous walls and pus mixed with a sero-sanguinolent or sero-purulent liquid, are more frequently found. In such cases a probe introduced into the lancet wound enters easily into the broken-down tissue in every direction, to a distance even of three to six centimetres, (several inches), according to the size of the tumefaction. I have seen fatal hemorrhages from such gangrenous destructions; therefore the treatment must be both timely and energetic. The incision must not be delayed too long. When the skin assumes a purplish hue or is simply discolored, it is time to incise and to apply concentrated or nearly concentrated carbolic acid to the interior, unless the neighborhood of very important blood-vessels or nerves yields a contraindication to concentrated applications. In that case a milder preparation is advisable, but the application should be repeated often, until the suppuration becomes more normal. Then mild disinfectant injections into what has now become a cavity will be found satisfactory, particularly when meanwhile the general condition of the patient has been improved.

Treatment of Nasal Diphtheria.--Especially during the prevalence of an epidemic of diphtheria must we be careful not to allow a nasal catarrh to have its own way; we must likewise guard against considering the thin and flocculent discharge in infected cases as a mucous secretion. Whatever be the origin of nasal diphtheria, whether primary or the result of a similar affection in the throat, local treatment should at once be instituted, and if this be done the great majority of cases will terminate favorably. The danger in this form of disease consists in an excessive absorption of putrid substances and in the breathing of contaminated air. The interior of the nasal cavities must be thoroughly cleaned and disinfected. If this be commenced early, the original seat of the affection may be reached, and the disinfectant process will, as a rule, have good results. It is not necessary to select very energetic disinfectants; a solution of twelve to twenty-five centigrammes (two to four grains) of carbolic acid in thirty grammes (an ounce) of water is at once mild and effective, and hardly gives rise to more discomfort than lukewarm water. Nasal injections must be made very frequently, until each time the stream of fluid has a free exit through the other nostril or through the mouth. They must be made at least every hour, and even oftener if necessary; at the same time it is advisable to be careful that the fluid does not enter the Eustachian tube. This can be prevented, to a certain extent, by compelling the patient to keep the mouth open during the procedure. I have seldom seen evil or even disagreeable results from the administration of nasal injections in diphtheria. It is likely that the mucous membrane of the pharynx is swollen as far as the openings of the Eustachian tubes to such a degree as to render the entrance of fluids into the latter improbable. {711} The hardness of hearing, which is of so frequent occurrence in the course of a severe catarrh or of a diphtheritic attack, seems to indicate that the mucous membrane of that part is in a state of swelling. An ordinary syringe will suffice. However, when administered by parents or nurses the blunt nozzle of an ear syringe is preferable. Occasionally here, as in local applications to the mouth and pharynx, the atomizer may be used to advantage, but the tube must be properly introduced into the nostrils. There are cases of nasal diphtheria, however, which are far more troublesome to manage than the foregoing would seem to indicate. I have seen cases in which the nasal cavities, from the anterior to the posterior nares, were filled and completely occluded by a dense, solid membranous mass. I was then compelled to bore a passage with a silver probe, to gradually introduce a larger-sized one, and then to apply the pure carbolic acid, in order to remove the densest and thickest masses, and finally was able to make injections; even in such cases I have had the gratification of being able to give a favorable prognosis. The dangerous secondary swelling of the glands will often subside after a steady employment of disinfectant injections for from twelve to twenty-four hours. It will be found that children frequently do not object to this method of treatment; I have even met with some who, after convincing themselves of the relief afforded thereby, asked for an injection. When we are about to bring each injection to a close it is well to press together the nasal cavities for an instant with the fingers. By this procedure the fluid is forced backward to the pharynx, and is swallowed or ejected through the mouth, and thus washes the pharynx and mouth at the same time. Frequently, however, this latter object is obtained with every injection; for, the palate being swelled, oedematous, and paretic, the fluid is not prevented from reaching the pharynx, even in the average case. In regard to the choice of a disinfecting agent, I have but a few words to say. I believe that no one of them has important qualifications above the others. I avoid those which stain or which produce firm coagula. For the latter reason I do not use the subsulphate and perchloride of iron; for the former, the permanganate of potassium. I employ, as a rule, carbolic acid in solution, of the strength above mentioned. Where there is but a slightly fetid odor I have frequently employed lime-water or water with glycerine, or a solution (1:100, 1:50) of chloride of sodium, or of bicarbonate of soda or of borax, or a saturated solution of boric acid. Disinfecting agents and antiseptics, whether carbolic acid, salicylic acid, or iron, are of no service when administered internally only, unless the seat and cause of the septic infection be attended to previously. Under the local employment of antiseptics, as described, or by simply washing out with water or salt water, most cases recover; without them, death will result. Of late, in many cases, the local applications, injections, etc. of the corrosive chloride of mercury in water (1:5000-10,000) has proved very effective. It has this advantage over carbolic acid, that the swallowing of the former is not so dangerous. This much, after all, my experience has assured me of, that there is a certain number of cases which terminate fatally; but it is likewise true that the mortality need not be excessively great. I cannot grant that it is hard to carry out the exact and apparently barbarous treatment necessary for a favorable result, for it is certainly more barbarous to sacrifice than to save life.

{712} It is a positive fact that when children suffering from nasal diphtheria, with its peculiarly septic character, are permitted to sleep much--and they are apt to be drowsy under the influence of the poison--they will certainly die. To allow them to sleep is to allow them to die.

The first symptom of improvement is often a rapid diminution of the glandular swelling wherever it exists. It is not present in all cases, but chiefly in those in which a bloody serum was discharged in an early period of the disease. In these the blood-vessels appear to be very vulnerable, superficial, and apt to absorb; these are also the most dangerous cases, and require the greatest attention and care, and also prompt disinfection.

Treatment of Laryngeal Diphtheria.--The severest form of diphtheria is that located in the larynx, constituting membranous croup. Its general treatment, whether the disease has originated primarily in the larynx or trachea or has been communicated from the pharynx, does not differ from that laid down for diphtheria in general. Naturally the larynx calls for special treatment on account of the symptoms of suffocation which result from its stenosis. The main indication of removing viscid mucus or partly-detached membranes is best met by the administration of an emetic. Such is their only indication in my experience. The selection of the emetic, when indicated, is of great importance. Antimonials ought to be avoided because of their depressing and purgative effect. Ipecacuanha is but rarely effective. The sulphates of zinc and copper, and particularly the latter, deserve preference. Turpeth mineral acts promptly and satisfactorily. When no emesis can be obtained the prognosis is decidedly bad. Recourse must then be had to tracheotomy, the good results of which are however only too often delusive and transient.

When, after the operation, there is scarcely any relief, and particularly when the case takes a very rapid course, it is probably one of ascending croup which commenced in the trachea. Mechanical relief by pushing down a hen's feather or a bundle of them, and turning it about and twisting, must be tried. It is a much better instrument than pincers of all sorts and shapes. But what relief will be accomplished is but of very short duration. When fever sets in within a few hours it means very much more frequently pneumonia than diphtheritic fever. It is apt to be soon complicated by that disproportion between pulse and respiration so characteristic of inflammatory diseases. Then quinia in larger doses, 0.25 or 0.5 (grs. iv-viij) every two, four, eight hours, at the same time doses of sodium salicylate 0.25-0.40 (grs. iv-vj) every hour or two hours until the temperature goes down, and small doses of digitalis where the heart requires it, must be given at once. Procrastination is dangerous; the patients want careful watching; many of them die within two days after the operation.

Diphtheritic conjunctivitis requires great attention and permits of no loss of time. Cold applications to the affected eye must be made constantly. Pieces of linen or lint kept on ice (better than in ice-water) of little more than the size of the eye, must be changed every minute or two day and night. The danger to the cornea is so imminent that constant watchfulness is required. Boric acid in concentrated solution should be dropped into the eye once every hour. Care must be taken that the well eye shall not get infected; for that purpose it is best to cover it {713} with lint and collodion, or with lint or cotton held in place by adhesive plaster.

Cutaneous diphtheria requires the destruction of the membrane or of the infected surface by carbolic acid, either concentrated or somewhat diluted with glycerine, or the application of the actual cautery. After that the use of ice or iced cloths, or diluted carbolic acid, is indicated. As soon as the surface is no longer diphtheritic the local and general treatment is to be continued on general principles.

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