Chapter I: Front Matter (1)

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°).