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TEXT BOOK
OF
VETERINARY MEDICINE

BY

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

Copyright by

JAMES LAW

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:

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.

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.