Text book of veterinary medicine, Volume 4 (of 5)

TEXT BOOK OF VETERINARY MEDICINE

JAMES LAW, F.R.C.V.S.

Director of the New York State Veterinary College Cornell University, Ithaca, N. Y.

VOL. IV.

INFECTIOUS DISEASES.

ITHACA PUBLISHED BY THE AUTHOR 1902

PRESS OF ANDRUS & CHURCH ITHACA, N. Y.

VETERINARY MEDICINE.

PYÆMIA AND SEPTICÆMIA.

Multiplicity of Septicæmias. Pyæmia and Septicæmia, distinction between. Multiple secondary abscesses in pyæmia; no secondary abscesses in uncomplicated septicæmia. Septico-pyæmia. Pyæmia. Causes: bacteria, deep wound infection, susceptibility, debility, shock, illness, narcotic ptomaines, partial immunization, complexity of infection, mutual decomposition of toxins, dose, lesions of intima of blood vessels, thrombosis, embolism, action of microbes on hæmatoblasts and blood globules, viscidity of cells, adhesion to endothelium, coagula, solution of clot, escape of microbes. Lesions: wound, abscess, thrombus, emboli, infarction, abscesses, ulceration, endocarditis. Spleen. Blood coagulates. Symptoms: rigor, hyperthermia with remissions, pulse weak, soft, rapid, perspiration, diarrhœa, sweet breath, fæces, urine acid, dulness, prostration, mucosæ dusky or yellow, blood shows leucocytosis, hæmolysis, cardiac murmur, arthritis, stupor, coma, palsy, dry, puffy sore, source of infection. Prognosis grave. Prevention: largely surgical, antisepsis, asepsis, excision of infected vein. Treatment: antiseptics, locally and internally, stimulants, tonics, nourishment. Septicæmia: microbes, toxins, septic intoxication, septic infection, fermentation fever, sapræmic fever. Lesions: blood dark, incoagulable, spleen enlarged—gorged, petechiæ, cloudy swellings, coagulation necrosis, organs as if parboiled, congested glands, kidneys. Symptoms: chill slight, hyperthermia without marked remissions, weak, rapid pulse, hurried breathing, anorexia, emesis, yellow mucosæ, nervous disorder—dulness, apathy, stupor, paraplegia. Value of precursory conditions. Prognosis grave. Prevention, Treatment: remove source of poison, antiseptics, drainage, internal antisepsis, strychnia, quinine, iron chloride, stimulants, supporting, easily digestible food, sponging.

At first introduced to indicate the supposed results of pus and septic material respectively in the blood, these terms have come to represent the clinical phenomena which come from the introduction into a susceptible system of pyogenic and necrogenic microbes and their toxic products. Gradually different affections, which would have been included under the same general terms, came to be identified under specific names, and a number of these will be described as individual diseases—strangles, mouse and rabbit septicæmias, metritis, phlebitis, omphalitis, rouget, barbone, chicken cholera, septicæmia hæmorrhagica, etc.—yet a certain number have been left to be referred to under the generic terms, though respectively due to different microbes.

Distinctions between Pyæmia and Septicæmia. Pyæmia is a morbid condition characterized by the formation in different organs of multiple metastatic abscesses, dependent on the transference, in the blood stream, of infected clots, or particles containing pus microbes, and their arrest at distant points, so as to cause foci of suppuration commencing with the intima of the vessels.

Septicæmia indicates a general infection often by the same microbes, but showing its results in enlargement and blood engorgement of the spleen and lymph glands and necrotic foci of the liver, kidneys and other organs, but without the formation of multiple abscesses. The presence of the microbes in the different organs affected, shows that it is not due to the diffusion of the toxic chemical products alone, as at one time supposed, and the lack of abscesses appears to be due to the absence of clots or of modified and adhesive leucocytes or hæmatoblasts, which adhering to the epithelium of the vessels predispose to suppuration.

The two conditions are, however, often combined, constituting what is known as septico-pyæmia.

As in the occurrence of other infecting diseases, the condition of varying susceptibility must be taken into account, one individual, or one species resisting an inoculation which would be deadly to another.

=Pyæmia.= Causes. The causation microbes are most commonly staphylococcus pyogenes aureus, or albus, the streptococcus pyogenes, and less frequently bacillus pyocyaneus, bacterium coli commune, and probably any pus producing microbe. Many conditions must however be accepted as contributing to the general infection.

Inoculation on a mere abrasion or surface sore is not to be dreaded so much as if the virus is lodged subcutaneously or in a deep wound. The ready escape of the toxic products, the active leucocytosis which takes place in the granulations, and the action of the oxygen of the air are more or less protective in the exposed sores.

The native susceptibility of the subject,—horse, ox,—conduces to the disease, while the insusceptibility,—bird—tends to obviate it.

The debility of the system or of individual tissues attacked, lowers the resistant power, and especially that of leucocytosis, and thus favors survival and encrease of the microbes and their chemical products. Thus the shock succeeding a serious operation, the general depression attendant upon severe illness, or the poisoning by narcotizing ptomaines and toxins, may easily become the extra weight which causes the system to succumb. On the contrary, pre-existing or long standing disease, with consequent general debility appears at times to prove to some extent a protective factor, the previous exposure to the invading germ having educated the leucocytes to resist the toxins and to produce the defensive sera which neutralize the latter or keep the invading microbes in check. A measure of immunization has been secured.

The resulting immunization cannot be looked on as very perfect, nor permanent, as a specially strong inoculation by a virulent microbe, or large dose, or different conditions of life, will entirely overcome it, and the pyæmic fever appears. Yet in chronic cases of secondary abscesses from a deep source of infection, the resistance is often such as to ward off febrile pyæmia. In a horse with primary abscess situated deeply under the humerus, free evacuation and healing of the wound, have, in my experience, been followed by the formation of abscesses in distant points for a period of seven years, but without any marked febrile reaction.

The complex nature of the infection appears at times to overcome the vital resistance more effectively than will the presence of even a potent microbe alone. Some of the worst cases follow on a wound, the seat of complex infection, and even saprophytes are to be dreaded in this connection. This may operate in various ways, either by mutual combinations or decompositions of the toxic products of associated germs producing more deleterious products, or by the individual action of one ptomain or toxin on leucocytes, hæmatoblasts, sera, or tissue, laying it more open to the attacks of those of another microbe which by itself would have been comparatively harmless.

Koch’s experiments showed that the attack is violent in ratio with the size of the dose: one-thousandth part of a drop of pyæmic blood was harmless to the rabbit, while one tenth of a drop killed in one hundred and twenty-five hours, and a syringe full in forty hours.

In ordinary cases of pyæmia the occurrence of internal phlebitis or arteritis with the inevitable thrombosis is an important step in causation. Any inflammation of the inner coat of the vessel leads promptly to the formation of a coagulation of the contained blood, and blocking of the lumen. Beginning on the diseased or abraded surface, the clot forms backward along the line from which the blood normally comes (proximal in the arteries; distal, in the veins), until it reaches the next considerable colateral branch. The clot is firmly adherent to the intima except at the free end, which is conical and projects into the blood current.

If small portions are detached from the thrombus and washed on in the blood stream they become arrested when they reach a vessel too small to admit them, it may be a smaller artery, or it may be a capillary, and always in the line of the circulation,—from the systemic circulation to the lungs, or from the lungs to the system at large. This is =embolism=. Wherever arrested, the contact of the leucocytes and hæmatoblasts with the inner coat of the vessel, leads to metabolic changes and firm adhesion, and the pus microbes in the clot determine suppuration and abscess.

Eberth and Schimmelbusch have shown that the hæmatoblasts, even more than the other blood elements, when acted on by the pus microbes become viscous and stick not only to each other, but to any floating body, and to the inner serous coat of the vessel, particularly when the latter has been abraded or injured. This clumping together of the hæmatoblasts forms white clots which block the smaller vessels, but in the viscous condition they further the coagulation of the fibrine, and again when they come in contact with the intima, instead of passing through, or moving on, they remain adherent and start the formation of thrombi. This is above all common in given tissues, and the medulla of bone has in this respect a bad preëminence, so that acute suppurative osteomyelitis, is a familiar lesion and is liable to become chronic, and determine distant abscesses and general infection long after.

The thrombus thus formed is an infective coagulum, tending to constant encrease, as the clot is a favorable culture-field for the microbes, and the tendency is to coagulate more and more of the adjacent blood. It tends further to disintegration, as the action of the microbes and their toxins on the leucocytes, transforms these into pus cells, inducing softening of the mass, and the washing on of individual infective pus cells and minute portions of the clot to form infective centres and abscesses at distant parts.

If the pathogenesis of the invading microbe is weak and the resistance of the leucocytes potent, such clots may remain circumscribed or may even be absorbed, but in the opposite conditions with potent and numerous microbes and abundant and effective toxins, the disposition is not only to a continuance of infection, but to an acute febrile pyæmia.

Pyæmia does not supervene at once upon a trauma as may septicæmia, but only after a variable number of days, (3 to 8), a peculiarity which is explained by the temporary protection of the clot. By the constant accretions on its exterior, of the new layers of hæmatoblasts and fibrin, the microbes are at first imprisoned, and it is only when softening has taken place, or when the coagulum has extended into the free flowing current passing into a colateral trunk, that the infection is liable to be washed on in dangerous amount.

The mere presence of pus microbes or their toxins in the blood, does not determine pyæmia: a modification of the intima of the vessels leading to local infections with thrombosis or embolism and abscess is an essential condition. This lesion of the vessels may be a trauma, as from bruise, puncture, operation, ligature, or it may be the extension of a disease process as in arteritis, phlebitis, atheroma, the growth of a tumor from adjacent tissues, or parasitism. The seat of the secondary abscess depends primarily on the location of the original suppurating centre. As such centres are most commonly in the systemic circulation (osteomyelitis, omphalitis, wounds, traumas) the lungs are most commonly attacked, the pulmonary capillaries acting as a sieve and arresting the floating infective coagula. When the primary infection comes from the chylo-poietic viscera, the liver is likely to show the first crop of secondary abscesses. When, on the other hand, the primary abscess is in the lungs, the great flow of blood through the kidney renders it especially subject to secondary suppurating foci, though these may form in any part of the body.

Lesions. Pyæmia may result from a wound or abscess in connection with which will usually be found a vein containing a thrombus more or less softened or liquefied. If from a deep seated injury or from osteomyelitis, the same condition is met with. The thrombus and circulating blood furnish abundance of the infective microbes, and at distant points, in the complimentary circulation, most commonly in the lungs the arteries are found to be the seats of embolism from arrested clots. The arrest always takes place where the vessels are diminished by bifurcation, or the giving off of a considerable colateral trunk, and the appearances will depend on the duration of the embolism. If quite recent, a wedge-shaped mass of tissue supplied by the vessel is ischæmic and pale, its blood passing on into the veins without further arterial supply; if later, this tissue forms an infarct being gorged with deep red or black blood which has filtered in from adjacent anostomosing capillaries and distended those of the exsanguine area. This area becomes of a deep red or black color, consolidated by an exudate of lymph, and rapidly invaded by suppuration. The microbes determine suppuration and softening, first in the clot and intima, and next in the outer coats of the vessel and the surrounding exudate, so that an abscess of variable size may result. Abscesses are usually smaller and more numerous in the acute forms of the disease, and larger and less numerous in the more chronic.

Ulcerative endocarditis with coagula on the valves is not uncommon. The spleen is often the seat of small abscesses in the centre of solid exudates, with in many cases softening and enlargement of the organ. The blood tends to retain its normal bright red color, and clots firmly, contrary to the usual condition in septicæmia.

Symptoms. The formation of emboli and secondary abscess is usually marked by a violent rigor, lasting from a few minutes to an hour and which may be repeated at irregular intervals, serving, in some measure, to distinguish pyæmia from septicæmia. The temperature rises with the rigor, (102° to 105°) but shows marked remissions especially in the morning, when it may not exceed the normal, and rising again with the recurrence of chill or staring coat. The pulse is usually encreased in frequency even during the remissions and is soft and compressible. Remissions may be attended by profuse perspirations or even, in the advanced stages, by fœtid diarrhœa. The breath has a peculiar sweetish or mawkish odor. Blood passed with the fæces may indicate intestinal abscess, and albumen or pus in the acid urine, bespeaks suppurating foci in the kidney. The cloudy mucus from the pelvis of the kidney in the horse must not be mistaken for this. Cough or dyspnœa will indicate abscess of the lungs, and intercostal tenderness, pleurisy.

The buccal mucosa may be dry and cracked, and the tongue coated. From the first the animal is dull, and prostrate, and the visible mucosæ become dusky brown or even yellowish from the liberated hæmatin. Blood abstracted, will show the microörganism, an excess of leucocytes and diminution of the red globules. The poison determines hæmolysis. A cardiac murmur, usually with the first sound, betrays endocarditis. This is especially characteristic of chronic pyæmia. Again multiple suppurating arthritis may appear. Stupor, coma or paralysis will indicate cerebral or meningeal lesions.

In pyæmia following trauma there is drying up of the pus which becomes serous or bloody, a puffy condition of the granulations, and the evidence of a thrombus in one or more veins leading out from the wound.

In other cases the occurrence of pyæmic symptoms, consequent on parturition, metritis, omphalitis, bone-abscess or osteomyelitis, on suppurating internal inflammations, ulcerative endocarditis, or infective fevers like strangles, influenza, contagious pneumonia, cattle plague, distemper, rouget, hog cholera, etc., serves to identify the disease.

The prognosis of pyæmia is always grave, and death may be expected in six to fourteen days in acute cases. Chronic forms last much longer.

Prevention is the great object in regard to surgical cases, and this means the prevention of suppuration in the wound. As far as possible, however, this is to be sought by asepsis, or the use of weak non-caustic antiseptics only, as cauterized tissues form favorable culture media, when the action of the antiseptic is spent, there being no longer any living and resistant leucocytes present. The early excision of veins, the seat of thrombosis, has proven successful.

In purely medical cases, the seat of the primary suppuration is not always obvious and one is thrown back on medical treatment which is rarely satisfactory in severe cases.

Treatment. When accessible even the secondary abscesses may be opened, washed out with a weak antiseptic (3 per cent. carbolic acid solution), and covered with antiseptic dressing. Antipyretics are worse than useless, because of the resulting depression of the vital powers, and the reduction of the natural powers of resistance. Calomel in small and repeated doses tends to assist in elimination, and to counteract complications through sepsis of the contents of the bowels. Quinine and chloride of iron continued in large doses have been especially relied on as antiseptic tonics. Liberal feeding, if the appetite will admit, is all important, to tide the patient over the period of depression. In the chronic cases tepid bathing is of great value (Senn). Senn has great confidence in the stimulating and supporting action of alcoholic liquors—beer, ale, porter and even whisky, and in human beings accustomed to the daily use of these beverages they are more imperative than in the lower animals.

=Septicæmia.= The micro-organisms causing septicæmia are the same as those of pyæmia, but they differ somewhat in activity, and act upon a system with a modified susceptibility, and above all one void of lesions in the internal membrane of the vascular system. The symptoms can be developed by the introduction of the ptomaines and toxins alone, which hypothetical condition has been named septic-intoxication. In case of excessive doses of septic material, death occurs so early as to indicate simple narcosis. If, as is usually the case, the microbes also gain access to the blood and multiply there, the condition has been known as septic infection. In any prolonged case of septicæmia, the tendency is to the formation of suppurating foci (septico-pyæmia), so that the two affections may be looked upon as probably the same, with modifications of the earlier phenomena.

In connection with septicæmia must be mentioned the fermentation fever of Bergmann, (aseptic or resorption fever) which follows on extensive wounds, even if aseptic, on the intravenous injection of the blood of healthy animals or even of fine foreign particles (charcoal, flour), of a normal salt solution, or of well water, or of pancreatin, pepsin or trypsin. It has been attributed to the introduction and metabolism of fibrine and other elements, but manifestly arises also from the solution of blood globules, (hæmolysis). It comes on within a few hours after a severe operation or other cause and lasts from one to three days, terminating in recovery, unless complicated by some intercurrent infection.

The sapræmic fever, of Mathews Duncan (sapros—putrid, haima—blood) may also be named in this connection. It is associated with one or more of the common saprophytes (Bacillus saprogenes 1–2 and 3 of Rosenbach, Proteus Vulgaris, Proteus Zenkeri, Proteus mirable, etc.) These are propagated with difficulty in the blood, but grow readily in pus or necrotic tissue from which their toxic products can pass into the blood.

Again the observations of Brieger and Maas, Ruine, Vaughan, Bourget and others show that the isolated toxins from putrefactive fermentation of animal matters, apart from the living bacteria are capable of producing the characteristic symptoms of septicæmia.

It is now generally concluded that the septicæmic phenomena can be produced by the introduction of such poisons, whether they are the product of septic fermentations outside the animal poisoned, or of fermentation in dead matter in the economy of such animal.

Lesions. In fermentation fever no tissue lesions are known. In septicæmia gross lesions are usually lacking unless the case has been prolonged to allow of secondary abscesses (septico-pyæmia). The blood however is dark and coagulates feebly if at all. The spleen is enlarged, softened, dark in color and gorged with blood. There are petechial hæmorrhages into the serosæ and mucosæ, and the solid organs; cloudy swelling of internal organs from coagulation necrosis; a parboiled appearance of heart, liver, kidneys and voluntary muscles; congestion of the lymph glands and usually the presence of the specific microbes in the blood and local lesions. The kidneys are always congested, and their epithelia granular and swollen, and there may be exudation between the glomeruli and their capsules.

Symptoms. Septic intoxication or septic infection may be ushered in by a staring coat or slight chill, but it rarely shows a violent rigor, such as inaugurates pyæmia. There is a rapid rise of temperature (102° to 104°), which persists for three to seven days without the marked remissions of pyæmia; weak, compressible pulse; great muscular debility; hurried, shallow breathing, usually without cough; anorexia; emesis in vomiting animals; dusky or yellow mucosæ from dissolved hæmoglobin; scanty, high colored urine, rarely albuminous; dulness, sometimes nervous twitching, delirium, apathy, stupor or paraplegia; and either constipation or, later, diarrhœa. When such symptoms supervene on a gangrenous sore, septic abscess or fistula, retained placenta, blood clot in the uterus or elsewhere, suppurating tubercle, or other morbid product, gangrenous lung or other internal organ, purulent pericarditis, pleuritis or peritonitis, or any febrile affection which is complicated by necrosis, septicæmia is to be suspected. “Septicæmia should always be suspected during the course of any disorder the lesions of which afford an opportunity for the growth and development of septic microörganisms, when the symptoms of that disorder depart from the usual type and an elevated temperature continues beyond the usual duration.” (Atkinson). “The final diagnosis of septic infection must be based on the existence of an infection atrium, through which pus microbes have entered the tissues, and from which they have reached the general circulation.” (Senn).

Prognosis is always grave. A slight infection, overcome by the leucocytes or a simple septic intoxication may get well in two or three days, but an acute progressive septic infection will usually prove fatal in from one to seven days.

Prevention does not differ from that recommended for pyæmia.

Treatment is virtually hopeless unless it can secure the removal of the necrotic tissue or fermenting material from which the poison is derived. When the poisoning is due to the absorption of septic products only, with little or no introduction of microbes (septic intoxication) the removal of their source of supply may bring about a speedy and permanent improvement. The removal of a putrid placenta, or liquid from the womb, followed by irrigation with an antiseptic lotion, the evacuation of a putrid abscess, empyema, or ascites, followed by a similar disinfection, or indeed the extirpation of a sloughing and putrid mass of any kind may be followed by a lowering of temperature within a few hours, and a steady improvement in the general symptoms. The antiseptic agents employed must be sufficiently potent, and persistently applied to render the surface sterile and yet not so caustic as to destroy more tissue to become a future culture medium for the septic microbes. Mercuric chloride (1:2000), aluminium acetate (1:100), powdered iodoform, or aristol will often serve a good purpose, to be followed, when necessary, by efficient drainage and a covering of antiseptic gauze. When the primary source of infection is in the intestinal canal, calomel, naphthalin or B. napthol may be tried.

For the weak heart strychnine is the most safe and reliable agent. Quinia in large doses acts as an antipyretic, without the attendant dangers of the coal tar products. It may be advantageously combined with tincture of chloride of iron.

Ammoniacal and alcoholic stimulants are largely resorted to to tide the patient over the period of depression, and nourishing and easily digested food should be given so far as the stomach can make use of it. Skim milk, eggs, and beef tea may be given even to the herbivorous patient.

The thirst should be met by plenty of pure water to favor elimination of the toxins, and the surface frequently sponged with tepid water, not only on the ground of cleanliness and disinfection, but also as calculated to lower the febrile temperature.

MALIGNANT ŒDEMA.

Definition. Causes. Bacillus septicæmiæ gangrenosa, anærobic, rarely in living blood. Source of germ in soils. Pathogenic to man and domestic animals except cattle. First attack immunizes. Infects deep wound, exudates, dropsical and gangrenous parts, womb, intestine, debilitated parts, large dose intravenously. Lesions and symptoms: excess of exudate, boggy swelling, watery discharge, fœtid gas bubbles, œdema of lungs and bowels. Complex infection. Minimum dose—abscess. Diagnosis: from black quarter and anthrax. Treatment: free incisions, hydrogen peroxide. Prevention: disinfection of skin and wounds. Immunity.

Definition. An acute bacteridian disease of domestic and wild mammals, and of man, manifested by doughy, painful and often crepitating swelling in the vicinity of the affected part, and proving fatal in many cases in twenty-four to forty-eight hours.

Cause. The essential cause is the bacillus of malignant œdema, the septic vibrio of Pasteur, bacillus septicus gangrenæ of Arloing, the bacillus of septicæmia gangrenosa of others.

Morphology. This is a staff-shaped microbe 3–4 μ. long by 1 μ. broad, often united in chains of three or more to form long flexuous filaments. They are furnished with numerous flagella by which they are rendered very actively motile. The movements are tardy or simply flexuous in the filaments. Spores form in the isolated bacilli (not in the filaments) in suitable culture media and at a temperature of from 20° to 38° C. They occupy a place near the centre of the bacilli, not the ends as in the bacillus of emphysematous anthrax. The bacilli are anærobic and die quickly in air, but the spores are unaffected by oxygen. The spores are similarly resistant to most disinfectants. They will grow readily in ordinary culture media if oxygen is excluded, for example under an atmosphere of hydrogen, nitrogen or carbon dioxide, and liquefy gelatine. Even the oxygen present in the circulating blood is highly inimical to them, so that they are rarely found in the blood during life, but rapidly invade both it and the tissues after death, and the suspension of respiration. In peptonised and glucosed gelatine the colonies are characterized as globules of liquefaction usually combined with gas. The germ is widely distributed in soils in general and not confined to limited areas like the bacilli of anthrax and black quarter.

Animals susceptible. The bacillus attacks man, horse, ass, goat, sheep, pig, mouse, Guinea pig, rabbit, white rat, cat, dog, chicken, pigeon, and duck. The mature ox is immune, but calves suffer. Dogs are often immune having already suffered from the disease. A first attack gives immunity from a second.

Infection Channels. Inoculation on an abrasion of the skin or surface sore is not usually infecting, the oxygen of the air destroying the germ. If, however, it is inserted deeply in the connective tissue, subcutem, it grows readily in a susceptible animal. Hence the danger of infection in deep wounds the recesses of which are not exposed to the air, and in such it becomes a most redoubtable surgical complication. If such wounds are the seat of active inflammation, with abundant exudate and more or less exclusion of the air-bearing blood, and in cases of blood stasis the field is specially inviting to the bacillus.

The debility of the injured tissue is a further invitation to the attack. Chauveau injected 4 to 5cc. of virulent liquid of malignant œdema into the veins of a ram and then practised bistournage, with the result that an invasion of malignant œdema of the scrotum and tunica vaginalis followed immediately. Pure cultures may be harmless, whilst an admixture of proteus vulgaris or micrococcus prodigiosus renders them most deadly (Penzo). Granulating wounds are even less favorable to invasion than simple abrasions. In these the bacillus cannot enter at once into the lymph channels and is exposed to destruction by the combined influence of the air and leucocytes.

Wounds in dropsical or gangrenous parts are equally favorable, to the development of the bacillus. Under such conditions the tissues are wanting in oxygen and resemble the condition of the entire body after death, when the bacillus of malignant œdema quickly penetrates its whole substance. Petri has traced the infection through the genital passages of newly delivered rabbits, producing a fatal metro-peritonitis and cutaneous œdema. A similar invasion may take place in other susceptible parturient animals. Lustig in a certain number of cases satisfied himself that he had traced the invasion through the intestine of the living horse. Invasion by the lungs, even by spores, is usually rendered impossible by reason of the presence of the inspired air.

A large dose of the virus is most likely to effect a successful invasion, since the toxins tend to debilitate and lower the defensive powers of the tissues and leucocytes. The effect of the toxins is shown under injections into the arteries, veins or trachea. A certain amount of hyperthermia follows, but there is rarely any colonization and reproduction of the bacillus in the connective tissue. In dogs and rabbits large doses given in this way induce short inspiration and broken or double expirations. In fatal doses death is preceded by extreme dyspnœa and convulsions. (Rodet and Courmont).

Lesions and Symptoms. The tissues where invasion occurs, become the seat of an abundant œdematous exudation, which feels boggy and painful and may even crepitate when pressed or manipulated. In case of an open wound, there is a profuse liquid discharge of a yellowish watery or serous aspect, and bubbles of gas or froth having a somewhat fœtid odor. The center of the swelling may become soft and flaccid while the peripheral parts where the disease is advancing are tense and resistant.

In fatal cases the mucosæ of the small intestine and lungs are usually the seats of œdema in which the bacillus is found. The bacilli may also be found in the liver. It is noticeable that gross lesions of the spleen and kidneys are usually absent, in marked contrast with anthrax. The microbes found in the tissues may be in the form of bacilli, micrococci (spores, or m. prodigiosus), and sometimes filaments.

Inoculation with a minimum dose usually results in local abscess only.

Diagnosis. From emphysematous anthrax, with which malignant œdema is most likely to be confounded, it is to be distinguished by its appearance anywhere outside the black quarter areas, by the immunity of cattle which are so obnoxious to emphysematous anthrax, by the susceptibility of man, who does not contract black quarter, by the formation of the spore near the middle of the bacillus in place of at one end, by its resistance to the action of ordinary disinfectants, and by the greater tendency to form filaments.

From anthrax it is differentiated by its appearance outside the anthrax localities, by the absence of the bacillus from the blood and from the surface layers of the skin, by the normal size of the spleen, and by the active motility of the bacillus. It cannot be cultivated like anthrax in the free air or on the surface of culture media, and unlike anthrax bacillus, its cultures produce bubbles or gas.

Treatment. This is essentially surgical and consists in free incisions to admit air freely to all parts of the œdematous tissue, perfect drainage and a liberal use of peroxide of hydrogen. Other disinfectants may be employed but are much less promising. The free disinfection of the adjacent skin is an important element in treatment.

Prevention. This consists essentially in the thorough disinfection of all accidental and surgical wounds, the careful cleansing and antisepsis of the skin before an operation, the exclusion of earth, manure, or water from driven wells or fountains, from all wounds, and above all the exclusion of proteus vulgaris, and micrococcus prodigiosus.

Immunity may be secured by a first, non-fatal attack of the disease.

INFECTIOUS FEVERS OF SWINE.

One name for several affections. Differentiation, swine erysipelas, hog cholera and swine plague. Complex infections. Effects of large, medium and small doses, of more or less potent germ, of greater or less susceptibility.

Until comparatively recent years the various infectious fevers of swine have been confounded and described as a single disease, the name varying in the different countries in which they were observed. In America it was Hog Cholera; in England, Swine Fever; in France, Rouget; and in Germany, Schweineseuche. A closer study showed a marked tendency to a particular class of lesions in different epizoötics, and bacteriological research associated plagues in given localities with different microbes, so that progress has been made in differentiating one from another to a certain extent.

The first clear distinction was made in setting aside the swine erysipelas (rouget, rothlauf,) from the rest as distinguished at once by its small, delicate bacillus, differing notably from the others in its staining and cultural peculiarities, as well as in the predominance of the cutaneous lesions.

What remains after eliminating erysipelas, constitutes a group having so much in common that attempts at further differentiation have led to much disputation, and not even to-day is there such accord in different countries as the writer of a text-book would find desirable. One class of pathologists claims but one common disease with many varieties under different conditions, just as the term septicæmia or blood poisoning has been made to designate a whole class of local and general infections, irrespective of the particular microbes that cause them. Others with greater precision give the disease a name according to the causation by one particular microörganism, or by another, which may be closely related to it in many respects, but which in successive subjects and outbreaks, maintains its own individual characteristics as regards morphology, cultural and staining habits, pathogenesis, etc. The question has been rendered all the more trying, by the occasional association in the same animal system, or in the same outbreak of two distinct varieties of microörganisms, in place of one, giving rise of course to modifications in the symptoms, lesions, progress, mortality, etc.

Apart from the microörganism the whole class tends to show a close family relationship in their pathological phenomena shown under different conditions :

1st. Under a large dose, or specially virulent germ, in a particularly susceptible animal, all tend to a manifestation of an acute septicæmia, with generally diffused petechiæ of the skin, mucosæ, serosæ and internal organs, blood extravasations, and an early high mortality.

2d. Under a smaller dose, or a less potent germ, or in a less susceptible animal the tendency is to necrotic processes in the seat of inoculation or the point of election of local lesions. Necrotic ulcers are especially common in cases that survive one, two or three weeks, or that develop in a subacute or chronic form.

3d. With a minimum dose of a germ of little potency, and in a very resistant subject even the necrotic lesions may be absent, and there may be suppuration only or ulceration of serosæ and joints.

The question of the primary identity, or disparity of the whole class of germs, causing the septicæmic swine plagues, may be practically ignored in this work; it is important rather with our present knowledge to note the diseases associated with particular germs, or varieties of germs, and to describe these as far as possible as independent affections. This is as permissible as it is to describe smallpox, sheeppox, and cowpox as distinct affections, no matter what may be the truth or falsity as to their alleged original identity.

Rouget in Europe and Hog Cholera and Swine Plague, as the best established types in the United States deserve primary mention, to be followed by references to additional types which have been found to be associated with other distinct microörganisms.

ROUGET, ROTHLAUF. RED FEVER OF SWINE. SWINE ERYSIPELAS.

Definition. Comparative immunity of sucking pigs. Disease unknown in America. Causes: Bacillus erysipelatos suis, mature age, infection through yards, buildings, troughs, dust, mice, rabbits, pigeons, men, dogs, vermin, birds, butcher’s and kitchen scraps, swill, hot weather, damp seasons, close pens, movement of swine, stockyards, fairs, public conveyances, public highways. Symptoms: incubation three days, chill, violet mucosæ, hyperthermia, recumbency under litter, muscular weakness especially behind, inappetence, thirst, costiveness, later diarrhœa, tenderness to touch, lymph glands swollen, red, blue, violet or black discoloration of skin, cutaneous swelling and pitting. Course: death in 12 hours to 6 days, or convalescence prompt. Mortality 20 to 80 per cent. Lesions: congestion of capillary vessel, blood extravasations, petechiæ, affecting cutis and subcutaneous fat, lymph glands congested, discolored; lungs engorged; spleen enlarged, liver and kidneys congested, petechiæ general, blood little altered. Bacillus 1.5 μ, anærobic, easily destroyed in pens, in pork. Pathogenesis: swine, rabbits, mice, rats, pigeons and sparrows suffer. Rabbit germ less fatal to pigs. Immunization, advantages and drawbacks. Technique.

Definition. A microbian disease of swine manifested by high fever, great prostration and muscular weakness, a violet tint of the visible mucosæ, red or violet discoloration of the skin in spots and patches or universally, enlarged lymph glands, encreased size of the spleen, and general congestion of the capillary plexus.

Contrary to the habit of hog cholera and swine plague, rouget attacks mature swine mainly, the sucking pig showing a remarkable power of resistance. It does not appear whether this is due to the animal (milk) diet or to the absence of infection from feeding in the trough used by the adult animals. Up to the present this disease has not been recognized in America.

Causes. The one essential cause of rouget is the presence of the bacillus. The other conditions are either such as predispose the animal to receive it, for example, mature age: or they are such as favor diffusion of the poison, such as the introduction of an infected animal, the feeding of the healthy from the same manger with the infected, the introduction into the manger of the feet or snout which have become soiled with the infected manure or urine, the distribution of the infection in dust, the introduction of the bacillus in the bodies of mice, rabbits, or pigeons, or on the feet of those animals, of men, dogs, birds, and vermin. We may add the distribution of infection in dried butcher’s scraps used in pig feeding, and in uncooked scraps from the kitchen or in hotel swill.

It has been noted that the highest mortality prevails in hot summer weather, in damp seasons, and in narrow, confined, badly ventilated pens. Under such circumstances the introduction of a diseased pig will lead to the infection of most of the others in a few hours. Infection is quite as prompt through public pens in stock yards and fairs, and in public conveyances (cars, stock wagons, steamboats, ferry boats, etc.) and public highways.

Symptoms. After a period of incubation of three days or more the subject is seized with shivering, the limbs are hot and cold alternately, respiration and heart beats are accelerated, the mucous membranes assume a dark violet tint and the rectal temperature rises to 104° to 108° F. From the first the pig tends to bury itself under the litter, and refuses to move unless absolutely forced to do so, and then only with painful grunts, swaying and staggering limbs (especially the hind ones), and straight drooping tail. There is inappetence, but thirst remains, and the bowels are at first costive, the manure being covered with a film of mucous or even streaks of blood; later they become relaxed and diarrhœa becomes often a prominent symptom. The pig seems to suffer and often squeals when handled, and he may give a weak, dry cough. The external inguinal glands may often be felt perceptibly enlarged. The red discoloration of the skin appears early and extends and deepens to the end in fatal cases. It may be of a bright red, or of a bluish red, violet or black. The first indications appear as spots, by preference around the roots of the ears, on the breast and abdomen, inside the arms and thighs, and in the perineum. These isolated spots run together into great patches, which extend over the whole ventral aspect of the body, and may cover the entire dorsal aspect as well. In some instances the skin is swollen and retains an impression made by the finger.

Course. The disease may reach a fatal termination in twelve hours: more commonly it endures for forty-eight hours, and at times it will last for four, five or six days. In the most rapidly fatal cases, the violet discoloration of the skin may be absent or only a little marked, while in the protracted cases it acquires its greatest extensions and its darkest shades. In the protracted cases too the prostration becomes extreme, the animal may find it impossible to raise himself on his hind limbs, the diarrhœa becomes profuse, liquid and fœtid, the respiration labored, cyanosis sets in and the temperature is reduced below the normal standard.

In case of recovery, convalescence is usually prompt and complete, differing in this from cases of swine plague and hog cholera. The more favorable issue in rouget probably depends on the comparative integrity of the intestinal mucosa and mesenteric glands, which are subject to slow healing lesions in swine plague and hog cholera. Slow convalescence is however not uncommon, yet in such cases, the concurrent, speedy and complete recoveries in other animals in the same herd serve to identify the disease as rouget.

Mortality. The mortality among grown hogs averages eighty per cent.

Morbid Anatomy. The most prominent lesion is the general congestion of the capillary blood vessels, and the numerous minute extravasations or petechiæ. The skin shows in the red patches a general dilatation of the capillaries which have become at the same time elongated and tortuous, with minute, often microscopic, ruptures and extravasations at frequent intervals. This usually extends to the whole thickness of the cutis, and to a considerable depth in the subcutaneous fat. Where swelling occurred or pitting on pressure, a serous infiltration of the tissues is found. The lymph glands are uniformly enlarged and discolored, of a dark red, almost black, color, the congestion and extravasation being extreme in the cortical substance, while the medullary is paler, soft and cellular. The lungs are usually gorged with black blood suggesting death by asphyxia. In tardy cases there may, though rarely, be centres of broncho-pneumonia. The spleen is enlarged, with dark color and uneven surface from rounded swellings, and is filled by a soft black, bloody pulp. The liver is congested, the kidneys congested, enlarged and petechiated, and the gastric and intestinal mucosa congested and thickened, with desquamating epithelium, and swollen solitary and agminated glands, the degree of alteration usually bearing a ratio to the duration of the disease. The serosæ are usually extensively petechiated and serous effusions occur into the serous cavities. The muscular substance of the heart and the endocardium are also the seats of petechial extravasations. Unless in some protracted cases the blood appears to be unaltered as regards its power of taking up oxygen, or coagulating.

Bacillus of Rouget. The germ of this disease is found in small numbers only, in the blood and vascular tissues, but very abundantly in the lymph glands, the spleen, the kidneys, and the red marrow of the bone. It is also present in enormous quantities in the urine and the bowel dejections, the former (urine) offering a ready means of diagnosing the disease microscopically.

The bacillus is 1µ to 1.5µ long by 0.1µ to 0.15µ broad, is nonmotile, and stains readily even in Gram’s solution. They occur either solitary or in pairs tending to unite at an angle. In old artificial cultures chains of considerable length may be formed. In the blood the bacillus is usually found in the leucocytes, as many as 20 or more being often present in a single cell. In the lymph networks of organs they also invade the leucocytes but are found in free masses as well. The bacillus is anærobic, but facultative ærobic, its preference being manifestly for the absence of oxygen. It is non-liquefying. In gelatine cultures no development takes place on the surface, but along the line of puncture a delicate cloud-like branching growth takes place which extends horizontally in parallel masses from the central puncture. This resembles but is not quite so delicate as that formed by the bacillus of mouse septicæmia with which it is supposed to be identical. It grows scantily on the surface of nutrient agar or blood serum, but not at all on bouillon, in the bottom of which, however, it forms a slight grayish white deposit. It does not grow on potato. The bacillus sometimes shows refrangent granules which have been supposed to be spores, but this idea appears to be negatived by the ease with which its vitality is destroyed by heat and disinfectants. The thermal death point is 68° C. (137° F.) maintained for 10 minutes (Sternberg). Boulton found that it was killed in 2 hours by mercuric chloride (1:10000), by carbolic acid solution (1:100), and by sulphate of copper solution (1:100).

It is killed by desiccation, by quick lime and by chloride of lime. At a temperature of 18° to 27° F. it perished in 13 days. In salted pork it lost vitality in one month.

Pathogenesis. The bacillus is pathogenic to swine, rabbits, white mice, house mice, white rats, pigeons and sparrows. Field mice, guinea pigs and chickens are immune.

Mice and pigeons take the disease most certainly, and die in three days to five, the whole body swarming with bacilli. Rabbits take the disease less certainly or rapidly, inoculation in the ear causing first an erysipelatoid inflammation and recovery with immunity often takes place.

Immunization. When inoculated continuously from rabbit to rabbit it encreases its potency for that animal, which it comes to kill in 24 to 48 hours, but in the same ratio it loses its virulence for swine upon which it can then be inoculated without danger to their life.

It was on this basis that Pasteur and Thuillier established in 1883, their preventive inoculation for rouget. The method has been most extensively employed in Europe, and where intelligently employed has prevented this disease. From the laboratory at Buda-Pest alone, there was sent out in one year material for 249,816 swine.

The objections to the method are: the danger of mistaking hog cholera and swine plague respectively for rouget, as the rouget mitigated germ would be in no sense protective against these; and the danger of spreading the germs of rouget in fresh localities and thus introducing a new plague instead of controlling and preventing an old one. In the Baden experiments 5.4 per cent. of inoculated pigs died, and of 118 unprotected pigs exposed to them 62 per cent. contracted the disease and one died. In France and Hungary, on the other hand, 1 to 1.45 per cent. died of the operation, instead of 20 per cent. when the disease was contracted in the ordinary way.

It is held that the danger lies largely in the inoculation of very young pigs, and Nocard advises to operate only on those of four months and upward.

The danger of spreading the germ by inoculation may be the more easily guarded against, considering that it is very destructible by disinfectant agents (heat, dryness, cold, chloride of lime, quick lime), and that it does not readily survive in a locality, where it cannot find a constant succession of victims. Yet the practice ought to be confined to herds exposed to infection, and under special precautions, as regards the exposure of other herds.

The technique of the Pasteurian inoculation is to inject, subcutem, on the inside of the thigh, 0.1cc. of the weaker preparation (premier vaccin), and twelve days after a similar dose of the stronger one (deuxieme vaccin).

This produces a mild attack of the disease from which the great majority recover, and though they still react somewhat to a second and third inoculation yet the disease so produced is rarely fatal.

CHOLERA SUIS; HOG CHOLERA.

Definition, Synonyms, History, Losses. Bacillus choleræ suis, 1.2–2μ., ærobic, biology, table of germs; accessory causes, roaming pigs, railways, car litter and manure, boats, trucks, loading banks, chutes, runways, stockyards, pens, fairs, watershed, butchers, dealers, etc., wagons, dogs, birds, vermin, insects, offal of abattoirs, butcher’s and kitchen scraps, unburied carcasses of dead hogs, convalescent and immune hogs, susceptibility, parasites and infection atria, putrid food, infection from ground carried into feeding trough by snout and feet, large herds, rapid carriage of swine for long distances. Lesions: hæmorrhagic spots and petechiæ on skin, mucosæ and serosæ, circumscribed capillary congestions, congestion of spleen, lymph glands, stomach, intestines, necrotic processes. Button-like ulcers on intestinal mucosæ. Incubation, 6 to 14 days. Symptoms: fulminant cases. Acute Cases: dulness, anorexia, recumbency on belly, weakness, paresis behind, thirst, tenderness of skin and abdomen, hyperthermia, easily blown, blush on skin, dark red spots and patches, enlarged inguinal glands, cutaneous exudate—greasy or drying black, bowels costive, later pultaceous and finally diarrhœaic, petechiæ on mucosæ, emaciation. Chronic Cases: symptoms more slight, but great loss of condition. Diagnosis: from swine erysipelas, swine plague, Widal test, table of differential symptoms. Prevention: expense of extinction prevents effective measures; removal of accessory causes, comfort, air, light, food, salt, powdered soaps, mouldy bread, cotton seed, space, green food, precautions against introduction of bacillus, special shipping provisions for fat hogs, exclusion of stock hogs from infected localities, precautions by purchasers. Immunization, Disinfection. Certificates. Extinction in herds and districts. Treatment: chronic cases, food, antiseptic medication, antithermics stimulants, tonics. Serum therapy, method, merits, demerits.

Definition. A contagious bacteridian disease of swine, acute or subacute, and characterized by hyperthermia and other febrile disorders,—congestion, exudation, ecchymosis and necrotic ulceration of the intestinal mucosa and of that of the stomach and of other parts,—by a profuse foul, liquid diarrhœa, by enlargement of the lymph glands with congestion and blood extravasation,—by effaceable blotches, and petechiæ (ineffaceable) of the skin, snout and visible mucosæ, with a tendency to necrotic changes—less frequently by pulmonary congestions, and degeneration,—and by a high mortality.

Synonyms. The earlier designations were mostly drawn from the red or black discoloration of the skin and mucosæ and applied indiscriminately to the other forms of hæmorrhagic septicæmia which we now differentiate as erysipelas (rouget, Rothlauf) and swine plague. They included measles, erysipelas, scarlatina, red soldier, purples, blue sickness, carbuncular fever, etc. Others basing their nomenclature on the prominent intestinal lesions, etc., designated it typhoid fever, pig typhoid, typhus, carbuncular gastro-enteritis, pneumo-enteritis, and diphtheria. Even in Europe while the pig erysipelas (rouget, Rothlauf) is now recognized as a distinct disease there is no clear distinction made between hog cholera and swine plague. In England we find these more or less confounded under the names of swine fever, swine plague and hog cholera, and on the continent of Europe under those of schweineseuche and schweinepest, or pneumo-enteritis infectieuses. Differences in different epizoötics or outbreaks are recognized, and the field is left open for the future identification of different forms of this common group of swine fevers, but the existence of constant bacteriological distinctions are not always insisted on, as we do in the United States in the case of the two great leading types swine plague and hog cholera.

History. Definite history of this disease may be said to begin with the discovery and demonstration of the actively motile hog cholera bacillus by the U. S. Bureau of Animal Industry in 1885. Yet in the history of animal plagues, even in early times, deadly epizoötics are described which undoubtedly represented one or other of the contagious affections of modern times. Among the more definite may be named a destructive gastro-enteritis (magen seuche) in Germany in 1817, a pleuro-pneumonia in France and Bavaria in 1821, a cholera with blotching of the skin (morbus niger) in Ireland, and an erysipelas in pigs in France and Switzerland in 1836, and in Ohio in 1833, there was a fatal affection afterward recognized as hog cholera. Writers conjecture that it was imported into America from Europe in improved pigs, and from one European country to another in the same way, but we have no absolute proof of times and shipments and their immediate effects, so that these theories are but more or less reasonable deductions from the familiar extensions of the disease in more recent cases. Under the great commercial activity of the latter half of the 19th century, the active movements of animals by canal, steamboat and rail, and the massing together in one market of many animals drawn from widely different sources, hog cholera has made extraordinary extensions on both sides of the Atlantic, until Friedberger and Fröhner pronounce the schweineseuche and schweinepest the most widely disseminated and dangerous of swine epizoötics, and Dr. Salmon estimates the losses in the United States at $10,000,000 to $25,000,000, per annum.

Bacteriology. Prior to 1885 bacteria had been found in the different outbreaks of contagious fevers in swine, and the bacillus of swine erysipelas had been demonstrated in 1882, but it was only two years later (1884) that the motile bacillus choleræ suis was first described by Klein, and in 1885 that Salmon and Smith demonstrated it as the essential cause of the disease, together with its biological and cultural peculiarities.

It is a short bacillus, 1.2 to 2μ × 0.5 to 0.8μ, but varying considerably in size according to the stage of its growth and the genera of animal or culture medium in which it is grown. It has rounded ends and is usually in pairs connected by an invisible band. It stains promptly in all the aqueous aniline colors, but loses the stain in a solution of iodine (Gram’s). Prolonged exposure of artificial cultures produces an uniform stain, while a transient exposure, and especially of bacilli obtained from the tissues, stains them most deeply at the ends (polar) and periphery, while the centre remains somewhat clear. This is less marked than in the bacillus of swine plague, yet serves to show the relation between this microbe and the colon group.

It is ærobic (facultative anærobic), non-liquefying, and, in fluids, very actively motile, the movements lasting for months in preserved specimens (Smith). It grows luxuriantly in various culture media, and especially in alkaline ones, at the room temperature, and most actively at 85° to 100° F. It may grow as low as 60° to 70° F. and as high as 104°. (Swine plague bacillus grows at 55.4°).

On peptonized gelatine the surface colonies are usually round and flattened, those in its substance globular and smaller, and those at the bottom expanded next the glass and rising in the center into the gelatine like a knob. At 48 hours they appear as opaque whitish points and slowly increase to ½ to 2 mm. They may be brown by transmitted light, the depth of color increasing with age. On agar the colonies are grayish, shining and translucent and may reach the size of 4 to 6 mm. On potato (alkaline) a straw yellow film is formed, darkening with growth. In bouillon a turbidity appears in 24 hours, and in 1 or 2 weeks a precipitate and surface film.

The bacillus is usually larger in the gelatine and smaller in the bouillon than it is in the tissues. It seems to produce neither phenol nor indol.

Its behavior with sugars is significant. It ferments glucose producing acid and gas; does not ferment saccharose nor lactose, but turns the saccharose solution alkaline (no gas). In bouillon containing muscle glucose, it may without additional glucose form a little gas. The swine plague bacillus ferments saccharose producing acids but no gas: it ferments neither glucose nor lactose but turns the former acid.

Milk is neither coagulated nor soured by the hog cholera bacillus, but in 3 to 4 weeks it undergoes a change, becoming saponified.

Cultures have no special nor offensive odor. Some varieties in close tubes may cause a faint acid odor.

Oxygen is not essential to the success of a culture. The colonies form as promptly and as large in the depths of gelatine, or in a vacuum, as if in free air.

The following table will serve to show differences between the hog cholera bacilli, and related pathogenic microbes:

=Hog Cholera.= =McFadyean’s.= =Swine Plague.=

B. Choleræ Suis Swine Fever B. B. Pestis Suis

1.2 to 2μ × 5 to 0.8μ 2 to 2μ × 0.6μ 0.8 to 1.5μ × 0.6 to 0.8μ

Ends rounded Ends rounded Ends rounded

Involution forms Involution forms

Actively motile in Actively motile Nonmotile liquids

Flagella No Flagella

Stains throughout, Polar or uniform faint From fresh organs polar lighter in center stain stain, from old cultures uniform

Bleaches in Gram’s (I) Bleaches in Gram’s (I) Bleaches in Gram’s (I) Solu Solu Solu

Ærobic (Fac. Anærobic) Ærobic Ærobic, (Fac. Anærobic)

Vigorous growth in Slight growth in Weak growth in alkaline alkaline nutrient alkaline nutrient nutrient fluids fluids fluids

Active growth on potato No growth on potato On potato at 37° C. a yellowish, becoming slight, thin gray, darker waxy layer

On gelatine, small, On gelatine light On gelatine feeble round brownish bluish colonies growth or none colonies shading off insensibly at edges

Nonliquefying Nonliquefying Nonliquefying

On agar conical On agar slight, On agar, grayish colonies, grayish, transparent, almost translucent, or white, semi- invisible growth brown, knobbed, translucent shining waving edges

In milk grows freely, Grows in milk, no clot Grows in milk, no acid, no acid, no clot: no clot Saponifies in 3 or 4 weeks

Forms no indol in Forms no indol in pancreatic bouillon pancreatic bouillon

Ferments glucose, Does not ferment forming acid and gas glucose, forms acid, no gas

Lactose not fermented Lactose not fermented

Saccharose not Saccharose fermented, fermented; forms acid, no gas alkalinity; no gas

Thermal death point Thermal death point 58° Thermal death point (moist) 58° C. in 15 C. in 10 minutes (moist) 58° C. in 7 minutes minutes

Desiccated it dies Dies quickly, if dried Dies in 3 days if dried according to bulk in at body temperature 7 to 49 days

Dies in water in 3 to 4 Dies in water in 10 to months 15 days

Dies in soil in 2 to 3 Dies in soil in 4 to 6 months days

Pathogenic to swine, Pathogenic to swine and Pathogenic to swine, rabbits, guinea pigs, rabbits hens, pigeons, mice, pigeons pheasants, sparrows, mice, rabbits, cattle, deer, guineapigs, etc.

Guinea pigs immune

=Swine Erysipelas.= =B. Coli Commune.= =Typhoid Fever.=

B. of S. Erysipelas B. Typhi Abdominalis

1 to 1.5µ × 0.1 to 0.2µ 2 to 3µ × 0.4 to 0.6µ 1 to 3µ × 0.6 to 0.8µ

Ends rounded Ends rounded Ends rounded

Involution forms Involution forms

Nonmotile in liquids Nonmotile or very Motile slightly so

No flagella No flagella Flagella

Stains readily and Stains uniformly or Stains uniformly uniformly polar (points clear)

Stains in Gram’s (1) Bleaches in Gram’s Solu

Anærobic (F. Ærobic) Ærobic (F. Anærobic) Ærobic (F. Anærobic)

Active growth in common Grows well in usual Grows well in usual nutrient liquids at nutrient liquids, nutrient liquids 37° C. even if acid

Usually no growth on Yellowish thick white Grows on potato; potato; variable growth on potato transparent glistening surface

In gelatine In gelatine amber On gelatine clear stab-culture delicate colonies, becoming colonies with feathery branching brown; may be bubbles radiating and growth of gas encircling lines

Nonliquefying Nonliquefying Nonliquefying

Grows in milk; Acidifies and clots Acidifies milk growing acidifies, often milk in 8 to 10 days freely coagulates it

Thermal death point Thermal death point Thermal death point (moist) 58° C. in 10 (moist) 60° C. in 10 (moist) 56° C. in 10 minutes minutes minutes

Loses virulence rapidly when dried

Dies in water in 18 to 20 days

Lives and even Lives and grows in multiplies in rich fæces soils, manure, etc.

Loses virulence slowly in light and air

Pathogenic to swine, pigeons, sparrows, rabbits, white and house mice, white rats

Guinea pigs, field mice and hens immune

=Hog Cholera.= =McFadyean’s.= =Swine Plague.=

Hen or pigeon has Hen or pigeon dies in slough where 48 hours, after inoculated, diarrhœa, drowsiness, drooping ruffled plumage, wings, sunken head, somnolence ruffled plumage, liquid stools, soft black comb and wattles, prostration

Rabbits getting 0.1cc. Rabbits getting 0.5 to Rabbits getting 0.01cc. virulent culture 1cc. culture subcutem culture subcutem die subcutem die in 5 to had tumor like walnut in 16 to 20 hours, 7 days with enlarged but recovered with inflamed serosæ spleen and necrotic and lung; Petechiæ liver foci

Weaker culture kills in Weak cultures kill in 4 10 to 20 days with to 10 days, with enlarged spleen, or inflamed serosæ and recovery ensues suppuration

Guinea pigs die in 7 to Not pathogenic to Guinea pigs die in 1 to 12 days Guinea-pig 4 days

Swine inoculated Swine inoculated have subcutem have often local lesions only, local lesions and only exceptionally bacilli, also in fatal lymph glands, only exceptionally fatal

Ingestion of virulent Ingestion of 30cc. by Ingestion of virulent cultures by fasting pigs proved always cultures by pigs is pig causes bowel fatal usually harmless lesions and death

Intravenous inoculation Intravenous inoculation in pig causes causes septicæmia and septicæmic lesions death in 1 or 2 days and death, or chronic diseases and typical bowel ulcers

Intrapulmonary infection causes pleuro-pneumonia

Swine erysipelas kills inoculated pigeon in 3 to 8 days, and rabbit in 4 to 8 days.

Accessory Causes. These are especially those conditions which favor the transmission of the germ from animal to animal. They include the reprehensible habit of allowing swine to run at large so that herd mingles with herd; the freedom to wander along the lines of railroad by which hogs are carried, and where the infected excretions fall on the ground; the scattering of infected litter or manure from a car or boat; the use of the same cars, boats or trucks for the conveyance of infected and sound pigs in succession, without intermediate disinfection; the use of the same loading banks, chutes, runways, yards, pens and feeding and watering troughs by strange pigs from all sources in succession, without constant disinfection; the purchase of stock swine at public markets; the return of swine from public fairs and exhibitions; the feeding and watering of pigs on the line of streams that have drained pig pens or pastures higher up; the use for pigs of premises that have harbored infected ones at an earlier (even distant) date; the supply of food or litter from barns where pigs have recently died; the admission to the pens or yards of butchers, dealers or others who are likely to carry infection on their persons; the admission even of wagons, dogs or other animals, including birds, tame and wild, which are liable to carry infection. Of all birds the buzzard is the most to be shunned as having presumably just come from infected carrion, but barnyard fowl and small birds that feed from the same trough with the pig are to be feared as well. The same remark applies to rats and mice, squirrels, skunks, woodchucks and rabbits which may easily carry the infection on their paws. If the infection is near, flies and other insects, in the warm season, will convey it for some distance from herd to herd. A common cause is the feeding of swine about abattoirs where they devour the offal and waste in a raw condition. Another is the feeding of boarding house, hotel or other kitchen slops, raw, or without the most exhaustive precautions in the way of cooking. Many outbreaks can be traced in this way to the consumption by the animals of the products of infected swine. Some indeed are fostered by the utter neglect of the parties in charge of an infected herd, in leaving the infected carcasses exposed so that they are eaten by wandering hogs, or portions are carried away by buzzards, carrion crows, dogs and other animals. In some cases a strong wind will carry the infection on dust, straw or other light object into sound herds at a distance. The introduction into a hitherto healthy herd of an apparently sound pig may be the occasion of a deadly outbreak. The strange new pig may have already had the disease, and in a condition of immunity, may without hurt to itself, carry the germ which becomes so fatal to the susceptible.

This susceptibility is one of the most important factors. It may be inherent in a given family or strain of blood. It may be enhanced by a constitutional weakness, engendered by too close breeding, by breeding from the young and immature, or from the old and worn out. It may be favored by a general debility from starvation, faulty or injudicious feeding, as exclusive feeding on corn (maize), an unbalanced ration, feeding cotton seed, irregular feeding, etc. It may result from parasitism, as round worms in the lungs, bowels, muscles, fat, kidneys or liver, from trichinosis, from cysticerci, echinococci, or from distomatosis. These not only lessen the force of constitutional and phagocytic resistance, but they also in many cases open the way for the entrance of the microbe by the wounds which they inflict. Perhaps nothing operates more effectively in this way than the attacks of other pathogenic microbes. The treatment of the domestic hog is often such that it would almost appear as if it were designed to destroy health and vitality. He is used to clear up the soiled and spoiled provender which has been rejected by other animals. Decayed vegetables and flesh of all kinds, which is no longer fit for other use, is supposed to be good for him and is furnished raw. Worse still, this is conveyed in barrels that are never washed, but are sent for each new supply reeking with abominations which render them a nuisance on the highway. It is left standing till wanted in these barrels, or in still larger receptacles, which are never emptied nor cleaned, but are allowed in the hottest weather, to continue a hotbed of the foulest fermentations. On a smaller scale the kitchen swill barrel becomes a similar centre of decomposition. Even at the creamery and cheese factory the surplus or waste products often remain in a common tank breeding larvæ, toxins and ptomaines, before they are fed to the hogs. In the hog pen, or yard, corn in the ear is thrown on the ground, already filthy with the solid and liquid excretions and is eaten with the rotting, if not infecting, filth in which it has been rolled. From grubbing in this filth with his snout, the pig plunges the latter in the liquid food in his trough and too often he gets his feet into the food as well, and further charges it with the injurious ferments. Again the kitchen swill is liable to contain various inorganic poisons and notably the carbonates and bicarbonates of potash and soda which are used to excess in the form of powdered soaps and, as shown by experiment, are deadly poisons to pigs.

The gastro-intestinal disorders caused by these poisons; (it may be botulism from stale or decomposing flesh, fish or fowl, the poisoning by mouldy bread or musty grain, or meal, or by the toxins of the many and varied saprophytic fermentations), often prove as deadly as outbreaks of genuine hog cholera, and are habitually mistaken for them. They do not, however, as a rule extend beyond the particular herd which has been exposed to the faulty management, and introduce no risk of a general spreading infection. The careless owner suffers and adjacent herds escape, unless exposed to similar causes. But if the hog cholera germ is present these pave the way for its destructive advance and tend to enhance the mortality. It may even be that the combination of the two factors is a condition of the eruption of a severe attack. The faulty feeding or food or poison by itself could be resisted, and the comparatively non-virulent hog cholera bacillus might have been resisted, but with the weakened system and digestive apparatus, the microbe finds a specially inviting field in which it can multiply destructively, and where it can gather a virulence which will enable it to invade and sweep away herd after herd in a deadly epizoötic.

I may add, as a prominent factor in the great modern extensions of hog cholera, the habitual aggregation of swine in large herds. This with the rapid steam transit of modern times, and the great aggregations of hogs in one common market, probably contributes more than anything else to the extraordinary diffusion of the infection. By accident, purchase or otherwise, a large herd becomes infected, and the owner, knowing that delay is ruin, at once ships the apparently healthy animals to market; these infect anything they or their excretions come in contact with; if sold in smaller lots they carry infection into every locality where they go, and along the route; if sold for slaughter, they still diffuse infection through the herds that receive their butcher and kitchen trimmings.

Finally other domestic animals may bring in an infection which becomes manifested by symptoms similar to those of hog cholera, and which if really different, yet serves to pave the way for such an outbreak. Galtier’s remarkable experience with a pneumo-enteritis in sheep, introduced into five separate flocks by infected pigs from the same market, is significant in this respect. It is further significant that the hog cholera bacillus is a very protean microbe. Th. Smith, to whom we owe more than to any one else the identification of the germ, gives seven varieties, which showed well-marked distinctions in their morphology, in their modes of growth on culture media, in the amount of gas they respectively produced in a glucose bouillon, or in their pathogenesis for rabbits. One of these modified germs which has largely parted with its virulence for pigs and some other animals, may under specially favorable conditions, resume its former potency and proceed on a new career of infection.

Lesions in the Acute or Septicæmic Form. The skin and subcutaneous fat are the seats of diffuse blotches or spots of a deep red varying from dark purple to light red, confined it may be to the inner sides of the arms and thighs the belly, the ears, eyelids, and muzzle, or it may be all but uniformly diffused over the body. When pressed so as to expel the blood, the greater part of the surface may be momentarily whitened, but red points remain representing the minute extravasations. Under the microscope the red points show tortuous and enlarged capillaries with here and there a rupture and minute clot. The visible mucosæ may show similar petechiæ, as may also the serosæ of the chest, cranium and abdomen. In the latter blood extravasations are liable to be more extensive. The spleen and lymph glands (particularly those of the bowels and omentum, the sublumbar and subdorsal regions) are usually enlarged, gorged with blood and softened. Many of the lymph glands may escape, and in others the congestion is largely confined to the cortical portion. The lungs may show petechiæ and even extensive hæmorrhages into their substance. The kidneys may show petechiæ in the glomeruli, the medullary substance, the papillæ or the pelvic mucosa, or there may be larger circumscribed hæmorrhages.

The stomach in its greater curvature especially is usually deeply congested and petechiated, with small submucous extravasations, and these conditions are liable to be still more marked in the small intestines and especially in the large, which may have a dark red or port wine hue. Blood may be present in clots among the contents. Necrotic ulcers are absent.

Lesions in the Protracted and Chronic Forms. The lesions of the skin are usually less extensive than in the acute type, and may be almost entirely absent. The lymph glands are enlarged and congested, though the discoloration may be largely confined to the cortical layer. The spleen is as a rule normal in size. The liver is firm, but it may show softening of the secreting acini and encrease of the fibrous framework. Petechiæ or circumscribed hæmorrhages may or may not be present on or under the serosæ or in the tissues.

The characteristic lesions belong to the gastric-intestinal organs. Congestions and ulcers may be found on the gastric mucosa, on that of the small intestine, and rectum, but they are above all common on the ileocæcal valve, cæcum and first half of the colon. In the earlier stages of these lesions the mucosa and submucosa are the seat of a congestion and exudation, but later the round button-like ulcer usually stands out prominently with its necrotic centre dirty white, brown or black, and composed of superposed layers, the whole resting on a congested and thickened submucosa. This contains small round and giant cells and may show considerable encrease in connective tissue. The ulcers may be seated on the agminated or solitary glands but do not show the same predilection for these parts which is seen in typhoid fever.

Incubation. This varies according to the dose and susceptibility from two or three to as many as thirty days. With the short incubation the disease tends to assume its most acute and deadly type, while the prolonged incubation bespeaks a milder form. During ordinary outbreaks from six to fourteen days represent the average interval between exposure and the onset of active symptoms. During the extreme heats of summer and the excessive cold of midwinter in our northern states incubation tends to be shortened.

Symptoms in Fulminant Type. In violent outbreaks some pigs are found dead without observed preliminary symptoms, and have been set down as fulminant examples of the disease. When these occur during very hot weather, in open yards or fields, there is reason to believe that insolation, acting on a system rendered specially susceptible by the toxic fever, has much to do with the early death. Though seldom observed during life, it has been said that such cases, show extreme dulness, prostration, stupor, weakness, unsteady gait, thirst, hyperthermia, persistent recumbency, and at times red blotching of the skin and even convulsions.

Symptoms in Acute Type. In contrast with erysipelas these may advance slowly and insidiously, there is a lack of the customary life and vivacity, the tail droops, appetite is impaired, the pig creeps under the litter and lies there, preferably on its belly, a great part of its time, there may even be tremors suggestive of slight chill, when moved it shows weakness, may stagger, or it may have difficulty in rising on its hind limbs and there is encreased thirst and heat of the skin. Even in the absence of shivering or chill, the skin is usually tender to the touch, calling out plaintive grunting or squealing, and the same is often true of manipulation of the belly. The temperature is raised, yet this must be compared with the previous temperature under the conditions in which the pig has been kept. That may have been anywhere from 100° F. in a confined, cold, draughty pen, to 104° F. in a warm, dry pen and with plenty of exercise. In hog cholera it may rise 1° to 3°. The patient is breathless under exertion, the circulation is accelerated and the mucosæ congested.

Sooner or later, (usually by the second or third day) the skin shows an erythematous blush, especially on the ears, breast, belly and inner sides of the thighs and forearms, in greater part effaceable by pressure but promptly reappearing and complicated by darker spots of extravasation which retain their color under pressure. The blush may appear in spots of ⅒ to ⅓ inch in diameter, or it may cover the region, or indeed the whole body uniformly. At first of a brighter red it tends to pass in succession through the different shades of purple and violet. Appetite becomes more and more impaired, and in exceptional cases vomiting may occur, but often the pig will drink liquid food to the last. A marked symptom is the enlargement of the inguinal lymph glands, which may even be tender. An early symptom is watering of the eyes, and later a muco-purulent exudate may form, and drying, gum the lids together. An abundant exudate appears on the skin as the disease advances, most abundantly about the eyelids, roots of the ears, axillæ and groins, but often covering the whole body, forming a foul greasy inunction, and later a black scaly covering.

The bowels may be costive at first, with fæces, firm, moulded, and covered with mucous, and this may continue to the end. In most cases, however, about the second or third day they become soft, pultaceous and finally liquid, profuse, fœtid, and mixed with abundance of mucous or even blood. The color varies, they may be whitish, yellowish (on maize diet), red, or black (on swill).

Petechiæ usually form on the mucosæ and small sloughs and ulcers may be found on the lips, tongue or elsewhere on the buccal mucosa.

A cough may be present but is by no means a marked symptom.

Emaciation advances with great rapidity, the patient arches the back, tucks up the abdomen, moves weakly and unsteadily or is unable to rise, and dies in one or several weeks, it may be quietly or in a state of coma, but usually without convulsions.

Symptoms in Subacute and Chronic Forms. In this type the disease may be obscure, and even overlooked, so that infected animals carry the microörganism into fresh herds, without rousing a suspicion as to its true source. In other cases, after a slow and progressive development, it takes on such a distinct pathognomonic character that its diagnosis becomes more easy.

In the slightest cases there may be only a capricious or irregular appetite, drooping tail, enlarged inguinal glands, and a progressive emaciation, with loss of life and strength and occasional irregularity of the bowels. The greasy exudation on the skin and black scaly encrustation is not uncommon. Such patients usually survive but they are liable to prove unthrifty and unprofitable.

In other cases the pig becomes dull and listless, leaves its fellows, creeps and lies much under the litter, has impaired or irregular appetite, some costiveness followed by a fœtid diarrhœa, abdominal tenderness, enlarged inguinal glands, progressive emaciation, arched loins, hollow flanks, skin exudation, and oftentimes in the end erythematous eruption with petechiæ and black scaly exudate on the skin. It is in these protracted cases especially that the formation and detachment of the necrotic intestinal sloughs take place and these may pass in the fæces as flattened rounded masses or more extensive plaques. Necrotic ulcers are also liable to show on the buccal mucous membrane or skin. The patient may finally die of colliquative diarrhœa, of exhaustion and marasmus, in a state of coma as in the more acute cases. The mortality may be high and the survivors are liable to prove unthrifty and unprofitable.

Diagnosis. With a group of plagues in swine bearing a strong family resemblance, and maintained by microörganisms, which, though maintaining distinct characters, yet show so much in common that it seems not impossible that they may have been originally derived from a common ancestor, and in face of the not infrequent complication of two of these microbes in one patient, it becomes a task of great difficulty to diagnose at once the particular outbreak that is met with in the field. In some outbreaks, however, the differential features are clear enough to allow the veterinarian to pronounce at once on the true nature of the disease. In others he must withhold his diagnosis until he can put it to the test of microscopic examination, bacteriological culture, the Widal test, or inoculation.

Hog Cholera may be decided upon, when upon wholesome food, in healthy environment, without any change of food, and in six to fourteen days after the introduction of pigs from outside, or the arrival of strange pigs in the near vicinity, or higher up on the watershed, sickness appears tardily, taking one or two daily, with or without a sudden hyperthermia, petechiæ on nose, eyes, belly, axilla, or groin, a general soreness of the skin and abdomen, stiffness or weakness, hiding much under the litter, enlargement of the lymph glands, costiveness with dark red rectum and glazed dung, followed by a profuse, watery, fœtid, bloody, black or yellow diarrhœa, and death mostly after one or two weeks or more. The absence of cough, and the presence of ulcers bearing necrotic sloughs on the lips, mouth or skin, and above all the presence of the button-like necrotic ulcers on the mucosæ of the cæcum, colon or ileum may be accepted as conclusive evidence on this point. So also its prompt fatality to rodents, but not to pigeons.

Swine erysipelas has a much shorter incubation, more rapid and violent onset, deeper, darker congestion of visible mucosæ, more extensive petechiæ of skin, mucosæ, serosæ, and tissues generally, a comparative absence of inflammatory and necrotic lesions of bowels, a very early and high mortality in swine, rabbits and pigeons, and a harmlessness toward the inoculated Guinea pig.

Swine plague also shows a shorter incubation, a speedy elevation of temperature, more mucous congestion, less indication of abdominal tenderness or of diarrhœa, more cough, dyspnœa, wheezing and objective symptoms of pulmonary consolidation, less congestion or engorgement of the spleen, or ulceration of the bowels, and finally is very much more fatal to pigeons, and spares neither rabbits nor Guinea pigs.

Widal test. The cessation of movements and the agglutination of the bacilli of hog cholera, noted by Dawson, is a valuable test, but as in the case of typhoid fever in man is not to be implicitly relied on in all cases. Some of the forms of bacillus coli commune and other allied microbes act in a similar way. It necessitates the maintenance of fresh (24 hours) active, artificial, agar cultures of the hog cholera bacillus and is thus virtually reserved for the bacteriological laboratory. A drop of blood is drawn from the suspected pig smeared very thinly on the cover glass and about 10 times the amount of sterile water added. Then the smallest possible addition of the agar culture of the bacillus is made. Immediately, or in ½ hour the bacilli cease their active motility and mass together in clumps in which they can be seen individually clear and distinct but absolutely still and crossing each other in all directions forming a kind of network. A few isolated bacilli remaining in the intervals between the clumps and even showing a slight motility are not to be considered as invalidating the reaction.

The table on the next page will serve to place in contrast the differential phenomena of the diseases caused by bacilli of hog cholera, swine plague and swine erysipelas in uncomplicated infections.

Prevention. As in all other contagious diseases, effective preventive measures imply the destruction of the pathogenic germ and all sanitary measures should aim at the early and final extinction of this organism and its subsequent exclusion from the country. This, however, entails an outlay and governmental control which it seems idle to expect in the very near future so that palliative measures, and those looking toward success over limited areas must still be resorted to. It should be here distinctly stated, however, that the extinction of a plague, though often the most expensive at the start, is in the end by far the most economical resort.

Removal of accessory causes. The health and vigor of the animal exposed is not without its influence in case of attempted invasion by a virus of diminished potency.

DIFFERENTIAL SYMPTOMS AND PHENOMENA.

=Hog Cholera.= =Swine Plague.= =Rouget.=

Incubation 6 days + Incubation 1 day to + Incubation 1 day

Mucosæ not necessarily Mucosæ congested Mucosæ deeply congested congested, dark red, violet

Petechiæ on snout, Petechiæ on snout, Petechiæ extensive eyes, mouth, etc. eyes, mouth, etc.

Necrotic ulcers on Necrotic ulcers rare Necrotic ulcers less snout, mouth, skin, frequent etc.

Furred tongue, vomiting Vomiting less likely Vomiting not uncommon common

Temperature high in Temperature high in Temperature very high, acute cases (104° to acute cases 107° to 109° 108°)

Lies on belly mostly, May lie on side May lie on side abdomen hot, tender

Moves stiffly, feebly, Stiff but less so, Stiff, weak, paraplegic unsteadily with Paretic. grunting, may be paraplegic

Bowels 1st costive, Diarrhœa less marked, Diarrhœa usually sets fæces molded, glazed; may be entirely in 2d or 3d day, or absent before death, diarrhœa, profuse, watery, fœtid, bloody, black on slops,—yellow on corn (maize)

Everted anus dark red Anus may not be deep Anus may be less red, red, less everted less everted

Cough often present, Cough, hard, frequent; Cough absent, save in hurried breathing wheezing breathing. latter stages with Auscultation and pulmonary percussion may show consolidation lung consolidation toward lower border. May bleed from nose

Spleen slightly Spleen usually little Spleen enlarged, soft, enlarged altered grumous

When death is deferred Necrotic, button-like Necrotic ulcers on 1 to 2 weeks, ulcers on cæcum bowels rare necrotic button-like rarely marked ulcers on ilio-cæcal valve, cæcum, colon, or ileum

Lobar pneumonia Lobar or lobular Pulmonary and enteric uncommon pneumonia a marked inflammation rare lesion

Kills rabbits (5 to 7 Kills rabbits (1 to 12 Kills pigeon (3 to 8 days) and Guinea pigs days), Guinea pigs (1 days), rabbit (4 to 8 (7 to 12 days). to 4 days), pigeon days), Guinea pig Pigeons sicken but (48 hours) resists survive

Blood serum of hog cholera patient causes agglutination of bacilli in cultures; (not constant, occurs with other bacilli)

Dry, warm beds with plenty of air and light are essential to vigorous health and the usual damp, filthy, dark pens are depressors of the vital forces and virtually invitations to hog cholera as to other diseases. The close packing of swine under manure or under rotten piles of straw where they often suffocate each other is to be carefully guarded against. It is a sufficient commentary on this to say that for every kilogramme of its body weight, the horse consumes daily 13,272 grammes oxygen, the cow, 11,040 grammes, and the pig, 29,698 grammes. This is in perfect keeping with the high normal temperature maintained by the latter animal. In the interest of health the pig requires twice the breathing space for every 100 lbs. of his weight that is demanded by either ox or horse. What violence is done to this demand of nature in the daily treatment of the hog!

Fresh, sound, wholesome food is no less a desideratum. Yet the omnivorous pig is condemned to become the scavenger for the kitchen, the stable, the feeding pen, the slaughter house, the creamery, the sugar works, the brewery and even the rendering works. Whatever is considered unfit for human use is thrown into a swill barrel, and as this is never emptied it becomes the field of endless decompositions with the production of the most varied toxins, ptomaines and enzymes. Many of these chemical toxic products cause gastro-intestinal inflammation with vomiting, bloody diarrhœa and tenesmus, and derangement of the nervous and other functions as manifested in weakness, staggering, dulness, stupor, etc. Death may follow in a few hours and the cases are set down as acute forms of hog cholera, rather than the simple poisoning that they are. All the same they pave the way for the attack of hog cholera if its germ is present even in a form of little potency. All such foods should, on the contrary, be fed fresh and after boiling.

Salt in excess, the brine of salt meats or fish (containing toxins), the powdered soaps used in kitchens and added to swill, mouldy bread, cotton seed meal fed in any considerable proportion in the food, and even an exclusive diet of corn (maize), must be guarded against.

The crowding of many pigs in a small yard where they root continually in each others’ droppings and their own, should be avoided. Individual pens, or pens holding two or three only and kept clean are to be preferred, and still more a wide grassy range where they may escape from their own filth. The long feeding trough should be discarded in favor of one into which the pig can introduce his nose only. The nose itself will introduce filth ferments, but, where there are not specific-plague-germs, it is the quantity that tells and the exclusion of the foul feet is an important consideration. To these various poisonous products of saprophytic ferments it often happens that the older swine have by continuous exposure, acquired a comparative immunity, while the young growing pigs perish in large numbers.

Feeding pigs in confinement, without green or animal food is very liable to induce costiveness and indigestion which pave the way for the inroad of the hog-cholera germ. A certain allowance of green food, slops, and, above all, a variety of food constituting a well-balanced ration are always desirable.

Again, the constitution of the pig is often material. On the continent of Europe it is the high bred English pigs that suffer most, and in all cases a lack of the rugged vigor attained through an active, open air life lays the system more open to a violent attack. Too close breeding must be similarly avoided, together with breeding from the immature, the weak and the debilitated. In this connection it is important to rid the herd of parasitisms which not only weaken the system and lessen the power of resistance, but by the bites or the inflammation induced, open channels for the introduction of the hog-cholera bacillus.

Prevent the Introduction of the Bacillus. The above precautions are important in obviating infection and favoring a milder type of the disease when the germ has been introduced, but they are but palliatives at best, and will not hinder the development of a plague in the presence of an active and potent virus. Adopted alone they are worse than useless as a means of extinction of the germ: they tend to preserve it. The exclusion of the hog-cholera germ is the one essential thing in prevention and whatever comes short of this must have at best but a partial effect.

Avoid pens, pastures or streams that drain swine enclosures higher up. Discard all provender or litter that has come in contact with other pigs or their products. Allow no visitors to the herd such as butchers, dealers, drovers, that have habitually come in contact with other herds. Exclude as far as possible domestic animals (dogs, sheep, cattle, fowls, pigeons), and even vehicles coming from places where hogs are kept. Wild animals such as buzzards, and other carrion feeders, must be especially guarded against. Wild rabbits and hares (jack rabbits), skunks, wood chucks, minks, rats and mice should be exterminated. Small birds and flies are difficult to deal with but the latter may be destroyed by acids, copperas, or sulphites on the manure and the former may even be exterminated when hog-cholera exists in the vicinity.

Sows should not be sent from herd to herd for service or otherwise, and any swine that have been hired out, or sent to an exhibition, and all that are acquired in any manner, should, on arrival, be excluded from the herd and held in quarantine, well apart for three or four weeks, and finally washed with carbolic acid soap before they are admitted.

The pestilential prevalence of hog cholera and other swine plagues to-day is largely the result of the great industrial and commercial activity of modern times. In America the disease was comparatively unknown until after 1830, and in Europe even later. But with the advent of steamboat and railroad, the few pigs raised in separate pens, or secluded localities, and killed and cured near by, gave place to the large herds, sent when fattened to great markets where pigs were collected from distances of many hundreds of miles, the stock animals and the fat occupied in succession the same boats, cars and yards, and, as a matter of course, the virulent germs were concentrated and diffused through the infected places and things. We cannot go back to the antiquated safer methods, but it would be possible to so regulate our commerce, that the evil could be reduced to a minimum. Separate cars, loading banks, chutes, alleyways, and yards can be reserved for fat swine going to immediate slaughter and no animal having passed through any of these should be allowed to be taken out for stock purposes, unless it has been passed through a rigid quarantine. The places and things used for such fat swine should be disinfected at intervals, and the manure and offal should be disinfected, or exposed to a boiling temperature for a sufficient length of time before removal from the premises. Stock swine on their part should be shipped only on a certificate of the complete immunity of the herd and locality from which they come from swine epizoötics, and of the roads or vehicles by which they reached the shipping point. They should be debarred from all yards, loading banks and cars or boats used for fat hogs, and admitted only to such as have just passed through a thorough disinfection. They should be sent directly to their destination, or if to a market, for purposes of sale, it should be well apart from that used for fat swine, and the loading banks, chutes and yards should be entirely distinct and should be thoroughly disinfected on every occasion after use. The millions now lost yearly from swine epizoötics might well warrant the inconvenience and expense entailed by such precautions. Heavy penalties should be imposed on those shipping pigs from infected localities, on those making false certificate, and on all who in any way violate the law.

Independently of State or local authorities the stock owner can do much to protect himself. He can make a number of pens large enough to hold 2 or 3 pigs each, safely fenced off from one another and so constructed that no drainage can take place from pen to pen. Then in winter in the absence of flies, and with rats, mice, and birds excluded the opportunity for the extension of infection from pen to pen can be kept at its minimum. All pigs must be kept apart from the manure heap, and in summer the manure must be so treated as to destroy the larvæ of flies. All food and water that might convey infection must be guarded against. Then if one pig is attacked it will only be necessary to destroy it and its two fellows in the same pen, and even if those in adjacent pens are killed or quarantined the loss will be a trifle as compared to the ruin of the whole herd, as usually happens. Prompt disinfection of the pens and manure is imperative, and the same would apply to the person and clothes of the attendant, and to all stable utensils.

Immunization by injection of sterilized products of the bacillus, has not proved satisfactory. In 1880 I applied this to two pigs, causing a transient fever, after recovery from which, the subjects resisted exposure to infected pens and pigs, and even virulent inoculations. But they failed to thrive well. Later experiments by Drs. Salmon and DeSchweinitz respectively, also proved unsatisfactory. The latter separated and injected the enzymes, but lost 50 per cent of his cases, the survivors proving immune, with the drawback of troublesome local lesions. The enzymes obtained from cultures in milk could be used safely on guinea pigs in the dose of 0.01 grams and in some cases even up to 0.04 securing immunity. But the great risk of an overdose, the frequent local lesions, and the subsequent unthrift, have prevented the adoption of the method.

Disinfection. The experiments of the Bureau of Animal Industry show that, apart from freezing, four months in the soil, serves to render the bacillus harmless.

From .75 to 1 per cent of quick lime added to soil in the form of lime water, destroyed the virulence in 11 days.

Lime can be employed as a thick whitewash on pens, fences, yards, etc., the precaution being taken to see that it is newly burned, caustic and applied in sufficient amount. Lime that has been kept absorbs carbon dioxide and loses its disinfectant property. If ¼lb freshly made chloride of lime is added to each gallon of the caustic lime white wash the certainty of success is insured. Lime water has the advantage of being applicable to grassy surfaces, without proving hurtful to the vegetation. For buildings and yards it furnishes a ready means of estimating the thoroughness of the application.

Sulphuric acid (1:100 or 1¼ oz. to 1 gallon) makes a good disinfectant for buildings and yards. Like lime this can be used freely without fear of poisoning the animals.

Carbolic Acid, 5 per cent, can be used with great safety. The Bureau of Animal Industry advises the combination of this with sulphuric acid, which adds greatly to its solubility.

Formalin may be employed, diluted one to forty of the solution (1 per cent of the gas) in buildings and on woodwork generally. It may also be applied in the form of gas by heating the solution in closed rooms. Like carbolic acid it is especially applicable to cars, boats, and other vehicles.

Corrosive Sublimate (1:500) makes a convenient and cheap disinfectant, with the drawback that it is poisonous, and destructive to metals. Mercuric Iodide though more potent is also more expensive. Blue stone (2:100) and zinc chloride (10:100) are also effective but poisonous.

The failure to stamp out hog cholera in England and America has been largely chargeable on the appointment of laymen to do the work of the expert, and no less so on the attempt to deal with the disease in hogs in transit or in the market rather than in the farm where they have been raised or kept. Let the fat and stock markets be kept rigidly apart, together with the means of conveyance to and from these, and let no stock swine start for a market or destination without a certificate of the soundness of the locality from which they came, and the purity of the means of transit, and we shall have taken a long step toward the final extinction of the pest.

State limits and rights stand in the way of successful work, but this can be partly met by a frontier supervision by national officials, and should be further, by a prompt and hearty coöperation of the sanitary officers of the two states involved. When it becomes possible to trace infecting hogs, back to the infected place in another commonwealth, and punish the offender who shipped them, we shall be within sight of a satisfactory control or extinction of hog cholera.

Extinction of Hog Cholera in Herds and Districts. As in all deadly plagues this should be a recognized governmental function to be carried out at public expense. It is a question of political economy and its neglect is subversive of prosperity not in Agriculture alone but in all public industries whose workers must subsist on the fruits of the soil. The $10,000,000 lost yearly by the farming community, is a dead loss, not to agriculture alone, but to the prosperity of the nation, the markets of which would be revived and improved by such a yearly sum expended.

The existence of the disease at any point should be reported by the stockowner or guardian, under penalty in case of failure. When the nature of the outbreak has been certified by the expert, the district should be scheduled, and the herd appraised, slaughtered and all products disposed of in such a way as to prevent any escape of infection. The carcasses may be burned, buried deeply, or boiled and rendered. The buildings, yards, utensils, fences, manure, cesspools, and infected fields should be thoroughly disinfected, or secluded from all animals for a year. The owners of the herd should be indemnified according to appraisment, and not to exceed ¾ths of the actual market value, provision being made that no award shall be made if the herd sickened within a fortnight after their arrival from another State, or in case the owner, has concealed the existence of the illness, or has otherwise deliberately or carelessly contributed to its spread.

Many minor rules and restrictions will be required to fit the general measures to individual cases and local conditions, and these require the direct supervision of an expert, and not of a mere business manager or layman.

Therapeutic Treatment. With state, county or municipal measures for the extinction of hog cholera, treatment is to be condemned, as calculated to encrease and spread the infection. But until the states can be educated out of the past wasteful system, into economical measures of extinction, the swine breeders are entitled to whatever salvage they can secure through therapeutics. For acute cases there is no hope. For the chronic a clean, dry, comfortable pen, well disinfected, and a moderate diet of varied and laxative food are essential. Wheat, bran or middlings, with corn, oat, barley or linseed meal may be allowed in form of a mash. A little green vegetable food may be added. Medicinal agents may be used to meet special indications, but when a whole herd must be treated at once, antiseptics and febrifuges have apparently proved the most generally helpful. The Bureau of Animal Industry especially recommends the following: Wood charcoal, sulphur, sodium sulphate and antimony sulphide, of each 1 lb.; sodium chloride, bicarbonate and hyposulphite, of each 2 lbs.; mix thoroughly and add to each feed in ratio with the size of the patient. In suitable cases, this is said to improve the appetite and contribute much to convalescence. Modifications will readily suggest themselves to meet individual conditions and different stages of the disease—antithermics, eliminants, calmatives. stimulants, tonics, etc.

Serum Therapy. This has been especially exploited and advocated in America by De Schweinitz of the Bureau of Animal Industry, and Dr. Peters of Lincoln, Neb. In Europe, Perroncito has prepared an antitoxin. The serum is produced in the body of the cow or other animal which is inoculated repeatedly with gradually encreasing doses of living hog cholera cultures and with solutions of the bacilli and their products, for a period of eight months, or until no reaction takes place from large doses, and the blood serum added to cultures of hog cholera bacilli causes agglutination of the latter. The serum is further tested as to its power of preserving Guinea pigs inoculated with a lethal dose of live hog cholera cultures. After separation from the blood the serum is concentrated until it reaches a standard at which 10cc. proves curative to a pig of 40 to 60 lbs. weight.

It proves most successful in animals in which the subacute or chronic form of the disease has just begun. One injection only was given to each animal. Of 1923 cases treated (1897–8) 30 per cent. died, and 70 per cent. recovered. Of 3197 in abandoned herds (checks), 81.24 per cent. were lost. (De Schweinitz.)

One drawback was found in the short period of immunity secured, the susceptibility reappearing as soon as the antitoxin had been eliminated from the body. This was met in part by using sterilized cultures (toxins) along with the serum.

Another desideratum was a speedy means of distinguishing in field work between hog cholera and swine plague, as the antitoxin of the one was not protective against the other. To meet this, serum was obtained from an animal immunized to both diseases, or a mixture was made of the sera of two animals respectively made resistant to the two affections.

De Schweinitz was very optimistic in the matter, claiming that the serum is absolutely harmless, can be used on pigs freely, and will cost but 15 cents for each animal. He estimated that of the $15,000,000 per annum lost by Hog Cholera and Swine Plague in Iowa alone, $11,000,000 can be saved at a comparatively small cost.

The method is scientifically sound in availing of the defensive products of the immunized system for imparting to the animal attacked, the power of vital resistance, and after allowing for enthusiasm, for the inevitable mistakes, when used on a large scale, of other deadly swine diseases for hog cholera, for the many accidents incident to its application by operators who are not specially trained like the employés of the Bureau, for its demand for acute and deadly outbreaks, as well as for chronic and mild ones, and taking into account that in other hands it has not fully borne out the promise made for it; yet it seems to have some measure of merit, and where no systematic attempt is made by the authorities for the extinction of the disease and its germ, it is an available resort for the owner of herds.

The fundamental objection is that it entails the preservation, encrease and spread of the poison, and like all temporizing measures, stands as a barrier to the complete extinction of the plague. Giving such a very transient protection, its repetition may be demanded in a few months or a year, and proceeding on the ground that the pest must continue for all time, the apparent economy of the process will prove, in the long run, but a permanent and grievous tax.

The soundest and only truly economical course in dealing with this and other deadly infections of swine is the radical extinction of the germ. When the people can be educated up to this we shall see the dawn of a brilliant future for our animal industries. Until then we must be satisfied to fall back upon, and make the best use of the temporizing measures now in vogue or that may hereafter be devised. Even if it should be shown that hog cholera is at long intervals developed from a ‘sport’ of the usually harmless bacillus coli commune, the fact remains that its great extensions and the resulting fatality are due to the contagion alone, so that extinction remains the true watchword of success and economy.

SWINE PLAGUE: SEPTICÆMIA HÆMORRHAGICA SUIS.

Definition. Synonym. Bacillus pestis suis, 0.8–1.5μ, nonmotile. Pathogenesis. Accessory causes, as in hog cholera: less vitality than in virus of hog cholera, bacillus in apparently healthy, deadly to birds and rodents. Lesions: like as in hæmorrhagic septicæmia, lungs suffer more than bowels, lymph glands swollen hæmorrhagic, liver and spleen may seem almost normal, bowels slightly congested, marked emaciation. Symptoms: Acute cases like hog cholera, shorter incubation—1 day, troubled breathing when driven, cough, congested petechiated skin, hyperthermia, costiveness followed by diarrhœa. Diagnosis: constancy and predominance of lung lesions and symptoms, nonmotile bacillus with polar staining, not gasogenic with glucose, very fatal to birds and rodents. Prevention: as in hog cholera. Immunization. Treatment: as in hog cholera dangerous. Serum-therapy.

Definition. A contagious bacteridian disease of swine, acute or subacute, characterized by a short incubation, hyperthermia, marked congestion of the mucosæ, petechiæ and circumscribed blood extravasations in the skin, subcutis, mucosæ, submucosæ, and tissues, swelling, congestion and petechiation of the lymph glands, and a marked tendency to inflammatory localization in the lungs.

Synonyms. Th. Smith identifies this affection with the “Schweineseuche” of Germany.

Bacteriology. The bacillus of Swine Plague (B. Pestis Suis) has already been described in the differential table of allied bacteria given under hog cholera. It is a short rod, with rounded ends, 0.8 to 1.5μ. × 0.6 to 0.8μ, staining readily in aqueous basic aniline colors and bleaching in Gram’s iodine solution. The staining is distinctly polar, the colored portions being more or less crescentic with the concave or straight border turned inward toward the central clear space. It is destitute of flagella and distinctly nonmotile unlike the very active bacillus of hog cholera. It further differs in its growth on potato which is slight, gray and waxy. On gelatine, too, it gives a feeble growth (or none) unlike the brownish colonies of the bacillus of hog cholera. It fails to liquefy gelatin. On agar the growth is more active, being grayish, translucent or brown. Those forming under the surface are like flat horizontal discs with a small microscopic elevation or knob in the center. It grows in milk producing little or no acid and no clot. It produces gas with none of the sugars—glucose, lactose, saccharose—in contrast with the gas production in glucose by the hog cholera bacillus. It shows much less vitality and hardihood than the hog cholera bacillus, growing but feebly between 65° and 70° F., and most actively at 97° to 100° F.; dying in 7 minutes at a temperature of 58° (moist); dying in 3 days when dried, in 4 to 6 days in the soil, in 10 to 15 days in water and instantly in 0.04 per cent solution of lime water.

Pathogenesis. It is pathogenic to swine, hens, pigeons, pheasants, sparrow, mice, guinea pigs, rabbits, cattle, deer, etc., showing not only a wider range than the hog cholera bacillus, but a more deadly action outside the genus suis. Inoculated birds die in 2 days, rabbits in 16 to 20 hours and guineapigs in 1 to 4 days.

Accessory Causes. These agree in the main with those of hog cholera already described so that it is needless to repeat them here. The principal distinctions depend on the lesser vitality of the swine plague bacillus outside of the animal body, and its wider range of pathogenesis outside the genus suis. Infecting materials that have been thoroughly dry for a week may be considered harmless, also that which has been more than two weeks in water, and that which has been more than a week in the soil. If, therefore, the buildings have been thoroughly disinfected, the simple disuse of yards and pastures for a fortnight, and of ponds of water for three weeks may suffice. In the case of hog cholera it may be necessary to abandon such places for 5 months or for the season.

Abandonment by swine is, however, insufficient: all susceptible animals, wild and tame, (see pathogenesis) must be excluded as any one of these may maintain the infection. The preservation of recovered swine on the premises, or the early return of the immune may become a means of preserving the bacillus for the next susceptible pigs that may be introduced. The bacillus of swine plague may be found on the air passages of swine and other animals that are not themselves, at the time, susceptible to the disease, and these animals accordingly become the occasions of what have been thought to be spontaneous outbreaks, and of invasions of fresh herds after the introduction of healthy pigs which have been thought to be beyond suspicion. The danger of the communication of the germ by wild birds and rodents would be enormous, but for the fact that it is so much more deadly to these animals than the microbe of hog cholera, that few survive to maintain the infection. Yet the rule ought to be, to exclude from the fields or premises occupied by new or susceptible pigs, all animals, that may by any possibility become the means of introducing the infection so recently prevalent. Though so easily destroyed when outside the living body, the microbe of swine plague can be carried by the apparently healthy living animal and we must rigidly exclude the possibility of this occurring.

Lesions. Acute and rapidly fatal cases of swine plague furnish lesions indicative of a hæmorrhagic septicæmia. The abundance of petechiæ on the skin, mucosæ, serosæ, and tissues generally, with circumscribed hæmorrhages, congestions, inflammations and exudations, agree in the main with what is observed in the acute examples of hog cholera. If the congestive or inflammatory lesions, concentrate in the lungs rather than the bowels it assists in the diagnosis of swine plague. The swelling and blood engorgement of the lymph glands are nearly alike in the more acute types of the two diseases. The spleen is less constantly enlarged than in hog cholera or swine erysipelas. In the subacute and chronic forms the lesions may be almost entirely confined to the enlarged and congested or hæmorrhagic lymph glands. Usually, however, the lungs are the seat of lobular or lobar pneumonia, affecting by preference the lower portions of the anterior and median lobes, and sometimes also the posterior lobe. The pleuræ are often involved, showing arborescent congestion, thickening, exudate, false membranes and hydrothorax. The exudate may at times fill up the interlobular connective tissue, even before the pulmonary tissue is materially involved suggesting a local infection starting at the pleural surface. The hepatised lobule has a general red color varying in depth at different points, and showing lighter yellowish or grayish spots representing the purulent air sacs and terminal bronchia, and necrotic foci. On section the bronchia often yield pus, while the pulmonary tissue oozes a bloody liquid rich in small lymphoid cells.

The liver and spleen may be all but normal, though in a number of cases they may be congested and softened. The stomach and bowels may be virtually sound, or they may show extensive congestion, petechiation and thickening of the mucosa at different points, with, in some cases ulcers, but these latter are mostly excavated and rarely assume the projecting, button-like, laminated form which is so characteristic of chronic hog cholera. Emaciation is a marked feature as in hog-cholera.

Symptoms. In the most acute type these may not differ from those of similar cases of hog-cholera. If there has been any opportunity of estimating the incubation it will be found to have been shorter, the skin and mucosæ have a darker red blush, showing first on the ears, breast, belly and inner sides of the thighs and forearms, the lymph glands are enlarged, and there is cough and dyspnœa if the patient is roused to exertion. The presence of petechiæ on the skin and of a very high temperature (107° to 109°) is to be specially noted. There are great prostration and dulness, complete anorexia, hiding under the litter, indisposition to rise, often weakness, staggering, paresis or even paraplegia, somnolence, and death in coma or convulsions.

In the subacute and protracted cases, there is the short incubation (1 day), followed by hyperthermia, drooping tail, hiding under the litter, flushed eyes, nose and mouth, impaired appetite, arched loins, hollow flanks, retracted abdomen, cough easily roused by driving, and signs of consolidated lungs in their lower parts (crepitation, suppressed murmur, abdominal or heart sounds etc.). After a day or two the skin becomes flushed and together with the visible mucosæ the seat of petechiæ. The superficial lymph glands are enlarged. The bowels are usually confined but as the disease advances diarrhœa may set in. There is rapid loss of condition, and the patient may die as the result of exhaustion, toxin poisoning, colliquative diarrhœa, or other condition.

Diagnosis during life is based largely on the shorter incubation, the greater reddening of the visible mucosæ, the comparative absence of abdominal tenderness, and offensive diarrhœa, and the constancy of the cough and other symptoms of broncho-pneumonia.

Post-mortem. It is marked by the constancy and predominance of the lung lesions, and the comparative absence of ulceration of the ileum, cæcum and colon, and especially of the projecting, laminated, button-like, necrotic sloughs.

The morphology of the bacillus, its habit of polar staining, its lack of automatic movements, its comparatively poor growth in alkaline bouillon, on potato, gelatine and agar, its inability to ferment glucose with the production of gas, its rapidly fatal action on hens and pigeons as well as on rabbits and guinea pigs serve to distinguish it from the microbe of hog cholera. (See table p. 38).

Prevention. In this connection the reader is referred to the precautions, given under hog cholera, against conditions, hereditary, hygienic, climatic, dietetic, parasitic, etc., which lay the system more open to microbian invasion. In the matter of exclusion of the bacillus, the swine plague germ is less difficult to deal with, because it is so much more easily destroyed. Disinfect the buildings, and all contaminated objects as advised under hog cholera, clean yards, and shut up these and pastures or runs, and all infected water for one month. In case of public market yards and alleys, and railway loading banks, chutes, and cars, a thorough cleansing and disinfection may warrant that they may be put to use again immediately. No animals that occupied the yards before disinfection should be allowed to mingle with the new stock, as they at times carry the microbe, though themselves apparently healthy and immune. All regulations as to railway and boat transit, recommended under hog cholera, are equally applicable to swine plague. The possibility of protecting private herds, by keeping them in special pens, holding two or three each, is also the same for swine plague.

Immunization is somewhat more promising than in hog cholera. Metchinkoff and Th. Smith working independently found a fair measure of success in inoculating rabbits and guinea pigs with three to five small injections of sterilized bouillon cultures, agar cultures or blood, intravenously, intraabdominally or hypodermically. But as applied to swine it has not proved satisfactory, and the irregularity of the results and the tendency to induce unthriftiness have caused it to be abandoned.

Treatment. The therapeutics of swine plague like that of hog cholera is essentially unsatisfactory. Benefit might be derived in individual cases from a careful and judicious use of drugs to meet the special indications, but with the comparatively low value of the individual animal, the certainty of the multiplication of the deadly poison by the preservation of the diseased, and the extreme danger of its diffusion and extension, treatment is anything but commendable.

Serum-therapy has been advocated for years by De Schweinitz, and under the auspices of the Bureau of Animal Industry it has been given a wide trial, but it has not met with the full success that was at first claimed for it. The serum is prepared in a similar way to that of hog cholera and is similarly employed. It is open to the same class of objections, and though when skillfully employed it will reduce the mortality, it does not yet seem to have reached the point at which it can be recommended as a profitable investment. Like all temporizing measures it draws attention from the sounder and more economical measure of extinction and is indirectly a means of the perpetuation and even the diffusion of the infection. So long as extinction cannot be secured, this is a less valuable alternative for the adoption of owners of high priced hogs.

MODIFIED AND COMPLEX FEVERS OF SWINE.

Double infections. Varieties of bacillus choleræ suis, and bacillus suis pestis. McFadyean’s swine fever bacillus. Marseilles swine plague bacillus.

We accept fully the duality of the Hog Cholera and Swine Plague, though this duality has been hotly contested on both sides of the Atlantic. Many of the best observers in Europe now support this position. These include Selander, Bang and Jensen who are familiar with the svinpest (hog cholera) of Scandinavia; Kitt, Friedberger and Fröhner who are familiar with the Schweineseuche (swine plague) of Germany; Raccugla, Canova and others in Southern Europe; and Lignieres and others in France who have studied the hog cholera and pasturellose porcine (swine plague).

But the conceded duality of these two diseases as they occur in typical examples in swine, does not account for all the infectious fevers of swine, in which these microbes or others closely allied to them may figure. Salmon, Smith and their coadjutors describe double infections in the same system, in which both the bacillus choleræ suis and the bacillus pestis suis figure, and in which there result a combination of symptoms and lesions, that together represent both of these germs. It may be that one or other of these germs in a given outbreak, shows a predominance in potency so that the symptoms are more characteristic of it than of its companion; it may be that the more potent germ kills the victim, quickly by an acute septicæmia and gross lesions that would apply almost as well to one germ as to the other; or it may be that both act moderately and the attack is protracted with resulting lesions in both lungs and bowels that respectively suggest the plague and the cholera.

Then as regards varieties in the individual germ. Th. Smith recognizes this as a frequent condition and describes no less than seven different types of bacillus choleræ suis which he had studied and which varied in morphology, cultural qualities and virulence. Lignieres found that the virulence especially of bacillus suis pestis is very easily affected by successive passages through the bodies of small experimental animals. We ought not to be surprised then if we find in different epizoötics, in different countries and even in the same, bacilli which for the time at least show characteristics different from those to which we have been accustomed. These give us varying phases of septicæmia which however come together in one great class. Two of these types which have been placed on record may be here named. For others see septicæmia hæmorrhagica of cattle and sheep.

=McFadyean’s Swine Fever Bacillus.= The characters of this microbe found constantly by McFadyean in swine fever, approximates closely to the hog cholera germ in morphology and motility and in its deadly action when eaten, while it approaches toward the swine plague germ in its cultural habits on potato, gelatine and agar, and in alkaline culture liquids, and finally it differs from both in the absence of pathogenesis to Guinea pigs and in its very moderate action on rabbits. The symptoms and lesions of the swine fever of Great Britain are those of the hog cholera of America rather than of swine plague.

=Marseilles Swine Plague Bacillus.= This microbe was found by Rietsch and Jobert in a febrile epizoötic of swine at Marseilles, and was studied by Caneva and Bunzl-Federn separately. The latter identified it with the bacillus of ferret septicæmia, as described by Eberth and Schimmelbusch. It was longer and thicker than the hog cholera bacillus, twice as long as broad, actively motile, with flagella, and differed from bacillus choleræ suis, in its polar staining, its free growth in acid media, in acidifying and coagulating milk, and in its forming both indol and phenol in peptonized bouillon.

In this case the source of the disease was in importations from Africa (Fouquet), and it spread widely in Southern France for nine months. It proved almost constantly fatal, in from four days to two or three weeks. The symptoms were weakness especially in the hind limbs, with more or less fever, constipation often followed by diarrhœa, an infrequent cough, and red blotches on the skin. In chronic cases ulcers formed in the mouth and intestines especially the cæcum and colon. Appetite was often retained to the end. The young, under a year old, were the chief sufferers. It made 20,000 victims in several months in the province of Bouches-du-Rhone.

SEPTICÆMIA HÆMORRHAGICA OF BOVINE ANIMALS.

Synonyms. Definition. Historic notes. Resemblance to black quarter. Bacteriology; saprophytic cocco-bacillus, nonmotile, ærobic, related to microbe of swine plague, chicken cholera, and rabbit septicæmia. Pathogenic to deer, buffalo, cattle, horses, swine, rabbits, rats, mice, goats, and sheep. Variability. Vitality: great in soil, dies in 6 to 20 days when dried, and quickly in antiseptics, resistant to heat. Accessory causes: rise of soil water in winter or in spring, drying of marshes in summer, wet, rich, swampy, mucky soils; youth, gregariousness, carnivorous habit, insects, vermin, wild animals and birds, epizoa, entozoa, wire fences, wounds of all kinds, hard, woody provender; inoculations in wounds the most fatal. Symptoms: superficial with hyperthermia, functional disorder; muscular tremors; violet mucosæ; segregation; swelling in intermaxillary space, tongue, throat, neck, dewlap, or elsewhere, not pitting on pressure. Petechiæ. Death in six hours to four days; thoracic form kills in four to eight days; abdominal form with colics, and bloody often frothy fœtid fæces. Chronic forms usually pulmonary. Lesions: straw-colored exudations subcutem or intramuscular; blood extravasations; in lungs resembles lung plague; on bowels blood effusions, and exudates; softened, blood-stained lymph glands. Spleen usually normal in size. Blood black. Petechiæ extensive. Chronic lesions. Bacillus in exudate, blood and bronchial mucus. Diagnosis: from anthrax, black quarter, lung plague, rinderpest, and malignant œdema. Mortality 50 to 80 per cent. Prevention: isolate and kill affected; destroy or disinfect carcasses and infected things and places, feeding and drinking troughs and manure. Close and drain infected fields. Immunization, by three inoculations with cultures made at a high temperature (86° to 90°) in free air; or with virus that has been grown in pigeon. In case of deer, drive a few days into a noninfecting enclosure, and then on to a sound range. Treatment.

Synonyms. Wild—und Rinderseuche (Bollinger), Buffalo Disease, Barbone (Oreste and Armanni), Cornstalk Disease (Billings, Moore), Sporadic Pneumonia (Smith), Pneumo-enteritis (Galtier.)

Definition. An acute bacteridian disease of domestic and wild herbivora and swine, characterized by sudden onset, rapid and fatal course, marked hyperthermia, accelerated breathing and pulse, and extensive gelatinoid or sanguineous extravasation in the intermaxillary space, tongue, skin, subcutaneous or intermuscular connective tissue, lungs, pleura, pericardium or intestine.

Historic Notes. It is almost certain that in earlier times this affection was often mistaken for gloss-anthrax, blackquarter, or even lung plague. Metaxa, in 1816 in Italy, manifestly describes it. Oreste and Armanni, in 1882 and 1887, traced Italian cases to the microbe. In 1854 it destroyed many cattle and deer in England (Veterinarian). In 1878 Bollinger records its great fatality among the deer, wild boars, cattle and horses in and near the royal parks at Munich, and for a number of years after in Bavaria. Friedberger records its presence in Schlüchtern, Prussia, in 1885–6, Condamine in Cochin China in 1868, and Guillbeau and Hess in Switzerland in 1894. In America, what appears to be the same affection is noted as corn-fodder disease in Nebraska (Billings), as Wildseuche in Tennessee (Norgaard), and as hæmorrhagica septicæmia in Minnesota (Reynolds). I have repeatedly met with the affection in New York in cows arriving from the west, and in the indigenous cattle on wet, mucky, undrained land in spring, about the period of the melting snows.

Bacteriology. The essential cause of the disease is a saprophytic cocco-bacillus, ovoid, with rounded ends, about 1μ long by 0.3 to 0.6μ broad, but showing involution forms and a variable size. It is nonmotile (Kitt claims motility), ærobic (facultative anærobic), takes a polar stain with clear centre in aniline colors, bleaches in Gram’s (1) solution, shows neither spores nor flagella, grows readily in bouillon, on gelatine, (a bluish transparent layer without liquefying), serum at 98° F., milk (without acidifying or coagulating), and alkaline potato (not on the acid). The cultures have a peculiar odor and yield no indol.

The microbe shows a very close relationship with those of swine plague, chicken cholera and rabbit septicæmia, but it sometimes differs in showing little or no pathogenesis for the Guinea-pig.

Animals susceptible. It is pathogenic to deer, buffalo, cattle, horses, swine, rabbits, rats, mice, and to a lesser extent to goats and sheep.

The pathogenesis varies with the immediate source of the microbe. When obtained from cattle a drop of blood kills rabbits in twelve to twenty hours, with intense hæmorrhagic laryngitis and tracheitis. Guinea pigs die in forty to eighty hours. When obtained from the buffalo it killed horse, ox, or pig in twenty to forty-eight hours. That obtained from barbone (buffalo) appears to be more potent than that from septicæmia hæmorrhagica (cattle).

Vitality of the microbe. Simple drying destroys virulence in six to twenty-two days. Virulence is retained for nine days in putrid flesh. It is preserved, and the microbe multiplies in soil or water containing organic matter and nitrates. It is easily destroyed by ordinary antiseptics 1:5000 of mercuric chloride destroying its vitality in one minute (Hueppe). On the contrary it shows a great resistance to changes of temperature. It grows in the soil at 55° to 60° F. (Hueppe), and in old cultures may resist for an hour a temperature of 175° to 195° (Oreste and Armanni).

Accessory Causes. These are such conditions as favor transmission of, or receptivity to the microbe. In Southern France the disease is most common in the winter months, probably because the soil water rises then; on the Roman marshes on the other hand, it prevails especially from May to October, when the water is lowest and most impure. In New York I have seen it especially at the breaking up of the winter frosts, when the water, pent up in the rich organic soils, is suddenly released. It is pre-eminently the disease of wet soils, rich in the debris of decomposing organic matter, of the rich prairies and bottom lands of the Mississippi Valley, of springy, swampy or mucky soils elsewhere, of the Pontine marshes at Rome, of the Delta of the Nile, of the rich virgin soils in Asia. Youth has the greatest receptivity, the older animals having probably acquired immunity through an earlier attack. The animals that live in herds infect each other by contact, fighting, licking, etc., others are affected by eating the vegetation or drinking the water soiled by the diseased, wild boars by eating the carcasses, and all animals by the attacks of biting or blood-sucking insects which have just come from the diseased. It is claimed that the infection is carried by men and animals, and by the sale in villages of the flesh of infected animals. Dogs, wolves, foxes, and other carnivorous animals and birds will also carry the infection for long distances. Finally, it will travel to a greater or lesser distance with running water.

The entrance of the microbe by wounds must always be counted on, and explains the casual inoculations, by bites of dogs, insects, worms, by barbed wire fences, by wounds with horns, tusks, or feet, by nails, etc., and in winter by hard, woody aliment scratching the lips, mouth, fauces or pharynx. Shedding of teeth, diseased teeth or gums, and everything that causes abrasion of the alimentary mucosa must be admitted into the list of causes. Infected traumatisms of any kind, like intratracheal and intravenous inoculations usually prove fatal, while infection by ingestion is not necessarily so. The pathogenic potency appears to be impaired in the stomach or intestines.

Symptoms. These vary widely according to the subject, the seat of infection and the violence of the attack. They may be classed under three principal heads: superficial, thoracic and intestinal, and in addition into acute and chronic cases.

In the superficial, external or cutaneous form there is usually a sudden onset with high fever (104° to 107° F.), accelerated pulse, (70 to 90), and breathing (24 to 50), anorexia, suspended rumination, muscular tremors or shivering, staring coat, dry, hot muzzle, burning of ears, horns and hoofs, suppression of milk, and more or less stringy salivation. The visible mucosæ are of a deep red or violet tinge, and the patient will often remain apart by himself when the herd has moved elsewhere. Soon there develops a tense, hard, hot, painful swelling of the intermaxillary space, tongue, throat, neck, dewlap or elsewhere, amounting to perhaps six inches in thickness, extremely resistant and not usually indented on pressure with the finger. The breathing becomes stertorous and deglutition difficult or impossible. The mouth is hot and filled with tenacious saliva, and the tongue may hang pendant while on its borders and lower surface are projections of the mucosa swollen by infiltration, yellowish and semi-transparent, or blood-stained. At other points petechiæ are more or less abundant.

Death may take place from pharyngeal obstruction or closure, or as the disease advances, there may be indications of implication of the viscera, of the chest or abdomen: encreasingly difficult breathing, a mucous or suffocative cough, colicy pains, tenesmus, and the passage of moulded glazed fæces, of pseudo-membranous casts, or of profuse liquid stools. The animal may move the hind feet uneasily, lie down and rise alternately, may remain persistently recumbent until death, or he may stand up until he falls to perish of asphyxia. Death may occur in six hours, or may be delayed four days.

In the thoracic form the extreme hyperthermia is complicated by early lesions in the lungs, while the muscular or cutaneous ones are omitted or deferred. So long as the lesions are confined to the chest, they are betrayed by hurried and even oppressed breathing or dyspnœa, a frequent, moist, suffocative cough, persistent standing to favor respiration, and there are the percussion and auscultation indications of consolidated lungs or hydrothorax. The mucosæ are usually of a darker red, than in the external form, cyanotic indeed, and the peculiar asphyxial position, with legs apart, head extended, dilated nostrils and open mouth may be very significant. These symptoms are likely to be modified or supplemented before death, by those caused by intestinal or renal disorder. In the thoracic form in young animals death by suffocation may occur in a few hours, but more commonly the disease progresses slowly and a fatal result is not reached until the fourth day or even the eighth. This form is common in the deer, and less so in cattle.

In the intestinal or abdominal form the usual sudden onset and high fever, are complicated by inappetence, tympany, rumbling of the bowels, uneasy movements of the hind feet, perhaps twisting of the tail, looking at the flanks, and even lying down and rising. There is frequent, violent straining with the passage of fæces at first glazed, later streaked with blood, or mixed with pseudo-membranous casts, and very soon soft, watery, frothy and fœtid. These are usually black or reddish black from contained blood.

The urine may also be blood-stained.

Before death, complications on the lungs or skin will often come in to assist in diagnosis.

In the chronic and subacute types the lesions are often concentrated on the lungs, and there are a moderate fever cough, hurried breathing under exertion, dulness on percussion over limited pulmonary areas, blowing sounds, mucous râles, crepitations and more or less muco-purulent expectoration. These phenomena are all the more significant if complicated by digestive disorders, costiveness, fœtid mucous diarrhœa, tympany, or by the eruption of the superficial swellings.

Lesions. The swellings on or under the skin or among the muscles show extensive straw-colored exudations, colored at points with blood, with enlargement, infiltration and staining of the adjacent lymph glands. On the chest walls the sero-sanguineous exudate may extend from the root of the lungs, through the intercostal spaces to the skin in the breast, the axilla and behind. The tongue is often enormously swollen and black, charged with extensive blood extravasations in addition to the yellowish exudate. Along its sides and on its lower surface, the mucosa stands out in projecting masses of yellowish infiltration, which may show equally on the fauces, pharynx, larynx, trachea and bronchi.

In the lungs the pleuræ and subpleural and interlobular tissue are extensively infiltrated and thickened by a profuse yellowish serous or sero-sanguineous exudate, so that the appearance may closely resemble that of lung plague. The lung tissue is consolidated, hepatized and dark red, with at some points emphysema. The pleural sac is usually filled by a serous or bloody effusion (2 to 25 quarts) and there is often extensive implication of the pericardium. The tracheo-bronchial mucosa and bronchial glands show extensive infiltration and thickening.

In the abdomen are found extensive infiltrations and blood extravasations in the mucosa and submucosa of the stomachs and intestines, softening and shedding of the epithelium, infiltrations of the peritoneum, diaphragm, and sublumbar adipose tissue, and softening and degeneration of the liver and kidneys. The intestinal gastric and mesenteric glands are usually infiltrated, softened and blood-stained. Engorgement of the spleen is exceptional.

The blood is very black but not usually materially changed in consistency nor coagulability. Petechiation of the different serosæ and other tissues is a prominent feature.

In chronic cases the lesions are mostly shown in the lungs and lymph glands. The lungs show circumscribed lobular islets of congestion, induration or caseation, offering a suggestion of tubercle, which is all the more deceptive when cretifaction has set in. The caseous centres may vary in size from a pea to a walnut, and some may have ruptured to form a vomica discharging into a bronchium. Bronchia leading to affected lobules are blocked with muco-purulent matter, yellowish, thick and tenacious, and their mucosa is thickened and puckered. The enlarged lymph glands are especially those of the bronchia, trachea, mediastinum, bowels, mesentery and sublumbar region.

The bacillus is present in the exudate but is especially abundant in the blood, and in the chronic cases in the bronchial mucous.

Diagnosis. From anthrax (gloss-anthrax) this affection is easily distinguished by the absence from the blood and exudates of the large, square ended anthrax bacillus, by the absence of enlargement and blood engorgement of the spleen, and of the softness and diffluence of the blood clot which characterize anthrax. Swine which are with difficulty inoculated with anthrax are very susceptible to hæmorrhagic septicæmia. Sheep which are very receptive to anthrax are somewhat refractory to the disease now in hand. Pigeons resist anthrax but readily contract septicæmia hæmorrhagica.

From black quarter it is readily distinguished by the absence of emphysema and crepitation and of a secondary cooling in the external swellings, by the presence of the germ in abundance in the blood, by its smaller size, its bipolar staining, and its lack of motility and of spores. Inoculation with black quarter bacillus kills the guinea pig, but spares the pigeon.

From lung plague it is distinguished by the suddenness of its attack and rapidity of its progress to a fatal issue; by the usual coincidence of skin and bowel lesions, while the lung plague affects the chest only; by its communicability to pigs, sheep, pigeons, and even horses, which are all immune from lung plague; and by the usual absence of lung lesions of different ages, which are so characteristic of lung plague. The abundance in the blood of the cocco-bacillus with bipolar staining in hæmorrhagic septicæmia is characteristic. Lung plague spreads slowly to exposed cattle, but spares all other domestic animals.

From Rinderpest it is differentiated by the history of its advent, by the presence of the surface œdematous swellings, by the absence of the whitish epithelial concretions on the mouth or vulva, and of the deep dark portwine discolorations of the mucosæ of the mouth, rectum and vulva, and by the fact of its inoculability on domestic animals generally. Rinderpest spreads rapidly to all exposed ruminants, but spares pigs, rabbits, Guinea pigs, horses and birds.

From malignant œdema it differs in its inoculability on the surface in place of subcutaneously only, in the presence of the cocco-bacillus in the blood during life, whereas in malignant œdema the germ is confined to the local lesion, in the absence of crepitation, which may be present in the swelling of œdema, in the greater facility with which cultures can be made of the septicæmic cocco-bacillus and in the absence of gas production in such cultures. The malignant œdema comes from a single accidental deep inoculation from almost any rich soil, and is not a malady spreading widely and generally on given limited damp, rich lands which have become infected. Finally the cocco-bacillus of septicæmia hæmorrhagica is found singly in the blood or exudate, whereas the microbes of malignant œdema may be found in form of sporeless filaments intermingled with the bacilli.

Mortality. The hæmorrhagic septicæmia of cattle cuts off from 50 to 80 per cent. of the animals attacked.

Prevention. The first consideration is to isolate and kill all the affected animals, to destroy the carcasses by burning or boiling and to burn or disinfect all objects that may have become contaminated. The buildings, yards, and fences, must be disinfected, and as the bacillus is very resistant a solution of corrosive sublimate and sodium chloride, a drachm of each to the gallon of water may be freely used after thorough cleansing. Or a whitewash containing ¼ lb. chloride of lime to each gallon may be substituted. Feeding and drinking troughs may be burned. Manure may be freely treated with sulphuric acid. Infected fields should be closed for years and if possible drained.

Immunization of buffalo and sheep has been secured by making cultures of the microbe in free air at 86° to 90° F. and inoculating the animals with the weakened virus, on three successive occasions with intervals of several days. It induces a transient fever, with no serious phenomena (Oreste and Armanni). A second available method is to pass the virus through the system of the pigeon and inoculate with the pigeon’s blood, on three successive occasions, the animals to be protected. It is manifestly impossible to put such immunizing methods in force on wild deer, and for these probably the best course is to drive them from the infected range, to an uninfected one, having retained them for a few days interval in a confined area, to allow of any already infected animals developing the disease. A similar avoidance of waters running from the infected tract is imperative.

Treatment, has been unsuccessful. Friedberger failed with hypodermic injection of carbolic acid, and internal administration of salicylic acid. Gal gave subcutem 5 per cent. solution of creolin, and doses of 1½ oz. of the same agent by the mouth. Five buffaloes out of seventeen recovered. Friedberger suggests deep incisions of the swellings so as to admit the air, and treatment of the wounds with strong antiseptics.

SEPTICÆMIA HÆMORRHAGICA OF THE SHEEP: LOMBRIZ.

Synonyms. Definition. Geographical distribution, Argentina, France, etc. Causes: bacillus; intravenously, etc., youth, verminous affections, low condition. Bacteriology: ovoid bacillus with polar stain, bleached by Gram’s solution, ærobic, nonmotile. Symptoms: Chronic form in summer, diarrhœa, arched back, stiffness, emaciation, flattened wool, segregation, impaired or depraved appetite, shedding wool, anæmic skin, dependent dropsies, sunken eyes, weak small pulse, temperature variable—elevated, nasal and buccal discharge, weakness, paresis, dulness, torpor, lung symptoms, arthritis. Diagnosis: from distomatosis and strongylosis. Acute form with high fever, constitutional disorder, colics, diarrhœa, death in 24 to 36 hours, subacute form. Lesions: black blood, congestions, and general petechiæ. Lungs, liver, kidneys and spleen, congested, swollen. Subacute cases have lighter blood, and lesions. Chronic cases anæmic, blood diffluent, lymph glands enlarged, congested; connective tissues and serous cavities dropsical, gastric, intestinal and hepatic worms, spleen shrunken. Mortality: great in acute, less in chronic. Prevention: segregation, exclusion of all sheep from unknown or suspected flocks, antiseptic dip and quarantine for new purchases, expose a few as a test; cleanliness, disinfectants, avoid watershed from infected lands, wide range, outdoor life, generous diet, remove weak, emaciated, anæmic. Immunization. Treatment.

Synonyms. Pasteurellosis Ovina. Infectious Pneumo-Enteritis.

Definition. An infectious febrile affection of the sheep, chronic or acute, characterized by dulness, stiffness, or paresis, anorexia, thirst, disorder of the breathing and digestive organs, black diffluent blood, petechiæ, reddish effusions in the serosæ or connective tissue, and congestive or inflammatory lesions of the lungs, liver, kidneys and intestines. The presence of a cocco-bacillus (diplococcus, strepto-cocco-bacillus, pasteurellosa) in the lesions is especially characteristic.

Geographical Distribution. Though Lignieres first demonstrated this as a bacteridian disease in the Argentine Republic, he was, after his return, able to identify the same affection in the flocks of almost every department of France, in newly imported English Lincolns and German Merinos, so that there can be little doubt that the malady exists in all or nearly all countries engaged in sheep husbandry, though it has been usually attributed to parasitisms of the lungs, liver or alimentary canal alone.

Causes. The essential cause is manifestly the bacillus, which Lignieres has isolated, cultivated in vitro, and successfully inoculated intravenously in the sheep, which he also infected by feeding the pure cultures. Intravenously it proved fatal to Guinea pig, rabbit, pigeon, chicken, rat, mouse, horse, ass and ox. Yet many other accessory causes must be admitted as operating in different cases.

Youth shows the greatest susceptibility whether the victim be mammal or bird. So marked is this influence that the principle sufferers are lambs just weaned or yearlings. Yet mature animals, that are debilitated from any cause, also fall victims. The measure of immunity usually noticed in mature sheep may well be attributed to a previous mild and non-fatal attack of the bacillus.

Verminous affections are undoubtedly predisposing causes, hence, the common practice of attributing the malady to the worms alone. This again in part explains the susceptibility of the young which so often harbor worms to a dangerous extent. It seems to matter less what worms are present than, that they are in sufficient numbers to greatly deteriorate the health. It is noticeable, however, that those worms that make breaches in the mucosæ, have been noted as infesting the victims of this malady. In the stomach worms sent from Argentina, Railliet identified Strongylus Contortus, S. circumcentus, and S. instabilis and in the duodenum S. filicollis and S. Curticei. These, like the distomata often found in the liver, are blood suckers and not only render the animal anæmic, but make numerous perforations to act as infection-atria. The various lung worms, encysting themselves in the air sacs and determining local congestions may act in the same way, opening channels for the entrance of the microbe.

Low condition or a low tone of health from any cause predisposes. Old, worn out animals, ewes in lamb, or those just lambed, sheep that have been shut up and denied proper exercise in winter, those on poor feeding and perhaps nursing twins, those that have suffered from any debilitating disease of any kind are especially obnoxious to a dangerous attack.

Microbiology. The microbe, which Lignieres found in the pulmonary lesions, is one of the colon group of pathogenic bacteria that have been classed together as pasteurella. It usually appears as a very minute ovoid bacillus which stains promptly and deeply at the poles in fuchsine or gentian violet, leaving a clear median part, so that it seems a diplococcus. It bleaches readily in Gram’s solution. Its form varies in different culture media sometimes showing long bacilli, and sometimes streptococco-bacilli, but the usual and characteristic appearance is that of a cocco-bacillus, and to this it constantly returns. The microbe is ærobic and nonmotile (the slow zig-zag motion sometimes seen does not seem to be automatic). In peptonised bouillon it produces opacity in 18 hours, or in simple bouillon in 24 to 48 hours, the best temperature being 100° F. Gelatine plate cultures are slow because of the compulsory low temperature, yet in 36 to 48 hours it forms pale blue, translucent, round colonies the size of a pin head. It never liquefies. In coagulated blood serum it forms only a thin transparent pellicle hardly visible, and there is no growth on potato.

Symptoms: Chronic Form. In Argentina, Lignieres observed the disease especially during the hot summer months (December to May), and after weaning in the lambs. This may be from the marked change of food, from the greater activity of microbian life at this season, from the exhausting effect of the heat, or from a combination of two or more of these conditions. It appears alike in the sheepfold, and on the open prairie. In considerable flocks the symptoms may be at first overlooked, so that the death of several sheep may be the first thing to draw attention. Then a certain number are found to scour, arch the back, walk stiffly, lose condition, and have the wool flattened and devoid of yolk (clapped wool). The sheep may be dull, lagging behind its fellows, or lying apart by itself, ruminating infrequently and for shorter periods than natural, and there may be inappetence, or depraved appetite (eating earth), though some eat well to the end. Irregular and at intervals capricious appetite is a frequent condition. When caught and examined, the wool is easily torn out, the muscles are soft and wasted, (the leg muscles may have practically disappeared), the bones stand out at all points, the skin is pale, thin, bloodless and devoid of its subcutaneous fat, (paper skin), there may be œdemas along the ventral aspect of the body, pitting on pressure, and between the branches of the lower jaw (poked), the eyes are sunken, the conjunctiva may be puffy and œdematous, but like the muzzle and mouth they are pale and anæmic and the pulse is small, though the excitement may have roused cardiac palpitations. The temperature varies from time to time often reaching 105° or 106° F. There is liable to be a muco-purulent discharge from nose and mouth especially noticeable during drinking. As the disease advances the subject becomes weak, paretic, dull and stupid, it remains down without interest enough to seek food, though still eating if it is brought to it. The head is usually rested on the flank, and the animal often lies so for days in a state of semi-stupor without disposition or ability to rise, paretic or paraplegic. Auscultation may sometimes detect a mucous râle or crepitus, and percussion a flatness of sound over some part of the lung. Chronic arthritis is an occasional symptom.

Diagnosis. The symptoms closely resemble those of distomatosis or strongylosis, and the disease is often complicated with one or more of these, so that it may become difficult to judge how much is due to the microbian infection and how much to the helminthiasis. The presence, continuously or intermittently, of the hyperthermia is almost pathognomonic of the operation of the microbe.

Acute Form. This has been particularly observed in the ewe just after lambing, when the system is especially susceptible to microbian invasion, and little able to cope with it. There are hot ears, nose and feet, temperature of 104° to 106° F., accelerated pulse and breathing, anorexia, ardent thirst, deeply congested mucosæ, colicy pains, pawing the ground, frothy or bloody diarrhœa, arched back, pendent head, ears and eyelids, muscular trembling, albuminous urine, plaintive cries, dark red vaginal discharge, muco-purulent or glairy nasal discharge, and death in 24 to 36 hours. Such animals may be in fair condition or even fat, no time having been allowed for emaciation.

In other cases death may be delayed for three or four weeks, with the same general symptoms, only less marked. In such cases, pregnant ewes are likely to abort, and the lambs are born dead, or prove weak and listless, and die when a few days old. Some have too little energy to suck; others suck heartily but perish all the same on the second or third day, after diarrhœa, thirst, hyperthermia, prostration, and stupor.

Lesions. These vary according to the type. In the rapidly fatal cases there is dark colored blood, with congestion of the serous and mucous membranes, which, together with the skin and often the solid tissues, are covered with petechiæ, and even circumscribed hæmorrhages. The lungs, liver, kidneys, spleen, and many of the lymph glands are congested and swollen, seeming at times of a black hue as if blood-saturated. The lesions, indeed, indicate an acute septicæmia.

In cases that have survived three or four weeks, the morbid changes are slighter, the blood is brighter in tint, and the congestions less deep in color, ecchymoses may be especially confined to the heart, abomasum and small intestines, which may also show hæmorrhages. Enlargement and congestion of the lymph glands are the rule, while pulmonary consolidation and gastro-intestinal mucous inflammations are frequently found. As in the more acute types the urine is albuminous.

In chronic cases the anæmia is prominent. The clot is soft, relatively small, elastic and black, the serum is relatively very abundant and pale. The red globules are greatly reduced in numbers, and there are a number of giant cells which stain deeply as in chlorosis. The lymph glands are usually enlarged, softened and slightly congested but rarely the seat of blood extravasation. The tissues generally are pallid, soft and shrunken. There is a marked absence of subcutaneous and intermuscular fat, while the connective tissue is more or less infiltrated with a transparent, watery lymph. The serous cavities usually contain more than the normal amount of fluid, transparent or straw-colored, and with few globules or granules. Congestions and even shreds of false membrane are sometimes present on the serosa. In some cases the lungs and bronchia are the seat of inflammatory exudates, causing nodular consolidations of from one-half to one inch in diameter. Not unfrequently the lungs show strongylosis as the fourth stomach shows strongylus contortus, the small intestines strongylus filicollis, tæniae (expansa, fimbriata, etc.), the large intestines æsophagostoma Columbiana, and tricocephalus affinis, and the gall ducts distoma hepaticum and distoma lanceolatum. In these chronic cases the spleen is usually shrunken, and the liver firm, sometimes even cirrhotic.

Mortality. The acute cases are usually fatal. Those that assume a chronic form, if free from local lesions in important organs, well-fed, and, above all, kept in the open air, and changed to a different pasture, tend largely to recovery.

Prevention. The propagation of the infection from animal to animal is slow and somewhat uncertain, and when introduced by the purchase of a new ram or other animal, it may take a considerable time to affect the stock extensively, but for this reason, and because an apparently sound sheep may harbor the germ, it is difficult to oppose it successfully by segregation. All the same, it is desirable to take all possible precautions against its advent, and among these, the exclusion of strange sheep from noninfected pastures and flocks. When the time comes to make an outcross from the home strain, the ram must be selected not only for his pedigree and individual qualities, but no less for the soundness of the flock from which he is taken. If the lambs of that flock have been decimated by disease, the best blue blood, and most faultless form should not tempt the flockmaster. He should be rejected in favor of one taken from a flock that is above suspicion. It matters little if it can be plausibly argued that the mortality came from worms of the lungs, liver, or digestive organs; these in themselves may soon ruin any flock, but they, too, often coexist with the microbe of infectious septicæmia, and, when this is the case, they prepare the system and open a way for its invasion.

New purchases should not only be selected from apparently sound and guaranteed stock, but they should be passed through an antiseptic dip on arrival, and then if possible quarantined in a special enclosure until they shall have proved their freedom from infection. A valuable ram may be placed with some lambs or yearlings in close quarters to ascertain whether he has brought the infecting matter with him. If all escape after some months the presumption is that he is sound. Perfect cleanliness of the fold should be maintained, and disinfectants may be freely used in it.

The water supplies should be watched, rejecting streams that have drained sheep-pastures where there have been marked losses of lambs and ewes. Water from deep wells without any surface leakage is to be preferred.

When new stock (ram, ewes, lambs) are of necessity mixed with the sound herd, a wide range, an open air life, and abundant dietary must be secured. The system that is full of strength and vigor can better resist the microbe and even throw it off entirely, whereas the weak, confined subject succumbs. For the same reason, the weak, emaciated and debilitated subjects should be at once separated from the sound flock, and kept in a special enclosure, in the open air, on a rich diet. Should they harbor worms, this seclusion is even more imperative. (See parasites of lungs, liver, stomach and bowels).

Lignieres advocates immunization by serum prepared on the Pasteur method, but, as he has not divulged the exact technique of its preparation, it is impossible as yet, to give this an unqualified endorsement. It has this in its favor that the mature sheep, in full vigor of middle life, though in an infected area, usually resist the infection, while the young, old, debilitated and verminous suffer. Opposed to it are these considerations that are recognized by Lignieres himself;—1st, The acquired immunity is not perfect, as shown by occasional relapses in sheep that have survived a first attack; 2d, The serum inoculation is not only useless, but dangerous in animals that already harbor the germ; I may, add 3d, Any acquired parasitism or debilitating disease may tend to break down the immunity and prostrate the system under the infection. Lignieres advises that the serum treatment should be restricted to the new born lambs in infected herds, or herds in infected areas. The first three or four weeks after birth are to be preferred for the operation, though failing this it may still be ventured on, up to a few days before weaning. The longer it is delayed the greater the danger of a preëxisting infection, and of untoward results from the new access of infecting material, on the back of an infection which varies so extremely in its pathogenic potency. Even among the new born lambs, Lignieres would restrict the serum therapy to the strong, robust and healthy, and, if they survive the resulting fever, would repeat the treatment after the hyperthermia has ceased. No satisfactory treatment of the disease has been made. An open air life, a generous diet, and a course of iron, and bitters will, however, be of use in serving to improve health, digestion and vigor, to solicit a better production of red globules, and to enable the patient to survive the period of anæmia, prostration and debility. Antiseptics like quinia, the sulphites and the iodides might be used as adjuncts.

PNEUMO-ENTERITIS IN SHEEP: HÆMORRHAGIC SEPTICÆMIA: SWINE PLAGUE.

Historic note. Microbiology: ovoid bacterium, motile, with polar stain, non-liquefying, chains, grows freely on culture media. Pathogenic to sheep, goats, dogs, hens, rodents, calf, ass. Views of Lignieres, Lienaux, and Conte. Symptoms: Acute form in young; hyperthermia, rapid pulse, troubled breathing, dulness, prostration, sopor, anorexia, congested petechiated mucosæ, offensive diarrhœa, emaciation, wheezing, cough, râles, crepitus, percussion flatness, abortion. Death in 6 hours to 3 days. Subacute form in mature: symptoms moderate, recoveries the rule. Lesions: fœtid carcass, blood staining of skin and organs, exudates, petechiæ, swollen congested lymph glands, peritoneal exudate, congested liver and spleen, gastro-enteritis, pleural effusion, lobular and peribronchial exudates, caseation, congested womb, placenta and brain, bacterium in lesions. Prevention: isolation, disinfection, secretions, manure, drainage, exclude tame and wild animals. Disinfectants.

Among the different forms of hæmorrhagic septicæmia in sheep, that observed by Galtier in 1889 in Basses Alpes, and later elsewhere in southern and western France and in Algiers, must be specially noted. It seems to be the same affection studied later by Lienaux, Conte, Besnoit and Cuillé and which prevailed from Tarn in the south of France, to Vendée in the west, and Somme in the north.

Microbiology. The pathogenic factor found in the lesions was an ovoid bacterium, a little larger than that of fowl cholera, motile, non-liquefying, with polar staining, and often showing in short chains of two or three joined end to end. It grows easily and abundantly in all common culture media, even on potato which fails to propagate the cocco-bacillus of Lignieres. This, with its ready transmission from swine to sheep and vice versa, apparently serves to differentiate it from the cocco-bacillus, and the disease from the hæmorrhagic septicæmia of Lignieres.

Pathogenesis. In Galtier’s first observations in Basses Alpes four separate flocks were infected by pigs brought all from one market, and placed in or by the pens of the sheep where they sickened and one in seven died in a few days. Then the mortality began among the sheep and ranged as follows: 1st flock lost 10 in 37: 2d flock 16 in 25: 3d flock 8 in 20: 4th flock 12 in 22. On one farm 10 sheep were sent to a neighbor’s just before the arrival of the sick pigs and escaped, and on another a second flock kept in outlying pens well apart from the home flock kept perfectly sound.

With cultures of the microbe in vitro, he successfully inoculated sheep, goats, dogs, chickens, Guinea pigs, rabbits, and, finally, a calf and an ass. The cultures were inoculated in different cases; intravenously, into the trachea, pleura, lung, and subcutaneous connective tissue, and one goat was infected by ingestion.

Lignieres claims that Galtier must have worked with a complex infection in which his (Lignieres’) cocco-bacillus was an essential constituent. The evidence of this is, however, lacking, and we must recognize that Galtier made cultures which showed the close relationship of his organisms to swine plague, and their lack of complete identity with those of the Lombriz.

Lienaux and Conte had pathogenic results in a limited number of animals only (rabbit, mouse, Guinea pig) illustrating the familiar truth of the variability in the pathogenesis of different specimens of septicæmic bacteria of the colon group.

Symptoms. 1. Acute Form. There is a sudden marked rise of temperature, often to 107° F., with acceleration of pulse and respiration. Sometimes death follows so early as to prevent the observation of other symptoms. If otherwise there supervene marked dulness, prostration, somnolence, anorexia, suspension of rumination, and more or less tympany of the rumen. The patient is found lying down, apart from the flock, indisposed to rise, with deep red, congested, arborescent conjunctiva and other mucous membranes, and petechial spots on these and on the white portions of the skin. The fæces, at first moderately firm and moulded in pellets, marked here and there with lines of mucus, or even blood, become on the second or third day soft, pultaceous, or watery and highly offensive. Parallel with this, emaciation advances with rapid strides. Breathing becomes more hurried, wheezing or snuffling, with a muco-serous, often bloody discharge from the nose, and an infrequent cough. Careful auscultation and percussion will often reveal the blowing or mucous râles, the crepitation or flatness on percussion of broncho-pneumonia. As the disease advances the petechiæ on skin and mucosæ extend, and extensive deep violet areas show especially on the inner sides of the arms and thighs, on the under surface of the tail, on the perineum and under the belly. Abortion is a common result, the lambs coming dead.

Death may occur in six hours, more commonly in two or three days, or even longer, the temperature going down to below normal in the last stages. In case of recovery, convalescence is slow, the animal remaining emaciated and weak, with lung lesions and persistent cough for a length of time. These poor imperfectly recovered animals continue to harbor the microbe and transmit it. Lesions of the liver and other organs, the result of this disease, are found in sheep that have survived the affection and are afterward killed for mutton.

Symptoms: 2. Subacute and Chronic Form. This is seen in mature sheep of two or three years, that have been infected when in the full vigor of life and health, during an open air life and by a limited dose of the virus. The temperature is less elevated, the circulatory and respiratory functions less disturbed, the dulness and prostration only moderate, the interruption of feeding and rumination transient and tympany slight. Cough and nasal discharge are however present and rather persistent, diarrhœa may be manifested, and marked emaciation occurs. There may be congestion of the mucosæ, but petechiæ and extensive bloody discoloration of the mucous membranes or skin are rarely seen. Abortion is not uncommon.

Recoveries are the rule in this type of the disease, though in some cases it will be delayed for weeks and may even then be imperfect.

Lesions. In the acute types of the disease decomposition advances rapidly after death, and the carcass from the first exhales a peculiarly heavy odor. The skin is discolored, the nasal mucosa is the seat of a muco-purulent or sanguinolent discharge, the anus is soiled with liquid fæces, the subcutaneous connective tissue marked by red arborescence and blood-stained areas, or by a gelatinoid exudation, the muscles at times deeply colored and petechiated, the lymph glands, especially the bronchial and mesenteric, are enlarged and congested of a deep red—the color being highest in the cortical zone. In some old standing cases these may have softened and acquired a grayish hue. They are rich in the specific bacterium.

The peritoneum is congested, petechiated, thickened, and more or less covered with thin false membranes, and it contains from a pint to three quarts of a sero-sanguinolent liquid which coagulates loosely on exposure. The liver is congested, with points of blood extravasation, and zones of degeneration (fibroid, fatty or necrotic), and sometimes abscess. The congestion extends to the spleen and pancreas. The abomasum and intestines are the seat of mucous gastro-enteritis. The mucous folds of the pyloric sac of the stomach are congested, reddened and petechiated, the small intestine has tracts and patches of congestion, thickening and softening, Peyers’ patches and the solitary glands are enlarged, and ulcers may be present on large or small intestines.

Effusion is usually found in the pleura, clear, grayish or bloody, with flocculi and false membranes, and further branching redness of the serosa. The mediastinum may be thickened by exudate especially around the glands, œsophagus and blood vessels. The lung shows lobular, interlobular and peribronchial exudates approaching at times to the appearances shown in lung plague, along with the atelectasis, emphysema and, in prolonged cases, caseation.

Less constant are congestions and petechiæ of the pericardium, heart, kidneys, vesical mucosa, testicles, ovaries or womb. The blood is dark and forms a loose coagulum. In case of abortion the umbilical cord is infiltrated and the placental membranes ecchymotic. The brain and spinal cord and their membranes are sometimes congested and infiltrated and a serous effusion exists in the arachnoid.

The bacterium is found more or less abundantly in each of the morbid lesions.

Prevention. Absolute seclusion of the sick and of all their products is the prime essential. The general distribution of the lesions throughout the body and the uniform presence of the bacterium in the lesions indicate that no part of the body and no secretion can be considered as free from infection. All parts of the body, all expectoration, saliva, fæces, urine, milk even must be withheld from all other animals, at least until they have been thoroughly cooked or disinfected. Manure must be burned, or buried deeply in quicklime. Contaminated pens, yards, wallows, streams and fields must be abandoned or thoroughly disinfected.

Galtier found that the virus remained active for six days in putrefying organic matter at 39° to 75° F.; in 25 days in water, at room temperature; the refuse litter, fodder, manure, and drainage matter from the infected place must be carefully guarded against. The virus steadily loses in force in such media, but remains infecting to animals injected with it. The most active disinfectants may be used on the pens and yards (copperas 5%, sulphuric acid 2% solution, or mercuric chloride .2%) while the contaminated fields should be abandoned for the season. All droppings may be treated with sulphuric acid (2%), creolin, lysol, phenic acid or copper sulphate. The susceptibility of practically all the animals of the farm, demands the exclusion of these, while that of rodents, renders necessary the further exclusion of wild mammals; and we may add birds, wild and tame, and if possible flies. The plowing of the contaminated soil will do much to obviate danger, yet the sheep folds and pastures should be separated by a considerable distance from any place where infected animals and objects have been. If drinking troughs for sound animals have been used by the sick or suspected they should be emptied and washed with a disinfectant (sulphuric acid 2:100).

ULCERATIVE (ERYSIPELATOID) INFECTION OF THE LIMBS IN CATTLE AND SHEEP.

New York outbreaks. Causes: wounds by sharp pebbles, streptococci, pure cultures, inoculations. Symptoms: swelling on lower limbs, abscesses, implicating tendons, bones, joints, and under hoof. Prevention: avoid septic or frosted mud, irritants, etc., disinfect surface, keep dry and clean, open abscesses, use disinfectants, separate infected.

This affection was seen in several herds in Oneida Co., N. Y., in the Spring of 1897. The geological formation of the region was a calcareous rock with a surface soil thickly impregnated with pebbles and small flat shaly masses. Sheep suffered in Western New York.

Causes. In Oneida, the subjects were dairy cows, which in the early spring, when the frost went out of the ground, had to wade through chilly soft mud reaching to the knees or above, and mixed with small stones with sharp edges, and with semiliquid manurial products. The abrasions made by these stones furnished convenient infection atria for septic microbes in the manure. In the pus obtained from the ulcers were found in abundance the bacillus coli commune, and a long streptococcus representing on an average from 20 to 40 cocci in a chain. Dr. Moore made pure cultures of these and produced the same symptoms in a cow by injecting the streptococcus subcutaneously in the back of the pastern, and in another animal by simply abrading the surface and rubbing on the streptococcus culture. As the inflammation, suppuration, and resulting ulcers implicated not only the skin but also the subcutaneous connective tissue, the affection had many of the characters of erysipelas.

Symptoms. The affection commenced by swelling in the region of the fetlock, pastern, metacarpus or metatarsus, and exceptionally, the forearm or tibial region, and advanced to a tense swelling, which pitted on pressure, and the formation of centres of suppuration, which burst and discharged. If the exposure to the septic mud were continued the sores ulcerated and extended both in the skin and subcutaneous connective tissue, but when the dry weather came and the mud disappeared, the tendency was to spontaneous recovery. In some instances ulceration extended beneath the hoof threatening its evulsion, and in other cases it extended deeply to the tendons and ligaments.

Treatment. The main object should be prevention, to be secured by protecting the stock against contact with septic mud, and especially such as is near the freezing point and intermixed with such sharp stones and pebbles as would wound the surface and open channels for infection. When infection has taken place we should seek to limit it by lotions of an antiseptic character. Bandages soaked in a solution of hyposulphite of sodium, 1 dr. to the ounce will often succeed. A more potent application is iodized phenol, prepared as follows: tincture of iodine 2 drs., carbolic acid crystals 4 drs., glycerine 1 oz., alcohol 1 oz., water 8 ozs. When applied on a bandage this may be diluted with water to make 1 pint. For circumscribed application to forming sores the undiluted iodized phenol, made of one part each of iodine and carbolic acid crystals, may be applied twice a day with a glass rod. Other favorite applications are a lotion of lead and laudanum; a saturated solution of boric acid; ninety-five per cent. alcohol; a mixture of creolin 1 part, iodoform 4 parts, and lanolin 10 parts; ichthyol and collodion; ichthyol and vaseline; or iodol, iodoform, salicylic acid or resorcin as dusting powders.

Internally, tincture of muriate of iron 3 drms. every three hours helps to keep the affection in check.

GANGRENOUS INFECTION OF THE CORONET. HORSE. POTCHETCHOUI.

Seen on rich, damp lands. Symptoms: lameness, small areas of congestion, erection of hairs, vesiculation, pustulation, gangrene as deep as tendons, depilation, desquamation, fistulæ, slough of hoof, early fever, impaired appetite, recovery in 14 to 21 days in most cases. Staphylococcus and streptococcus. Prevention: segregation, different attendants, avoidance of infecting land while damp, smear limbs with antiseptics. Treatment: antiseptic bandages.

Under this name Sotsevich describes an infectious disease of the horse, which prevails in the Don province, and especially on rich, low, damp lands. Before the appearance of any local lesion, the horse goes very lame on one limb. Afterward there appears, usually on the coronet or pastern, an area on which the hairs stand erect, with elevation of the epidermis and the formation of vesicles as large as barley corns, filled with a yellowish white liquid and later with pus. Gangrene follows, extending from the skin to the subcutaneous connective tissue, aponeurosis and tendons, and forming large sores, one to two inches in diameter and discharging an abundant yellow, fœtid pus. The adjacent skin takes on a yellow tint and sheds its hair and epidermis. The disease may extend into the interphalangean joints or under the hoof, leading to offensive fistulæ or evulsion of the hoof. If it extends to the higher parts of the limb it becomes less destructive.

At the onset there is some fever (101° F.), dulness and inappetence, but these gradually subside, and in favorable cases complete recovery has taken place in two or three weeks.

Bacteriological investigation has detected in the contents of the vesicles, staphylococcus pyogenes aureus, and streptococcus pyogenes.

Prevention is largely secured by a rigid separation of the diseased from the healthy. Other obvious precautions would be to exclude those dressing the sores from handling other horses until after thorough disinfection of the hands, and to keep the sound animals, during wet seasons, from the damp infecting soils, or when they must work on these, to smear the lower parts of the limbs with antiseptic ointments (tar, carbolic, iodine, mercuric, etc., etc.)

Treatment with sublimate bandages proves very satisfactory, yet any comparatively non-irritating antiseptic lotion may be used.

STRANGLES, INFECTIOUS RHINO-ADENITIS.

Synonyms. Definition. Historic notes. Bacteriology: streptococcus coryzæ contagiosæ equi in pus, chains of 3 and upward, free cocci, arthrospores, clumps, ærobic, growing freely in serum, or glycerined bouillon; pathogenic to horse and white mouse; relation to other streptococci; clinical evidence; accessory causes, youth, primary susceptibility, dentition, training, impure stable air, grain ration, excitement, sudation, fatigue, chill, change of climate, trading, crowding, sea voyage, catarrh of air passages. Infecting products, pus, ingesta, blood, manure, fodder, litter, water, secretion of mucosa of healthy. Wounds, castration, mangers, racks, troughs, buckets, poles, shafts, harness, halters, twitches, blankets, rubbers, combs, brushes, men, etc. Pathology: infection of lymphatics, through inhalation, sore, ingestion, congenital, milk; congestion of nasal mucosa, epithelial degeneration and desquamation, discharge little viscid, corded lymphatics rare, submaxillary swelling rarely small or nodular, pus creamy, indolent cases, pharyngeal, thoracic, buccal, gastro-intestinal, hepatic, pancreatic, splenic, muscular, arthritic, cutaneous, nervous. Forms: mild, malignant, regular, irregular. Incubation 3 to 5 days. General symptoms: hyperthermia, dulness, apathy, costiveness. Specific symptoms: nasal, congestion, sneezing, purulent discharge; epiphora, submaxillary phlegmon; pharyngeal and laryngeal; parotidean; pulmonary; abdominal, hepatic, pancreatic, splenic, perirenal, cutaneous, genital, nervous, septicæmic. Diagnosis, from catarrh, glanders. Prognosis, favorable, apart from malignancy. Prevention: exclude strange equine animals; avoid public stables, yards, drinking troughs and buckets; also manure, stable utensils, hay, fodder, litter, or watershed from infected places; disinfect cars, wagons, etc. Seclude inmates of infected stable, yard, park, etc., temporarily close public drinking and feeding places, make sale or exposure of infected animal penal; temporarily close dealers’ stables; sale with general guarantee only. Disinfection. Immunization; inoculation from mild case. Treatment: hygienic, antipyretic, eliminating, antiseptic, surgical, tonic, antisuppurant.

Synonyms. Distemper; Coryza Contagiosa Equorum; Gourme (Fr.); Druse (Ger.); Cimurro (Ital.).

Definition. An infective, streptococcic, febrile disease of solipeds, usually manifested by a catarrhal inflammation of the upper air passages, and phlegmon of the adjacent lymph glands, or less frequently by phlegmonous inflammation of lymph glands elsewhere or of the skin.

Historic Notes. Strangles was fairly indicated in the writings of the ancient Greek veterinarians, and was clearly described and attributed to contagion by Solleysel in 1664. It was so evidently infectious that it was experimentally inoculated by Lafosse in 1790, by Viborg, in 1802, and later, by Erdelyi (1813) and Toggia (1823) and others. Rivolta, in 1873, found a streptococcus in the pus of its abscesses, and to this the contagion was definitely assigned by Baruchello (1887), Schütz, Sand and Jensen (1888). Priority in this demonstration is accorded to Schütz.

Bacteriology. The streptococcus coryzæ contagiosæ Equi (Streptococcus rhino-adenitis or S. equi) is easily found in the pus of gland abscesses sometimes in pure cultures (impure in the nasal discharge), stains readily in aniline colors and in Gram’s solution so that it stands out clearly among the pus cells. The decolorizing agent must be weak (not muriatic acid) and applied only for a very short time. Beside the chain forms, there are isolated, oval cocci, some of which, larger than others and more elongated, have been held to be arthrospores or mother cells. The number of elements articulated in a chain varies from two to four and upward. The chains are straight or sinuous, and may be grouped in bundles, radiating masses, or clumps like staphylococci.

They are ærobic (facultative anærobic), grow freely as transparent droplets on blood serum at 99° F., and in glycerine bouillon, and less vigorously on agar and gelatine. On agar the colonies reach the size of a pin head in two days with projecting alæ, and on gelatine in three to five days, and then dry and shrink. Multiplication takes place by transverse division, and at such a time the organism may seem to be a chain of diplococci.

Pathogenesis. Inoculation of cultures on a susceptible horse produces the unquestionable phenomena of strangles, and solipeds alone take the disease casually. In white mice it produces abscess in the seat of puncture and in the adjacent lymph glands. If the action is delayed the abscess may be in lung, spleen, kidneys, liver, or other distant organ. Rabbits, Guinea pigs, pigeons, pigs and cattle are immune unless large doses are employed. Intravenously large doses kill the lamb.

The identity of the microbe with other streptococci of animals and man has been claimed. Arloing alleges that, by culture of the microbe in the blood or peritoneum of the live rabbit, he exalted the virulence, and obtained in succession a streptococcus capable of producing erysipelas; gangrenous erysipelas; suppurating, sloughing erysipelas; pseudo-membranous peritonitis; metastatic abscesses; and fulminant septic peritonitis. Hill, Jensen and Sand, and Lignieres, as the result of cultures and inoculations claim that strangles streptococcus is identical with that of contagious pneumonia. Courmont, on the other hand, as the result of his cultures and inoculations, concludes that the microbe of strangles and that of erysipelas are independent organisms.

The clinical evidence is decidedly against the theory of identity. In epizoötics of strangles we meet with a constant succession of cases of strangles and in districts into which contagious pneumonia has never been introduced, no single case of that disease ever comes in to break the monotony of the sequence and to start a series of cases of the latter affection. Conversely, in an outbreak of contagious pneumonia in a locality heretofore free from strangles, strangles do not develop. Again, no matter how prevalent nor how constant strangles may be in a locality, and how habitually men have their wounded hands covered with the pus of the abscesses, no epidemic of erysipelas is entailed in man. Strangles spreads with remarkable rapidity through a stable, but not to the often more than equally exposed human attendants, nor to any animal apart from the genus equus. The absence of strangles from Iceland (Jonsson) endorses that view.

As a practical question of sanitary science, we occupy a sound position in differentiating the germs of strangles and contagious pneumonia, and further that of erysipelas of man, as a wise health officer would differentiate the microbes of cowpox and smallpox. Whatever may be true or false as to their primary identity, or as to the transition of one to the other in successive inoculations on animals of other genera, they are essentially diverse pathogenically as we meet with them in practice, and our measures may be safely based on this practical diversity.

Accessory Causes. Youth strongly predisposes, most cases occurring between two and five years, and seventy per cent. before five years. It may, however, appear at any age, being congenital in some cases (Nocard, etc.), in others appearing a few weeks after birth, and in still others at over twenty years, if the subjects have not contracted it earlier.

Dentition which is active in these early years, induces congestion about the head and general constitutional disturbance, which make the system more receptive.

Training or breaking is another reason for the predisposition in the young. The first experience of the hot, impure, infected air of the stable, the unwonted grain feeding, the excitements and perspirations attendant on the first handling all contribute to temporary loss of resistance.

Fatigue like other weakening conditions lays the system open to attack.

Chill is a most efficient cause, hence the disease often prevails most extensively in spring and autumn, at the time of changing the coat, and of passing from stable to field and the converse. Joly relates that in Russia where large numbers die of strangles through imperfect stabling in winter, immunity is sought through a milder first attack, brought on in the milder autumn weather by turning the young animals into a deep pool for half an hour and then exposing them freely to cold winds and giving cold water to drink. The omnipresent germ takes occasion to attack the cold debilitated system.

Any change of latitude or of locality acts in the same way. Riquet even alleges that this will bring about a second and even a third attack. It is common, he says, for newly bought young horses to have the disease at Hamburg, and after recovery to have a second attack at Hanover and finally a third one after they join the regiments in France. A similar exhaustion of immunity has been repeatedly noticed in the case of canine distemper.

Horse trading and the stabling of large numbers together is naturally the most fruitful of infection and hence strangles is a virtual plague in dealers’ studs. The buildings in such cases are reinfected at short intervals with virulent types of the streptococcus, and fresh susceptible animals are being constantly introduced to keep it up. Riquet says that in Northern Germany dealers avoid this largely by traveling their purchases in bands of 100 or 150 head, from ten to twelve miles a day, feeding sparingly, and turning them like sheep into an open park at night regardless of the weather. Much of the advantage is doubtless from the avoidance of stable infection and the warm relaxing air of indoors.

A sea voyage especially favors infection and a single victim placed on board will speedily contaminate all susceptible animals present.

Finally the predisposing influence of catarrh of the air-passages must not be overlooked. The inflamed mucosa furnishes a most inviting infection entrance.

Infecting products. The streptococcus abounds in the local phlegmons and abscesses, in the exudate of the submaxillary, pharyngeal or other glandular swellings, in the pustular eruption on the skin, and in the catarrhal discharge from the air passages. It further exists in the alimentary canal, in the ingesta and in the blood to a limited extent. In the bowels of an immunized animal it may remain virulent for months. Thus it comes that the manure is a source of infection, and that soiled fodder, litter and water may prove dangerous. The infected soil can not only harbor but can multiply the microbe, keeping it in readiness to attack any receptive horse. On his part the horse that is immune and in vigorous health may carry the infection for months and transmit it to his less resistant fellow.

While the streptococcus is usually found in the blood, in limited numbers only, its presence there implies its general diffusion and especially in the lymph plexuses and glands. Hence, the danger of operations on the subjects of strangles, the weakened tissues of the wound forming a most inviting field of growth. Castrations, occurring as they do mostly in the growing animal, are especially to be guarded against, and I may cite the case, familiar to many, in which seven cryptorchids died with phlegmon in the seat of the wound, the first one operated on having had strangles.

The nasal and buccal discharges are especially liable to convey the infection through mangers, racks, fodders, drinking troughs and pails, harness, poles and shafts, halters, twitches and the like. Infection through blankets, brushes, rubbers, and the clothes and hands of attendants, dealers, veterinarians and others, is not to be overlooked.

Pathology. The streptococcus shows a special disposition to enter and advance along the lines of the lymphatic circulation. The paucity of the germ in the blood and its abundance in the lymph plexuses, vessels and glands show that its election is preëminently for the lymphatic system. Then the ordinary primary lesions in and around the upper part of the air passage (nose, pharynx, submaxillary, parotidean and pharyngeal lymph glands) bespeak infection by inhalation, rather than with the ingesta. Primary solitary lesions on or near stomach or intestine are almost unknown; nearly all such being secondary. Next to inhalation, the most prominent channel of entrance is through castration and other wounds. Abrasions and sores of skin diseases must rank after wounds as entrance channels. Transmission by copulation the microbe being lodged on the genital mucosa is well established, also transmission from mother to fœtus through the placenta, and from dam to offspring through the milk.

In the most familiar type of the disease the nasal mucosa is red, congested and somewhat thickened with exudate, and the epithelium is softened and desquamating. As the result of this desquamation there may be slight abrasions or raw sores but these do not show indications of the irregular outline, excavations, or progressive extensions that characterize the ulcers of glanders. The surface is usually plentifully covered with a muco-purulent material with less disposition to adhesiveness than in glanders. It is rare to see any exudate into, and thickening of the walls of the lymphatics running from the nostrils toward the submaxillary glands. The predominance of the streptococcus in, and the entire absence of the glanders bacillus from the discharge and inflamed mucosa are conclusive. In the regular cases in which the submaxillary lymph glands are implicated, both right and left are usually involved, though not to the same degree, the exudate fills not only the gland tissue, but a large amount of the surrounding connective tissue as well, there is a great accumulation of lymphoid cells, and more or less extensive pus cavities, containing usually a white, creamy product. In the early stages the glands may be hard and nodular, as in glanders, but this condition is very transient, so that the rule is to find an extensive surrounding exudation filling up the whole intermaxillary space, and having a great abundance of small round cells with double or triple nuclei. In the older cases there is usually the open abscess, and if the case is an indolent one there may be extensive organization of the exudate with formation of dense, fibrous tissue. In some instances the nasal sinuses are filled with muco-pus.

When lesions extend farther implicating the pharynx and larynx, the mucosa of these parts shows the same redness, congestion, cloudy swelling and desquamation with, in some instances, small, submucous abscesses, and in others extensive infiltration of the submucosa with lymph so as to narrow or even close the lumen of the larynx. The guttural pouches may be filled with pus though this is far from constant. The pharyngeal lymph glands, are nearly always involved and often the lymph gland in the parotid so that a general infiltration of the surrounding parts is met with.

If the chest is implicated there is congestion of the bronchial mucosa, engorgement of the smaller bronchia, air sacs and cells with pus, collapse, carnification or congestion of lobules, in some cases pulmonary abscess, and, finally, swelling and not infrequently abscess of the bronchial glands. Pleurisy is a not uncommon accompaniment, appearing it may be as a simple extension, from the lung, or, in the worst forms, from rupture of mediastinal or glandular abscesses into the cavity and severe infection of the entire pleural walls. The pericardium is exceptionally involved and coagula on the tricuspid valves have been met with (Zschokke).

Circumscribed phlegmonous exudates and small abscesses are sometimes found in the mouth (tongue, soft palate, cheeks) and less frequently in the œsophagus.

The stomach may show congestions, petechiæ, circumscribed hæmorrhages, ulcers, and abscesses of the gland tissue or submucosa. Rupture of the walls may follow abscess (Cadeac).

The intestines may show congestions, colorless or hæmorrhagic exudate, and suppurations in the agminated or solitary glands, or submucosa. The intestinal, mesenteric and sublumbar lymph glands may be the centres of abscesses of varying sizes.

Abscesses may also be found in the liver, pancreas, spleen, of variable size and usually as secondary formations.

The muscles and intermuscular tissue may be the seat of more or less extensive exudation, and abscess, and the bones may be congested and swollen especially in their epiphysis. This may extend to suppuration or necrosis.

The synovial membranes of joints and the tendinous sheaths are not infrequently inflamed causing distension and even suppuration.

Congestions of the skin are sometimes met with developing as multiple papules or hard nodules which advance to the formation of pustules or small abscesses. These often appear especially where the skin is thin and delicate as around the lips, nose and eyes, close to the anus or vulva, in the perineum, sheath or mammæ, inside the thighs or elbow. They may be of all dimensions from a millet seed upward, and may merge into or become complicated by the extensive engorgements of petechial fever.

Finally lesions of the nerve centres are to be looked for in the protracted or irregular types of the disease. There may be simple congestion, or serous effusion, intraventricular or subarachnoid, or finally abscess in the brain, spinal cord or meninges.

Forms of Strangles. The types of strangles vary, special forms characterizing given epizoötics or seasons, or at other times as individual deviations from the current type. Division has been made into two groups—mild and malignant, or again into regular and irregular, under each of which come several varieties. Many of these varieties consist simply in a difference in the seat of the principle lesions, which start in lymph glands or tissues at a distance from the nasal mucosa, or they depend on secondary foci of infection supervening on the primary disease in the head.

Incubation. In inoculated cases this lasts from three to five days, in those due to simple exposure it may appear to extend over eight days.

General Symptoms. In nearly all cases alike there is a marked constitutional disturbance the temperature often rising at once to 104° to 106° F., and oscillating on successive days between this and 102°; the pulse is usually normal at first and the breathing is either slightly accelerated or may be made so under slight exertion. There is more or less dulness, or at least a lack of the vivacity of youth, the head is somewhat pendent, the eyes may be semiclosed, the patient may be tardy or even stiff in his movements and the appetite may be diminished or capricious, oats being rejected by some and hay or grass by others. The bowels are somewhat confined, the stools consisting of a few small, hard, balls covered with mucus.

Specific Symptoms in the Mild Form. In the vast majority of cases the local symptoms are concentrated on the mucosæ of nose and mouth, and the submaxillary lymph glands. Along with the general febrile phenomena, there appear redness and often mottled congestion of the nasal mucosa, which not infrequently extends to the mouth and eyes, as well. Heat of the mouth, the collection of a more or less tenacious mucus, and even uneasy movements of the jaw may be seen. The nasal mucosa, at first dry, is soon the seat of a watery exudation, passing into a cloudy sticky material, and finally a thick, opaque, muco-purulent flow. This may become colored of a variety of tints, dirty white from inhaled dust, brownish or yellowish from exuded blood, or greenish from food materials. The discharge is usually profuse in the young and may be scanty in the old. Most commonly it flows from both nostrils alike, though exceptionally it is unilateral. In this it differs from glanders which is more often unilateral though at times bilateral. Small abrasions and sores may appear in connection with the softening and shedding of the epithelium, but these are not ragged, irregular and spreading as in glanders. Sneezing or snorting is an inevitable symptom. Epiphora is usually present. Exudations into the nasal sinuses are to be recognized by heat of the forehead and flat sound on percussion.

Very early in the attack a swelling is noticed in the intermaxillary space, which may be at first confined to the nodules of the lymph glands, thus forming distinct, rounded, hard swellings, but they are early covered by a diffuse exudation into the surrounding connective tissue, that completely envelopes and obscures the form of the swollen glands, and forms a more or less uniformly rounded, pasty swelling, extending to the median line of the intermaxillary space, or filling the whole space from one maxilla to the other and projecting downward below their level. This early, diffuse, pasty, evenly rounded swelling, hot and tender, is distinctive of strangles, and usually exclusive of glanders.

Another characteristic of the strangles swelling is its steady, and usually speedy, advance to suppuration and abscess. It becomes hard, tense, and resistant, then, in the centre, or at various points of the surface, small areas of circumscribed softening can be detected, and soon show distinct fluctuation. Two or more of these may coalesce or they may form several distinct abscesses, which may early point, burst and discharge, when the remainder of the exudate softens and degenerates into pus, and the cavity closes by granulation. In some cases after the formation of the swelling it disappears by resolution, the exudate becoming liquefied and absorbed. In glanders the nodular, insensible, swelling tends to persist without extensive pasty exudation or suppuration.

Cases of strangles catarrh in which the submaxillary lesions are omitted, are quite common. These occur during the regular strangles epizoötic, and protect against a second attack.

Symptoms of Pharyngeal and Laryngeal Strangles. Extension of the morbid process from nose to pharynx is exceedingly common. When concentrated on the pharynx there are extension of the head forward with elevation of the nose, swelling of the throat laterally or downward, uneasy movements of the jaws, salivation, difficulty of swallowing, return of ingested liquids through the nose, gulping, and a loose suffocative cough. The swelling of the throat tends to attain to large dimensions, and may threaten suffocation by interfering with the breathing. This is still further aggravated if the laryngeal mucosa is the seat of exudate. The breathing may become loud and stertorous, the mucosæ of a dark leaden hue and the animal dull and stupid from the venous condition of the circulating blood.

Abscesses forming on the lateral parts of the throat usually make their way to the surface though this may be below the level of the parotid. If from the parotidean lymph gland, one of the ducts may be opened thus forming a salivary fistula. If from the retro- (supra-) pharyngeal glands the rupture into the pharynx is more likely to take place, but in some cases the investing sac, meeting with equal resistance in all directions, fails to undergo degeneration and softening at any one particular point, and the contents remain pent up indefinitely. If the liquid is absorbed a cheesy or putty like mass may be the final outcome, with chronic cough, some stertor in breathing and it may be difficulty in swallowing.

If the guttural pouches should be involved, there is deafness, parotidean swelling, which may eventuate in a fluctuating swelling at the lower border of the parotid, and a free discharge when the head is lowered, which is likely to last after general recovery. (See Guttural Pouches, pus in).

Laryngeal paralysis and roaring often follow laryngitis in strangles.

Pulmonary Symptoms in Strangles. Tracheitis and bronchitis are forms of extension of strangles from the upper air passages, and pneumonia follows of virtual necessity. In many cases these are primarily dependent on the descent into the lungs of the infecting discharges, complicated in many cases by the inhalation of food materials. There are the usual symptoms of broncho-pneumonia complicating those of strangles and the percussion and auscultation signs usually imply circumscribed areas of congestion and consolidation with intervening areas of pervious lung. There may be at such points the blowing or mucous râles of bronchitis, the sibilant sounds of emphysema, the crepitation of congestion and the abnormal clearness of sounds carried from distant organs through the consolidated lung. On percussion there may be the non-resonance of the consolidated areas, and the excess of resonance over emphysematous portions or open gas-filled vomicæ. In these last cases there may be an amphoric sound on auscultation and a crack-pot sound on percussion. These pulmonary lesions are often fatal, or the recovery is slow on account of a succession of lobular congestions and abscesses.

Abdominal Symptoms in Strangles. The abdominal lesions in strangles are usually secondary, the infection reaching the part through the blood, or by the lymphatics from a castration or other wound, or from infection by coitus. The phlegmon and abscess may be in the mucosa, especially in the agminated or solitary glands, in the adjacent lymph glands at the connection with the mesentery and in those of the mesentery itself. The animal is dull, listless, with dry, staring coat, tympany and slight colicy pains after eating, costiveness, retracted, tender abdomen, insensible loins, and groaning when rising, when walking down a steep incline, or turning in a very narrow circle. These symptoms following an apparent or partial recovery from strangles are significant, and rectal examination may detect a hard, tender mass connected with the bowel or mesentery.

If rupture takes place into the peritoneum there is general infective inflammation of that structure with sudden access of fever, marked prostration and an early death. In more favorable cases its adhesion to the bowel or to the abdominal wall opens the way for rupture into the gut or externally and there may be a slow healing of the cavity by granulation. It may be a month or two before such an abscess opens and for a length of time thereafter the health is poor, and the animal lacking in condition and endurance.

When the abscess is formed in the liver there is high fever with shivering fits, irregularity of the bowels (bound up or loose), dusky or yellowish hue of the visible mucosæ, anorexia, followed by peritoneal infection or pyæmia (secondary abscesses).

Abscess of the pancreas or spleen is even less definite in symptoms. These may terminate in rupture and peritonitis, or the splenic abscess may become chronic and indolent and in a measure harmless.

Perirenal Abscess is betrayed by specially sensitive loins, stiffness and groaning in rising or in turning sharply on himself, drooping of the back under a load, and by albuminous urine. In a small animal the part may be reached and the tenderness ellicited by handling.

Cutaneous Symptoms in Strangles. Though by no means a common form, strangles sometimes attacks the skin, more particularly that of the face, head and neck, appearing in the form of pustules or small abscesses, or it may be of a rounded nodular elevation, which may disappear without forming either vesicle or pustule. The points of election are around the lips, nose and eyes, upon the mucosa inside the lips, along the line of the facial lymphatics running toward the submaxillary gland, and at points where there is special friction, as under the halter, collar, saddle, crupper, in the hollow of the heel, under the tail, on the perineum, in the groin and axilla. They may extend more or less up the limbs, or around the point of primary attack attended by more or less engorgement. When this engorgement has reached extensive dimensions and is mixed with sanguineous extravasation it is considered as having merged into petechial fever.

Symptoms of Coital Infection. From four to seven days after copulation there appear fever, dullness, stiffness, anorexia, swelling and heat of the lips of the vulva, a yellowish opaque discharge from its lower commissure, a deep dark red blush of the mucosa, with points of distinct infiltration and thickening, developing into vesicles and pustules. The perineum, the groin and mammæ often show an extension of the congestion and eruption. In exceptional cases deep abscesses form and Letard records a fatal case with extensive suppuration among the muscles of the hind limbs and the haunch, inside the pelvis and along the line of the aorta.

Symptoms of Nervous Lesions. The lesions of the brain and spinal cord are usually secondary and often appear when the less dangerous superficial manifestations, are tardy and indolent, when the exudates are indurated and indisposed to soften. There may be violent delirium, pushing of the head against the wall, movements of the limbs as if walking or trotting, roaring, plunging, striking with fore or hind feet, trismus or other muscular spasms. More frequently there is great dulness, prostration, debility, vertigo, drowsiness, amaurosis, paraplegia, general paralysis, coma. If the lesion is in the spinal cord the spastic or paralytic symptoms are likely to be confined to the hind parts.

Fulminant or Septicæmic Form. Bigoteau describes a rapidly fatal, septicæmic form, with sudden onset, anorexia, extreme prostration, uncertain stumbling gait, a deep blue color and ecchymosis of the visible mucosæ, violent heart action, pulse weak and small, hurried breathing (45 per minute) temperature 102° to 106° F., often inability to rise and death from asphyxia in from two to five days.

Diagnosis. In mild and regular cases this is easy. The attack in rapid succession of all the young, and still susceptible horses in a stable or locality, and the uniform coincidence of a profuse nasal catarrh, and the formation between the branches of the lower jaw, of a diffuse, hot, painful swelling rapidly advancing to suppuration and discharge are virtually conclusive. Simple catarrhs even if infective and attacking all young horses do not cause phlegmon of the submaxillary lymph glands as occurs in the great majority of cases of strangles. Glanders which is attended by both nasal discharge and submaxillary swelling, is slower in its onset, usually with little or no fever, has usually a more adhesive discharge, ragged, unhealthy ulcers on the nasal mucosa with a disposition to extend, often it shows cord-like thickening of the lymphatics on the side of the face, and the submaxillary swelling is smaller, made up of a number of small, hard, insensible rounded nodules which show virtually no tendency to suppurate. (See diagnosis of glanders). In cases of doubt it may be advisable to inoculate a Guinea-pig and a white mouse. The Guinea-pig resists a small dose, while the mouse forms abscess in the seat of inoculation in the dependent lymph glands. The Guinea-pig is very susceptible to glanders, and the white mouse immune. Or mallein may be used.

Prognosis. The mild type of strangles almost invariably terminates favorably. In the irregular types with internal abscess the prospect is grave in ratio with the size and multiplicity of the foci and the vital importance of the organ invaded. In 15,421 cases collected by Friedberger and Fröhner, and representing the total in a series of outbreaks, but 3 per cent proved fatal. Much, however, depends on the special potency of the germ. Horses contracting this in a particular year or from a given stable in the same year convey the disease to others in a malignant form, while others that contracted it in another year or a different stable infect with the mild form only.

Prevention. In the older countries horsemen too often accept strangles as inevitable. They expect that all horses will have it sooner or later, and it is not worth while to guard against it. The too absolute doctrine of the identity of the germ with the microbe of erysipelas, puerperal fever, contagious pneumonia, influenza, of the suppurations of the limbs and feet in sheep and cattle, and other streptococcic infections seems to corroborate this view. But on the other hand the absence of strangles from given countries like Iceland where erysipelas and its coadjutors are common, its absence from secluded breeding farms and districts in America, though prevailing all around them, the rapidity of its spread when introduced in a sick colt, and the entire failure to extend in the same way from an erysipelatous man to susceptible young horses with which he comes in contact show that preventive measures may be successfully applied for its restriction and extinction. The conceded family resemblance of the microbes and the experimental production, by their inoculation, of lesions showing many points of similitude leave them still sufficiently distinct in their pathogenesis to warrant measures for the suppression of the variety which produces strangles.

Precautions for the private owner. During the existence of strangles in the district, exclude strange horses, asses or mules from the farm or stable. Keep young susceptible horses from public stables or yards (livery, feeding, training, fair, market, and above all, dealers’ and sale stables) and even from public drinking troughs and buckets used in common. Provide against their contact with manure from strange or infected stables, or with pastures, fields and wagons on which this has been put, also against the use around the stable or on fodder of forks or other implements that have been used for such manure. Avoid hay or other fodder or litter from a strange barn or one that is open to any suspicion of infection. Avoid running water that has drained land, stables, or yards where strange horses have been, or those open to suspicion. In shipping by car or other public conveyance disinfect the latter before the animal is loaded. If a second hand wagon, shafts, pole, harness, blanket or other object is brought on the place or used, disinfect the same before using.

Measures for Sanitary Police. Make it compulsory to report, under penalty for failure, all cases of strangles, or of horses with nasal discharge, or submaxillary swelling. Forbid removal from the stable, or secluded enclosure, of all horses, etc., suffering in this way or which have been pronounced by the official veterinarian to have strangles. Provide for exclusion of all other solipeds from such stables, or from contact or dangerous proximity to animals held in them, also from infected yards, parks, cars, boats, etc. Close public drinking troughs during an epizoötic; let each owner use his own bucket. Circumstances may demand closure of public feeding stables as well. Forbid, under penalty, sale, exposure or movement on any public highway or unfenced place of any infected (diseased or exposed) soliped. Enjoin certificate of sanitary conditions of stable and stud with each animal sold. Close dealers’ stables, or forbid any sale from them until all infection has ceased and the buildings have been thoroughly disinfected. Compel thorough disinfection of stables, yards, cars, boats and other public conveyances that may be open to reasonable suspicion of infection.

Immunization. An attack renders the subject immune, but this may be early overcome by marked change of location, and exposure to a virus of greater intensity or modified quality. Besides the crude and reckless Russian method already referred to, direct inoculation of the virulent products has been often resorted to from the time of Gohier onward, in the different countries of Europe. By selecting the matter from the abscesses or nasal discharge of a mild epizoötic, and preserving the inoculated subjects in clean, dry, pure aired stables, on nourishing diet, and under the best conditions of hygiene, a fair measure of immunity was conferred with absolutely no loss. The same as after casual cases, second attacks will sometimes be shown, but even in severe outbreaks, of a less violent type. The pus from the abscess, or the preceding exudate in the swelling may be simply rubbed on the nasal mucosa, or injected subcutem in another part of the body. In many cases there follows merely a local cellulitis, while in others the general infection leads to the nasal discharge, with or without the submaxillary abscess.

This method is open to the individual owner where no concerted effort is made to stamp out the infection. When, however, police measures for suppression are in force, it must be strictly prohibited, or adopted only under official control, and with absolute seclusion and thorough disinfection.

Treatment. In mild regular cases hygienic measures only are demanded. Cleanliness, dry stalls, pure air, warmth (a sunny exposure if available), nourishing, easily digested food, (grass, green corn stalks, bran mashes, roots, carrots, turnips, apples, potatoes, ensilage, scalded oats or hay) and pure water, or linseed tea, grooming and, in cold weather, blanketing may suffice. Rest is indispensable, though exercise may be allowed in a sheltered or sunny field or yard in fine weather.

Castrations and all other surgical operations are forbidden.

For costiveness or tardy action of the bowels 1, 2 or 3 ozs. of sulphate of soda may be allowed daily in the drinking water.

To soothe the inflamed air-passages it is well to steam them with the vapor of hot water to which has been added an antiseptic such as oil of tar, tar, phenic acid, or creolin. This may be placed in a bucket, and a bag with its bottom cut so as to form a tube drawn over the bucket and nose of the horse. It may be continued an hour or more at a time, or a nasal douche of creolin (1:100) may be employed. In case of tardy softening of the submaxillary swelling it may be assiduously fomented, or covered with a linseed meal or other poultice to which a little antiseptic (carbolic acid, creolin) has been added. It may be applied on a cotton hood having holes for eyes and ears and furnished with ends to tie back of the ears and down the middle of the face. If still indolent the swelling may be rubbed with soap liniment or smeared with soft soap, or finally a cantharides blister may be applied.

As soon as any indication of softening or fluctuation is detected a free incision should be made to allow the exit of the pus. This further tends to hasten the liquefaction and removal of the adjacent exudate. If the pus lies near to the surface, with little more than skin to penetrate, it may be freely incised with one thrust of the knife, but if there is intervening glandular or other tissue, the skin only should be first incised, and the connective tissue bored through with the finger nail, or the point of a sterilized director, or of closed scissors. In this way the important vessels, nerves and salivary ducts are pushed aside and troublesome bleeding and saliva fistula alike avoided.

Fever usually subsides on the opening of the abscess, but if it fails to do so, or if it reappears from slight absorption of septic matters it may be desirable to favor elimination by small doses of sodium bicarbonate, ammonium chloride, or potassium nitrate. In extreme cases a few doses of acetanilid may be given, or full doses of quinia.

When the discharge from nose or abscess threatens to persist, such agents as sulphur, yellow or black sulphide of antimony, are given with bitters, but a more prompt effect can usually be had from injections of weak solutions of creolin, cresyl, lysol, etc. When the cough is troublesome it may be quieted by belladonna, or, in case of weakness of the heart, by digitalis.

The various complications require treatment appropriate to their nature. Collections of pus in the nasal sinuses may demand trephining and antiseptic injections. Swellings about the throat threatening asphyxia and which cannot be relieved by evacuation of pus may necessitate tracheotomy until suppuration occurs. The cutaneous pustules and abscesses are dealt with by pricking the collections and washing daily or oftener with astringent antiseptics (phenic acid and alum). Bronchitis and broncho-pneumonia may be benefited by sinapisms applied to the sides of the chest, the internal administration of potassium iodide, ammonium chloride, sodium hyposulphite, terpene or terpinol; or by inhalation of weak sulphur fumes, or tar vapor.

For abscesses in the bronchial or mesenteric glands, the brain, spinal cord, or other internal organ, little can usually be done but to sustain the patient and await the course of events. If the abscess can be accurately located it may be aspirated and then injected with an antiseptic; if in the encephalon, trephining may be resorted to; death is certain in such a case in the absence of treatment.

During convalescence it is very important to avoid overexertion and chill, which are very liable to bring on petechial fever. Also, to feed nourishing food, give pure air and water, and to see that no suspension of action of bowels, or kidneys threatens to shut up toxins and waste products in the system. Apropos of impure water Williams quotes the case of a foul stream near Bradford, England, on the banks of which every case of strangles did badly.

CONTAGIOUS PNEUMONIA IN THE HORSE.

Synonyms. Definition. Historic notes. Accessory causes: youth, native susceptibility, inclement weather, exposed stables, nasal and bronchial catarrh, sores as infection atria, lack of stable hygiene, crowding, underfeeding, overwork, excitement, exhaustion, infection from stables, etc., convalescents; doctrine of recrudescence. Bacteriology: streptococcus pneumoniæ contagiosæ equi: pathogenic to mice, rabbits, and Guinea pigs. Cocco-bacillus of Lignieres in early lesions. Lesions: bilateral, multiple foci, congestion, consolidation, purulent, necrotic, infarction, sequestra in purulent sacs, pleuritic effusion; enlarged, congested liver with centres of degeneration and necrosis. Congested spleen, kidneys, lymph glands and gastro-intestinal mucosa. Yellow mucosæ, mahogany colored muscles. Incubation, 3 to 10 days. Symptoms: staring coat, early extreme hyperthermia, accelerated pulse and breathing, cough, icteric mucosæ, anorexia, dulness, defervescence in 3 to 5 days; convalescence in 10 days; or prostration, swollen eyelids, trembling or interrupted labored breathing, cough, nasal flow yellow, multiple centres of percussion flatness, crepitation, râles; urine scanty, yellow or reddish, albuminous, acid, alkalinity as a symptom; throat symptoms, inhalation bronchitis, cardiac phenomena, swelling of legs, stupor, trembling, staggering, vertigo, paresis. Course: duration 2 to 3 weeks, defervescence. Fatal cases, toxin poisoning. Diagnosis: by age, history, tardy infection, prostration usually less than in influenza. Prognosis: gravity depends on violence of attack, susceptibility, hygiene, treatment. Mortality 1 to 20 per cent. Permanent lesions from sequestra, adhesions, cardiac, hepatic, nervous or arthritic disease. Treatment: pure air, sunshine, comfort, hygiene, pure water, rest, cold rectal injections, damp compresses, hot bath, diaphoretics, expectorants, alkaline diuretics, antipyretics, heart stimulants, derivatives, antiseptics, nerve sedatives, tonics. Prevention: early removal, disinfection, quarantine new horses, disinfection of public and sale yards and stables, certificates. Immunization: by a mild attack; serum-therapy.

Synonyms. Ataxic or Adynamic Pneumonia; Stable or Hospital Pneumonia; Pleuro-Pneumonia Contagiosa Equorum; Contagious Pleuro-Pneumonia; Bilious Pneumonia; Edematous Pneumonia; Brustseuche.

Definition. An infectious adynamic type of pneumonia occurring in horses, asses and mules, characterized by marked hyperthermia; by infiltration of lung tissue, often bloody, infarcted or caseated and usually circumscribed; by a deep yellow discoloration of the visible mucosa and other white tissues; and by complicating lesions of the pleura, heart, pericardium, liver, bowels, or kidneys.

Historic Notes. This affection was formerly confounded with equine influenza, and it was only in the second third of the nineteenth century that the differentiation was attempted. S. Prangé describes this as a special epizoötic disease in the French hussars in 1841, Leconturier in Belgium in 1845, Seidamgrotzky in Germany in 1882 (strongly emphasizing the contagion), and Dieckerhoff in Berlin in 1883. The latter showed that horses, recovered and immune from influenza, still contracted brustseuche and perished. This distinction was fully corroborated by Lustig, Cagnat (1884), Brun, Delamotte (1886), Jolly, Benjamin, Leclainche, Trasbot, and others. The presence of a particulate, living, self-multiplying cause (microbe) was recognized as the essential condition of the disease (as we still recognize the necessity for such an organism to explain rabies) though the micro-organism itself was as yet undiscovered.

At the same time many concurrent factors had to be considered as accessory in different cases.

Accessory Causes. Young horses often show a greater susceptibility than older animals, mainly because they retain all the unimpaired susceptibility of the colt, while old horses have already passed through the disease and become immune. On the other hand, in the absence of acquired immunity, the older, worn out and debilitated animals are the most susceptible and tend to have the disease in its worst form. Susceptibility and immunity are therefore more important factors than mere age. Immunity usually lasts for several years, or throughout life, yet in some animals, or under given conditions, it is overcome much earlier. Inclemency of the weather, or special exposure of any kind, as in severe rainstorms, or working with the feet and legs in water, may become the occasion of an attack. Exposure to cold northwest storms (America, Atlantic Slope), or northeast (Europe), standing without blanket in a temperature at zero, confinement in draughts of cold air between doors or windows, without clothing and after severe exercise, weaken the whole system and increase susceptibility. The presence of a nasal or bronchial catarrh, or of another debilitating disease may act in the same way. The weakened tissues seem to invite the entrance of the germ. Palat, Boiteux and Trasbot found that horses with local sores or suppurations fell readier victims than others;—perhaps the germs entered by the traumas; perhaps the tone of the whole system was lowered, so that the resistance was lessened.

Close, foul air, bad ventilation, imperfect sewerage, and overcrowded stables not only contribute strongly to infection but tend to aggravate the cases. Underfeeding and overwork act in the same way and in this connection may be named the excitement and exhaustion attendant on a long journey by rail. This, like the foul, crowded stable, furnishes many more opportunities for infection and reinfection, so that the invasion of the exposed animal system is all but certain. Infection clings to the loading banks, yards, feeding stables, mangers, troughs, buckets, cars, litter, and manure, so that young horses shipped from the west to the Atlantic Coast States, very frequently come down with contagious pneumonia, and contaminate the stables in which they are placed. Peters suggests that the germ is preserved in the soil water, so that after apparent subsidence it may be again brought to the surface in time of rains or freshets, to start a new epizoötic. Convalescent horses may carry the germ for weeks, on the mucosa or in sequestra in the lungs, and contaminate horses with which they come in contact.

It is remarkable that the contagious pneumonia is far less diffusible on the air than influenza, so that it is much more constantly the result of direct contact of a sound, with an infected animal, or with a place or thing that the sick animal has contaminated. It therefore spreads much less rapidly, remains confined to individual stables for a length of time, and in the absence of active interchange of horses tends to die out of its own accord. As the infection is not generally and speedily acquired, so immunity fails to become general, and the infection tends to fix itself permanently in places where many strange horses congregate, (market stables, sale stables, livery stables, etc.), and the constant influx of fresh animals keeps the flame burning by accessions of fresh fuel. In such cases it is manifest that the germ outside the animal body either rests in a dry condition, or lives as a saprophyte in earth or organic matter, and often loses much of its virulence. Under such circumstances animals that would prove readily susceptible to a virulent germ, prove nonreceptive to this resting germ, until under some special devitalizing influence, like exposure, exhaustion or local disease, it finds its opportunity and the weakened system succumbs. Then, acquiring new force through its life in the debilitated system, it starts on a recrudescence, and an epizoötic is mistakenly supposed to have started without a preëxisting microbian cause.

Cadeac even advocates the theory that the same germ possessed of greater or lesser virulence, is always present in ordinary stables and horses, and habitually causes in exposed or debilitated animals an ordinary fibrinous pneumonia with no perceptible tendency to transmission by contagion; that, in other cases when a considerable number of horses have their defensive powers impaired, it gains a wide extension; and, that in some such cases, the germ that has been living as a comparatively harmless saprophyte, suddenly acquires an unwonted potency, and breaking down the barrier of partial immunity, attacks exposed animals on a large scale and irrespective of weather perturbations, or debilitated conditions. He quotes from Trasbot instances that seem to support this hypothesis, which is not at all in disaccord with the habits of bacterial life, yet we require a solid basis in bacteriological experiment to make it unassailable.

Bacteriology. Siedamgrotzky (1882) found in the hæmorrhagic centres in the affected lung and in the pleural exudate micrococci. Dieckerhoff (1882) and Mendelsohn (1883) found in the pleural exudate streptococci. Chain cocci were also found by Peterlein (1884), Perroncito (1885), Delamotte and Chantemesse (1888), and Mosselman and Lienaux (1893).

Schütz (1887) found a diplococcus which he studied very fully and this is corroborated by Lustig’s ovoid bacterium, by Cadeac’s micrococcus and diplococcus. In Dr. V. A. Moore’s cultures at the N. Y. S. Veterinary College cocci were found constantly in pure culture, sometimes as a diplococcus, but under slightly altered conditions the streptococcus form predominated. As the difference between two, and three or more cocci in chain form is merely a question of early or late separation of cocci which multiply in line, the apparent discrepancies in the above observations do not imply any real difference in the microbe.

Inoculated in pure cultures the Schütz diplococcus killed mice in 24 to 48 hours with enhanced virulence of the germ. In the rabbit, subcutem, it usually killed in 24 to 48 hours, but some survived; intravenously or intratrachealy it killed more certainly and speedily and in either case with pleural, pericardial and even peritoneal lesions. In the Guinea-pig, subcutem, it caused extensive effusion, and death in two to six days with chest lesions. In the dog it caused hyperthermia, but no marked lesion and no mortality. In the horse there were no infectious resultant lesions. A pure culture thrown into the lung tissue of an old horse at the N. Y. S. V. College, determined an extended pleuritic adhesion and lung hepatization. The age of this subject was opposed to any marked susceptibility. The apparent immunity of the horse in Schutze’s cases might depend on the insusceptibility of the animals selected during or after an epizoötic, or on the absence of the predisposing causes so strongly insisted on by Cadeac.

Rats, chickens and pigs proved immune.

On peptonized gelatin at 98° F., and less rapidly at ordinary temperature, it grew as white, opaque, colonies which gradually extended and united in many cases. The gelatin was not liquefied. In peptonized bouillon it produces turbidity for one or two days, after which the microbe precipitates leaving the liquid clear. The reaction is unchanged.

It lost virulence rapidly when kept in artificial culture or at a temperature of 122° F., and was killed by a temperature of 150° F. Yet it survived drying at moderate temperatures. Cadeac found that the dried expectoration or blood, diffused in the inspired air produced pneumonia with certainty in solipeds. Schütz and Fiedaler injected pure cultures into the lung, and in other cases into the trachea, thereby inducing pneumonia. Twenty grammes of the culture injected into the trachea raised the temperature 2° or 3°, but this lessened on repetition and after four or five treatments the subject proved immune.

Lignieres (1897) discovered his cocco-bacillus in the exudation in the tissues in the early stages of contagious pneumonia, from which it disappears, giving place to other bacteria, and usually streptococcus, as the disease reaches its maximum. (See Equine Influenza for description). His theory is that the cocco-bacillus, which is slightly smaller than the bacillus of chicken cholera, and appears like a diplococcus when stained, and which may not be found after the first eight days of infectious pneumonia, is the starting point of disease, in this and influenza, making the system very receptive of the streptococcus of strangles and of other bacteria, the identity of which determines the nature of the malady. The diplococcus or streptococcus of Schütz in his opinion is none other than the strangles streptococcus which finding a congenial home in the animal invaded by his cocco-bacillus, pervades the system and determines the pathological phenomena of contagious pneumonia.

There are certain obstacles to the unreserved acceptance of Lignieres’ conclusions, among the chief of which is the absence of evidence that horses, successfully inoculated with his cocco-bacillus in pure cultures, can infect others standing near them with the same rapidity and certainty, as does the casual case of influenza, or even of contagious pneumonia. The same holds true of the supposed identity of the streptococcus and that of strangles. Abscesses containing streptococci, were formed in the seats of inoculation with Schütz’s organism, but there is no evidence that the horses suffering from such abscess affected susceptible horses standing beside them, as do ordinary cases of strangles. The cocco-bacillus may be a concurrent cause of contagious pneumonia, but we need more proof to show that it is the essential cause, even as we need proof of the absolute identity of the streptococcus of strangles and brustseuche.

Lesions. The pneumonia is far more likely to be double than in the fibrinous form, and the area invaded, in its ratio with the high intensity of the fever, is usually less. The consolidations are especially common near the lower borders of the anterior parts of the lungs. There may, however, be a number of centres in each lung, to be accounted for by the inhalation of the germ and the starting of the morbid process at the various points on which it falls. This, like the double character of pneumonia is therefor in keeping with the contagious origin. Each centre of condensation shows a small area, hepatized, purulent or necrotic, with a surrounding zone of dark bluish red congestion. The consolidated areas are less dry and granular than in fibrinous pneumonia, seeming to be largely infiltrated with a still liquid exudate and dark blood, and thus tend to a greater tenacity, and less friability. Black areas of infarction form in the lung, the thrombosis of the arteries, cutting off the free normal circulation and the isolated portion fills up with dark blood globules and forms a sequestrum. In the inflammatory and still living parts the color is lighter with, it may be, some straw colored exudate, and always an active leucocytosis, as in other inflamed parts. When infiltration is located near the root of the lung, it is usually attached to the primary bronchi, or larger bronchia and may extend into the upper portion or almost the entire substance of the lung.

Simple abscess is rare, yet purulent sacs containing the gangrenous masses or sequestra are common.

Pleuritic areas are common over the congested and hepatized foci, yet as these are usually circumscribed in extent, an excessive hydrothorax is exceptional. Yet the pleuritic effusion may at times become abundant. Friedberger and Fröhner say seven gallons or more. It may become purulent or even septic, exhaling an offensive odor. Adhesions and fringes on the pleura are frequent.

The heart and pericardium may be affected, the first showing the pallid, soft, or parboiled appearance of high fever, with at times fatty degeneration or petechiæ, and the latter congestion, exudation, thickening, false membranes and liquid effusion.

The enlargement of the congested liver is a marked feature. It frequently attains the weight of 30 pounds. It may ooze dark blood freely from the cut surface, has usually a yellowish tinge, and shows points of fatty degeneration or even of commencing necrosis. The spleen is like the liver, charged with blood, and shows an increase of pulp and even petechiæ or circumscribed hæmorrhages.

The kidneys are congested, friable and petechiated.

The bronchial lymph glands and less constantly the mediastinal and abdominal ones, are congested, pink to dark red and somewhat enlarged.

The gastric and intestinal mucosa may be congested, thickened, hæmorrhagic or ulcerated.

The white tissues generally tend to an icteric hue, and the muscles assume a mahogany aspect.

Incubation appears to be longer than in equine influenza, varying in different cases from 3 to 10 days.

Symptoms. These vary greatly in different cases, mild and severe. Some, in the same stable with the severe cases, simply refuse food, are a little sluggish in work, cough, have hyperthermia (104° to 106° F.), respirations 20–25, pulse 60, with conjunctiva only moderately yellow, a slightly yellowish discharge from the nose, and no observable lung consolidation. The temperature descends to normal in three to five days, the symptoms generally abate, and the animal may be convalescent in eight or ten days.

In the more severe cases there may be seen a shivering fit, or it may pass unobserved. Then the first morbid phenomenon is usually a rapid and extreme elevation of temperature which may reach 104° or 106° F. in a few hours. With this there is great impairment or complete loss of appetite, and a loss of life and energy. In some cases the depression, stupor and muscular weakness suggest influenza but this is not the rule. Still more rare is infiltration of the eyelids and free watering of the eyes, yet in the absence of this, drooping of the upper eyelids is not uncommon. The respiration may be accelerated and short, from 20 to 30 per minute, and the pulse, which is usually small and weak in spite of the fever, may rise to 50 or 70 per minute. The breathing may be trembling or distinctly interrupted in the course of inhalation or exhalation, short and with no interval between inspiration and expiration. Cough may or may not be a marked feature, heard at long intervals only in some cases and frequent and painful in others. It is liable to be dry and husky rather than hard, loose or gurgling. The eye and to a less extent the nasal and buccal mucosa tend to show a yellowish shade, and this may even at an early stage show a distinct brownish orange, or even a dark mahogany hue. Yet dropsy of the lids or even epiphora are uncommon. A yellowish discharge from the nose is an almost constant feature and this may dry up into a yellow crust on the floor of the anterior nares and adjacent skin. The percussion and auscultatory indications of lung consolidation are rarely obtainable before the end of the second or third day and when at all extensive can usually be detected on both sides. Trasbot considers the double pneumonia as almost pathognomonic of contagious pneumonia. When confined mainly to the lower parts of the lungs and occurring in isolated areas, with lung tissue still pervious to air in the intervals, it comes more nearly to being so. Crepitation round the border of consolidated areas, is a more marked feature than in equal consolidations in influenza. It often becomes inaudible again as the disease advances. Blowing murmurs, coarse mucous râles, heart and intestinal sounds can often be heard with unusual clearness, in unusual situations, when an area of consolidated lung is immediately beneath. A transient dry friction sound of commencing pleurisy is sometimes detected over a tender intercostal area, but soon giving place to the uniform quiet of effusion rising to a given horizontal level. Later still there may be the creaking sound of organizing false membranes in process of being stretched, and which is so often confounded with crepitation. The indications of pneumothorax (tympanitic resonance, and metallic tinkling), are rare. In advanced stages there may be tympanitic sound from the cavities of abscesses or the sacs containing sequestra.

The urine is always scanty and high colored and may at times prove red and hæmorrhagic. Albuminuria is usually present when the disease is at its height. The same is true of uric acid, which replaces the hippuric acid, in cases of high fever and complete abstinence so that the products are drawn from the disintegrating tissues alone. The returning appetite, and the restoration of a neutral or alkaline condition of the urine, therefore tend to occur simultaneously, and to mark improvement.

Great tenderness of the throat, protrusion of the nose, and difficulty of swallowing mark the localization of the lesions on the pharynx and larynx. It is liable to be accompanied by the introduction of exudation and food materials into the larynx and trachea with the occurrence of inhalation bronchitis and pulmonary gangrene.

Symptoms of pericarditis, endocarditis and myocarditis, are especially common in the more severe types of the disease. With soft, weak or imperceptible pulse and tumultuous heart beats they may be suspected, and further indications are a transient friction sound, synchronous with the beat of the heart, intermissions, murmurs with first or second heart sound, and an increasingly low, distant, or muffled heart beat, as pericardial fluid accumulates. As in the case of troubles with the kidneys or liver, stocking of the legs, or dropsical swellings elsewhere may appear.

Exceptionally, acute nervous symptoms may appear, due to functional derangements caused by circulation of the toxins and metabolic products, or even to congestion or inflammation of the brain or its membranes. This may occur at the outset of the disease indicating the election of the nerve centres for the colonization of the microbe, and advancing to a rapidly fatal issue (Friedberger and Fröhner). It may set in with hepatization (Rey), or it may coincide with pulmonary gangrene (Cadeac). There may be merely dulness, prostration, or stupor; or trembling, unsteady gait, or falling; there may be rolling of the eyes, or amaurosis, or vertigo occurring intermittently; or there may be epileptic attacks or paraplegia.

Course. In moderate cases the disease may last from two to three weeks, and in well conditioned horses, with strong constitutions, tends to recovery. On the third to the eighth day all the symptoms appear better, appetite, expression, alertness, breathing, pulsation and temperature. The temperature which has been a degree, or more, higher in the afternoon than in the morning, remains about the same from morning to night, or is even slightly lowered; it is lower still next morning and in two or three days may have reached 101°, still rising a little in the afternoon. The pulmonary exudate is usually quickly absorbed though less so than in favorable cases of influenza. Convalescence may be completed by the end of the third or fourth week.

In violent and fatal cases the general symptoms tend to encrease in violence, though the temperature may descend to 103°, and in the final collapse to 100° or lower. In a mare presented at the college clinic after three weeks illness and treatment elsewhere, prostration was extreme, the head rested in the manger, the nose discharged a fetid, glairy, frothy liquid, with grumous, bloody debris; breath offensive; pulse 92, almost imperceptible; respirations 30, very labored; nostrils widely dilated, flapping; temperature in vagina 103.6°, anus was open with constant ingress and egress of air, and a watery glairy, frothy discharge; extensive dropsy under the sternum; percussion and auscultation indicated consolidation of lungs from the lower border up, crepitation, creaking, and loud clucking bronchial sound. The mare survived for forty-eight hours, the temperature descending to 100.5° in the morning and rising to 102° and upward in the afternoon. At the necropsy the right lung was consolidated throughout, the left had pervious areas anteriorly and posteriorly; there were large areas of infarction, necrosis, with encystment, caseation, and lobular and perilobular exudation and hepatization.

Liver, enlarged, tense in its capsule, but soft and friable on its cut surface, with areas of softening and necrosis. Both kidneys congested, with pale zones of necrosis; right enlarged. Beside the substernal exudate, there was extensive hæmorrhagic exudate between the serratus magnus and ribs. The blood, very dark, brightened on exposure to air.

Diagnosis: This may be based mainly on the prevalence of the disease in the district, or the fact that the victim has come from a long railway journey with risks of exposure, or has stood by a horse just arrived; on the prompt loss of appetite and sudden and extreme rise of temperature, without notable lung lesions; on the deep brownish yellow discoloration of the visible mucosæ, especially that of the eye, and on the yellow discharge from the nose, the tardiness with which successive cases follow each other comparatively to influenza, and the absence in large measure of the early extreme prostration of that affection. (See table under influenza).

Prognosis varies with the progress of an epizoötic, and the youth and susceptibility of the animal together with the favorable or unfavorable conditions of life. The death rate is usually high at the outset when the more susceptible animals are attacked, and for the same reason, in the young that have not been previously exposed. Old and debilitated animals with broken down constitutions suffer severely, and bad hygiene contributes much to the mortality. The deaths vary from one to twenty per cent. But short of death, permanent injury follows in a number of cases. Encysted sequestra remain in the lungs for months and when liquefied and absorbed, leave fibroid masses in place of healthy lung tissue. The fibrous organization of peribronchial exudates, impairs respiration, and the same is true of the fibrous development of false membrane. Thus the horse is left permanently broken-winded or short-winded, or from interference with the recurrent laryngeal nerve, laryngeal hemiplegia (roaring) ensues. In still other cases permanent adhesions of the pericardium, or insufficiency of the cardiac valves, or disease and distortion of joints or tendons, or nervous, hepatic or renal degenerations destroy or seriously impair the value.

Treatment. Hygienic measures are of prime importance in treatment. A dry, clean box stall with pure air, and genial warmth (60°–70° F.)—in warm summer weather outdoor air—must be secured. In cold weather a sunny outlook, and clothing—blanket, bandages, and it may be a hood—to counteract any sensation of chill. Tepid drinks, pure water changed often, linseed tea, barley water, are of importance in allaying thirst, lowering temperature and favoring elimination. Absolute rest is all essential. Keeping at work after the onset of the disease is nearly equivalent to signing the patient’s death warrant.

The high temperature at the outset of the disease seems to demand antipyretics, and in times past, in Southern Europe especially, bleeding was a constant resort. But even under favorable conditions this does not lower the temperature more than 1.5° F., and the resulting debility is such that it has been long discarded in Germany, England and America. In cases of acute extensive pulmonary congestion it is helpful in relieving the vascular tension on the lungs and allowing the tissues to better reassert their natural functions, in antagonism with invading microbes and their poisons, but even this action is transient, and when it saves life it is probably only by tiding over safely a very transient and urgent danger.

The same decline of temperature can usually be secured by injections of cool water into the rectum, and with the added advantage that this relaxes the bowels, and removes dried irritant masses from the rectum and floating colon.

As in other pneumonias the application of cold to the skin is liable to bring on a chill unless the temperature is very high. A safer and hardly less effective method is to apply around the chest a thin blanket or sheet wrung out of tepid water and cover it closely with dry blankets holding these close to the skin by elastic circingles. No part of the damp compress must be allowed to remain exposed to the air under pain of causing chill. Damp cotton wool applied next the skin tends to maintain its contact by its own elasticity, so that it requires less care in the elastic dry covering. This moist warmth draws a free circulation of blood to the skin, so that it is cooled and sent back internally to cool the burning fever, without sensation of chill. The abstraction of this large mass of blood to the skin, acts like bleeding in diminishing the blood tension in the chest and allowing the resumption of the normal vaso-motor and nutritive functions without the dangers of venesection. The soothing action on the skin, soothes by sympathy the infected and inflamed tissues.

A steam or hot air bath may serve a similar purpose. Conjoined with an aloetic laxative and aconite, I have seen this reduce the temperature from 104.5° F. to 102.7° F. at the next taking 18 hours later. It only once again reached 103° F. in the subsequent course of the disease.

To secure diaphoresis, warm mashes or gruels may be freely used. Alcoholic drinks have been freely used (the weaker wines 1 to 2 qts., sherry, brandy, whisky ½ to 1 pint), camphorated spirit (2–3 drs.) subcutem, ipecacuan (1 oz.), tartar emetic (2 drs.), liquor of acetate of ammonia (4 ozs.), pilocarpin (2 grs. subcutem). If the alcoholic liquors produce a free circulation and glow in the skin, better still if diaphoresis, they are useful antithermics, but, if they fail in this, they may do harm by reducing the vital activities of the leucocytes, and their power of resistance. Trasbot has had uniformly unfortunate results with alcohol in large doses. The same objection attaches to tartar emetic and other depressant diaphoretics, though valuable if free diaphoresis is secured.

Constipation may be met by cold water injections, calomel (½ to 1 dr.), pilocarpin (3 grs.), eserine (1½ gr.), sodium sulphate or other agent graduated to requirement.

An expectorant and alkaline diuretic action may be obtained from potassium iodide (1–2 drs.), ammonium chloride (2 drs.), or ammonium acetate. These not only liquefy the exudate, and facilitate expectoration, but secure elimination of toxins, ptomaines and waste products from the blood and system. The iodide is besides somewhat antiseptic.

In the early stages especially medicinal antithermic agents may be called for: acetanilid (2–3 drs.), phenacetin (2–4 drs.), sulphate of thallin (2–3 drs.), sodium salicylate (½ oz.) or in the weaker cases, caffein—natrium salicylate (1 dr.) or quinine sulphate (2–3 drs.) Acetanilid will sometimes relieve dullness, and materially improve the general condition.

In weak conditions of the heart we may resort to digitalis (10–15 grs.), strychnia sulphate (2 grs.), strophanthus tincture (3 to 4 drs.), caffein, or alcohol. Care must be taken not to overstimulate and exhaust a weak and intermittent heart.

Derivatives are often of material value from the first, in mild cases or to succeed damp compresses in the more violent ones. One of the best and most convenient is essential oil of mustard and alcohol (1:12 or 20). This may be rubbed on the surface and like mustard itself, covered with stout paper to prevent evaporation. In the absence of this, soap liniment, or even tincture of cantharides may be used.

The use of antiseptics has been tried with variable results. While it is impracticable to saturate the system, safely, with sufficient antiseptic to destroy the microbes in the blood and tissues, yet when the balance of force between the microbian attack and systemic defence shows little variation either way a slight increase on the side of the patient may serve to give it the preponderance, and to restrict the increase of the microbes and their products. Above all when the center of morbid activity is largely on and near the bronchial mucosa, antiseptic inhalations serve to hold them somewhat in check and to moderate the amount of both microbes and toxins that enter the system at this point. For this purpose camphor, oil of turpentine, or oil of tar volatilized from hot water may be inhaled in a close room. Or we may use carbolic acid, terpene, terpinol, creolin lysol, thymol, eucalyptol, or oil of cinnamon. The fumes of burning sulphur diffused in the air of the room and just short of that concentration that will cause cough, suffering and headache, is an excellent resort. The sulphites, bisulphites or hyposulphites may be given by the mouth.

When there are indications of encephalitis cold to the head and the internal exhibition of bromides, iodides, and acetanilid may be resorted to.

During convalescence nourishing and easily digestible food may be given, and iron, strychnia, quinia and common salt may be employed. In protracted or chronic cases with fœtid breath and indications of sequestra or opened vomica in the lungs these may be continued along with one or more of the disinfectants referred to above.

Prevention. This is much more promising than in equine influenza. The extension of incubation to three days and the indisposition of the infection to spread beyond the stable into which it has been brought, or the near vicinity of the diseased animal, gives us a great relative advantage. The early, extreme rise of temperature of the infected horses gives the opportunity of removing these horses to a special stable or shed, where they can have special attendants, and the stable drainage and manure can be kept apart, and disinfected, or spread and plowed under by oxen. The infected stable should be emptied, the soiled hay, litter and manure burned, and the walls, partitions, floors, ceilings, and above all the mangers and racks must be thoroughly disinfected. Lime wash with chloride of lime or mercuric chloride will suffice. The gutters should be cleaned, washed and drenched with mercuric chloride, followed by the whitewash. If there is rotten wood work or filth-saturated soil these must be effectually treated. In many stables it will be impossible to do all this thoroughly, yet closing the empty building tightly, and filling it with chlorine gas, or even sulphur fumes, concentrated until they extinguish the burning sulphur, and keeping shut up for twenty-four hours will usually suffice. Washing with a solution of formalin (1:40 or 1 per cent of formaldehyde), or even the evaporation of this agent by heat in the closed building is very effective, with the serious drawback that it is very irritating to the lungs. It can however be conveniently used for the sterilization of harness, stable implements, halters, and all movable objects in the building.

Strange horses, such as new purchases, should be placed in quarantine for one week in a separate stable, and not hitched up with sound horses. If they show evidence of recent illness this may be extended to six weeks.

For horses that have been shipped long distances, and stopped for rest or feeding in public stables or yards, a similar quarantine is essential. This might be obviated if a system of thorough disinfection of such stables, yards and cars, could be enforced, between any two successive lots of horses, and if the latter were accompanied by certificates of the absence of contagious pneumonia and all other infectious diseases from the localities from which they were shipped and through which they had come. Such certificates should be made by veterinary officials in the employ of the government, which would thus become responsible for their genuineness.

In view of the frequent persistence of this malady in a given stable for a great length of time, successive animals being attacked at long intervals, and where isolation was impracticable, Beckmann rubbed the nasal discharges of the sick on the nasal mucosa of the unaffected, producing the disease almost invariably in a mild form. The infected animals were placed in the best hygienic conditions, the duration of the infection was shortened, and the horses being rendered immune, the stable was then disinfected with a satisfactory result.

Schütz, Hill, Pilz and a number of others have sought artificial immunity, by the injection of blood serum from a horse that has recently recovered from the malady. The results were very contradictory. In some cases the disease came to a sudden end. In other stables no new cases appeared either in those treated with serum or in those left without treatment. In other experiments, new cases occurred among those treated with the serum;—in Weishaupt’s cases after a lapse of one or two months. This is exactly what might be expected. If the horse supplying the blood serum had really recovered, and if the microbes (streptococci) had disappeared from the blood, the latter would of necessity retain little of the toxins, but much more of the antitoxins, the active production of which would be continued by the stimulated leucocytes. These antitoxins would neutralize the toxins, in case of invasion and prevent that from reaching the maximum of intensity that it would otherwise have reached, but would be powerless to stimulate the leucocytes of the inoculated animal into the habit of themselves producing antitoxins. This would act rather as a curative than a prophylactic agent, and its value would be spent as soon as the injected antitoxins were eliminated from the system.

The true line of inquiry would have been, whether injection of the toxins, which acting on the leucocytes would have stimulated these to the habit of producing antitoxins in large amount, might not be expected to give an immunity as lasting as that which follows on a casual attack of the disease. Lignieres appears to have approximated to this, in his experiments on mice and rabbits. In horses suffering from contagious pneumonia it lowered the temperature, but did not materially affect the result of the attack. If we adhere to Lignieres’ own theory of causation by cocco-bacillus and later by streptococcus or some other complicating infection, we can scarcely hope that the toxins of the streptococcus or other complicating microbe will immunize against the cocco-bacillus or mutually against each other. If complete protection is aimed at, the toxins of his cocco-bacillus, and of Schütz’s streptococcus, and of any other possible microbe which may produce a secondary complication, ought to be employed.

At the date of this writing no satisfactory sero-therapy for this disease has been worked out and publicly demonstrated.

INFECTIOUS STABLE BRONCHITIS. SCALMA.

Definition. An infectious inflammation, of the upper air passages and bronchia, attended by high fever, special nervous irritability and a protracted convalescence.

Dieckerhoff gave the name scalma (rogue) to outbreaks in given stables of an infection, showing the high temperature of brustseuche, (104° to 107° F.) a similar incubation (6 to 7 days), a correspondingly tardy extension from animal to animal, and duration of the disease. The apparent differences are in the absence of the profound dulness, the yellowness of the mucosæ, and the yellow or rusty nasal discharge, in the ready response to the voice or touch, the disposition to bite or kick, the spasms of the larynx and sudden dyspnœa, in certain cases, and the paroxysmal cough in others. Apart from these transient respiratory troubles the pulse and breathing are unaffected, relatively to the elevation of temperature. Sometimes the jaws are kept in constant motion, from nervousness or pharyngeal trouble.

In the absence of any conclusive bacteriological investigation, it may be surmised that this is a form of brustseuche which has not advanced to the same grade of destruction of red globules and prostration of the nerve centres, the latter showing only an excited and irritable condition.

Treatment and prevention do not differ materially from what is required in contagious pneumonia. The irritable cough may be soothed by inhalations of warm water vapor, with alcohol, camphor, eucalyptol, or opium, or electuaries of bromides, belladonna or stramonium, and local derivatives to the throat.

Most cases are mild and recover in a week, the cough lasting for two weeks more.

OTHER INFECTIOUS PNEUMONIAS OF THE HORSE.

Claims have been made for infections by a variety of other germs which it would be difficult or unreasonable to deny. In given conditions of the horse’s lung it may succumb to the attacks of pathogenic microörganisms which at other times or under other conditions would be practically harmless. Thus the round ended bacillus of Friedländer is claimed by Jacquot and others to cause one form of pneumonia in the horse as it does in man (Vol. 1 p. 216). Again Galtier and Violet have claimed a form of pneumonia transmitted through musty or spoilt fodders and attacking the bowels as well as the lungs (pneumo-enteritis). Two micro-organisms are accused, a diplococcus and streptococcus, which is strongly suggestive of the now familiar germ of brustseuche.

EQUINE INFLUENZA. ADYNAMIC CATARRHAL FEVER OF SOLIPEDS.

Synonyms. Definition. Historic notes. Equine influenza of 1872–3; its indication of infection. Other evidence: through stables, cars, manure, clothes, coition, inoculation. Bacteriology: streptococci; diplococci; cocco-bacillus, latter pathogenic to rodents, dog, cat, sheep, pig, ox, ass, pigeon, chicken. Inoculations on horse. Present in early stages only. Uncertainty. Accessory causes: chill, electric tension, high barometer, impure air, overwork, poor feeding, season, youth, primary susceptibility, acquired immunity. Incubation 1 to 3 days. Symptoms: Forms: sudden attack, anorexia, profound prostration, weakness, hyperthermia, epiphora, brownish red conjunctiva, pulse, heart beats, catarrhal symptoms, thoracic, pulmonary, pleuritic, cardiac, digestive, urinary, diarrhœal, ophthalmic, nervous, rheumatoid; complications, abortion, laminitis, strangles, contagious pneumonia, cerebro-spinal meningitis, etc. Lesions: inflammation of mucosæ of nose and air passages with blood unaffected; in severe attacks, with heart clots, or later with blood black, diffluent, red globules crenated or dissolved, without viscidity or rouleaux, reddish serum, and hæmatoidin in masses, acid reaction, petechiæ; congestion of mouth, stomach, small intestines or large,—ulcers, tumid follicles, peritoneal effusion, enlarged congested mesenteric glands; liver as if parboiled, with petechiæ and necrosis; spleen large and gorged; kidneys infiltrated, mottled, petechiated, swollen; may be meningeal or ophthalmic congestion; pulmonary lesions, pleural effusions, adhesions, infiltrations, consolidations, infarctions, sequestra. Diagnosis: sudden attack, great numbers attacked, marked prostration, conjunctivitis, great hyperthermia, digestive disorder, evidence of infection. Table comparing croupous and contagious pneumonia and influenza. Prognosis. Mortality low,—high in some epizoötics, in horses kept at work, under bad hygiene. Treatment: good diet and hygiene, rest, shelter, stimulating diuretics and diaphoretics, venesection, antipyretics, alkaline eliminants, inhalants—water medicated, derivatives, collyria, guarded laxatives, antiseptics, cardiac stimulants, nerve sedatives, tonics, transfusion of blood, normal salt solution,—technique. Prevention: quarantine difficult, yet possible; examples, applicability to countries, to districts, lines of restriction.

Synonyms. Epizoötic Catarrh; Catarrhal Fever; Nervous Fever; Epizoötic; Rheumatic Catarrh; Cocotte; Gastro-enteric Epizoötic; Gastro-entero-nephro-hepatitis; Gastro-Conjunctivitis; Gastro-Hepato-meningitis; Entero-pneumo-carditis; Pink eye; Epizoötic Cellulitis; Typhose; Typhoid Fever; Blitz Catarrh; LaGrippe; Septicæmia Hæmorrhagica etc.

Definition. An infectious fever of solipeds, of a specially low or adynamic type, and with a tendency to localization on the respiratory or gastro-intestinal mucosa, on the eyes, lungs, pleura, heart, liver, kidneys, subcutaneous connective tissue, joints, fascia, or nervous system.

This disease was long confounded with the influenza of man and while compelled for the identification of the affection, to retain this name in combination with the qualification equine, yet we would prefer to discard it entirely as conveying the idea that the illness is caused by Pfeiffer’s bacillus, which it is not. The term typhoid fever which is in common use in France, has been selected to convey the impression of its two prominent features of hyperthermia and stupor. But it is open to the same objection for it has been long applied to a specific disease in man having its own bacillus which is not present in the equine influenza. Septicæmia Hæmorrhagica which has been adopted more lately, however correct it may be as indicating the tendency of the local lesions has a generic meaning rather than a specific one, and requires much more qualification to correctly designate the disease. The term adynamic catarrhal fever of solipeds has this recommendation, that it expresses the prostration and debility which is such a marked feature of the disease, its great tendency to become localized on mucous surfaces, and the genus of animals that prove its victims. A better designation is still desirable and may perhaps be reached, when the pathogenic microbe shall be demonstrated beyond question.

Historic Notes. Among catarrhal fevers and epizoötics of early times it is impossible to distinguish this from widespread nasal and bronchial catarrhs, and from contagious pneumonia (brustseuche), yet when the epizoötic attained a sudden and wide extension without any direct climatic cause, the presumption is in favor of the disease now before us. Hints are obtained from Titus Livius of a Sicilian equine epizoötic of this kind 412 B. C. This is corroborated by an account by Hippocrates of a similar outbreak in Greece. Later, Virgil (Georgics), Columella, Absyrtus and Vegetius give similar hints. In 1299 in Seville horses suffered with drooping head, watery eyes, beating flanks and anorexia and 1000 died (Laurentius Rusius). The horses of the French Army in Germany suffered severely in 1648 (Solleysel), horses in England in 1688 (Short, Rutty), again in 1693 (Webster, Short, Foster) and again in 1699 (Webster). In 1712 horses suffered extensively in Europe (Lancisi, Kanold) and in 1727–8 in England and Ireland (Rutty), in 1732–3 (Arbuthnot, Gibson) and again in 1736–7 (Short). Other such equine epizoötics are recorded for Europe in 1729 (Löw), for Ireland in 1746 and 1750–1 (Rutty, Osmer), for Europe and the British Isles in 1760 (Bieset, Rutty, Webster), and again in 1762 (Rutty, Webster) and 1767 (Forster), also in America (Webster), in Europe in 1776 (Fothergill etc.), in Europe and Asia in 1780–2 (Gluge), in England in 1798 (Wilkinson, White), in Europe and England in 1814–15 (Heusinger, Wilkinson, Youatt), in England in 1819, 1823 (Field) and 1827 (Brown), in Europe in 1833 (Prinz, Wilkinson, Hayes, Spooner), 1834 (Hensinger), 1835–6 (Prinz, Friedberger), 1840, 1846, 1851, 1852, 1862, 1870, 1873, 1881, 1883, 1890, 1891, 1892 (Friedberger).

In the United States as in Europe the affection has in the main smoldered in the large cities in ordinary years, to break out without obvious cause, in given years into an advancing epizoötic which sweeps the whole continent. Such were the great outbreaks in Europe in 1881 to 1883, and in America in 1872–3, and 1900 to 1901. The great recrudescence of the disease in North America in 1872–3 was so remarkable in its progress and limitations that it seems desirable to recal its more prominent historic features. The unquestionable demonstration of the microbe of the affection may make such a record superfluous, but until then, and so long as books are published which attribute the disease to the environment, or to the soil, it is not altogether unnecessary.

PROGRESS OF EQUINE INFLUENZA OF 1872–3.

Last week of September, 1872. Toronto, Ontario; (30th) and neighborhood.

First 2 Weeks of October. Barrie, Collingwood, Owen Sound, Guelph, Ont.; St. John, N. B. (13th); Niagara Falls, (11th), N. Y.; Montreal (8), Ottawa (12th), Stratford, Brantford, London, Can.; Buffalo, N. Y. (14th); Detroit, Mich. (13th).

Third Week in October. Goodrich, Kingston, (19th), Ont.; Rochester (18th), Syracuse, Lockport, Canandaigua, Geneva, Albany, (19th), Ogdensburg, (21st), New York, (21st) N. Y.; Bangor, Me.; Port Huron, Mich.

After Third Week in October. Quebec, (28th) Can.; Utica, (29th), Watertown, Oswego, Schenectady, Saratoga Springs, Poughkeepsie (28th), Elmira, Binghamton, (28th), Jamestown, Ithaca, (31st), Port Jervis (29th), Nyack, N. Y., (30th); Revere, (22d); Springfield, (23d), Worcester, (27th), Fall River, New Bedford, Mass.; Waterbury, (27th), Norwich, (23d), New Haven, Hartford, Conn.; Providence, (23d), Newport, R. I.; Burlington, (26th), St. Albans, Vt.; Concord, Nashua, Portsmouth, (23d), N. H.; Bath, (28th), Portland, Me.; Philadelphia, (26th), Harrisburg, Lancaster, York, Erie, Corry, Titusville, (28th), Pittsburg, (29th), Pa.; Baltimore, (25th), Md.; Washington, D. C., (28th); Norfolk, (31st), Richmond, Va.; Cleveland, O.; Chicago, (29th) Ill.

First Week of November. Kingston, N. Y., (1st); Rutland, Vt., (3d); Meadville, (2d), Pottsville, Williamsport, (6th), Reading, Easton, Bethlehem, Pa.; Trenton, N. J., (2d); Wilmington, Del., (6th); Jackson, Mich., (7th); Milwaukee, Wis.; Raleigh, N. C.; Charleston, S. C., (4th).

Second Week in November. Scranton, Pa., (13th); Lynchburg, Va., (11th); Wheeling, (13th), Parkersburg, W. Va.; Dayton, Sandusky, Toledo, O.; Adrian, Kalamazoo, (9th), Grand Haven, Mich. (8th); Davenport, Ia., (14th); Janesville, Green Bay, Wis.; Louisville, Ky., (9th); Wilmington, N. C., (12th); Columbia, S.C.; Savannah, Ga.

Third Week in November. Steubenville, (15th), Columbus, (16th), Zanesville, (16th), Springfield, O.; Indianapolis, (17th), Fort Wayne, Lafayette, Evansville, (21st), Ind.; Bloomington, Galena, (21st), Ill.; Dubuque, Iowa City, Ia.; Madison, Fond du Lac, Wis.; St. Paul, Minn.; Memphis, Nashville, Chatanooga, Tenn.; Augusta, Atlanta, Ga.; Helena, Fort Smith, Ark.; Havana, Cuba, (20th).

In November after third Week. Terre Haute, Madison, Ind.; Peoria, Galesburg, Ill.; Keokuk, Muscatine, Des Moines, Ia.; Paducah, Ky.; Knoxville, Tenn.; Charlotte, New Berne, N.C.; Macon, Rome, Columbus, Ga.; Jacksonville, Lake City, Fla.; Mobile, Montgomery, Selma, Ala.; Natchez, Vicksburg, Miss.; New Orleans, (25th), La.; Galveston, (29th), Houston, (28th), Tex.; Little Rock, Ark.

First week in December. Cairo, Ill.; Lincoln, Omaha, Nebraska City, Neb.; Yankton, (5th), Vermilion, Dak.; Tallahassee, Fla.; Camden, Ark.; St. Louis, Kansas City, Mo.

Second Week in December. Quincy, Ill. (8th); Shreveport, La.; Hanibal, Mo.; Fort Scott, Lawrence, Leavenworth, Topeka, Kan.

December after the Second Week. Denver, Central City, Col.; Cienfuegos, Cuba.

January 1873. San Antonio (3d) Tex.; Cheyenne, Wyo.; Cimarron, (1st week), Elizabeth City (2d week), Alberquerque (4th week), N. M.; Salt Lake City, (2d week), Corrinne (3d week), Utah; Santiago, Cuba.

February. Brownsville (3d week) Tex.; Winnemucca, Nev.; Monterey (1st week), Mex.

March. Prescott (1st week), Tucson (2d week), Yuma (4th week) Ariz.; Boise City, (3d week), Ida.; Helena (4th week) Mont.; Virginia City, (1st week), Nev.; Carson City, Nev., Santa Barbara, Visalia, Cal.; Guaymas, Mazatlau, Manzanillo, Mex.

April. San Diego (1st week), Mariposa, Stockton, San José, Oakland, Sacramento, Marysville and Shasta (2d week), San Francisco, Vallejo, Nevada City and Weaverville (3d week), and Lava Beds, Cal. (4th week); Baker City (2d week), Jacksonville, Ore. (4th week); Walla Walla, Wash. (4th week); Acapulco (1st week), Mex.

May. Eugene City, (3d week), Dallas and Portland, Ore. (4th week); Olympia, Wash.

June. Seattle, Wash. (3d week).

July. Guatemala City, Guatemala (2d week), Victoria, B. C.

August. La Union, San Salvador (1st).

Among the deductions from this record are:

1. The affection advanced gradually from Toronto over the whole continent of North America, where horses are kept, taking full ten months to accomplish this. Nothing checked its advance, over lowland and highland, swamp and arid land, in summer as in winter, with a temperature at 0° or at 100° F., in country pasture or in city street or stable, idle or overworked, on all kinds of soils and geological formations, under all successive conditions of meteoric and terrestrial electricity, in all conditions of the air—pure, impure, dense, light, moist and dry. No one condition of the environment operating on the animal system, can be conceived of that could advance as this disease did from place to place in regular sequence for this length of time.

2d. The rapidity of its progress was manifestly subordinate to the activity of the movement of the equine races from points already infected. Its most rapid advance was along the lines of railway while the back districts shut out from railway traffic were much later in being invaded. The larger cities situated on the through railroad routes suffered earlier than the smaller places on the same lines. The outbreak was several days earlier in Montreal than in the nearer and smaller cities of Kingston, Ottawa, Belleville, Port Hope, Peterboro, Stratford, Brantford, Guelph, London and Owen Sound. The important port of St. John, N. B., suffered two weeks earlier than Quebec. Along the N. Y. Central and Erie Railways etc., Boston and New York suffered nearly a week earlier than Utica, Poughkeepsie, Binghampton, Elmira, and Jamestown, while the smaller places like Kingston, Nyack, Ithaca, etc., were later still. In Baltimore the disease was seen a day earlier than in Philadelphia, and in these cities and Washington over a fortnight before it was seen in Scranton, Pa. So it was almost everywhere and in these large cities the outbreak could in nearly every case be traced to horses just arrived from a pre-existing centre of infection. In Detroit, Syracuse and Chicago it spread first in stables that had just received Canadian horses, in Ithaca in one which had received horses from an infected centre in Northern New York and in Pittsburgh and Washington in stables that had just admitted horses from infected New York.

3d. It advanced with much greater rapidity eastward than westward, being in the line of greatest horse traffic, the animals being mainly raised and fitted in the West and shipped in large numbers to the great cities near the Atlantic seaboard.

4th. In the absence of this active railway traffic In horses, the advance was most rapid through other lines. In Pa., in a number of valleys opening to the south, the disease reversed its general direction, and extended northward up these valleys. In Lehigh Co., Pa., it followed the course of the canal, being carried by horses and mules employed on the towpath. In Davidson and Sumner Cos., Tenn., it followed the track of a circus which came through an infected locality. It reached the Pacific coast at Santa Barbara (not at the railway terminus at San Francisco) having followed a mule stage route in the absence of an active, westward progress of horses by rail.

5th. The affection failed to overstep any serious gap over which there was no movement of equine animals. It prevailed in Victoria, B. C., in July, but, owing to a strict quarantine on horses and mules, it failed to reach Vancouver Island. It ravaged New Brunswick and Nova Scotia in November but failed to reach Prince Edward Island which was then ice bound and shut off from all traffic with the mainland. It ravaged Cuba to which it was brought by American horses landed at Havana, but no other West Indian island was attacked. Its southward course was finally arrested at Central America, where horses are few and horse traffic nearly unknown.

Every fact in connection with its eruption and progress agrees perfectly with the hypothesis of transmission by contagion alone, and taken altogether the history excludes all other causes from being anything more than accessory. Before the days of modern bacteriology we had ample proof that glanders, rabies, sheeppox, lung plague, and Rinderpest were due to contagion alone as an essential cause, and so now we have the same evidence concerning equine influenza.

Other testimonies to Contagion. Trasbot says the virulence is “almost equal to that of Rinderpest or aphthous fever,” and adds “all practitioners have become assured that the bringing of an affected animal into a stable constantly introduces the malady to the others.” Cadeac says “the diseased or infected animals are the main channel of propagation of the malady” and again the disease is “essentially infectious.” Friedberger and Fröhner are more definite—“influenza which is as highly infectious as any other disease can be produced only by infection.” Cadeac implies nearly as much in saying: “in all the epizoötics that have invaded Paris, the disease has been carried into the four quarters of France by horses bought in this city. In most regiments the malady shows itself after the arrival of horses from remounts where it was prevailing. At Sibourne it is through horses from St. Jean d’Angely. At Lyons it is by a horse from Cæn. At Bourges the source was not traced but it spread from the garrison to the whole surrounding country. The Omnibus stables in the Rue d’Ulm were invaded when a horse was introduced from Clichy where influenza raged.”

Stables are fruitful sources of infection hence dealers’ horses and horses travelling from place to place have long been objects of just suspicion (Trasbot, etc.).

Cars are often infected, and spread the disease widely. (Poucet, Salle, Trasbot, etc.).

Manure is especially dangerous. Trasbot gives a number of cases of the infection of farms, by the manure taken from the Alfort Veterinary College, and other infected stables in Paris. Friedberger conveyed the disease experimentally in the manure.

The conveyance of the virus on the clothes of attendants has been alleged by Friedberger and Fröhner, and considering that it has been noted to pass over intervals of about half a mile without the intervention of any horse, it must have been wafted on the air, or conveyed on the surface of man or non-equine beast.

Jensen and Clark allege that the contagium may be conveyed to mares by coition, for months after the stallion has shown all outward signs of recovery. This would be entirely in keeping with the analogous fact in swine plague.

Inoculation. Experimental inoculations have transmitted the disease with difficulty and uncertainty. Those of Hertwig, Nocard, Arloing, Labat, Friedberger, Trasbot, Pasteur and others came to naught. Even the transfusion of the blood of the sick, proved as harmless as the inoculation of the serous exudate. A probable explanation is found in the extreme diffusibility of the germ of equine influenza, which spreads over a city or county in a few days, attacking practically all equine animals. Inoculation is necessarily made at the time of the prevalence of influenza and at such a time all horses in a wide area are likely to be suffering from the affection. Those that are unaffected and therefore apparently available for experiment, are the immune animals. If they were susceptible the probability is that they would speedily show the disease through infection drawn from another source than the inoculation. If the inoculated animal failed to contract the disease, and yet very shortly afterward became infected by simple exposure, there would be some basis for alleging that inoculation was always inoperative. Dieckerhoff, on the other hand, transmitted the disease to healthy horses by subcutaneous and intravenous inoculation of the blood of the sick, and the same seems to be true of inoculations of the cultures of the cocco-bacillus by Lignieres.

Bacteriology. Our knowledge of the bacteria of equine influenza is as yet very imperfect and uncertain. Galtier and Violet found streptococci and diplococci in the blood and tissues of cases showing intestinal lesions, and held that they were derived from musty fodder. Injections of infusions of such fodder into the trachea of the horse produced broncho-pneumonia, double pleuro-pneumonia, and at times intestinal or meningeal congestion. But there is no proof that the malady so caused, passed with the certainty and rapidity of equine influenza from horse to horse in the same stable.

The cocco-bacillus found by Lignieres in the blood and exudate of the patients has more plausible claims to being the specific germ. This is an ovoid bacterium, somewhat smaller than that of chicken cholera, and like it pigmented at the poles and clear in the central part, a characteristic feature of the group of Pasteurella of Trevisan. This group includes the nonmotile germs of swine plague, the septicæmic pneumo-enteritis of sheep, wildeseuche, and septicæmia of rabbits and chickens, as well as that of fowl cholera; all stain easily in gentian violet and fuchsin, and all cause some form of hemorrhagic septicæmia. The germ is ærobic and grows best in peptonized bouillon to which a little serum has been added. It forms, in peptonized gelatin, round colonies, at first transparent and later opaque or milky, and without liquefaction. The cultures when inoculated subcutaneously proved fatal to Guinea pig, rabbit, rat, mouse, dog, cat, sheep, pig, ox, ass, pigeon and chicken.

Intravenous inoculation on the horse of 1 to 2cc. of the culture kills in a few hours, the temperature having risen to 104° F., the mucosæ acquire a dull brown tint, the eyes are swollen and weeping, enteritic colics appear, the limbs may swell and there may be painful arthritis and jaundice. At the necropsy the blood is black and incoagulable, the muscles as if parboiled, the liver a deep violet, the intestinal mucosa congested, a yellowish or reddish effusion in the pericardium and numerous petechiæ on the serosæ.

Subcutaneous inoculation causes an enormous inflammatory œdema resulting in a sanguinolent abscess, in case the subject survives. There are also hyperthermia (106° F.), dulness, stupor, weakness, staggering, and congested, swollen, weeping eyes.

Intratracheal injection is harmless to the horse.

Lignieres finds his cocco-bacillus in the expectoration at the outset and in the nasal and guttural forms of the disease later, but not in the blood nor lungs after death, as it is then replaced by streptococci, the great reproduction of which is favored by its presence. In ordinary cases of equine influenza it is often impossible to find the cocco-bacillus in the lung or other organs after an illness of 8, 10 or 15 days. (Lignieres).

Lignieres appears to have omitted the obvious test of the infection of other horses in the same stable, from the cases produced by his experimental cultures, so that we must still call for more confirmatory proof. Cadeac, indeed, assures us that cultures of cocco-bacilli taken from cases of equine influenza, are often innocuous. Deadly as the germ cultures of Lignieres prove, they appear to lack that element of extreme infectiousness shown by equine influenza when the susceptible animals come into proximity with the sick.

Accessory Causes. The recognition of the one essential cause in the microbian invasion, need not exclude as accessory factors the many unwholesome conditions which have long been recognized as contributing to the severity of epizoötics. As the seed requires the rich field, the rain and sunshine to bring it to an abundant harvest so the microbe of equine influenza flourishes best where the conditions are most favorable and the antagonisms least.

The chill which comes from a sudden extreme fall of temperature, or the standing in a cold draught when wet or perspiring, lays the system open to this as to other microbian invasions.

The electric tension preceding a thunderstorm, to which many of the lower animals are excessively susceptible equally prepares the system to succumb to the germs. It may here be noted that September 1872, the last days of which witnessed the start of the great epizoötic, had no less than eleven thunderstorms, while in September of the previous year there were but two in the vicinity of Toronto. It is just possible that the great and frequent electric tension, lowered the animal vitality, allowing a violent invasion by the hitherto slumbering germ, and gave to the latter that encreased potency which sent it forth on that year of almost unparalleled epizoötic record.

The high barometer and low dew point similarly affect the animal economy and encrease receptivity to disease. Rain fell at Toronto 16 days in September 1872 and but 8 days in September 1871.

Impurities in the air whether originating in volcanic eruptions, telluric emanations, close, filthy overcrowded buildings or compartments or large collections of decomposing organic matter, impair the animal vigor and lay the system open to a more violent attack. For this among other reasons epizoötics of equine influenza are nearly always more deadly in the closely packed city stables than in the pure country air.

Overwork and poor irregular feeding and watering pave the way for debility, prostration and severe invasion.

Sudden vicissitudes of temperature, which are so common in spring and autumn, associated as they are with the shedding and growth of the coat, materially encrease susceptibility and sometimes determine an encreased severity in the attack.

Youth has its influence, even if it means only that the system that has never before been exposed to the poison, retains all its native susceptibility, and has none of that acquired immunity which comes from a previous exposure to the virus and successful resistance.

Acquired immunity must of course be reckoned with. After a non-fatal attack this is usually to be relied on for several years or even for the rest of the lifetime, yet it varies with the individual animals, and, under the baleful combination of a specially potent germ and strongly conducive accessory causes, it may become worn out in a year. Yet the older horses can always be trusted to show a large measure of this immunity, so that in the absence of extraordinary epizoötics it is mainly the young that suffer, and it is only when a country has had no general invasion for a length of time, or when the germ has acquired an unusual pathogenic potency, or when these two conditions conjoin, that the invasion of the equine population becomes universal, as it virtually was in the United States and Canada in 1872–3. Under other circumstances the germ, temporarily shorn of its power, lingers in city and dealers stables, biding its time until circumstances become more favorable for a new general outbreak.

Immunity largely explains the comparative mildness of the last cases in any particular locality. The more susceptible animals are attacked first and most severely, while the partially immune ones, which for a time resist, throw off the disease with greater readiness. The explanation has been sought in a lessening potency of the germ, but though this may hold true of some cases, it manifestly does not apply when slight lingering cases only are left in one locality, and the disease is advancing over the neighboring state with all its original force and vigor.

Incubation. This appears to vary within certain limits. When during an epizoötic a sick horse is brought into a new locality and stable, other cases usually develope in from one to three days. Trasbot gives examples of one day, Salle, Cadeac and others of two, others claim four, seven and even, exceptionally, fifteen days. One reason for an apparently prolonged incubation may be found in the seclusion of the germs in the alimentary canal, so that they escape only when passed with the fæces. The pathogenic potency of individual germs, and the varying susceptibility of the animals exposed must also be taken into account.

Symptoms. Equine influenza is liable to show a special predilection for a given set of organs in different epizoötics, so that we find descriptions of the different forms as independent types or even separate diseases: as the catarrhal form, thoracic form, abdominal form, bilious form, nervous form, pink eye, infectious cellulitis, and rheumatic influenza. These forms may, however, appear in different subjects in the same epizoötic, and when they are not due to complications, may be looked on as a concentration of the morbid processes on one class of organs rather than another.

Initial pathognomonic symptoms. Certain prominent and striking symptoms are so constantly present in the earlier part of the disease that they may be held as virtually diagnostic. These are the suddenness of attack, the anorexia, the profound early prostration and weakness, the high temperature, the swelling and watering of the eyes, and the specially brownish red coloration of the conjunctiva and other visible mucosæ. The attack may come on with almost lightning rapidity. The animal which yesterday, or it may be but an hour or two ago, appeared to be in the most vigorous health and spirits, is found with pendant head, resting perhaps on the manger, ears drooping, eyelids swollen and half closed, epiphora, conjunctiva of a brownish red or violet, lips loose and drooping, and one or two legs partially flexed, while the body is balanced on the others. The patient is indisposed to move, and when compelled to walk may sway and stagger from nervous and muscular weakness. The arched back, cracking limbs, and their stiff, rigid movement further indicate the suffering in muscles or joints or both. Appetite is greatly impaired or lost, thirst marked, and hyperthermia 102° to 105° or upward. Sneezing, cough or symptoms of some other special localization may be present, but the above occurring in a number of horses at once, without appreciable climatic cause, when one or two new horses have been very recently acquired, or when influenza has been prevailing in the vicinity or in a neighboring place, will usually stamp the nature of the attack.

Cadeac considers the sudden attack, high fever, and profound nervous prostration and stupor as the manifestations of the uncomplicated disease, while the localizations in the lungs, bronchia, pleura, liver, bowels, etc., are indications of complications by germs of other diseases, which find the debilitated influenza system especially open to attack. The fever which always sets in early may be little above the normal in mild cases, and may reach 107° or 108° F. in the more severe ones. It may last thus for five or six days and then rather suddenly descend to near the normal. In other cases it descends a little daily, the lowest temperature for the day being seen in the morning. Shivering is often nonexistent or passes unperceived.

The pulse does not usually encrease in ratio with the temperature. It may be at first only 40 or 50 per minute, though later, and especially with extensive disease of important organs, it may reach 60, 70, 80 or even 100. It usually lacks in firmness and force, even when the heart beats forcibly, being soft, somewhat compressible, and often irregular in successive beats, the weakest corresponding to the last part of the inspiratory act, or when the lungs are full and the heart compressed. The heart impulse behind the left elbow is usually forcible and may show variation in rhythm or even intermissions.

Mild catarrhal symptoms of the nose and throat are usually present, the discharge being at first serous and later muco-purulent. As a rule this is complicated with more or less bronchitis, but this does not indicate anything serious. Acceleration of the breathing, sneezing, and cough are present. Cough may be at first nervous, husky and paroxysmal, but later as the discharge is established it assumes a looser, mucous character. It is liable to be roused by excitement, by drinking cold water, by inhalation of dust, or by giving medicine. In connection with these symptoms there are some indications that the digestive organs are involved. The pharyngeal and submaxillary glands may be swollen and tender. If the subject has been seized just after a full meal, there may be slight tympany, and in any case, the fæces are passed in small balls, a few at a time, hard and with a baked or glistening surface. These may have an unusually strong or heavy odor, and laxatives are liable to act with dangerous energy. The urine is scanty and high colored, sometimes icteric.

In such mild attacks, which constitute the majority, improvement may be noted as early as the fourth day, and a prompt recovery follows.

With extensive thoracic lesions, the symptoms are much more severe and the danger greatly enhanced. These may occur in any patient, but there appears to be a special predisposition in the young and still very susceptible animals, in those crowded together in close, badly aired buildings, in the overworked, poorly fed or in any way debilitated subject, and in horses that have been especially excited and exposed, as by railway travel.

In exceptional cases congestion of the lungs may be so acute as to lead to speedy death, and the objective symptoms do not differ greatly from those of ordinary cases of this condition, if we except the very high temperature in influenza, associated as it is with the fact of the epizoötic prevalence of the disease.

In pneumonic cases the lesions are usually double and have a tendency to develop toward the lower borders of the lungs, just behind the elbow or farther back, and less frequently in the centre of the organ. It may be impossible to detect crepitation, but sounds of distant organs (heart beats, bronchial blowing, intestinal rumbling) are heard with unwonted clearness over the consolidated parts. A mucous râle can usually be detected behind the shoulder blade, along the line of the larger bronchia. Percussion sounds may be indefinite, as the area of consolidated lung is usually small in ratio with the hyperthermia. The area of flatness in ordinary fibrinous pneumonia is usually much greater with a high fever, and if the lesions are on one side only, right or left, it is still more suggestive. The crepitation too in pneumonia is significant. When the pulmonary lesions are extensive by reason of œdema, a marked infiltration may often be noted on the lower surface of the trunk or in the limbs as well.

Pleuritic symptoms may show in the same connection. The breathing becomes more hurried and shorter, friction sound may be heard but it is very transient and soon superseded by an absolute flatness on percussion, rising to a definite horizontal line, representing the boundary of the effusion in the lower third or half of the chest, and usually rising to the same height on both sides. Tenderness of the intercostal spaces may or may not be present. As the disease advances creaking sounds may be heard from the stretching of the consolidated false membranes. The combination of double pleuro-pneumonia constitutes a very fatal type of the disease.

The symptoms of pericarditis and of cardiac disorder usually accompany those of pleurisy. The tumultuous heart beats, often associated with soft, weak or even rapid pulse, and later, a deadening or muffling of heart sounds, as in hydropericardium are characteristic when present. With endocarditis the early tumultuous heart beats, with small weak pulse, irregular and sometimes intermittent, become complicated by a blowing or hissing murmur with the first heart-sound. In such cases clots of blood are liable to form in connection with the valves, and may cause sudden and early death. When the heart is involved the tendency to extensive infiltration of limbs and lower aspect of the trunk is much enhanced. (See diagnosis for table of phenomena in influenza, fibrinous pneumonia and contagious pneumonia respectively).

Symptoms of digestive disorder are usually in evidence. Even in the thoracic forms the mouth is dry, hot, and has an offensive odor; the tongue coated above, has often red margins and tip; it may even be yellowish; the gums may be swollen and dark red or violet especially around the incisors; mastication may be slow and unwilling; the pharynx maybe swollen; the pharyngeal and submaxillary lymph glands may be tumid and tender; and swallowing may be difficult.

Congestions of the stomach and intestines are indicated by inappetence, sometimes flatulence, passage of flatus, constipation with small, round, mucous-coated balls passed in small numbers, and by slight transient colics, pawing, looking at the flanks, and retraction of the abdomen. The retention of bile and destruction of blood elements are indicated in a deeper yellow of the conjunctiva and visible mucosæ, and in a yellow, brown or red color of the urine. There may be tenderness of the abdomen, but this, like the colics, is moderate, the senses being blunted by the attendant stupor which is usually even greater than in the thoracic forms. Urination may become frequent with straining, and the urine may become turbid, opaque, with flocculi of cystic epithelium and mucus, and even albumen. In from three to five days diarrhœa supervenes, the fæces becoming soft, pulpy, watery, glairy or bloody, and escaping through a permanently dilated sphincter. The diarrhœa may alternate with periods of torpor or complete inactivity, otherwise tenesmus of the rectum is marked. The exposed rectal mucosa is congested, of a deep red or it may be of a dark violet hue. Eversion is not unknown.

In the worst cases death may ensue by the third or fourth day, but in others the diarrhœa is critical and heralds an improvement which goes on to a speedy recovery. In still other cases the bowel troubles continue, the fever does not give way and the privation of food and rapid metamorphosis of tissue produce steady emaciation and fatal marasmus.

A striking feature of the gastro-intestinal disease is the extraordinary susceptibility to laxatives. So much is this the case that I have known of two drachms of aloes proving fatal by superpurgation in a large, mature Percheron horse. It is never safe to use laxatives in equine influenza until one has ascertained whether in the special form of the epizoötic in question the gastro-intestinal organs are or are not especially involved.

Disorders of the eye are so common or constant as to have procured for certain epizoötics the name of pink eye. They set in suddenly, and equally in both eyes, with infiltration of the lids and particularly of the mucosa which is of a more or less deep red, and may bulge between the margins of the eyelids, (chemosis). The flow of tears is profuse, seropurulent matter accumulates at the canthi and in the lachrymal sacs, vision is impaired and there is intolerance of light. The cornea becomes bluish, cloudy or milky white, with a red zone around its margin and, above all, on the adjacent sclerotic. In some cases the aqueous humor becomes turbid or flocculent, and the iris changes its clear, healthy dark lustre for a dull brown or yellow tint. The tension of the globe may be materially encreased. They are readily distinguished from recurrent ophthalmia by the attendant weakness, stupor and hyperthermia, and by their non-recurrence in case the patient survives.

The nervous symptoms are especially manifest in the sudden seizure, great prostration, extreme weakness, profound stupor or lassitude, the staggering gait, in bad cases, insensibility to voice, slap or, it may be, even to the whip, the rigidity of the loins, their insensibility to pinching, the difficulty of turning in a short circle, or of backing. The high fever, disproportionate to the appreciable local lesions, and its sudden improvement at the critical period, the excessive weariness and the disposition to lie down contrary to the habit of other inflammatory chest diseases are further indications.

This may go on to coma, there may be more or less complete anorexia, muscular trembling, paresis, especially of the hind limbs, or delirious manifestations indicating meningitis.

Rheumatoid attacks of the muscles and joints usually appear in the advanced stages of the disease, but may appear earlier. They may occur in any latitude but seem to be especially common in cold, damp, inclement northern regions, and at seasons when climatic vicissitudes are sudden and extreme. These may appear suddenly and disappear with equal rapidity, or they may last for a time during and even after an apparent recovery in other respects. When the joints are involved they usually become engorged with exudates in the synovial membranes.

Lameness in either fore or hind limb may assume an intermittent type developed by exercise and subsiding with rest, evidently bespeaking local arterial embolism, and in such cases it is likely to persist for months.

A tendency to transudations and dropsical effusions is common in severe cases, showing especially in the filling of the legs, but in certain epizoötics, these become strikingly prevalent and have secured for such a special name (epizoötic cellulitis). Apart from the limbs these affect particularly the inferior surface of the chest and abdomen. The swellings are not necessarily hot nor painful nor petechiated as in petechial fever, yet they may merge into that affection or they may become phlegmonous and develop abscess.

Complications of many kinds are to be looked for, pregnant mares may abort; laminitis may set in; the microbes of strangles, contagious pneumonia, cerebro-spinal meningitis, septicæmia, pyæmia, etc., may take occasion to attack the debilitated system, and thus complex diseases and manifestations are developed.

Morbid Anatomy. The lesions may predominate in different organs in different subjects and successive epizoötics. It is a protean disease and may expend its main energy on any one of a number of different organs or systems of organs.

In the slighter cases the lesions are often largely confined to the anterior part of the respiratory organs. The fauces, pharynx, larynx, guttural pouches and nasal mucosa are tumified, congested, red and covered with mucous, and this condition may extend down to the bronchia. In such cases the blood is normal or may coagulate with undue readiness and firmness. The pharyngeal and intermaxillary lymph glands are red and congested in their outer zone.

In the more severe cases the alterations in the blood are perhaps the most constant of the morbid features. The blood is fluid and incoagulable, or the clot is soft, diffluent and black, the red globules are crenated or broken up, and show little tendency to adhere in rouleaux. The escaped hæmatoidin accumulates in masses in the serum in crystalline forms, giving it a high staining power when a line is drawn with it on white paper. Fatty globules also float in the mass. The leucocytes are relatively very much encreased and the red globules diminished. Dieckerhoff found 30,000 and Trasbot 40,000 leucocytes in a cubic millimetre.

The diffluence is not constant. Blood drawn in the earlier stages of the disease, coagulates with extraordinary firmness, influenced, doubtless, by the encrease of the leucocytes, the disintegration of the blood globules, and the liberation of globulins. This serves also to partially explain the early and sudden deaths from coagula in the heart and large vessels, which are occasionally met with. Such clots in the heart are often found adherent to the valvular or ventricular endocardium which at such points shows cloudy swelling, thickening, cell proliferation and even encreased vascularity and granular elevations.

In advanced cases, however, the prominent features are usually acidity, blackness, and incoagulability of the blood, its resistance to oxygen, altered and broken down red globules, free coloring matter, relative encrease of white cells, and, if necropsy has been delayed, the abundance of septic microbes (cocci and bacilli). Petechiæ are abundant on the serosæ especially on the pericardium.

Lesions of the alimentary mucosa are very constant. There may be stomatitis, with tumid follicles and even ulcers (Kowalavsky). In the stomach the right sac has its mucosa thickened, softened, red, congested, petechiated and discolored. The summits of the folds may be ulcerated (Labat). Similar lesions are presented in the small intestines. The agminated glands may show many rounded elevations, with or without open discharging follicles. The mucosa is covered with a muco-purulent material. Otherwise, the small intestines, like the stomach, are usually empty. The large intestines present similar lesions, the nodular elevations often representing the solitary glands, and the masses of ingesta are likely to be dry and indurated, in the earlier stages or semiliquid in old standing cases. The peritoneum may be congested, petechiated and at points infiltrated and usually contains a reddish serum in variable quantity. The mesenteric glands are more or less enlarged and congested.

The liver shows more or less congestion as in other infectious diseases localized in the bowels. It usually has a parboiled appearance, and yellowish gray areas of necrosis may be manifest, or again, fatty degeneration may be present. Petechiæ, and even small blood clots may be found on or beneath the capsule. The pancreas, and, still more, the spleen may be the seat of congestion or engorgement but this is far from constant.

The capsule of the kidney may be petechiated or elevated at points by serous exudate or extravasation. The surface of the organ and of sections show a mottling with darker and lighter areas, and petechiæ and patches of congestion may be found on the bladder and urethra.

The nervous centres exceptionally show meningeal congestions, and exudations, and petechiæ as has been noted of other serosæ.

Lesions of the eye may be confined to the mucosa, or they may extend to the membrane of the aqueous humor, the iris, or even the deeper structures.

Other lesions such as laminitis, bursitis, arthritis, like those attendant on abortion need no special description.

When pulmonary lesions are extensive, the bronchial mucosa is not only softened, opaque and covered with a serous, or muco-purulent discharge, but deeply congested and petechiated. When the chest is opened there is usually an effusion, pale straw, red or bloody and more abundant than in contagious pneumonia. False membranes may exist and show a blackish tint from extravasated blood. The lung fails to collapse and shows on the surface and throughout its substance petechiæ and small black infarctions. In some instances the whole lung is blood gorged, black, almost jelly like, as in acute congestion. In others these are limited infiltrations, concentrated especially in the anterior and lower parts, and almost invariably affecting both right and left lungs. The infiltration is circumscribed in area in comparison with the attendant fever and constitutional disturbance, resembling in this respect, the lesions of contagious pneumonia. It differs however in having a greater tendency to liquid infiltration of the connective tissue, and but for the lack of such tissues in the horse’s lung it would tend to approximate to the lesions of lung plague in cattle. It shows a distinct thickening of the interlobular septa, a tendency to extension to the pleura, and to issue in pleural and subpleural infiltration, and to a more copious effusion into the pleural cavity than in either fibrinous or contagious pneumonia. The lung tissue may be granular and hepatized, but far more frequently it is only splenized, the lung being the seat of a bloody infiltration, yet retaining much of its elasticity and coherence. Portions may be infarcted and black and large areas may have a pale or parboiled appearance, and gangrene is by no means uncommon.

Diagnosis. This is based largely on the suddenness of the attack, its epizoötic character, the numbers attacked in rapid succession, and over a large area as contrasted with contagious pneumonia, the sudden and extreme prostration and weakness, the swelling, watering and discoloration of the eyes, the mildness of the average case, the congestion of the upper air passages, and in the mild cases a comparative immunity of the lungs, the irritability or congestion of the gastro-intestinal mucosa, and the history of the case:—the arrival of the infected horses within a few days from an infected place, or coming through infected channels, or the attack of new arrivals in a previously infected stable, or the known advance of the disease towards the place where the patients are, will usually serve to mark the true nature of the affection.

As a help to correct diagnosis we give below some of the prominent conditions and phenomena of the three forms of lung disease known as fibrinous pneumonia, contagious pneumonia, and the pneumonia of equine influenza:

=Pneumonia=: =Pneumonia=: =Pneumonia=:

Croupous Fibrinous. _Contagious, of Equine of Equine Influenza. Animals._

From climatic Slow succession of Rapid succession of vicissitude, cases in the same cases in the same exposure, etc. stable, irrespective stable or locality, Attacks exposed of climate or irrespective of animals only, and all exposure climate or exposure at once

Prevails in inclement Any season: worse in Any season: worse in seasons, spring, inclement season inclement season autumn, (Winter)

Infection from close Infection spreads proximity, contact, widely and rapidly stall, manger, rack, through the air. bucket, trough, etc.: Spread rapid and Spread slow often general

Carried in manure, on Carried in manure, on harness, wagons, harness, wagons, clothes, etc. clothes, etc.

Incubation, 3–10 days Incubation, 1–2 days

Rigor may be late: Rigor early and well Rigor not always well after exudation has marked, before marked commenced exudation

Sets in slowly or with Sets in slowly, cough, Profound nervous acute congestion; dulness, impaired prostration like appetite and pulse appetite, pulse opium poisoning, vary with rapid, prostration appearing early and inflammation slight suddenly

Nasal discharge, watery Nasal discharge, yellow Nasal discharge, or rusty, later watery, may become muco-purulent yellow

Eye pink, dark red Eye yellow, rarely Eyelids bloodshot (pink swollen or watery eye), violet, madder hue, swollen, watery, closed

Temperature rises with Temperature rises early Temperature rises early inflammation and extremely, before and extremely, in exudation, 104°–107° some hours, 104°–107°

Swelling of limbs rare Limbs swell rarely Limbs often swell greatly

Rheumatoid arthritis Rheumatoid arthritis may follow may set in; often in advanced stage

Crepitation more Crepitation less Crepitation may escape constant around the constant around the recognition exudation exudation

Exudation Exudate affects lower Exudate less granular (Hepatization) in or anterior border of than in pneumonia; lung, lower, lung; often in small forms in or posterior, anterior, isolated areas or gravitates to lower or central, usually around bronchia; less part of lung. undivided area blood engorgement Congestion passive than in fibrinous pneumonia

If pleurisy effusion Pleural effusion Pleural effusion may be copious infrequent, or frequent and abundant limited, though pleurisy is common

Abscess not infrequent Abscess rare Abscess not infrequent

Pulmonary gangrene Pulmonary gangrene and Infarctions, sequestra, infrequent sequestra frequent and cavities not uncommon

Pericarditis infrequent Pericarditis frequent Pericarditis frequent

Blood, decrease of red Less altered than in Blood at first clots globules; encrease of either of the other firmly, later white, hæmatoblasts, forms. Shows becomes, thick, fibrine formers and cocco-bacilli in the black, sizy, soda salts earlier stages: hæmatosis tardy. streptococci later Reaction acid.

Coagulation firm, buffy Coagulum loose, buffy coat coat slight

Hepatic congestion, not Hepatic congestion Hepatic congestion hepatitis excessive, hepatitis, excessive, necrotic changes hæmorrhagic; fatty degeneration

Prognosis. Mortality. As usually met with and under favorable conditions, equine influenza is a mild disease. In 1872 when the disease, sweeping the continent and hardly sparing an equine animal, might be assumed to have reached its maximum, the actual deaths varied from 2 per cent. in country districts to 7 per cent. in large cities. The same holds for Europe where Friedberger and Fröhner gives 4 to 5 per cent. Früs (Denmark) 1 per cent., Aureggio (Italy) 3 per cent., Siedamgrotzky 10 per cent. Much depends on conditions: In horses infected in transit on a long railroad journey it may be 100 per cent. and in fat dealer’s horses, out of condition for active work it usually reaches a high figure. If the patients are kept at work the complications and mortality run very high. The same applies to debilitated animals kept in close, foul, ill-aired stables, or reduced by exhausting or long standing diseases. The very young and the senile suffer more than animals in middle life and vigorous condition. Finally the parts invaded have a controlling effect. The milder cases affecting the upper air passages only, nearly all recover, in those showing abdominal lesions the indications are still favorable; while with double pulmonary and pleural lesions the patient is too often in a hopeless condition. Brain lesions are almost equally redoubtable.

The actual money losses, in an epizoötic of influenza, are more in the way of the loss of work and the complete stagnation of trade in all departments, than in the number of deaths. Yet even in this sense it may prove more ruinous than would a disease having a less universal sway, though far more fatal to the animals attacked.

Treatment. A disease like this, which tends to spontaneous and perfect recovery, needs mainly dietetic and hygienic care in the vast majority of cases. Rest is a prime consideration in a pure genial atmosphere. In the summer season, in the absence of rainstorms, an open air life, at pasture is the best. Shelter must be had in case of storms, and in the cold season a clean, sweet, roomy well-aired loose box, with a sunny exposure, is important. Clothing, bandages, blankets and even hoods may be required if there is any tendency to chill. Food should be laxative, cooling and of easy digestion. Bran mashes, scalded oats or barley, ensilage, roots, potatoes, apples, fresh grass or scalded hay may be suggested. Milk has been strongly advocated, from twelve to fifteen quarts a day, and linseed tea as being especially adapted to the irritable stomach and bowels. Food should be given often, in small quantities so as not to destroy the appetite.

Costiveness is best met by injections of water, blood warm, or if there is much hyperthermia, of cold water. This latter stimulates the peristalsis more actively and at the same time lowers the temperature. By unloading the large intestines it removes irritants, without danger of encrease of congestion or diarrhœa.

If anything more is wanted for these mild cases, small doses of stimulating diuretics or diaphoretics may be given. Sweet spirits of nitre ½ oz. or liquor of acetate of ammonia 2 oz. may be given twice a day, the latter in the drinking water or gruel. In the absence of these saltpeter ½ oz, or potassium acetate ½ oz. may be given.

In the more severe cases more active treatment is resorted to, but in all cases one should avoid measures that tend to greatly depress the vital powers and especially the circulation. Heroic treatment has been all but universally condemned and yet Trasbot claims to have had excellent results from a moderate venesection (2–5 qts.) in strong, muscular, well conditioned animals. The blood became more fibrinous, the general symptoms improved and complications were far less marked. During twenty years, in a large number of cases, it had constantly the same results, restoring appetite, opening the closed eye, imparting new life, lowering temperature, and checking congestions. The results were best in all cases when it was employed early, but they were almost equally good when later congestions set in, or when the ordinary inflammatory localizations were advancing, and he found the measure hurtful only when, in the advanced stages, the animal was worn out, and destitute of all power of recuperation.

Antipyretics have been lauded and decried, and it is doubtless best to use them with due discrimination and caution. Acetanilid, the agent in most common use, is a powerful cardiac depressant, and in this disease the heart is often already dangerously weak. Yet in cases with very high temperature, seriously threatening life, acetanilid in doses of 2 drams, repeated every second or third hour until the temperature falls, and thereafter twice or thrice daily, for a day or two, may save the patient. Similarly, where there are indications of violent headache (drooping head, eyelids and ears, congested and watery conjunctiva, stupor or irresponsiveness) a dose or two of acetanilid with the same amount of sodium bromide will often give material relief. The general suffering and disorder attendant on the cephalalgia, if allowed to continue, prove a direct bar to improvement, and endanger complications that might otherwise be escaped. On the other hand, there is constant danger from too large doses, or a too long continued use of acetanilid in influenza. Phenacetin may be substituted in 2 dram doses, the action being somewhat more prompt and transient. As less dangerous than the coal tar antipyretics, we may fall back on such agents as sodium salicylate, ½ to 1 oz., or sulphate of quinia, 20 grs.

Elimination of toxins and waste products is to be secured and this is more safely conducted by the kidneys or skin than by the irritable alimentary canal. Plenty of pure cold water is one of the best and simplest resorts. Aside from this, where there is much hyperthermia, bicarbonate of potash or soda will serve the various purposes of an antidote to the acid blood, an eliminant and an antithermic. Under the same circumstances saltpeter may be resorted to in ½ oz. doses twice daily. When, however, the heart is weak it is better to employ ammoniacal or etherial diuretics:—spirits of nitrous ether, 1 oz. or liquor of acetate of ammonia, 2 to 4 ozs. By combining these with extract of belladonna and camphor a fairly standard prescription may be prepared.

Inhalations of warm water vapor, rising from hot water or a hot mash in a bucket, over one end of which a bottomless bag is drawn, while the other end receives the nose of the horse, will greatly relieve the irritation and the cough. It can be made even more soothing by introducing a little alcohol, eucalyptol, menthol, camphor, poppy-heads, or other anodyne. Or the water vapor may be set free in a close stall from a boiling tea-kettle or a steam pipe, and an admixture of sulphurous acid made by burning a few pinches of sulphur, more or less according to the size and closeness of the stall. If the stall is tight enough a steam bath may be given with much profit in the early stages.

Counter irritants applied to the throat, or, if need be, to the breast and sides of the chest will often give material relief, acting as derivatives and probably also by modifying the globulins in the exudate and thus influencing the course of the disease. In case of sore throat of a very high type it may be best to apply a compress or poultice, or even a piece of sheepskin for a day or two, until, by antithermics, cooling diuretics and soothing inhalations, the severity of the inflammation has abated. The common mustard pulp made with tepid water, rubbed in, and covered by paper, may be applied for an hour; or the soap liniment (soap 6 ozs., camphor 3 ozs., and proof spirit, liquor ammonia and linseed oil aa 1 pint) may be rubbed on repeatedly; or a blister of cantharides may be used.

The ophthalmia may be treated by a moist atmosphere, a few drops twice daily of a solution of atropine beneath the lids, a similar treatment with pyoktanin, (1:1000), or a solution of mercuric chloride (1:2000).

In case of gastro-intestinal inflammation elimination is to be sought by ⅓d the usual laxative dose, supplemented if need be, by injections. Half a pint of olive oil with 20 grs. calomel will usually be well borne. Counter irritants may be applied to the abdomen, and the bowels must be carefully watched and any inactivity or derangement corrected. A slight diarrhœa is not to be too hastily checked as it may serve at once to eliminate offensive matters and subdue mucous inflammation. Solutions of flax seed, gum, or slippery elm in the drinking water may serve a good end.

In case of cardiac weakness with intermittent or irregular pulse, hurried breathing, and an undue contrast between the violence of the heart action and the weakness of the pulse, circulatory stimulants are called for. Digitalis 10 grains twice daily, strophanthus tincture 1½ dr., strophanthin subcutem ¼ grain, caffeine 5 grains, veratrine ⅒th grain, or strychnia 2 grains.

Nervous symptoms will exceptionally demand the application of cold water or even ice or snow to the head, with counterirritants to the sides of the neck or chest, and the internal use of bromides, iodides, chloral or other nerve sedative.

Other complications must be treated according to their indications.

As the skin becomes cooler and more moist, and the pulse slower and fuller, a tonic and stimulating treatment may be desirable. Gentian 4 drs., saltpeter 4 drs., sal-ammoniac 2 drs. may be given night and morning, or in case of great debility ammonia carbonate may replace the sal-ammoniac. Or the gentian may be replaced by nux vomica, and the ammoniacal preparations by alcoholic ones.

When prostration becomes extreme and stimulants and bitters appear inadequate, transfusion of blood from a healthy horse may save the patient’s life, or a normal salt solution sterilized may be introduced into the vein.

The first method is accomplished through a caouchouc tube with a short tube of silver inserted in each end; the jugular groove of each horse is washed and disinfected, and the vein opened; the tube disinfected with a salicylic acid solution, and cleared out with boiled water is inserted upward into the vein of the sound horse, and when the blood begins to flow the other end is inserted downward into the vein of the sick one. In this way the blood is allowed to flow from the one to the other, the finger being kept on the pulse of the patient to detect any faltering, which like heaving up of the head or rolling of the eyes, may be taken to indicate undue arterial tension, or disturbed brain circulation, and should be the signal for an arrest of the flow. To effect this, pinch the tube in the centre, and wait a minute or so; if the symptoms subside the current may be reopened and a little more carefully admitted, but if not the tube may be withdrawn and the wounds pinned up.

The normal salt solution, .6 per cent., is sterilized by boiling, and placed in a sterilized vessel where it is allowed to cool to the body temperature; then a caouchouc tube furnished with a silver tube at one end and sterilized as for transfusion of blood, is filled with the solution and the vessel containing the latter having been placed at a level higher than the patient, the tube is used as a syphon. When the liquid flows in full stream the silver tube is inserted downward into the jugular of the patient and the liquid is allowed to flow in, subject to the same precautions as regards sudden blood tension as in the case of the transfusion of blood.

Prevention. No country appears to have attempted the absolute exclusion of the disease or the extinction of the germ by a compulsory quarantine and disinfection. The nearest approach to this is in Prussia where in the event of an outbreak of equine influenza, the official veterinarians and police authorities must send in reports to be published in the official papers and communicated to the directors of government breeding studs and to the army authorities. We have here the germ of an effective system of extinction, for if those in charge of government horses in an infected country can protect them against infection, much more could such protection be secured by putting an end to the infection which is now allowed to remain generalized. Moreover in our great outbreak of 1872–3, when germ-potency and all but universal susceptibility were so remarkable, effective quarantine showed the most signal successes, in the resulting immunity of Vancouver’s Island, Prince Edward Island, the whole of the West Indies except Cuba, Central and South America, and isolated districts in Mexico.

Sanitary police in this disease has been abandoned mainly because the virus is so diffusive on the air that quarantine must be more than usually comprehensive to prevent extension of infection, and because the disease is fatal only in a small percentage of cases, so that the loss is apparently minimized. But a panzoötic like that of 1872–3, prostrating 1,000,000 horses, asses and mules in the United States for one to two weeks, and paralyzing the agriculture and commerce of the continent for that length of time, may well make one hesitate to supinely accept for all time an evil, which, experience has shown, can be circumscribed and stamped out. When horse owners, legislatures and veterinarians can be educated up to the needs of the case our yearly local losses from equine influenza, and the occasional all pervading epizoötics of this disease can probably be abolished by the extinction of the germ on the Continent. To achieve this result an immediate large outlay would be well spent. In a new generation, or a new century perhaps, this desirable object may be achieved.

Meanwhile the individual owner can do something to secure a partial protection. On farms and in barracks the animals may be secluded from all other equine animals during the local prevalence of the disease. Men, dogs, and wild animals can be similarly excluded. Litter, fodder, bags, clothing, manure, vehicles, etc., from infected stables and places must be carefully guarded against. Newly purchased animals, carried in any public conveyance, or kept or fed in any public yard or stable must be quarantined at a considerable distance from others, and treated by disinfectant sponging and fumigation before they are allowed to mingle with other equine animals. Stables where the disease has occurred must be thoroughly disinfected, together with all manure made during the epizoötic and for some time thereafter.

EPIZOOTIC CELLULITIS: PINK EYE.

Williams follows a popular fashion in describing under the above names an affection which may be only a form of equine influenza, but which may be named by itself until its true place can be defined by proof of its actual pathogenic microörganism.

Beside the general constitutional disturbance, this condition is distinguished by marked hyperthermia (103° to 104°), swollen, congested, watering eyelids, cough, strong pulse becoming gradually feeble, firmly coagulating blood, irritable bowels, painful passage of fæces, and, above all, a frequent movement of the feet indicative of discomfort and followed by swelling, often excessive, of the limb or limbs, by a cutaneous and subcutaneous exudate. These various phenomena may all be but manifestations of the rather protean disease, equine influenza, and the cellulitis but variations of the rheumatoid and arthritic forms which are so common in the regular type of that disease in cold or wet climates, or seasons. Williams claims that a prominent danger is the formation of clots in the heart and large vessels and advocates the free use of the salts of ammonia and potash with stimulants. The treatment does not essentially differ from that of equine influenza except in the call for special applications to the inflamed eyes and infiltrated limbs.

PETECHIAL FEVER. ACUTE HÆMORRHAGIC—ANASARCOUS—TOXÆMIA.

Synonyms. Definition. Causes, obscure, bacteria variable, pus microbes no active contagion, toxic products, any toxin causing vaso-dilatation, examples, toxins from fermenting ingesta, debility; impaired innervation, nutrition and function; gravitation; primary and secondary forms: predisposing diseases. Lesions: petechiæ and slight blood extravasations in skin, subcutis, mucosa, submucosa, serosæ, and solid tissues, largest in soft tissues; round cutaneous swellings one to two inches across, patches, cracks, oozing, fissures, sloughs, section shows yellow serous and blood infiltrations, capillaries greatly dilated, infiltrated thickened mucosæ, blocked nasal passages, ulcers, serous and bloody discharges, pharynx, larynx, lungs, stomach, intestines, kidneys, blood firm or diffluent. Symptoms: Hyperthermia, nasal petechiæ, extravasation, pink or yellow oozing, swellings on nose, lips, face, limbs, oozing, cracks, sloughs, turning up of toe from detachment of the flexors, metastasis from skin to lungs, or abdomen, dyspnœa, colics, serous or bloody diarrhœa. Course. Duration: acute two days, average one to three weeks, tardy one to two months, Diagnosis: from glanders, anthrax, urticaria, malignant œdema, horse pox. Mortality. Prognosis: 50 per cent.: hopeless and grave indications. Sudden retrocession. Treatment: excellent sanitary conditions, cleanliness, air, light, green food or mashes, pure water, laxative food, or salts, diuretics, alkaline diuretics, vaso-motor contractors, antiseptics, quinine, strychnine, phenic acid, lysol, ichthyol, sulphites, etc.; locally aluminium acetate, cold water, scarification, nasal injections and tubes, tracheal iodine injections, argentum colloidale intravenously, antistreptococcic serum subcutem, Menveux’s solution.

Synonyms. Purpura Hæmorrhagica; Morbus Maculosus; Anasarca (Fr.); Typhus: Anthrax; Dropsy of Connective Tissue; Mal de Tete de Contagion; Coryza Gangrenosa; Malleus Gangrenosa; Charbon Blanc; Diastashemia; Leucophlegmasia.

Definition. An acute (or subacute), toxæmic, generally secondary disease, manifested by capillary dilatation and petechiæ on the mucosæ, skin, serosæ and elsewhere, and attended by extensive effusions of lymph and blood into the skin and connective tissue, to form hot, tender, nodular, diffused, or general swellings.

Causes. The causes of petechial fever are not clearly made out. Bacteria are found in the early exudate, but these are not constant in kind and it is not unreasonable to suspect that these may be results rather than causes of the lesions. On the other hand there may be an as yet undiscovered organism present, the products of which are capable of producing the disorder. Or the latter may be due to a combination of the toxins of two or more. Among the bacteria found may be named: The pus microbes, cocci, streptococci, staphylococci, and bacilli, have been found and adduced as causes, also diplococci, the bacillus hæmorrhagicus of Kolb, the streptococcus of strangles, the microörganism of contagious pneumonia and that of influenza, with a variety of others too great and too inconstant to be accepted as proof of cause. The fact that rarely more than one animal suffers in the same stable at the same time might be held to oppose the idea of contagion and of a definite organized germ.

Hence the theory of its causation by the presence in the system of the toxic products of bacteria rather than the bacteria themselves. (Dieckerhoff.) Cadeac supposes that any toxin which causes capillary dilatation may determine the disease, and calls attention to the fact that the injection of mallein (a vaso-dilator) aggravates the phenomena of petechial fever and determines enormous local exudations and engorgements. He notes further the potent vaso-dilator action of the products of strangles, contagious pneumonia, and influenza which are among the most frequent antecedents of petechial fever. Dieckerhoff also looks on the phenomena as the result of poisoning by the absorbed toxins of the microbes of suppuration, which modify the nutritive changes in the walls of the capillaries and determine exudations and hæmorrhages. Zschokke thinks that there is infection of the intima of the capillaries, with the formation of coagula. Clots are not found, however, apart from hæmorrhages.

The toxin theory receives indirect support from the absence of the same specific lesions in simple mechanical congestion of the capillaries and veins. Ranvier had no such results from tying the veins of a rabbit’s ear. Roger tied the auricular veins of the rabbit, and then cut the sensory nerves without effect: he then destroyed the cervical sympathetic ganglion, when there supervened marked exudation, lasting for three days. The complete blocking of veins by pressure or aseptic ligature, does not produce a spreading œdema, whereas in ordinary suppurative phlebitis, with abundance of toxins in the tissues this is a constant result.

The toxin theory does not fully account for those cases that occur suddenly, without any manifest pre-existing disease, and as the result apparently of cold and chill. On the other hand, it is only a very small proportion of horses exposed to the same degree of cold and chill that contract petechial fever, and it might well be surmised that in these few an unknown focus of suppuration or other lesion existed prior to the chill or that toxins having the requisite devitalizing and vaso-dilating properties had been absorbed from fermentations in the bowels or elsewhere. The mere exposure is harmless to the very great majority of subjects.

In any case it must be accepted that the debility and impaired local innervation, nutrition and function, that attend on the exposure to cold and toxins must be looked on as potent contributing causes. The predilection of the swellings for dependent parts (limbs, venter, face) shows the influence of gravitation and congestion. Whether there is present any special microbe which has yet eluded discovery, but which is the main pathogenic factor, must be left to the future to decide.

In cases that appear to be due to cold or chill alone, the disease is held to be primary; in those following on another affection, secondary.

Among the diseases on which petechial fever supervenes as a secondary affection contagious inflammatory affections of the lungs and air passages hold a bad preëminence. Strangles, influenza and contagious pneumonia, about in the order named, are especially causative factors or occasions of petechial fever. Among the other affections on which it supervenes may be named pharyngitis, abscess of the nasal sinuses, hepatic, renal and other internal abscesses, acute coryza, laryngitis, or bronchitis, enteritis, abortion, aggravated grease, suppurating wounds of the skin, infective abrasions by harness, suppurating sores after firing, infective arthritis with open joint, amputation of the tail, and castration.

Lesions. In certain cases these may be largely confined to petechiæ and slight blood extravasations, which are distributed very generally throughout the tissues, but show especially in the skin, subcutis, mucosa and submucosa of the nose, eyes, pharynx, guttural pouches, larynx, trachea, bronchia, mouth, stomach, intestine, bladder, vagina and womb; also in and on the lungs, pleura, pericardium, heart, liver, spleen, kidneys, peritoneum, pancreas, ovaries, bones, lymph glands, brain and nerves. The largest extravasations are liable to be in the softest tissues, and in the lungs they may reach the size of the closed fist, though usually they vary from a mere spot up to this. The spleen is sometimes engorged even to rupture. Beside the extravasations, and associated with them in position, and probably largely as an effect of them, there is more or less serous effusion infiltrating the tissues, congestions, suppurations, degenerations, and necrotic changes.

The skin, if white, and the dark skins on section, are seen to be marked by petechiæ. The cutaneous swellings may appear on any part, commencing with nodular thickenings varying in size from a pea to a walnut, and merging together into extensive elevated areas terminating abruptly at their margins in the smooth skin. The larger and more persistent engorgements settle on the lower aspect of the body and other dependent parts like the limbs and face. Cracks, oozing, deep fissure, and extensive sloughs are not uncommon. When the skin is incised it shows serous infiltration and thickening, with spots and patches of blood extravasation. The subcutaneous connective tissue is similarly infiltrated and discolored, and often in the limbs, face, and under the breast, sternum and abdomen so as to form a tremulous gelatinoid cushion of several inches in thickness. The capillaries may be distended to more than 20 times their normal calibre. The exudate may extend deeply between the muscles, and sloughs may lay these freely open and invade their substance. The muscular tissue is mottled with petechiæ, and apart from these it is pale, yellow, or grayish, having to some extent undergone granular or fatty degeneration. Detachment of the perforans and perforatus from their insertions is occasionally met with.

The nasal mucosa may show only petechiæ and circumscribed blood staining, but in fatal cases it is more likely to present extensive blood extravasations involving it may be the whole mucosa, and narrowing the lumen almost to complete occlusion. Sloughing is not rare, and the resulting ulcers may extend into the subjacent tissues, so as to penetrate the septum nasi or the thin plate of the turbinated bone.

The buccal mucosa and submucosa are often involved in common with the skin of the lips, cheeks, and intermaxillary space, the tissues being involved in one common infiltration of blood and serum. In some cases circumscribed necrosis and ulcerations are formed.

In the pharynx and larynx infiltration of the mucosa and adjacent parts of a deep blood red, with or without ulceration, causes serious narrowing of the passage, that on the vocal cords threatening suffocation. Suppuration of the pharyngeal glands and guttural pouches is not uncommon. Alimentary matters are frequently found in the larynx, and bronchia.

Beside the petechiæ and hæmorrhages in the lungs, œdematous infiltration in dependent parts, hepatization, abscess, and limited areas of necrosis are met with. The pleural sacs often contain a sanguineous effusion.

The stomach and intestines are usually more or less mottled with petechiæ involving mucosa, serosa or muscular coat; they are raised in rounded or irregular elevations by œdemas; or they are the seats of more or less extensive and even perforating ulcers. The contents of the bowels may be deeply discolored by the escaping blood.

The kidneys may be pale except where blood stained and œdematous infiltration of the surrounding tissue may be marked. Serous effusion into the peritoneum is not rare.

The eyelids are often implicated, infiltrated thickened, and rigid, and the conjunctiva, bulbar and palpebral, the seat of extensive petechiæ.

Barreau mentions extravasations on the divisions of the lumbosacral plexus causing sudden paraplegia.

Petechiæ and hæmorrhages mark endocardium, pericardium and cardiac muscle, otherwise the muscle is pale. The blood is sometimes in firm clot, at others diffluent or nearly incoagulable.

Symptoms. If hyperthermia is not already present as a feature of the pre-existing malady it usually shows itself early, at first slight, it may be (101° F.), and afterward rising in some cases to 104° to 106° F., or even higher. The general symptoms are usually those of the pre-existing disease (strangles, contagious pneumonia, influenza, nasal catarrh, pharyngitis, bronchitis, etc.), pursuing, it may be, a persistent course, or attended by special toxæmic symptoms of prostration and other signs of depression of vital functions. In some cases the hyperthermia is either absent at this stage or overlooked. On the prostration supervene the petechiæ on the visible mucosæ, and often also the swellings of the skin and subcutis. One of these may be seen before the other and it is difficult to decide whether the petechiæ always appear first as has been claimed. Cadeac claims that when œdema is first seen it has been preceded by petechiæ in that tissue (skin).

The petechiæ are usually first noticed on the nasal mucosa as fine red points, pin’s heads, or up to half an inch in diameter, or a number of these have coalesced to form extensive patches, and by and by to cover the entire wall. At first the mucosa is spotted with purple, without any marked elevation of the surface, but as the lesions extend it becomes swollen and raised at the points of extravasation and immediately around them and oozes a serous, sometimes a pinkish or yellow fluid. Even in the smallest petechiæ the color is persistent and does not disappear on pressure like the blush of the adjacent mucosa.

Usually cutaneous swellings coincide with the petechiæ, or appear within two days thereafter. The first manifestation is in the form of rounded abruptly elevated nodules, about 1½ inch to 3 inches in diameter, strongly resembling the eruption of urticaria. These show a certain predilection for the more dependent parts of the body,—limbs, abdomen, sheath, mammæ, sternal or pectoral region, nose, lips, face, etc.,—but they may develop on any part or on the whole surface. Neither tenderness nor heat is usually excessive. The swellings tend to run together so as to form extended elevations enveloping the entire limb up to a given point, forming a great pad under the chest and abdomen, or distending the whole face or head so that it seems more like that of a hippopotamus than of a horse. In such cases the lips and nostrils become so thick and rigid that prehension is impossible, and breathing if it can be accomplished at all is accompanied with a marked snuffling. The swollen eyelids are closed, and the general turgid surface of the face is hard and resistant and no longer pits on pressure.

Under the chest and abdomen the swellings show as a continuous pad or cushion, on one side mainly or extending across continuously on both sides, and from the breast to between the thighs. It usually pits on pressure, and may shed the hair and become rough and scabby or ooze a serous fluid from the surface.

On the limbs the swelling usually shows first on the fetlock or pastern and gradually extends upward until it reaches the body.

As the disease advances chaps, cracks and fissures tend to form on the swellings, showing about the head, on the lips or on the nose and maxilla where the noseband of the halter crosses; on the lower part of the body where the circingle crosses, or where the part is pressed upon in lying down, and in the limbs in the flexure of the joints—behind the pastern, or knee or in front of the hock. In many cases the skin and connective tissue sloughs, and drops off exposing the muscles, the tendons or the ligaments of the joints. In other cases the tendons are involved in the degenerative process or necrosis and become detached from their lower insertions so that the toe may be turned up or the fetlock pad may come to the ground. The matrix of the hoof wall (coronary band) may separate from the horn, leaving a gaping opening which exudes liquid freely, and if the animal survives, the entire hoof may be shed.

In other cases, and often quite early in the disease, the swellings may suddenly subside and disappear, with it may be, a recovery, or, in other cases, with an exudation into the lungs or chest, the digestive organs or abdomen. In case the lungs are attacked, there is hurried oppressed breathing merging into dyspnœa or asphyxia. In case the bowels suffer there are colicy pains more or less acute, with much constitutional disturbance, marked prostration and serous or bloody diarrhœa. These mostly prove speedily fatal. Less redoubtable are those cases in which the swellings alternately subside or moderate, and reappear or increase, without implication of the internal organs. The absence of internal lesions and the moderation and intermissions, of the external ones, give good hope of the preservation of the vitality of the tissues and of recovery.

Course and Duration. These vary much with the severity of the case. In subacute and tardy cases with few petechiæ and restricted swelling in the limbs, the symptoms become remittent and recovery finally takes place after one or two months. In other cases the morbid phenomena which developed rapidly may subside as quickly and recovery occurs in a few days. In the more typical case the visible lesions may encrease or remain stationary for one, two or three weeks and then terminate in death or recovery. In the most violent types death may occur within forty-eight hours. The average duration of the affection is found to be about 16 days.

Differential Diagnosis. In typical cases of petechial fever, diagnosis is easy. The supervention on a protracted or debilitating disease of the respiratory passages of an access of hyperthermia, and marked prostration, with the appearance on the nasal or other mucosa of petechiæ and swellings of a dark red color throughout, and of cutaneous swellings in the form of nodular elevations and more extended salient patches, having a tendency to ooze blood or serum, to crack and fissure is virtually pathognomonic.

Acute glanders may resemble it but lacks the extended sloughs of petechial fever, and the nasal ulcers that form in glanders are on a yellowish base and periphery, whereas the purpura ulcer is on an uniformly dark red base, and without the elevated margin seen in glanders. In cases of doubt the mallein test is not available as the purpuric patient is already fevered, or liable to be so at any moment, and any wound in such a subject will give rise to extensive swelling.

In glanders the nodular submaxillary enlargement is almost pathognomonic and still more so if the facial lymphatic vessels are thickened (corded) and both symptoms fail in purpura. In cutaneous glanders with swollen joints or limbs the attendant pain is much more severe, and the farcy buds, forming on the thickened and indurated lymph vessels, bursting and discharging an albuminoid fluid like oil have no counterpart in petechial fever. In cases of doubt the search for the glander bacillus, and above all the inoculation of a male Guinea pig in the flank and the discovery of the bacillus mallei in the resulting exudate and diseased testicle will decide.

From anthrax and emphysematous anthrax petechial fever is distinguished by the absence of the large bacilli of these respective diseases from the exudate. It is not communicable, like anthrax, to the sheep, Guinea pig and rabbit, and does not crackle on manipulation, like emphysematous anthrax. The swellings are much more generally diffused than in anthrax and the hyperthermia much less.

Urticaria furnishes a skin eruption which may be indistinguishable from the earlier skin lesions of petechial fever, but these lesions are not associated with the petechiæ in the nasal and other mucosæ, and the swellings do not advance to great sanguineous engorgements, cracks, fissures, necrosis, and deep and extensive sores as in purpura. Urticaria is, moreover, usually traceable to some digestive disturbance and fault in feeding.

Malignant œdema is usually confined to the seat of the inoculation wound and an extension around that, the exudate is very watery and may be mixed with fetid gas bubbles, so as to crepitate slightly, and it contains an abundance of its specific, round ended bacillus, often in chain form. The carcass putrefies with great rapidity.

Horse pox affecting the pastern and limb with attendant swelling is distinguished by the absence of petechiæ on the mucosæ, and by the formation on the affected part of little pea-like papules, which early exude an abundant liquid, the concretion of which on the hairs forms a remarkable yellowish encrustation, embedded in the angry red sores beneath.

Mortality. Prognosis. The mortality has generally averaged about 50 per cent. Much, however, depends on the violence of the attack, and the reduced and worn out condition of the patient. The most hopeful cases are those in which the temperature remains near the normal, the strength and appetite are well sustained, the swellings are comparatively slight, and there is no indication of any internal complication. The unpromising symptoms are: persistent high temperature; complete anorexia; great dulness and prostration; excessive swellings not only cutaneous but in the nose and throat as well; a marked oozing from the swellings with a tendency to form cracks, fissures and sloughs; the serious obstruction of breathing and prevention of hæmatosis by blocking of the nose, pharynx or larynx by sanguineous and serous exudate; the appearance of oppressed breathing and other indications of exudate with the lungs and chest, or of colics, diarrhœa, and other suggestions of effusion on the bowels or in the abdomen. Extreme fetor of the expired air and of the fæces is a bad symptom, though not always a fatal one. Sudden retrocession of the cutaneous swellings, may be the precursor of internal exudations and death, yet in the absence of marked acceleration of the pulse, and of the objective symptoms of disease of the chest or abdomen, it is rather to be taken as a herald of recovery.

Treatment. Whatever may be the precise cause of petechial fever it is largely connected with and maintained by an unhealthy condition of the blood, and especially with the presence of toxins and waste products in that liquid. The first consideration is to secure for the patient the best possible sanitary conditions. A roomy loose box, dry, clean, well lighted and well aired, nourishing, easily digested food—green food, carrots, turnips, or mashes—and pure water are desiderata. A sunny exposure is desirable especially in winter, and everything like chill should be guarded against. Blanketing may be called for in cold weather, but the circingle like the halter should be avoided as being calculated to cause indentation, cracking or sloughing of the swellings.

A moderate action of the bowels should be secured by the nature of the food (linseed meal or tea), or by small doses of saline laxatives (sodium sulphate) or calomel. Suppression of the urine too, must be counteracted by diuretics (saltpeter, oil of turpentine) when necessary.

Further internal medication has been aimed to correct the dilatation of the capillaries, and to prove antidotal to or to eliminate the poisons present in the blood.

As vaso-motor stimulants have been employed ergot, belladonna, tannic, sulphuric and hydrochloric acids, oil of turpentine, iron sulphate, potassium bichromate and chlorate, quinia sulphate, and strychnia sulphate and arsenate. The value of any one of these is dependent on its early employment, the slight character of the lesions and the remissions that so often occur even in severe attacks. None are of much account in a violent attack at its worst.

In the slighter cases ergotin, 5 grains daily in two doses, has been apparently useful. An objection is that its continued action on the nerve centres and digestive organs is liable to prove depressing and injurious. Of the acids, tannic is liable to engender constipation, locking up the injurious products to which, however, it acts to some extent as an antiseptic. Sulphuric and hydrochloric acids have a tonic effect, and the latter is a stomachic under ordinary conditions. The same may be said of the iron salts and to some extent of oil of turpentine, which have both proved useful in favorable cases. Cadeac condemns ol. terebinth as calculated to abolish kidney secretions. The potash salts, bichromate and chlorate, and quinia sulphate are decided antiseptics and though the admissible dose would not ensure the destruction of bacteria, yet, acting in the system, with leucocytes and leucomaines, they may serve by keeping them in check. The chlorate of potash is given to the extent of an ounce the first day, and of half an ounce on succeeding days. The quinine salt is given in half ounce doses once or twice daily. In combination with bitters they seem to be of material value. Nux vomica (1 dram) or strychnia sulphate or arsenate (2 grains) given twice daily has seemed to be among the most promising agents of this class. As a potent vaso-motor stimulant, a bitter tonic and stomachic, strychnia has seemed at times to rouse the vitality and enable the system to throw off the load of poison that depresses it. The wonderful power of adrenalin chloride as a vaso-motor stimulant more than warrants its use both locally and generally. In using any one of these agents, we should not neglect concurrent attention to the bowels and kidneys, to antisepsis internally and externally, to hygienic and tonic measures generally.

Antiseptic agents have been given by the alimentary canal, the skin, the subcutis, and the air passages.

By the stomach the following have proved more or less useful in checking gastro-intestinal fermentations, and perhaps in hindering absorption of toxins from the specific lesions on this track: phenic acid, creolin, lysol, ichthyol, boric acid, salicylic acid, sodium salicylate and hyposulphite, and calomel.

To the superficial swellings, fissures and sores the same agents may be freely applied, alone, or combined with astringents, such as alum, lead acetate, aluminum acetate. In the hot season they may be applied cold, whereas in the cold weather hot applications are often preferable. Aruch claims excellent results from covering the engorged head with a woolen cloth and irrigating it with cold water.

The question of drainage of the worst cutaneous swellings by scarification, has been variously dealt with, Dieckerhoff advocating deep incisions, while Friedberger and others forbid them as encreasing the tendency to necrotic infection and sloughing. In the slighter cases it can well be omitted, but in extensive swellings the disintegrating and debilitating action on the tissues is so great as to well warrant its prevention by incisions and drainage. It is well to first give the surface a soapy wash, then apply a mercuric chloride or carbolic acid lotion and lance it in the prominent and tense portions. As a further precaution against septic infection it may then be covered by cotton soaked in one of the above lotions and covered with a bandage. For swellings beneath the abdomen or chest this may be held in place by loose circingles. Scarifying becomes imperative in case of paraphymosis arresting the flow of urine. Deep fissures and sores following sloughing may be treated with mercuric chloride solution, (1:1000), creolin or phenic acid (2:100), iodoform, dermatin, naphthalin or salol.

Disinfection of the nasal passages has been attempted by pervading the air with carbolic acid, creolin, cresyl, lysol, or naphthalin, by hanging saturated cloths in the stall, or spreading them on the floor. Perhaps a better method is to flush out the nose, by injecting each chamber in turn with a piece of rubber tubing, one end of which is introduced into the nose, and the other raised four feet and furnished with a funnel. The injection may be 1 dram creolin to 2 quarts water, or carbolic acid or alum may be substituted or alternated.

The swelling of the nostrils may be so great that it becomes requisite to hold them open mechanically. The suture of the two altogether, across above the nose has been practiced, or a tube of light wood or aluminum can be inserted in each nostril.

Injection of the trachea and bronchia with a solution of iodine 1 part, potassium iodide 5 parts, and water 100 or 200 parts, was advocated by Dieckerhoff and met with a fair measure of success in mild cases. In some cases, however, granular tracheitis and bronchitis followed, and in others necrotic tracheitis and pulmonary gangrene, so that the method has not been widely accepted. If resorted to, the weaker solution is to be preferred, and may be injected through a tracheal ring, or the membrane between two rings twice a day in doses of 3 to 5 centigrammes (45 to 75 drops).

Injection into the veins of Argentum Colloidale, 1 per cent solution in doses of 1⅔ oz. (50 grammes) at intervals of 2 hours has been very strongly advocated by Dieckerhoff who in four successive cases had complete recoveries in from three to six days. After disinfection of the skin a small trochar and cannula, or a hypodermic needle is introduced into the jugular and the injection made. Local treatment for the swellings was also applied.

Injection subcutem of the antistreptococcic serum of Marmorec, has been lauded as promptly overcoming the capillary dilatation, and enabling the leucocytes to neutralize the toxins.

Finally Menveux recommends an artificial compound as possessing all the good qualities of the antistreptococcic serum. This is composed of sodium chloride 5 grammes, sodium phosphate 1 gramme, sodium sulphate 20 centigrammes, sodium carbonate 1 gramme, caffein chlorhydrate 10 grammes, boiled filtered water 100 grammes. Inject daily in three doses 135 grammes.

PETECHIAL FEVER IN CATTLE.

Synonyms. Causes: microbes, maturity, hard work, chill, poor hygiene, drying of damp lands in summer and autumn, impermeable soils, corrupt water, bacillus, diplococcus; resemblance to hæmorrhagic septicæmia. Lesions: petechiæ and hæmorrhages on mucosæ, serosæ and skin; gelatinoid exudates gravitating to the lowest parts of face, chest, belly and legs; chaps, oozing, sloughs, depilation, exudate in tongue, bloody diarrhœa, duration 14 to 40 days, mortality light; indurations. Diagnosis: from anthrax, black quarter, malignant œdema and acute hæmorrhagic septicæmia. Prevention: avoid infecting soils in summer and autumn; drainage, cultivation; chills. Treatment: venesection: laxatives, diuretics: intratracheal injections of iodine: colloidal silver. Locally: antiseptic astringents: remove eschars: facilitate breathing by surgical or mechanical means: good hygiene.

Synonyms. Purpura Hæmorrhagica. Anasarca. Inflammatory Œdema. Yellow Water. Morbus Maculosus.

This malady presents phenomena very similar to those found in the horse, and shows itself in mild and severe types. It has been noted by writers on diseases of cattle from Vegetius down, though under quite a variety of names.

Causes. These are uncertain, though much seems to point to microbian invasion or intoxication by microbian poisons. In France, it has been seen mainly in mature and robust working oxen after a hard day’s work, when the animal has had time to cool off. Also in cows used in the yoke and milked at the same time. Poor food, starvation and low condition have also been cited as causes. In other cases, high feeding and plethora have been incriminated. It shows itself most commonly in summer and autumn, so that cold or chill must be looked on as a cause secondary to another—probably microbian or toxic. Again, it is by far the most common in the adult animal. What is more suggestive is its relative frequency in localities characterized by swamps, springy fields, hollow basins, damp hill-foots, bottom lands, and damp, impermeable or undrained soils. Again, on heavy clays where the water is preserved through summer in open ponds and often in a very corrupt condition. This at once accounts for its common appearance in summer and autumn when the offensive products of fermentation are most abundant, and corroborates the doctrine of a toxic ferment. But its origin has not been definitely traced to such products as yet. This, notwithstanding that Kolb attributes it to bacillus hæmorrhagicus, and Robert, Fabert, and Dinter found the exudates swarming with diplococci. This may assimilate it to septicæmia hæmorrhagica.

Lesions. In cattle killed during the early stages, circumscribed hæmorrhages and petechiæ are found in the nose, trachea, bronchia, gastric and intestinal mucosæ, cerebral membranes, pleuræ, peritoneum, bladder, and skin. In many cases these are accompanied by congestion and thickening of the walls of the lymphatics, and effusion in and under the skin in different parts of the body, but especially along its lower aspect—(belly, sternum, dewlap, limbs, lower jaw, tongue)—of a gelatinoid exudate, which raises the skin abruptly in the form of a thick cushion. At first this is soft and tremulous, but later it may have coagulated giving a great degree of resistance to the structure. Extensive cracks, fissures, and sloughs, and unhealthy sores form on these swellings. Franck especially notes the enlarged tongue gorged with blood and yellowish exudate as in gloss-anthrax. The blood extravasation may be further evidenced in the black or blood-streaked fæces, the reddish urine, and a rosy tint of the milk.

Symptoms. The animal is dull, sluggish, moves stiffly and with difficulty, and shows hyperthermia, (102° to 106° F.), inappetence, impaired or suspended rumination, heat of the roots of the ears and horns, and of the dry muzzle; the spine, and usually certain points beneath the sternum or abdomen at which swellings are about to appear, are tender to the touch. On the affected parts of the skin the temperature is raised, and there may be detected pea-like elevations which become surrounded and enveloped in extensive swellings that pit on pressure. The swellings show a preference for the thinner and looser parts of the skin, and gravitate rapidly toward dependent parts. Thus, the eyelids, roots of the ears, intermaxillary space, throat, muzzle, dewlap, ventral aspect of the body, axilla, mammæ, scrotum, groin, thigh, knee and hock are favorite spots, the liquid rapidly gravitating downward through the loose connective tissue to the lowest points. The face becomes infiltrated to unsightly dimensions, interrupting prehension and threatening suffocation, the dewlap swells up to a great size, the forearms or thighs become rounded and tense, and a thick pad forms along the ventral aspect of the body. The white skin on such swellings becomes red, they may ooze a yellowish liquid or blood, the surface becomes depilated, scaly and rough, chaps and cracks appear, going on, it may be, to deep fissures, more particularly at the flexures of the joints, on the throat or muzzle, or on other points that are subjected to pressure. Necrosis of great patches of skin is not uncommon, and these sloughing off leave large wounds with unhealthy, indolent surface and little disposed to rapid healing.

The petechiæ show early on the muzzle, the nasal and buccal mucosæ, and on other mucous membranes. Exudations also appear and a serous, often bloody, discharge escapes from the nose and concretes in colored encrustations around the nostrils. The nose may be obstructed causing the animal to breathe through the open mouth, protruding the tongue which is often also the seat of extensive swelling, discoloration and induration.

As the disease advances there is encreased dullness and prostration, marked emaciation, and anæmia, sunken eyes, encrusted eyelids, extensive areas of depilation including even the long hairs of the tail, and quite often an abundant bloody diarrhœa.

The affection may last for 24 to 40 days and under rational treatment the majority survive. There remains, however, in a certain number of cases, a permanent enlargement and fibrous induration from the organization of the exudate.

Diagnosis. A fully developed case is easily recognized. The fever and constitutional disorder, complicated by petechiæ on the mucosæ and skin; the extensive swellings suddenly formed, oozing serum or blood, and tending to fissures and necrosis; and the discharge of blood from the nose, bowels, kidneys and udder, in the absence of the bacilli of anthrax, emphysematous anthrax, malignant œdema, and wildeseuche; the slower progress; the low mortality; the occurrence on a damp, springy, or impermeable soil, or one known to produce this disease; and especially if in late summer or autumn, become virtually pathognomonic.

Prevention. Seclude cattle in late summer and autumn especially, from soils known to be productive of this affection and above all from damp wet clays, underlaid by hardpan, from swamps, from drying up ponds and basins, from wet river bottoms and deltas and from springy fields generally. Fields of this kind may be reserved for cultivated crops or for raising hay. The fundamental remedy is thorough drainage, and a subsequent abandonment of the land for a year or two to other crops to allow of a dissipation of the poison. Sudden chills after being heated or fatigued, and exposure in the pasture in cold nights are to be avoided.

Treatment. The French writers up to the present extol bleeding for the early stages. Its benefit must apparently depend on the diminution of the blood tension allowing the distended capillaries to resume their normal contractility, and in the lessening of the tendency to exosmosis, and the encrease of endosmosis so that much of the poison in the blood is removed and what remains is largely diluted and rendered comparatively harmless. However well this may operate in the strong and plethoric, it cannot be considered as applicable to the weak or anæmic, nor to advanced cases in which the vital powers are already seriously reduced by the abundant exudations and extravasations, and by the narcotic and devitalizing action of the circulating toxins.

With us the demand is usually met by laxatives and diuretics, under the idea that these are less debilitating and that if the morbid process can be arrested recovery is more prompt and perfect. A purge of sulphate of soda is followed by full doses of nitrate or acetate of potash, in combination with iodide of potassium, or chlorate of potash; or bicarbonate of soda associated with hyposulphite of soda. These or other diuretics should be pushed so as to produce free diuresis. Stimulating antiseptic diuretics like ol. terebinth, may be added. Iodine solutions injected into the trachea have been recommended as for the horse (Huber, Heuberger, Rohr,) and the serum or silver preparations or adrenalin may be tried.

Locally astringents and antiseptics have given good results. Solutions of alum or lead acetate with carbolic acid and iodine; frictions with soap liniment, with a mixture of aqua ammonia, oil of turpentine and oil, or with mixtures of oils of origanum, cajeput and peppermint, and iodine, or simple painting with tinct. of iodine may be cited. Fissures and open sores may be dressed with mercuric chloride solutions (1:1000), Lugol’s solution, phenic acid lotion, solution of creolin, lysol, or chloronaphtholeum, camphorated spirit, or other antiseptic agent. The nose should be injected, cleared of eschars, and if necessary propped open.

An abundant, wholesome, easily digested diet, pure air, a dry stall and protection against cold are essential.

CHICKEN CHOLERA. FOWL CHOLERA. CHICKEN TYPHOID. CHICKEN PASTEURELLOSIS.

Definition. Historic notes. Bacteriology: Bacterium choleræ gallinaceæ, nonmotile, with polar stain, bleached by iodine, non-liquefying, causes septicæmic lesions. Lignieres’ bacillus, culture features non-gasogenic, acidifies dextrose; vitality in disinfectants; survives drying. Accessory causes: new birds in flock, or eggs for hatching, mingling of flocks, manure, watershed, streams, ponds, dust, wild birds, buzzards, rabbits, insects, infected soil. Susceptible animals: hens, doves, peafowl, pheasants, parrots, ducks, small birds, guinea pigs, rabbits, white and gray mice. Effect on sheep, horse, man, cow, frog. Incubation 18 to 48 hours. Symptoms: in fulminant cases rarely seen, in acute, anorexia, depression, debility, apathy, ruffled feathers, sunken head, neck, wings, tail, tremors, nasal and buccal discharge, hyperthermia, sighing, violet comb and wattles, thirst, pultaceous fæces, later glairy, green and fetid. Temperature becomes subnormal, inability to rise, stupor, convulsions, death in 1 to 3 days. Mild cases last 7 days. Cases caused by one microbe have slough only. Lesions: congested, petechiated, hæmorrhagic intestinal mucosa; contents of bowels watery, frothy, bloody; epithelial degeneration and desquamation; abrasions, croupous exudates, enlarged congested lymph glands, fermenting contents of crop. Petechiæ general, spleen and liver swollen, congested, friable; kidneys congested; lungs hyperæmic or blood gorged. Blood diffluent with microbe. Anæmia. Emaciation. Arthritis. Diagnosis: by rapid spread, infection origin, early excessive mortality, hæmorrhagic lesions, microbe in blood and liquid ingesta. Prognosis: Mortality 90 to 95 per cent. at outset. Prevention: Quarantine new birds, inside screens in summer; burn or acidify manure; exclude buzzards, vermin, wild birds, and visitors; separate sick, kill, burn, disinfect; divide infected flock in small lots; prevent wandering in fowls, destroy insects. Phenic acid subcutem. Immunization: inoculate in breast with one microbe (Salmon): or with weakened virus (Pasteur). Limitations. Treatment: gastric and intestinal disinfection—copperas, mineral acids, carbolic or salicylic acids, aromatics, quinine, naphthol, tar, phenic acid subcutem.

Definition. A febrile hemorrhagic septicæmia of chickens and other fowls (pigeons, ducks, geese, parrots, etc.) communicable to certain rodents and other animals, and characterized by a short incubation, rapid progress, great prostration, violent diarrhœa usually greenish, and a high mortality (90 to 95 per cent.).

History, Geographical distribution. It is quoted as prevalent in Lombardy in 1789, in East India in 1817, in France in 1825, and generally in Europe and America in the last half century.

The losses from the ravages of this disease are far greater than the average value of the individual animal would lead one to suppose, but with domestic fowls numbering 300,000,000 and a yearly egg crop bordering on a billion dozens it may well be called enormous.

Bacteriology. Chicken cholera is caused by a very small ovoid bacterium (B. Choleræ gallinaceæ) about 0.3 to 1.8μ long, as found in the blood and tissues of the fowl. It has the general characters of the groups which cause hemorrhagic septicæmia, thus: 1. It fixes, above all at the poles, the ordinary anilin colors; 2. It is decolorized by the methods of Gram and Wiegert (iodine solutions); 3. It grows on gelatine without liquefying it; 4. It produces acute septicemic lesions; 5. It tends to polymorphism when grown under different conditions. In the peritoneum of the guinea pig it forms cocco-bacilli tending in acute and violent cases to diplococci. Fed to rabbits it appears in the fæces as a minute bacillus. Even the mode of staining causes a difference in appearance. Fixed in alcohol-ether, and then stained in Ziehl’s phenated preparation, coloring is polar, and the central area clear. If in place of Ziehl’s fluid, hot fuchsin solution is used warm for ½ a minute, bacillus or cocco-bacillus is shown (Lignieres). It is nonmotile, though some observers have been misled by Brownian movements. There are no flagella. In old bouillon cultures short chain forms are met with. No spores are formed.

From fresh cultures, in flask or in animals, the bacterium grows readily in alkaline culture media. In bouillon a turbidity ensues, and after some days pellicles form on the surface and walls, and the liquid slowly clears. The addition of a little blood serum, sugar or glycerine encreases and hastens the growth, while acid retards or prevents. This is common also to other septicemic germs. In gelatine growth is tardy, but in two or three days there are whitish glistening colonies, becoming opaque later, and appearing granular if slightly magnified. In punctures minute colonies form along the line of culture and one at the surface, at first translucent; later opaque. On agar the colonies grow faster with similar appearance. On gelose at 37° C. the colonies are blueish and iridescent, at first, and later opaque. If the germ has been repeatedly passed through the Guinea pig, they are more translucent. On potato with alkaline surface, there is a delicate grayish yellow growth after 48 hours; if acid, growth ceases. In milk there is no coagulation nor acidification for four weeks; then it becomes slowly clear and opalescent. With sugars it is not gas producing. With dextrose it forms an acid solution; with saccharose or lactose an alkaline one. Cultures in peptone gave a strong indol reaction (V. A. Moore). Lignieres found no indol in cultures in pancreatic bouillon.

The bacterium perishes when heated to 58° C. for fifteen minutes. It dies in carbolic acid solution (1:100) in five minutes; in sulphuric acid solution (0.25:100) in ten minutes; in lime water in ten minutes; and in sulphur fumes in three hours. Easily destroyed by disinfectants, it remains potent for months in flasks or buildings that are not subjected to disinfection. It is not killed by drying (T. Smith and V. A. Moore) nor by zero temperature maintained for seventeen hours.

The cultures, especially those made in agar have a very characteristic odor.

Accessory Causes. Birds sent to poultry shows will often contract the disease and introduce it into the home flock on their return. It may also be imported in newly purchased birds, or on eggs obtained for hatching. It is even alleged that it has been propagated by feeding healthy hens on the eggs of diseased ones. When chickens run at large it passes easily from flock to flock in the immediate vicinity. The infected manure is, however, the most common channel of infection. Carried on the feet or bill this contaminates the food and drinking water, and washed into streams and ponds, it finally in any case reaches the alimentary canal of the susceptible bird. Or drying up and raised as dust it is inhaled into the lungs. Or finally from any such source it infects any open sore. As granivorous birds, wild and tame, suffer from fowl cholera, it is often introduced by the wild, especially coming from infected poultry yards. Predatory birds, like hawks and buzzards, but the latter especially, are common bearers of infection. Rabbits, which contract the affection so readily, transmit it equally with birds, but man or beast, soiled by the manure will convey it. Insects are among the most prolific bearers, hence, as noted by Salmon, the infection may fail to overstep a close fence in winter, but is subject to no such limitation during the fly season. In this respect chicken cholera agrees with Asiatic cholera, typhoid fever and other affections in which the virus abounds in the alvine discharges. The sale and transportation of the guano from the infected poultry yard is a direct cause of new outbreaks. Feeding on the carcasses or offal of the infected birds is a further cause. It must not be forgotten that the microbe is largely saprophytic, living indefinitely in the organic matter in soils, and determining new outbreaks when brought in contact with susceptible animals. Thus a period of immunity may be followed by infection when new birds are brought in or when young and susceptible ones grow up.

Susceptible Animals. Fowl cholera is preëminently a disease of chickens, but the microbe is successfully transferred to pigeons, peafowl, pheasants, parrots, ducks, canaries, sparrows and other small birds, also to Guinea pigs, rabbits, white and gray mice. Guinea pigs have abscesses in the seats of inoculation (Pasteur); the same is alleged of sheep and horses (Kitt), and man (Marchiafava, Celli). Injection into a cow’s teat caused chronic catarrhal mammitis in which the microbe persisted for a long while (Kitt). Like other members of the group of microbes causing septicæmia hæmorrhagica, the pathogeny and even the morphology are liable to material modification as grown in different environment (genera). Some of the forms of cholera occurring among domesticated birds and held to be distinct diseases may find in this an explanation. Rabieaux claims that under favorable conditions it has been transmitted to the frog.

Incubation. This varies from 18 to 48 hours, the usual being 24 hours.

Symptoms. In some fulminant cases the animal is found dead a few hours after apparently blooming health; it may even have died on the nest or fallen dead from the roost. Cadeac speaks of transient symptoms even in such cases—extreme dulness, prostration, somnolence, seclusion in a cool, dark place, ruffling of feathers, sinking of the head between the wings, drooping, trailing wings and tail, violet comb, gaping, discharge of glairy mucus from the bill, convulsions and death. These symptoms last from two to five hours.

In acute but less fulminant forms there is loss of appetite, depression, debility, apathy, erection of the feathers, sinking of the head, swaying when made to walk, drooping wings and tail, sitting on the breast, convulsive tremblings, discharge of filmy or frothy mucus by the nose or mouth, vomiting, hyperthermia (108° to 111° F. ), sighing, breathing, inflation of the crop, violet colored comb, wattles and mucosæ, great thirst and diarrhœa, at first pultaceous and light yellow, later glairy, green and fetid. The feathers round the anus become soaked and matted with the discharge. Temperature becomes subnormal, the patient falls and is unable to rise, and finally dies in a stupor or convulsions, the illness having lasted 1 to 3 days.

Milder cases occurring chiefly towards the end of an outbreak when the less susceptible animals only are left, or when the microbe has become less virulent, show a larger ratio of recoveries. These show a lack of spirit and vigor, impaired appetite, diarrhœa, emaciation, dulness, prostration, moping, ruffling of the plumes, dark discoloration of the comb, and often swelling of one or more important joints (femoro-tibial, etc.). These may burst and discharge a reddish pus, or simply form dark or grayish swellings. These cases may drag along for a week or more and finally die in marasmus. The minute bacillus is not obtainable from these (Lignieres).

Cases inoculated in the pectoral muscles with only one or two microbes usually have only a circumscribed slough, with loss of condition, and after the elimination of the slough and the healing of the sore the bird proves immune.

Lesions. The alimentary canal is the main seat of morbid changes. The intestinal walls, and especially the mucosa, have points and patches of blood extravasation, extensive areas of congestion with ramified redness, exudation and thickening. The intestinal contents are watery, frothy, browned or blackened by effused blood, and swarming with ferments including the specific bacterium. The mucous surface is brownish or blackish, and epithelial degeneration and desquamation with abrasions are not uncommon especially on the summits of the duodenal folds and villi. Croupous exudates and swelling or ulceration of the follicles are met with. The lymph glands at the base of the cæcum are often enlarged and congested. The crop is full of watery, pulpy, frothy or slimy contents, and its mucosa and that of the pharynx may be deeply congested.

Elsewhere the lesions suggest rather the action of destructive toxins and the profound changes in the blood. Pericardium and endocardium are usually studded with dark petechiæ, and congestion and even slight exudation may be present. The spleen is enlarged, soft, and gorged with blood. The liver is swollen, congested, extremely friable, and mottled, grayish white from degenerations. The kidneys are dark red, and friable. The lungs may show slight hyperæmia only, or a blood engorgement and consolidation, and are then easily reduced to a dark red pulp. Friedberger and Fröhner say that respiratory changes are most frequent in land birds; and intestinal and cardiac in water fowl.

The blood is diffluent coagulating loosely if at all, of a brownish red color, reddening slowly and imperfectly in contact with air, and like the tissues contains an abundance of the characteristic bacterium staining deeply at the poles and clear in the center.

In birds that survive a few days there are marked anæmia and emaciation, and the muscular system is of a grayish red color, with fatty degeneration. In acute and fulminant cases on the other hand the muscles may be full and of the normal red color.

In arthritic cases the congestion and thickening of the soft tissues, and the excess of synovia, are supplemented by destruction of the articular cartilage and by areas of bone abrasion. In the more tardy cases collections of caseous matter are found.

Diagnosis. This is based on the demonstrably highly contagious character of the disease, its rapid spread in a flock, and from the first to nearby adjoining flocks in summer, the short period of incubation, the constancy and nature of the diarrhœa, the speedy and great mortality, and the hemorrhagic lesions of comb, bowels, heart, lungs, liver, kidneys, spleen, and serous membranes. The demonstration of the bacterium in the blood and affected tissues is conclusive. Kitt points out that inoculation of a pigeon kills the bird in 12 to 48 hours, with dry yellow exudate in patches of from ½ to ¾ inch in diameter on the surface of the muscles, and yellow discoloration and nodular induration beneath.

Prognosis. The mortality reaches 90 to 95 per cent. The negative chemiotaxis exerted on the leucocytes by the microbe, precludes defensive phagocytosis, and the progress of the deadly microbe is comparatively unhindered. Toward the end of a severe outbreak, and in certain mild epizoötics the recoveries are much greater.

Prevention. All birds bought or otherwise acquired and all birds returning from shows should be quarantined for one week before being allowed to mingle with the flock. In summer this should be conducted inside fly screens. The manure should be burned, carefully secluded, or treated with dilute sulphuric acid. Buzzards and vermin as possible bearers of the infection should be excluded from poultry yards. So with human beings, dogs, etc., coming from infected places. In an infected flock the sick should be at once separated, killed and burned or treated with sulphuric acid. All manure should be treated in the same way. Buildings, yards and runs should be thoroughly cleaned and liberally sprinkled with a dilute sulphuric acid (2:100). If the birds can be divided up in small groups (say of 5) the appearance of the disease will only endanger that group. In small flocks or with very valuable birds it may even be well to take the body temperature morning and night and separate at once any bird showing a rise. Any diseased or suspected flock should be kept where its manure will not be washed into wells, running streams or ponds to which other birds have access. In a locality where the disease exists fowls should not be allowed to run at large. In winter this is very effective; in summer owing to the danger from insect bearers, it must be supplemented by the most scrupulous cleanliness of poultry houses and yards, and by a liberal sprinkling with dilute sulphuric acid, or other disinfectant, to be made especially abundant and frequent on the manure. Nocard cuts short the disease by injections, subcutem of a 5 per cent. solution of carbolic acid.

Immunization. With valuable birds it may be desirable to secure immunization by non-fatal inoculations. Salmon secured this by first estimating the number of microbes in an mm. of the blood, then diluting until five drops would contain but one, or at most two of these organisms, and injecting this amount into the pectoral muscles. A sequestrum forms in the muscle and is gradually sloughed out, and the cavity heals, with resulting immunity.

Pasteur produced a weakened virus by exposing the artificial bouillon cultures to air for from three to ten months, the strength decreasing with the length of exposure. The weaker form produces slight illness only, from which recovery is prompt. A second and stronger virus is used ten or twelve days later and produces a real immunity.

The drawbacks to these methods are: 1st; that fowls are of too little value, to warrant inoculation in healthy flocks; 2d; that in infected flocks, where it is employed, the more susceptible birds are usually already contaminated, and a large proportion die in spite of it; and 3d; that it becomes a means of planting the infection in new localities (Kitt).

Treatment. The disease is so deadly that little can be hoped from medicinal treatment. It has been directed mainly to gastric and intestinal disinfection. Copperas and sulphuric or hydrochloric acid in the drinking water ½ to 1 per cent. of each is at once prophylactic and curative. Friedberger and Fröhner add fennel or peppermint, and give a tablespoonful every hour to an affected chicken. Other agents recommended are: carbolic acid (5:100) by the mouth or subcutem (Nocard), salicylate of soda, quinia (Cadeac), tannic acid (2:100), salol, naphthol, tar water, etc.

DISTEMPER IN DOGS AND CATS.

Definition. Synonyms. Animals susceptible: dog, fox, jackal, hyena, wolf. Historic notes. Causes: contagion, inoculation, immunity, contact with sick, clothing, bedding, kennel: infection fixed—little diffusible, dogs at large, chill, domestication, high breeding, special breeds, shows, public conveyances, vegetable diet, debilitating conditions, catarrhs, change of climate, recurrent attacks, youth, native susceptibility, teething. Microbiology: micrococci, bacilli, mixed cultures, Shantyr’s observations, Lignieres’. Virulent products—all secretions and exudates. Vitality: virus survives drying, freezing, dilution in water. Destroyed by disinfectants. Forms of distemper: catarrhal, ophthalmic, cutaneous, gastro-hepatic, bronchitic, pulmonary, nervous. Duration 20 to 30 days. Mortality 20 to 70 per cent. Prognosis: unpromising conditions. Incubation 4 to 7 days. Symptoms: hyperthermia (103° to 104°), dulness, debility, anorexia, staring coat, tremors, seeking warmth, early fatigue, dry burning nose and footpads, irregular temperature, simultaneous congestion of all visible mucosæ; Respiratory phenomena; sneezing, congestion of nose, discharge, blocking, snuffling, rubbing, cough, retching, vomiting; percussion flatness in lungs, in islets or along the lower part; auscultation râles, wheezing, crepitus, creaking, etc.; epiphora, swollen eyelids, weeping, photophobia, muco-purulent discharge, sticking of lids together, opacities, vesicles, ulcers; red, hot, buccal mucosa, costiveness, fetid diarrhœa, tenesmus, weakness, emaciation; skin eruption, on delicate areas, papules, vesicles with colored contents, pustules, sticky, greasy exudate; irritability, restlessness, taciturnity, depraved appetite, spasms, delirium, paresis, epilepsy, chorea. Lesions: inflammation, degeneration, ulceration on air-passages, alimentary tract, lymph glands, kidneys, liver, cerebral and spinal meninges, leucocytic infiltration: offensive odor. Lignieres’ views of microbes. Prevention: quarantine new dogs for 14 days, wash, disinfect all collars, etc., avoid shows and meetings, exclude street dogs, protect against mice, rats, birds, shut up all dogs during an epizoötic; separate a pack into small lots; seclude the sick and all belonging to them. Immunization: by lung exudate, by weakened cultures. Treatment: hygienic, dietetic, warm baths, antipyretics, antiferments, calomel, phenic acid, eliminants, expectorants, collyria, emetic, demulcents, bismuth, etc., pepsin, quinine, nerve sedatives, tonics.

Definition. A contagious, febrile affection attacking dogs (and by inoculation cats), and tending to local inflammatory and degenerative lesions in the mucosæ, lungs, bowels, liver, skin, kidneys, and nervous system,—a first attack usually immunizing against a second.

Synonyms. Contagious catarrhal fever; Dog ill; Bronchial Catarrh; Intestinal Catarrh; Fr. Maladie des Chiens, Maladie du jeune age, Typhoïde, Typhus des chenils, Variole du chien; Ger. Staupe; It. Cimurro.

Animals susceptible. Dogs, especially puppies and young dogs, and other members of the canine race, fox, jackal, hyena, wolf. Cats suffer from inoculation (Laosson), also apes (Cadeac). Old cats and dogs are often immune, also all animals that have passed through one attack of the disease.

History. The older English veterinarians quote the epizoötics in dogs described by Virgil, Aristotle and even Homer as probably distemper. Laosson attributes to it a canine epizoötic which prevailed in Bohemia in 1028. It appears to have been unknown in Europe in the earlier third of the 18th century though prevailing in Peru. According to Ulloa, it was introduced from Peru into Spain in 1735, whence, it spread into France (1740), Germany (1748), Ionian Isles, Greece (1759), England (1760), Italy (1764) and Russia (1770), Sweden and Norway (1815), Siberia (1821). Since that time it has prevailed in Europe and many dependencies of European nations.

Causes. Its advent in Europe as a new disease in the second third of the 18th century, its steady spread, its continued prevalence, and extension, concur with the infection of kennels and districts by the introduction of a sick dog, in demonstrating its purely contagious nature, and this implies a living microbe transferred from animal to animal. If any doubt remained it must be dispelled by the inoculations which have been constantly successful when made on young puppies, or dogs that have not previously suffered, and on cats. A first attack confers immunity.

Among accessory causes may be especially named contact with the sick dog, its clothing or bedding, and above all its kennel. A kennel may retain infection indefinitely, especially if there is a constant accession of puppies or susceptible dogs. On the contrary it is not readily carried on the clothes of attendants, and the inmates of a kennel often remain sound, though only separated by a yard from the infected one, and though cared for by the same attendant. Yet so universally diffused is the contagion that few dogs escape it until they are a year old.

The habit of letting dogs run at large, to meet in roads and fields is a most prolific cause, which might easily be done away with where distemper is prevalent.

A chill is a common condition, hence injudicious washing, swimming in cold water, exposure of house dogs to cold storms, or outdoors at night, sleeping in cold, damp cellars, on cold stones or metal plates, or in passages in a current of cold air are frequent factors. Yet it often spreads rapidly in the summer, the heat favoring the preservation and diffusion of the germ.

House dogs as a rule suffer more severely, as their systems are more sensitive to the cold, and the resisting power to invading microbes is lessened. Country dogs and those living in the open air are hardier and more resistant and often have the disease in a mild form.

High bred dogs suffer more severely probably largely from the greater protection and care lavished on them and their consequent diminished power of resistance. Newfoundlands, great Danes, pointers, pugs, poodles, spaniels and greyhounds may be named as especially liable.

The exposure to infection at shows, and in traveling by rail, steamboat or other infected conveyance must be considered as among the prominent causes.

An exclusively bread diet has been recognized as a predisposing cause, by reason of its lowering the stamina of the carnivorous animal.

Any condition which induces debility whether severe or continued disease, parasitisms, impure air, under feeding, improper food, rachitis, or scurvy, etc., must be admitted to operate in the same way. Any catarrhal disease of the nose or bronchia is especially conducive to the affection by weakening the mucosa and making an easy entrance channel for the germs.

Change of climate is a strongly predisposing condition, which not only hastens an attack, but even, at times, arouses anew the susceptibility in dogs that have passed through a first attack. Dogs that suffered in England have had a second attack in India, and some have even had a third attack when brought back to Europe. Four attacks within a year, in the same dog, and without change of climate, are recorded by Friedberger and Fröhner.

Youth is much more susceptible than age, even apart from the immunity which comes to the mature dog from a first attack. Yet some puppies are insusceptible from birth.

Microbiology. No one pathogenic organism has been proved to be the constant infecting agent, yet two classes of investigators have contended in favor of micrococci and bacilli respectively.

Micrococci, 1 to 3μ in diameter, singly or in chains of 6 or 8 have been found in the blood, lungs, liver, kidneys and spleen (Semmer, Friedberger, Krajewski, Rabe, Mathis, Marcone, Meloni, Kitt).

Bacilli were found associated with micrococci by Semmer, Legrain and Jacquot, Laosson, Millais, Schantyr, and Galli-Valerio. As observed by the latter they were 1.25, to 2.5μ long, by 0.31μ broad and took the Gram stain. Cultivated on gelatine the colonies were waxy, lustrous points, which indented the gelatine without liquefying it.

Cultures of the mixed bacteria (cocci and bacilli) and their inoculation on young dogs produced the symptoms of distemper with subsequent immunity (Laosson, Millais). Legrain and Jacquot claimed immunity, as resulting from inoculations with the cocci in pure cultures. Galli-Valerio, using the mixed cultures produced all the symptoms (pulmonary and cerebro-spinal) of distemper.

Schantyr, ignoring the cocci, describes three bacilli which cause three different diseases (distemper, abdominal typhus, and typhoid), but the distinctions are not clear nor generally accepted.

Lignieres and Even, in Argentina, and dealing with the more susceptible high bred dogs (fox terriers, great Danes and carlins), found constantly in the blood of the dog, in the early stages of the disease, a long, delicate bacillus, nonmotile and easily stained in aniline, but not by Gram’s method. Inoculated on the Guinea pig it shortens, approximating rapidly in successive passages to a cocco-bacillus, and assumes the general characters of Lignieres’s pasteurella. Different bacteria may be found in the lungs, bronchial and nasal mucus, tears and vesicles.

Lignieres’s pasteurella is inoculable on the Guinea pig, mouse, rabbit, and dog, producing the symptoms of local or general infection. Two centigrammes, subcutem, in the Guinea pig, produced a local œdema, disappearing in four or five days and securing immunity. Five cc. subcutem proved fatal in 48 hours; intraperitoneal in 24 hours. In the rabbit 1cc., subcutem, caused local œdema for 2 days and hyperthermia (104°) for 3 days; 1cc. intravenously, caused fever for 3 weeks, diffluent blood and hæmorrhagic lesions in lungs, liver, kidneys, bowels, spleen, and serosæ. In the mouse, 4 to 8 drops, subcutem, caused œdema, and recovery or death in 2 to 4 days. In such cases the microbe was found in pure cultures in the blood or inoculated tissues.

Inoculations of the pure cultures on dogs produced in different cases, gastro-enteritis, pneumonia, pleuro-pericarditis, and arthritis, in various combinations. If the animal survives it is immune.

Grown on peptonized bouillon, neutral or slightly alkaline, the bacillus forms, in 24 hours, small granular colonies which fall to the bottom, leaving the liquid clear. The addition of serum renders this more abundant without causing opacity.

On pancreatic bouillon the growth is very free without indol.

On gelatine plates there are fine punctiform colonies, transparent, but becoming white and opaque in 8 or 10 days. Similar colonies form in stab and streak cultures. The gelatine is not liquefied. Cultures in milk cause neither coagulation nor acidity. There is little or no growth in hay tea, on potato, nor in vacuum. The cultures have the peculiar odor of the pasteurella.

Virulent Products. Infection is present sooner or later in all the morbid animal products. The nasal mucus, bronchial exudate, saliva, tears, contents of the cutaneous vesicle, milk, contents of the bowels, and the blood have been successfully inoculated on susceptible subjects. Inoculations with blood failed with Bryce, but proved successful with Konnhauser, Krajewski, Even, Lignieres and Physalix, so that the first named cases may be explained by a prior immunity, or by a too advanced stage of the case which furnished the matter. The virulence is not lost nor even diminished by drying at ordinary temperatures, freezing (10° F.), nor by moderate dilution in water. Prolonged exposure at ordinary temperature, however, reduces the virulence, which is greatly impaired in 15 to 25 days (Laosson), or, if dried, in three months and upward (Krajewski). Virulence is easily destroyed by disinfectants,—thorough washing (Menard) hypochlorous acid (Trasbot), chloride of lime, mercuric chloride, etc.

Forms of Distemper. This disease is extremely protean in its manifestations. Many cases, in country districts especially, are manifested by a slight fever, with a catarrhal condition of the mucosæ of the nose, eyes, and throat. In other cases there may be simply a slight conjunctivitis or keratitis, and in still others a cutaneous eruption, papular, vesicular or pastular. In some instances there is slight gastric or hepatic disorder with inappetence nausea, and vomiting or some irregularity of the bowels. In such cases recovery may take place in eight or ten days.

In the more severe forms, especially seen in house and city dogs, and in high bred and confined dogs generally, the fever is high and persistent and the disorders often predominate in particular organs, hence we see a catarrhal form, a conjunctival, a bronchitic, a pulmonary, a gastro-intestinal and hepatic, a cutaneous and a nervous. The severe cases may last for twenty or thirty days or even in their sequelæ for several months. Exposure to cold contributes greatly to a pulmonary attack even in inoculated cases (Lignieres).

The mortality varies greatly. In country dogs it may be below 20 per cent., whereas in city dogs and those kept confined in close quarters and in large numbers it may rise to 50, 60 or even 70 per cent.

Prognosis is especially unfavorable in severe cases; in those profoundly affecting the brain, lungs or liver; in high bred or pampered dogs; in the very young; in the debilitated, anæmic or rhachitic; in those that have been recently imported from another climate and are as yet unacclimated. Puppies from debilitated dams, or those raised in a large litter with insufficient nourishment, or older dogs confined to a purely vegetable diet show less power of recuperation. Profound prostration and offensive odor, from excess of toxins are always to be dreaded.

Incubation in inoculated cases varies from four to seven days (Krajewski). When contracted by simple exposure it may seem to have been extended to fourteen or even eighteen days.

Symptoms. The earliest symptom is hyperthermia (103° to 104° F.) This is accompanied and followed by prostration, dulness, impaired appetite, erection of the hairs along the spine, shivering, trembling, seeking a warm place, fatigue on slight exertion, hot dry nose, burning pads of the feet, sometimes taciturnity. Later the temperature may descend even to the normal or there may be alternations of rise and fall. One of the most characteristic symptoms of distemper is the implication of more than one set of organs, so that morbid manifestations referable to the nose, eyes, throat, stomach, skin and nervous system occurring in the same subject are to be especially noted. In enumerating the prominent symptoms caused by disease of one set of organs therefore, it is not to be implied that the absence of others referring to a different class of organs is to be understood. On the contrary a complication of several is especially significant of this disease, though the predominance in one class of organ will signify a special form of the disease.

Respiratory Symptoms. One of the earliest symptoms is usually sneezing with redness of the nasal mucosa, followed by a muco-purulent blocking of the nose, and rubbing of it with the paws. With the implication of the throat there is usually local tenderness and a hard, painful cough, which may be accompanied by retching or vomiting. The breathing becomes snuffling, especially in pugs and bull dogs, and rapid and even oppressed in case of implication of the smaller bronchia and lungs. The nostrils may become glued together, the discharge red or dark in color, vesicles and sores may appear on the mucosa, and the cough gets paroxysmal, small, weak and husky or gurgling.

Percussion of the lungs may reveal small areas of flatness from exudate or collapse, and in case of pleurisy and hydrothorax there is a lack of resonance up to a given horizontal line, varying in position according to the position of the animal and always keeping to that part of the thorax which may at the time be lowest. Auscultation will reveal various sounds according to existing lesions. There may be a loud blowing murmur over the large bronchia, or at points to which this sound is conveyed through consolidated lung. Or a coarse or fine mucous râle may be present indicating the second stage of bronchitis, or a line of crepitation, around a non-resonant area indicating pneumonia, or there may be friction sounds or, later, creaking murmurs from false membranes. Wheezing and sibilant sounds are not uncommon, also sounds of the heart, bronchia or bowels, heard in unwonted situations to which they are conveyed through consolidated lung tissue. Dyspnœa may become extreme, with puffing out of the cheeks, labial soufle, and violent inspiratory action. Fœtor of the breath is common. Emaciation, marasmus, sunken, pale or dark red eyes, putrid diarrhœa and nervous disorders usually precede death.

Eye Symptoms. Conjunctival congestion is one of the earliest and most constant symptoms. Weeping, swollen eyelids and red turgid mucosa. Photophobia may bespeak keratitis. Soon the watery tears become muco-purulent, matting together the lashes and even the lids, during the night especially, so that they must be sponged to get them apart in the morning. The exudate may accumulate under the lower lid, or may become flocculent, and usually flows down the cheeks causing matting and even shedding of the hair. Vesicles exceptionally appear on the conjunctiva; more frequently it becomes cloudy and opaque, and at points near the centre, degeneration of the epithelium leads to the formation of ulcers no larger than pinheads, but extending into the cornea and sometimes perforating it so as to allow protrusion of the membrane of Descemet or the escape of the aqueous humor. The formation and extension of the ulcers are favored by the general debility, the rubbing of the eye with the paws, and the infection of abrasions, by pus microbes. This infection may extend to the lining member of the anterior chamber and even of the posterior with panophthalmia, but, in the absence of perforation, internal ophthalmia is rare. When the ulcers heal, white cicatricial spots, or black points caused by the adhesion of the uveal pigment remain.

Digestive and Hepatic Symptoms. Anorexia and vomiting may usher in the disease. Buccal congestion, dryness, clamminess and fœtor are marked symptoms and there may be some yellowness of the mouth and eye. The patient is at first costive, but diarrhœa often sets in early, with tenesmus, much fœtor, mucus, froth and even blood, also abdominal pain and tenderness. The abdomen is habitually tense and contracted. The alvine flux may rapidly exhaust the animal, or it may continue for a month in dysenteric form with intense fœtor, weakness, emaciation and exhaustion. Ulceration of the mouth, gums and rectum, invagination, prolapsus ani, jaundice, septic pneumonia, paralysis, chorea, convulsions, or cutaneous eruptions are occasional complications. The abdominal type of distemper is especially fatal. Even in its early stages debility, prostration and even drowsiness are marked features.

Cutaneous Symptoms. Skin eruptions are observed in the great majority of cases, at some stage of the disease, and may remain as a sequel for a time after apparent recovery. Friedberger and Fröhner note cases in which the high fever and skin eruption are the only prominent symptoms, and recovery may be looked for with some confidence. The lesions are most patent on white skinned dogs with short hair, and on the more delicate parts of the skin (abdomen, scrotum, perineum, inside of the thighs and elbows) but they may extend over the whole body and even extend on the mucosæ. They vary much in different cases and stages. There may be punctiform reddish spots, changing to hard elevated papules, and, in the case of a certain number, to vesicles and even pustules. Some vesicles may be small and pointed, but more commonly they are rounded and flat, and as large as a lentil or small pea. When first formed, the contained liquid exudate may be clear and transparent, but often it is reddish or even violet. The individual vesicles tend to speedily burst, and dry up, but others appear, and thus the eruption will continue for weeks, the skin meanwhile exuding a sticky, greasy, offensively smelling exudate which mats the hairs together. Itching is usually slight, yet in given cases excoriations and sores are produced with considerable moist discharge. It tends to spontaneous recovery when the general health improves and appears to be little affected by local treatment.

Nervous symptoms. These are shown more or less from the beginning. The great dulness, depression, apathy and weakness, which usually usher in the disease, are indications of this. Drowsiness may be early shown. Even the early nausea and vomiting may be largely central in its origin. In some cases, however, the brain symptoms are more active and violent. The dog is restless and irritable, getting up and moving from place to place, starting from sleep, yelping, snapping, with twitching of the muscles of the face or limbs, rolling of the eyes, and excessive heat of the head. Krajewski even describes rabiform paroxysms, depraved appetite, spasms, furious delirium, fawning, or threatening, and finally paraplegia and maxillary paralysis Occurring in a country where rabies is familiar it would have been more satisfactory if inoculations had been made from such cases with results negativing rabies. Epileptic attacks may appear at any stage of the disease. Chorea, tonic spasms, paresis and paralysis are on the contrary habitually late manifestations and often seem to be sequelæ determined by toxin poisoning of the nerve centers, or degenerations of their structure. Choreic movements may be confined to the head, or a limb, or they may affect the whole body. Tonic spasms often affect the neck, turning the head rigidly to one side. Among other nervous disorders may be named, amaurosis with dilated pupil and atrophy of the optic nerve, deafness, anosmia, and dementia.

Lesions. These vary as do the symptoms. The nasal pharyngeal, and laryngeal mucosæ show congestion, swelling, infiltration, ecchymosis with vesicles, pustules and ulcerations. They are covered by a foul muco-purulent exudate. The same condition may often be traced to the final ramifications of the bronchial system. In pulmonary cases, the lungs show inflammation, inflammatory exudation and consolidation, collapse, splenization, œdema, and even suppuration in points or large areas. The bronchial lymph glands and often the pharyngeal are enlarged, congested and may be suppurating. The pleura over the congested lung may be the seat of exudation and false membrane, and a bloody serum may occupy the pleural cavity. The heart may show parenchymatous degeneration.

In the digestive organs there may be buccal congestion, with degeneration and the desquamation of the epithelium and formation of more or less extended ulceration. The stomach shows similar congestions and degenerations, the ulcer appearing particularly on the summit of the folds. Together with the intestines this often presents numerous petechiæ and ulcerations, and is covered by a foul but often tenacious mucus. The agminated and solitary glands are usually swollen and infiltrated, and the mesenteric glands are swollen, congested and infiltrated.

The kidneys are often congested, and show points of blood extravasation and tissue degeneration.

The meninges of the brain and cord are often inflamed with infiltrations, false membranes, and especially exudation into the subarachnoid and ventricles. Centres of congestion and softening have been noted in the brain and cord with embolism of capillaries and softening and degeneration of their endothelium. Nocard and others have noted a leucocytic infiltration of the perivascular lymph spaces. In old standing cases sclerosis is an occasional feature.

In nearly all cases there is marked emaciation and a very heavy offensive odor comes from the skin, the tissues, the contents of the bowels and the exudates on the respiratory passages.

Lignieres alleges that in the early stages, the specific bacillus is found in the blood and viscera, but that later it is only exceptionally found and that other bacteria (streptococcus, etc.,) usually take its place. In the nasal discharge it may be found at times, but in the more tardily appearing cutaneous vesicles its absence is the rule, and in the brain matter and meningeal and ventricular fluids, in cases of paralysis or chorea, it is not to be detected by culture. Hence the case cannot always be diagnosed by a successful search for, or culture of the germ, and hence also the frequently unsuccessful inoculations with the blood, tears, liquid of vesicles, and even the lung tissues or nasal discharges.

Prevention. Distemper, like any other contagious malady may be excluded from a city or district by the simple expedient of shutting out animals that bear the infection. From a kennel or pack of hounds, new arrivals should be quarantined for a fortnight, until danger is past, and should only be admitted after a good soapy wash. All clothing, collars, brushes and other material that came with them should be thoroughly disinfected. Dog shows and other meetings are to be avoided as far as possible, and any animal that has returned from one should be quarantined and all his belongings purified. Dogs that run at large should be carefully excluded from kennels where valuable dogs are kept, and from all possible contact with them. Even mice, rats, and birds have to be considered if the disease exists in the near vicinity. When the disease exists in a district a sound sanitation would demand the shutting up of all dogs on their owner’s premises, unless carefully led on chain and prevented from coming in contact with other dogs.

When the disease has broken out in a pack of hounds, or a populous kennel, the dogs should be separated into small lots of 3 or 4; the temperatures of all should be taken twice a day; any lot in which one shows a high temperature should be instantly removed to a safe distance and placed in quarantine; and the enclosure where they have been and all their belongings should be thoroughly disinfected. The enclosures where the sick are kept must be carefully quarantined so that no infection may escape on food, water, brushes, utensils, clothing, attendants, cats, vermin, or even birds.

The dogs that are still healthy should have spacious, well-aired dwellings, open air exercise (as much as possible in the fine season), good but not too stimulating food (in part at least fresh animal food), pure water, and protection against undue fatigue, cold, icy baths, especially when exhausted, rain or snow storms and cold stone or metallic beds. In the cold season artificial heat in the kennel is desirable.

Immunization may be sought in various ways based on the use of the toxins and antitoxins on the one hand, and of a weakened type of virus on the other. Bryce (1882) and others inoculated with the blood and pulmonary exudate, and produced in three-months-puppies, local swellings mainly, with subsequent immunity. The mortality from the inoculation did not exceed 10 to 15 per cent. These losses imply that in certain cases the material inoculated conveyed the microbe of the disease, and the survivors acquired all that immunity which comes from a first attack. In the cases that show local lesions only, it may be presumed that few microbes or none were inserted, while the results came mainly from the toxins or antitoxins. This would be entirely in keeping with Lignieres’ observation that the blood and pulmonary lesions often failed to furnish the pathogenic microbe, as tested even by attempts at artificial cultures. The protection secured from the antitoxins alone is shortlived, terminating with the elimination of these elements, while that coming from the action of the toxins on the leucocytes, and the stimulation by these to the production of defensive products, is much more lasting and in ratio with the quantity of the stimulus introduced and the profundity and duration of its influence on the leucocytes. This may partly explain the occasional early exhaustion of the immunity and the reinfection of the animal within a year after inoculation.

Physalix working in Chauveau’s laboratory has found the best results from the use of weakened artificial cultures. He cultivated the microbe of Lignieres in peptonised bouillon having 6 per cent. of glycerine, and allowed successive cultures to rest (without reseeding a new culture fluid), after they have attained to their full growth. The strength of the culture is in inverse ratio to the period that elapsed between successive cultures, leading up to this one, and the first inoculation is made with the weakest product that will produce a very limited local swelling which is fully developed in 48 hours, and disappears in a few days. Three or four inoculations are made successively with cultures of gradually encreasing potency, after which immunity persists for years. It is to be understood, that an overdose will overcome the immunity at any time; also that the passage of a culture of lessened potency through a dog or Guinea pig will raise it to its original virulence. Physalix operated only on young dogs, that had not shed their milk teeth, and injected 2 to 3 c.c. of the culture as a dose with only 2.5% mortality. Others had less success.

Treatment. To secure good results in the treatment of distemper every attention must be paid to good hygiene. An open air life in summer, and a roomy, clean, well-aired, warmed building in winter are most important. Chills, foul air, and filth generally are to be carefully guarded against. Food should be moderate in amount, easily digested and nutritious. Milk is especially good (sweet, skim or buttermilk); then biscuit and milk, or in patients accustomed to animal food, lean meat, minced, scraped or pulped. Warm baths are often advantageous, but they must be given with great caution to avoid chill.

Medicinal treatment is largely symptomatic. An excessively high temperature (104° and upward) may be met by warm baths, or antipyretics—quinine, acetanilid, salicylate of soda, antipyrine, phenacetin, or even damp compresses to the sides. As a rule, however, it is not well to continue such agents as acetanilid, antipyrine or phenacetin longer than is absolutely needful to reduce excessive temperature.

Attempts have been made to check microbian proliferation by antiferments, such as quinine, calomel, creolin, phenol, and phenacetin. The tonic action of quinine specially recommends it but like all bitters it is obnoxious to a dog with a delicate stomach. Calomel is especially recommended by Fröhner as a gastric and intestinal antiseptic and its indirect action on the liver renders it valuable in many cases. Creolin and carbolic acid exhaled from saturated cloths tend to disinfect the air passages and give tone to the mucosa. My colleague Dr. P. A. Fish gave carbolic acid, 2 per cent., and afterward 4 per cent. in normal salt solution, and in doses of ½ to 1 drachm, subcutem once and twice a day. In the initial stages, it seemed often to be of great value, quieting the nervous excitement, improving the general symptoms, and in some instances apparently cutting short the affection. Trasbot recommended strong infusion of coffee, and Zippelius sodium chloride, while others gave ergotin, or better hydrogen peroxide in spray or as a draught.

Eliminative treatment. As in all depressing contagious diseases, we must favor elimination of the toxins, and in this case without risking any material encrease of debility. Calomel (7 grs.), sodium salicylate or benzoate (4 grs.), sodium bicarbonate (7 grs.), potassium iodide (4 grs.), chlorate (7 grs.), or nitrate (7 grs.) may be cited. Digitalis (1 gr.), strophanthus, or caffeine are especially recommended by their power of encreasing the tone of the heart when that has become weak or exhausted.

For the respiratory symptoms we may employ the antiseptic inhalations already named, or, in place of these, iodine or sulphurous acid. The nervous cough may be met by syrup of poppies, or anise, by morphia, or codeia. (Recipe: morphinæ hydrochloras 0.1 grams: aquæ amygdal. amar. 10 grams, aquæ distill. 150 grams. M. A teaspoonful three or more times a day. Fröhner). As expectorants, ammonium chloride (5 grs), or acetate, senega, or apomorphia (⅒ gr.), may be used. In vigorous subjects ipecacuan (½ to ¾ gr.), or antimonial wine (1 drop). Hydrogen peroxide in doses of a teaspoonful is often useful. Among counterirritants and derivatives the warm bath and cold compresses are especially valuable, or tincture of iodine, or camphorated spirit, or equal parts of aqua ammonia and olive oil serve a double purpose as furnishing at the same time an expectorant inhalant.

Special pulmonary complications must be dealt with on general principles as advised for the special diseases, bearing in mind always the profound prostration and the need to avoid depressing agents.

For conjunctival symptoms bathing with tepid water to soothe irritation and remove adhesions and crusts, may be followed by a drop of aqueous solution of pyoktanin (1:1000) under each lid, twice a day, or cocaine (3:100), or silver nitrate (½:100); may be used. Fröhner advises creolin (½:100); Cadeac, cresyl (½:100); Müller, mercuric chloride (1:2000) or boric acid (1:40). Other Collyria may be substituted (see diseases of the eye). In violent inflammations atropia will find a place and in ulcerations boric acid, silver, pyoktanin, calomel, or hydrogen peroxide. When irritation and rubbing are persistent a cocaine solution may be dropped into the eye every few hours. When the ocular troubles persist during general convalescence tonics with good nourishment and hygiene are demanded.

With digestive symptoms the attendant vomiting will usually have cleared the stomach of irritant contents. In the exceptional cases it may be unloaded by apomorphia (¹⁄₁₀₀ gr. subcutem), or ipecacuan wine a teaspoonful by the mouth. More commonly a check must be placed on persistent vomiting by bismuth nitrate (3 grs.), laudanum (5 to 10 drops), creosote (5 drops), or chloroform (5 to 10 drops), and small pieces of ice. A derivative to the epigastrium is sometimes useful. The food should be of the simplest and most easily digested kind, milk, meat-soup skimmed of fat, meat juice, scraped or pulped raw meat. Demulcents like gum water, slippery elm bark, or decoction of marsh mallow may be resorted to, and in case of extreme irritability nourishment may be given by rectal injection. As vomiting may be kept up by irritants in the intestines a tablespoonful of tincture of rhubarb may be required to be repeated twice a day until relief is secured. Calomel and chalk (1:12) in grain doses will sometimes serve a good purpose. Also dilute hydrochloric acid in water (1:60) in doses of a teaspoonful with pepsin, gentian, quinine or nux vomica will often contribute much to restore tone and function. Septic intestinal fermentations may be met with beta-naphthol, naphthalin, (7 grs.), chloral hydrate (10 grs.) lactic acid (buttermilk), or salol (5 grs.). The attendant fœtid diarrhœa may demand in addition opium or silver nitrate (½ to 1 gr.). The gastric secretion is usually suspended so that it largely passes into the intestines unchanged. Of course it should not be used along with muriatic acid.

The skin eruption is usually considered of little consequence, or, by some, beneficial (Cadeac). If treatment is desired it may consist in dusting powders, demulcent soothing dressings and perhaps stimulating liniments as found under skin diseases. It usually disappears with the elimination of the toxins and the restoration of vigorous health.

For the nervous symptoms treatment must correspond to the morbid phenomena. Extreme prostration may demand diffusible stimulants. Spasms and other indications of congestion may be met by cold to the head, and inhalations of ether, followed by potassium or sodium bromide (8 grs.), sulphonal (20 grs.), trional (15 grs.) chloral hydrate in mucilage, or hypnal (15 grs.). Paralysis must be met by tonics, stomachics, easily digestible, rich food, and good hygiene. Pepsin, muriatic acid, nux vomica (½ gr.), arsenite of soda solution (5 drops), arsenite of strychnia (¹⁄₂₀ gr); orexin(3 grs.), strong coffee infusion, wine, and electricity may be tried, in addition to stimulant liniments. Chorea must be treated on the same corroborant plan. Cold douches after which the patient is carefully rubbed dry are sometimes successful, (see Chorea).

During convalescence and in all cases of debility and anæmia a similar corroborant treatment is demanded. Pulped raw meat, rich soups, stomachics, tonics including the preparation of iron, and in extreme cases transfusion of blood or a normal salt solution may be resorted to.

In cats a parallel course of treatment may be pursued, allowance being made for the smaller size of the animal and the great susceptibility of the feline patient to phenol.

INFECTIOUS BRONCHIAL CATARRH. BENCH SHOW DISTEMPER.

Under this name Glass describes an affection, milder than the usual distemper, but showing similar lesions and demanding an equivalent treatment. It is not self-limiting the same patient having suffered twice in the same year (an occurrence which is occasionally seen in distemper.) The incubation is 3 to 5 days. Diarrhœa is invariably present from the first, and the fæces slimy and at the end of a week slightly bloody. The affection is characterized by the predominance of the digestive disorder, the absence of skin eruption, the free shedding of the hair in long coated animals, the ulceration of the gums, tongue and lips, and the low mortality.

Bacteriological research must be invoked to determine whether this is only a form of distemper or if it is one of a group of diseases which have hitherto been known by that name.

EMPHYSEMATOUS ANTHRAX.

Definition. Historic notes. Geographical distribution. Animals susceptible: Young cattle after weaning, sheep, goats; horses, asses and white rats, have local swelling; dog, cat, pig, bird and man immune. Immune animals succumb if injected with lactic acid, or proteus vulgaris, or violently exerted (sarco-lactic acid). Causes. Bacillus anthracis emphysematosa, 3 to 10μ by 5μ, stains violet with iodine, anærobic, sporulates in living body, hence seen as rod, club, and round, spore. Lives in exudate, not in blood nor on surface. Table comparing with anthrax bacillus. Vitality: resists drying, cold, 98° F., weakened by 139°, sterilized by 212° F. for 20 minutes, by strong antiseptics. Lives in dense clay, hard pan, and waterlogged soils holding little oxygen. Accessory causes: lactic and other organic acids, overwork, potash salts, alcohol, salt, proteus vulgaris, micrococcus prodigiosa, low condition, debility, plethora, chills, change to warmth, youth, melting snows, freshets, drying of wet lands. Symptoms: incubation a few hours, disease 12 to 70 hours. Hyperthermia, swelling in loose connective tissue, shoulder, quarter, arm, thigh, neck, trunk, palate, base of tongue, pharynx, tender point, rapidly enlarges, spreads, crepitates, percussion resonance, finally cold, insensible, and withered. On incision black, bloody pulp, or frothy. Peripheral gelatinoid exudate. Subsidiary lymph glands enlarged. Cases with deep seated exudate. Diagnosis: from malignant œdema and anthrax. Lesions: early decomposition, bloating, in swelling blood extravasation with gas bubbles and lymph exudate, muscle beneath dirty brown or black, breaking down when pressed, shows waxy or fatty degeneration, and many leucocytes and cell forms. Lymph glands and plexuses blood gorged. Extravasation may be in internal organs. Liver congested. Spleen rarely enlarged. Treatment: Chloride of iron internally, ammonia iodide and ol. terebinth externally. Scarify and use hydrogen peroxide or potassium permanganate. Antitoxins. Prevention: drain and till soil, apply quicklime to muck, exclude new animals just from infected districts, disinfect buildings, close infected wells and streams, seclude the sick, burn, cook or dissolve carcasses, or fence graves. Bleeding purgation, diuresis, uniform good feeding, setoning. Immunization by heated and sterilized culture; by toxins passed through a porcelain filter; by minimum dose intravenously; by injection into trachea; by inoculation on tip of tail; by inoculation with Pasteur weakened virus; by heat sterilized virus.

Synonyms. Symptomatic Anthrax; Black Quarter; Quarter Ill; Black Leg; Rauschbrand; Charbon Symptomatique.

Definition. An acute infectious bacteridian disease manifested by hyperthermia, lameness, and a localized, hot, painful swelling on the shoulder, quarter, leg, neck, trunk or elsewhere, tending to emphysema, and gangrene and when incised showing black extravasated blood, clotted or frothy.

This affection was long confounded with anthrax proper, but was differentiated by the observation of Wallraff (1856), Boulit-Josse, Vernant, Pfisterer, Feser, and others and finally Bollinger in 1875 found the motile bacillus. Arloing, Cornevin and Thomas (1879–84) thoroughly substantiated this position, and devised a method of immunizing by inoculation. Feser had however seen the motile sinuous rods in the exudate as early as 1860, and even produced the disease by the inoculation with mud from infected Alpine pastures.

Geographical distribution. Emphysematous anthrax prevails in limited areas, and particular buildings in Europe, Asia, Africa, Australia and America, and in all climates from the tropics up to the sub-Arctic. It is however most prevalent in spring, summer and autumn. It is not uncommon at the breaking up of the winter snows. It is especially prevalent on damp, undrained land or on such as has dried up in the heats of summer, and has become less prevalent in many localities in connection with drainage and careful cultivation.

Animals susceptible. The disease is especially common in young cattle, from three months to four years of age. Calves fed on milk are rarely attacked, being in a sense carnivorous and sometimes immunized by toxins from the dam. Cattle over four years usually escape, having already become immune if kept in an infected locality. If brought from a noninfected place they are, at any age, as susceptible as the young. Sheep and goats contract the disease only exceptionally, but like the Guinea pig are easily infected by inoculation. Horses, asses and white rats have only a circumscribed swelling in the seat of inoculation, and foals and buffalo calves sometimes contract it casually. Carnivora and omnivora, (dog, cat, pig, bird, man), and the rabbit are virtually immune.

Immune animals may, however, be made to succumb under special treatment. In a rabbit inoculated at the same time with the microbe of black quarter and proteus vulgaris, or micrococcus prodigiosus, or if injected with a little lactic acid, the disease develops promptly and fatally. Over-exertion, producing sarco-lactic acid will also lay the system open to attack. The reduction of the vitality and resistance of the muscle of the rabbit by a contusion, bruise or lacerated wound, or by injecting it with acetic acid, potash salts, alcohol, or common salt, will render the inoculation pathogenic. Again, the introduction of the black quarter microbe into the aqueous humor of the rabbit, where there are so few defensive leucocytes, entails an active proliferation and a fatal result.

Causes. The essential cause of emphysematous anthrax is a rod-shaped germ, variously known as =bacillus anthracis emphysematosa=, =bacillus Chauvæi=, =Rauschbrand bacillus=. This is a rod-shaped microbe, with rounded ends, found singly or connected in pairs, or very short filaments. The bacilli are 3 to 10µ long, by .5µ broad, or when sporulating, 1.1 to 1.3µ. They form spores even in the body of the affected animal, often assuming a club shape by reason of the spore formation near one end. If the spore develops in the center they appear fusiform. They take aniline colors readily, and iodine slightly, assuming in the last case a violet tint. The staining is unaffected by heating in melted balsam. The bacillus grows readily in ordinary culture media, (peptonized gelatine, bouillon, milk, etc.), but, being anærobic, only under the surface in stick cultures, or under a neutral gas or vacuum. It grows most rapidly at a temperature of 36° to 37° C. but also as low as 15° C. The bouillon at 37° C. becomes milky and opaque in 24 hours, and later it clears up, the microbes being precipitated as a free white powder. In gelatine cultures liquefaction takes place in three days, and in twenty days the whole mass may be dissolved and the microbes precipitated to the bottom. Spores may form in the living body and as these are set free by the granular degeneration of the bacilli, the virulent exudate and cultures usually show the microbe in three different forms: 1st; the straight, motile bacillus of one thickness throughout its whole length; 2d; club-shaped or fusiform bacilli, the thickening of the end or median part being due to the endogenous formation of a refrangent spore or spores; and 3d; the free refrangent spores which have been set free by the degeneration and destruction of the sporulating bacilli. The microbe is not found on the surface of the living animal, nor in the blood, for in both the supply of oxygen is too abundant; it forms its colony under the skin, in the tissues, and above all, in the mass of extravasated blood or gelatinoid exudate which its irritation has produced and where air is lacking.

The most marked differential features of the microbes of anthrax and emphysematous anthrax are contrasted in the following table:—

=Bacillus Anthracis.= =Bacillus of Emphysematous Anthrax.=

5 to 20μ × 1.25μ. 3 to 10μ × 0.5 to 0.6μ.

Ends square or cupshaped. Ends rounded.

Occurs singly in the living body. Often in pairs or threes in body.

Long filaments in cultures. No long filaments.

Nonmotile. Motile (sluggishly).

Ærobic. Anærobic.

No spores formed in living body. Sporulates in living body.

Sporulates in air; in surface Sporulates in vacuo; deep in soil. soil.

Bacilli only. Bacilli; sporulating bacilli; free spores.

Multiplies freely in blood stream. Dies in blood stream unless charged with toxins.

Rabbit very susceptible; man less Rabbit, pigeon and man immune. so.

Produces no gas. Gas producing.

Inoculation swelling very Inoculation swelling very restricted. extensive.

Bacillus destroyed by Not destroyed by putrefaction. putrefaction.

Resistance of bacillus of black quarter to physical and chemical agents. The microbe is possessed of great vitality. Thoroughly dried at a temperature of 95° F. it retains its virulence. The spores may be preserved indefinitely in dry soil, buildings, fodder, litter, harness, etc. Cold is equally harmless to it. It has been exposed to a temperature of 98° F. below zero without losing its virulence. Its virulence is lessened by exposure for an hour to 139° F., and it is sterilized at a temperature of 212° F. for twenty minutes. The dried spores are virulent after six hours of the boiling temperature but are sterilized at 230° F. if maintained for the same length of time. Diffused in water the virus is sterilized in thirty-five minutes at the boiling temperature. Some waters at ordinary temperatures destroy the virulence in twenty-four hours; others not for many months. It is destroyed by the more potent disinfectants, mercuric chloride (1:1000), silver nitrate (1:100), acid salicylic (1 to 2:100), acid carbolic (2 to 4:100), copper sulphate (20:100), boric acid (20:100), muriatic acid (1:2). Quicklime, copperas, zinc chloride, sulphuric acid and an alcoholic solution of phenol have proved unsatisfactory.

In clay soils, hard pans, waterlogged soils, and in some that are over manured so that the atmospheric air is excluded, it may be preserved indefinitely. Feser, Gotti and others have produced the disease by inoculating with the washings of infected marshy soils, and this is doubtless a common source of casual cases of the malady.

Accessory causes are important. The predisposing influence of lactic acid, of other organic acids, and of overwork have been already named. Potass salts, alcohol, common salt and the products of proteus vulgaris, or micrococcus prodigiosus increase the susceptibility. Low condition, debility, or suddenly induced plethora have a similar influence. Sudden changes of weather, chills, and particularly the access of hot weather in spring, when the animal is changing its coat lays, the system open to attack. Youth, after the period of suckling, and under three years old, seems to increase the predisposition, though this is largely the result of the absence of a previous exposure. Then impermeable, clay, wet, marshy soils, or those charged with organic matter are conditions of the presence of the microbe. It often appears in spring in connection with the melting of the winter’s snows, the occurrence of freshets, and the washing out of soil infection which would otherwise remain buried. Also in advanced summer and autumn when swamps, ponds, basins, deltas, river bottoms, etc., are drying out and furnishing pasture. Pease records its great prevalence in the rainy season in the swamp districts of the Punjab and North Western provinces of India, and the same is largely true of our Gulf coast states.

Symptoms. Emphysematous anthrax develops suddenly, the incubation in experimental cases, lasting only for a few hours, and the whole course of the disease does not usually exceed ½ to 3 days. The local swelling may be the first observed symptom or there may be first febrile disturbance followed by the local swelling. The swellings show where the connective tissue is loose and abundant as on the shoulder, quarter, arm, thigh, neck, face, or trunk, and practically never where the areolar tissue is very spare and dense as on the end of the tail, or ear, or on the limb below knee or hock. They sometimes form on the palate, base of the tongue, or pharynx. The muscular system is especially liable to suffer, the looseness of the texture and the presence of lactic acid making a particularly favorable field for the propagation of the microbe. The comparative absence of muscle in the region below the metacarpus, the tail and ear is an important cause of this immunity.

The swelling is at first very small and tender, but it encreases rapidly, and in a few hours may extend to one, two, or three feet in diameter. At first smooth, rounded, pitting on pressure and destitute of crepitation on handling, it becomes softer and less sensitive and when pressed or kneaded it gives a crepitant sensation and sound, or it even appears to gurgle. When percussed the resonance is drumlike. Finally, the skin may become cold, insensible, and withered like a piece of parchment. When incised the tissues are found to be gorged with blood, and of a black or dark red color; they break down under pressure into a bloody pulp, and from the wound flows a bloody fluid which may be red in the early stages, black in the advanced, and frothy in the latest. Where the connective tissue is very loose and abundant, the bloody extravasation is surrounded by an extensive straw colored œdematous infiltration. The swelling is sometimes single, but more frequently several appear and become confluent. The lymph glands in the vicinity become greatly enlarged.

Fever is a constant condition as the swelling advances and sometimes it precedes the local engorgement. There is erection of the hair, with it may be, distinct shivering, recurring again and again. Then general stiffness, dulness, prostration, loss of appetite and rumination, accelerated breathing sometimes attended by a grunt or moan, and rapid pulse. The temperature usually reaches 104° F., and may rise to 109° F. The breathing becomes more and more labored and plaintive, colicy symptoms may set in, the prostration advances to complete adynamia, the patient can no longer stand, the temperature drops to 100° F., or 98° F., and death supervenes in from eight hours to two days from the first sign of illness.

In some cases the swelling may be invisible because it is situated deeply or it may perhaps be entirely absent, and the constitutional symptoms are the only ones observed.

Diagnosis. From malignant œdema, which it resembles in producing gas and crepitating tumors, emphysematous anthrax is distinguished by the greater length of the microbe, by its formation of spores at the pole and not in the centre of the bacillus, by the more sluggish motions of the germ, by the restriction of the germ to given infected districts instead of being generally diffused as in malignant œdema, by its not attacking man, rabbit, nor pigeon, which are subject to malignant œdema, by its deadly action on mature cattle which are usually immune from malignant œdema, and by the abundant blood extravasation on the swelling.

From anthrax it is distinguished by the motility of the bacillus, by its polar sporulation and club shape, by its rounded ends, by its absence from the blood in the earlier stages, by the presence of gas and crepitation in the swellings, and by the deadly action of the infection on Guinea pigs, but not on rabbit, man, nor pigeon. Anthrax is easily inoculable on a cutaneous sore or intravenously whereas emphysematous anthrax is not.

Lesions. The carcass is liable to be bloated with gas and a reddish, frothy liquid often escapes from mouth nose and anus. Gas is particularly abundant in the substance of the tumor, and the skin covering it may be dry and crackling. An incision made into the swelling exposes a mass of blood extravasation and lymph exudate, the blood predominating in the centre so that it may appear clotted and black, and mixed with gas bubbles, while the yellowish lymph forms the periphery of the tumor, yet streaked more or less with blood, or even pink throughout. The abundance of gas is usually in inverse ratio to the amount of œdema. The muscles beneath or surrounded by an exudate are of a dirty brown or black, and are disintegrated so as to break down readily under pressure of the finger into a blackish pulp. They are infiltrated with gas, crepitate under pressure and assume a golden yellow color on exposure to the air. The gas is comparatively inodorous immediately after death, being mainly carbon dioxide and carbide of hydrogen. Later it may show distinct and even offensive odor, from the formation of hydrogen sulphide, or lactic acid. The muscular fibres are easily teased apart, and show under the microscope masses of blood globules, leucocytes, lymph cells, free nuclei and granules, with, in some points, fatty or waxy degeneration of the fibres, or granular masses that are stained black by osmic acid. The bacillus is present in large numbers, and this with its absence immediately after death from the blood becomes characteristic. The lymph glands near the swelling are usually enlarged and gorged with blood. The lymph plexuses and vessels contain bubbles of gas.

The swellings may be subcutaneous, or submucous in the tongue or pharynx, but they occur also in the pleuræ, lungs, heart, pericardium, mediastinum, the peritoneum, the sublumbar connective tissue, and even the walls of the stomach or intestine. It is not uncommon to find a pink effusion into one of the serous membranes. The liver is usually hyperæmic, as may be also the kidneys, but the spleen is rarely enlarged. In this and in the integrity of the blood globules this affection differs from anthrax.

Treatment. This disease is so often speedily fatal, cutting off its victim in eight hours, often during the night, that no opportunity is allowed for treatment. Even in those that survive for two days, the affection must always be looked on as exceedingly grave, and as little amenable to treatment. Yet much depends upon the patient and the country. Dr. Phares in Mississippi found that it yielded readily in many cases to ½ oz. doses of tincture of chloride of iron every four hours, and a local application composed of equal parts of tincture of iodine, aqua ammonia and oil of turpentine. Galtier tells us that recoveries are frequent in Algeria, while they are rare in France. Tisserant gives the French recoveries as 2 per cent. It is probable that in districts and countries where the malady is all but ubiquitous, the surviving animals are racially immune, or they have been largely exposed and in some degree virtually immunized at an early age.

Wallraff mentions a success from applying a tight ligature around an infected limb, above the seat of the tumor and freely scarifying the latter so as to freely admit the air. For swellings elsewhere, scarifications and the free application and injection of peroxide of hydrogen or potassium permanganate (2 to 3:100) would be rational treatment. The same agent might be given by the mouth in doses of 2 or 3 ozs. at frequent intervals. Antiseptics and tonics have been freely employed, including phenol, salicylic acid, sodium salicylate, potassium iodide, quinia, alcohol, phosphorated oil, ammonia acetate, and as an eliminant soda sulphate, but with no very good result. Locally, scarification, antiseptics and caustics, have been employed.

Another line of treatment which deserves to be further exploited is the use of antitoxins on infected animals. An immunized animal may be again and again inoculated at intervals of a week or two until it has been stimulated to produce antitoxin in large amount. Then after three weeks interval its blood serum or blood, may be sterilized by heat, the resulting coagulum washed in distilled or boiled water, and filtered, and the filtrate injected subcutem on the infected animal.

Prevention. This is most effectively secured by sanitation of the soil and buildings. Thorough drainage to secure perfect and constant æration leads to destruction of the anærobic germ, or the suspension of its pathogenic quality. Thorough culture contributes largely to this sanitary æration, while baking of the surface counteracts it. When thorough drainage is impossible it may be desirable to subject the land to gardening or to the production of crops that are to be used for human consumption and not for domestic animals. Kitt’s suggestion, to soil cattle on hay, produced on such lands, and to exclude from the infected lands all animals that by wounds or sores near the feet, or by raw gums from shedding of teeth, furnish infection atria for the poison, is insufficient, as stalled cattle occasionally suffer.

When an open porous soil maintains the infection by reason of the presence of an excess of decomposing organic matter, that may be largely remedied by a free application of quick lime. This hastens the decomposition of the organic matter and after a year or two, when that has been largely disposed of, the good effects may be expected.

An important measure is to exclude from fairs, markets, and above all from clay or other dense wet soils into which they might convey the germs, all animals brought from infected soils.

Disinfection of the buildings where diseased and infected animals have been is an essential measure. Wells and streams receiving the drainage of infected lands must be carefully avoided.

Diseased animals must be carefully isolated, and all their droppings, and products of every kind disinfected.

The carcasses are best cremated or rendered under superheated steam under pressure. Solution in sulphuric acid may be employed. If none of these are available they may be deeply buried in dry porous soil well apart from any risk of drainage into wells or water supplies. The area occupied by the graves should be fenced in so that no cattle nor sheep can gain access to it, and any vegetation grown on the graves should be burned. The danger of the germs being raised to the surface by soil water or earth worms must be recognized and any consequent evil guarded against. The carcass should not be cut open but buried in the hide, or if the latter is preserved it should be treated with a chloride of lime solution. If a carcass is opened for scientific purposes, great care must be taken to avoid the distribution of the bacillus in soil appropriate to its preservation. The meat should not be preserved for human consumption unless it has been cooked under pressure at a temperature of 240° F. The object is not to destroy any poison which would be fatal to man, but rather to prevent the spread of the spores on new soil and the extension of the area of infection.

The reduction or prevention of sudden plethora was formerly availed of to lessen the number of victims and it is well to still bear in mind that this has an appreciable though limited effect. As a means of reducing plethora a free bleeding was resorted to when the period of yearly prevalence approached, and no less when the disease had already appeared in a herd. I can mention an instance in which infection was carried on the fleam from the first animal bled (the sick one) and caused the fatal infected swelling around the phlebotomy wound in the next seven animals operated on. Another objection to phlebotomy is the tendency to a rapid reproduction of blood, which the depletion brings about, and the supervention of a greater danger than before, in the course of a month or more. Purgatives and diuretics are somewhat less objectionable in this sense. Careful feeding to keep the animal constantly in good condition does something to obviate sudden plethora and its attendant dangers, and thus an allowance of grain or linseed cake through winter and early spring, or when the pastures are bare, will bring the animals through in fine condition, and ward off the danger that comes from a sudden access of rich aliment.

Another measure was the insertion of a seton in the dewlap. The theory was to counteract plethora but the benefit probably came rather from the formation of an actively granulating wound, which came in contact with the ground and received the bacillus, but in which the abundance of air, and of active leucocytes checked the propagation of the germ and the occurrence of a fatal infection. A certain grade of immunity was the natural result in many cases.

Immunization. As the first attack of emphysematous anthrax secures for the subject of it immunity against a second, we are furnished with a reasonable basis for the practice of artificial immunization. This has been attained by a variety of methods, the essential feature of each being the subjecting of the system of the animal to be treated, to the action of the toxins of the specific bacillus.

1st. A culture of the bacillus made in the thermostat at 42 C. (107.6° F.) so as to prevent the formation of spores is then sterilized by heating to 100° C. for one hour and then injected subcutem in a dose of 2 drams, to be repeated on the second day. This, like all the other methods named should be done by some one accustomed to bacteriological manipulation and the sterilization completed by superheating the neck of the vessel containing the mixture. Any germs escaping on the hands, instruments or other objects used will prove fatal in spite of all the appearance of precautions.

2d. Roux sterilized his cultures by filtering them through a porcelain (Pasteur) filter and using only the filtrate for injection. This requires even greater precaution in manipulation as what is left in the filter is most virulent, and must be thoroughly sterilized to obviate dangers from its dissemination.

3d. Intravenous injection of a small quantity of virus, containing but a few bacilli produces no local swelling, but only a slight temporary hyperthermia and permanent immunity. The greatest care is necessary in the manipulation, to prevent any contact of the bacillus with the subcutaneous tissues or the walls of the vein. The virulent exudate swarming with bacilli is taken and a drop or two added to a normal salt solution, which is diluted and shaken in a stoppered bottle, until each drop contains but one, or at most two bacilli. Then the hands having been thoroughly washed with soap and warm water and rinsed in a 5 per cent. solution of carbolic acid, and the instruments having been boiled, the vein is raised as for bleeding, and penetrated by a short cannula and trochar, which after boiling has been dipped in the carbolic acid solution, the trochar is withdrawn, and the nozzle of the syringe containing the virulent solution is inserted through the cannula, so that its point is free in the centre of the blood stream, into which a few drops of the virulent solution are discharged. The nozzle is left in place for a few seconds to ensure the washing of any infecting matter from its point, when it is withdrawn, followed immediately after by the cannula. Great care should be taken to avoid any scratching of the inner coat of the vein with the cannula, trochar or nozzle.

4th. Another method of immunizing is by the injection of the virulent liquid into the trachea and bronchia. This appears to bring it so directly in contact with the blood, that the microbes are destroyed as rapidly as if it were introduced into the blood stream direct. The injection is made between two tracheal rings, the manipulation being essentially the same as in the cases of the vein, the tissues being first perforated by a sterilized cannula and trochar, and the sterilized nozzle subsequently inserted through the cannula.

5th. Inoculation into the tip of the tail can be successfully employed, the coldness of the region and the scantiness of the connective tissue preventing any dangerous increase of the bacilli in the cooler season. In the heat of summer, however, this is to be avoided as dangerous. The tail is first washed with soap and water followed by a 3 per cent. solution of phenol. It is then punctured with a fine trochar or needle, (sterilized), within two inches of the tip and in a downward direction and the instrument is moved slightly from side to side so as to form a small sac, and is then withdrawn. The sterilized nozzle of the hypodermic syringe is now inserted in the opening and a few drops of the virus injected into the sac. When the nozzle has been withdrawn the thumb may be placed on the external orifice and the end of the tail manipulated to diffuse the virus in the connective tissue. This is usually followed by an insignificant swelling, and a slight rise of temperature. Should the swelling exceed the size of a duck’s egg or if others appear higher up on the tail, they may be freely scarified and covered with a carbolic acid bandage. Or the tail may be amputated above the highest swelling and the stump treated with antiseptics.

6th. The virus prepared by the Pasteur institutes, that of Arloing, Cornevin and Thomas, is the most extensively employed. Forty grammes of the diseased muscle are dried rapidly at 32° C (90° F.) and triturated in 80 grammes of water. This is divided in 12 equal parts and put on plates in two thermostats, six at 100° C. (212° F.) and six at 85° C. (185° F.) where they are kept for six hours, when it forms a dry, brownish powder. One tenth of a gramme (1½ gr.) of this powder is dissolved in five grammes of distilled or boiled water and will furnish ten doses. The animal to be protected is first injected in the tip of the tail or elsewhere with the virus prepared at 100° C., and ten days later with that prepared at 85° C.

By the use of this method in hundreds of thousands of animals on infected lands the mortality has been reduced to less than one tenth of its former amount. It is attended by the one danger which is not always duly appreciated, that unless its use is restricted to herds on ground that is already infected, it endangers the infection of new districts. The spores are not absolutely sterilized at 85° C. Arloing and Cornevin and later, Nocard and Roux have shown that the addition of lactic acid to the liquid which has been weakened for inoculation, restores it to its former virulence, making it a most deadly agent. Galtier says that the virus weakened by heating to 100° C. for seven hours until it will no longer kill a mature Guinea pig, will still kill a new born Guinea pig and acquire all its original virulence in the act. Also that the injection of large enough doses will not only kill the full grown Guinea pig, but at the same time restore the microbes to their former virulence. While recognizing the great economy of the judicious use of such weakened virus, we cannot but condemn the reckless sale by the Pasteur institutes of their products, to be used on animals on all kinds of lands, the uninfected as well as the infected. A great and valuable prophylactic measure should not be used in such a way as to increase the area of prevalence of the disease which is to be prevented, and also the yearly demands for more of the preventive agent. This may appeal to the business instinct, but this should ever be held subordinate to sanitary considerations. The danger might be avoided by making the state the sole distributor of such prophylactic agents, but in any case their use should be forbidden, and as far as possible prevented, upon dense and wet soils that are not yet contaminated by the bacillus.

7th. Kitt secured immunization by inoculating once only, with dried virus which had been subjected for six hours to steam at 100° C.

8th. In different outbreaks, I have taken the blood from the sick animal, or one that has just died, and heated it for over one hour in a water bath, at 100° C., then broken up the coagulated mass in well boiled water, filtered the liquid and used the filtrate for inoculation in doses of 2 drams, repeated the second day. Great care is taken in keeping the whole mass at 100° C. for the requisite length of time; then in heating the upper part of the vessel, which was above the contents and the water so as to char anything adhering to it; to see that hands, instruments, and all articles used have been thoroughly sterilized; and to dip the hypodermic nozzle in carbolic acid before each injection.

It is not claimed that this method is perfect, since severe, advanced cases may have bacilli and even spores in the blood, and the latter would not be sterilized but only weakened. It has, however, several manifest advantages that may be held to more than counterbalance this danger.

a. It almost infallibly secures the toxins of the disease prevailing in the particular herd, thus escaping the danger of using the weakened virus of emphysematous anthrax on some other disease (anthrax, Wildeseuche, Barbone, etc.), which has been mistaken for it, and which may not be prevented by this purchased product.

b. During life the blood of emphysematous anthrax is usually free from the microbe, and even where that is present it is liable to be in very small numbers, so that we secure either the pure toxins, or if a few germs are present they are so scanty, that weakened as they are by heat, they are without danger to the animal operated on. I have never had occasion to note evil results.

c. There is no danger of the spread of the bacillus to new territory, as we secure the material from a herd in the already infected territory, and use it only on the animals on the same land.

The certainty of results with this method, and the comparative absence of danger of injury to the animal operated on, and of all risk of the extension of the area of infection appeal to me so strongly, that I would not willingly resort to the purchased products, except where it proves impossible to secure the virus on the spot.

ANTHRAX.

Definition. Synonyms. History and geographical distribution. Etiology: Bacillus anthracis. Susceptible animals: small rodents, sheep, horse, camel, ox, goat, deer, stag, man, swine, dog, white rat and bird when chilled, frog when heated; young most susceptible, races long exposed to infection are least. Soils, wet, dense, impermeable, basins, swamps, rich river bottoms, deltas, rich meadows, below tanneries, alkaline soils, wells with surface drainage; season: wet, hot and dry, late summer and autumn; flies; infected buildings, harness, vehicles, fodder, litter, butchers’ knives and wagons, surgical instruments; insolation; privation of water: plethora, starvation: overwork, exhaustion. Bacillus anthracis: rod, nonmotile, 5 to 20μ by 1 to 1.5μ, square ends, isolated in blood, often filamentous in cultures, sporogenous, ærobic, stains easily in aniline and iodine, killed at 131° F. (spores at 203° to 282° F.), action under chemical disinfectants, or septic ferments: air favors sporulation and survival; in shallow graves, water. Infection atria: ingestion, inhalation, inoculation, insects, placenta. Forms: fulminant, internal, febrile, local,—external,—gloss-anthrax, pharyngeal, hæmorrhoidal, subcutaneous. Lesions: blood normal in fulminant, dark, diffluent, crenated or disintegrated globules in prolonged cases, tissues brown or yellow, heart pale; liver enlarged, softened, pale, hæmorrhagic: spleen enlarged, blood-gorged, ruptured; lymph glands hyperæmic; serosæ congested, petechiated, hemorrhagic; lesions embolic and like the blood swarm with bacilli. Toxins, ptomaines. Incubation 1 to 6 days. Symptoms: internal cases: hyperthermia, constitutional disorder, mucosæ dusky, brownish, yellowish, bleeds, bloody urine, rectal mucosa congested, blackish, colics, pharyngeal anthrax, blood diffluent, black, broken down red globules, bacilli, abortions, death in 12 to 48 hours: fulminant cases in cattle and sheep. Local (external) anthrax, cutaneous, swellings: gloss-anthrax; pharyngeal, hæmorrhoidal; sheep and goats; horse; swine; dogs; cats; birds. Differential diagnosis: deductions from symptoms, condition of blood, animals attacked, environment or conditions of life, presence of the bacillus. Examination for bacillus. Post mortem lesions; gelatinoid, bloody exudate, petechiæ, blood-gorged spleen, lymph glands, and liver, diffluent blood, bacilli in capillaries. Inoculation intravenously. Cultures. Prognosis. Mortality often 70 per cent.

Definition. Anthrax is an acute infectious bacteridian disease occurring casually in the herbivora and omnivora and, under favorable conditions, communicable to carnivora, birds and batrachians. Its special features are the presence of the bacillus anthracis in the diseased parts, the destruction of red globules, the arrest of hæmatosis, the occurrence of capillary embolism, extravasations and exudations, and of necrotic processes in the affected parts, and a sanguineous engorgement of the spleen.

Synonyms. Malignant pustule; Splenic apoplexy; Splenic Fever; Charbon; Miltzbrand; Woolsorter’s Disease; Malignant Carbuncle; Contagious Carbuncle.

History and Geographical Distribution. As anthrax prevails in damp, undrained lands where agriculture is backward, it is not wonderful that it can be traced to near the dawn of human history when the whole race lived under primitive conditions. Moses records its ravages on the bottom lands of the Nile (Ex. ix. 9), Homer, on the plains of Troy (Iliad, Bk. 1st), Ovid, Plutarch, Dionysius, Livy, Lucretia, Columella, Virgil, Pliny and the Arabian physicians all show a familiarity with a disease of this nature. Later, Heusinger collects evidence of its prevalence in certain areas in all parts of the world from the equator to the Arctic circle. The mortality was often very high, thus Kirchner records the death of 60,000 people in a single epidemic in 1617, in the vicinity of Naples, Placide-Justin, that of 15,000 in St. Domingo in six weeks in 1770, and on the Russian and Siberian Steppes it is not uncommon for hundreds of thousands of domestic animals and thousands of human beings to suffer in a single year.

The geographical distribution of the disease is largely influenced by soil and climate. On dense, impermeable clays and hardpan subsoils, on river bottom lands, dried lake basins and deltas, rich in organic matter, and with the air driven out by water or gaseous fermentation products, the germ is preserved and propagated if once introduced. Thus it is common around the mouth of the Nile, and along the occasionally inundated banks of the Vistula and Danube, the Spree, Oder, Elbe, Rhine, Eure, Loire, Seine and Marne, and in England in the Fen district. On the rich, undrained, black soils of Siberia it is extremely prevalent and fatal. In the rich Genesee Valley, N. Y., the writer has seen 200 cattle in one herd and three human attendants attacked in the course of a fortnight, and in different meadows receiving the drainage of tanneries, the affection prevails every summer and autumn. It is much more prevalent in the rich lands of the Southern States and a widespread and deadly epizoötic prevailed in Louisiana in 1896. Where the soil is favorable, the germ may be preserved indefinitely, even in mountainous districts, and near Los Angeles, Cal., where the disease was introduced in imported sheep some years ago it has become permanently domiciled, on the dry ranges which have moist lands (Cienegas). When an outbreak occurs, the herds or flocks are usually moved to higher soil, and the carcasses being left unburned and unburied the infection is spreading year by year (McGowan, Morrison).

Etiology. Nothing is more certain than that the disease is due to the introduction into the blood or tissues of the bacillus anthracis or its spores. These microbes are always found in the anthrax lesions and in the blood of the victim in the advanced stages. When grown in bouillon cultures to the hundredth generation they retain their virulence unabridged and determine the same lesions in the animals inoculated. When the infecting culture has been passed through a Pasteur filter the virulence is lost with the removal of the bacilli. The fresh anthrax blood containing bacilli but no spores when subjected to compressed oxygen (50 atmospheres) becomes noninfecting. The same liquid when boiled proves non-virulent.

Certain conditions, however, contribute to the propagation and reception of the bacillus and these may be considered as accessory causes.

Animals susceptible. The receptivity of the animal exposed is of first importance. Young animals are the most susceptible. The small rodents, the mouse, Guinea pig and rabbit are susceptible in the order named, followed by the sheep and horse and these again by the camel and ox. Among the wild herbivora the goat, deer and stag have a high susceptibility. Man is less susceptible yet contracts the disease readily by inoculation, inhalation or ingestion. Swine and dogs are comparatively little susceptible, yet they often contract the disease by eating the carcasses or discharges of anthrax animals. White rats and birds are held to be insusceptible, yet the latter contract the disease readily when the vitality of the system has been reduced by immersing the body in water, or giving antipyrine. A similar result is observed in the otherwise immune frog if the body is heated above the normal cold blooded temperature. The receptivity may vary, however, in the same genus and species. The Algerian sheep is virtually immune from anthrax, perhaps because its ancestors have been so constantly exposed that only the insusceptible strains survived. Swine, birds and carnivora may have similarly acquired a fair measure of immunity by the survival of the fittest. Apart from this, however, a flesh diet is to a certain extent protective, thus Feser’s rats if fed vegetable food proved susceptible to inoculated anthrax, while if fed on animal food they were comparatively immune.

The animal that has survived an attack of anthrax is thereafter strongly immune. This serves to partly explain the apparent immunity of animals bred in an anthrax district, the young animal becoming habituated to infinitesimal doses of the toxins, conveyed in the secretions of the uterine glands or mammæ.

Soil is a factor so far as it preserves and propagates the bacillus. As already stated, soils that are naturally wet by reason of their impermeable character, their position on or near the water level, their conformation in basins which dry out in late summer or autumn, are especially favorable to preservation of the bacillus. Again soils that are specially rich by reason of an excess of decomposing vegetable and animal remains, or because of excessive manuring, tend to preserve and multiply the microbe. Rich, flat meadows below tanneries or abattoirs, and irrigated from these or occasionally overflowed are especially dangerous to stock placed upon them. Soils with an alkaline reaction from the lime, potash or ammonia present are very favorable to anthrax. Wells receiving surface drainage are common factors in carrying infection.

Season is a contributing factor in various ways. Damp seasons sometimes bring the germ to the surface of the soil by the gradual elevation of the water level, or by causing inundations and the deposition of the bacillus on areas of pasture or forage that were previously free, or finally by bringing the earth worms to the surface and leading to the deposition in their casts of the bacillus brought from the infected graves or retentive subsoils. Dry seasons are, however, the anthrax seasons par excellence, as they dry up swamps, fens, ponds, lakes, basins, deltas and bottom lands, and render them available for pasture. The germladen mud of these drying lands is also raised in dust and deposited on the vegetation to be taken in by the animals. Again on the drying basins and bottom lands the tempting green vegetation is often pulled up by the roots with adherent, infecting mud. For the above reasons, even in an anthrax region the malady is most prevalent in the late summer and fall, and in certain valleys like those of Corsica the stock is considered safe until the dry autumn weather demands their removal to the mountains.

Another reason for the summer epizoötics is found in the transference of the germ by flies. House flies, horse-flies, blowflies, mosquitoes, etc., carry the bacillus on their feet, mandibles or piercing apparatus, and even in their stomachs (Bollinger) and transfer it from one individual to another. It is worthy of note that the great majority of cases of local anthrax in man occur on the habitually uncovered parts of the body (face, neck, hands and arms) and start from a centre like the bite of an insect.

Stables, stable utensils, harness, shafts, poles, fodder and litter are familiar bearers of the virus. Butchers’ knives and wagons and surgical instruments are further media of contagion.

Certain conditions of the animal system expose it to attack. The fever and constitutional disturbance which are caused by the extreme heats of summer and autumn are strongly predisposing, especially if alternated with frigid nights as seen on the Siberian Steppes. Privation of water raises animal temperature and thus the drying up of the customary drinking places becomes an important factor. Plethora and starvation are alike predisposing, probably by lessening the resisting power of the system. Overwork and exhaustion predispose, as Roger showed by making the immune white rat turn a wheel until worn out and then successfully inoculating it. The addition of lactic acid to the virulent liquid (1:500) greatly encreases its potency (Arloing, Cornevin and Thomas) and the further addition of fermentescible sugar and rest enhances this still more (Kitt). The production of lactic acid by muscular overexertion is thus a potent accessory cause in fatigue.

Bacillus anthracis. This was first demonstrated in anthrax blood and exudates by Pollender and Brauel in 1849 and 1850 but as they failed to find it in all cases they concluded that it was not the essential cause. Davaine who found the bacilli in 1850 suspected that they were pathogenic and by 1863 he had shown that blood which contained no bacilli was non-virulent, while that in which these organisms were present was constantly infecting. Klebs and Tiegel in 1871 filtered anthrax blood through an earthenware vase and found that the clear filtrate (bacillus-free) was noninfecting.

The bacillus anthracis as found in the blood is a nonmotile rod-shaped organism, 5 to 20μ long by 1 to 1.5μ broad with ends apparently square, but really slightly cup shaped as seen in the stained specimens when two have remained connected end to end. Under favorable conditions a clear hyaline envelope may be seen around the bacillus. Though usually isolated in the living blood, yet in bouillon cultures the bacilli grow out into long flexible filaments, made up of separate segments which are easily distinguished in the stained specimen. In all cultures out of the living animal body, in the presence of air and at a suitable temperature spores form endogenously in the bacilli and are set free by the granular degeneration of the latter. In peptonized bouillon this may occur in four days at 14° C., or in eight hours at 37° to 40° C., but not above 42° C. (Schreiber. Centr. S. Bact. 1896). Sporulation never occurs in the living animal body.

The bacillus is ærobic, yet it will grow at the bottom of a stick culture in solid media. It fails to grow in an atmosphere of CO_{2}, H, or N. It stains readily in aniline colors, and also by Gram’s method. It grows freely on a variety of culture media (blood serum, aqueous humor, urine, vegetable infusions, milk, meat bouillon, peptonized gelatine, potatoes, etc.) at a temperature of 20° to 38° C. Growth ceases below 12° C., and above 45° C. Growth is most active in neutral or slightly alkaline media, and is arrested by that which is decidedly acid.

Action of physical and chemical agents on the bacillus anthracis. The bacilli survive a temperature of −45° C. (−49° F.), but they perish in 10 minutes at a temperature of 100° C. (212° F). A temperature of 55° C. (131° F.), proves fatal if sufficiently prolonged. The spores are much more resistant. They have survived −130° C. (−202° F.) and though they may die in 10 minutes in liquid media kept at 95° C. (203° F.), yet when old and dry it may require several hours at 140° C. (282° F.) to sterilize them.

Even the bacilli are comparatively resistant to ordinary disinfectants, and, as spores form in the body very rapidly after death, and in virulent products, it is always best to assume their presence. In a moist medium Cl. 44.7% destroyed the spores in 3 hours: HCl (1:1100) in 2 hours: HgCl (1:1000) in a few minutes: HgI_{2} (1:20000) in 2 hours: Malachite green (1:40,000) in 2 hours: Methyl violet (1:5000) in 2 hours: Aseptol (1:10) in 10 minutes: Carbolic acid (4:100) with HCl (2:100) in 1 hour.

Action of septic ferments on the bacillus anthracis. Rapid putrefaction in the anthrax carcass which has not been opened tends to speedy granular degeneration and death of the bacillus anthracis, so that the blood and tissues may be no longer infecting after six days in summer. In such cases the irrespirable gaseous products of decomposition drive out the oxygen without which the bacillus cannot live. If, however, spores have already formed or if air is freely admitted the infection survives in spite of decomposition. The search for the bacilli may thus be fruitless as soon as decomposition is well advanced and the material can only be virulent through any spores that may have formed. Eventration serves to retard sepsis and admit air to form spores, and salting operates in a similar manner.

The infected hides, the nasal, buccal, kidney and bowel discharges, and spilt blood and exudates mingling freely with the air tend to form spores and to preserve and propagate the contagion. On the contrary prompt and deep burial, without opening the carcass and before spores can have formed will usually ensure its destruction. The main danger in such cases comes from infecting matter (adherent to the surface of the body) which sporulates easily. This serves to explain the great danger of working in anthrax hides, leather, horn, wool, hairs and bristles. It also explains sporulation and preservation of infection when the virulent excretions, blood, etc., mix with the surface layers of soil. This may happen at a greater depth (3 or 4 feet) in a very porous soil and where the temperature is sufficiently elevated (above 14° C.) It may even occur in water. The dried spores are mostly carried in dust, hay, fodder, and running streams.

Since 1892 anthrax has prevailed along the banks of the Delaware river for a distance of 40 miles in N. J. and Del., destroying from 70 to 80 per cent of the farm stock. The great morocco industry on this river draws infected hides from India, China, Russia, Africa and South America, and the spores are carried and distributed by the tides.

Infection-Atria. Infection may occur by a variety of channels as: 1st, by ingestion, giving rise most commonly to anthrax of the mouth, throat or intestines; 2d, by inhalation, giving rise to pulmonary anthrax (wool-sorter’s disease): 3d, by inoculation through contact of abrasions, wounds, etc., with infecting bodies, including surgical instruments: 4th, by flies and other insects: and 5th, by transmission to the fœtus in utero. This last form is very rare in the larger animals, but has been repeatedly seen in Guinea pigs, rabbits, goats and even in one case (Pangalli) in man.

Forms of Anthrax in Domestic Animals. In the lower animals anthrax manifests itself differently according to the seat of invasion and the amount of the virus. The worst forms, seen especially in cattle and sheep, are so sudden that they have been called apoplectic or fulminant. Without premonitory symptoms there is sudden loss of appetite, trembling, haggard expression of face, uneasy shifting of the feet, irregular movements backward or to one side, dyspnœa, cyanosis, plaintive cries, convulsions, ejection of blood by the nose or with urine or fæces, and death in a time varying from a few minutes to four hours. The second type is the anthrax fever, known also as splenic fever, splenic apoplexy, or internal anthrax. In this form there may be prodromata, especially in sheep, excitability, restlessness, and above all, a rise of temperature of often 3° or 4°. There may be distillation of drops of blood from the nose, eyes or ears, the mucosæ become congested, and in sheep this may show on the finer parts of the skin, as inside the forearm or thigh. Tremors, erection of the hairs, dulness, prostration, lagging behind the flock or herd, insensibility of the loins to pinching, inappetence, ardent thirst, grinding of the teeth, colics, tympany, mucus coated, bloody or liquid fæces, bloody urine, tumultuous heart beats, dyspnœa, dark, congested mucosæ, amounting to cyanosis, and spasmodic contractions of the muscles of the back, neck or eyes. If blood is drawn it may appear abnormally dark in color and very slow to brighten under the action of the air, it may have a thick, tarry appearance, and form a very loose clot. Death, (usually in coma or convulsions) will supervene, in sheep under 24 hours, in cattle in 2 to 5 days, and in horses in 1 to 6 days. The third type is the local or external anthrax, assuming in cattle the special forms of gloss-anthrax, pharyngeal anthrax, hœmorrhoidal anthrax, cutaneous and subcutaneous anthrax. In horses most of the same forms appear, in the tongue, throat, neck, shoulders, withers, flank or thigh. These swellings have a firm or doughy feeling, are comparatively and sometimes wholly insensible and show a marked tendency to necrotic changes. When incised they show extensive blood extravasation, or a pale, straw-colored exudate mixed with sanguineous lines or patches, and manifest no tendency to suppuration, nor to emphysematous crepitation. These features distinguish them from phlegmon and emphysematous anthrax. When suppuration ensues it is tardy and indolent and is, on the whole, a favorable indication. In all cases the bacillus may be found on microscopic examination of the exudate.

Lesions. Putrefaction of the carcass is usually rapid. In the very rapidly fatal cases the changes in the blood and tissues are often little marked, and after the removal of the enlarged, engorged spleen and infiltrated internal organs, the carcass might often be placed on the market without much suspicion. In more prolonged cases the blood is profoundly changed, being very dark, not subject to rapid æration, and incapable of coagulating firmly or at all. The red globules are crenated or otherwise distorted, adhere to each other in irregular masses, and have parted with much of their hæmoglobin which diffused in the serum stains the intima of the blood vessels and other white tissues. The leucocytes are relatively very much encreased. The bacteria are easily found in the intervals between the globules. The heart is often soft, discolored, as it were parboiled, with the endocardium deeply stained and the contained blood dark and diffluent or liquid. The liver is usually enlarged, softened, friable, and as if parboiled, with many hæmorrhagic patches. The spleen is materially, often enormously enlarged, irregular in outline from extreme engorgement with blood, and in exceptional cases even ruptured. An encrease to two or three times the normal is common. The bacilli are present in great numbers in the spleen, alike in the pulp, in the blood vessels and in the trabeculæ. The lymph glands are almost always hyperæmic, hypertrophied, and softened, especially in the vicinity of the localizations of the tissue lesions. They may be merely petechiated, or they may seem like a mass of black blood, and under pressure may break down readily into a sanguineous pulpy mass. Like the spleen they are favorite centres for the accumulation of the bacilli. The marked alterations in these glands will often indicate the channel by which the infection entered the body. The serosæ are usually hyperæmic, with many hæmorrhagic points and even extensive exudations, and they often enclose a sanguineous liquid. The hyperæmia and points or patches of extravasation are to be found in any part of the body in which the bacilli have been colonized, thus they are common in the tongue, the throat, the lungs, the stomach or bowels, the mesentery, the omentum, the skin, the connective tissue, or the muscular system. There may be bloody or gelatinoid exudation, but there are always the capillary embolisms by irregular masses of blood globules, and bacilli. These embolisms, the arrest of hæmatosis and the destructive action of the toxins on the red globules go far to account for the extreme fatality of the disease.

Morbid poisons. Hoffa found in anthrax cultures a ptomain which killed with anthrax symptoms. Hankin obtained a deadly albumose which in small doses procured immunity. Brieger and Fraënkel separated a toxalbumin, and Martin too, a protalbumose and a deuteralbumose together with a ptomain. Marmier separated a toxin which did not give the reactions of the albuminoids, albumoses, peptones nor alkaloids. This was not poisonous in small doses, to animals possessing immunity—natural or artificial. It was weakened but not destroyed by 110° C., and was rendered harmless by treatment with alkaline hypochlorites. Immunity could be induced by its use in small non-fatal doses. This is present in the bacilli and being soluble in water can be secured from these by diffusion in watery fluids and especially so if aided by heat.

Incubation. The implanted bacillus begins at once to multiply in the tissues, but the encrease is at first slow and the resulting morbid phenomena slight, so that there appears to be a period of incubation. In experimental inoculations in which this can be certainly noted it extends from one to two and even three days in the rabbit and Guinea pig, from two to four days in sheep, and from three to six days in horses and cattle. It may be shortened by giving an overdose and especially if this is introduced intravenously, the chemical poisons apparently acting at once. In young animals, too, the period is shortened, unless they have been rendered refractory by a milk diet or otherwise.

Symptoms. These vary according to the species affected, and the seat of the disease, general or local, internal or external. In the latter case the febrile and constitutional disturbance is delayed. In the internal cases the fever is early and of a high type. Even before the animal appears to be seriously ill, while still keeping with the herd and showing life and vigor, there may be high temperature, 104° to 106° F., pulse and breathing accelerated, heart beats tumultuous, tremors or shivering or perhaps only staring coat, anorexia, and grinding of the teeth. Later there may be drooping head and ears, dulness, a disposition to lie, apathy, stupor and somnolence. Nervous excitement and delirium have been noticed. The patient becomes weak, especially behind, comatose, and the temperature declines to, it may be, 97° or even 94° F., prior to death. The visible mucosæ becomes dusky, brownish or yellowish, and streaks of blood may appear in the nose or elsewhere. The urine may be red, the fæces covered with mucus, or blood streaked, and the rectal mucosa of a violet tinge, or blackish and blood gorged. In this the vulvar mucosa often participates. Local swellings may appear in the tongue or pharynx, even if not on the surface, or colics indicate implication of the digestive organs. The examination of the blood early reveals the presence of the bacillus, and as the disease advances, its black, incoagulable, tarry, or coffee-grounds appearance becomes characteristic. Pregnant animals are liable to abort. Death occurs in 12 to 48 hours. Most cases are fatal at the beginning of an outbreak, while later the great majority often recover.

Fulminant cases (Anthrax acutissimus) occur mostly in cattle or sheep, in high condition, the victim being found dead in pasture or stall, without previous observation of illness, or, if seen during life there is the sudden attack, leaving food, muscular tremors, anxious expression of countenance, hyperthermia, dyspnœa, dark red mucosæ, it may be streaks of blood on them, plaintive cries, rolling of the eyes, spasms or coma, and death in a few minutes to one or two hours. In sheep there may be separation from the flock, pawing, stretching, shaking of head, turning in circle, dyspnœa, falling, convulsive struggling, passing of blood by nose, kidneys or bowels and death.

Local Anthrax in Cattle. Symptoms. In cutaneous anthrax the circumscribed swellings appear suddenly, and may grow to considerable dimensions on different parts of the skin, head, neck, breast, shoulders, abdomen, axilla, sheath, udder, or flanks. There may be one or many, and they lack the acute early tenderness, and later crepitation of black quarter. On white skins they are dark red, or violet, and when incised, show a gelatinoid, bloody, non-suppurating mass, abounding in bacilli.

Gloss-anthrax implicates the whole, or it may be the roots only, of the tongue and the fauces. There is profuse salivation, perhaps bloody, intermaxillary and pharyngeal swelling, anorexia, and the tongue is found protruding, swollen, violaceous, vesiculated or with rounded nodules, or sloughs and ulcers, with lardaceous or blood stained bottoms. Hyperthermia and constitutional symptoms are present.

Pharyngeal anthrax is manifested by swelling of the throat, profuse salivation more or less marked with blood, complete dysphagia, attending on the marked febrile and constitutional symptoms already described.

Hæmorrhoidal anthrax, a common complication of the constitutional disease, is manifested by infiltration, blood extravasation, violet discoloration and often enormous swelling of the rectal mucosa, seen mainly during straining, but sometimes also as a constant protrusion.

=Local Anthrax in Sheep and Goats.= External anthrax swellings may form on the face, throat or udder with the general characters of those of the ox, but this form is much more rare than in cattle and horses. The usual form is the internal one, with engorgement of spleen, liver, and perhaps some other internal organ, and it is relatively very fatal.

=Local Anthrax in the Horse.= Symptoms. In anthrax districts, tumors form in the seats of inoculations on sores, insect bites, or sometimes without apparent local cause, as a result perhaps of a general infection. The infiltration takes place suddenly into or beneath the cutis, mostly on the head, tongue, throat, neck, breast, shoulder, inguinal region, mammæ, croup, or thigh, encreases rapidly, but without crepitation, or suppuration, the incision showing the general characters described in the ox, and early attended by the constitutional disorder. The general fever is often later in developing, less intense, and, on the whole, less fatal than the purely internal forms.

=Anthrax in Swine.= Symptoms. Swine are, on the whole, less susceptible than cattle, and on the strength of his laboratory experiments Pasteur denied their susceptibility. The mistake gained a wide acceptance, yet experienced practitioners knew that they were occasionally infected by eating the carcasses or droppings of anthrax cattle. I had seen a number of swine die in common with cattle in an outbreak at Swineshead, Lincolnshire, in 1863, and a like occurrence took place in East Lothian, and similar cases are reported by McFadyean, Trombitas and Von Ratz, while Crookshank and Perroncito have respectively inoculated the pig with success. In my experience at East Lothian a shepherd skinned an anthrax bullock and then castrated several litters of pigs, all of which died of anthrax. Much doubtless depends on the condition of the animal as regards food (flesh or vegetable), the presence of lactic or other organic acid, the coincidence of infection with anthrax bacillus and one of those conditions, which habitually enhances its virulence. There may be named venesection (Rodet) or its counterpart anæmia, the presence in the blood of inert powders—precipitates (Bardach), fatigue—sarco-lactic acid (Charrin and Roger), starvation—dyspepsia (Canalis and Morpurgo), privation of water (Pernice and Alessi), the products of previous or coincident illness (Galtier).

The pig, infected by ingestion, suffers especially from pharyngeal and intestinal anthrax. There is marked swelling of the throat with stiffness, dysphagia, champing of the jaws, salivation, frothing about the lips tinged with blood, dark, violet discoloration or ulceration of the fauces and tonsils, retching, vomiting, hoarseness of grunt, extension of the swelling to the face, with petechial spots and patches, diarrhœa with frothy or bloody fæces, great muscular weakness, a disposition to lie, it may be actual paraplegia, with the usual accompaniments of hyperthermia, constitutional disorder, cyanosed, or dusky brown, reddish or yellowish mucosæ, and the black, incoagulable blood, with destruction of the red globules.

=Anthrax in Dogs.= Symptoms. In the outbreak at Swineshead, Lincolnshire, in which the pigs suffered, one shepherd dog contracted the disease from eating the carcasses. It took the pharyngeal and intestinal form, with dysphagia, vomiting, bloody diarrhœa and high fever. Straus found that young puppies were very susceptible and old dogs refractory probably because of flesh diet and exposure. The excision of the spleen encreased the susceptibility to 76 per cent. instead of 20 per cent. (Bardach). Cornevin saw 5 dogs die the same night out of 7 that ate from an anthrax carcass. Much depends on the previous exposure and existing condition of the dog.

Cats have been observed to suffer under similar conditions. At Geneseo in 1877 I found that a cat and three young horses died from licking the blood from a stoneboat on which an anthrax hide had been carried.

=Anthrax in Birds.= Symptoms. Birds (chickens) are naturally less susceptible than swine, yet they succumb readily to inoculation, when the body has been cooled by partial immersion in cold water. Caplewsky found that, apart from artificial chilling, young pigeons of certain breeds were easily infected, and Œmler successfully inoculated small birds, sparrows, finches, canaries, yellow hammers, red breasts. The larger birds are more resistant but succumb readily if dosed with chloral hydrate, or antipyrin (Wagner). Birds of prey seem to be immune.

In chickens the disease is very acute, of rapid progress and fatal. A few hours after inoculation they are seized with dulness, debility, sunken head, drooping wings and tail, ruffled feathers, and dark red or black discoloration of comb and wattles. Dark colored anthrax swellings may appear on these last, on the eyes, tongue, palate or feet, and the obstruction of breathing may cause general cyanosis. Weakness is extreme, the bird staggers or is unable to rise, has violent tremors or convulsions, with bloody diarrhœa and perishes after a few hours or a day’s illness. The presence of anthrax in the locality, or in other species, will be to some extent a safeguard against confounding chicken cholera, entero-hepatitis or malignant œdema with this affection. The crucial diagnosis is based, as in other animals on the discovery of the characteristic bacillus.

Differential Diagnosis. The suddenness of the attack, hyperthermia, dusky, cyanotic, petechiated mucosæ, the escape of blood from mucous surfaces, the dark, tarry blood, brightening imperfectly on exposure to the air, its comparatively loose coagulum, the crenation and destruction of red globules, the staining of the serum with hæmatoidin, the leucocytosis, the engorged, enlarged liver and spleen, and the gelatinoid or bloody swellings, not gasogenic as in blackquarter or malignant œdema, together present a picture which is strongly suggestive of anthrax. If the malady affects domestic animals generally, is especially virulent in cattle, sheep and horses, and attacks even man; if the district is subject to anthrax, or of a rich damp soil which would be favorable to the preservation of bacillus anthracis; if it is in the line of watershed from stock markets, abattoirs, tanneries, rendering works, glue factories, packing houses, sausage factories, or phosphate works; if forage or new stock has been introduced from an anthrax district; and if the outbreak has taken place with a high water level, or during a dry hot season the case for anthrax will be strengthened.

The final tests are, however, by the microscope and inoculation. To discover the bacillus a power of 400 to 500 diameters is desirable. From the living animal take a drop of blood, exudate, or hæmorrhagic extravasation, make a thin film on a cover glass by drawing across it the straight edge of another one, dry the film, then pass it three times through the alcohol flame film downward, stain in anilin dies, or clear with acetic acid and examine. The bacillus is large (5 to 20µ by 1 to 1.5µ), nonmotile, of uniform thickness throughout, and sharply cut off at the ends. The bacillus of blackquarter is shorter, often club-shaped because of a spore in one end, has rounded ends, is flagellate, motile and gasogenic. That of malignant œdema is much thinner, has rounded ends, sluggish movements and is gasogenic. The bacillus subtilis (hay bacillus), is short, thick, with rounded ends each bearing a flagellum and is motile. The proteus vulgaris (common septic saprophyte) is small, short, with rounded ends, and very active movements. If the subject is dead we may examine the blood, or the scraping from the cut surface of the spleen, liver, kidney, congested lymph gland or other part bearing the lesion.

If we find in the carcass exudates gelatinoid or bloody (especially the latter), petechiæ, dark, uncoagulated blood, brightening little on exposure, blood gorged spleen, congested or hæmorrhagic condition of one or more internal organs, muscle or connective tissue, (particularly of the lymph glands), if the muscles of the loins, quarters, thighs, diaphragm or elsewhere, are soft, as if parboiled or salmon-colored, clammy, friable, or if reddish, yellowish, brownish, with petechiæ, and capillary embolism the case will require critical examination. If the first examination fails to show the bacilli, repeat it from different lesions until thoroughly satisfied of their absence, or until another cause for the condition has been discovered. The blocking of the capillaries with bacilli in the various lesions is a most important point, never to be overlooked.

In case of uncertainty, inoculation of a Guinea pig, mouse or rabbit should be made. The blood or scraping from the seat of a lesion is made into an emulsion if necessary, and injected subcutem. A single bacillus will destroy a mouse or Guinea pig in from one to four days, and the blood shows the characteristic bacilli.

One must, however, exclude the possibility of septic bacteria, excluding or obscuring the bacillus anthracis, by taking the inoculating material from the blood of the living animal, or from the same or the tissues as shortly after death as possible. Fifteen hours may be altogether too late for inoculation. To exclude the anærobic bacteria of black quarter, malignant œdema and septic affections, make an emulsion of the suspected material in sterilized water, filter through a boiled cloth and inject a strong dose into the auricular vein of a rabbit. The anærobic bacteria perish in the blood and if anthrax bacilla are present they are found in pure cultures.

In inoculating suspected water or infusion of forage the intravenous method should be adopted.

Another resort is to make two artificial cultures, one in free air, and the other in an atmosphere of nitrogen or carbon dioxide. The bacillus anthracis develops in the first, the anærobes in the second.

Prognosis. Mortality. Fulminant cases are uniformly fatal. Acute intestinal cases are usually fatal in 70 to 90 per cent. of the subjects at the beginning of an outbreak. Toward the decline most cases may recover. In a herd of 200 head, at Avon, N. Y. in 1875, 40 fat bullocks died in two weeks, and 50 more showed a marked hyperthermia, yet under a change of pasture, and antiseptics, all but two of the latter recovered. As serving to identify the disease, three attendants suffered from malignant vesicle, but recovered.

SUPPRESSION AND PREVENTION OF ANTHRAX IN HERDS.

Less simple or easy than in plagues. Germ survives in soil and water. Extinction not always possible. Killing: conditions demanding it: when unwarranted. Kill without shedding blood, or opening carcass. Body burned: if buried, 5 feet deep, in porous soil, distant from wells, ponds, and rivers. Fence graves, burn grass. Disinfection of hides, litter, fodder, manure, excretions, stalls, etc.: of bodies that must be moved, of buildings, yards, utensils, etc. Isolation of unaffected on porous soil; surveillance. Sales interdicted. Milk, butter, cheese. Immunization: by toxins which stimulate leucocytes to form defensive products: antitoxins. Eosinophile cells, action of spleen, and liver. Mellituria. Protection by a minimum dose: by weakened virus—modes of lessening potency, Pasteur’s “vaccine”, its drawbacks and dangers, its technique; by soluble toxins in sterile solution, author’s experience, apparent failures, advantages. Drainage—Æration of land. Prevention of importation and diffusion. Therapeutic treatment.

Prevention of anthrax in animals is equally important for the sanitation of herds and human beings. It involves the purging from the anthrax bacillus of the infected lands and the drinking supplies, and in this respect the disease is much less amenable to thorough and speedy extinction than is a simple plague in which the germ does not live and multiply outside the animal body. In some localities the extinction of the germ may be confidently counted on and secured; in others, it may be impossible and other measures of protection must be resorted to.

Killing of the Sick and Disposal of the Carcass. This is not always so imperative as in the obligatory parasitic infections, since the destruction of the sick, still leaves the germ present in the soil and water. If, however, the infection has just been introduced, on hitherto uninfected soil, by the arrival of new animals, and, if the new location is in any way favorable to permanent colonization by anthrax bacillus, and, if the diseased and suspected animals cannot be kept secluded so as to absolutely exclude these dangers, or again, if the diseased herd or its remnant is to be moved on to another locality, slaughter is the obvious sanitary measure.

The animal should be killed on the premises to avoid the danger of scattering the infectious discharges in transit; it must not be bled, nor cut open, as the admission of air determines the formation of the resistant spore; and the carcass must be burned, boiled, or rendered in superheated steam under pressure, or finally dissolved in strong mineral acids. If buried, it must be in open, porous soil, well apart from any well, pond, river, or bank where the liquids may leach out, and the body must be wholly covered to a depth of at least five feet. The graves must be well fenced in from all stock, for a number of years, and no forage grown on them can be safely fed to animals, as the bacillus can be brought to the surface by earth worms. I have known cattle to become infected through licking the fluid which escaped above a stratum of clay, on the deep bank of a river, at some little distance from where an anthrax carcass was buried in the surface sandy loam. A covering of coal tar, chloride of lime or of sand charged with sulphuric acid is an admirable precaution.

As a measure of economy the skins may be removed, if at once, on the spot, plunged for 12 hours in a 5 per cent. solution of carbolic acid, or cresyl, or creolin, or in a two per cent. solution of sulphuric acid, and, if the knives and other implements used are placed in boiling water for half an hour. The same will apply to fleeces.

Disinfection. All litter, fodder, manure, urine, and other excretions, or products; all stalls, feeding troughs, sheepfolds, covers, halters, harness, wagons, poles, shafts, and other objects used about the animals, or soiled by them or their products, should be disinfected by burning, flaming or scalding (boiling), when applicable, by one of the above-named disinfectants, by mercuric chloride (5:1000), by formalin, or other potent antiseptic. Extensive dung heaps, too wet to burn, may be sprinkled freely with strong mineral acids, or mercuric chloride in solution, piled into compact mass, covered with chloride of lime, and finally with a thick layer of earth, and fenced in from all stock.

If carcasses must be moved to the grave, rendering works, or elsewhere, they should be sponged with carbolic acid solution, formalin, or mercuric chloride, and each of the natural openings firmly plugged with tow or cotton soaked in the same material, so that no infecting material may drop on the way. They should on no account be dragged on the ground, but carried on a wagon or stone boat, which should be afterward carefully disinfected. Men or animals, entering an infected place, should be disinfected on leaving; especially hands and feet.

All roads, yards, and pastures where the sick have been, and, above all, where manure, urine, or saliva has fallen, should be subjected to thorough disinfection, or the surface layer removed and deeply buried. Where available, a concrete or asphalt floor should be placed in the buildings.

Isolation. Movement from Infected Ground. It has long been known that the movement of an infected herd from the contaminated pasture to another, will often, at once, check the development of new cases. In Sardinia and Auvergne the flocks and herds were yearly moved on the approach of autumn, from the rich valley, and bottom lands, to the drier hill pastures, to avoid or lessen the decimation that otherwise inevitably overtook them. This is in keeping with the enzoötic nature of the malady which arises more from the microbe preserved in the soil than from the sick animal direct. Two precautions are necessary in making such a change of locality: 1st, Animals already infected should not be moved on such new pasture; and 2d, the pasture to which the stock is moved should be entirely free from the impermeability (clays, hard pans), and saturation with water (swamps, basins, low bottoms), which would ensure the permanent preservation of any microbe planted there. Elevated, sandy, argilaceous or loamy soils are to be selected. To these the animals of the infected herd which by their appearance and thermometry may be pronounced sound, should be removed, and kept under careful supervision, especially as regards thermometric tests. Any showing symptoms of anthrax should be at once taken back to the infected herd. If they have stood in stalls, for milking or otherwise, these should be disinfected, and they should be carried in wagons, or driven by unfrequented roads. Their droppings should be carefully disinfected.

If, in the absence of anthrax symptoms, animals must be kept in the infected lot, or returned to it, they should be immunized.

Interdiction of Sales. No animal in the infected herd which shows a rise of temperature, should be sold even for slaughter. No animal should be sold for stock purposes until the disease has completely subsided. Any animal in the infected herd, which shows no hyperthermia nor other sign of anthrax, may be sold for immediate slaughter, subject to a critical expert examination of the cadaver for anthrax. Milk, the product of an infected herd, and butter and cheese made from such milk, should not be used as food. If those members of the herd, that show no hyperthermia or other symptom of anthrax, can be held apart as a separate herd, in a disinfected place and under careful thermometric observation, their dairy products may be used.

Immunization. A number of different methods have been practiced of rendering animals refractory to the bacillus anthracis, but all are apparently based on the production in the system of defensive products, as the result of a nonlethal poisoning with anthrax toxins. It is true of anthrax as of many other infections that a first attack protects against a second. In all animals there is a certain measure of defensive power against the bacillus anthracis, amounting in some cases to virtual immunity and in others having a very little effect. The object in immunizing is to stimulate to the increase of these defensive products in quantity or power until an ordinary dose of the bacillus will fail to colonize the tissues or the blood. In considering this subject a clear distinction must be made between the simple bactericidal and the antidotal or antitoxic products found in the serum of immune animals and the toxins which are produced by the bacilli. The soluble antitoxic and bactericidal agents found in the serum of the immune, may be employed for therapeutic purposes to preserve life in an animal which has received a lethal dose of the bacillus anthracis, but as these are rapidly eliminated from the system, their protective power is very short lived, and if some bacilli survive the period of their presence and potency, or if they are introduced into the system later, the animal may fall a victim to anthrax as if no such protective agent had been used. Behring showed that the blood serum of the white rat proves fatal to the bacillus anthracis, but Metchinkoff pointed out later that it must be brought in contact with the bacillus in order to prove effective, whereas if the serum and bacillus were injected at different parts of the body no protection was obtained. The antidotal or bactericidal action of the serum of an immunized animal acts at once, whereas a permanent immunity cannot be established before about fifteen days. The serum of the immune animal contains the following elements antagonistic to anthrax: Antitoxin or leucomain which may be poisonous to the bacilli, or chemical antidotes to their products: globulicidal principles which distort or disintegrate the blood globules and release their contents including the bactericidal nuclein, and probably others. All such agents when injected into the system are present only for a limited time and while they may be made subservient to a temporary immunity, they can give no permanent protection and must be considered mainly as therapeutic agents.

A permanent immunity must depend on a stimulation or education of the system to the production of these protective agents de novo or in increased quantity. This must be done by exposure of the tissues to the toxins of the bacillus anthracis, and is accomplished slowly. Precisely what tissues are stimulated to the production of the defensive agents is not fully known, though certain indications may be drawn from observant facts. The eosinophile cells of the blood are presumably important factors as the natural sources of the leucomaines. The spleen as the seat of important blood changes and as preëminently the seat of election of internal anthrax is probably involved. The dogs from which Bardach had removed the spleen were found to be three times as susceptible to anthrax as were the dogs that had not been operated on. Leo’s rats, in which he had produced mellituria by the administration of phloridzin were found to be much more susceptible to anthrax. The liver is also a favorite seat of election of internal anthrax. The products of the healthy liver, are probably in some measure protective.

No matter where the defensive products are formed, the practical problem is to secure their production without imperilling life.

By Minimum Dose. Chauveau and Colin secured this in the larger animals by intravenous injection of a minimum dose,—one or two bacilli. This is more lasting in effect if a second and stronger dose is injected some days later.

By Weakened Virus. This has been secured by heating the defibrinated blood to 55° C. for ten minutes (Toussaint); Pasteur, Chamberland and Roux accomplished the same end by making anthrax cultures at 42° to 43° C. in presence of air; Chauveau by subjecting the virulent culture for eight days to oxygen under a pressure of 8 atmospheres at a temperature of 38° C.; Chamberland, Roux and others have cultivated the bacillus in weak antiseptic bouillons as phenic acid (1:600 or 1200), bichromate of potash (1:2000 or 5000), sulphuric acid (2:100).

Other methods have been followed, as growing the bacillus in the blood or serum of immune animals (dog, chicken, pigeon, white rat, frog).

Of these different methods that of Pasteur has been most extensively adopted. The temperature of culture (42° C.) prevents the formation of spores and the duration of exposure to air gradually lessens the virulence until in 12 or 13 days it is not fatal to the Guinea pig and after 31 days it fails to kill the young mouse. Thus preparations of varying grades of virulence, and adapted to the varying susceptibility of different animals, are secured. The protective inoculation is made by preference in spring, when there is less chance of complication by a coincident accidental infection, it is to be avoided if possible in animals at hard work, in advanced gestation, in full milk, in extreme youth, or in ill health. To secure the best results it should be repeated with a stronger preparation 12 to 15 days after the first injection. The acquired immunity lasts a year and over, and it is probably perpetuated by new and non-fatal doses taken in casually, on the anthrax pastures. Hundreds of thousands of live stock in all parts of the world have been treated in this way with the result of reducing a mortality of two, five or ten per cent. to insignificant proportions. It can only be safely adopted on anthrax lands, as elsewhere it may lead to the stocking of new areas with a malignant germ which in young and susceptible animals reacquires its original virulence.

It can never be safely ignored that we are dealing with the living seed of a most deadly infection. Though robbed of a large part of its virulence by artificial culture at 107:5° F., yet many accidental conditions, contribute to a relapse to its original potency, and when it has once killed a victim, the reacquired virulence is usually persistent. If the virus employed for protective purposes in cattle and sheep, is inoculated on Guinea pigs of 1 to 30 days old, from these on those of several months, and from these last on sheep, the virulence is constantly and persistently enhanced. The same is true of the microbe which is inoculated on a succession of pullets of steadily encreasing ages (Roux and Chamberland), or on a succession of pigeons (Metchnikoff). The germs reinforced in potency in any such way are liable to be the starting points for dangerous infections in animals and permanent contamination of soils and waters. Fortunately an occurrence of this kind is rare, yet with a wide application of the Pasteurian inoculation the opportunities also are great, and with the free sale and distribution of the mitigated virus (anthrax “vaccine”), the evil may grow indefinitely. The method departs from the ideal one, aimed at a final extinction of the disease, and accepts in place a mere temporary protection of the herd or flock, and though in this affection eradication cannot always be secured, every effort should be made to gain it and above all to prevent an encrease of the area of infection.

Technique. The weakened virus (1st “vaccin”) is sold in tubes holding enough for 100, 200, or 300 sheep. Of this ⅛ cc. is injected subcutem on the inner side of the thigh of the mature sheep, and 12 or 15 days later a similar dose of the stronger preparation (“2d vaccin”). For the ox or horse double the amount (¼th cc.) is used, being injected behind the shoulder, and on the side of the neck in the respective animals. The dose is graduated in the different subjects according to the size and age, yet a considerable latitude is permissible. The syringe must be disinfected before and after inoculations by a 5 per cent. solution of carbolic acid, or by boiling, and the nozzle should be dipped in strong carbolic acid immediately before and after each insertion. This will greatly obviate infection of the liquid used, and of the wound by any virulent germs lodged on the surface of the skin. The liquid to be injected should be used as soon as possible after preparation, and if kept should be in a dark cold place, and if the tube is once opened the whole of its contents should be used the same day,—never kept over. The second, stronger preparation should never be used until the system has been prepared for it by the use of the first.

By the Soluble Toxins in Sterile Solution. In 1884, in an outbreak of anthrax in Skaneateles, N. Y., I drew blood from an anthrax cow, subjected it to 212° F. for 30 minutes, dissolved out the soluble toxins in boiled water, and injected the product subcutem, in the dose of 2 to 4cc. according to size, into every apparently healthy member of the herd, excepting one, which was left as a check. The check animal died of anthrax while all of the others escaped.

Since that time I have personally used it in every herd where opportunity offered, and with equally good results. In an outbreak near Elmira, Dr. Moore adopted it in a large dairy herd, and the disease was suddenly arrested.

In several experimental cases (one cow and 2 Guinea pigs) at the N. Y. S. V. College, the outcome was not so satisfactory and in a herd in Oneida Co., N. Y., it is said to have failed to check the disease.

Notwithstanding these untoward results in other hands, I am still confident that we have in this a measure of no small value, and worthy of application in suitable cases. A certain percentage of failures in immunization are to be looked for. Even cowpox vaccination is not always protective against itself; I knew one man who was successfully vaccinated every three years in a comparatively long series. Many habitually self-limiting diseases relapse in particular individuals. Even in the case of anthrax excess of glucose in the system, and the lack of some unknown influence of the spleen are respectively destructive of immunity. Even after the Pasteurian inoculation a certain number of inoculated animals are lost, it may be between the first and second injection, or it may be “two or three months” after the latter (Galtier). We must also bear in mind that in an infected herd or flock, there are always a certain number already infected at the time of the protective inoculation, and as the protective conditions are slowly established, through the action of the leucocytes, it is unreasonable to expect that serious illness and death can be obviated in such animals.

In inoculation with the Pasteur lymph, the bacillus is held not to enter the blood, a position supported by the researches of Bitter, Perroncito, Wissokovicz, Lubarsch, Metchnikoff, Chamberland and Roux, so that the resulting immunization must come from the toxins. Add to this that Chauveau (1885), conferred immunity on a sheep by injecting intravenously, anthrax blood, defibrinated and sterilized by heat: Arloing obtained immunity in the sheep by injecting, subcutem, the clear supernatant liquid from old bouillon cultures of anthrax, from which all bacilli had been precipitated. Roux and Chamberland obtained the same result by using the pulp of an anthrax spleen treated with essential oil of mustard, so as to destroy the life of the bacillus, and then evaporated in vacuo to remove the essence. Smaller doses proved effective, than when the splenic pulp had been filtered or sterilized by heating to 58° C.

The advantages of using sterilized toxins are numerous:—

1st. As the material can be derived from a case of the outbreak in hand, there is no risk of using the anthrax protective inoculation for black quarter, hæmorrhagic septicæmia or other disease which is so often confounded with it.

2d. There is no danger of the sudden enhancing of the potency of a weakened microbe on account of some condition of the animal inoculated, as no living microbe is employed.

3d. There is no possibility of planting the anthrax bacillus, on new soil, as is so liable to take place in using the weakened microbe.

4th. There is no necessity for the care and cost of holding the inoculated animals apart by themselves, under official veterinary control for 15 days, of withholding their products from market, or of disinfecting the place where they have been kept. On the contrary the animals inoculated can be treated in every way as if no such injection had been made.

Thorough Drainage and Æration of Land. The most thorough and permanent method of eradicating anthrax is by thorough æration of the soil. In dry, sandy, or gravelly soils, having a good natural or artificial drainage, and not underlaid by an impermeable damp stratum, the bacillus is never permanently found, and, if introduced, is slowly robbed of its virulence by the action of the oxygen. When a soil can be well and permanently ærated by thorough underdrainage, a few years suffice to rob it of its infecting property and render it salubrious. In many localities, however, this is actually or economically impossible, so that the owner is thrown back on the alternatives, of abandoning the soil for stock, or of immunizing all the animals placed on it.

Prevention of Importation of Anthrax. To prevent the introduction of anthrax into a country or district, the usual control must be exerted on trade in cattle and their products, as in the case of other infectious diseases. The exclusion of livestock from an anthrax-infected country or district, or the admission after 6 to 10 days of quarantine and the disinfection of the surface of the animal. Dried hides, horns, hoofs, hair, wool and bristles are even more dangerous, as they are liable to hold the microbe in the spore form which will survive indefinitely and plant the disease widely. The recent great extension of the disease along the Delaware River, in connection with the morocco factories, which draw their hides from the most virulently anthrax regions (India, China, Russia, Africa, S. America) is a strong case in point, and nearly every tannery planted on a favorable soil is an example on a smaller scale. Disinfection of all such products on arrival is essential. But this should be thorough, and no question of trouble nor expense should stand in the way. If the trade cannot stand the expense, it has no right to exist where it is, at the expense of threatened ruin, local and ultimately general, of agriculture, on which all other industries are based. Similar control is demanded of live stock products from infected regions in America.

The control of home markets, stockyards, and abattoirs is no less important. Fortunately the disease is shortlived and deadly, and is much more easily discovered and arrested than in the case of plagues with prolonged incubation and frequently occult form (glanders, tuberculosis). An inspection of the various markets, and the detention of herds that have shown anthrax infection would do much to limit extension. This would entail the disinfection of the infected places, cars, boats, harness, clothing, and other things, and of the skins of the healthy animals of the infected herd.

The Therapeutic Treatment of anthrax in animals must in the main follow in the same lines given below for the human being; locally, antiseptics (mercuric chloride or iodide, Luzol’s solution, hydrochloric acid, phenic acid, iodized phenol, creoline, cresyl, oil of turpentine, formalin, salicylic acid, scarification, excision of the primary sore or swelling with antisepsis, antiseptic injections into the swelling.) Internally, there have been employed, dilute phenic acid, creolin, terebene, calomel, quinine, hydrochloric acid, bichromate of potash, tincture of iron chloride, etc. (see below).

ANTHRAX IN MAN.

Causes: infection from animals and their products, from soil, by flies, by dust. An industrial disease, of workers among animals and animal products. Wounds as infection atria, ingestion anthrax, inhalation. Lesions: malignant vesicle, anthrax œdema, intestinal anthrax: pulmonary anthrax. Symptoms: malignant vesicle, œdematous anthrax, intestinal, pulmonary. Prevention. Treatment: caustics: antiseptics, excision of nodule and subsidiary glands, mercurial ointment, iodine, sodium bicarbonate. For intestinal anthrax: emetic, oleaginous purgatives, potassium iodide, sodium salicylate, iron muriate, heart stimulants. For pulmonary anthrax: inhale chlorine, iodine, bromine, phenic acid, eucalyptol, oil of cinnamon, sterilized cultures of prodigiosus, pneumococcus of Friedländer, bacillus pyocyaneus, staphylococcus aureus, or streptococcus: blood serum of immune animals: blood serum (sterilized) of anthrax cattle.

Causes. Anthrax in man is usually the result of contamination by infected animals or their products. It is quite possible that man, like animals, may be infected directly from the soil or water, or from the same source through the medium of flies or windblown dust, yet undoubted cases of this kind are rare or unrecognized. The animal origin of the disease, as regards man, makes this largely an industrial affection, attacking shepherds, cattlemen, horsemen, farmers, drovers, butchers, veterinarians, tanners, and workers in hides, wool, hair, bristles, furs, hoofs, bones, rags, felt, glue, and even leather. The sound skin is sufficient protection, but the slightest abrasion may form an infection atrium. Workers in tanneries and those who live near them are notoriously subject to anthrax. The hides must of course be drawn from an anthrax region. Russian, Armenian, South American, Australian and African hides have an especially bad reputation. The British Medical Journal, May 21st, 1898, records cases occurring in postal clerks who had to handle foreign parcels bound with strips of hide. Proust records cases from handling Chinese goat skins (Bull. de l’Acad. de Med. 1894). Infection may also occur through leather made from infected hides as proved experimentally on Guinea pigs.

Hair has long been recognized as a frequent medium of infection and outbreaks among brushmakers have been recently recorded by Gerode, Sarmont and Chauveau. (Compt. Rend. de l’Acad. des Sc. 1893). Trousseau reports twenty cases in Paris, all contracted from South American horse hair. Wool from infected countries is often dangerous and has given rise to special names for the disease (wool-sorter’s, rag-picker’s) which may be developed in the lungs from inhalation of the dust. In the same way those who handle bones about fertilizer, glue and rendering works, are particularly exposed. The agency of insects in man is undoubted. In sixty cases recorded by Dr. Bell, fifty-four were on the face, two on the hands, one on the wrist and one on the forearm. This is mainly due to blood-sucking flies, yet Heim incriminates the coleoptera as well (Compt. Rend. de Soc. de Biol. 1894). Wounds of all kinds contribute to inoculation, hence, the presence of burdocks, thorns, thistles and the like in the matted wool or hair is often a direct cause of infection.

The infection may be transferred on surgical instruments, and in these days of hypodermic medication the greatest care is necessary to prevent infection through the needle.

As in animals man suffers from ingestion and inhalation of the bacillus; and sometimes widespread mortality comes in this way. Meat just killed may be thoroughly disinfected by the secretions of a healthy stomach, yet the bacillus may pass through in an envelope of fat, in an undigested mass or during an attack of dyspepsia, and infect the intestines. The spores are proof against the gastric juice, and as they are produced in a few hours after death the meat of an anthrax animal must always be considered as exceedingly dangerous.

Man is much less susceptible than some other animals and the disease wherever inoculated tends to remain for a time localized, in the skin, the lungs or the bowels. The forms of the disease are malignant carbuncle (pustule), malignant œdema, intestinal anthrax, and pulmonary anthrax.

Lesions. The morbid histology is in the main the same as described in animals. In the protracted cases there is the same dark nonærated blood, forming a loose coagulum, the crenated or distorted blood globules aggregated in irregular masses, the escape and solution of the hæmoglobin so as to stain the white tissues, the enlargement of the spleen which is gorged with dark blood, and the hyperæmia of the liver and lymph glands. There is in the affected tissues and usually in the blood the characteristic large bacillus anthracis.

In the malignant vesicle there is first a minute, firm central, dark nodule like an insect bite with a lighter colored areola, and showing not only hyperæmia, but blocking of the capillaries, and minute areas of extravasation. Somewhat later the dark centre is surmounted by a small vesicle, beneath which the tissues are becoming necrotic, and the area of congestion and extravasation has extended and thus the local disease advances by a constant invasion of new tissue which in its turn becomes the seat of coagulation necrosis. On microscopic section the central necrotic part shows the cells of the rete Malpighi separated by a finely granular coagulum, and the papillæ are greatly swollen by serous and hæmorrhagic exudate. The cell nuclei are necrotic and no longer take a stain. The capillaries are gorged with red globules and bacilli. In the surrounding tissues there is much congestion and exudation, with numerous points of extravasation, but the abundant multinuclear cells retain their staining power.

In Anthrax Œdema, which appears in parts like the eyelids, neck and forearm where there is an abundance of loose connective tissue and a scanty blood supply, there is no firm central nodule, but a diffuse soft infiltration, with points or patches of a yellow or reddish color. The capillaries are congested, with minute emboli and extravasations and there is an excessive and rapidly spreading exudation. It shows a great tendency to early general infection and may end in vesication and local gangrene or in favorable cases in resolution.

In Intestinal anthrax (intestinal mycosis) the lesions are usually concentrated on the small intestines, while the stomach and large intestines in the main escape. The walls of the bowel are of a dark red, and greatly thickened by exudation and extravasation which also mixes with the ingesta giving it a dark bloody tinge. At intervals on the mucosa are nodular hæmorrhagic swellings, from the size of a linseed to a pea, with commencing necrotic changes or the formation of sores. The mesenteric glands are swollen, infiltrated and hæmorrhagic, and like the other lesions abound in bacilli. Hyperæmia and engorgement of the liver and above all of the spleen are the rule.

In pulmonary anthrax (wool-sorter’s disease) a sanguineous liquid is found in the lower trachea and bronchia, and not infrequently in the pleuræ and pericardium. The bronchial glands are swollen, hyperæmic and often hæmorrhagic, and exudations and extravasations may be found in the mediastinum and lungs. Lesions of the intestines and spleen are common, and in all alike the bacilli are found.

In certain cases the anthrax lesions may be found in the brain, or any part of the body but in all they show the same general characters and the same specific microbe.

SYMPTOMS: DIAGNOSIS.

Malignant Vesicle (pustule). Symptoms may vary somewhat but are in the main as follows: An itching papule appears in the seat of inoculation, which might be mistaken for an insect bite but for the dark red color of the centre. Occurring on an uncovered portion of the skin, in an anthrax district, or near a factory where anthrax products are likely to be used, this should at once create suspicion. Soon the dark centre is covered by a small vesicle with clear contents which later become bloody. Within 24 or 48 hours the vesicle dries up, becoming firm, resistant and brownish red or blackish gray, and apparently gangrenous. The swelling has meanwhile extended to ½ or ¾ inch in diameter and a row of fresh vesicles may appear which in their turn give place to a necrotic slough. In this way extension may take place, the sore retaining a more or less rounded form, and necrosis extending from the centre in every direction. The necrotic mass, however, remains firmly adherent to the adjacent tissues until separated by the work of suppuration which ensues in favorable cases. The disease is attended with more or less fever, chill, hyperthermia, nausea, diarrhœa, with aching of head, back, and limbs and unfavorable cases may merge into acute and fatal general anthrax. The mortality is about 20 per cent., though in special epidemics it has reached 80 per cent. (With the pustule on the face 25 per cent.; on the lower limb 5 per cent., Norris). The prognosis is favorable with a free concentration of leucocytes, a moist condition of the wound and above all a liberal invasion of pus cocci. It is unfavorable when the wound is dry, when the drying slough remains firmly adherent and when the adjacent lymph glands become implicated. In non-fatal cases it may be difficult to find the bacillus.

Anthrax Œdema. This is less easily diagnosed than malignant vesicle, and appears where the connective tissue is loose, abundant and little vascular, from direct local inoculation, or as a concomitant of internal anthrax. It is a flat, rapidly extending swelling, with the skin comparatively unaltered, though at points yellowish or reddish discoloration indicates congestion and extravasation. Not being limited by firm tissues nor aggregations of accumulating leucocytes it tends to a speedy general infection with all the febrile manifestations of that condition. Thus chills, nausea, hyperthermia, dusky reddish or brownish mucosæ, cephalalgia, rachialgia and profound prostration assist in diagnosis. The bacilli in the blood and exudate would serve to confirm the conclusion.

Intestinal Anthrax. Here again the ingestion of anthrax products, and the simultaneous attack of a number of people who have taken such materials will often assist in diagnosis. There may have been for some days indications of local bowel lesions, such as chilliness, elevation of temperature, nausea, headache, and giddiness. Suddenly these become more violent, there is vomiting and sanguineous diarrhœa, extreme anxiety and debility, cyanosis, dyspnœa, and it may be the appearance of petechiæ on the skin and mucosæ or even of local swellings. In some cases there are convulsions or other symptoms of nervous disorder and in others extreme prostration and collapse. The bacillus is not always to be found in the circulating blood, but may be detected in sanguineous excretions, or by cultures.

Pulmonary Anthrax. (Woolsorter’s disease). Here again the occupation of the patient assists in diagnosis. For two to five days prodromata similar to those of intestinal anthrax may be noted. The difficulty in breathing, dyspnœa, cough, cyanosis and sense of constriction of the chest are especially diagnostic. Suddenly all these symptoms are aggravated, respirations become 30 to 40 per minute, the pulse 120 to 150, the temperature 104° to 106°, and there is a frothy bloody expectoration in which the bacilli may be detached. There may be indications of intestinal, cerebral or nephritic lesions, and bloody discharges. Death usually occurs in 12 to 48 hours from collapse, or coma, from asphyxia or in convulsions. The few recoveries are tardy and tremors and spasms persist for a length of time. In the most favorable cases the disease does not proceed beyond the initial stage.

PROPHYLAXIS AND TREATMENT.

Prevention is the most important consideration and this will include all that has been stated above with regard to the restriction of the disease in flocks and herds, the drainage and improvement of anthrax lands, the seclusion, destruction, deep burial or cremation of carcasses without autopsy or incision, the disinfection of stalls, secretions and all contaminated products, and the suppression of all traffic in anthrax products—meat, milk, blood, guts, bones, horns, hoofs, hair, wool, bristles, etc., or the thorough disinfection of the same. Above all, is the adoption of personal precautions. No one should handle anthrax animals, nor suspected products who has any sore or abrasion on hands or face, or such sore may be temporarily covered with a film of albuminate of silver, or the hands may be washed with a solution of mercuric chloride (1:500), or chloride of lime (1:200). If persons must work in wool or textile products which are open to suspicion a respirator is an obvious precaution, and this may be disinfected by live steam at intervals.

Treatment of malignant pustule is mainly surgical. At the outset the thorough destruction of the dark central point or nodule with a red hot needle or powerful caustic will be sufficient. Even when the pustule is fully formed, its free excision with as much of the surrounding infiltrated tissue as can be safely accomplished and the free application of caustics will usually succeed. Potassa fusa, or zinc chloride (1:3), or mercuric chloride or iodide in powder with or without calomel, or pyoktanin, or formaline, or iodized phenol may be named as especially applicable. Injections of carbolic acid (5 or 10:100) into the indurated centre and infiltrated periphery have proved very successful. In the case of Kaloff, when the excision of the nodule followed by the local use of carbolic acid solution, failed to prevent implication of the inguinal and pectoral glands, violent fever, prostration, and diarrhœa; the excision of the affected glands and the free use of phenic acid solution (5:100) in the adjacent tissues led to speedy improvement. Some surgeons make a crucial incision of the pustule and apply caustics freely. Muskett has been successful in excising the nodule, filling the wound with ipecacuan powder and giving the same agent internally. Many mild cases, or those that occur in refractory systems will however recover spontaneously or under a less drastic treatment. In the anthrax districts of Russia mercurial ointment is rubbed on the sore, and the application of tincture of iodine or iodized phenol to the raw sore or incised nodule and surrounding infiltration is often successful.

Camescasse has claimed great success by incising the swelling, applying tincture of iodine freely, and then wrapping in cloths kept wet with a solution of 5 drachms of bicarbonate of soda in a quart of tepid water.

When systemic reaction has set in it is desirable to have resort to general medication as for internal anthrax.

Treatment of Anthrax Œdema must follow the same rule. Free incisions into the œdematous tissues with the application of antiseptics, solution of mercuric chloride or biniodide (1:1000), or the injection of the whole infiltrated area and around it with the same agents, with phenic acid (5 or 10:100), or with pyoktanin (1:1000) will prove useful, and as in the malignant pustule the surface should be kept disinfected by a compress wet in solution of the mercuric chloride or biniodide, carbolic acid, iodized phenol, formalin or pyoktanin. If the pain of these applications is very acute cocaine will be demanded or even ether. If ether is applied to the surface its evaporation will cool the parts and retard the proliferation of the bacillus. Under other conditions cold water, pounded ice or snow may be applied.

Treatment of Intestinal Anthrax. When anthrax flesh has been eaten, or when there are symptoms of incipient intestinal anthrax, the first resort is an emetic of ipecacuan, followed by an active oleaginous purgative to clear the prima viæ of bacilli and their toxins. To these may be added potassium iodide, pyoktanin, sodium salicylate, quinine or tincture of muriate of iron, by way of keeping in check the multiplication of bacilli. To counteract depression and heart failure digitalis, strophanthus or strychnia with alcoholic stimulants may be resorted to.

In Pulmonary Anthrax the same principles are applicable. The patient may be made to cautiously inhale gaseous chlorine, iodine or bromine or a solution of iodide of potassium in an atomized condition. The vapor of carbolic acid, eucalyptol, or oil of cinnamon may be tried.

The irritable stomach may be soothed by oxide of bismuth, with milk, beef tea and other bland nutritive or stimulating draughts.

The grave character of internal anthrax, however, is such that resort may be had to one of the various antitoxins, antidotal cultures, serums, and immunizing agents that have proved useful in different hands. Unfortunately such agents do not seem to act in the same manner on all genera, and what has been effective in one of the lower animals may fail in the human being. Thus Roger found that sterilized cultures of bacillus prodigiosus retarded or obviated anthrax in rabbits, but hastened its progress in the Guinea pig.

The sterilized cultures of the pneumococcus of Friedländer (Buchner) of the bacillus pyocyaneus, or of the staphylococcus pyogems aureus, (Pawlowsky) when injected subcutem have proved antidotal to anthrax. Emmerich has successfully used erysipelas serum subcutem in the treatment of anthrax. (Münch. Med. Woch. 1894). The sterilized cultures of the streptococcus erysipelatos therefore offer themselves as promising curative agents. The same is true of the sterilized cultures of the bacillus pyocyaneus (Woodhead and Cartwright-Wood).

The blood serum of animals that are naturally immune (frog, white rat, pigeon, dog,) is bactericidal and to a certain extent antidotal to the bacillus anthracis, but that of an animal which is naturally susceptible but which has been artificially immunized has proved much more potent. In the experience of the writer this potency attaches no less to the blood of an animal in the advanced stages of the disease. In adult cattle he has found the symptoms of anthrax subside under two successive daily doses (4cc.) subcutem of the sterilized blood serum of one of the herd which had just died. Relapses were observed several days after the serum treatment was abandoned. In experiments on rabbits two check animals with anthrax inoculations died at the end of 3½ and 4 days. Of six inoculated with anthrax and injected from one to three times with sterilized (anthrax) blood serum one recovered, and the others died, one at the end of the 7th, two of the 6th and two of the 5th day. In this connection it may be stated that successful treatment by leucocytes is claimed, (Pawlowsky) and that one of the effects of serum treatment is the destruction in part of the globules and the release of nuclei, and in this we may have an explanation in part at least of the therapeutic action of the serum from the infecting and immunized animal.

Protective serums may be utilized by hypodermic injections daily or every second day for a week, giving time for the disposal of the bacilli present in the system. In the intestinal anthrax they may be given by the mouth and injected into the peritoneal cavity. In pulmonary anthrax they may be introduced into the trachea, bronchi and pleural cavity.

GLANDERS.

Synonyms. Definition: Acute, infectious, microbian disease, often localized in lymph glands and plexuses of nose and air passages, etc.; with hyperplasia, degeneration, necrosis, liquefaction. Affects solipeds, and, by inoculation, man and all domestic animals save cattle, chickens and (usually) swine. Geographical distribution and historic notes: known in Ancient Greece; now where solipeds live and fresh subjects are exposed; Central Europe; great horse trade and movement; war, Franco-German, Napoleonic, Afghanistan, American Civil War, Boer War. Unknown in Australia. Susceptibility: solipeds, Guinea-pig, rabbit, goat, cat, dog, pigeon, sheep, and swine in low condition. Cattle, chickens, white and house mice, linnets, chaffinches, and frog immune. Microbe lives in frog in water at 86° F. Cause: Bacillus mallei. Accessory causes: trade in solipeds, mingling of sound and sick, crowding, common feeding and drinking troughs or buckets and racks, debility, low condition, starvation, overwork, damp, dark, draughty stables, carriage in transports or cars. Insular quarantined lands—Australia, Tasmania, and New Zealand exempt. Bacteriology: Bacillus Mallei; 2 to 5μ by 0.5 to 1.4μ, nonmotile, ærobic grows in ordinary culture media, stains tardily but is easily bleached. Spores uncertain, easily killed by disinfectants, preserved in stables, does not grow in infusion of hay, straw or horse manure, lives 15 to 20 days in water; infection by coitus, and through placenta, by ingestion, by blood transfusion, through dust; microbe in all lesions and discharges, (unless sometimes in milk, sperm, etc.). Infection-atria: skin wound, mucosa, hair follicles, lungs. Forms: Acute, chronic, nasal, pulmonary, cutaneous (farcy), orchitic, arthritic, abdominal, occult. Symptoms: nasal; incubation, 3 to 5 days, languor, weariness, stiffness, horripilation, tremors, inappetence, thirst, hyperthermia, epiphora, snuffling, nasal discharge, serous, viscid, agglutinating, purulent, swollen alæ, violet mucosa, elevated spots and patches with central ulceration, may become confluent, and involve submucous tissues; submaxillary lymph glands swollen, nodular, not tender, non-suppurating, swollen (corded) facial lymphatics, from nose, eye or lymph glands; swellings, cutaneous and lymphatic in skin of limb or body, ulcers (farcy buds), deposits in throat or lungs; chronic cases; slow, indolent, persistent, nasal discharge—unilateral (or bilateral), viscid or not, nodules on mucosa with whitish centres or points; red areolæ, later ulceration, puckered white cicatricial lesions, submaxillary swelling, nodular, large or small, insensible; cutaneous cases; arthritis with lymphangitis, skin engorgement, corded lymphatics with ulcerating nodules, sanious discharge, intermuscular abscesses. Occult cases: lesions in internal organ;—cough, leucorrhœa, enlarged testicle, low condition, weakness, lack of endurance. Diagnosis: inoculation of male Guinea-pig in flank or peritoneum,—ulcer and orchitis, cat, dog, old soliped; mallein test,—swelling, involving lymphatics, fever, 1.5° to 2.5 F. and upward above normal, at 10th to 18th hour, lasting two days. Lesions: cell proliferation in nests in fibrous stroma, pea upward, central degeneration, fatty debris, ulcer or abscess, hyperplasia of lymph vessels, on nasal mucosa like sand-grains, peas, patches, centre grayish or yellowish, blood extravasation, necrotic degeneration, ulcer with ragged edges; fibroid degeneration—cicatricial lesion; lesions in guttural pouch or tube, larynx, trachea, bronchia; lungs—peribronchial, lobular or interlobular inflammation, cell proliferation in foci, degeneration—nodules—and caseation; skin,—cell proliferation, degeneration, rupture, fibroid hyperplasia of lymphatics, exudates in connective tissue; dependent lymph glands congested, hypertrophied, cell proliferation, caseation; lesions in pharynx, spleen, kidney, heart, brain, testicle, scrotum, mammæ, vagina, uterus, joints, bones; bone fragility. Glanders in swine, sheep, goat, rodent, dog, cat.

Synonyms. Malleus, Equinia, Farcy.

Definition. An acute infectious disease caused by the bacillus mallei, which tends to localize itself in the lymphatic glands and plexuses, especially of the nose and upper air passages but also in other parts of the body, where it produces a progressive hyperplasia, with a strong tendency to degeneration, necrosis, and liquefaction. It occurs casually in horses, asses, mules and other solipeds, and is communicable to man and all domestic animals except the bovine races, chickens, and, under ordinary circumstances, swine.

Geographical Distribution. Glanders (Malis) appears to have prevailed in asses in Greece as noted by Aristotle. Its contagious prevalence in horses is recorded by Absyrtus in the time of Constantine, and again by Vegetius Renatus in 381 A.D. At the present time its existence is almost coextensive with the equine family, but its prevalence is in a direct ratio with the facilities for the infection of fresh subjects. In the central countries of Europe where the equine population is greatest and where there is the most extensive trade and movement among horses it secures the greatest relative number of victims. War with its constant opportunities for infection, in crowded cavalry and artillery stables and the successive changing of place, tends greatly to enhance its ravages. Thus in the German army it rose from 966 to 2058 per 100,000 per annum in the year of the Franco-German war; in Spain it was practically unknown until the Napoleonic war in the Peninsula, but after this it proved a veritable scourge; in Hindostan it was hardly known until the Sepoy rebellion yet its ravages greatly hampered the army movement in Afghanistan in 1879; and in the United States it became very prevalent in the armies during the Civil War of 1861–4, and was widely scattered over the whole country on the sale of the army horses and mules. Since that time, as before, it has been most prevalent in the car stables of the great cities, though it has also gained a wide extension in many great horsebreeding establishments in the Rocky Mountain region, where however it proves much less destructive than in the East.

It is unknown in Australia, whence it is excluded by a rigid system of quarantine.

Susceptibility of Different Animals. Horses, asses and mules are the most susceptible, and it is only exceptionally that the disease is contracted casually outside the class of solipeds. The Guinea pig and rabbit are susceptible to glanders in the order named and the former is especially available for experimental diagnostic inoculations. The goat, cat and dog sometimes contract the disease from living in stables with glandered horses, but infection is much more certain when they are inoculated. The pigeon is also susceptible. In the dog the disease is rarely fatal, but the ulcerations tend to heal in 14 days and recovery ensues. In sheep and goats too, many cases recover though in other cases an internal infection takes place followed by death. Swine are comparatively insusceptible, but they may be successfully inoculated when in ill health and low condition. (Spinola, Cadeac and Malet). Cattle and chickens have uniformly proved refractory even on inoculation. White and house mice and rats, have proved immune, also linnets and chaffinches and the frog at ordinary temperature. If however the frog is placed in water at 30° C., he may be successfully inoculated and, though it does not prove fatal, the bacillus may be found in the blood and tissues after a lapse of 50 days.

Etiology. As already stated this disease is due to the presence of a microörganism, the bacillus mallei. Many secondary causes, however, contribute to its propagation. The activity of movement and commingling of horses has been already noticed. Crowding in close yards where the animals bite each other, snort out the virulent discharges on each other and eat and drink from the same troughs, leads to a rapid extension. Even on the western ranges where the disease tends to be mild, Billings observed a deadly extension when yarded during winter storms. Debility from chronic ill health, starvation, overwork and damp, dark, draughty stables, is so conducive to the disease that it was at one time considered as the sole cause. Close confinement in impure air is at once a cause of increased susceptibility and a means of concentration and transmission of the poison. Hence confinement, between decks, of military and other horses, carried by sea, is a source of wide extensions. On the other hand insular places from which strange horses are excluded or into which they are admitted under careful inspection and quarantine have succeeded in preserving immunity. Australia, Tasmania and New Zealand are examples.

Bacillus Mallei. Christot and Kiener claimed to have found a bacillus in the lesions of glanders in 1868. In 1881 bacilli were found by Bouchard in a glander abscess in man, and these were cultivated in vitro and inoculated in a number of animals, by Capitan and Charrin in 1882. Independently in the same year (1882) Löffler and Schütz discovered the bacillus, cultivated it in vitro, and successfully inoculated it on animals. The microbe is rod-shaped, 2 to 5μ long, by 0.5 to 1.4μ thick, the same length as the bacillus tuberculosis but thicker. It is nonmotile, ærobic (facultative anærobic) and grows readily in a variety of culture media at a temperature of 37° C. On neutral bouillon of the flesh of horse, ox, calf or chicken with or without peptone, it grows readily, producing cloudiness in one or two days. In peptonized gelatine it forms a whitish flocculent mass. On glycerine agar with milk it forms in 48 hours a milk white layer, changing to yellowish brown. On potato it forms long slender filaments, in yellow, viscous, glistening colonies, changing to fawn and darker. It grows best at 35° to 39° C. and growth ceases below 25° C., and above 42° C. It stains tardily in aniline colors, and not at all by Gram’s or Weigert’s, but will readily take Kuhne’s stain prepared as follows: take of phenic acid in solution (5:100) 50cc., absolute alcohol 10cc., and 1 to 2 grammes methylin blue. The stain is very easily bleached by acid, differing in this from the bacillus tuberculosis. For decolorizing Löffler recommends 10cc. distilled water, 2 drops of strong sulphuric acid, and 1 drop of a 5 per cent. solution of oxalic acid. Sections should be left in this not longer than 5 seconds. The bacillus often appears granular, and unequally stained in its different parts. It may be difficult of discovery in old standing lesions of horses, but comes out clearly in recent lesions of experimental cases in Guinea pigs and donkeys.

Baumgarten claims sporulation but this is uncertain.

The bacillus has only limited power of resistance to destructive physical and chemical agents. It is killed in 10 minutes at 55° C., in 2 minutes at 100° C., or by mercuric chloride solution (1:5000), or by phenol (5:100), or by permanganate of potass (1:100). In warm dry air and sunshine it is sterilized, in thick layers in 2 months (Peuch), in moderate layers in 4 to 15 days (Galtier), and in very thin layers in 3 days (Cadeac and Malet). In moist, cool air and in the shade it is much more resistant. In stables it may remain virulent for three or four months, and thus the disease has often reappeared among the newly introduced horses after a stable has been abandoned for a length of time. The microbe does not grow in infusions of hay, straw or horse manure, and it is doubtful if it can maintain an active saprophytic existence. Its vitality and virulence, however, persists in putrefying materials for 14 to 24 days, and in water from 15 to 20 days. Hence it is largely propagated through drinking troughs and occasionally through ponds, lakes and sluggish streams. Again the virus is likely to be preserved in and transmitted by rotten or even sound woodwork, as of mangers, racks, buckets, shafts and poles, and by harness, halters, blankets, combs, brushes and rubbers. Sometimes direct transmission takes place in snorting or coughing, or by the animals biting or licking each other. As the virus is spattered on surrounding objects, the walls, stable utensils, soiled fodder and feed, and even the attendant’s clothes may be the medium of transmission. Contagion during copulation is not unknown, nor infection of the fœtus in utero from a diseased mother. Carnivora (dog, cat, lion) fed on the diseased carcasses have become infected. Experimentally infection has been conveyed by administering, by the mouth, balls containing the virus (Renault, Coleman, etc.), and again by transfusing the blood from a bad case of glanders into the veins of a sound horse (Viborg, Coleman, Renault, Hering, Chauveau, Nocard). Transmission through the air on dust is counteracted by the speedy destruction of virulence on dust, and horses often stand side by side in adjacent stalls for months without communicating the infection. Such escapes may, however, in some of these cases, be attributed to the immunity secured by a previous exposure and slight attack. That the germs may be exceptionally conveyed through the air appears to have been proved by Viborg and Gerlach, who collected the floating dust in a stable containing infected animals and successfully inoculated with it.

The microbes are especially found in the visible lesions of glanders, in the mucous, cutaneous and subcutaneous swellings and abscesses, in the swollen lymph glands, in the nodules and ulcers of the mucous membranes and skin, in the morbid discharges, from the nose, eyes, pharynx, guttural pouches, larynx, trachea and bronchia, and in the discharge of farcy buds and abscesses. They are not necessarily distributed through all the tissues, and in chronic cases, with strictly local lesions, the infection appears to be often confined to these or nearly so, and the contamination of other animals is slow and uncertain. When, however, the disease is acute and advanced, or generalized, every part must be looked upon as probably infecting. Thus virulence has been shown in the blood, the exhalations of the serous membranes, saliva, the aqueous humor (Cadeac and Malet), the tears, (Viborg), the muscles, and the bones. Galtier says the milk, sperm, bile and intestinal mucous are non-virulent, also the vaccine lymph raised on glandered animals, but much must depend on the grade and stage of the disease and no one would care to run unnecessary risks with these liquids.

Infection Atria. Inoculation on a skin wound or abrasion, is a most effective mode of transmission, but the virus undoubtedly enters in certain cases with the air, food or water, or by accidental lodgment of a speck of the virus on the mucosa of the nose or eye or other natural opening. Through the healthy mucosa the bacillus may enter by penetrating the soft epithelium, or entering the mucous follicles, but it will find the way smoothed for it, if there has been friction, abrasion, desquamation or congestion. The skin in its healthy state is usually resistant, but Babes has conveyed infection by rubbing on the virus mixed with vaseline, and without displacing the epithelium. The channel of entrance was the hair follicles. Injected into the blood, intravenously, or into a serous cavity, the bacillus infects with great certainty and promptitude.

There is ample evidence that primary lesions appear not only in the skin and nasal mucosa, but also in the bronchia, intestines, and other parts. Much time and ink have been wasted in attempts to prove that pulmonary lesions are always secondary, and doubtless many are so, but the cases in which the lesions are confined to the bronchia or parenchyma, and the many parallel cases of direct infection of the lungs by other diseases (tuberculosis, lung plague, contagious pneumonia, influenza, etc.,) furnish conclusive enough evidence that the germ may be inhaled and colonize this part first. Cases of inhalation bronchitis, are equally corroborative, and not only may the grosser solids be aspired, but infection droplets can easily gravitate down when from congestion or inflammation the action of the tracheal and bronchial cilia, is suspended.

FORMS AND LESIONS OF GLANDERS IN SOLIPEDS.

Glanders appears in two primary forms—acute and chronic, and each of these is further divided according as the lesions are exclusively or mainly seated in one part of the body or another. The generic term glanders is habitually used to designate that form in which the lesions are situated in the nose, the nasal sinuses, and the submaxillary lymphatic glands—nasal glanders. When the principle lesions are situated in the lungs and lymph glands of the chest, the case is one of pulmonary glanders. When the skin and subcutaneous lymphatics are most prominently affected it is known as farcy or cutaneous glanders. When the skin and nose are simultaneously affected the name farcy glanders is sometimes applied. But as the bacillus may enter by very varied channels the primary lesions may appear in still other organs. Thus in stallions the first symptom is often a glanderous orchitis. In other horses it may be a glanderous arthritis, and in still others infected by ingestion it may be an abdominal infection.

Symptoms of Nasal Glanders in Solipeds. Acute. After an incubation of three to five days the subject shows prostration, weariness, stiffness, erection of the hair, and even tremor or shivering, inappetence, thirst, hyperthermia, rapid pulse, weeping eyes, the discharge becoming purulent, snuffling breathing, and a discharge from the nose, at first serous, with a remarkable viscidity which tends to glue together the long hairs or even the margins of the nostrils. This discharge may be reddish, greenish, or brownish and may become distinctly purulent and opaque. The alæ nasi are swollen, hot and painful, and the mucosa red, congested, thickened, with a blackish or violet tint especially along the median part of the septum nasi. On these, violet patches appear on the second or third day, pronounced elevations of very varying size indicating the centres of active hyperplasia. They are usually yellowish or grayish, surrounded by a deep violet areola, and may become confluent forming patches. The centre of each undergoes rapid degeneration, forming a rounded ulcer with salient edges, a yellowish base, more or less pointed or streaked with red, and a viscid seropurulent or bloody discharge which may concrete in crusts or scale. The whole septum may become one continuous ulcer with excavations of various depths surrounded by hyperplastic elevations, and involving not only the mucosa, but even the cartilage and leading to perforations.

From an early stage of the attack the submaxillary lymphatic glands and the investing connective tissue become swollen, forming a mass of firm bean- or pea-like nodules, with no excessive heat nor tenderness, and with little disposition to suppurate and discharge. If this has lasted for some time the glands often become more firmly attached to adjacent parts (maxilla, tongue) by the contraction of the exudate.

The swelling of the alæ nasi also often extends to the skin of the face, and firm, rounded cords formed by the swollen lymphatics stretch upward toward the eye, or the submaxillary glands. Upon the turgid lymphatics may appear more or less rounded nodules from the size of peas to hazel nuts, which, unlike the submaxillary glands, tend to soften, burst and discharge a viscid, glairy, sanious liquid.

At the same time the morbid process is liable to show itself in the cutaneous lymphatics of one limb, usually a hind one, in the form of firm cords, with degenerating or ulcerous nodules (farcy buds) and pasty patches. Or the throat or lungs may become involved, with local swellings, violent cough, dyspnœa and fever. The swellings of the cutaneous lymphatics usually follow the course of the veins, in the hind limbs the branches of the saphena, and extend from below upward, and the first nodules may be on the fetlock or hock.

Symptoms of Chronic Nasal Glanders in Solipeds. The chronic form of the disease follows an indolent course, and local symptoms are often so slight or equivocal that the true nature of the malady is unsuspected. If the patient is well fed and cared for and not overworked, the malady may run a course of three, five or seven years, and the victim may pass through many hands leaving infection in every stable it occupies. Diagnostic symptoms, more or less clear, may be obtained from the discharge; the lesions of the mucosa and the submaxillary glands.

The nasal discharge may be bilateral, but if confined to one nostril is strongly suggestive of glanders. It may be profuse or scanty, continuous or intermittent, of a yellowish, purulent tint, or greenish, or grayish and with a special tendency to viscidity. In some indolent cases the nostrils may be clean but if there is any matting of the long hairs, or adhesion of the alæ nasi, the case is specially suspicious. If it is sanious, flocculent, or bloody it is all the more characteristic, and suggests the supervention of an acute attack.

The lesions of the pituitary membrane are varied. Hyperæmia of a purple or violet color is common, especially along the septum, and the mucosa is liable to be somewhat tumid or œdematous. Nodules the size of a pin’s head, a pea or larger appear inside the inner ala, or on the septum or turbinated bones, and at first red from extravasation and, as it were vesicular, become grayish, whitish or yellow with points of red and surrounded by a deeply congested areola. Larger nodules forming in the submucosa approach the surface and stand out the size of the tip of the finger and with the same general character as the smaller. Sooner or later these degenerate and form ulcers which bear a resemblance to those of acute glanders but are less angry, and when small and solitary may be taken for simple erosions. In other cases they become thickened and indurated with sharply defined projecting margins, and a yellowish base with points or lines of red. The presence of red, black, green, or brown crusts may also be noted.

Another lesion frequently observed in indolent cases is a cicatricial white spot or patch in which the hyperplasia has become partially developed into tissue and shows no tendency to ulcerate. The mucosa may even be drawn or puckered around the cicatrix, making the illusion all the more complete.

The submaxillary swelling is even less sensitive than in acute glanders and produces the same sensation as of an aggregation of small, hard, pea-like, masses with no tendency to ulcerate.

Symptoms of Cutaneous Glanders (Farcy) in Solipeds. Acute cutaneous glanders has been already referred to under nasal glanders. The chronic type is often less characteristic, yet may be detected by careful observation of the symptoms. The main symptom may be the swelling of a joint with more or less engorgement of the limb from attendant lymphangitis. There can usually be detected around the margins of such swellings firm, tender cords representing the larger lymphatic vessels and often branching in their course. In the absence of the engorgement, or when it is slight, these cords may be the main evidence of the disorder, and in the hind limb usually follow the course of the flexor tendons on the inner side of the digit, metacarpus and thigh. At intervals along the line of the cords appear nodular masses (farcy buds) varying in size from a pea to a hen’s egg, and showing a great disposition to soften and discharge a glairy, sanious or more or less bloody liquid. The inner sides of the fetlock and tarsus are favorite seats of these nodules but they may form at any point. On the trunk also the corded lymphatics and nodules follow the lines of the veins and lymphatics, and here there may be the complication of large intermuscular abscesses often in connection with the groups of lymphatic glands.

Latent or occult glanders is often met with, the indolent, specific lesions being confined to some internal organs, like the larynx, lungs or womb, or to the testicles, the nasal diagnostic symptoms being absent. A chronic cough, with a slight purulent discharge from the nose, a chronic leucorrhœa, a swollen testicle, or simply a persistent low condition or weakness without apparent cause, may be the only indications, and special means of diagnosis are demanded.

Special Means of Diagnosis. In occult cases, the disease may be identified by inoculation, or by the mallein test.

Inoculation is best performed on a very susceptible animal. If the suspected discharge from the nose, vagina, open sore or preferably from a freshly incised nodule is inoculated subcutem in the flank of a male Guinea pig, or better in the peritoneum, there develops a local ulcerous sore and on the second or third day a violent orchitis in which pure cultures of the bacillus can be obtained. The caseous and purulent centres are found not only in the testicle but along the line of the spermatic cord, affecting the tunica vaginalis and connective tissue. Death usually follows in four to fifteen days. The cat and dog can also be utilized, inoculation being made on the forehead. Old wornout, but otherwise healthy asses, and even horses make very available subjects, inoculation in the nose speedily developing acute glanders. In the absence of a good subject the suspected animal is sometimes availed of, scarifications being made in the nose and the morbid product rubbed in freely. The rapid development of ulcerous wounds is characteristic. If, however, the case is chronic, and if a fair measure of immunity has been acquired this test may prove misleading.

Test by Mallein. Mallein is the sterilized and concentrated toxic product obtained from a pure culture of bacillus mallei in a peptonized glycerine bouillon. When injected hypodermically in a small physiological dose this has no effect on a sound horse, but in one affected with glanders it develops in several hours an extended swelling in the seat of inoculation, hot, tense and painful, which continues to enlarge for 24 to 36 hours and does not subside for 4 or 5 days. From the margin of the swelling, swollen lymphatics may often be traced running toward the adjacent lymphatic glands. There is also decided dulness, prostration, inappetence, staring coat and tremors. The body temperature rises 1.5° to 2.5° and upward from the eighth hour after inoculation attaining its maximum from the tenth to the eighteenth hour and subsiding slowly to the forty-eighth to the sixtieth.

Mallein must be used under precautions like tuberculin. It must be obtained freshly prepared from a reputable maker. If preserved for months its force may be largely lost. The animal to be tested should be in his customary environment, and not just arrived from a railroad journey nor other cause of excitement. He must not be fevered as any rise of temperature is then equivocal, and a fall of temperature, which sometimes occurs in the febrile system under mallein, is no sure evidence of glanders. Reaction sometimes fails in advanced cases of glanders, but in such a case other symptoms are usually diagnostic so that mallein is superfluous and should not be misleading. The greatest care should be taken to prevent infection from the syringe, nozzle, skin, hands, etc., as other infections may give rise to local swelling and hyperthermia (see tuberculin test). If a first test leaves the matter in doubt, the animal should be secluded and tested again in a month (some prefer 3 months).

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Text book of veterinary medicine, Volume 4 (of 5)