Text book of veterinary medicine, Volume 4 (of 5) (part 3 of 3)

Text book of veterinary medicine, Volume 4 (of 5) (part 3 of 3)

A strong argument for the appreciable influence of the bovine bacillus upon man (acting directly or indirectly through the pig) is that the relative death rate of Jews from tuberculosis is materially less than that of other races. It is constantly claimed that orthodox Jews who eat only kosher (rabbi inspected) beef and no pork, suffer least of all the population from tuberculosis. Dr. Gerster, judging by the burial returns of the United Synagogue and the English Registrar General’s returns, concludes that only about half the relative proportion of Hebrews suffer from consumption as do other races in the same country. Some remarkable facts come out in the report of the Royal Commission on tuberculosis in England. In England and Wales the disease had decreased 39.1 per cent, in thirty-five years, but this decrease has been mainly in pulmonary cases, while the abdominal forms decreased only 8.5 per cent. Sir Richard Thorne, indeed says, that in children of the first year there had been an actual encrease of 27.7 per cent. Northrup and Still, on the contrary, present statistics showing that in children the pulmonary form of tuberculosis is the most common (Brit. Med. Jour. 1898). If in the face of this there has been a very material encrease of the abdominal form, coincident with the notorious encrease of the disease in dairy cows and of the bottle-feeding of infants, may we not enquire how much of this is due to the greater prevalence of bottle-feeding and the infected cow’s milk? It is not for a moment supposed that the majority of infections in children come from the cow. The question is whether this encrease in the minority is not in measure chargeable on the cow. The impaired nutrition resulting in some instances from the use of cow’s milk cannot well be charged with a marked encrease of cases in which the mesenteric tubercles point so directly to infection through the food. If it is held that the tubercle bacilli in the milk are harmless, we wait for evidence of the real cause of such encrease and localization.

The experiments of Adami show that tubercle is directly transmissible from man to ox though usually with decreased virulence. More recently, Ravenel using the bacillus derived from the mesenteric glands of a child, injected intravenously two tuberculin-tested calves, with 5cc. each of the culture producing exalted hyperthermia, miliary tuberculosis of the lungs, tuberculosis and caseation of the bronchial and mediastinal glands, and death in 17 days. Dr. Garnault’s experiment on himself, now in progress, has already shown the great danger to a susceptible man, of the bovine bacillus.

As showing accommodation to environment, Battaillon and Ferre found that the bacillus (mammalian and avian) grown in frogs, Dubard that grown in fishes, Kráhl that grown in frogs, snakes, fishes and lizards, and Müeller that grown in the glow worm, thereafter grew at summer temperature (68° F.) and grew poorly or not at all in the bodies of mammalia.

The tubercle bacillus is primarily and essentially one, but this must not close our eyes to the fact that in different hosts and environments it takes on very different habits, so that for the time and in these surroundings, it is materially modified in its pathogenic attitude toward different races. Yet its ready variability when conditions are favorable to change, renders it desirable to destroy it in all its forms, and especially in those which approximate most closely to those that prey on man and animals.

An impartial review of the whole field warrants the conclusion that the nineteen young (and therefore comparatively insusceptible) cattle which in Koch’s hands failed to develop generalized tuberculosis after inoculation with the virulent sputum of man, and the smaller numbers that resulted in the same way under similar treatment in the hands of Th. Smith, Dinwiddie and Adami, while showing a very marked limitation in the susceptibility of the sound bovine system to weak bacilli from man, cannot disprove the many well authenticated cases of the transmission of tuberculosis from cow to man and the reverse. The greater potency of the bovine bacillus over that of man, in its action on the small rodents and pigs, utterly forbids the unproved assumption that it is on the contrary harmless to man.

If the object of the sanitarian were merely to delay a fatal result in his tuberculous patient, while he accepted the prevalence of tuberculosis as inevitable for all future time, the acknowledged lessened receptivity of the ox for the bacillus from man would mean more and would be at least worthy of a hearing, but as the extinction of a disease germ and its representative plague must ever be the first object, any movement toward the preservation in cattle of a germ which is deadly to man and much more so to cattle, must be held as subversive of the prime purpose of sanitary work. This is true even if we allow, for the sake of argument, that only a few of the bovine bacilli are capable of dangerously colonizing the human body, and that special environment is needful to allow of such successful colonization. On the other hand the limited receptivity of the ox for the bacillus from man is the greatest encouragement to active work to exterminate tuberculosis from our herds. It is impossible to adopt in man the summary measures that are so successful in the speedy stamping out of the plagues of the lower animals, so that tuberculosis in the human family can only be eradicated by slow degrees, and therefore there will long continue for our herds the danger from the human side, but just so far as the susceptibility of cattle to human tuberculosis is limited, in the same ratio are our hands strengthened in effective work for the extinction of consumption in our herds and for preserving their soundness after they have once been purified. If they were to be reinfected by the presence of any consumptive person we might well despair of success in face of a wide prevalence of tuberculosis in man, but since it is only exceptionally that cattle suffer from man, outbreaks coming from this source can the more easily be taken care of. In this view tuberculosis is approximated somewhat more closely to the other bovine plagues (lung plague, rinderpest) which can be stamped out with the greatest ease and certainty, so that as a purely economic measure the argument for the speedy extinction of tuberculosis in our herds is reinforced.

TREATMENT OF TUBERCULOSIS.

Like all deadly infectious diseases in the lower animals, tuberculosis is not to be profitably treated as a rule. In the case of specially valuable breeding animals, in which the prospective progeny will pay for large outlay, and when the disease is in its incipient stage, treatment may be warranted. The patient should be thoroughly separated from other animals, kept in the open air, or, in our northern winters, in roomy, well ventilated buildings facing the south, well lighted, kept immaculately clean, frequently whitewashed, and well drained. If there are more than one case every precaution named under the head of prevention must be adopted. Exercise to keep the muscular system in good tone is called for, but never to fatigue. Hence, a sheltered pasturage is ideal. Feeding must be liberal including a ration of grain or seeds, and oil bearing seeds like linseed, rape seed or cotton seed may be specially named. Cod liver oil alone, or etherized is often of great value, with iron and bitters continued for weeks or months. In the case of specially valuable animals one may use a pneumatic cabinet the principle of which is to diminish the air pressure on the body at large by an exhaust, while pure air for breathing, at the ordinary atmospheric pressure, is introduced through a tube furnished with a face piece fitting around closely beneath the eyes. This serves the purpose of attracting (sucking) the blood toward the skin and other tissues from the lungs, which in their turn are compressed by the air at the atmospheric pressure. Pulmonary congestion is in this way lessened, exudates are absorbed, necrotic tissue removed, sepsis counteracted, hæmatosis encreased, circulation of both blood and lymph stimulated, digestion and nutrition improved, and general health invigorated.

Active grooming and even the stimulating effect of cold douches may be invoked, the skin being rubbed actively until dry and warm.

If the circulation is poor, a stimulating steam or hot water bath of fifteen minutes followed by a cold sponge and rubbing till dry may be profitably substituted. In such cases it is well to put a cold sponge on the head while in the bath.

Medicated inhalation is often valuable especially when the lesions are on, or near the bronchial mucosa. In 1868, Dewar met with most successful results from inhalation of sulphurous acid gas impregnating the atmosphere as strongly as the patient can breath without discomfort. His own groom who had given up work because of advanced phthisis, under treatment of half an hour three times a day, became ruddy, gained weight, and betook himself to work again. In rabbits which I inoculated with human sputa, the same year, all died tuberculous excepting one which I fumigated three times a day for weeks. This rabbit remained plump and well.

As an example of a still more irritating inhalant, I watched the case of a phthisical man who secured employment on the government disinfecting corps, in Chicago, in purifying the lung-plague-infected stables with chloride of lime solution, and who very soon began to improve, gaining weight and strength, his cough meanwhile subsiding.

Cervello’s use of formalina by inhalation though well spoken of by its inventor would seem too irritating on the delicate lungs, however good it is as an antiseptic.

Inhalants may be conjoined with the pneumatic cabinet.

Among agents used to moderate the cough may be named codeine, morphia, cherry laurel water, wild cherry bark, guaiacol, menthol, syrup of Tolu, or chloroform, or alcohol inhalation.

As an internal antiseptic, carbonate of creosote has often proved beneficial.

Mustard blisters on the skin covering the tubercle is claimed by Knopf to act beneficially by attracting the microbes from the delicate lungs to the more robust skin and connective tissue, where they can be better disposed of by the more abundant leucocytes.

He has also found excellent results in complex infections in animals from the use of Marmorek’s streptococcic serum in doses of 10cc., followed after the second dose by 5cc. every 24 hours. In other cases it failed of the effect (reduction to normal temperature) evidently indicating that the hyperthermia was maintained by other microbes than the streptococcus. The principle is good, and perhaps at some time in the future a bacteriological examination of the sputum may reveal the microbes present and suggest the sera for such complications.

The introduction of air into the peritoneum has long been known to exercise a retarding and curative action on abdominal tuberculosis. At the present writing my colleague, V. A. Moore, is experimenting by pumping air and oxygen into the peritoneum and pleuræ in cattle slightly affected, with encouraging results.

I should add that isolated superficial tubercles may often be excised to advantage, and the part dressed antiseptically.

It is only in exceptional cases, however, that one is warranted in preserving and running the danger of spreading the tubercle bacillus for the advantage that can be secured to individual animals from treatment.

EXTINCTION OF TUBERCULOSIS IN CATTLE.

As cattle are the great propagators of tuberculosis on the farm, the question of extinction necessarily centres around this race. As in all other dangerous infections, the most prompt and successful method would be in the time honored one of destroying the infected and thoroughly disinfecting all their products. The only barrier to success in such a case would be the conveyance of infection anew from man to cattle after the herd had been purified. The demonstration that cattle are less susceptible to infection by the human sputa than many had supposed does away largely with this objection, as in a generally purified bovine race, the few primary cases contracted from man could be easily taken care of. Then, if tuberculous persons were interdicted from attendance on cattle, the danger in this direction would become very nearly a negligible quantity.

There remains the question of expense and many honestly consider this as absolutely prohibitory. The estimate of 5 per cent. of our 68,000,000 head to be killed and paid for at $25 per head, would be $85,000,000. But there is no necessity for this. Our fat steers at the packing houses are tuberculous only to the extent of 0.02 per cent., speaking well for their dams and nurses. The estimate of 5 per cent., based upon the testing of those few herds that have been taken because they were already known to be tuberculous, is unquestionably far above the actual ratio for the United States. It may apply to dairy cattle in some infected districts, but, for the bovine race of the whole country, it is absurdly high. If we had 10, 20 or 50 per cent. infected, as in some countries of Europe, the objection of expense might be a formidable one, but when the ratio of the infected is but 2:10000, we have every encouragement on the score of expense to enter on a campaign of extinction. But again, we do not need to deal with 68,000,000 cattle as we can omit the steers which are so little affected and which will all come to the slaughter house in two or three years. The source of their infection (a few cases excepted) is in the older cows and bulls of the dairy and breeding herds, and this brings down our total to a little over 17,000,000. The average census price for dairy cows is $29 and, as the condemned cows are depreciated by their condition, it would be a high average to estimate them at $20. Again, the average infected ratio of cows for the entire country would be set high at 2 per cent., and on this basis it might well be that the required indemnity would not aggregate much over $6,000,000. Five or even ten times that amount would be a mere trifle in comparison with the $3,000,000,000 value, constantly encreasing, of our domestic animals, with the $99,210,272, representing our yearly product of beef and beef products, with our annual dairy products, worth $500,000,000, (Alford), or with our yearly loss of 100,000 of our population in the very prime of life when they are of the greatest value to the country, representing a yearly drain of $100,000,000, beside all the suffering and loss entailed by their prolonged and too often helpless idleness. Though this last item is doomed to continue for a length of time after the disease has been extinguished in our herds, it is receiving constant accessions from the latter, and can never be entirely done away with until our cattle are above suspicion.

An even more serious problem is the demand for tuberculin and above all for accomplished, experienced and honorable veterinarians fitted to conduct the sanitary campaign over the entire country. The tuberculin cannot be produced in a week or a month, yet the problem of its production in any required amount in a few months is merely one of the encrease of existing plants under the management of the same careful hands now engaged upon it. As to veterinarians it would be impossible to secure at once the required staff of men capable of carrying out the work over the whole country. But this is not essential. The work can be begun in the counties supplying the large cities with milk, and in the great butter and cheese producing areas where it is so urgently needed, and it must be made to include all thoroughbred herds, which are so constantly drawn upon to improve the blood elsewhere, and each herd, county and district, as freed from infection must be scheduled and no additions made to it from outside, except under the guarantee of the tuberculin test, repeated in six months. The reacting animals, must be appraised, excluded from the herd, and disposed of, it may be to the butcher to be killed under official expert inspection, and the salvage, if any, to be deducted from the appraised value; or to be rendered and the salvage estimated; or to be buried as the case may be. In all such cases the other animals (horses, pigs) that occupy the same buildings and yards should be tested, although the risk of the infection of cattle from these animals is comparatively small. Unless in badly infected herds, steers and young cattle, which can be kept in a separate herd need not be tested. Vermin must be killed. Thorough disinfection must be applied to buildings and yards, and the dairy herd must be retested at the end of every six months until no more reactions are met with.

In this way the campaign in any State can be begun with a small staff, which may be steadily encreased as men are trained to the work, and in no great length of time the dairying and breeding herds can be purified and the investigation carried into the more purely agricultural fields, where herds are small and usually free from infection. Many minor points would require the attention of a competent superintendent of the work. My object here is to make a plea for the approved and attested method which has never failed in the case of other animal infections on enclosed farms, and which is based on the absolute destruction of every seed of the disease in the area under sanitary control. The method has the apparent drawback, that it demands a greater relative outlay at the start, than do others proposed, but in view of its certainty, and the confident hope of an early abolition of all infection, loss, and expensive expert control, it must, in my opinion, be looked upon here, as it has always proved in the past, the course of the truest economy. It may be compared to the treatment of a field of thistles by removing the offensive weeds, root and branch, before they have advanced to seed, instead of merely cutting them down with a mower, and leaving the roots, to grow anew, to leaf, to blossom and seed, in spite of the temporary partial drawback. But as the prospect of early legislation along this line is not a bright one, the expert must accommodate his aims and efforts to what can be done under the existing laws.

Breeding Healthy Stock from Parents with Latent Tuberculosis. When a State is not pledged to exterminate tuberculosis by prompt and radical measures, it is quite possible to raise healthy stock from sires and dams that have the disease in a latent form. It is very exceptional that calves are born tuberculous. If, then, they are kept in a pure environment and furnished with the milk of sound nurses, or even with the milk of their own tuberculous dams, after it has been heated for one-quarter of an hour to 180° F. or 212° F. they can be preserved in perfect health.

This is especially adapted to herds of valuable thoroughbreds, the destruction of which would be a serious loss, and the preservation of the strain of blood a most desirable object.

The whole herd should be tested with tuberculin, and the advanced and generalized cases, that can be detected by objective symptoms, should be at once destroyed and safely disposed of. The animals in good condition and that have not reacted should be placed in a new barn and yard, or where no tubercle has been, or in places that have been thoroughly disinfected, under special attendants. There will remain the animals in good condition with no objective symptom, but that have reacted, and these are placed in separate barn, yard and pasture well away from other stock, under their own attendants, for breeding purposes. They should have the best of food and air, clean, well lighted, roomy buildings with shelter from storms, clean sheltered yards, and in summer, pasturage. Any cow showing indication of active advance or generalization of the disease (cough, wheezing, dyspnœa under exertion, excessive pallor of mucosæ, unthriftiness) should be at once separated and destroyed as endangering the reinfection of others, and the stable subjected to disinfection. The calf, as soon as born, must be removed to a special building or park, where it shall get milk from a sound cow or that of its own dam after it has been carefully sterilized. After sterilization the milk cannot safely be returned to the unscalded pail into which it was drawn from the cow, and it should be fed by separate attendants who have not milked nor handled the affected animal. Any loss of condition, unthriftiness, cough or scouring on the part of any of the calves should be the signal for its separation from its fellows, subjection to the tuberculin test, and, if it reacts, for its destruction and the disinfection of the building where it was. It is well to test each calf at six weeks old and to remove the reacting ones. The success of this method is now well established.

Goodman, of Dorpat, applied it largely as early as 1891, rearing the healthy calves of reacting cows on the milk of cows that had stood the test. Bang, of Denmark, raised such calves to sound maturity on sterilized milk. Reynolds, of Minnesota, reports the raising of twenty-four healthy calves from infected cows on the milk of tested cows, while three fed on milk of reacting cows, which was supposed to be sterilized, all became tuberculous. McEachran (1899) in an extended experiment succeeded perfectly with the milk of tested cows only. I have now in hand a Jersey herd in which the progeny, fed on the milk of their reacting dams, became tuberculous without exception, and in the years following, those fed on the milk of the same reacting cows after it had been kept at 180° F. for half an hour all grew up healthy.

Under this method, inasmuch as the infection is not at once extinguished, but temporized with for the benefit of the stock owner, State indemnities are not necessarily called for. Yet the State can profitably test the cattle at public expense, mark indelibly those that react, schedule them and control them, so that they will not be allowed to change hands nor to mingle with sound animals until finally butchered, dead or recovered. The State should see to the thoroughness of the seclusion, disinfection, the safe disposal of all products from milk to manure, and the testing at intervals of three or six months of both cows and calves.

Raising Healthy Offspring Without Sterilizing the Milk. In the northwest territories cows and heifers that have reacted to tuberculin, but which otherwise appear to be in good health, are made into a herd by themselves and placed on a special range apart from all other cattle. They live in the open air, slight shelter being allowed in winter only, and their calves are allowed to suck the dams until winter. The wide range, the open air life, and the early destruction by oxygen and sunshine of the discharged bacilli, tend in the main to ward off infection, except such as comes in the milk, and the majority of the calves grow up in apparent health and are fattened for market. A small minority are born tuberculous or contract the infection from the milk, but this does not seriously impair the financial success, and living in the open air they bring little danger to others. The loss is infinitesimal as compared with the expense of milking a large herd, sterilizing the milk and feeding it by hand. Advanced cases, with objective symptoms, should always be removed, and the cows may be tested at intervals if compatible with profit. The seclusion of the herd should be complete, by distance, by the configuration of the country, or by fence.

For this system the climate of our Southern States, where stock can remain out of doors all the year, offers a better field than the semi-arctic northwest.

Removal of all Unthrifty Animals and Those Showing Physical Symptoms of Tuberculosis. Before the days of tuberculin testing I succeeded in extinguishing tuberculosis in several herds by the prompt removal of all unthrifty animals and such as showed objective symptoms of tuberculosis, the disinfection of the buildings, the restocking from sound herds, and the strict separation of the new stock from the old. In one herd of 200 this entailed the final destruction of the whole original herd; in others the destruction was in the main limited to particular (susceptible) families. But in these days, with the tuberculin test available, a resort to a method of this kind would produce an unnecessarily slow, uncertain and expensive result.

Removal of Animals Showing Objective Symptoms or Reaction under Tuberculin. The Bang (Danish) method is the chief example of this, and is so considerate of both state outlay and stock owner’s interests that it is deserving of high praise. Under it the State usually waits for the stock owner to take the initiative, but to encourage applications from the owners, it furnishes tuberculin testing without expense, and even allows a small indemnity for animals killed because of advanced tuberculosis. In return for this the stock owner agrees to furnish separate buildings (or enclosures), yards and pasturages, new or, when necessary, disinfected, one set for the high conditioned, nonreacting, healthy herd, and a second for the animals that reacted but which show no further sign of tuberculosis, with separate attendants, utensils and other appointments for each. This reacting herd is furnished with the best of food, air, accommodation and hygiene generally, and the milk is sterilized before it is allowed to pass into consumption by man or for calves or pigs or for the production of butter. The quarantined herd is marked, registered, and kept under government surveillance; it cannot be parted with for stock uses, but it is at the disposal of the owner to keep it for milk, or fatten at once for the butcher. Finally every member of this herd is slaughtered under government inspection, and the beef put on the market or sent to the rendering works as may be decided. The system secures the hearty coöperation of dairyman, dealer and government, and while it comes short of the speed and efficiency of a generally applied method of extinction, it is accomplishing a great work for Denmark, putting an immediate stop to the advance of the disease in the worst infected herds, and placing the latent cases of such herds in a safe seclusion for the rest of their lives. At first the tested herds showed 40 per cent. affected; now less than 20 per cent.

The feature which would be likely to work the least satisfactorily in the United States, is the disposal of the sterilized milk as such. It is to be feared that this milk would find but a poor market with us, and if it proved unsalable, the preservation of the reacting herd would be no longer an economic success.

In Pennsylvania where practically the same method is in force, leaving it in the option of the owner to keep the reacting latent cases and sterilize their milk, or to abandon them to the State, have them appraised and slaughtered with indemnity, the uniform practice has been to accept the latter alternative. Not a single owner, I believe, has elected to keep a herd in quarantine and sell the milk sterilized. The result has been that four times the number of applications come in that the appropriation will warrant the officials to take in hand.

A special feature of the Pennsylvania method is the provision that a stockowner can have his herd examined, and tested with tuberculin, at his expense, the State to furnish a certificate setting forth the condition of the animals. In case of infection, the owner has the option of abandoning the reacting ones to the State, to be secluded, or appraised and slaughtered, he meanwhile guaranteeing that he shall introduce no new animals into the herd except by tuberculin test under the direction of the State Board.

The usual provision is in force that no indemnity is allowed for any animal that entered the state not more than three months before, and without the tuberculin test demanded of all such stock animals.

Indemnities are restricted to $25 per head and under for non-registered animals and grades, and $50 for registered thoroughbreds. The average appraised price has been $23.

On the whole an excellent work is being done in Pennsylvania, and herds now tested are found to contain not more than half as many infected animals as did those tested a few years ago. A better showing would doubtless have been made if the State appropriation had permitted the board to give attention to all applications made.

The good results may be attributed to the adoption of a system which secured the confidence and trust of the stockowner: he sees that the State has no desire to oppress nor injure him; he is in no dread of a high-handed confiscation of his remunerative property without indemnity; while advanced cases are destroyed he is left the option of segregating his latent cases and marketing their products under the precaution of sterilization; he can raise the progeny of these animals if he will, under similar precautions; he can sell his stock and its product under government certificate if they prove sound; he can avail of government assistance in protecting his herd against reinfection, by the testing of animals to be purchased. Under such a system there is no object in secreting infection, and in underhanded sale of tuberculous animals, with the spread of the disease into new centres. Even the tardy or inimical stockowner is roused to action by public opinion, when he finds the market for his suspected product growing more and more uncertain, and feels the daily encreasing pressure of opinion among neighboring owners, that he is exceeding his rights in maintaining an infected herd in the very midst of their purified ones.

A most important item of the system of Pennsylvania, and of sixteen other states, is the compulsory testing of all stock cattle introduced into the State. This has the further support of the Federal Government which demands a tuberculin test of every stock bovine animal imported into the United States. This is a natural corollary of every attempt to restrict or extirpate tuberculosis from a State, but when through willful blindness a great State like New York, repudiates a measure of this kind, it but makes its dairy and breeding herds the depository of the reacting animals that other states wisely exclude. The sifting process goes on at Buffalo and other centres and the New York herds are loaded with the rejected, diseased animals. Under the operation of this, and the denial of indemnity for animals slaughtered, it will be wonderful, if the New York stock owner is not soon roused up from his idle dream of fancied security, by a great extension of the infection.

Generally Applicable Measures. Under any system many special rules will be demanded in individual cases, which it will require the skill of the expert sanitarian to apply, and which cannot be referred to here. The following are generally applicable whether by the owner in his particular herd, or by the State or other authority dealing with the subject.

1st. On discovery of a case of tuberculosis, test the whole herd with tuberculin. (See Tuberculin Testing.)

2d. Remove all animals that show a typical reaction.

3d. Destroy and burn, boil or deeply bury all cases of the disease, unless it is decided to form an isolated herd of latent cases which are in good condition and apparent good health.

4th. In case of doubt or disturbing influence which may have caused rise of temperature (calving, heat, exposure, concurrent disease, changes in management, etc.), keep the suspected animal apart for four weeks and test again.

5th. Repeat the test every six months, and if two successive tests show no indication of tuberculosis, the herd may be accounted sound.

6th. As soon as tuberculous animals have been removed from a stable, let it be vacated and thoroughly disinfected with chloride of lime, 4 ozs. to 1 gallon of water, and enough quick lime to make a good whitewash which will show if even a square inch is missed. When chloride of lime is objectionable because of its tainting the milk, use mercuric chloride 1 dr. to 1 gallon water, with enough sal ammoniac to make it freely soluble. The roof, walls, and especially the floor, gutter and feeding trough must be first thoroughly scraped, washed and cleaned, all rotten wood work must be removed, and, in case of double boarded walls, the boards must be removed on one side to permit of a thorough application. Utensils should be scalded and dressed with carbolic acid, 1:20. A stable incapable of disinfection should be abandoned for a length of time or burned.

7th. In making new purchases, avoid any herd in which tuberculosis has appeared, or that has had sickness or deaths in recent years.

8th. Do not purchase from city, suburban nor swill stables.

9th. Do not take a cow that is in ill health or low condition, especially one with cough, nasal discharge, foul breath, wheezing breathing, hard nodules under the skin, diseased udder, swollen bones or joints, or a tendency to scour or bloat.

10th. Test every animal with tuberculin before admitting it into the herd.

11th. Do not admit strange cattle to house, field or yard. Keep apart from the herd until tested.

12th. Keep each animal strictly to its own stall and manger.

13th. Board up between the stalls in front so that no two cows can feed from the same manger.

14th. Be especially watchful of the older cows and on the slightest sign of ill health, separate and subject to the tuberculin test.

15th. In case a herd of cattle is found to be tuberculous, subject to the tuberculin test all domestic animals that have mingled with them freely and fed from the same troughs. Remove those that show a reaction.

16th. Exterminate the vermin (rats, mice, sparrows) in a building where tuberculosis has prevailed.

17th. Let no consumptive person attend on cattle nor prepare their food.

HYGIENE OF MILK AND MEAT. SANITARY POLICE MEASURES.

This has a reference to both man and beast and involves measures of private and public hygiene alike. In man, as we have seen, milk is the source of greatest danger, being habitually taken uncooked, whereas meat has been usually subjected to a high temperature before it comes to the table.

Milk. The unsterilized milk of the tuberculous cow must always be regarded with grave suspicion. Especially is the drinking of milk warm from the cow to be strongly condemned. The feeding experiments of Vilemin, Gerlach and others, in 1866 to 1869, demonstrated the virulence on the lower animals of the milk of infected cows, and many accidental infections have shown the same for man. (See relation of the bacillus of man to that of animals). This conceded, the question arose as to the virulence of milk drawn from the sound udders of tuberculous cows. Many experiments of Nocard, Galtier, McFadyean and others seemed to decide against such infection. Others have had a different experience, and especially when the test was made by inoculation. Ernst found tubercle in 30 per cent. of the cows he examined, though no affection of the udder could be made out. Theobald Smith, Hirschberger, Bang and others found tubercle bacilli in milk from sound udders. Pearson, injecting the milk from sound udders intraperitoneally into Guinea pigs had ten in sixty-three affected. Rabinowitsch and Kemper found tubercle bacilli in ten out of fifteen cows with sound udders. While it must be allowed that often a very small proportion of tuberculous cows with sound udders pass the bacilli in the milk yet a sufficient number of exceptions are found to deter one from endorsing such milk as safe. Much more is this conclusion justified by the consideration that commencing mammary tuberculosis is in many cases unrecognizable by ordinary examination intravitam or post mortem. Again when the bacilli are circulating in the blood (generalized tuberculosis) they can escape from such a vascular tissue as the mamma without the formation of a local lesion, as they can pass through the intestinal walls or lungs and colonize the adjacent lymph glands. Nocard’s injections of the bacilli into the veins seem to show that they disappear from the blood in 4 to 6 days, but with a generalization of the infection from within, the presumption is against a single isolated entrance of bacilli, and in favor of a continuous introduction. In such generalization therefore the bacilli circulate in all vascular tissues, and are liable to escape with any normal secretion, but especially with the milk or urine on account of the great vascularity of the glands.

When the udder is itself tuberculous the case is incomparably worse. The milk can scarcely fail to be infecting, and the bacilli, grown in these highly vascular tissues, apart from the air, are usually of a very virulent type. Of these Martin writes in the report of the Royal Commission (England): “The milk of cows with tuberculosis of the udder possesses a virulence which can only be described as extraordinary. All animals inoculated showed tuberculosis in its most rapid form.” Woodhead is equally positive in this position. Galtier says “we should absolutely avoid the consumption of milk from cows in which the udder is tuberculous, and boil before using, the milk of all cows affected with, or suspected of tuberculosis in any form.” Finally we should never consume without boiling, milk of which we do not certainly know the origin, and especially in cities, we ought not to omit this precaution in the case of milk furnished by milkmen.” Rabinowitsch and Kemper add: “Milk from cows that react to tuberculin must be suspected of being tuberculous in every case.”

It may well be allowed that the mixed milk from a large dairy, containing but one or two tuberculous cows, is much less infecting than that of the tubercular cow herself, and that skim milk that has been passed through the separator has been robbed of many bacilli which have been precipitated in the albuminoid material that collects on the inner side of the bowl. But these mean dilution not purification: they reduce the danger but do not altogether remove it, and sanitary police should aim at sterilization in every case where available.

Butter, cheese, whey, and other dairy products have been proved virulent in different cases (Galtier, Heim, Lasar, Bang, Obermüller, Roth, Groëning, Gasperimi, Petri, Rabinowitsch). This was true for butter 120 days old, and cheese 330 days. In a number of cases Rabinowitsch found a bacillus, similar to the tubercle bacillus and producing tubercle-like lesions, but differing in its staining, morphology and culture, and she supposed that other observers had mistaken this for the tubercle bacillus. Petri, Morgenroth and Hormann, found the bacillus of Rabinowitsch in company with the real tubercle bacillus in butter, and Rabinowitsch, later, in fifteen samples of butter found the bacillus tuberculosis in two.

Bacilli coming from the mouth, bowels, or lungs, are also liable to get into the milk, through the floating dust of the stable, or from the teats, udder, tail, etc., (Gaffky).

Oleomargarine cannot be considered as free from this indictment, for though the tuberculous glands, etc., from the mesentery, may be sterilized in the preliminary heating process, yet the subsequent mixing with milk is liable to convey the infection.

The ideal course with milk, if the herds cannot be purified from tuberculosis, would be to compulsorily remove from the herd every cow that shows objective symptoms of tuberculosis, or any internal disease of the udder, and to subject all the milk of the remainder to Pasteurization at a temperature of 155° F. for twenty to thirty minutes. This, however, requires skilled and faithful management to avoid renewed contamination from the lips of the vessel which may have escaped the heat, or from hands, vessels and objects that were in contact with the milk before. The boiling temperature for fifteen minutes would be a safer resort, as requiring less careful handling, yet even this may be contaminated afterward under poor management. It has the further drawback of the boiled milk taste and the coagulation of the albumen. But the outlay for such careful sterilization will soon amount to more than will the tuberculin test.

Meat. For various reasons meat must be held less virulent than milk, but mainly because it is less frequently the seat of tubercle than the udder, and because it is usually cooked before being eaten. The muscular tissue of the ox appears to be unfavorable to colonization by the bacillus, and although the intermuscular lymph glands do not partake of this inherent resistance, yet as the glands are very frequently affected from the tissues which they drain, they necessarily partake in some degree of the comparative immunity of the muscles. This immunity is, however, far from complete, as the frequent implication of the intermuscular glands (prescapular, axillary, prefemoral, etc.), sufficiently show. Again in estimating the virulence of meat we must never forget that in the great majority of cases, in ordinary infected herds, the tubercle is still essentially local; no generalization has taken place. The muscle is vascular throughout, and in cases of generalized tuberculosis is infecting, yet a single transient escape of tubercle bacilli into the blood does not ensure permanent infection of that fluid, which can usually purify itself in six days or less (Nocard). On the contrary, when the escape of bacilli into the blood is constant, so becomes of necessity the virulence of the blood and a rapid generalization ensues. Such continuous escape may occur in actively advancing tuberculosis at any point, but it is more certain if the degenerating tubercle has opened through the walls of the vessels (capillaries), so that the infecting bacilli can pass into the blood in a continuous stream. The pus and other microbes, in complex infections, hasten this degeneration and contribute to generalization of the tubercle and emaciation. The transient infection of the blood with the pure tubercle bacillus does not, however, lead to emaciation and marasmus, and hence the frequency of high condition in spite of extensive tuberculosis.

Ostertag gives the following as indicating blood infection: “When with emaciation there is evidence of recent blood infection, enlargement of spleen and all lymph glands, miliary tubercles of the lungs, liver, spleen and kidneys.” In the absence of these indications, though there may be numerous old standing tubercles, caseated, calcified or sclerosed, he considers that there is no reason to dread infection of the blood and carcass. Even a tuberculous intermuscular gland does not, in his opinion, condemn the adjacent muscle. When vomicæ (caverns) are present in the lungs and internal organs the flesh may still be used “if embolic tubercles of different ages, indicating repeated eruptions of tubercle bacilli into the blood stream are absent from the spleen and kidneys.” This meat is, however, to be sterilized before marketing (Ostertag).

The United States Bureau of Animal Industry orders the destruction of all cases of “extensive or generalized tuberculosis;” “any disease or injury causing elevation of temperature or affecting the system of the animal to a degree which would make the flesh unfit for human food;” also “any organ or part of a carcass which is * * * affected by tuberculosis * *.”

In most countries of Europe even emaciated animals are used for food for animals or even man, provided the wasting is not too extreme. The carcass must, however, first be subjected to a temperature of 230° F. for a period of three hours. This is sold in a special market as low priced meat and labelled as such. Ordinary cooking does not always sterilize, as Martin and Woodhead, like Vilemin, found living bacilli in the centre of a cooked six-pound roast.

TREMBLING IN SHEEP. LOUPING-ILL. INFECTIVE MYELO-MENINGITIS. IXODIC TOXÆMIA.

Definition: infective, tick-borne disease, characterized by meningo-myelitis. Animals susceptible: sheep, and possibly swine (Meek, Greig-Smith) and cattle (Williams). Known in North Britain only in spring (in Skye also in autumn), on rough pasture with much brush, and wood ticks, (Ixodes ricinus, erinaceous, marginatus or other). Experimental infection. Bacteriology: Bacterium fluorescens β and γ found in exudate and infecting. Accessory causes: dried grass of previous year, brush, low condition, cold, youth. Symptoms: incubation 10 to 30 days; impaired innervation, hyperæsthesia, timidity, excitability, trembling, jerking, lack of coördination and balance, falling, convulsive struggling, jumping, rolling of eyes, stiffness, opisthotonos, paresis, paralysis of hind—later of fore limbs, apathy. Wry neck, arched back, stiff joints. Diagnosis from myelo-meningitis by its enzoötic appearance, in spring, on tick infested ground: from paralytic rabies, also by absence of that disease locally; from tetanus by its general prevalence, the absence of tonic spasm, and presence of palsy; from braxy by the lack of emphysematous swellings, and of speedy sepsis; from anthrax by usually healthy spleen and its confinement to sheep. Lesions: cerebral meningitis with encrease of subarachnoid fluid, of myelon, reddened, softened, also of other serosæ, stomach, bowels, liver and kidneys. Prevention: destroy ticks in winter by burning grass and brush, by ploughing and cropping; or fence off ½ the pasture one year and the other half next; or lime soil; or dip repeatedly in April, May and June to keep off ticks; avoid moving sheep in these months: Give liberal feeding. Mortality 10 to 20 per cent.

Definition. All infective disease of sheep, inoculated by ticks, and producing a meningo-myelitis, with drowsiness, hyperæsthesia, irritability, paresis and other nervous disorders.

Animals susceptible. This is almost exclusively a disease of sheep, yet Meek and Greig-Smith claim to have seen it in swine that have eaten the raw carcasses of louping-ill sheep, or that have ranged the tick infested pastures, and in rabbits inoculated with the microbe from the wound caused by the tick. W. Williams claims to have seen well marked cases in cattle, and heard of cases in horses and swine. He speaks, however, rather obscurely of “the tick disease” and seemingly includes in this all affections inoculated by ticks.

Geographical Distribution. This disease has been hitherto described as existing in the northern part of Great Britain only, but given the presence of the tick, and of the infection which it carries and the malady might easily be extended indefinitely. It is known to prevail in Northumberland north of the Tyne, in Kirkcudbright, Dumfries, Ayrshire, Lanark, Peebles, Roxburgh, Berwick, Argyle, Inverness, and Ross. In Berwick it is less prevalent than in the other countries named, while in the Western Isles it is not only widely spread rising on the hills 2000 feet or as high as the sheep range, but in Skye there are two distinct outbreaks, in spring and autumn respectively, apparently coinciding with the appearance of two successive generations of ticks. This may be due to the prevalence of warm winds from the Gulf Stream. Further investigation will doubtless show a much wider distribution—the author has seen an affection bearing the same general characters on the spurs of the Lammermoors in East Lothian, and the supposed adaptation of the Norse word hloupa (staggering) suggests that it is probably not unknown in Scandinavia. W. Williams notes its prevalence on the Silurian formation, but ticks confine themselves to no geologic stratum, and the tick is the main agent in carrying infection.

Causes. 1st, Sheep Ticks. The sheep tick is not the ked (Melophagus ovinus) which is common on long wooled sheep everywhere and is an example of a wingless, degraded dipterous insect.

The sheep ticks, on the other hand, are true ixodes, and of the same family with our common wood tick and of the cattle tick (boöphilus bovis) of the Southern States and the West Indies. The ticks collected from the sheep by W. Williams were identified by Mr. Moore, of the British Museum, as ixodes ricinus, ixodes erinaceous and ixodes marginatus. Those obtained by Meek and Greig-Smith showed the following characters: The male is 2.48 mm. long, by 1.30 mm. broad; the female is 5 to 5.5 mm. long, by 3 mm. broad, or when gorged with blood, 10 mm. long, by 7 mm. broad. The fasting female is yellowish green, and when full of blood, blue. Following the rule of their genus, the mature tick has eight legs, the larva but six. The fasting larva has head, legs and dorsal plate (scutellum) brown, the remainder of the body yellow. Scattered hairs appear on the body, legs and maxillæ.

In all ticks the rostrum is a characteristic feature. It consists centrally and interiorly of a dart covered below and on each side by rows of teeth turned backward, which, when imbedded in the skin, hold so firmly that the parasite may be pulled in two in any attempt to pull it out. Above this dart and on the two sides lie the cheliferæ (horns), each furnished with three or four teeth turned outwardly and more or less recurved, by which the dart is worked into the skin. Finally, on the lateral sides of this central apparatus, are the two maxillary palpi, which are not inserted into the skin, but applied against it and operate as feelers prior to and during the insertion of the dart and cheliferæ. The maxillary palpi are club-shaped and soft.

Ticks pass through three moultings before they attain to the sexually mature eight-legged form, and though the hexapod larvæ attach themselves to animals and irritate the skin by their bites, it is only the mature, impregnated egg-bearing female that lives exclusively on blood and sucks this to excess.

While given species of ticks show a preference for particular genera of animals, yet ticks generally in their vagabond life will leave the long grass and brush where they have been hatched to become temporarily the guests of any passing animal. It is, therefore, premature to seek to identify any single species of tick as the only bearer of the infection, and it is quite possible that any one of several species may contribute to its propagation.

Experimental Infection by the Tick. W. Williams muzzled four sheep from a healthy district and turned them for several hours a day on a tick-infested field, and two sickened—one on the eighth day and one on the sixteenth. Twelve ticks sent out of the district and put on a healthy sheep caused illness on the tenth day. In a second experiment with ten sheep, during a colder spring, when there were fewer ticks, no deaths occurred.

Meek and Greig-Smith turned twenty sheep on a tick-infested louping-ill pasture, six of the number wearing muzzles to prevent grazing, seven having been dressed with a mixture of sweet oil, 2 quarts; castor oil, 1 quart; train oil, 1 quart; pitch oil, 3 gills, and cade oil, 1 gill, while the remaining seven were unmuzzled and undressed. The muzzled sheep were regularly taken out and fed on food from a healthy locality. At the end of a fortnight oils were reapplied on the second lot (seven sheep). No ticks appeared on these sheep, while many were found on the undressed ones. On the fifteenth one of the unmuzzled and untreated sheep sickened and died with lesions of louping-ill. On the twenty-second day one of the muzzled sheep sickened, and died of louping-ill next morning. On the thirty-first day another of the muzzled sheep took ill and on the thirty-eighth was killed. It showed characteristic symptoms and lesions. The seven salved sheep, on which no ticks could at any time be found, remained healthy throughout.

Bacteriology. W. Williams describes a bacillus which he figures as forming filaments of very uneven breadth, with frequent branching (contrary to the habit of bacilli), and forming spores in clusters. These were obtained from the coagulum of the cerebro-spinal fluid and Meek and Greig-Smith conclude that the alleged mycelium was but the filaments of fibrin.

McFadyean found pus microbes.

Meek and Greig-Smith (Veterinarian, 1896–7) found in the black bloody swellings under the skin, where the ticks had inserted their proboscides, a variety of microbes which in pure cultures did not provoke louping-ill. These included staphylococcus cereus albus, sarcina lutea, bacterium putridum, bacterium coli commune, micrococcus sulphurous, micrococcus bicolor, and micrococcus caudicans. He also found penicillium glaucum. Two organisms allied to the bacterium fluorescens and designated as β and γ (G) respectively, were found in these sores and produced in rabbits and sheep nervous disorders and lesions which could be fairly identified with louping-ill. These are about 1.5 to 1.7μ long by 0.7μ broad, and chromogenic with a special fluorescent appearance. Microbe β inoculated on a rabbit caused on the second day rhythmic movements of the head downward and to one side, the eyelids closing as the head dropped, as if the animal were constantly falling asleep. In another rabbit it caused stiffness of the legs only and in a third it had no effect. Microbe γ when cultivated ærobically was harmless to rabbits, but when grown anærobically on mutton bouillon to which a drop of blood had been added, it caused on the second day general paralysis of the neck and limbs, spasmodic twitching of the muscles, dyspnœa and feeble heart action. Two rabbits which survived the early effects developed large axillary and inguinal abscesses four months later.

A lamb inoculated with the bouillon culture of γ showed after thirteen days, lameness of one hind limb, with paresis, and a disposition to fall to one side or the other. Two months later, when it had greatly improved, a second inoculation of microbe γ grown anærobically in bouillon and blood, caused, on the third day, a severe aggravation of the lameness.

Accessory Causes. Much depends on the abundance of old dried grasses of the previous year in which the larval ticks may hibernate. Land that has been burnt over in winter, that is cleared of brush, or in which the aftermath has been killed by free salting or liming will be largely cleared of the ticks.

Whatever disturbs or undermines the general health lays the system open to the disease and many flockmasters in tick-infested districts have succeeded in greatly reducing the mortality by feeding sound hay and oats in winter. Sudden changes of weather have long been noticed to coincide with outbreaks of the disease. A change to cold and wet is especially dangerous as causing a chill and robbing the system of its tone and vigor. But a sudden access of warm spring weather, especially if at the same time moist, may have a decidedly predisposing effect by lowering the general tone. A fatal paresis common in the flocks of New York, in the absence of ticks, shows a similar tendency to select the atonic animal. This occurs mainly in spring, when the sheep have been shut up in close confinement for weeks or months, with flaccid muscles and fatty livers, and above all if they are in advanced pregnancy with twin lambs, and if their fleeces are extra heavy. In both affections the majority of the flock escape, while those that are specially predisposed succumb. Lambs suffer most, doubtless because of relative weakness, and on account of their innate and unexhausted susceptibility.

Symptoms. After an incubation varying from ten days to thirty some impairment or disorder of the innervation is shown, varying widely, however, in different cases.

The two names “trembling” and “louping-ill” long used by shepherds as characteristic of the disease indicate spasmodic disorder of a clonic kind, the paresis which is essentially passive having been very naturally overlooked, or held to be subordinate. There is hyperthermia the temperature rising at times to 105° or higher, and often marked hyperæsthesia and excitability at the outset. On approaching the patient it is very much frightened, and when caught, struggles and twitches in a remarkable manner or trembles violently. If merely raised or disturbed the trembling or clonic spasms are very marked, the nose is jerked forward and upward from the contraction of the muscles attached to the occiput; the legs may be lifted jerkingly as in stringhalt; when raised they are moved stiffly or sway uncertainly before the foot is once more planted; or the sheep loses its balance, falls to the ground and struggles convulsively in its efforts to get up and escape. As the result, it will in certain cases jump to its feet, rising meanwhile to an undue height in the air. In other cases there is squinting or rolling of the eyes, and movements of the jaws with frothing from the mouth. Or the spasms may be tonic affecting especially the muscles of the back and loins, and causing extreme stiffness or rigidity or even opisthotonos. Lambs are unable to suck.

But whether the early spastic symptoms are well marked or not, paresis and even paralysis set in sooner or later. This usually begins as paraplegia, or exceptionally one limb only may be affected at first, causing the animal to walk on three legs. For a time the fore limbs may be free, and the patient attempts to move by dragging the hind limbs, which are extended backward. When the fore limbs become involved the animal remains down helpless and after awhile apathetic. Temperature and sensibility are both greatly lowered in the paralyzed limbs. Sometimes the spasms are lateral and the head may be drawn to one side.

In the animals that survive the early attack, there is likely to remain some lasting deformity, such as wry neck, arched back, stiff or swollen joints. Abscesses, which appeared in the inoculated rabbits after a lapse of four months, are a not uncommon sequel in sheep, the pus collecting in the neighborhood of a joint, or of the lymph glands of the axilla, inguinal region, breast or shoulder.

The succession of symptoms are in the main such as are observed in other cases of myelo-meningitis, first exalted function and later depressed and abolished.

Diagnosis. From other forms of myelo-meningitis it may be distinguished by its enzoötic occurrence on tick-infested pastures, which already have a reputation for causing this malady, by its appearance only in the season of the development of the tick, by the presence of the tick or of its sores on the skin, and by its entire absence from adjacent fields which are free from ticks. From paralytic rabies it is differentiated by the same conditions, and as a rule by the absence of rabies from the district and of any evidence of a bite. In tetanus the tonic persistent nature of the spasms, the absence of paralysis, the marked spasms of the muscles of the eye, and the usually isolated condition of the case should prevent any confusion. Braxy is to be distinguished by its emphysematous swellings near the surface of the body, and by the comparative absence of hyperæsthesia, spasm, or paralysis. The carcass in braxy undergoes much more rapid decomposition. Anthrax is more rapidly fatal, shows no such marked nervous disorder, has a dark, nonoxygenated and often incoagulable blood, an enlarged sanguineous spleen, and the characteristic anthrax bacilli. It attacks the larger herbivora as readily as the small.

Lesions. The most constant and striking lesions are found in the nerve centres. In many cases there have been found cerebral meningitis, involving the choroid plexus (Fair, Hamilton, Klein, Murray, McFadyean) with an encrease of the ventricular and subarachnoid fluid (Murray, Hamilton, Williams). The exudate may be yellow or rosy from contained blood globules (Klein). The meninges are thickened and the seat of ramified redness. In the region of the spine inflammation is found not only in the meninges but also in the cord, which may be blood-stained, softened (Mathewson, Goodwin, Robertson), or in older cases indurated (Robertson, Hamilton, Williams, Young). In this last condition there is a sclerotic condition of the neuroglia, and it may be a distinct atrophy. The exudate is usually abundant and more or less coagulated into a soft, diffluent jelly.

In many cases there is inflammation of the serous membranes of the chest (pleura, pericardium, endocardium), and even of the lungs (Fair, Hamilton, Klein). In some instances there has been inflammation of the stomach and intestines (McFadyean), liver and kidneys (Klein), and enlargement of the spleen has been noted. The most constant lesions appear to be those of the nerve centres, but the wide variety of organs involved in different cases sufficiently accounts for the variability of symptoms.

Prevention. As the ticks are the chief media of infection, the disease may be eradicated by their destruction. The burning of all withered grass and brush during the winter months will do much in this direction. Their destruction is rendered even more complete by ploughing and putting the land under a series of cultivated crops. By this means not only is the winter shelter of the tick removed, but the animal host which it requires for its complete development is denied it, and it must perish before the land is again seeded to grass. When the land is unsuited to cultivation, the same end may be in some measure secured by fencing off half the pasture, and leaving it unpastured for a season, meanwhile burning the dry grass or temporarily suppressing it by a liberal application of salt. The following year the pasture so treated may be restored to pasturage, and the other half subjected to the same course of treatment. In the absence of such thorough treatment, a liberal application of lime to a virgin soil will often bring a growth so fresh and appetizing that the stock keeps it closely cropped and thus removes the shelter for the offensive ticks. Finally, the ticks may be prevented from attacking the animals, by repeated use during April, May and June of a dip in which tar oil, cade oil, heavy petroleum or other odorous insecticide forms a component part (see the dip of Meek and Greig-Smith).

A very obvious precaution is to avoid the movement of sheep during April, May and June, from tick-infested pastures to others which furnish rank grass, brush or other suitable shelter for the preservation of the parasite.

It has been noticed that sheep indigenous to the tick-infested and louping-ill pastures are less susceptible than those that have been introduced from outside, but, as yet, no attempt appears to have been made to secure immunity by the use of sterilized products of the microbe, nor therapy by the resort to antitoxin. A liberal and tonic diet is an important element in prevention. Grain and hay should therefore be allowed whenever necessary to bring the sheep to early summer in good condition.

Treatment can hardly be said to have been attempted, though mild cases are allowed by the shepherds to recover. According to Meek, the deaths often average 10 to 20 per cent. of the flock.

BRAXY, BRADSOT, GASTRO-MYCOSIS OVIS.

Definition: Acute, infectious, bacteridian disease of sheep, with colic, enteritis, emphysematous swellings, dark, diffluent blood, and after death rapid putrefaction. Geographical distribution: Iceland, Norway, Faroe Islands, Scotland. Causes: inclement weather, exposed localities, low condition, winter food, chill, frosted grass. Bacteriology: Bacillus gastromycosis ovis: 2 to 6 μ by 1 μ, in pairs or filaments, sporogenous, polar staining, anærobic liquefying, gasogenic, found in the gastro-intestinal congested mucosa, serosa, liver, kidneys, blood. Pure cultures by boiling five minutes. Pathogenic to sheep, Guinea pig, mice, pigeons, hens and less certainly rabbits. Symptoms: resemble blackquarter, sudden, rapid, fatal, back arched, stiff hind parts, crepitating swellings on hind parts or elsewhere, colics, tympany, anorexia, pulse and breathing hurried, separation from flock, lying, drooping head, ears and eyelid. Usually found dead in morning when apparently well previous night. Lesions: early putrefaction, slight, transient rigor mortis, tympany, fœtor, sero-sanguineous exudates under skin, on fourth stomach and bowels, and elsewhere. Contents of large intestine dry, hard. Effusions in serosa. Spleen enlarged or not. Liver and kidneys congested, softened, small, pale necrotic areas containing bacillus. Prevention: drainage and cultivation, winter feeding, abandon infected pastures in late fall and winter as pasture for young, avoid overstocking, burn old fibrous heather. Immunization by sterilized kidney extract. Treatment.

Definition. An acute infectious disease of sheep, manifested by sudden attack, colicy pains, inflammatory and sero-hæmorrhagic lesions of the bowels, and sanguino-emphysematous swellings occurring subcutaneously and especially in the hind quarters. The blood is dark, tarry and comparatively incoagulable and after death putrefaction advances with extraordinary rapidity.

Geographical Distribution. Braxy is generally prevalent in Iceland where it was described over a century ago (1778) by Ketilson as “vinstrarfár” or “vinstrarplága” (“Omasum disease”). In Norway it prevails on the whole Atlantic border to as far north apparently as the sheep industry extends (Stavanger to Tromso Amt). The Faroe Islands are said to be affected throughout. In Scotland it prevails like louping-ill along the west coast especially, and embraces Caithness, Ross, Cromarty, Banff, Inverness, Aberdeen, Argyle, Bute, Ayrshire, Lanark, Galloway, Dumfries, Peebles, Selkirk and Roxburgh.

Causes. Like louping-ill this affection is associated with inclement seasons, exposed localities, and insufficient or indigestible food, but it differs in being an affection of autumn and winter rather than spring. It is rarely seen in summer. At a time when it was looked upon as an acute indigestion, its coincidence with hard frost or deep snow, was explained on the basis that the victim had been driven to eat dry, fibrous, indigestible grasses, brakens and heather. W. Williams who formerly identified the disease with anthrax, seemed to go back to this theory of indigestion. Though that is no longer tenable, yet it would be wrong to ignore the effect of inclement weather and unwholesome food in predisposing the animal system, and robbing it of the healthy tone which would otherwise have successfully resisted the infection in many cases. The occurrence of deaths after frosty mornings more than during mild weather, suggests at once the chill effected in the animal, the chilling of the paunch by the frosted grass eaten producing a subsequent congestive reaction, and the known facility with which frozen vegetables undergo rapid fermentation.

Cowan and Borthwick, (Transactions of Highland Society 1863) agree that the disease is especially prevalent when the land has been overstocked in summer, or when there has been a drought which withered up the pastures, and later a free growth of green herbage from the autumn rains. This they attribute to the “foul and unwholesome” character of the autumn growth, but it suggests no less the low condition of the sheep on the overstocked lands and the soft, aqueous character of the herbage grown rapidly in a comparatively cold season. Cowan quotes cases in which the lambs, weaned early and put in a separate pasture (hogg hirsel), suffered a mortality of 50 per cent., while in later years when allowed to remain with the ewes until winter, the deaths were reduced to 10 or 15 per cent. Here the more rugged health and vigor were manifestly strong prophylactic factors.

Both Cowan and Borthwick incriminate the withered heather and the dry, fibrous (“tathy”) and innutritious tufts of grass which make up a large proportion of many hill pastures in autumn and winter.

Cowan strongly condemns heavy smearing with tar, which he believes to encrease the mortality, by lowering the general tone of the system: “Hoggs are very dull and listless for some time after being smeared with tar, more especially if heavily smeared; ... when the skin is taken off, every shed or opening in the wool where the tar has been laid on, is as distinctly visible upon the flesh as the stripes upon a piece of printed calico.”

It has been further alleged that the deaths are especially common during the full of the moon, the usual explanation being that the sheep are tempted to feed in the night and overload the stomach. It may be added that at such times the grass is taken in a cold—(often frosted) condition so as to chill the stomach and cause a congestive reaction, and that short of this, under the night dews the microbian ferments are moist and ready to start into full activity, while the herbage if it has been partly frosted is particularly susceptible to bacteridian attack.

Bacteriology of Braxy. The essential cause of braxy was revealed by Ivar Nielson in 1888, who demonstrated on the local lesions of the alimentary canal and the capillaries of various internal organs a bacillus which he named bacillus gastromycosis ovis. This is 2 to 6μ long by 1μ broad, occurring in pairs or filaments. The organism has an elliptical form and stains deeply at the extremities, while the central, bulging portion fails to take the color, is highly refrangent, and represents the spore. The non-spore-bearing bacilli are long, uniform rods with rounded ends. The germ is anærobic, grows readily in serum glycerine agar, and is gas producing and foul smelling. Liquefies gelatine. It is found abundantly in the congested parts of the abomasum and to a less extent in the bowels, in the mucosa, and in the submucous and subserous tissues. It was also found in the blood and in the small areas of degeneration in the liver and kidneys. Jensen obtained pure cultures through the survival of the spores when impure cultures were boiled for a few minutes.

Animals Susceptible. Inoculation of the cultures subcutem produces an affection resembling malignant œdema, or braxy, in sheep, Guinea pigs, mice, pigeons and hens, and less certainly in rabbits. Inoculation of a calf had no deleterious effect, while a second succumbed in forty-eight hours. In its pathogenesis this microbe appears to be more closely allied to that of malignant œdema than that of black quarter, as the latter attacks cattle very readily and has little effect on rabbits, pigeons and chickens.

Symptoms. The more obvious manifestations of braxy bear a resemblance to those of black quarter, so that the two affections have been often confounded. In both the attack is sudden, the course rapid and fatal, the back arched, the step short, especially with the hind limbs, and there are swellings which crepitate on pressure on the hind quarters or some other part of the body. Symptoms of colic soon appear, the sheep lying down and rising frequently and moving the hind limbs uneasily, and the abdomen becomes distended, tympanitic and tender. Rumination and feeding are promptly suspended, and as a rule defecation as well. Urine may be passed frequently in small amounts and of a high color. The pulse is rapid and often irregular and the breathing hurried and labored. In some cases the abdominal pain is less acute, the animal standing apart with drooping head, ears and eyelids and frothy lips, or lying by itself at a distance from the flock. Sooner or later emphysematous swellings appear on some part of the body, but most commonly on the hind quarter, which have a soft, doughy feeling and crackle or gurgle on pressure. In the great majority of cases, however, the disease runs a rapid course and ends in death in a few hours, and as the attacks are mostly in the cold of the night, the victim, which appeared well at night, is found dead in the morning. Cowan has often noticed that those that stepped short at night were dead next morning. In certain cases the sheep stood obstinately to the end and fell dead as if shot. When death was deferred for several days a common result was shedding of the wool.

Pathological Anatomy. A marked feature of braxy is the early putrefaction of the carcass. The rigor mortis quickly passes and the carcass bloats up and exhales a putrid odor. On removing the skin one sees extensive sero-sanguineous exudations, mixed with bubbles of gas of an offensive odor. The abdomen is tense and tympanitic and the anus protrudes. Visceral lesions are especially marked in the fourth stomach, the walls of which are thickened in patches or throughout by a hæmorrhagic or sero-hæmorrhagic exudation of a dark purplish color. If killed in the early stages this may be very restricted in area, but becomes general in animals that have died of the disease. Similar exudations are found on the walls of the first three stomachs, or on the small or large intestines. The fourth stomach and duodenum are, as a rule, empty of food, though containing a sanguineous liquid. The contents of the large intestines are usually dry and hard. Some serous exudate is usually present in the peritoneum, pleura and pericardium. The spleen may be normal or slightly enlarged. The liver is pale, soft and friable. The kidneys may be congested and swollen and usually show brownish areas of necrosis in which the bacillus is readily found. The blood is dark, and though it may be coagulated, the clot is usually soft and diffluent.

Prevention. Much may be done in the way of drainage and above all cultivation and liming of the braxy pastures, and again laying them down in grass. Cowan found that braxy diminished largely in ratio with the improvement and cultivation of the soil. A rotation of crops and the free æration of the soil tends to destroy an anærobic microbe or to render it non-virulent. Winter feeding is another well attested source of protection. Hay with turnips, oats, linseed cake or oil cake seems to encrease the tone and vigor, and to counteract the fermentations in the digestive organs which lay the system open to attack. Wholesome and nutritious food then must be a main stay whenever the health threatens to be undermined by insufficient or unwholesome pasture, by dried or withered grass, ferns or heather, by the watery grass of recent and rapid growth, by frosted and partially decayed herbage, or by pasture exhausted by overstocking or drought.

Fields and hills known to be infecting must be abandoned especially in late fall and winter and in the case of the younger and more susceptible sheep. Understocking is always better than overstocking as the flock is kept better nourished, stronger and with a greater measure of tolerance and resistance. Upon land covered with old, fibrous, astringent heather, burning is often of great value. The new growth of young heather is much more digestible and nutritious, and destitute of injurious astringency, and maintains a stronger and healthier flock.

Finally the question of immunization arises. Nielsen attempted this by drying and heating to sterilization the diseased kidney and injected small quantities of this suspended in water. Sheep treated in this way in Norway and Iceland have had a circumscribed inflammatory swelling and afterward appeared to resist casual infection when placed on the braxy fields. Jensen carried the experiment a step farther and inoculated his artificially immunized sheep with 2½ cc. of a virulent serum-gelatine-agar culture. It was rather unwell for half a day and walked lame but soon recovered. A dose of ¹⁄₃₀ cc. of the same culture killed in fifteen hours a larger sheep that had not been artificially immunized.

Treatment. Though some cases of braxy recover yet the treatment of the disease can hardly be seriously considered as yet. A disorder which is so rapid in its progress, so early associated with such great and rapidly extending lesions of the most vital organs, and which proves fatal so early and almost invariably, leaves little room for a successful treatment. In the milder cases, likely to recover of their own accord, this may be hastened by the internal use of antiseptics and purgatives, and perhaps even by antitoxic serum from the blood of an immunized animal.

SOUTH AFRICAN HORSE SICKNESS. ŒDEMA MYCOSIS. DUNPAARDZIEKTE. DIKKOPZIEKTE.

Definition: Geographical distribution: S. Africa; enzoötic or epizoötic on damp soils; damp, humid atmosphere. Pathogenesis: horses, and more mildly mules and asses, quagga; (cattle and goats?). Causes: green forage, from rich, damp lands, eaten dewy; cut and fed with dew on; dried in sun safe; so of horses stabled or corralled; in hot summer only; inoculable; penicillium; cultures cause the disease; debility. Forms: lung sickness—head sickness—blue tongue. Symptoms: incubation 8 days. Fulminant form asphyxiates in an hour. Acute lung form has rigor; remittent hyperthermia; prostration; dyspnœa; cyanosis; serous nasal discharge; frothing; gurgling breathing; cough; death in 3 or 4 days. Head œdema; general swelling and oozing of serum. Blue tongue: great lingual swelling; cyanosis; coldness; projection from mouth; salivation; stertor; asphyxia. Three forms combined. Mortality. Lesions: serous exudate coagulates with heat or blood; intermuscular exudates; whole head densely infiltrated; excessive bloody pleural effusion; punctiform petechiæ; lungs pale, yellow, great interlobular infiltration; or, if worked, hepatization; dark, congested mucosæ; blood diffluent; heart pale; spleen enlarged, blood-gorged; kidneys infiltrated; gastro-intestinal congestions; cerebro-spinal effusion. Prevention: keep indoors during summer and autumn; allow no fresh damp forage; or cut only after dew is off; check rein or muzzle; pastured horses must be stabled at night or in damp weather. Immunization: by protective inoculations; recovered horse is re-inoculated until a high grade of resistance is secured and his blood used to immunize.

Definition. An ectogenous, infective disease of solipeds in South Africa, characterized by intense vascular congestions, destructive changes in the blood and the profuse exudation of liquor sanguinis into the tissues of the affected parts.

Geographical Distribution. The affection is not known out of South Africa, where it has been observed since 1780. It appears yearly in certain areas in the Transvaal, Orange River Colony, Natal, and adjacent States, but only in certain years in Cape Colony and especially in its southern portion. In certain years it makes wide extensions so that it has appeared to become epizoötic instead of enzoötic. The habitual enzoötic prevalence is in the areas that are relatively lower, damper and richer than the surrounding country, where the vegetation is luxuriant and the surface of the ground moist. Thus it is a disease of low meadows, basins, river bottoms, drying marshes or ponds, and the Boers have been in the habit of protecting their horses by sending them to high, dry tablelands, from the first appearance of the disease until the first frost. Yet elevation in itself is no protection, thus Johannisburg, 6000 feet above the sea, is habitually ravaged and Rhodesia loses 90 per cent. annually. A humid atmosphere, mist, or rain with a high temperature are directly connected with the outbreaks.

Animals susceptible. Horses take the disease in its most fatal form. Mules suffer like horses, while in asses the disease is relatively somewhat more benign, and the virus after having passed through the ass, has lost part of its potency. A disease of a similar nature is seen in cattle and goats. The quagga is also alleged to suffer (Edington).

Causes. The disease has been traced to the green forage, grown in damp, hot seasons on the rich moist bottom lands, in basins, gullies, etc., and which has been consumed while damp with night dews or fog. Few suffer that are only turned out to pasture after the sun has dried up the dew, and that are shut in the stable or kraal before sunset. Coley who witnessed a loss of 60 per cent. of the stabled horses at Eshowe, Zululand, found that the deaths were among horses that had been allowed to eat their fodder wet. The Guinea or Ubaaba grass and Indian corn were cut at night and fed to the horses next day. The horses that ate this wet from the bundles were attacked, while those that had it only after it had been opened and dried in the sun escaped. Race horses that receive no green fodder very rarely suffer. Horses that are corralled (in kraal) at night escape.

The hot season is the season of greatest prevalence, the disease beginning in November and proving especially fatal from the end of December to the first of March. It appears in a modified form until May when the first frosts appear.

Though the disease can be fatally inoculated by transferring the blood from one horse to another, it is the rarest possible occurrence to have it propagated in this way. It can be absolutely prevented therefore by attention to the diet.

The real cause of horse sickness is a mold having the general characters of a penicillium, and which enters the system with the moist, dewy food. Edington, who discovered this cryptogam, has found it in the blood in all his necropsies of horses dying of horse sickness. Why this should be no longer infecting when dried does not clearly appear. It has been alleged that the disease has gradually extended to the higher grounds which were formerly free from it, and the introduction of diseased or infected horses has been advanced as the cause, but in the unfenced state of the veldt and the former abundance of wild animals this should have ensured such extension long ago, if it is really a permanent one. The deadly prevalence of the malady in particular areas in given years, and its entire absence from such localities in others may explain the instances of apparent extension. The dryness and cold of winter is the factor which usually extinguishes the poison in a given district. We have as yet no absolute proof of a progressive acclimatisation of the germ in a colder and drier region. Wittshire observes that it will prevail on one side of a narrow river, while the other at an equal elevation is practically free from it. There is no mention of shade which might have explained such a difference in the growth of cryptogams on the right and left banks.

Such limitations, together with the activity of the infection in damp seasons, and during damp hours of the day, and its inactivity in dry air and vegetation, would strongly suggest a microbe which is conveyed in the body of some invertebrate, but this appears to be nonessential because Edington has cultivated his mold in vitro and inoculated its products on horses so as to secure immunity.

Debility doubtless renders an animal more susceptible, yet the disease usually kills nearly all horses attacked, excepting such as have been immunized. This is the same for casual and inoculated cases. When, however, the virulence has been lessened by culture or by passing through the body of an unsuitable animal the results are very uncertain; some horses it will kill, while in others it produces a slight and harmless fever.

Forms. Two leading forms of the disease are known: 1st, the lung sickness (Dunpaardziekte), and 2nd, the head sickness (Dikkopziekte). A variety of this last is blue tongue (Blautong), which has been confounded with gloss-anthrax.

Symptoms. The lung sickness may appear as a fulminant affection following on the usual incubation of about eight days. Suddenly, in the midst of apparently full health and vigor, the breathing becomes accelerated and dyspnœic; this encreases for about an hour, then the patient staggers, falls, ejects a mass of white froth from mouth and nostrils and dies. When death is more delayed, there may be noted a rigor, and in the evening a rise of temperature to 103° F., lowering a little next morning and rising again toward night, yet making an encrease day by day until near the end, when it becomes subnormal. Death in such cases occurs on the third or fourth day, preceded by great prostration, hurried, labored breathing, dark red or cyanosed mucosæ, loud rattling over the large bronchia or lower end of the trachea, coughing and dropping of a serous fluid from the nose, or accumulation of white froth around nostrils and mouth. The froth soon condenses in part into a straw-colored liquid, which collects in considerable quantity. The abundance of froth blocking the air passages produces death by suffocation.

In the head œdema, the muzzle, lips, head and neck become the seat of excessive exudation, the swelling of the face drawing back the lips so as to expose the teeth of the lower jaw. The skin is rendered tense and exudes the straw-colored serum, as do also the buccal and pituitary mucosæ.

In blue tongue the exudate is concentrated in the lingual organ, which swells to an enormous size, forcing the jaws and lips apart, and hanging out as a dark blue, cold mass. A foul, liquid mixture of saliva and exudate drivels from the mouth. The pressure on the larynx may cause marked stertor, advancing to asphyxia.

While these three types may seem to be distinct and uncomplicated in some cases, more commonly the exudation appears to a slight extent in all three situations, and it is only the predominance of the symptoms in one particular part that assigns the attack to one type rather than another. All are very fatal, but the lung sickness is preëminently so, very few such surviving.

Lesions. There is usually a mass of white froth around the mouth and nostrils. The serous exudate coagulates readily in the presence of minute traces of blood, and forms a solid mass of clot when heated. A yellow gelatinoid exudate is found in streaks or patches, subcutaneously and between the muscles, but especially along the jugular furrow. In the head sickness the whole subcutaneous and intermuscular tissue in the head and neck are infiltrated, and the straw-colored liquid escapes abundantly when the part is scarified. The same is true of the tongue, which is stained throughout with blood that has gravitated into it.

The pleuræ contain an abundant exudate more or less deeply stained with blood. The same is true of the pericardium. In the latter Edington has found 140 fluid ounces. On the surface of the lungs and pericardium are extensive yellowish exudates. They are covered with petechiæ mostly small or punctiform. If the horse has stood at rest throughout the illness the lungs seem pale, yellowish, yet swollen and indisposed to collapse. The interlobular tissue especially is infiltrated with serum so that toward the free margin the lobules may be separated by intervals of half an inch in breadth as in lung plague of cattle. In horses that have been worked during the illness the whole organ is congested and firm, resembling the condition of croupous pneumonia. The trachea and bronchia show dark congestion of the mucosæ and a mixture of froth and serous exudate. The large blood vessels contain diffluent blood clots of an intensely dark color. In the vascular furrows of the heart and along the large vessels are yellow exudates or blood extravasations. The muscular tissue of the heart appears normal or rather pale, and under the microscope the striæ are found to be obscured by cloudy swelling, and minute blood extravasations and hæmatin are met with. The endocardium is cloudy, with blood extravasations, and exceptionally ante-mortem clots are found. The spleen is usually swollen, very dark, blood gorged and covered with petechiæ. On section there are found extensive extravasations, with masses of blood pigment and crystals. The kidneys are enlarged, the capsule easily detached, the epithelium of the glomeruli and convoluted tubes swollen and their nuclei multiplied. A gelatinoid exudate is usually present in the renal pelvis. Congestions have been found in the right gastric cul-de-sac and less frequently in the intestines. Exudations have also been found in the cerebro-spinal nervous system, the laryngeal mucosa and the conjunctiva. The latter is usually cyanosed.

Prevention. The first consideration is to keep work horses indoors or in a kraal during the summer or sickly season. Here they must be fed on dry hay and grain only, grass being strictly withheld. If it becomes absolutely necessary to feed green fodder of any kind it should not be cut until all dew or rain has completely dried off in the heat of the sun, and if kept over night should be kept under cover and again dried before feeding. When taken out to work the animal should wear a check rein or muzzle so that he cannot by any chance reach the green vegetation. This rule must be most strictly adhered to at night or during damp weather.

For horses turned to pasture a fair amount of protection may be secured by shutting them in a stable or kraal before sundown, and until the vegetation has been thoroughly dried by the sun the next morning.

Immunization. A horse that has recovered from the sickness has been long held to be immune and will bring from six to ten times its former price. As any disease is liable to be called the sickness this enhanced value is too often insubstantial. Wiltshire even says that all “salted” horses eventually die of horse sickness if allowed to live long enough. Be this as it may Edington appears to have established a reasonable measure of immunity by his protective inoculations. He takes a recovered (‘salted’) animal and reinoculates it at intervals with encreased doses of virulent blood. After the last of these inoculations the subject is allowed to rest for a long period of time, and is then re-inoculated with a small dose of virulent blood. A definite amount of this horse’s virulent blood is mixed with 50cc. of serum and injected subcutaneously; some days later 30cc. of the same serum with the same dose of blood is injected; at a later date the procedure is repeated, with a reduced dose of serum, and fourteen days later pure virulent blood is injected.” The result has been perfectly satisfactory.

DOURINE.

Synonyms. Definition: Contagious disease of breeding solipeds, with special lesions in generative and nervous system, and skin, and caused by a trypanosoma. Susceptible animals: horse, dog, rabbit, rat, mouse, ass. History: in Europe and America. Causes: contagion; coition; microbiology; trypanosoma equiperdum; its successive stages: 1. granules and refrangent spherules; 2; chromatin bodies with two prolongations; 3. fusiform body with nucleus and nucleolus and two flagella; 4. pyriform bodies with flagella; 5. fusiform body with nucleus, nucleolus and undulating membrane: in blood, sperm, milk, vaginal mucus, sores; disappears from blood in intermissions and rapidly after death. Lesions: phlegmons of generative organs, papules, vesicles, mottling, swollen inguinal glands, penis, testicles, caseation or atrophy, thickened lymphatics, nervous lesions, friable bones, arthritis, liver, spleen, kidneys, lungs, lack of red globules, anæmia, muscular atrophy; in mare, in dog. Symptoms: Horse: incubation 11 days, variable; preputial, scrotal, sub-abdominal swelling, catarrh of genital mucosa, vesicles, sores, swollen penis, semierections; paraphymosis, slight fever, tender loins, frequent micturition, paresis, swollen joints, tendons, emaciation marked anæmia, apathy, dementia, nasal ulcers, submaxillary swellings. Mare: vulvar swelling, distortion, leucorrhœa, eruption, spots of depigmentation, erection of clitoris, urine in driblets often, inguinal swellings, sterility or abortion, lameness, trembling, great anæmia and emaciation. Diagnosis: from urticaria: from glanders, generative lesions, no response to mallein, paresis: from chronic paraplegia, by its coition cause, and in horses only; from vesicular exanthema by gravity and nervous phenomena. Prognosis: Mortality 70 per cent. and upwards. Symptoms in ass slight: in dog severe and fatal; in rabbits severe. Treatment: prevent copulation, castration, local antiseptics early. Prevention: prevent copulation of infected and suspected animals, castrate, import only on certificate and on long quarantine.

Synonyms. Venereal Disease of Solipeds; Equine Syphilis; Maladie du Coit; Chancrous Epizoötic; Breeding Paralysis; Epizoötic Paraplegia.

Definition. A contagious affection of solipeds, transmitted by copulation, and attended by specific lesions in the generative organs and nervous system, such as local venereal swellings, chancrous ulcers and cicatrices, dementia and paralysis.

Susceptibility. As occurring casually the disease is essentially an equine one, yet the following species are susceptible to experimental inoculation in the order named: dogs, rabbits, rats, mice, asses. While the horse shows the greatest susceptibility, the ass is comparatively very resistant to the poison.

History. The malady has probably long prevailed in the east, yet it was first clearly distinguished in 1796 when described by Ammon as prevailing in the royal stud at Trakehnen in Northern Prussia. We have later descriptions of the disease in the same locality in 1801 (Hertwig), and 1807 (Ammon). It was found in Bromberg in 1817 to 1820 (Waltersdorf), also in Hanover (Haveman), in Austria and Bohemia in 1821–8 (Fischer), in Styria in 1821, in Switzerland in 1830, in France in 1830–2 (Lautour), in Silesia and Pomerania in 1833–40 (Fischer), in Italy in 1836, in Russia in 1843, (Fischer), in Silesia and Poland in 1830–40 (Freidberger and Fröhner), in Algiers in 1847–55, and in Syria and Asia generally and perennially (Daumas and Signol).

It appeared at Bloomington, Ill., in 1882, the first affected animal being a brown stallion that had been imported from France and which bore on his neck a brand like the letter D. In this locality it extended to a considerable number of breeding mares and stallions, and having been recognized by Dr. W. L. Williams, was largely stamped out by a rigid quarantine of diseased and exposed animals. Some exposed animals had, however, left the district, and isolated centres of infection have been since found in Nebraska and elsewhere in the United States.

It is not known to have invaded Belgium, Scandinavia, England, South America nor Australasia.

All indications point to Asia or North Africa as the primal home of the disease, as they still prove its perennial one.

Causes. The disease is transmitted by contagion and almost exclusively in the act of coition. Hayne has seen the affection in geldings, and Haxthausen in mares that had never been served. Schneider, Buffard, Nocard, Blaise and others have transmitted it freely by inoculation of blood and nervous matter, so that the possibility of infection through other channels than the generative organs must be admitted. But such irregular means of casual infection are so rare, and the probability of transmission of the virus from a non-breeding animal is so remote that in the practical measures of sanitary police, the breeding horses alone need be taken into account.

The extra vascularity of the male and female generative organs at the period of coition undoubtedly favors infection, as a latent or apparently recovered case will relapse under its frequent repetition. The abrasion of the epithelial surface also forms infection atria and favors new multiple points of infection.

The disease has occurred congenitally (Rodolff, Jessen). It has been claimed that the higher bred horses with lighter frames are the more susceptible (Fischer), but this is probably a delusion, the disease having been often introduced by the Barb and Arabian and propagated among their grade descendants. The heavy Percheron shows a very ready susceptibility and a virulent and fatal form of the affection.

Microbiology. That the affection was due to a microbe was clearly shown by its absence from every part of the world into which infected horses had not been brought. The secluded countries, Belgium, England, Scandinavia, that breed their own horses, the distant Australia, New Zealand and South America remained free in face of the constant presence of the infection in different parts of Central and Southern Europe, in Africa and Asia. The horses of America and South Africa showed a ready susceptibility to the virus brought by infected horses, and rigorous sanitary police control speedily cleared a district of the trouble.

Thanhoffer found in the blood, vaginal mucous, testicle, semen, spinal fluid, myelon, and roots of the dorsal and lumbar nerves cocci, especially streptococci and less constantly bacilli, to which he attributed the malady. More recently Schneider and Buffard have apparently demonstrated that an infusorian, the trypanosoma of dourine, is the essential pathogenic agent.

The Trypanosoma Equiperdum varies greatly in form at different stages of its growth or in different media. In the exudate of the slight early tumefaction, without as yet other symptoms, it is found as minute granules in groups, as larger spherical very refrangent bodies like very large cocci, each having a strongly staining nucleus, and as larger bodies in which a delicate membranous covering encloses one, two or three masses of chromatin and extends to form one or more points (club-shaped or fusiform). Each chromatin mass has a nucleolus on its outer surface or slightly apart from it. Twenty-four hours later there may be added: First, short, thick chromatin bodies, with two slightly undulating, pointed, membranous prolongations. Second, more delicate, fusiform bodies, each with one chromatin nucleus, a detached nucleolus, and the membrane prolonged into two actively moving flagella. Third, larger pyriform bodies with chromatin nuclei and nucleoli and the membrane prolonged into one or several flagella. Fourth, fusiform bodies, thick or delicate, each having a chromatin nucleus and nucleolus, and arranged singly or in groups of two, four, six or more, united together at one end and diverging at the other to form a stellate mass. These last, 20 to 30μ long by 1.5 to 2μ broad, may perhaps be the adult form of the parasite from which the small granular or spore forms found in the most recent lesions are derived. The fusiform outline, the deep staining central mass, with its adjacent nucleolus, and the pointed or flagellate membranous prolongations, more or less motile or undulating, are characteristic features.

In its morphology and evolutionary forms the trypanosoma of dourine has not been shown to differ from that of surra, nor the nagana or Tsétsé disease, the granule form, the spherical, the club-shaped or pyriform, the fusiform with more or less stellate grouping, are characteristic of all (Lydia Rabinowitsch, Kemper, Schneider, Buffard). The distinction is found in the pathogenesis of the two diseases.

With active cutaneous or mucous lesions, the parasite is usually found abundantly in the blood, sperm, milk, vaginal secretions, and the erosions of the vaginal mucosa or penis. During intermissions, however, and in the absence of local lesions, examination of the blood may fail to detect it, yet its inoculation on a dog will usually produce the affection. It disappears from the blood and tissues with great rapidity after death, so that, to prove successful, inoculations should be made before death or immediately after. They are ineffective after 48 hours.

Schneider and Buffard, Nocard and others found the trypanosoma in the blood and exudates of horses, asses and dogs, suffering from dourine, and failed to find it, in the same localities, in animals of the same species which were free from dourine. The infected blood, preserved for 24 hours in sealed glass tubes, and then inoculated on two dogs produced characteristic dourine, with the extensive production of trypanosoma in the blood, the destruction of blood globules, and the pathognomonic local lesions. Inoculation of two other dogs, with the same material, at the end of 48 hours produced a slight transient hyperthermia only, without local lesions or propagation of the parasite in the blood. The same blood inoculated after 15 days produced neither local lesion nor fever.

Lesions. Horse. In the early stages are found a phlegmonous or œdematous swelling of the sheath, scrotum, penis and inguinal glands and a yellowish liquid effusion into the scrotal cavity. The skin covering these parts may show a papular or vesicular eruption or if this has passed, a mottling with white spots shows where the lesions have been. Later still the inguinal glands are shrunken and have undergone fibroid degeneration and induration and the testicles, swollen or shrunken, contain centres of caseation. The connective tissue of the epididymus and cord is the seat of a gelatinoid exudation. The walls of the scrotum may be greatly thickened and the seat of abscess or of caseous degenerated hyperplasia. In advanced cases the testicles are usually abnormally small even if the scrotal mass is enormously distended. The sheath and penis may be the seat of more or less numerous ulcers, and swellings, contractions and distortions of the latter organ are not uncommon. The penis may, however, retain its normal dimensions. The walls of the lymphatics in the inguinal region may be the seat of hyperplasia, the thickening causing them to stand out like cords as in glanders. In the advanced stages the muscles, especially those of the hind limbs, become pale and atrophied.

The nerve centres undergo profound changes which have been studied by Thanhoffer. The pia mater in the affected parts of the spinal cord is the seat of active congestion and thickening. The central canal of the cord is dilated (syringomyelia) more at one point than another, contains more than the normal amount of liquid, and the neuroglia around it is thickened and fibrous (sclerosed). The substance of the cord, both white and gray, shows congestion, blood staining, at points foci of softening, and at others induration (hyperplasia of the neuroglia). The nerve cells are modified in various ways, some being granular, some discolored by fine granular pigment, some having enlarged and multiplied nuclei, and some show vacuoles. The nerve filaments often show a granular degeneration extending from the nerve cell into the axis cylinder, and the latter is liable to be varicose or uneven in size. In the affected portion of the cord leucocytes are numerous and hyperplasia is often present. The neuroglia especially tends to encrease, and apart from the foci of softening tends to give a special firmness to the substance. At intervals, in the perivascular spaces, may often be found minute (microscopic or macroscopic) blood clots. The subarachnoid and subdural fluid is encreased and may be pinkish. At the roots of spinal nerves, especially in the dorsal and lumbar regions, a gelatinoid exudate may invest the nerve, distending the connective tissue beneath the neurilemma and even occupying the interval between the nerve filaments. Sometimes large corpuscular bodies are found between the nerve fibres.

The cerebral meninges, especially the pia mater, are congested and opaque. Foci of softening are by no means uncommon and the cerebral ventricles contain an abnormal quantity of fluid.

The bony tissue generally has lost its consistency and the medullary matter may be unduly reddened. The large joints contain an excess of synovia somewhat pinkish in color, and the ligaments of the hip joints are often congested, thickened and softened. The articular cartilage may even show patches of blood staining.

The intestines are usually nearly empty, soft, pale and flaccid, and Ruthe has in one case observed rounded ulcers on the mucosa. Fibroid thickening on the peritoneal surface may indicate a previous exudate.

The mesentery is thickened, with infiltration and has a yellowish discoloration and the mesenteric glands are usually enlarged, softened and friable, though sometimes firm and contracted. The lymph glands adjoining the generative organs are often swollen, pigmented and studded with foci of caseation, varying in size from a pea upward.

The liver is softened and congested or fatty. The spleen is small.

The kidneys are usually large, but flaccid, pale and bleached.

The thoracic organs may show little change, though hypostatic inflammation and foci of caseation or suppuration may be present.

The blood is pale and watery and forms a loose, pale, diffluent clot, while there is an extraordinary diminution of red globules and a relatively great encrease of leucocytes.

In advanced stages the muscles are pale, anæmic and shrunken especially those of the hind limbs.

Mare. In the mare in addition to the lesions of the internal organs and blood, the following may be noted in connection with the generative system. Phlegmonous or œdematous swellings, sores or ulcers on the lips of the vulva, and on the vulvar and vaginal mucosæ. The parts become variously distorted, and the vulva, habitually open may expose the swollen and ulcerated clitoris. A crop of papules or vesicles, running into sores or ulcers may appear on the urethral orifice, the vulva and adjacent skin, and even though overlooked, their seats are marked later by loss of cutaneous pigment and the formation of small white spots. The mammæ are sometimes inflamed, œdematous and tender, with suppurative or necrotic foci and the adjacent lymph glands are enlarged by infiltration or contracted by sclerosis.

Dog. These resemble those in horses. In the bitch genito-urinary congestion, inflammation and catarrh, subcutaneous infiltration under the belly and inside the thighs, swelling of the inguinal lymph glands, emaciation, and pallor and atrophy of the voluntary muscles are marked features.

Symptoms. Horse. Incubation may last from one to eight weeks (Maresch), but is usually 11 days from the infecting service. It may be abridged by a special susceptibility, and by repeated infections and hence the more acute cases are especially seen in the male in daily service. In some such subjects local genital infiltrations are speedily followed by paralysis or vertigo which cuts off the patient in a few days.

More commonly the malady is chronic though varying in different countries, epizoötics or even in particular cases.

The first symptom is slight swelling of the anterior border and raphe of the sheath, which gradually extends backward to the scrotum and inguinal region and forward on the abdomen it may be as far as the brisket. This may be hot and painful, but is usually œdematous, cool and painless. The infiltration affects the end of the penis, the meatus may be red and angry with a slight muco-purulent discharge, and red spots vesicles and ulcers may stand out clearly on the pigmented surface. Williams never saw such eruptions in the American cases and doubts their existence except as the result of injuries. There are frequent semierections and service is still possible. Later the engorgement extends to the specially pendent testicles, inguinal glands and others adjacent. Paraphymosis is occasionally seen or, more commonly, the penis hangs out of the sheath soft and flaccid and erection seems impossible. The local swelling may become excessive, pressing the testicles up against the inguinal ring, or suppuration and extensive abscess may follow. Appetite is retained and the temperature remains moderate (100° to 102° F.).

The local swellings may almost completely subside, except a slight tumefaction of the end of the penis, hence some (Fischer) have held that the cutaneous lesions are the primary ones, yet the start of infection at the generative organs and the fact that a stallion often infects a number of mares before there is any suspicion of his own infirmity is evidence enough of the genital seat of the earliest lesions.

The cutaneous lesions, which are essentially secondary, but highly characteristic, appear from forty to sixty days after the infection (Schneider and Buffard). They are from a quarter of a dollar and upward in size (in some old horses much smaller), and rise abruptly from the healthy skin, becoming the more marked that the hairs upon them stand erect. These may arise suddenly and subside again in one day, or give out a serous exudate which mats the hairs into a tuft. They may, however, last four or five days. These are more patent after a full drink of water, or after sprinkling or sponging with water. Even when they have been overlooked these results may often be seen later on colored skins, in the presence of many circular white spots entirely devoid of pigment. The most common seat of these cutaneous lesions is the hind parts (anus, tail, croup, quarters), but they may appear on the sides, neck, shoulder or thighs.

Tenderness of the loins may now be shown, with frequent, painful micturition, but the penis becomes more and more paretic, so that coition becomes encreasingly difficult or impossible. Paresis also shows in the hind limbs, the animal remains recumbent a great part of the time, rises with difficulty, starts suddenly forward at the fetlock, and drags the toe on the ground in walking. Swelling of the joints and tendinous sheaths, with attendant lameness, is not uncommon. The appetite remains good, yet emaciation and weakness make marked progress.

The advanced stages are characterised by marked anæmia, paraplegia and dementia. The visible mucosæ are pale, emaciation advanced, the patient stubs his toes and sways in walking, and finally drops unable to rise; or he stands with hind legs straddled and semi-bent, and largely oblivious of all around him. He may be too stupid to eat unless the food is placed in his mouth, and yet the neigh of another horse or a mare may draw forth a feeble retort, as if the deranged generic instincts remained. Swelling, or even abscess of the lymph glands, axillary, submaxillary or inguinal, is usually present, and muco-purulent discharge with ulceration of the nose or eyes is not uncommon. The joints crack when moved and fractures are common.

The duration of the disease is two or three months, the progress being more rapid in winter.

Mare. Vulvar swelling eight or nine days after service, with ejection of urine in jets, contraction of the vulva, redness, swelling and erection of the clitoris, and a muco-purulent discharge are marked symptoms. European observers note nodules, vesicles and ulcers on the mucosa and adjacent skin, but these were not observed in the American cases (Williams). Yet later they showed the characteristic white spots. Switching of the tail, stamping of the hind feet and painful straining to urinate are followed in certain cases by ejection of the urine forcibly in jets or in small dribblets. The catarrhal discharge is at first watery, but later becomes viscid, sticky and white, yellow or grayish, or even red. It mats together the hair of the tail and thighs, and putrefies, exhaling a repulsive odor. The swelling involves the space between the thighs and often implicates the mammary glands and even the floor of the abdomen. The inguinal glands are often involved, and hyperplasias with degenerations and even abscesses may appear in this region. As in the stallions the local lesions may have periods of advance and subsidence, and in favorable cases, that are not again served, there may seem to be a temporary recovery. The mare, however, remains infecting, and if served the local disease is at once roused into activity. The button-like skin eruptions appears on the quarter as already noticed of the horse and in grave cases may caseate or suppurate and burst, forming an indolent and intractable sore. The dark skin of the vulva and perineum becomes marked by white spots or by irregular patches caused by the confluence of several such spots, which for ordinary breeds of horses are highly characteristic of this disease. Many Arabian horses naturally acquire such white spots on the dark skin, and in pure Arabs and grades this appearance need not be held as evidence of dourine.

Infected mares rarely conceive, and any that do so are likely to abort before the sixth month.

The systemic symptoms, nervous, paralytic, tremulous, dyspeptic, atrophic, cerebral and cachectic follow a similar course as in the stallion.

In grave and progressive cases the lesions of the generative organs become very marked. The lips of the vulva become rigid and distorted so that it remains constantly open and the erect clitoris continually exposed. The skin of the vulva is tense, dry and shining. Lameness is shown in one or both hind limbs, knuckling over at the fetlock, shortening of the step, planting the toe first and the heel later with a jerk, lack of balance, paresis and even inability to rise.

A disposition to trembling is common to both sexes, as is also an intolerable itching of the skin which may make the animals tear the lower parts of the limbs with the teeth. In either there may be a local paralysis of a lip, an ear, an eyelid, or some other part of the body. In both sexes the disease tends to extreme anæmia, debility and emaciation, and to infective internal inflammations (lungs, bronchia) or septic or purulent infections.

Diagnosis. From urticaria this disease is to be distinguished by the absence of lesions of the generative organs in the former, by its association with change of food and digestive disorder and by the absence of all evidence of contagion.

From glanders it is to be distinguished in the same way by its casual transmission by sexual connection only, by its restriction to breeding animals, and by the irresponsiveness of the victim to the mallein test. The progressive paresis and hebetude are valuable diagnostic phenomena.

From chronic paraplegia it is distinguished by the same prevalence in breeding solipeds only, and by its mode of transmission.

The greatest difficulty is experienced with the slight and comparatively occult cases, and in some of these the history of the infection of a number of breeding animals, which have been served by the same horse may be the one guiding point for a number of the cases. For sanitary purposes it is well to treat as suspicious animals all mares that have been served by a stallion which is in the line of infection. This suspicion would attach also to any stallion that had served a mare which had been to a diseased or suspected stallion, and to all mares that have been served by the suspected stallion after he had been to the suspected mare.

From simple vesicular exanthema dourine is to be distinguished by its comparatively slow progress, and by the uniformity of the lesions of the generative organs and nervous system, which are lacking in the vesicular affection.

Prognosis. A certain number of animals recover from the milder attacks which have not become complicated by the grave trophic and nervous lesions, but as in glanders, recovery from severe attacks and in the advanced stages is practically unknown. The mortality is set at 70 per cent. and upward.

Symptoms in the Ass and Mule. The disease usually remains discrete, the lesions in the generative organs or other seat of infection being the marked symptoms, and recovery the rule. Œdema of the end of the penis, obliteration of the folds around the orifice of the urethra and eversion of the urethral mucosa are the most constant features, distinct even in semi-erection. Œdema of the sheath and skin eruption may follow. Exceptionally a mule proves as susceptible as the horse, and shows the disease with the same fatal severity.

Symptoms in Dog. A bitch, 15 days after vaginal injection of the infected equine blood, showed severe vaginitis and hyperthermia (100°). On the 23d day she aborted, followed by muco-purulent discharge, vulvar œdema, pallor of the mucosæ, anæmia, rapid emaciation, paresis and occasional convulsions. Blood drawn from the vulva contained the trypanosoma. She died on the 66th day. The temperature rose to 103°.

Two male dogs that lined the above infected bitch showed after 12 days, engorgement of the sheath and scrotum, muco-purulent discharge, and abundance of the trypanosoma in the blood of the affected parts. Cutaneous lesions on the loins, thighs, sides or forehead, showed erection of the hair, with infiltration, or shrivelling and bloodlessness.

Other dogs showed arthritis, corneal opacities and ulcers, hypopion, cataract, nasal discharges, facial periostitis, dyspnœa and syncope.

Symptoms in Rabbits. Rouget found in inoculated rabbits, extensive gangrene of the skin, involving even the cranial bones, ulcerative keratitis, hypopion, panophthalmia, following on the earlier genital troubles of vaginitis, swelling and discharge.

Treatment. Some cases recover spontaneously a few may be aborted in the earliest stage of the disease, but cases that have advanced to any extent and assumed a grave character are practically hopeless.

An important element in treatment is to do away as far as possible with the cause of generative excitement since the disease is aggravated and more rapidly advanced by frequent copulation. Rodloff from a very wide experience speaks highly of castration of the stallion. Castration of the mare has not been specially advocated and the absence of marked lesions in the ovaries, may deter the veterinarian, yet whatever promises to lessen in any degree the genesic excitement is not to be despised, and the measure has besides a sanitary value for other animals.

Early local treatment is the most promising, and especially if it can be applied to exposed animals during apparent incubation. Injection of the urethra, sheath, vulva, vagina and uterus with antiseptic lotions, and apply them to the external sores. Mercuric chloride 1:2000, carbolic acid 2:100, silver nitrate 1:250, calcium chloride 1:100, or chlorine water may be taken as examples. When local swellings have supervened it would be entirely appropriate to incise them freely or even to excise them and cauterize thoroughly with stronger agents.

Internal treatment by mercuric chloride 1½ to 3 grains, potassium iodide 2 to 5 drs., arsenic 7 to 14 grains, has been widely used but to little purpose. The same may be said of Rodloff’s treatment by tonics and carminatives (sal ammoniac, camphor, iron, angelica, gentian, ginger and valerian.)

Prevention. The one thing to be secured is the prevention of copulation with any animal that has been affected, or exposed to this disease in the past three years.

1st. Any stallion or mare once affected must be excluded from breeding for at least three years after apparent recovery.

2d. Every such animal that has been exposed by copulation with a suspected animal must be excluded from breeding for the same period even if no active symptoms have been shown.

3d. Every affected or exposed animal, should be quarantined in the hands of his or her owner and placed on an official register and the sale, gift or loan of such an animal, or its movement to a new place where it might propagate the disease should be made a misdemeanor.

4th. In any county or district in which the disease exists all stallions and mares should be registered and none should be allowed to be used for breeding purposes without an official certificate showing that each of the animals mated is free from all suspicion of having been exposed to this infection.

5th. If any stallion or mare is imported from a country in which dourine exists it should be accompanied by an official certificate showing that it has not in the past three years been exposed to the possibility of infection with dourine.

6th. In the absence of such certificate the imported animal (capable of breeding) should be kept in strict quarantine for the period of three years.

7th. A much more radical measure, which may be made to supersede all of the above, would be to castrate every soliped (stallion or mare) which has suffered from the disease in the past three years, and every such animal that has by coition been exposed during that length of time to even a remote opportunity for contagion. This would embrace all apparently sound mares that had been served by a stallion which had shown slight symptoms of the disease, or by a stallion which had not himself shown such symptoms, but which had served a mare that had shown such symptoms; or one that had served a mare that had not shown such symptoms, but that had been previously served by a stallion which had shown such symptoms, or that previously covered a mare that had shown such symptoms. In such cases the State might well afford to indemnify the owner for any reduction in value of the castrated stallion from that borne by the animal as a prospective breeder, the breeding for which indemnity is sought being understood to count only from a date of three years after the sanitary castration. A mare once attacked should be remorselessly castrated or killed. A perfect recovery in a horse can be better attested; that of a mare is always uncertain, and most secondary outbreaks after the apparent extinction of the poison have come from breeding mares that have apparently recovered, or that after exposure have shown no appreciable symptoms.

When a State is so lost to all sanitary considerations as to abandon an affection of this kind to take its course, the owners of stallions and mares cannot be too careful to avoid the exposure of their valuable breeders to the risk of infection. Each mare brought for service should be admitted only when accompanied by a certificate showing all previous services in the last three years, with the identification of the stallion, and this irrespective of whether the service has been fruitful or not. In such certificate the owner of the mare should bind himself to make good all damage or loss that may accrue from his failure to set forth in the certificate every such service and every symptom of illness affecting the generative organs from which the mare has suffered in the three years antecedent.

The owner of the stallion should give a similar guarantee that the horse has in the past three years served no mare that was in any way open to suspicion, and that the animal has not suffered from any affection of the generative organs which had any of the characteristics of dourine.

No mare should be served which shows swelling, nodules, distortion, or gaping vulva, a muco-purulent discharge, or too frequent or too prolonged heats.

No stallion in such locality should be allowed to serve which shows pasty swelling of the sheath, swelling, shrinking or distortion of the penis, red, angry, tender meatus urinarius, or a muco-purulent discharge.

Unless in case of Arabian horses the appearance of white spots on the dark ground of the sheath, penis, vulva, or perineum, should be ground for debarring from service until an absolutely stainless record covering a number of years has been shown.

MAL DE CADERAS.

This is a disease caused by Trypanosoma Equinum described by Voges who studied the affection in the Argentine Republic as it exists in a region extending from Santa Fe, and Corrientes on the south to Bolivia on the north. It resembles surra in prevailing in tropical heat, during wet weather, in its intermittent character, in the presence of the mature trypanosomata in the blood at the beginning of a paroxysm and their disappearance toward the end of it, in the supervention of rapid and extreme emaciation, debility and anæmia, in the destruction of red blood globules and the passage of the coloring matter by the kidneys, in the presence of paresis and œdemas, in its expending its energy mainly on the soliped and in the constancy of the mortality. Death occurs in two to five months in horses, and six to twelve months in asses and mules. Swine and water hogs contract the disease casually and it is inoculable on white and gray rats, mice, rabbits, dogs, goats, sheep, chickens, turkeys, ducks and monkeys, (Nyctipithecus felinus), and exceptionally on Guinea pigs. The same measures of prevention would be indicated as in cases of surra and dourine.

INFECTIOUS PARAPLEGIA OF SOLIPEDS IN MARAJA.

Synonym. Definition: Infectious, anæmic, dropsical paraplegia. Origin: Decomposition of myriads of horse carcasses in torrid heat; rodents; swine; horses. Causes: Microbe uncertain; infection in corral and vicinity; manure; rubbish; flies; hot dry weather. Symptoms: Decreasing severity; preliminary weakness, dulness, emaciation, dyspnœa. Paresis: Fifty per cent. paraplegic; marasmus; difficult defecation or urination; paretic penis; anorexia; ardent thirst with diuresis; rumbling of bowels. Œdema, epigastrium, abdomen, sheath, mammæ, head. Cutaneous sloughing, stupor, asthenia, rapid emaciation, hemiplegia, impaired peristalsis. Blood dark, viscid. Lesions: Intestinal congestion; petechiæ of serosæ; icterus; enlarged, soft, congested liver; spleen engorged, softened; kidneys swollen, congested; petechiæ on bladder; congested lungs, thoracic serosæ, cerebral meninges. Relation to surra. Mortality excessive or constant. Treatment hopeless. Prevention: Keep sound from sick and from infected places and things; kill and bury sick; disinfect harness, trappings, wagons, utensils, buildings, manure and rubbish heaps; destroy flies and mosquitoes, vermin (rodents), etc.

Synonym. Quebra Bunda: Broken Buttock.

Definition. An acute infectious disease of horses characterized by a condition of fever, with rapid loss of condition, resulting in rapid and extreme emaciation, local dropsies, cutaneous eruptions and ulcers, a rapidly advancing anæmia and debility, with lessening control of the hind quarters and death in almost all instances.

History of the Disease. Luis Calendrini da Silva Pacheco says the malady was unknown on the island until 1830, when, on account of the great excess of wild horses and their devouring the pastures needed for the more valuable cattle, great numbers were killed and their hides marketed. This continued for over a year without any attempt to dispose of the carcasses. These accordingly lay in heaps in a damp climate, under the equatorial sun, in a condition of putrefaction, exhaling the most offensive odors. Stimulated by frequent complaints, the government ordered that the carcasses should be burned to ashes, but no success was accomplished, in one case 800 bodies having been merely roasted a little on the surface. The district around Chaves contained the greatest number of horses, there the greatest number were killed, and there the disease broke out. A number, variously estimated at from 25,000 to 60,000 were driven into the little bay of Juncal and killed by burning the grass, which, however, did not at all consume the bodies. The disease attacked first the capivaras (rodents) in the district of Chaves, killing off the whole race; then the wild and domestic swine suffered, and finally it ravaged the equine race, and though confined to Chaves for two years it was extended through sales of horses and raged with such fury that in five years not a horse was left alive in the island, except a small remnant of a few hundreds in Chaves, where the infection started.

Causes. The microbian cause of the disease has not been definitely ascertained, so it is idle to speculate whether we have to deal with a saprophyte which has taken on deadly pathogenic properties, or whether the infection was carried to the island by winged insects or birds attracted by the decaying carcasses.

Certain conditions may be named as accessory or favoring causes. The wild horse often escapes so long as he is on the pasture, but when lassoed, taken to the corral and broken, he will die in four to six days. This suggests that the infection is laid up and preserved in the corrals or stables, the mangers or racks, or possibly in the water supplies. The contact with even the reins (harness) of other horses is alleged to be a prominent cause of infection. Another significant point is that around every hacienda, within a radius of a mile, there are numbers of carcasses, so that there is every opportunity for the infection of the wild and susceptible horses caught and brought in. Near the buildings, too, are accumulations of horse and cattle manure and rubbish heaps of all kinds, the breeding places of the flies, which are probably important factors in conveying the infection. Again, the attacks are more numerous and severe and death earlier in the hot, dry summer weather, while there is a pause and a lesser intensity in the cool or rainy season. All domestic animals, save when kept up for breaking or work, live in the open field day and night and subsist on the green food (capine, gramineæ), and are thereby exposed to all climatic changes.

Symptoms. At the first appearance of the disease (1830) it proved fatal in a few hours, but after a year’s prevalence, when the more susceptible animals had been killed off, the progress of the malady became slower, death being deferred to the 8th or 15th day, so that the symptoms could be more definitely followed. From 7 to 14 days before the more obvious symptoms, there were lifelessness, tardy movement, hurried breathing, debility, weakness and emaciation without work or other obvious cause. Exercise caused difficult breathing, dilated nostrils and great agitation of the flanks.

One of the most constant symptoms was the loss of power of the hind limbs which would sway and stagger, the femurs turning inward, as if dislocated, and on uneven ground the animal could not walk without falling. When down, he could not rise without assistance. In the earlier experience of the malady (1835) only 8 to 16 per cent. failed to show these paraplegic symptoms, whereas in recent years 50 per cent. or more escape them. In these cases the emaciation goes on alone, gradually encreasing until the patient appears like a living skeleton. Some retain an appearance of liveliness, yet all stand on three limbs, and change from one hind limb to the other every six or eight seconds.

The retraction of the abdomen is a marked feature, yet expulsive contraction is defective, the patient fails to put himself in the position for urination or defecation, and there is more or less detention of urine or fæces, the latter being dry, moulded, covered with mucus and of a reddish yellow color. After a time the urine escapes in fine jets, so small that in the absence of stretching to urinate, or raising of the tail, they are easily overlooked. The urine may be normally clear, or dark colored. The penis hangs out of the sheath several inches farther than in health.

Appetite is sometimes impaired, or completely lost, but usually the patient eats and drinks to the last, but without proper digestion or assimilation. It does not check the advance of marasmus. Thirst often becomes excessive and in such cases, there is diuresis together with frequent and excessive rumbling of the bowels. The loins are very sensitive to pinching.

About sixty to seventy per cent. in different outbreaks show œdema, in the epigastric region it may be six inches in diameter, or it may extend from the sternum back so as to include the abdomen, sheath, or mammæ, and perineum, and even the hind limbs. Considerable serous oozing takes place from this for four or five days after which it dries up.

In about seven to fourteen per cent. the head became œdematous and swollen, with an abundant fœtid purulent discharge from the nose and eyes, and extensive ulceration of the pituita and conjunctiva. Such cases became completely blind prior to death. In other cases extensive ulceration of the skin set in with the formation of most repulsive sores.

The nervous symptoms assumed various forms; in some there was stupor with head resting on the ground; in others extreme debility and paraplegia with phenomenally rapid emaciation; in a few hemiplegia, or even delirium was shown; in all there was a marked paresis of the digestive organs and especially impairment of peristalsis. The blood assumed a dark gluey aspect.

The most constant symptoms appear to be dyspnœa under exercise, paresis of the hind limbs and intestines, genital atony, a wonderfully rapid and extreme emaciation, œdema, and a tendency to impaired nutrition or ulcerous degenerations of the pituita, conjunctiva or skin.

Lesions. Congestion or inflammation of the intestines was usually noted, with petechiæ on the peritoneum, especially the omentum, and on other serosæ. The serosæ, mucosæ and other normally white tissues were of a yellowish color, more or less deep. The liver was enlarged, much softened, gorged with black blood, and sometimes of a greenish color. The spleen was more or less black, and friable sometimes coming to pieces in handling. The kidneys were always enlarged and gorged with black blood. The bladder was usually distended and showed petechiæ on its mucosa. The lungs and bronchia bore evidences of congestion, and the pericardium had become dull, rough and lusterless. The horses that had rested their heads on the ground showed meningeal congestion.

Sr. Calendrini claims to have had recoveries in some cases, followed by relapses, and states that a second relapse is usually fatal. Many features of the disease reminds one of surra—for example its relation to hot weather, its relation to buildings and enclosures with their accumulations of decomposing organic matter and swarms of flies, the decomposition of the blood, anæmia, icterus of the white tissues, petechiæ, extreme weakness, muscular atrophy, and marasmus. Calendrini’s cures followed by relapses suggest the further coincidence of intermissions. If now the trypanosoma were discovered in the blood it might be recognized as at least a near ally of surra.

Mortality. Prognosis. The disease is nearly always fatal. At the time of its first appearance (1830) Calendrini had 5,000 horses, and in 1835 he mounted his last horse a half-tamed animal lassoed on the Campo. One Haziendiero invested $25,000 in horses and in 30 days he had lost $18,000 worth. Others with 35,000 head lost the whole.

Treatment proved one continuous failure. Bleeding, purgatives, coloquintidas, saltpeter, cream of tartar, lemon, vinegar, nicotine, buchu, by mouth and rectum, strychnia, camphor, caustics, prolonged baths in the river, and a great variety of other measures, only seemed to hasten a fatal result.

Prevention. Calendrini finally struck the true note of rational prophylaxis, in the immediate killing and burial of all affected animals, and the strict separation of all sound horses from the places where they had been, together with the thorough disinfection of all harness, utensils, wagons, etc. For a number of years his district (Soure) had by this means been kept free from the plague.

This might be profitably extended so as to include the thorough disinfection of any buildings and yards where the sick had been, the removal of manure heaps and disinfection of their sites, also of all rubbish heaps as breeding places of flies, the use of petroleum on all stagnant water devoid of fishes and frogs as being the sources of mosquitoes, and the application of suppressive measures which would include the rodents (capivaras), and swine which have been shown to propagate the infection.

INFECTIOUS PARAPLEGIA IN SOLIPEDS IN EUROPE.

Definition: Infectious, non-febrile affection of solipeds with lesions of the genito-urinary mucosa and nerve centres, paresis and paralysis. History. Causes: Microbes varying; bacteria of colon group; infected urine, genital mucus, brushes, combs, rubbers, mares especially exposed; infection local or general. Lesions: Congestion, exudation, swelling, discharge from vulva, vagina, bladder, ureter, kidneys; lumbar spinal cord, brain. Symptoms: Mare, swollen open vulva, congestion and petechiæ, bloody mucus; horse, swollen sheath, pendant penis, congested papilla, discharge; paresis of hind limbs, falls, inability to get up, incontinence of urine; paresis of fore limbs, of thoracic muscles, asphyxia, fever in late stages. Recovery. Diagnosis: From hæmoglobinuria by absence of dietetic cause, the infectious progress and genital lesions. Prognosis: One-fourth to one-third die or fail to recover. Treatment: Antiseptic washes and irrigations of vagina, urethra, bladder, skin; internally oil of turpentine; slings. Prevention: Isolation, disinfection, separate attendants, litter, sponges, etc., fly nets, screens, insect powder, removal and disinfection of manure and garbage.

Definition. A contagious, non-febrile affection of solipeds, characterised by congestive and hæmorrhagic lesions of the genito-urinary mucosa, the spinal cord and its meninges, and by paraplegia or paresis of the hind limbs.

History. This was described in 1888 by Comeny, as occurring in a regiment of French cavalry. Other outbreaks have been observed in 1892 (Rancoule); in 1896 (Blin and Lambert). Earlier outbreaks have doubtless been confounded with cerebro-spinal meningitis, hæmoglobinuria or simple paraplegia, the genito-urinary symptoms having been overlooked or viewed as secondary.

Causes. The disease, as hitherto observed, has been invariably associated with microbian infection of the genito-urinary mucosa, but no one microörganism has been found to be constantly present. In the 1888 cases, Nocard isolated from the kidneys and lumbar cord a small, motile bacillus which was not stained by Gram’s method and the inoculation of which proved fruitless. Zschokke, in 1889, found in the kidneys, lungs, liver and spleen of both horses and cattle, the victims of a progressive infectious paralysis, a bacterium coli commune 1.5μ long by 0.7μ broad, which stained in methylin blue and grew in agar and gelatine, and when inoculated under the skin of a goat provoked paralysis. It had no effect on a pig. In keeping with this, Thomassen, in 1893, alleged that the bacillus coli communis in certain conditions, when colonized in the solid organs, produced a toxin which caused paresis and paraplegia. Blin and Lambert, in 1896, found in the urine, in pure cultures, a short ovoid microbe, motile, non-liquefying and bleached by Gram’s solution. It grew on gelose and peptonized gelatine as a creamy surface layer which did not extend into the medium, and assumed a brownish color as it became older. On potato it formed a superficial bright yellow film. In bouillon the surface film which formed gradually precipitated to the bottom of the vessel.

This microörganism was not found in the blood, liver, muscles nor spinal cord.

Inoculation into the pleural cavity of the horse induced pleuro-pneumonia.

The contagion appears to be transmitted through the urine and morbid discharges of the urino-genital canal, falling on the litter and floor and thus contaminating the tail, and indirectly the generative organs. The brushes, combs and rubbers used on one horse after another are similarly incriminated. The mares, having a wider exposure to infection, appear to suffer most. Comeny saw eighty sick mares to twenty-eight horses, and the mortality was thirty-four mares to three horses. The smallness and length of the male urethra and its frequent flushing throughout its whole length with urine seems to give a greater measure of immunity to the horse.

In the Blin and Lambert cases the indications pointed to a local infection and to the presence in the spinal cord of the toxins alone. It may be assumed that in such cases there was a purely local infection. In the Zschokke cases on the other hand, with microbian infection of internal parenchymatous organs the presumption is that the paralysis was due to a totally different infection, as appears to be further indicated by the morphology of the microbe. They may have been, however, but the advanced and generalized stages of a primary local infection.

Lesions. These appear to vary with the progressive advance of the malady. In an ass which was killed as soon as paraplegia appeared and the necropsy made at once, the lesions were confined to the vulva, vagina and bladder. In advanced cases the ureters and kidneys are visibly involved together with the spinal cord, especially in the lumbar region, and in certain instances the brain.

The vulva is swollen, held habitually open so as to expose the erect clitoris; the mucosa is irregularly swollen and petechiated, and there is a glairy or bloody discharge. The swelling usually extends to the inner side of the thighs, the mammary glands and the adjacent wall of the abdomen. The vaginal mucosa is congested, swollen so as to bulge irregularly at intervals and covered with a glairy muco-purulent matter often mingled with clots of blood. The urethra and bladder are red and congested, with marked thickening and ecchymosis of the mucosa and an abundant serous exudate which extends into the muscular and peritoneal coats as well. Minute extravasations are found in the two outer coats and petechiæ of the serosa is the rule. In fatal cases the ureters and kidneys are involved, the renal parenchyma is greatly congested and softened, the cortical part especially being of a dark red, and the glomeruli distinctly enlarged. An oily sanguineous liquid can be squeezed from the cut surface. The lumbar portion of the spinal cord together with its meninges, is congested and arborescent, and in bad cases this may extend upward to the head and involve the brain and its coverings.

There is general congestion of the venous system with black blood, especially noticeable in the arborescent lines on the inner surface of the skin and in the serosæ, and the liver and spleen are gorged with black blood, which, however, reddens on exposure to the air. Muscles and parenchymatous organs may show a parboiled appearance. In the male the swelling appears about the sheath and penis, the papilla, the urethral mucosa and that of the bladder are deeply congested and petechiated, and the kidneys and medulla may be implicated as in the mare.

Symptoms. In the mare the early symptoms are the swelling and gaping of the vulva, with the muco-purulent or sanguineous discharge and the presence of redness, congestion and petechiæ of the mucous membrane.

In the horse there is swelling of the sheath and a pendant condition of the penis, which in its turn may be irregularly reddened and swollen, and the papilla and orifice of the urethra are deep red and angry.

Most commonly these early local symptoms are overlooked until attention is drawn by some lack of control of the hind quarters. When moved the animal sways or staggers behind, knuckles forward at the fetlocks and drags the toe along the ground. This weakness encreases, and although for a time the animal can stand steadily, he is liable to fall when we make him take a step, and when down he will require help to get up. In advanced stages the animal remains recumbent and cannot be made to stand even with help, the fore limbs have become implicated in the paralysis, and in the end the respiratory muscles are involved and the patient dies asphyxiated. This marks the occurrence of severe lesions in the medulla oblongata. Incontinence of urine is a frequent symptom. Fever usually sets in, in advanced cases. Recoveries may take place from the first and second stages, the control of the muscular system improves, the animal lies down and rises with greater ease, the drooping penis is retracted within the sheath, incontinence of urine ceases, micturition becoming less frequent and more abundant at a time, and finally muscular control becomes once more perfect. Convalescence may be complete in eight days if it begins early, while it may require two or three months when the disease has been more advanced.

Some subjects survive without overcoming the paralysis, so that they simply eat their heads off if preserved.

Diagnosis. From hæmoglobinuria this disease is to be distinguished by the history which fails to show its supervention on a period of hard work and high feeding, followed by one or more days of rest and then sudden exercise; by the swelling ecchymosis and discharge from the vulva or sheath, and by the occurrence of several cases in animals that have had an opportunity for a common infection. In case of death the condition of the kidney, bladder and urethra, and the marked congestion of the lumbar portion of the cord is significant, the congestion, petechiæ and extravasations are deeper and the glairy discharge is present.

Prognosis. From one-fourth to a third of the animals attacked either die or are rendered permanently useless.

Treatment. Antiseptic washes and irrigations of the genito-urinary passages, and the adjacent parts, if employed early enough, would tend to abort the disease. Even if resorted to later, they would be of some value in limiting the multiplication of the microbe and the absorption of its toxins. For this purpose boric or salicylic acid, salicylate of soda, permanganate of potash, or silver nitrate may be taken as examples. They should be as thoroughly applied as possible, the bladder being thoroughly evacuated and injected several times a day. As internal medication, oil of turpentine and other stimulant antiseptics that are eliminated by the kidneys might be tried in small doses frequently repeated. Keep in slings. The patient that cannot stand up is lost.

Prevention. This consists in isolation of the healthy, thorough disinfection of the stalls, gutters, combs, brushes, rubbers, blankets, and the hands of attendants. Litter used for the sick should be burned and manure piles secluded and disinfected. Even flies are to be dreaded, so that darkness in the stable, fly nets, fly screens, and insect powder and other means of insect destruction will be in order. Sponges and other means of dressing should not be used indiscriminately on different animals.

PROTOZOAN CATTLE FEVER. TEXAS FEVER. PALUDISM OF CATTLE.

Symptoms. Definition: protozoan, tick-borne, febrile, affection, of wild damp lands, and warm seasons, with enlarged spleen and liver and hæmolysis. Historic Notes; Old World; Australia; tropical and subtropical America. Causes: contact of cattle from salubrious districts with the insalubrious or with cattle from such; Piroplasma bigeminum; a bovine parasite, reducing red globules by ¾ths.; successive forms of piroplasma; the cattle tick, boöphilus bovis, bearer of piroplasma; demonstration of the tick agency; toxic saliva of tick; toxic property in blood; question of identity of infection-bearing ticks. Lesions: putrefaction rapid, icterus, ticks, blood oozing in skin, hydræmia, hæmoglobinæmia, few red globules, small petechiæ, slight serous exudates and effusions: congestion, petechiation, sloughing, perforation of gastric mucosa, congestion of intestinal mucosa, in rectum like port wine; liver enlarged, congested, biliary radicles in acini gorged with bile; spleen enlarged, engorged; kidneys œdematous, blood-stained; bladder petechiated; urine opaque or red, in convalescence watery; womb; fœtus. Incubation three to ten days; delays due to hatching of ticks. Symptoms: Acute case: anamnesis; hot season; hyperthermia 104° to 109° F.; hurried breathing and pulse; anorexia; dulness; costiveness; icterus; prostration; weakness; delirium; urine turbid, red; blood hydræmic; diarrhœa; emaciation. Duration one to seven days. Fatal (90%) to exotic cattle; mild in indigenous, or cool season. Mild case; temperature 103°, anorexia, dulness, costiveness, enuresis, albuminuria, pallid mucosæ, emaciation, round protozoön in globules, ticks, oligocythemia. Differential diagnosis, from anthrax. Treatment: laxative; antiseptic; mucilaginous food; picking off ticks; anti-ixodic lotion; tick-free pasture or place. Prevention: destruction of ticks; picking; dipping or smearing with tick killing preparation, paraffin or extradynamo oil and sulphur, danger with shipping; dressing of all cattle at intervals during warm season; cultivation of tick-infected land; exclusion of cattle for one summer and two winters; soil cattle for three weeks in each of two tick free pens, to let ticks drop; danger of nonimmunized cattle in infested area; suggestions for extinction by States. Immunization: Infection of sucking calf; infecting by a few ticks: by graduated injections of piroplasma blood; technique; injection of blood from body of tick. Limited value of artificial tolerance. Marketing of the beef. Federal restrictions.

Synonyms. Splenic fever; Spanish fever; Mexican fever; Southern cattle fever; Australian tick fever; Tristeza; Red water; Black water; Bovine periodic fever; Bovine yellow fever; Maladie du bois; Holzkrankheit; Moor evil; Wood-ill; Ixodic Anæmia; Roumanian hæmoglobinuria.

Definition. A specific fever of cattle, enzoötic during the warm seasons in the low, malarious grounds and wooded or uncultivated districts of different countries, caused by a protozoön in the blood and red globules, which is conveyed from animal to animal by ticks, and leading to engorgement of the spleen and liver, destruction of the red globules, hæmoglobinuria, and oligocythemia.

Historic Notes. This malady has doubtless existed from time immemorial in different malarial districts of the Old World, where the wood and moor ill is now coming to be recognized as a protozoan tick-borne disease. The malady exists in Roumania (Starcovici, Babes, Gavrilescu), Turkey (Nicolle, Adil-Bey), Sardinia (San Felici, Loi), Southern France (Lignieres), Italy (Celli, Santori), Algiers, Tunis (Lignieres), Finland (Krogins, Von Hollens), West Indies, Mexico, Nicaragua, United States of Columbia, South America as far south as the Argentine Republic, German East Africa (Koch), Transvaal (Theiler), S. Australia (Pound). In Australia imported European cattle found the infection waiting for them in the uncultivated bottoms. In America it doubtless prevailed on the seaboard and islands of the Gulf of Mexico from the time of the importation of Spanish cattle, but for the first definite account of it we are indebted to Dr. James Pease, who records the widespread destruction of the native herds in Lancaster, Co., Penn., in connection with the introduction of cattle from the south. None of the southern cattle died, but wherever they traveled, the native stock perished all but universally. Other droves from South Carolina were equally destructive to all cattle along their track. The recorded symptoms of anorexia, great weakness, often inability to stand, trembling, groaning, bloody urine, bleeding from the nose, costiveness, congested kidneys, and decomposed, incoagulable blood serve to identify the disease.

Later, whenever southern cattle were moved north, the disease followed their trail. Florida cattle left infection along their route until they reached the border of Virginia, where it usually ceased. When taken from the Georgia mountains to the lowlands, they died without infecting the native stock, and, when such native stock of the lowlands were moved to the hills or the north, they conveyed the fever to the stock among which they came, though themselves well and improving all the time (Wilkinson). Similar experiences were had in all the middle states up to the war of 1861, but, in too many cases, the real source of infection was overlooked. It was observed that the disease was confined to the vicinity of the main highways and drove roads running north, and spared the lands lying somewhat back of these routes. Attention was drawn to the Texas cattle in 1853 when a herd of 450 which had wintered in Jasper Co., Mo. moved north passing through Vernon Co. in June, and causing losses of 50 to 90 per cent. of the native cattle along their course, and only along that line. Such invasions occurred yearly, and in 1858 $200,000 worth of native cattle perished from this cause in Vernon Co. alone (A. Badger). During the war (1861–64) the cattle, in Texas especially, encreased without meeting with an adequate market, and, on the opening of the trade once more, they were sent north in large numbers carrying infection with them. When Forts Smith and Gibson had been occupied by the Union soldiers, the southern cattle poured in along the military road and the Kansas farmers along this route suffered severe losses, as well as those to whom the southern cattle were finally distributed (Bray).

Causes. Up to 1889 the true cause of Texas fever was unknown. It was well established that cattle brought from the lowlands of the southern states, during the warm season, though themselves in apparently the best of health, proved deadly to northern cattle with which they came in contact, to those that followed them in the same pasture during the same warm season, and even in many cases to the mountain cattle of the south. In the same way northern cattle, removed to the infected regions in the south, contracted the fever and almost all perished. This was equally true of cattle taken from the northern states to Jamaica or other islands in the Gulf. In the winter season, after the first severe frosts of autumn and before the last keen frosts of spring, the southern cattle could be safely introduced into the northern states and on this a modus vivendi, for a trade in southern cattle in the winter only, was based.

Microbiology. Piroplasma bigeminum: Apiosoma bigeminum. (Apios pear, geminus twin). In 1888 Starcovici discovered pyriform organisms (Babesia bigeminum) in the red blood globules of Roumanian cattle suffering from hæmoglobinuria, and Babes, after a study of the organisms, named them Hœmatococcus. The following year Theobald Smith found them in the Texas fever blood, and recognized them as protozoa (Pirosoma bigeminum). Wadoleck proposed Apiosoma, Bonome Amœbosporidia, and Patton, Piroplasma. The latter pointed out that Pirosoma was already in use for another organism. Th. Smith’s discovery identified Texas fever with the Roumanian hæmoglobinuria, and stimulated the Bureau of Animal Industry to an extended research which, in the main, elucidated the true nature of the disease. In a long series of experiments the observers produced the disease in healthy susceptible cattle, by injecting them, in the warm season with the blood of sick animals, and as constantly failed in the experimental inoculation of similar blood on non-bovine animals such as sheep, rabbits, Guinea pigs and pigeons. In Australia, Pound had violent fever in two injected sheep but no pyroplasma, and their blood injected on the ox, had no effect. In none of these latter were the blood globules invaded by the parasite, nor were the corpuscles lessened in number. In the affected cattle, the red cells were reduced from the normal 7,000,000 per cubic mm. to 1,800,000 and even lower in some cases.

The Piroplasma Bigeminum passes through a series of forms in the blood. Theobald Smith found in the red globule and attached to its margin a pale round body 0.5μ in diameter, and staining freely in alkaline methylene blue and other basic anilin dyes and in hæmatoxylin, but not in acid coloring fluids. These he found in the red globules in acute cases, often in company with the pear-shaped bodies, and usually in the absence of the piriform bodies in chronic cases, in non-fatal relapses, in cases occurring in cooler weather, (late autumn or early winter) and in immune southern cattle. The red cells containing these rounded organisms were not crenated nor distorted, though 50 per cent. of them might contain the parasite. He looked on these as the earlier stage of the organism which later developed into the piriform body, by segmentation of its substance. The piriform or spindle-shaped bodies were usually found in pairs connected at their pointed ends by a filament and extending across nearly the whole breadth of the red globule. Free microörganisms, pear-shaped or round, he failed to find in the blood of the large vessels, but saw them only in the cardiac capillaries and especially in the kidneys. In some cases the dim remnant of the disintegrated blood globule could still be detected around the parasite.

Laveran and Nicolle, examining the blood of Italian cases by fixing and staining, found the two forms, round or oval, and piriform, and claimed that the first passed into the second by segmentation.

Lignieres working in Buenos Ayres with the most ample opportunity as regards fresh material and authority to use it, watched the successive changes in the living organisms, and reached further conclusions. He diluted the blood with a 7 per cent. salt solution, or with ox serum or both, until the globules stood apart in the field. The blood can be kept under observation for days under a cover glass luted with sterile paraffin, and the changes clearly traced. Securing the blood from a subject having a great abundance of infected globules (usually at the height of the hæmoglobinuria) he found mainly the piriform parasite intraglobular and free, and in the latter an active whirling motion was kept up by means of the flagellum at its pointed end. As usually arranged in pairs (gemina), whether inside or outside the globule, they are connected by the flagellum attached to their pointed ends. Careful observation enables one to detect in the pyriform mass a small brightly refrangent point like a nucleus. In this form the piroplasma is 3 to 4μ in length.

After 4 or 5 hours, and on toward the 8th, the piroplasma has assumed the round or oval form with a small linear prolongation (flagellum) and shrunken to 1 to 1½μ in diameter. All the piriform bodies pass into the rounded so that this last is the second stage of their development and not the first as was formerly supposed. The round forms are always present in great numbers in the cortex of the kidney in the second stage of the disease (toward the subsidence of the hæmoglobinuria). The refrangent nucleus is no longer to be seen.

After, one, two or more days there appears in the round parasite a chromatine mass, which breaks up into 2, 3, 4 or 5 smaller chromatic bodies, which Lignieres considers as germs. He has seen no division of the protoplasm, but on the contrary the germs escape, yet remain for a time attached to the outer surface of the parent organism. They show rapid jerking movements.

Lignieres claims to have followed all these changes in the blood kept in a sterilized glass cup at room temperature or in the thermostat, and in the stomach of the tick, as well as on the warm stage of the microscope.

He claims to have made a further success in cultivating the parasite in ox-blood serum highly charged with hæmoglobin. It was only occasionally, and by the use of blood extraordinarily rich in the parasites, that success was obtained. In one such case he produced five successive cultures, the product being the rounded forms only and within these the germs. There were no piriform bodies. These are not formed outside of the red globules. The third successive culture in this medium grew with great readiness, producing larger parasites with less disposition to contract, but the fourth and fifth cultures were encreasingly poor. Inoculation with these cultures failed to produce the disease. To explain this the doctrine of passive germs, strong for survival, but weak pathogenically, is hazarded.

To summarize, the successive stages of the piroplasma are: 1st. The intraglobular pear-shaped bodies, with flagellum often connecting two bodies. 2nd. The rounded bodies with refrangent nucleus—intraglobular or extraglobular. 3d. The free round bodies with the nucleus divided into 2 to 5 chromatin masses. 4th. The free chromatin masses, large, active, infecting germs, and small, passive, noninfecting germs. The insuccess of inoculations of cattle with the last-named bodies throws an air of doubt upon them as links in the pathogenic chain. Definite information on the antecedents, environment, food, etc., of the cattle unsuccessfully inoculated, including the season, shelter and meteorological conditions might have brought us a step nearer to the full life history of the piroplasma.

The Cattle Tick: Boöphilus Bovis: Ixodes Bovis: I. Dugesii: The Invertebrate Host of the Texas Fever Organism. As early as 1868 shrewd observers had noticed that in all outbreaks of Texas fever the affected animals were covered with ticks, and drew the natural inference that the disease was due to the bites of these insects. But the prevalence of ticks in localities where the disease was unknown served to draw attention away from the important fact that was suggestive of the true explanation of the disease. The truth, however, constantly obtruded itself that casual cases were never found in the absence of the tick. Finally, in 1889, Kilborne conceived the idea of putting the matter to the test, and with the approval of the Chief of the Bureau of Animal Industry, set aside special paddocks for this purpose. Five native cattle were placed, at midsummer, with three South Carolina cattle, from which all ticks had been carefully picked, and they completely escaped infection.

After seventy-one days, on September 6th, when the hottest weather had passed, two were turned into a lot with four South Carolina cattle of the original herd which had stocked the pasture with ticks. Of the two one died of Texas fever, September 20th, and the other sickened in the last week of September, and had a relapse in October, but finally recovered. Of eleven other native cattle placed in this tick-infested field up to September 30th, ten sickened and one escaped. One animal placed in the field October 19th escaped.

Again three North Carolina cattle and three natives were placed in a field September 14th and 15th. The new generation of ticks was retarded by the cool season, so that few larvæ appeared on the native stock yet one of the three sickened.

These results were confirmed by a series of other similar experiments.

In a further experiment, September 13th, thousands of ticks, mostly mature, from North Carolina, were scattered over a second lot and four native cattle turned into it next day. Three sickened and one, to outward appearance, escaped.

These results were corroborated by experiments made in succeeding years. In addition the disease was produced regularly in native stock by placing on their skin the six-legged larvæ of boöphilus bovis, which had been hatched in glass vessels in the laboratory. It was also shown that the Washington winter destroyed the ticks in infected pastures so that native cattle could be safely turned on them the following spring or summer.

To summarize:—

1. The blood of southern cattle containing the piroplasma produced the disease when injected into a healthy susceptible animal.

2. The animal with piroplasma in its blood, did not convey the disease, in the absence of ticks, to a susceptible animal kept with it.

3. The animal with piroplasma in its blood and covered with ticks conveyed the disease to a susceptible animal kept with it.

4. The ticks hatched and raised in glass vessels in the laboratory, when put on susceptible animals, infected them.

5. Ticks taken from cattle harboring the piroplasma, and put on the skin of susceptible animals, or on their pastures in the warm season, infected the exposed stock.

6. The six-legged larvæ developed in the laboratory from the eggs of mature ticks, taken from cattle having the piroplasma, conveyed the disease.

7. On bare pastures as far south as Washington the winter frosts destroyed the ticks so as to render the pastures safe on the following season.

8. Ticks artificially raised in a warm laboratory, produced the disease when placed on susceptible cattle in a warmed stable (65° to 80° F.) in winter.

9. In the Gulf states, in stables which the cattle occupy constantly or enter twice daily for milking or feeding, the ticks may live through the entire winter. The same has occurred in the warm swill stables in the north.

10. When taken into a new locality, it is rarely the mature ovigerous ticks that bite and infect the native cattle of the place, but the next generation of larvæ, so that time must be allowed for the laying and hatching of ova.

11. Ovipositing usually occupies about a week, while hatching varies with the temperature from two to six weeks.

12. Cases can be adduced in which native cattle followed, on the same pasture, the tick-bearing infecting cattle, and remained for a week or more, and yet escaped, the larvæ being as yet unhatched from the ova. Other native cattle, following these two or three weeks later, perished almost without exception.

13. This delay in the hatching may be indefinitely prolonged, and thus in the southern states, the winter may be tided over, without the loss of vitality in the ova, especially if it is covered by leaves, moss, wood, or decaying vegetable matter.

14. When dealing with lung plague in Chicago in 1888, I noted the facts that every cow that entered a city stable through the stock yards during the dry, hot, midsummer weather died of Texas fever within a month, while those that passed through the same yards during a particular rainy week, all escaped. Berkau has shown that, in the absence of the coating of the glutinous saliva, the eggs do not hatch, and here we may assume that this covering was washed off by the rains and the eggs perished.

15. It has long been noticed that the ticks are scarcely at all dangerous to young calves living on milk. This applies not only to calves born of cows native to infected localities, and therefore possibly having a congenital immunity, but also to the calves of northern and susceptible cows, and which were exposed simultaneously with their dams. It suggests a special defensive power in even the bovine system when sustained on animal food. In the Bureau of Animal Industry experiments, calves of four months, already using vegetable food freely, sickened but still, as a rule, recovered.

16. The Bureau fed three cattle with adult live ticks (2000 to one animal) but no infection resulted.

17. Four cattle were injected intravenously with the liquid charged by crushing ticks in a mortar with distilled water. In some cases the liquid was put through a Pasteur filter, in others only through two thicknesses of filter paper. No infection ensued.

18. Lignieres injected, subcutem, in different animals the pulp of the ticks at all stages of life, ground in a mortar with distilled water, but found in no case tristeza as the result nor any destruction of red globules.

The apparent paradox involved in the last three items probably finds its explanation in the statement of Nicolle and Adil-Bey that, in biting, the tick instils into the wound a venomous saliva which causes local congestion and infiltration and presumably operates on the blood globules as well. Curtice describes the two racemose glands situated under the head shield, the secretions of which are pressed out by the movements of the mouth ring and appendages. How much of this irritant and toxic action is inherent in the saliva, and how much due to the protozoan contained in it, has not been shown. Nicolle, Adil-Bey and, later, Lignieres showed a similar toxic property in the blood. Three to five cc. of blood taken from an acute case at the crisis and injected into the marginal vein of the ear in a rabbit, killed the subject in a few seconds. A similar amount thrown into the peritoneum of a Guinea pig destroyed life in a few minutes. It is probable that the dilution of the venom in the mass of tick pulp and distilled water reduced its toxic quality to such a low ebb that the red globules were comparatively unaffected by it and successfully resisted the attacks of the microbe.

The name Boöphilus bovis was given to the bearer of the Piroplasma by Cooper Curtice who made a special study of the tick, and its development. For the description see Parasites, Ixodes. Among the most marked and distinctive features of the female are the extreme shortness and relative breadth of the rostrum, the slender palpi, the eight rows of spines on the lower surface of the labium, the smooth mandibles with terminal hooks, the limbs long, slender, in seven segments, and each furnished with a terminal pad (pulvillus) and one hook (fore limbs) or two hooks (hind). Curtice has identified the ticks of hæmoglobinuria in various other countries with the boöphilus. The Garrapata of Mexico and the West Indies, the Hæmaphysalis rosea of Cuba (Koch), the Ixodes Annulata of Florida (Say), the Ixodes Dugesii of Italy (Nequin), the Ixodes Algeriensis and the Ixodes Egypti he found to be identical. There may be some doubt as to the Rhipicephalus Annulatus Microplus of Buenos Ayres, but as it agrees with the boöphilus in size, in the thickness of its rostrum, in the eight rows of hooks on the lower surface of the labium, in its host and habits, in the fact that it transfers the piroplasma to cattle, and that it prevails on the same continent in what were formerly colonies of Spain it is in all probability the same tick. Curtice holds that it was originally a North African tick, which was carried by the Spaniards to their American colonies. The Rhipicephalus Annulatus of Roumania is probably the same, together with the ticks that convey the Piroplasma in the other countries of Europe. There remain the Hæmaphysalis of South Africa and the “Scrub-tick” of Australia to be identified with, or differentiated from the Boöphilus. The life history of the Queensland “scrub” tick coincides with that of the boöphilus of America (Pound). As Australia derived her cattle from Britain it is improbable that the tick was imported from Europe.

Lesions. If the course of the disease has been short, followed by an early death, the carcass may be full and rounded, but if the animal has been sick for five or six days there is marked loss of condition and weight—emaciation. As after any other affection occurring during very hot weather, decomposition sets in early, though not quite so speedily as in anthrax, in which the subject dies full of rich blood. Something, too, depends on the condition at death, putrefaction being manifestly slower in protracted and debilitated cases. The color of the skin, the mucosæ and normally white tissues varies in the same way. As it has been largely seen in our northern States (and Australia) in fat cattle, which contracted the disease in railway cars, cattle markets, or dealers’ or butchers’ parks, etc., the deep orange hue of the white tissues is one of the most marked features, and even the muscles have a deep mahogany yellow hue. In poor milch cows and stock cattle in the South, on the other hand, the icteric hue is often conspicuous by its absence. Cattle killed early for experimental purposes may also show less icterus. The color appears to be influenced largely by the abundance of red globules in the blood when the animal was attacked, by the rapid destruction of these globules, and the saturation of the blood and tissues with hæmoglobin in solution. The presence of ticks on the skin, especially along the ventral aspect, inside of the thighs, on the scrotum, udder or perineum, sufficiently explains the number of minute infiltrations into the derma, the oozing of blood or serum, and the matting of the hairs into little tufts.

The pale, watery condition of the blood was recognized as one of the most constant features in 1868, together with the disappearance of the red globules. The clot is remarkably soft and, at the crisis of the disease, the serum is of a reddish hue by reason of the hæmoglobin in solution. When, however, the urine is no longer stained, the hæmoglobin having been eliminated, the serum assumes its normal pale amber hue. For the first counting of the red globules in this disease we are indebted to the Bureau of Animal Industry. The average count in healthy cattle approximated to 6,000,000 per mm. of blood, and in three days this would descend to 4,000,000, 3,000,000, 2,000,000 or even 1,183,000. The rates of decrease was ⅛ to ⅙ of the entire number in one day. In case of recovery the repair of the red globules was slow, from one to two months being required to bring them up to the normal standard. Lignieres claims recoveries after the count had gone as low as 300,000 per mm., and in fatal cases, a few hours before death, it may be but 31,000 per mm.

In high conditioned animals, with high fever often aggravated by travel, the muscles may be dark and firm, but in those out of condition and in the advanced anæmic stages of the disease the muscles are pale, and there may be subcutaneous œdema below the chest and belly. These last features are especially noted by Smith and Kilborne.

The lungs are usually normal. Sometimes limited congestions, punctiform petechiæ, emphysema and small areas of œdema or hepatization are noticed (Smith and Kilborne).

The pericardium contains a little bloody serum and is marked by petechiæ.

The left heart is usually empty, but the right heart full of fluid, or later, of clotted blood, in the latter case without buffy coat. The endocardium, and especially on the musculi papillares, is marked by petechiæ, punctuate or in considerable patches. The cardiac capillaries are full of blood, with numerous piroplasmata.

The peritoneum often contains a little reddish serosity, and a slight gelatinoid exudation is sometimes found around the kidneys or elsewhere in the abdomen. Petechiæ are frequent.

The stomachs usually show petechiated spots on the mucous membranes, and more or less diffuse congestion. Sloughing of the mucosa at such points is not uncommon, and even perforation of the folds of the third and fourth stomachs. The Bureau of Animal Industry and Lignieres both found these stomach lesions very inconsiderable. The smaller pinhead erosions described by Gamgee were identified by the Bureau of Animal Industry as bites of the strongylus convolutus. The small intestines are usually moderately congested.

The cæcum and colon show more congestion, becoming at times of a deep red or almost black hue, and considerable extravasation of blood may take place. This is especially marked in the rectum, which may be of a port wine hue, comparable to that seen in rinderpest or hæmorrhoidal anthrax. The fæces are often dry and massed in balls in cæcum and rectum, while if diarrhœa has set in, the discharges may be colored with blood or blood elements. Yet in the cases reported by the Bureau serious lesions of the intestines were rather the exception, and some subjects showed scarcely any lesion.

The liver is usually enlarged, averaging three to five pounds heavier than in a healthy ox of the same weight. In these enlarged and congested cases it is of a deep yellowish brown color, and often shows yellow spots on the darker ground. Microscopically each acinus has a bright yellow centre from which yellow radiating canals diverge to join the peripheral gall duct. In the superficial or portal portion of the acinus, the hepatic cells are granular from fatty change, yet the nucleus is usually still recognizable. Toward the central zone it may have disappeared. The further this has advanced, the softer, the more easily pitted and the more friable the liver. The congestion of these radical gall ducts with the dense colored bile, displays the structure of the acini in a clear and beautiful way, which no injection can accomplish. When the affected tissue is teased out and placed under the microscope the inspissated contents of the bile canaliculi may be seen as yellow cylindroid casts sometimes bifurcated to represent the union of the two canals. If stained in Ehrlich’s acid hæmatoxylin, the necrotic elements refuse to take the stain so that the contrast between the dead and the living tissues is enhanced. Fatty degeneration is common in the liver of healthy beef cattle so that this is less significant than the congestion of the acini, and the phenomenal distension of the radical gall ducts with inspissated bile.

The gall bladder is usually full (½ pint to 1 quart or more), and its mucous membrane congested and sometimes petechiated. The bile is thick and viscid, like tar, it may be yellowish green, darkening on exposure and contains hæmatoidin crystals and abundance of flocculi showing bright yellow or orange by transmitted light and reddish brown by reflected light.

The spleen is always enlarged, often enormously so. From an average weight of 1.5 lb. to 1.7 lb. for a 1000 lbs. ox, it will rise to 2, 7 or even 10 lbs. One measured 27 inches long by 7½ inches wide and in the centre 3 inches thick (Rauch). Even in apparent health the Gulf coast cattle have spleens averaging about 2½ lbs.

The spleen is gorged with blood which appears purple as seen through the stretched and attenuated capsule, and darker petechial spots are found at intervals. When cut into, the pulp alone appears dark, brownish red, grumous, and showing under the microscope many red blood cells, larger cells granular and undergoing fatty degeneration, yellow flocculi, crystals of hæmatoidin, and granules of black pigment. It is the excess rather than the nature of these agents that is significant. The pulp may be pressed or washed out, bringing the trabeculæ and Malphigian bodies into view.

The kidneys are most seriously affected in acute and rapidly fatal cases. There may be œdema, with blood staining and even extravasation on their lower surface and in the adipose tissue. The gland may be enlarged and the cortical substance congested of a dark brownish red or black. Its capillaries are gorged with red globules in which the piroplasmata are very numerous. The medullary portion is much paler, and with fatty granules in the epithelium, and oil globules in the tubules. The renal pelvis is more or less petechiated and marked by extravasations.

The bladder is marked by petechiæ and usually contains some quarts of urine more or less deeply stained with hæmoglobin. The depth of color is in exact ratio with the extent and rapidity of the destruction of red globules, and of the elimination of their coloring matter. When the destruction is proceeding rapidly the urine may be as dark as port wine; when their disintegration has lessened it may be pale though the temperature is still high (105° F.) In slight and tardy cases there is reason to believe that the redness of the urine may be omitted altogether as is the icteric discoloration of the mucosæ, and hence cases seen in animals indigenous to the protozoan fever districts, have been described as a distinct disease. In these mild cases and advanced stages there is usually a certain amount of albuminuria remaining. In the early stages the urine is strongly alkaline, effervesces with acids, and has a high specific gravity (1030–1040); later when abstinence and suspended digestion and assimilation causes the patient to subsist on its own tissues the reaction may become distinctly acid and the specific gravity reduced (1010–1020). It no longer effervesces. During convalescence while there is a great deficiency of red globules and other blood solids, the urine tends to become pale and watery, of a low specific gravity, and lacking in even its normal pigments.

The womb will at times show petechiæ and in pregnant cows the fœtus will show sero-sanguineous effusions or even extravasations in the chest or abdomen, and hæmoglobinuria (Lignieres).

Incubation. Outbreaks occurring in the North, in herds into which southern infected cattle have been brought, were at first held to indicate an incubation of thirty or forty days (or even sometimes sixty-five), but this is now explained by the time required for the laying and hatching of the eggs of the mature ticks and the evolution of infecting young larval or seed ticks. The actual incubation, as shown by the subcutaneous or intravenous injection of the blood of an infected ox, extends from three to ten days. The hyperthermia is usually shown on the third day, and the more manifest outward symptoms on the sixth. Extreme heat of the weather, a special susceptibility of the animal infected, and especially a large dose of the blood and protozoa will hasten somewhat the onset, but three to six days may be set down as the rule after the ticks have introduced the parasite into their victim. Cattle taken from the northern states and placed on southern pastures, or passing over trails already well stocked with the ticks, are infected at once and sicken in from three to ten days. Cattle in their northern home placed on a previously uninfested field with southern cattle just arrived, do not suffer for thirty, forty, sixty, and in exceptional cases, even ninety days. The paradox is explained by the time wanted for the laying of the eggs and the hatching of the tick larvæ. The female tick does not lay eggs until she is fully mature, and if the ticks on a southern ox are still immature there is a variable period of delay until the eggs are mature enough to be deposited. Then the ovigerous tick drops off her host and spends one week in laying her eggs. In warm weather these eggs take three to four weeks to hatch, so that usually five weeks elapse before the young (seed ticks) can climb upon the ox and infect him. Add three to six days more for the actual incubation and we account for about six weeks of delay in the appearance of the disease in northern cattle. If we consider further that a wet season occurring after the eggs have been laid and before they are hatched tends to divest them of their protective covering and to expose them to destruction, and that, in any case, a cold season will delay the hatching until the recurrence of warm weather, and that the absence of bovine victims will doom the new-born larva to an arrest of development, so that a further indefinite delay may be entailed, we have abundant explanation of the frequently delayed evolution of symptoms. Yet in general terms the apparent prolongation of incubation is due to fortuitous circumstances which delay the infection, and not to any actual extension of the incubation itself.

Symptoms of Acute Type. Cattle infected outside the area of habitual prevalence and stock from noninfected districts, conveyed into the infected ones in hot weather, usually contract the disease in its acute and fatal form. The period of the year is often significant, a number of animals being attacked at once in the hot dry period of late summer or autumn—July to September in North America, February to May in Argentina.

The first symptom is a rise of temperature, and this may last two or even three days before other morbid phenomena are noticed. It may rise to 104° F. in the first day and later to 107°, 108° or 109°. The more acute the case and the hotter the weather the greater the rise. The highest records are obtained late in the day, the lowest in the morning. The temperature often rises for two to four days, and then suddenly drops with the occurrence of collapse and imminent death. While the thermometer is of the highest value in taking the temperature, yet the extraordinary hyperthermia is easily detected by grasping the root of the horn or ear, or by feeling the nose, feet, anus or lips of the vulva.

After 2 or 3 days the respirations become accelerated to 60 to 100 per minute, and the pulse to 90 to 100 or more. There is complete loss of appetite and rumination after the development of these symptoms, the mouth is hot and it may be dry, the muzzle dry, the head pendent, the eyes dull or semiclosed and congested (usually icteric), the bowels confined, to be relaxed again as the fever subsides. A disposition to stand or lie down in water has been frequently noted. Nervous symptoms are usually present. The extreme dulness, languor, and apathy, the drooping head and ears, the unsteadiness of the support the animal staggering or propping himself up by spreading all four limbs, and the tendency to assume and retain a recumbent position, are marked phenomena in our domesticated northern cattle. The paresis may absolutely incapacitate the animal from getting up. In our wilder range cattle it may show itself in active delirium and Lignieres notes the same of the Pampas cattle in Argentina. The animal lying dull and apathetic (triste), on being approached may raise his head, open his eyes and glare threateningly at the intruder. Sometimes when trembling violently, and swaying ready to fall, he will marshal all his remaining energy to plunge at a man on foot or mounted. Some have become blind and unconsciously walked against obstacles, others have been noticed to run in wide circles.

The milk secretion is suppressed, any little that can be drawn in the advanced stages having a thick, creamy appearance. Abortion is common in the pregnant cow.

The condition of the urine has, however, always drawn especial attention and the names red-water and hœmoglobinuria have accordingly been largely applied to the disease. When, in infected areas, the milder types of the disease have failed to show red-water (Jamaica), the identity of the affection with Texas fever has even been denied. Shortly after the rise of temperature, the urine becomes turbid, and this gradually encreases to a more or less deep red. It assumes its darkest hue when the destruction of red globules is most active and during convalescence it disappears. The suppression of urinary secretion may account in some cases for the absence of this symptom even at the crisis of the fever, yet, as a rule, it is present at such time, and, even though it may have escaped notice during life, the red-water is found in the bladder at the necropsy. It may be of all grades, from the merest tinge of redness to a reddish brown, coffee-grounds, or blackish aspect. The coloration is not due to red globules, but to the hæmoglobin which has escaped from the disintegrating globules, and been eliminated by the kidneys. It is always associated with albumen, and, in the advanced stages and during convalescence, when the elimination of hæmoglobin has ceased, that of albumen continues in small amount for weeks.

The thin, watery appearance of the blood when the disease has reached its height, is constant and even more characteristic than the red-water. A single drop drawn from the skin will show to the naked eye the pale, thin, transparent appearance, but examination under the microscope will confirm this. It remains, too, for a length of time, being recognizable for a month in cases of recovery. In connection with the watery blood, the mucosæ and the muzzle (if naturally white) assume a pallid aspect. This is best marked in the absence of icterus, yet even with the yellow discoloration, the absence of ramifying red vessels is very characteristic.

The bowels are at first constipated and the fæces passed in small, hard balls. Later they may assume a reddish brown or chocolate color, and a covering of mucus and fine blood clots. Diarrhœa supervenes in some cases. In passing the fæces, the everted mucosa usually shows a dark red color.

Course and Duration. Acute cases, above all if traveled or otherwise excited, may terminate in death in 24 to 48 hours. More commonly death will take place in 4 to 7 days. Some patients survive longer, but owing to the extraordinary loss of blood globules and the lesions of important solid tissues they are unable to rally, become steadily weaker and perish in from two weeks to three months. Such animals are pale and bloodless, weak on their limbs, careless of food, and encreasingly emaciated. The pulse is weak and irritable and the eyes sunken. The temperature becomes normal or nearly so, soon after the suspension of the hæmoglobinuria. In cases of recovery there remains for a month or more an unnatural pallor, with marked loss of condition and weakness which are only gradually overcome. Convalescent animals are liable to die of indigestion when overfed.

The mortality averages not less than 90 per cent. in susceptible mature cattle from a healthy district in the hot season. Later, from October onward, the tendency is to a milder type of disease and a greater ratio of recoveries.

Symptoms of the Mild Type. This is seen mainly in cattle indigenous to the Texas fever district, in sucking calves, and in mature cattle from healthy districts but attacked during the cool or winter season. It can be produced at will by placing a limited number of ticks (5 to 20) on the skin of susceptible cattle, especially in the cool season. Again, it occurs as a relapse in cattle that have survived an attack earlier in the season.

Though there are all gradations from the violent type, yet we may set down as mild all cases in which the temperature does not rise above 105° F., running frequently about 103° F. There is loss of appetite, dulness, languor, costiveness, scanty urine, albuminous but not hæmoglobinuric, pallor of the mucosæ, and marked loss of condition. Examination of the blood shows the presence of the parasite in the red globules but usually in the coccus or round form only, and the destruction and disappearance of the globules is much less marked so that, though the blood is anæmic and watery, it is not nearly so much so as in the violent and fatal cases. Without the examination of the blood it may be impossible to distinguish these cases from other febrile affections, yet occurring as they do in the infected district in a number of animals at once, in the cooler season, and showing albuminuria, and marked anæmic symptoms, they should lead to suspicion and a search for the boöphilus on the skin, and the oligocythemia and the protozoa in the blood.

Differential Diagnosis from Anthrax. As anthrax is the one disease with which Texas fever is most likely to be confounded, it may be profitable to collect in tabular form their differential features:

=Protozoan Cattle Fever.= =Anthrax.=

A disease of given districts, Prevails in rich, swampy wooded, swampy, uncultivated, impermeable soils: not and places where cattle from permanently implanted on open these districts are taken. well drained lands.

Always shows Boöphilus, minute or Has no essential connection with mature, on the skin of the the Boöphilus: latter usually patient. absent.

Extends in warm season, as the Practically never conveyed by the Boöphilus from an infected Boöphilus. district is introduced.

Can be carried by the Boöphilus apart from cattle.

Infection destroyed by winter Infection not destroyed by winter frost above 35° of N. latitude. frosts.

Attacks bovine animals only. Attacks mammals, generally, especially herbivora.

Lapse of 5 to 6 weeks after Outbreak may occur at once after introduction, for tick introduction of infection. development, precedes outbreak.

Confined mainly to summer season. Occurs at any season: most prevalent in summer.

Sucking calves nearly immune. Sucking calves susceptible.

Mucosæ become increasingly pale; Mucosæ dusky brownish red, not icteric in violent attacks. pallid, nor icteric.

Urine red or blackish in acute Urine exceptionally red: blood cases at height of the disease. globules, in some cases. Hæmoglobin. Albumen.

Blood becomes increasingly thin Blood becomes thick, tarry, and watery: Oligocythemia. incoagulable; not watery nor oligocythemic.

Blood reddens more or less in air: Blood reddens little, or not at then becomes darker. all on exposure.

Spleen greatly enlarged, purplish, Spleen greatly enlarged; pulp very often firm: pulp reddens dark does not redden in air. slightly in air.

Liver enlarged, congested, often Liver enlarged, congested, dark yellow, with fatty and necrotic red or violet. areas: remarkable yellow injection of radical bile ducts.

Bile abundant, thick, tarry. Bile fluid.

Kidneys pale, or congested, black. Kidneys congested.

Lymph glands slightly enlarged, Lymph glands enlarged; often petechiated or (rarely) hæmorrhagic, black; peripheral hæmorrhagic. œdema.

Pallor in violent cases, in Tissues generally reddish, plethoric, icterus of tissues, bloodvessels dark, prominent. especially of white ones.

Muscles in acute cases mahogany Muscles pale, grayish, unless they colored. are seat of congestion or extravasation.

Blood and its red globules show Blood shows bacillus anthracis, the pyroplasma in different but no pyroplasma. forms.

Treatment. Up to the present medical treatment has been essentially unsatisfactory. Lignieres gave quinia sulphate in large doses by the mouth, and in doses of 2½ drams subcutem daily, before and during infection without any visible effect on the progress of the disease. Methylene blue to (¾ to 1¼ dr.), salicylate of soda (7½ drs. daily), arsenious acid (1¼ dr. daily), cacodylate of soda (7½ grs. subcutem) were also tried with no good result. The Metropolitan Board of Health, New York, claimed a succession of recoveries under the use of carbolic acid in the drinking water and sprinkled on the ground so that the animals inhaled it. The cases were, however, the survivors after the first and more acute cases had perished, and the results no doubt depended largely on the mildness of the attacks. The same agent in other hands has not been equally successful. A large number of other agents have been used in vain.

Among the most important measures are a laxative food, like flax seed gruel, a careful picking of all ticks from the surface, the washing of the skin with a 5 per cent solution of creolin, and the removal of the animals to a tick-free pasture, lot, or building. This at once arrests the introduction into the blood of fresh and continuous accessions of the pyroplasma and, if begun early enough, will determine a mild and non-fatal case.

Prevention. The prevention of the protozoan cattle fever is based on the life history of the parasite, and may be directed (1st) to the destruction of the Boöphilus Bovis; or (2nd) to encreasing the resisting power of the exposed animal, to the Piroplasma Bigeminum. 1st. Destruction of the Ticks. (a) On the cattle. The picking of ticks from the skin is effective if the object is to make the animal safe for a few days only as the boöphilus habitually clings to the skin of the one ox from the stage of seed tick to that of ovigerous female, ready to drop off and lay its eggs. An animal going direct to slaughter may therefore be sent through an uninfested district, even in the hot season with a fair amount of safety, after the careful gleaning of the ticks. The greatest care, however, must be taken to manipulate thoroughly all parts of the skin and above all, the ventral aspect, the inner sides of the limbs, the scrotum, udder and perineum. The animals must be shipped at once after such gleaning of ticks with no further opportunity of taking on a new supply, the cars and other conveyances must be cleaned and treated with acaricides and the litter burned as soon as they are vacated, and the cattle must be passed over no loading banks, chutes nor yards that may by any possibility be used for other cattle unless these are going into slaughter house.

The picking will safely remove all the larger larvæ, and the mature ticks which are ready to lay their eggs, but it cannot be implicitly trusted to remove also the all but invisible embryos or seed ticks, and if the host is preserved these grow up and mature, while if they are accidentally dropped or brushed from the surface, they climb upon the first available ox and mature on that. By passing from ox to ox they may be kept alive for a time in the pens adjoining the slaughter house, but fortunately they do not travel over a few feet and if no cattle escape from such pens there is small risk of their preservation.

Dipping or smearing to destroy the seed ticks on the skin becomes an essential adjunct to, or substitute for, picking. The Bureau of Animal Industry has experimented largely on dips with most important and valuable results, even if they have proved only in a measure successful and desirable. Aqueous dips they early discarded. Poisonous agents like corrosive sublimate and arsenic are liable to poison through absorption and licking, with the added drawback that neither these nor calcium sulphide are at all effective in destroying the ticks. Proprietary sheep dips were abandoned on similar grounds. Baths of cotton seed oil were introduced by Francis, but proved not quite effective even when phenic acid, benzine, gasoline, or different mineral oils were added. Paraffin oil gave the best results, and later a staple sold as extra dynamo oil, which in combination with sulphur (1:100) proved most destructive to the ticks, was adopted. But in the hot season, when such dipping is required, any one of these baths produced heating, and illness in the cattle, and together with the exertion and excitement served to rouse into dangerous activity the germs already present in the blood. Ophthalmia, too, was a very frequent result. If the cattle could be kept on their native pastures the dipping might be permissible, but this was to lose the object aimed at—the wholesomeness of these cattle on uninfected ranges. When shipped north in the hot weather the losses were so great as to be prohibitory.

If, however, it could be reserved for use on the southern pastures, to prevent the maturing of the ticks and the laying of eggs for a future generation, it might be employed to rid the infested pastures of the boöphilus, and consequently of infection. The question, then, is reduced to the comparative advantage of the destruction of the ticks, on the one hand, and the cost of frequent dipping throughout the warm season, on the other. The following season there ought to be no ticks left.

Cooper Curtice advocates kerosene 1 gallon in combination with an equal amount of lard, 1 lb. sulphur, and 2 lbs. pine tar. Melt the lard, add the sulphur and tar, bring to the boiling point, cool, add the kerosene with stirring. Rub daily with a brush on the whole skin but especially inside the arms and thighs. On tick-infested pastures it must be continued through the season, and if thoroughly done will leave the fields tick-free the following year. Like oil dipping it would manifestly be incompatible with immediate shipment on a long railway journey, but Curtice vouches for its efficacy as a means of eliminating ticks from southern pastures. The main question is the expense. What would be perfectly adapted to small herds of very domesticated cattle in North Carolina would be a herculean and expensive task in the large herds of Texas. Curtice mentions cotton seed oil, fish oil and even a small proportion of linseed oil as good substitutes for the lard.

Destruction of Ticks on Pastures. Fields, farms and larger areas can be freed from the boöphilus by the thorough application to the cattle pastured on them of one of the above-described methods, provided that no strange cattle are admitted on the land. The ticks are sluggish and, unless carried on the bodies of animals, do not crawl many feet from where they drop. If cattle are kept in the next lot, they should not be allowed to come in contact with the treated or protected stock, but a double fence with an interval of five or six feet, will prove a sufficient barrier to the advances of the tick, apart from its bovine host.

Cultivation of a tick-infested soil for one year or more, with complete exclusion of cattle from November or December until March or April of the second year thereafter, will exterminate the ticks. During the intervening summer there may be plenty of young live ticks on this land, but, in the absence of the bovine host, and blood, these cannot reach maturity, lay their eggs and thus leave new generations. In the course of the second winter therefore they are exterminated. In restocking such land, it is all important to see that the cattle placed upon it do not introduce any ticks on their bodies. Equally essential is it, to see that cattle are excluded from the cultivated land in winter as well as in summer. During warm days ovigerous female ticks, dropped from the skins of such cattle, may produce eggs and larvæ to start a new crop in the coming summer. But as has happened to the wood ticks of the North, so in the South, cultivation of the soil and the exclusion of cattle for a length of time, will exterminate the race of ixodes.

Exclusion of cattle for two winters and the intervening summer will eradicate the ticks even in the absence of cultivated crops. To reach full maturity and propagate its kind, the tick must have bovine blood. If therefore the ticks of a whole season (spring, summer and autumn) are denied bovine victims, and thus cut short in their development, no crop is left for the succeeding spring. If then a cattle pasture is divided in two parts by a double fence with an intervening space of 5 or 6 feet, and if the cattle are confined to one of these parts for a whole year and are transferred to the second half in January after dipping or smearing with ixodicide oil they may be kept entirely free from ticks thereafter. That half of the pasture which is abandoned in the second year, will be tick-free and salubrious in the third year.

Another resort, advised by Curtice when a large tick-free pasture is available, is to place the infected cattle in a pen, and soil them for three weeks, no longer. Then transfer them to another clean pen and soil them there for three weeks more. Then examine closely, and if entirely free from ticks they can be put in the large clean pasture. Should they still carry a few ticks they should be placed in a third clean pen for two weeks more, when they will be tick-free and may be turned into the large pasture without the formality of examination. This is substantially based on the period of parasitism of the tick on the skin of the ox, and its development from the newly hatched larva (seed tick), to the ovigerous female. This period is from three to four weeks. The greater number of the ticks are therefore dropped off as mature ticks to lay their eggs in the first pen, while the remainder are similarly left in the second pen. As the stock leaves the two pens in succession long before the deposited eggs have had time to hatch out, they can take on no more ticks and emerge from the second pen clear and safe. The same pens cannot be used repeatedly, as the eggs develop into seed ticks in 15 days in hot weather, and at once attack cattle.

A stockowner who, independently of his fellows, adopts one of the above expedients in an infested district, is however confronted by the risk of the infection of his herd, by the accidental or careless contact of his cattle with outside ones, and especially with the places where they have been. A broken fence and the entrance of tick infested cattle, or the escape of his tick-free cattle into infested lands, will be the death warrant of all that have not been previously exposed to the disease. Another consideration is that this rigid seclusion of the protected herd must be continued indefinitely so long as ticks are maintained anywhere in the district. The protected animals cannot be driven over a highway without exposing them to almost certain death. Even if a group of adjacent stockowners agree to purify their respective farms, they cannot debar their less careful neighbors from using the highways for tick-infected stock, nor from turning such out on adjoining fields. The veriest scrubs, admitted to the highways, woods and unfenced grounds, keep up the general diffusion of the fever germ and its tick bearer and undo the best directed efforts of any combination of owners of high class and valuable stock.

Well directed legislation, excluding cattle for one or two years, from all woods and unenclosed lands, and enforcing some one of the available methods for the clearing of fenced and stocked lands (cultivation, pasturage by cattle on alternate years, frequent dipping or smearing, passing the stock through a succession of pens), could be made to put an end for all time to the obnoxious tick. If even some other than bovine animals should be discovered to harbor the boöphilus and pyroplasma it could be included in the prohibition and the work made complete. The results would far more than compensate for any necessary outlay. Illinois, with 55,414 square miles of area has over 3,000,000 cattle. The coast states from Virginia to Texas, with Arkansas, Indian Territory and Oklahoma, amount to 767,215 square miles, and in the same ratio should sustain 43,340,040 head. A stock of 25,000,000 at $20 per head would amount to a capital of $500,000,000. Immune from the pyroplasma these cattle would draw freely on the best blood of the north and under the milder skies would compete with the northern cattle on more than equal terms. Living in the open air, they would in the main escape tuberculosis and the other stable-propagated diseases of the north, and their dairy and beef products would enter the market free from suspicion, and command a readier sale, if not a higher price. The stock themselves could be moved to northern markets at all seasons without restriction, and escape the serious losses that now come from a sudden transfer, while pyroplasma-infected and susceptible, to the violent excitement of travel, and the frost-bound destination. Their owners could watch the markets and sell in the best, in place of being compelled, as at present, to hurry them in during November and December, and to sell often at a ruinous sacrifice. With the extinction of the boöphilus the present unrestricted pasturage and all other privileges now enjoyed would return, freighted with a value never borne before, and the few Southern cattle and cattle products need fear no competition in the markets of the world, and could no longer be justly subjected to any restriction.

There would remain the constant danger of the introduction of the boöphilus anew from Mexico, the West Indian Islands and the Central and South American States, where in the absence of frosts the boöphilus cannot be extirpated in the same way, and here accordingly all importation must be forbidden. Cattle from Southern Florida and from islands on our Southern Coast may demand a similar exclusion. There is too much at stake to permit any laxity, and no infected area should be allowed to send out its cattle until it has been abundantly well proved that such district or State is absolutely tick-free.

2d. Immunization: Encreasing the Resistance to the Piroplasma Bigeminum. That cattle can be fortified to resist the attacks of the piroplasma is shown in the immunity possessed by the indigenous herds generally, in the regions infested with this parasite and the boöphilus. To begin with, there may be a survival of the fittest, the more susceptible strains of blood having been long ago cut off. But the immune southern cattle if kept for years outside of the infested area and then returned to it, suffer a mortality about as great as that of northern cattle in the same circumstances. Their earlier immunity, therefore, is not merely a racial difference, but must be due in greatest part to an acquired resistance, and further, this resistance is not permanent but must be renewed at short intervals. The immunity may be in part acquired in the womb of the infested dam, in the last months of gestation, but it is chiefly post-natal through the attacks of the ticks.

a. Infection of sucking calf. The indigenous cattle acquire immunity mainly through the attacks of the boöphilus, in the first month or two when they are still on an exclusively milk diet, that renders the piroplasma practically harmless. Following a parallel method, calves, living on milk alone, can be taken into the infected regions and exposed to the attacks of the ticks with safety, and with the result of protection for the future. Escaping the first invasion, they continue to harbor as many ticks summer after summer, as will reinforce yearly their acquired power of resistance, so that they continue measurably safe though spending the life in the area of the infection.

Francis and Connoway applied this to Jersey calves of two to six weeks old applying to each 25 to 50 ticks. It led to slight hyperthermia, some dulness and inappetence, but on recovery they all gained flesh and condition. Two died from exposure but necropsy showed no sign of Texas fever. The following summer all were infested with 200 to 500 ticks apiece but not one sickened in consequence. These were Jersey calves (the least susceptible breed) and the experiments were made in cool weather in autumn. The limitation of the practice to the cool fall or winter months renders the operation much more safe.

b. Infecting Older Animals by a limited number of Ticks. Yearling Jerseys, Holsteins and Shorthorn were subjected to 25 to 50 ticks in July, they showed only slight rise of temperature, and later resisted the free exposure to tick infestation. It must be recognized that these were still young animals, with presumably greater resisting power than the mature, but on the other hand they were of the susceptible northern herds, they were first infested in the hottest season, and the acquired resistance appears to have been perfect throughout the succeeding summer. The added precaution of subjecting them, in late autumn or winter only, to the ticks raised in a warm room or thermostat, would add greatly to the safety of the operation. After recovery from the effects of the first crop of ticks, a second crop of 50 to 100 should be placed on the skin so that the system may be thoroughly habituated to them and the measure of resistance correspondingly strengthened.

This measure may be advantageously applied to valuable cattle that are to be moved into the infecting territory, but it has serious drawbacks. The relative strength of the poison introduced by the ticks to the susceptibility of the animals on which they are placed, can never be perfectly gauged, and a certain small but appreciable number of deaths result from this first infesting. This has been observed in North and South America, Australia, Roumania and Turkey. Again, the plan entails the necessity for clean, non infected premises (lots or buildings) for each fresh lot of cattle, as the places previously used are left in a tick-infested condition, and are likely to furnish a dangerous excess of ticks to any susceptible animal. The buildings could, of course, be disinfected and purified, but this entails considerable expense.

c. Infection by Graduated Injections of Blood Containing the Pyroplasma. Up to the present this is the most promising method of securing resistance to the pyroplasma. It is advised to take the blood from an immunized northern animal or from one indigenous to the infected district. Such an animal is not, however, strictly speaking immunized. It has acquired a tolerance so that it is no longer in much danger of succumbing to the pyroplasma, but it does not exclude the pyroplasma from its system. The micro-parasite is still found in the blood, though mainly in the coccus-like form in the interior of the red globules. The animal to be fortified against the disease is therefore inoculated with the germ of the disease itself, though it may be, at the time, in a somewhat inactive form. If, however, the inoculated animal is specially susceptible, or if the dose is excessive, the disease is produced in deadly form. The virulence is less in the case of blood drawn from a northern animal just recovered from the disease, than from an animal indigenous to the infected district, and which harbors the pyroplasma, it may be in spore form (Lignieres), without showing obvious disease. The former source of the blood is therefore the more desirable, while the latter is the more easily obtained. The precaution, however, should be adopted of reducing the dose when taken from an indigenous animal. Another important precaution is to select the winter or cooler season for the operation rather than the summer.

The animal which is to furnish the blood may be fixed in stocks, or held with a bull ring, or it may be cast so that it can be kept still. The hair is clipped or shaved from over the jugular vein in the upper third of the neck and the surface is washed with soap and water and with a five per cent. aqueous solution of carbolic acid. A thick cord inch (¼ inch) is tied tightly around the back part of the neck so as to compress and raise the jugulars. With a sharp pointed bistuory sterilized by boiling, a small incision is made through the skin, directly over the centre of the jugular and a cannula and trochar ⅒th inch in diameter and sterilized by boiling, is passed obliquely upward through the coats of the vein and the trochar withdrawn. The blood flows through the cannula and is received in a sterilized (scalded) glass beaker. The blood is stirred slowly with a sterilized glass rod until all the fibrine has coagulated when the latter is lifted out and the remaining liquid blood is ready for use. The blood is injected with a hypodermic syringe which, with its nozzle, has been thoroughly sterilized by boiling. The point selected for injection is usually back of the scapula on the middle of the chest. The skin is clipped or shaved, washed with soap, soaked in a five per cent. carbolic acid solution, then pinched up, perforated with the point of the bistuory, and with the nozzle of the syringe passed through this wound the blood is injected into the subcutaneous connective tissue. The slight wound may then be covered with tar or collodion or merely left undressed. The mass of blood in the connective tissue may be diffused through its meshes by rubbing so as to favor absorption.

The dose of defibrinated blood employed is 5cc. if from an immunized northern ox, or 3cc. or even 2½ cc. if from an indigenous animal. The animal operated on should be in good health and condition, well fed, and kept if possible in the shade, in a cool stable, or under trees.

In some respects it is preferable to operate on the animals before they are moved from the north or other noninfected territory, but as there is danger of infection in preserving and carrying the blood, the treatment is more conveniently deferred until the animal reaches the infected region where the blood can be had fresh. In such cases the animals should be shipped in carefully disinfected cars, and before leaving they should be liberally oiled or larded so that the ticks will not climb upon them, in being led to their stable. They must be kept stabled until the febrile effects of the injection have entirely passed, usually a month or more.

d. Injection of Blood from Bodies of the Ticks. In view of the difficulty of shipping infected blood without danger of contamination or sepsis, and the occasional accidents that happen to animals injected with such blood outside of the infected area, attempts have been made with dried blood, or that charged with antiseptics (calcium oxalate), or that had been frozen, but in every instance the virulence of the pyroplasma was destroyed. Dalrymple and Dodson availed of the blood drawn by mature ticks, which, in their blood-gorged condition, were shipped to the points where the injections were to be made. The mature ticks charged with blood were taken from infected indigenous cattle, and at once shipped. On their arrival they were washed externally with a mercuric chloride solution (1:1000) to destroy any adherent saprophytic or other bacteria, mashed in a sterilized mortar, with a few cubic centimeters of boiled water and the fluid portion drawn off and injected subcutem, into the animal to be protected. From 3 to 12 mature female ticks were used for each animal. The results were the same, only milder than when the blood of the indigenous animal was used direct, and the subsequent tolerance of the pyroplasma proved satisfactory.

It is difficult to explain the moderate effect of the considerable mass of blood injected in such cases, as compared with the deadly effect of the small amount that could come from the insertion of the rostra of even 50 or 100 ticks. But perhaps the venomous saliva instilled in concentrated form into the bites, protects the pyroplasma in the very limited area, until it gains sufficiently in numbers and force to hold its own even in the circulating blood.

Limited Value of Artificially Induced Tolerance. It must be added that all these measures for securing a partial immunity in the individual animal, and which enable us to safely introduce previously susceptible cattle into an infected district, virtually imply the continuance of the infection and infection bearer (boöphilus) for all time. They give no promise of the extinction of the bovine infection at even a remote future time, nor the abolition of the taxes for prevention, which must oppress the southern cattle owner so long as the disease continues. They are most valuable measures truly, but mere temporizing ones at the best, and they could just as well give place to the more sanitary, economical and statesmanlike measures for its radical extinction.

Marketing of the Beef. The piroplasma is not communicable to man, so that the carcasses of well conditioned cattle, which bear the infection need not be rejected as human food. It is only in severe and advanced cases in which anæmia, emaciation and pallid innutritious muscles are marked features, that the flesh is objectionable, and then only as being somewhat lacking in nutriment and digestibility,—not because of poisonous qualities. Danger of infection to cattle might be apprehended, but, if used outside the infected area, the second condition of the disease—the boöphilus—is lacking, while within the existing area of prevalence of the fever, the propagation from the carcass to the animal is infinitely less likely than from one live animal to its fellow.

Federal Restrictions on Cattle within Infected Areas. The orders of the Secretary of Agriculture prohibit the removal of cattle from the following states and territory into any states that extend northward of the line indicated: California, Oklahoma, Indian Territory, Arkansas, Tennessee, Virginia and the states south of these to the Gulf of Mexico. Exceptions are made in the case of fat cattle, sent out of an infected area, for immediate slaughter at the point of destination; conveyed in cars or boats placarded as containing Southern cattle and receiving no other; fed and watered enroute in yards that admit no local or other cattle and which can be reached without passing over any highway or unfenced open ground; and unshipped at their destination directly into yards reserved for Southern cattle only and within the same enclosure as the slaughter house. If reshipped the cars used must be subjected to the same restrictions. The cars, boats, chutes, alleyways, pens and troughs are to be disinfected by thorough cleaning; by saturation of all wood work, etc., with a mixture of 1½ ℔s. lime, ¼ ℔. phenic acid and 1 gallon of water, or ¼ ℔. chloride of lime in a gallon of water, or a jet of steam under a pressure of 30 ℔s. to the square inch. The manure and litter must be mixed with quicklime, or saturated with a 5 per cent. solution of carbolic acid, or secluded in a well fenced enclosure from February 1st to November 15th of each year. This is made the duty of the stock yard companies.

Cattle may be freely moved north from the infected area at any time from November 1st to December 31st, if inspected by an officer of the U. S. Dept. of Agriculture and found free from infection.

Provision is also made for sending infected cattle northward at any season, if they have been first dipped and pronounced free from the disease by an inspector of the department.

Cattle from Mexico are admitted under analogous rules.

PROTOZOAN ICTERO HÆMATURIA IN SHEEP. PALUDISM OF SHEEP. CARCEAG.

This is described by Babes and Starcovici as prevailing among sheep in the delta of the Danube, and held by them to be identical with the Roumanian Hæmoglobinuria of cattle (compt. rend. de l’Acad. des Sciences, 1892). Its essential cause is a piroplasma affecting the red blood globules, and very analogous to that of the protozoön of Texas fever, but its especial election for the sheep shows a specific difference, inasmuch as the Texas cattle fever does not attack sheep. Not only the parasite, but the symptoms and lesions as well, furnish a close counterpart to those of the cattle infection. It remains to be seen whether the pathogenic difference is due to a distinction in the piroplasma or to the absence from the Southern States of America of the particular tick or other insect which attacks the Danubian sheep.

Bonome (1895, Virchow’s Archives) describes the same disease as prevailing in Italy, describing the parasite and lesions at great length.

Finally my colleague Dr. W. L. Williams, and later Dr. Knowles, have identified the disease in the upper part of Deer Lodge Valley and the lower part of Silver Bow Valley in Montana, prevailing among sheep only, extending year by year, and proving disastrous to the sheep husbandry. Sheep were introduced into these valleys as early as 1875, but it was only in 1891 that the flock masters recognized the existence of this disease. By 1895 it prevailed over an area of 300 square miles. It made its advent in 1891 in four or five large flocks (2,000 to 10,000 head each) on land which they had occupied for nine years, and so disastrously that several sheep ranchers, after an experience of a year or two, sold out to the butcher and abandoned the sheep industry.

All or nearly all cases seen in 1896 were in parturient ewes, (4 to 6 days after parturition), the constitutional condition attending on lambing proving a most potent factor in causation.

The protozoön repeated the characters of that found in the sick sheep in Italy and the Danubian delta, and the conditions of the blood and the structural lesions supported the idea of identity.

Altitude seems to have little or no effect as a causative factor, as the disease is domiciled alike on the low alluvium of the Danube and the Deer Lodge Valley of Montana over 5,000 feet above the ocean. In both regions there is the common condition of inundation or its equivalent irrigation, for the Montana range is dry and arid, interspersed with alkaline bogs inimical to vegetation, but prolific and fruitful under irrigation. The Montana disease has been attributed to mineral poisons carried on the winds from the extensive copper smelters in Butte and Anaconda, but the smelters had been in existence for eight or ten years before this disease was observed, and from its appearance the infection has gradually extended, attacking sheep only, and sparing other domestic animals, which would have suffered as well from a mere mineral poison on the vegetation. The doctrine of a mineral poison is equally contradicted by the habitual prevalence of the disease in spring and autumn, while it is dormant in winter and summer. In winter the flocks eat hay cut from the richer valley lands and meadows, while in summer they are pastured on the foothills and mountains, and drink from the mountain springs surrounded by alkaline bogs. The autumn outbreak occurs long after the mountain grasses have dried up, when the flocks are thrown back on the supplies obtained from the alkaline bogs and the valley pastures. In late winter and early spring the growth naturally starts first in the same boggy and valley areas, and both facts suggest a microbian infection—protozoan or bacteridian. If an intermediate host or bearer—insect or other invertebrate—is to be assumed it implies two generations of these, a spring and an autumn one, in the same season, or otherwise a restriction of such invertebrate to the low valley pastures and the alkaline bogs on the higher levels, and that they disappear from the drier, arid areas in summer. It cannot be an obligate parasite like a louse or melophagus which would be constantly present, nor a musquito absent in early spring. But up to the present no invertebrate host or intermediate bearer has been identified. Cases were at first reported in the Angora goat, but this animal is now known to be immune.

Microbiology. The parasite is formed in the red globules and blood serum of the affected sheep and closely resembles the microbe of Texas fever. In the blood globules the parasite is seen in different forms, round, oval, oblong or curved and from one tenth to one sixth the diameter of the red globule. A single red globule may show from one to four of the microörganisms. They may at times show indications of division, and at others, automatic amœboid movements, from one portion of the blood globule to another, or from the periphery toward the centre. The affected blood globules are usually enlarged, having lost their biconcave outline, and become biconvex or spherical, with irregular crenated surface, and a dull, lustreless appearance instead of a clear red or yellow aspect. The protozoön stains readily in anilin red or methylene blue.

Lesions. The condition of the carcass was good or even high, in sheep attacked when in good flesh, and in which the affection ran a rapid and fatal course. In sheep attacked while in low condition on the other hand, the case tended to be milder and more prolonged, and the body was emaciated and anæmic. Dropsical swellings were common on the ears and sides of the head and neck.

The skin, connective tissue, fat, and other normally white tissues were usually of a yellow color, varying from sulphur to lemon color. The muscles were pale and soft with a yellowish tinge.

The blood was pale, thin and watery, especially in protracted cases, formed a loose coagulum, or remained fluid with a grayish red color. There was marked leucocytosis (1:4 or 5).

The stomach and intestines were more or less icteric, and contained little ingesta.

The liver was congested, softened, shrunken in protracted cases, colored of a deep yellow especially in the interior, and with gorged biliary radicles so that the acini stood out very prominently. The gall bladder was usually well filled with a thick, flocculent bile, yellowish green, blackish green or chocolate color.

The spleen appeared shrunken, somewhat spherical, 2 to 3 ozs., firm, and with a dark, reddish brown pulp.

The kidneys were greatly enlarged, weighing 12 to 16 ozs., dark red or bluish black, friable, and on section exuding freely a bloody or chocolate-colored liquid. The capsule was easily detached. The bladder contained a bloody or chocolate-colored urine, but was sometimes empty.

The heart cavities were empty or contained small diffluent blood clots. Petechiæ were common on pericardium and endocardium.

Yellowish or yellowish green gelatinoid effusion was often present, not only on the head and neck, but also on the inner side of the thighs, and in one or other of the serous cavities.

Symptoms. The first indications noticed are dulness, listlessness, a dragging behind the flock, ceasing to graze, arched back, and stiff or unsteady movements. There is moderate fever, yellowness of the visible mucosæ and skin, and rosy, bloody, or reddish brown urine.

Puffy dropsical swellings are noticed, especially on the ears, sides of the face, on the neck or thighs, and the patient lies down most of the time.

The patient usually dies in a state of collapse which has lasted for several hours, yet in certain cases it is preceded by a convulsive agony.

It is certain that the affection may appear in a mild form, as sheep slaughtered in apparent health are found to show the general icterus, the congested liver, and the leucocytosis with crenation of the red globules which characterize the disease. The icteric carcasses are said to be recognized and condemned at Kansas City and Omaha.

The duration of the affection is from 1 to 5 days, though it may last longer, and severe attacks usually end in death.

The prevention of this disease can, as yet, be based only on the same principles that guide us in the case of Texas fever. Search should be made for an invertebrate host of the protozoön, by the extinction of which infection may be stopped. The spring outbreak could be opposed by feeding hay on safe ground until the higher pastures furnish sufficient vegetation. To counteract the autumn attack, the sheep might be fenced out from the alkaline bogs, and the forage supplied in the form of hay or soiling crops. If it should appear that any wild animals harbor or transmit the parasite, a campaign of extermination upon them would be in order. If, as seems to have been the case in the early nineties, the movement of sheep from the infected flocks and pastures tends to cause the disease, this should be legally interdicted. Finally, the complete extermination of the sheep on infected areas could be practiced, and their place supplied by the immune Angora goat.

PALUDISM IN DOGS. MALIGNANT PROTOZOAN JAUNDICE.

Distribution: Senegal, Lyons, E. Africa, Paris, Pas de Calais, Cape Colony. Microbiology: piroplasma: differentiation from that of Texas fever: pathogenesis: tick-borne. Symptoms: incubation 3 to 5 days; dulness, prostration, apathy, drowsiness, anorexia, thirst, hyperthermia, icterus, hæmoglobinuria, offensive odor, emaciation, protozoön in globules, loss of globules. Death in collapse. Lesions: body shrunken, emaciated, fœtid; dark tissues, mahogany yellow, petechiæ, enlarged congested liver and spleen; muco-enteritis; bloody urine. Treatment unsatisfactory. Prevention: keep from tick infested land; clear and cultivate land; smear dog with insecticide ointment when hunting.

In certain malarial districts dogs suffer severely and even fatally from a febrile affection in which violent shivering is followed by great hyperthermia and yellowish or brownish red discoloration of the visible mucosæ. It was frequently attributed to malaria, and even sought to be identified with intermittent fever in man. Marchoux in 1899 studied this disease on the malarious seaboard of Senegal, and recognized the existence of hæmoglobinuria and the presence in the red globules of a hæmatozoön. Leblanc, about the same date, found a protozoön in the blood of dogs at Lyons, suffering from “red water,” and Koch later found a double piroplasma in the red globules of suffering dogs in East Africa, both considering the disease analogous to Texas fever in cattle. Nocard and Almy in 1901, at Charenton, Paris, met with a similar affection in a dog which had just returned from a fox hunt, and was covered with ticks. Its urine was brownish red, like coffee-grounds, and highly charged with albumen and hæmoglobin. Many of the red globules were affected and contained minute, spherical refrangent bodies which, when stained with carbolized thionine, appeared like those of Texas fever. There were but 2,800,000 red globules in a cubic millimetre of blood.

The injection of 5 grammes of the blood into the jugular of an aged bitch caused in the 3d day hyperthermia (105° F.) and an extensive invasion of the red globules which still counted 6,100,000 per mm. On the 4th day the animal was thoroughly prostrated, refused to eat, had hæmoglobinuria, and many individual red globules enclosed from 4 to 8 hæmatozoa each. On the 5th day the count of the red globules was but 4,400,000 per mm. By the 6th day the urine was nearly normal, and appetite returned, but the red globules counted but 3,500,000 per mm. Menveux went to Pas de Calais with an Irish setter to hunt rabbits. The dog came in every night covered with ticks. In 5 days he sickened, with extreme prostration, diarrhœa and red urine and died on the 25th day.

Wm. Robertson describes the disease in Cape Colony. The piroplasma was first identified at Grahamstown by Purves and successfully inoculated by Spreul. By intravenous inoculation symptoms appeared on the fourth day and death followed about the sixth, while by subcutaneous inoculation the course was slower and the animal died about the eleventh day. Robertson inoculating from animal to animal carried it through a succession of thirteen dogs all of which perished. He found the blood to be infecting on the third day after inoculation subcutem, and the globules invaded on the fourth. They were especially numerous in blood taken from the spleen.

Microbiology. The protozoön resembles that of Texas fever, but is larger, longer, less pyriform, and more like an oat seed, staining slightly in the centre which shows one clear spot, and more deeply at two or three places in the margin. It stains well with carbol thionine blue or methylene blue, but not readily with hæmatoxylin. The dog’s blood, containing abundance of parasites, failed to infect horse, sheep, ox, cat, fowl, Guinea pig, rabbit, rat or mouse (Robertson).

Robertson found the ticks on every affected dog which had contracted the disease by simple exposure and which came under his observation. Specimens sent to Neumann were identified as Hæmaphysalis Leachi. Mature ticks from an infected dog were preserved and their eggs hatched in an incubator. The resultant six-legged larvæ, placed on susceptible puppies a month old proved harmless and no protozoa appeared in their blood. This was repeated when the same generation of ticks had reached the stage of nympha, and it was after two months from the hatching that the ticks, now mature, when placed on the same puppies conveyed the disease. On the thirteenth day the temperature reached 105° F., and the red globules swarmed with parasites, many single globules containing no fewer than eight. They were of various shapes, spherical, pyriform or cloveshaped many tapering finely toward the ends like an oat. The puppies died respectively 14 and 18 days after infection.

Experiments made on other dogs with the larval and mature ticks, fully confirmed the conclusion that the immature insect was harmless. A 14 days old puppy infected by mature ticks died on the 11th day so that the immunity of the other puppies cannot be due to a milk diet, as in the case of calves and Texas fever. Intravenous inoculation with the infected blood invariably conveyed the disease.

Symptoms. On the third day after inoculation the dog is dull, prostrate, apathetic and drowsy, refuses food and shows thirst. Temperature may reach 103° to 106° F. On the fourth day the mucosæ assume a yellowish tinge, and by the fifth this has encreased to a deep chrome yellow, which involves any white portions of the skin as well. Hæmoglobinuria is now well developed, the liquid being often as dark as claret, and the patient may lie perfectly prostrate, giving off an offensive odor from the skin, lungs, and especially from the mouth. The tongue is furred, the teeth dirty, and the gums may be congested or even ulcerated. Emaciation advances rapidly. The temperature may oscillate from day to day or it may rise steadily to a climax, and then descend suddenly when collapse occurs. In all cases the protozoön is found in the red globules, or free in the blood. In the worst cases the red globules may be so reduced in number that they can scarcely be found. Death comes usually by collapse. In some instances the hæmoglobinuria may be absent yet the disease advances to a fatal result.

Lesions. The carcass is usually shrunken and emaciated and exhales a fœtid odor. The mucosæ, white skin, and all naturally white structures (fat, connective tissue, fascia, tendons, ligaments, brain, spinal cord, etc.), are stained of a deep yellow. The muscles, liver and other darker tissues are of a mahogany yellow; petechiæ appear on the heart and serosæ; the liver is greatly enlarged and friable (10 lbs.) the spleen is swollen, gorged with blood and a soft, black, bloody pulp; the stomach and small intestines are empty, yellow and sometimes congested. The large intestines show muco-enteritis throughout with an abundant rusty red exudate. The kidneys are yellowish with cortex somewhat pale. The bladder also yellow contains dark colored urine. The red blood globules are greatly diminished in number, many are crenated, broken up and distorted and they contain the piroplasma in large numbers.

No system of treatment has proved successful. Essays would naturally be made with quinia and other antiperiodics.

Prevention would naturally be sought in keeping dogs off from the uncultivated land and brush during the tick season (summer, autumn), in clearing and cultivating the tick infested pastures, in drainage, or in smearing the coat of the dog with the oil of tar liniment or other insecticide when he goes hunting.

PALUDISM IN HORSES.

Alleged identity with ague. Geographical distribution. Points of difference from ague. Causes: low, damp, undrained, inundated localities, hot seasons; inoculation, congenital. Symptoms: restless, drowsy, stiff, shivering, hyperthermia, tremors, cough, frothy, rusty expectoration, excited breathing and pulse, anorexia; puffy, petechiated eyelids; epiphora; dyspnœa: albuminous, yellow or red urine with casts: hæmoglobinæmia: colics, constipation, fœtid diarrhœa. Death in a few hours to 6 days, or months. Lesions: reduction in blood globules, crenation, watery blood: petechiæ: enlarged, blood-gorged liver and spleen; congested, swollen, softened, kidneys; congested lungs with extravasations: in chronic—anæmia, dropsies, lung hepatization and suppuration. Prevention: keep susceptible horses from low, infected lands from June to November and from their water: protect from insect enemies. Treatment: quinia sulphate or bromide, hot baths, etc.

Cadeac and others describe an intermittent or remittent febrile affection of the horse, as identical with ague, and due, they allege, to the presence in the blood of the plasmodium malariæ of Laveran.

Geographical Distribution. It has been observed on the low marshy grounds of Sicily, the Danube bottom lands, Algiers, Tonkin, Madagascar, Soudan, Senegal and Cochin China (Dupuy, Lenoir, Pierre, Colin). Dr. Gelston informs me that in the American cavalry in the Philippines extensive losses are sustained from this disease.

Microbiology. The causation of the disease is attributed to the plasmodium malariæ, which is carried by the Anopheles and inoculated in the skin of man, in malarious regions at night, but we are confronted with the difficulty, that accepting the alleged identity, the disease in the horse should be coextensive with that occurring in man. Yet we have in the New World many areas characterized by the all but universal prevalence of intermittent fever in man, and at the same time by its entire absence in the case of the equine races. It may further be considered that protozoa, found in the red globules of birds, were at one time considered identical with those of malarious fever, but have been demonstrated to be entirely different so far as pathogenesis is concerned. There is every presumption that the protozoa of the red globules found in the horse in this disease are also distinct pathogenically.

Laveran has sought in vain for his plasmodium in the blood of the affected horses, while Pierre found in the blood globules of the Soudan victims refrangent, crescent shaped bodies, thickened and staining deeply in the centre, which in his opinion represented the growing hæmatozoa of Laveran. Gelston found the rounded and crescent shaped forms abundant in the red globules. The disease in the horse is said to be conveyed by direct contact, which would again distinguish it from intermittent fever of man. If the protozoön is the cause, and not a mere sequel or attendant on the disease of the horse, the indications are that it is peculiar to the equine race and distinct from the germ of human malaria.

Causes. Like malarial diseases in man, it is confined to low, damp, undrained or inundated localities, and shows in the hot seasons when the surface dries out. The elevated plains and tablelands which are habitually dry or well drained are exempt. Cadeac alleges that infection is usually inhaled in the floating dust. The mortality of Algerian horses taken to the Soudan is 90 per cent., while but 25 to 35 per cent. of the native horses in the Soudan or in Senegal suffer. This difference is manifestly the result of the survival of a comparatively immune strain of blood, or of immunity resulting from a previous invasion. Subcutaneous inoculation on a soliped failed, while transfusion of blood from the affected horse to a sound mule produced the disease. It is also claimed that it is transmitted from the affected mare to the fœtus in utero, which showed characteristic visceral lesions after birth.

Symptoms. Premonitory symptoms of restlessness, drowsiness, or stiffness, are followed by violent shivering, elevation of temperature (104° or 106° F.), muscular tremors, rapid breathing, hacking cough with expectoration of frothy mucus, tumultuous heart beats, and small irritable pulse. There is complete anorexia, an opaque, infiltrated, petechiated, mahogany colored, conjunctiva, epiphora, and sometimes blood extravasations into the vitreous. The lungs may become intensely congested, with rapid, panting breathing, dyspnœa, a frothy, rusty expectoration, and extended head and limbs. This may prove fatal in a few hours. Otherwise there may be remissions of the fever and dyspnœa at somewhat irregular intervals. Sooner or later are observed urinary changes, the liquid becomes albuminous, yellow, or red, or it shows distinct casts. These indicate the destruction of the red globules and the escape of hæmoglobin. In other cases there are slight colics and constipation alternating with a greenish yellow fœtid diarrhœa. The early nervous prostration and drowsiness may merge into vertigo, or paralysis. Vertigo is a very prominent feature in the Philippine cases (Gelston). The skin which, at first, may often be pricked without response, sometimes becomes tender, itchy and congested, with erection of the hairs and the formation of pustules, or small abscesses like hazelnuts.

Course. Duration. In very acute cases death may take place in a few hours. More commonly illness lasts from three to six days. In certain instances it becomes chronic and may last two or even three months, the early congestion of the mucosæ giving place to pallor and anæmia with advancing emaciation, dropsies and finally marasmus and death.

Lesions. These are mainly in the blood, red globules being distorted, crenated, massed in clusters and greatly diminished in numbers so that the liquid appears thin and watery. The mucosæ, internal organs and serosæ are petechiated and the serous cavities contain a yellowish serum. A yellowish tint pervades the white tissues generally. The liver is congested, virtually gorged with blood, enlarged and yellow or yellowish brown. The spleen is greatly enlarged, blood gorged, and shows irregular, rounded swellings indicating the seats of extravasation of blood. In some instances rupture has taken place. The kidneys are congested, enlarged, softened and of a brownish red or black color, with circumscribed extravasations especially in the cortical area. The lungs are violently congested, with many areas of blood extravasation, and they do not collapse when the chest is opened. The heart is petechiated, with a parboiled aspect and shows areas of commencing necrosis or fatty degeneration.

In the chronic form the watery condition of the blood is remarkable, the serous cavities (peritoneum, pleuræ, pericardium, arachnoid) contain considerable effusion, dropsical conditions of the limbs and dependent parts of the body are common, the lungs show hepatization and minute centres of suppuration, and other viscera may show fibroid degeneration.

Prevention. It is advisable to keep susceptible horses from the low marshy infected lands from June to November and to avoid especially water that is drawn from such lands. It is not needful to take the stock to any very marked elevation provided the land is dry and free from wet or swampy areas. The native horses or those that have been long in the marshy district and have thus secured a partial immunity may profitably replace the more recently imported and susceptible horses during the dangerous summer months.

The habit of the paludal protozoa of securing their transfer from one of the higher animals to another through the intermediation of insects in which they undergo developmental changes essential to their survival, would further suggest the adoption of especial precautions against such invertebrate enemies in the affected district.

Treatment. Pierre employed quinia sulphate or bromide 45 grs. in distilled water 1 oz., intravenously, Gelston, creolin, subcutem. Hot baths, 95° to 100° F. are claimed to lower the temperature and contribute to the arrest of an attack. Other complications are treated according to indications.

SURRA: ROT.

Synonyms. Definition: Acute protozoan remittent fever, of rainy season or after, with destruction of red globules, anæmia, emaciation, dropsy, icterus and cutaneous or mucous eruption or discharge. Distribution: India, Burma, Cochin China, Persia, Phillipines, etc. Trypanosoma Evansi: a fusiform flagellate infusorian with undulating membrane, attacking the red globules: agency of flies as carriers, infection of dogs; of crows; feeding, licking; rats; open sores; stables; yards; pastures; pickets; stagnant water; manure or rubbish heaps; abattoirs. Lesions: anæmia; trypanosoma swarms during relapses; leucocytosis; œdemas; effusions; blood extravasations; splenic enlargement; emaciation; gastric and intestinal congestions; gastric ulcers; kidneys petechiated, swollen; brain effusion. Incubation, 2 to 8 days. Symptoms: local swelling, 2 to 4 inches by 4th day; decreases to 14th day; the general symptoms; hyperthermia 102° to 104° F., night highest; dulness; sluggishness; inappetence; icterus; cutaneous eruption; remission in 1 or 2 days; exacerbation after 3 to 10 days; catarrhs; petechiæ; stocked legs; pectoral swelling; encreasing anæmia and emaciation; ulcers on mucosa or skin; generative excitement; fœtid diarrhœa; urine profuse, bilious, albuminous or with casts; thirst; intestinal rumbling; debility; marasmus; hair erect; skin dry, rigid. Duration variable. Diagnosis: based on above, confirmed by finding blood parasites, constantly fatal in horses. Surra in camel, ox, buffalo, rabbits, rats, mice, dogs, cats, apes. Treatment: unpromising; mercurials, iodides, chromates, arsenates, terebinthinate, phenic acid, santonin. Dry, clean, airy stable, dry grain, tonics. Prevention: keep horse and mule from infecting locality; use oxen rather: stables, pickets, etc., apart from marshes, pools, manure and rubbish heaps; disinfectants, insecticides, seclude all surra-affected animals: smudges. Sanitary police.

Synonyms. Sar, Zahrbad, Gumzahrbad, Kushkzaharbad, Sokra, Sokhra, Tap, Tapdik (Punjab): Phitgya, Purana (Meerut): Berbag (Bombay): Tarai, Tebersa, Wabai-ki-bokhar, Pernicious Anæmia, Trypanosomosis, Relapsing Fever, etc.

Definition. An acute, relapsing, protozoan fever of equines, camels and elephants, inoculable on other animals, occurring during or after the rainy season, and characterized by hyperthermia which is liable to be intermittent, remittent or relapsing, anasarcous swellings, petechiæ of the mucosæ, icterus, cutaneous eruption, nasal, ophthalmic, vaginal and other mucous discharges, rapidly advancing anæmia, emaciation and debility, and above all, by the presence in the blood, at intervals from one to six days, of swarms of protozoa, analogous to those found in dourine or nagana.

Geographical Distribution. Surra has long been known to the English veterinarians in India, occurring during or just after the rainy season, and especially on the low flooded lands, along canals, rivers, lakes, etc., and later in Burma, Cochin China, the Persian Gulf, Persia. Lingard claims its existence in East Africa, North and South America, Australia and Southern Europe, but he has evidently confounded it with nagana and other affections. The discovery of the disease by Dr. Slee in 1901, among American, Australian and Chinese ponies in the Philippines is suggestive of a very wide diffusion of the infection in Southern Asia and adjacent islands, with which an American work on veterinary medicine must deal.

Cause. Parasite. Trypanosoma Evansi. The essential cause of the disease, Trypanosoma Evansi, discovered by Dr. Griffith Evans, Inspecting Veterinary Surgeon, British Army, in 1880, is a flagellate infusorian, pointed at one end, near which is a dark centrosome, and from this a flagellum running along the free border of the broad undulating membrane to the extreme opposite end of the parasite and extended beyond this as a waving lash. The length of the Trypanosoma Evansi is 20 to 50μ, (10 to 14μ, Smith and Kinyoun, Manila), its breadth 1 to 1.5μ. By reason of its large size and active motion it is easily detected in a film of fresh blood under ⅙th inch objective, and no less easily when dried and stained on a cover glass. It must be borne in mind that the mature parasite appears in the blood at intervals in swarms, so that examination at one time of day, or on a particular day, may fail to detect it, while examinations made earlier or later are successful. The general structure and successive stages of growth of the parasite appear to be the same as described for the Trypanosoma Equiperdum of Dourine, to which accordingly the reader may turn for description. The distinction from that parasite is to be found mainly in the pathogenesis. In this respect it should be noted that the parasites are strongly attracted by the red globules, upon which they fasten themselves by the blunt ends, shaking the cell in the most vigorous manner and even breaking pieces off and carrying them away. They are most strongly attracted by the concave part of the disc, and when there are rouleaux they will bore between the globules and even push them apart (Evans).

The appearance of the disease at the conclusion of the rainy season when the waters dry up and become foul, has led to the idea that the parasite lives in waters, but as this is also the time of the great swarming and activity of flies, and as the trypanosoma is found in the bodies of tabanidæ and hippoboscidæ that have bitten affected animals (Lingard), and as horses crowded together so that the fly with piercing apparatus still wet can pass from horse to horse (Evans), the opinion has grown that it is a compulsory parasite which is transmitted through the bites of insects. In 1880, Griffith Evans found that the native Hindoos attributed the disease to the bites of a very large brown fly which was active in July (probably a tabanus), in 1897, Pease identified the incriminated fly as the tabanus tropicus. Finally, Rodgers, in 1901, took flies that had been on surra horses, kept them 4 days or longer and found that their bites failed to produce surra; whereas those that were allowed to go directly from the sick to the healthy animal produced the disease in the latter. The direct experimental inoculation from horse to horse infallibly conveys the disease so that the flies are not needed to pass the parasite through an intermediate stage of its existence, but merely to carry it. It follows that no particular fly is the bearer but any insect may carry the infection from a bite or sore to inoculate it on a sore or by a bite on a fresh animal. Different observers have noticed the tendency to the infection of dogs and other animals that fed from rubbish heaps, or upon the carcasses of animals dead of surra, suggesting at once the intervention of the swarms of flies that congregate at such places. This is probably another example of the shrewd insight of the common mind, as in the case of the tick-borne Texas fever.

Lingard finds another bearer in the crow which sits on the backs of affected horses, pecking at the wounds, and passes at once to other healthy horses to peck their sores.

Experiments in feeding the infested blood to sound animals, have apparently succeeded, and the observation that dogs and cats suffer from eating the carcasses is in favor of this view. Horses that lick the infested sores, or the blood drawn by the flies may readily infect themselves, and especially if the mouth bears scratches caused by fibrous food, leech bites, or sores from bits, or if the pharynx or stomach has been wounded by bots or spiroptera.

The water and food are blamed by the natives in some quarters, but Pease’s observations on the Bombay tramway horses, which all perished though kept on boiled water and carefully picked fodder from sound regions, would suggest that this if a channel of infection at all, is not the main one.

The bowel excretions of rats harboring trypanosoma, when mixed experimentally with the food of the horse, have been charged with causing surra, but there are objections to the acceptance of this as a common cause. The alleged period of incubation in the horse in such cases was 40 days in place of the usual 7 or 8 days, when inoculated from a horse first affected in this experiment on a second the usual incubation of 7 or 8 days was shown, and though the horse fed on rat’s dung in the infected region of Bombay contracted the disease, the experiment failed when the same dung was fed in a high dry region unaffected by surra. The natural inference is that Bombay experimental horses contracted the affection in the usual way, probably through insects.

In the rainy season the Indian rats swarm with the Trypanosoma Lewisi, an entirely different species, and though they can be successfully inoculated with the T. Evansi of Surra, the T. Equiperdum of Dourine, the T. Brucii of Nagana, and it is alleged the T. Equinum of Mal de Caderas, yet these are not their common parasite. The presumption is that the rat affected with Trypanosoma Evansi could transmit the disease to the horse through one of the many possible insect channels or otherwise.

Neither condition, sex nor age appears to affect receptivity. Open sores especially open the way for infection.

The position of stables, yards, pastures or picket grounds near stagnant water, manure or rubbish heaps, abattoirs or other places that breed or attract flies, is a much more important consideration. Foul stables, or those having light from both sides are more exposed to flies.

Pathology and Lesions. The pathology of the disease consists in the rapid destruction of the red blood globules by the trypanosomata. It is a form of rapidly advancing pernicious anæmia due to the great and active voracity of the trypanosoma. The swarming of the trypanosoma in the blood at the period of the relapse and the absence of the mature form in the intervals is remarkable. The trembling movement in the blood at the period of swarming results from their prodigiously active movements. The red globules may assume various forms, crenate, echinated, (Ranking), and more or less broken up or disintegrated, their numbers steadily decrease, leaving the blood thin and watery with rusty serum and yellow (icteric) staining of the white tissues, even the bones. Encrease of white globules, actual or relative, has been a marked feature (always present in typical cases, Burke).

Petechiæ are especially common on the conjunctiva, vaginal mucosa, endocardium, and less marked in the nose, mouth, and serosæ.

Œdemas are common, yellowish, gelatinoid exudate at the base of the heart, subcutem, between the muscles of the limbs or elsewhere, and as effusions into the pleuræ, pericardium or peritoneum.

Distinct blood extravasations have been noted beneath the endocardium.

The spleen is often enlarged, excessively so if death occurred during a paroxysm. The lymph glands are swollen and appear dropsical.

The whole body is emaciated and shrunken, the visible (unpetechiated) mucosæ are pale and bloodless, often yellow, yet rigor mortis is well marked.

Gastric ulcers are common (Steel, Burke, G. W. Evans) apparently preceded in many cases by capillary embolism, congestion and degeneration. Intestinal congestions are frequent (Steel, Burke), but ulcers are rare (Geo. H. Evans).

The liver may be normal (Griffith Evans), or especially during a paroxysm (Lingard) congested, inflamed and enlarged. The pancreas is usually normal.

The kidneys are petechiated, congested, œdematous, or the seat of blood extravasations.

Instances have been noted of cerebral and meningeal œdema (Steel, Lingard), encrease of fluid in the arachnoid or lateral ventricles, or in the spinal cord, with gelatinoid exudation in the lumbar portion (Lingard). Like other tissues, in advanced stages the nerve centres are usually anæmic (Geo. H. Evans).

Incubation. As made out by inoculation cases this extends from two to eight days, according to the dose—five to seven days being the most common. Infection by inoculation subcutem in mules showed a hyperthermia on the fifth day; or by ingestion (feeding the virus) on the sixth day (Steel). Longer (alleged) incubation depends mainly on the first slight paroxysms having been overlooked, or set down for the frequent bilious and icteric condition which is common in mules and horses in India (Steel), or to a later infection by insects or otherwise.

Symptoms. In experimental cases a small raised swelling in the seat of the inoculation, appears in 24 hours, encreasing to 2 to 4 inches in diameter, and 1 to 1½ inch high by the 4th day, and loosely connected with the parts beneath. From the 4th to the 14th day it decreases in size and softens and general symptoms set in.

In casual cases these general symptoms are the first to be observed. There is a transient fever 102° to 104°, highest toward night and without preliminary chill, hot mouth and skin, dulness, sluggishness, inappetence, yellowness of the mucosæ, petechiæ on conjunctiva or vulva, and sometimes nodules like those of urticaria on the skin. After a day or two these symptoms subside, the temperature is 101° F., or below, the mucosæ clear and pale, and spirit and appetite nearly normal. These slight first paroxysms are rarely seen by the veterinarian, having been looked upon as one of the oft-recurring bilious attacks of a hot climate. The remission lasts for 3 to 10 days when the second paroxysm sets in, like the first but often more marked: temperature 102° to 104°, eyes especially the membrana nictitans petechiated, epiphora, slight catarrh from nose or vulva, it may be stocking of the legs, or pitting swelling under the breast bone, or abdomen, or in the sheath. Like the first, the second paroxysm subsides, and after another interval a third sets in, to be followed in like manner by a fourth, a fifth and so on, if the patient survives. With each the symptoms become more pronounced, the mucosæ are left more pale and bloodless, debility and weakness are greater, emaciation is more marked, œdema of the limbs or body more extensive, hyperthermia may reach 105° or more, the pulse is weaker and the heart more liable to palpitation, and the respirations may reach 50 or 60 per minute. Yet in sparely built animals dropsy may be entirely absent (Steel). Steel often found superficial, circumscribed ulcers on the tongue, inner sides of the lips, nose, eye, or vulva, beginning as epithelial degeneration, followed by superficial erosion and early healing. Sometimes, similar erosions appeared on the skin. Generative excitement may be present, the mare appears to be in heat, while the horse has erections, which are supposed to depend directly on the implication of the generative centre in the lumbar myelon. The submaxillary glands sometimes swell and even suppurate and discharge a gluey pus (Griffith Evans). The bowels are usually costive at first, the fæces may be glazed, but in advanced stages they become soft, pultaceous and fœtid. The urine at first normal in amount, becomes later abundant or even profuse (Griffith Evans, Ranking, Nariman and Vaz, Lingard). It is at first yellow and turbid, later of a dingy green or greenish yellow. Sometimes it diminishes as the disease advances. It may contain bile, albumen, or even casts (G. H. Evans), though the latter appear to be exceptional. The reaction varies, sugar is absent, and the parasite has not been found in it. Appetite though interfered with during the paroxysms, remains fair or even voracious in the intervals and the animals may eat to the last (Burke). Thirst usually encreases with the advance of the disease, in keeping with the free urinary secretion. Rumbling and gurgling of the bowels are common and even tympany at times (Lingard).

In the advanced stages the picture is one of great anæmia, marasmus and general debility. When moved the animal will stumble over the slightest obstacle, even the litter, recovering himself with effort and difficulty. If he should fall he is liable to remain down indefinitely, the side next the ground becoming drenched with sweat though there is no general perspiration. The hair becomes encreasingly dry, withered and erect, the skin dry, powdery, rigid and more and more firmly adherent to the bones and muscles, losing all its natural pliancy and mellowness, and becoming like that of a dead animal. It is bloodless, and sloughs readily over the prominent bones, where compressed or bruised in lying, owing to the lack of nutritive and reparatory action. The visible mucosæ are absolutely bloodless. The muscles as a whole are wasted to an extreme degree, but this atrophy is most marked in the back and loins, along the longissimus dorsi and in the quarter in the gluteal muscles. The patient may remain recumbent, from sheer weakness, for a length of time at the last, or he may get up after a long recumbency and stand to the end.

Death may occur early with general anasarca and extreme hyperthermia (110° F.). In the great majority it appears to result largely from perforation of the stomach, clots in the heart, or general debility and heart failure.

Diagnosis. With symptoms such as are above described the discovery of the trypanosoma in the blood completes the diagnosis. Trypanosoma is found in dourine, nagana and other affections so that the discovery of it alone would not be conclusive as to the existence of surra. Nor can the discovery of the parasite always be made at the first or second attempt. The swarm of mature trypanosomata is found with the advent of a paroxysm, and as the veterinarian is often called during the decline of the attack the parasites have already retired and elude his investigation. It becomes needful to take the temperature and examine the blood daily sometimes for eight or ten days, and when with a sudden rise of temperature he finds also a swarming of the mature trypanosomata, the diagnosis is perfect. A drop of blood placed on a cover glass, pressed down upon the slide, and placed under the microscope, will show the parasite with eel-like movements among the blood globules. There may be very few during the first or second paroxysm, but they become numerous and very obvious as the disease gains its height. Evans recommends to use defibrinated blood.

They may be dried rapidly on a cover glass, fixed in absolute alcohol one or two minutes, then stained ten minutes in a mixture of the two following liquids united just before using:

A.—ONE PART OF THE MIXTURE.

Methylene blue 1 Grams. Borax 2.5 „ Distilled water 100 „

B.—FOUR PARTS OF THE MIXTURE.

Eosin .1 Grams. Water 100 „

The plasma of the trypanosoma appears blue, the flagellum red and the chromatin of a different shade of red. It may be permanently mounted in balsam.

Mortality. The disease is constantly fatal in horses, though the animal may survive for months.

SURRA IN CAMELS.

Haggar describes this as having remissions or intermissions as in the horse, the trypanosoma disappearing during the intervals to reappear with the hyperthermia. The temperature may rise to 106° F. and the animal wastes away to a veritable skeleton. A remarkable feature of the disease is the formation of immense abscesses containing a thick, cream-colored pus on the sides of the chest in the vicinity of the pad, and in the sheath and scrotum or udder near to the stifle pad. The mortality is nearly as great as in the horse or mule, yet the camel drivers say that a small percentage recover.

SURRA IN BOVINES.

The domestic ox, the sacred cow of India (Lingard) and the water buffalo (caribao) of the Philippines contract Surra. It is interesting to notice that in these animals the disease is relatively mild and recoveries are frequent.

In the Indian buffalo it causes dulness; advancing emaciation; slight temperature variations; muco-purulent inflammations of the conjunctiva, cornea, and pituita; and occasionally eruptions under the breast or belly.

Among lesions were atrophy, softening of lymph glands, enlarged liver and spleen (slight), petechiæ and blood extravasations on the pericardium, epicardium and other serosæ, and on the intestinal mucosa which sheds its epithelium in patches.

Stall enzoötics in cattle do not seem to affect horses casually. The disease is easily conveyed to rabbits, house rats and mice, dogs, cats and apes. Goats and ducks appeared to be immune (Penning).

TREATMENT OF SURRA.

In well established cases in the horse, ass or mule no treatment has succeeded in saving the patient. Almost every germicide has been called into requisition but without good effect. Among these may be named: mercuric chloride subcutem, iodine and potassium iodide intratracheally, iodoform subcutem and intravenously, oleum terebinthinæ subcutem and intravenously, potassæ bichromas by veins and stomach, cinchona alkaloids and arsenic, phenic acid and iodine, quinine, hydrargyri biniodidum, santonin, potash. The claims of different agents, notably arsenic and phenic acid, have been supported by the manifest improvement of condition under their use and the disappearance of the trypanosoma, but both these conditions may often appear during intermissions, without medication. The usual outcome is that the animal dies and the only claim that can be made is a slight extension of life. This is favored by dry, clean, airy stables, change of water, rich grain and succulent food (oats, rice, linseed, barley, gram sorghum, bran, middlings, salt, etc.), with iron, arsenic, and other tonics, yet the best that can be said for them is that they have deferred somewhat the inevitable death.

Prevention of Surra. The first consideration is to avoid placing equines and especially horses and mules, or camels in the infecting localities in the rainy season and just after it. Oxen and buffaloes can be used in such places with greater impunity. If they must be used in such localities, place the stables or pickets in dry locations well apart from marshes, and stagnant water. Keep the stables dark during the surra season, open to light on one side only and with screens in the windows. Make a deep pit for the manure, keep it well darkened and screened and turn every particle of manure into this several times a day so that the stable shall be perfectly clean. All rubbish heaps should be similarly dealt with. The flies breed in the manure and decaying organic matter. After each sweeping of the stable sprinkle the manure in the pit with some disinfectant, phenic acid, tar water, copperas, etc. Smear the skins of the animals with tar water, coal tar water, naphthalin, daily if necessary to prevent the attacks of the flies. Other suggestions in this line can be found under parasites.

An important consideration would be to seclude every animal attacked with surra. The flies can only carry and inoculate the poison when there is some source from which they can obtain it. Until we shall learn how many animals, tame and wild, casually contract the Trypanosoma Evansi we cannot speak of how effective this may be made, but it is at least a substantial advance in the line of restriction, since the infected horse or mule in the vicinity of healthy ones is a constant peril, and as given insects attack by preference, given favorite genera, the horse flies, coming from the diseased animal are much more likely than other flies to attack the sound horses. In a surra season it would be a wise economy to destroy the infected equine at once, as according to all past experience, sentence of death has already been passed upon him, and his preservation even for a hour is hopeless for him, but full of the gravest danger for others. The carcass and all pertaining to it, blood especially, should be promptly and deeply buried and the place thoroughly disinfected.

In the same way smudges made by burning green grass or other vegetation, tar, leather or other material producing empyreumatic products offensive to the fly may be employed.

Sanitary Police. The Department of Agriculture forbids the landing in the United States or its dependencies of any animal from the Phillipines. If the infection should by any accident be imported no cost should be considered too high to secure a prompt and thorough extinction of it.

NAGANA. TSETSE FLY DISEASE.

Trypanosoma Brucii: attacks horse, ass, mule, cattle, buffalo, antelope, camel, hyena, dogs, etc. Elephants and zebra, pigeon and hen immune. Tsétsé fly. Inoculation only certain channel; virulence in dead body 24 hours; in vitro 3 to 4 days, or when dried or heated (122° F.) Symptoms: hyperthermia; anæmia; leucocytosis; buffy coat; œdemas; catarrhs; wasting; debility. Lesions: as in surra; trypanosoma in blood at intervals, bone marrow, lymph glands, spleen. Immunizing unsuccessful. Prevention as in surra.

This is an infective disease caused by the Trypanosoma Brucii, which has been supposed to be identical with Trypanosoma Evansi but differs in its morphology and in its infectiveness toward a greater variety of animals. It is 25 to 30μ long by 1.5 to 2.5μ broad, less pointed at its posterior (nonflagellate) end, broader undulating membrane, more deeply staining protoplasm, and more sluggish movements. It invades the blood of horses, asses, mules, cattle, buffaloes, antelopes, camels, hyenas, and dogs, and can be inoculated on cats, rats, mice, rabbits, hedgehog, boshbok, zebra hybrids, Guinea pigs, goats, sheep, weasel, and monkey (Macacus rhesus). Elephants are immune though they suffer from T. Evansi, and the zebra is immune though a soliped.

The tsetse fly (glossina morsitans) is credited with being the main agent in transmitting the parasite to mammals, (see Diptera).

Kauthack, Durham and Blandford found that Guinea pigs were more resistant than rabbits, surviving the inoculation for a longer time. Bruce also found the native South African sheep and goats more refractory than others, yet their hæmatozoön was as deadly to other animals as that of horse or dog. Pigeons and South African hens proved refractory. Manifestly in Africa the present races of some animals are the products of the survival of the fittest.

Inoculation. The disease has been produced experimentally by inoculation only. Feeding experiments on rabbits, cats and Guinea pigs, the sucking by puppies of an infected dam for 14 days, coitus, and even the careful dropping of infected blood under the eyelid failed to convey it. Lousy rats with sores on face, one cat doubtless scratched by a bone, and one rabbit supposed to be infected by sexual congress (Rouget) offer exceptions, which in the light of the general results must be looked on as probable inoculations through wounds.

Successful inoculations were made with blood, lymph gland, spleen, bone marrow, aqueous humor, serum, œdema fluid, and testicular juice. The effectiveness of inoculation did not vary materially with the different fluids used, with the amount, nor with the point selected for its insertion, subcutaneous, intravenous, intraperitoneal, or on a mere scratch.

Virulence is lost in the dead body in 24 hours or less; when the infected blood is kept aseptically in vitro, in 3 or 4 days at most; or when completely dried. Heating to 122° F. for 30 minutes sterilized, while at 114.8° F. for half an hour the trypanosoma became nonmotile, but not quite non-virulent.

Symptoms. Hyperthermia is marked about the time of the appearance of the infusoria in the blood. (Horse 106.7°; dog 104°; rabbit 105.8°), and in the horse there was a paroxysm with each new swarm of the parasite. In one ass intermissions were not observed. In rabbits there was no constant ratio between the temperature and hæmatozoa, hyperthermia was constant or nearly so. The horse had marked hyperthermia up to death, dogs and cats showed a marked descent even to subnormal, before death.

Anæmia is a marked feature the red globules being greatly reduced, and they show a tendency to clump in masses instead of forming rouleaux. The serum added to healthy blood has the same effect on that. Leucocytosis is not constant nor excessive (15,000 to 34,000 per c.m. at the highest). In clotting the blood may form a buffy coat.

Œdema is common in horse, rabbit, cat and dog especially about the head, legs, belly and genital organs. Rabbits often show swellings, excoriations and sores of the labia, prepuce and penis favoring inoculation by this channel.

Conjunctivitis is common in cats, dogs, rats, rabbits, often in connection with facial œdema, and corneal opacities and ulcers, and turbidity of the aqueous humor may follow.

Nasal catarrh often interferes materially with breathing.

Muscular wasting and debility are prominent phenomena, especially in horse, dog, cat and rabbit, the loss of weight reaching 20 or 30 per cent.

Lesions. These are like those of surra. Enlargement of the lymph glands, spleen and liver, firmness, friability and dark color of the spleen; effusions, petechiæ, and even hæmorrhages of the serosæ, lungs and stomach, and great atrophy of the muscles and adipose tissue are prominent features. The liver is always fatty in rabbits. In the shafts of the long bones, the fat is replaced by red marrow. The bone marrow is sometimes red, at others pale.

The trypanosomata in the blood vary greatly. In infected rats and mice they appear 3 or 4 days after inoculation, are almost constantly present thereafter, and as a rule, encrease steadily up to 2,000,000 or 3,000,000 per c.m. In dogs they appear in 4 to 6 days, in cats in 5, in Guinea pigs in 5 to 7, and in horses in 7 days. In rabbits there were found 60,000 per c.m., in dogs 100,000 to 300,000, and in Guinea pigs 200,000 to 500,000. In one Guinea pig they did not appear until 6 weeks after inoculation and then rapidly encreased to a fatal termination. More commonly a few can be found about a week after inoculation, and then they disappear for a variable period. They have been found in the bone marrow when they could not be recognized in the blood. Again, after subcutaneous flank inoculation in the rat, they were found in the corresponding inguinal glands 1 to 3 days before they could be detected in the blood. After death they are found most abundantly in the bone marrow and spleen, but they have not been found in the intestinal contents nor urine except in the case of hæmorrhages or local sores.

No soluble toxin appears to be formed, and no immunization is effected by the serum. Blood serum kept several days until the infusoria had died and then passed through a Berkefeld filter had no apparent effect on the animal economy even in large doses. Blood heated to 122° F. was equally harmless. The same is true of extracts of organs and of bile from infected animals.

Attempts to secure immunity by injecting the blood serum of affected animals, after it had been sterilized by heat, filtration, or standing one week in vitro proved of absolutely no effect. The blood of the fœtus almost at full term proved valueless, and the young born of infected mothers proved fully susceptible when inoculated. The serum of the Guinea-pig, which is naturally somewhat resistant, proved no protection to other animals. Bile mixed with infecting blood in vitro, kills the trypanosoma, but such blood has no protective effect on animals. Sewer rats and white rats inoculated and re-inoculated with the common rat trypanosoma (T. Lewisi) until immune from that organism, show a full susceptibility to the trypanosoma of nagana.

Flesh feeding and vegetable feeding have made no difference in the susceptibility in the case of rats. Feeding with the hæmatozoa has produced no immunity.

It is evident that prevention must follow the same lines as in Surra, due consideration being had of the greater number of genera susceptible.

LUNG PLAGUE OF CATTLE.

Synonyms. Definition: infectious, cattle fever, with long incubation, insidious onset, excessive pulmonary exudation, infarctions and sequestra. History: ancient, modern; England, Norway, Sweden, Denmark, United States,—its extinction in 1887 to 1892—Massachusetts, New Jersey, S. Africa, Australia, Tasmania, New Zealand. Causes: contagion only. Bacteriology: Nocard’s organism cultivated in collodion capsules in vivo, as actively motile refrangent points, morphology uncertain. Modes of transmission, exhalations from sick inhaled by susceptible, ingestion of infected food, pastures, watering troughs, ponds, commingling of herds, attendants, dealers, stables, manure, unrestricted commerce, convalescent cattle, breed, hot seasons. Lesions: profuse exudation in lymph networks of lungs, marbling, parenchymatous cell proliferation, compression and gangrene of lobulets, thrombi, sequestra, infarction, fibroid sac, or stalactite-like fibroid peribronchial formations, hepatization, pleural effusions and false membranes, pericardial, bronchial, lymph glands congested. Incubation: 6 to 30 days, protracted cases, bearing on quarantine. Symptoms: conditions affecting gravity, breed, excitement, heat, chill, susceptibility, usually insidious, infrequent cough, roused by cold water, dusty food, exertion, etc., hurried breathing when driven, slight auscultation râles, hyperthermia (103° to 108° F.), dulness, anorexia, suppression of milk, stiffness, no pandiculation, troubled breathing, auscultation, and percussion signs of extensive consolidation, tenderness of chest walls, in bad cases stands obstinately, head extended, mouth open, tongue protruded, grunts with expiration, heavy breath, nostrils dilated, nasal and buccal discharge, rapid emaciation, fœtid diarrhœa, erect hair, pale, scurfy, adherent skin, varied chest râles, abortion. Mild in winter, severe in summer. Loss of one-third or one-half weight in one week. Chronic cases, fibroid and necrotic changes, sequestra. Diagnosis: Anamnesis, inoculation: from tuberculosis by high fever, rapid, extensive infiltration, early succession of new cases, failure to react under tuberculin, absence of tubercles; from bronchitis and pulmonary strongylosis, by the succession of cases in place of many at once, the extensive exudation, the evident cause (exposure or infected place), and by the lesions; from fibrinous pneumonia, by absence of climatic cause, the more extensive consolidation, more troubled breathing, and coexistence of old and recent lesions; from infectious pneumonia by the greater area consolidated, more exalted hyperthermia, more marked dyspnœa, the absence of white points of alveolar cell proliferation, and by the old and recent lesions; from septicæmia hæmorrhagica, by its occurrence at all seasons, on all soils, by the absence of sanguineous swellings at other parts, by the absence of cocco-bacillus from the exudate, and by its non-inoculability on sheep, horses, pigs and rodents; from needle in pericardium, by its epizoötic prevalence, fever, and the absence of preliminary gastric and later cardiac, morbid phenomena; from emphysema by the fever, absence of drumlike tympany, and presence of consolidation; from aspergillosis of the lung by the fever, more rapid progress and extended consolidation, by the harmlessness to birds, by the absence of aspergillus from expectoration and lung; from insolation by the absence of the causes of heat stroke, of the implication at once of a number of exposed animals, of the excessive hyperthermia, the brain symptoms and sudden deaths. Treatment: a poor economy, to be punished when extinction is attempted. Prevention: importation under three months quarantine, surveillance of three months more in case of single animals; applied to lung plague countries and those adjoining; disinfect cars and boats that have been used in lung plague country; exclude hay and fodder from lung plague country; also litter, bags, head ropes, horns, hoofs, hides, hair. To extirpate: stop all ingress of possibly infected cattle, stop movement of cattle, prohibit common or unfenced pasturage, kill without indemnity in case of violation, record all cattle, make necropsy of all dead, kill and pay for all infected herds, disinfect all infected premises and things, use horses in removing and plowing under manure. Unaided owner may: breed all his stock, in buying bull quarantine him, allow no intercourse between his herd and others, get new cattle from herds only that have had no illness nor losses for a year, and no exposure, and bring by thoroughly safe route, in disinfected cars or boats, then quarantine, under special attendants. Immunization; by a first attack, inoculation in tail, intravenous, of sterilized exudate. Conditions permitting and forbidding immunization.

Synonyms. Bovine Pleuro-Pneumonia, Contagious Pleuro-Pneumonia, Peripneumonie (Fr.), Lungenseuche Vieseuche (Ger.), Pneumosarcia, Peripneumonia Exudativa, Epizoötic Pleuro-Pneumonia, Pulmonary Murrain, Slijmlongziekte (Dutch), Pulmonea dei Bovina (Ital.), Phush phush pirdaho, Pheepree (Bengalee).

Definition. An infectious febrile disease, occurring casually in cattle only, so far as known, and characterized by a prolonged incubation (10 to 90 days), a tardy insidious onset, inflammation of the bronchia, lungs and pleuræ, a profuse exudation into the interlobular connective tissue and chest, a very extensive area of consolidation, pulmonary infarction, and sequestra.

History. It is difficult or impossible to identify this disease among the various animal plagues in ancient times. Yet when lesions are given it may be admitted in different cases. Aristotle, writing 350 years before Christ says “the cattle that live in herds are subject to a malady which causes the breathing to become hot and frequent. The ears droop and they cannot eat. They die rapidly and the lungs are found spoiled.” Here the facts that cattle alone suffered, that large herds suffered most, that the lungs were the seat of very marked lesions, and that fever and mortality were both marked, point forcibly toward lung plague. Valentini’s description of a fatal lung disease in cattle also stands out prominently in the obscure records. The first full and definite report is that given by Bourgelat of its prevalence in Franche-Compté in 1769. Later the records are frequent and from all over Europe, indicating its general prevalence before as well as after Bourgelat.

Much more important are its definite extensions into new countries after a long interval of immunity as showing that with trustworthy records such invasions can always be satisfactorily accounted for by the introduction of cattle or their fresh products from a previously infected area. Into Holland it was imported from Germany in 1835 by Vanderbosch a Guelderland distiller and spread over the whole country. Attempts were made in Friesland, and at first successfully, to stamp it out by slaughter and disinfection, but the demands of the trade toward England grew so enormously that it was being constantly introduced anew and the measure was abandoned. The British Consul at the Hague, in 1839 sent some Dutch cows to a friend in County Cork, Ireland, which led to the general infection of that island and indirectly of Great Britain. In 1842, under the Free Trade Act, England became at once deluged with lung plague cattle from Holland, Belgium and France on the one side, and Ireland on the other. Soon the whole island had been infected except exclusively breeding districts (Welsh and Scottish Highlands, etc.) into which no cattle were ever introduced from outside.

In 1847 an importation of English cattle into Sweden conveyed the disease, where it prevailed for some time and even infected Denmark through shipments of cattle, but was finally extirpated by the pole axe and disinfectants.

In 1860, Norway imported infected Ayrshire cattle for the Royal Agricultural College at Aas, but the imported and exposed stock were promptly destroyed and the previous immunity of the country has been maintained up to the present.

Denmark was infected in 1848 by importation from Sweden, and on different other occasions from Germany and England, but by prompt and rigid suppressive measures, stamped out the disease on each occasion. This was true also of Schleswig so long as it remained a part of Denmark, but the infection entered in the commisariat parks of the German army in 1864, and the principality remaining in German hands, the lung plague became permanently established.

Mecklenburg-Schwerin and Oldenburg also maintained vigorous suppressive measures and for long kept clear of the infection.

Into Brooklyn, lung plague was introduced in 1843 through the purchase of an English ship cow by a dairyman (Peter Dunn). From this centre the infection spread until it prevailed in Connecticut, New York, New Jersey, Rhode Island, Pennsylvania, Maryland, Virginia, District of Columbia, Ohio, Indiana and Illinois.

In 1879, measures were taken in New York and New Jersey to extirpate the disease but failed to receive the requisite continued support and were practically abandoned. It was only in 1887 when the infection had reached Chicago, the largest cattle market in the world, that the National and State Governments were aroused to the gravity of the danger, and, the Federal Government supplying the funds and the Illinois Government the authority, the beginning of a real attempt at extinction was seriously undertaken. The author acted as chief of the national veterinary force in Illinois in 1887, and takes great pleasure in recording that at the end of three months from the date of his arrival, the last acute case of the disease had been disposed of and the frightful danger that had threatened the nation through the Chicago stock yards had been removed. The supervision was maintained for a year later, and some old sequestra were later found in the lungs of cattle slaughtered, but no acute nor dangerous cases of the disease. This was followed by vigorous suppressive work in other infected states and by September, 1892, the quarantine was raised and the nation pronounced free from lung plague. The last cases were met with in New Jersey, early in 1892. In this last anti-lung-plague crusade the National Government inspected 1,605,721 cattle in 166,951 herds, made 356,404 necropsies, purchased 21,961 head of cattle, and disinfected 4,128 premises. 7,438 cattle were found affected at the necropsy.

Another line of infection was started by 4 Dutch cows, landed at Boston in 1859, and before the end of the year the infection had extended into 20 different townships in Mass. In 1860, a State Commission was created, with Dr. E. F. Thayer as veterinary commissioner, and in the next few years they destroyed 1,164 cattle, and stamped out the plague at a total cost of $77,511.07.

An importation of infected cattle into New Jersey was made in 1847, by Mr. Richardson, who on discovering the nature of the disease, made an end of that particular contagious centre, by slaughtering his whole herd at a cost of $10,000.

South Africa was infected in 1854 by the landing of a Dutch bull at Cape Town. As there were no railroads and all inland carriage was conducted by ox-wagons, it soon spread over the colonies and extended thence into the native states, and has continued to the present time.

Australia was infected in 1859 through an English cow landed at Melbourne. When the disease was identified, the whole herd was slaughtered and paid for, and the farm quarantined. But the quarantine was broken by a teamster turning his work oxen into the pastures under cover of night, and the infection escaped and has prevailed over Australia to the present day.

Later the disease extended in a similar manner, to Tasmania and New Zealand.

Causes. The one essential cause of lung plague is contagion from a preëxisting case. Before the days of bacteriology, this had been demonstrated as conclusively as any truth can be. All extensions into a new country or district could be traced to direct importation from a preëxisting area of infection. Until such importation such lands have been immune from time immemorial; at once after, the infection has spread from the imported animals as a centre; if the stock is divided up and scattered, several primary centres are formed from each of which the plague makes extension. Again, isolated islands (Channel Islands) and purely breeding districts (Scottish Highlands) into the herds of which no store cattle from outside are admitted, remain immune through centuries, no matter how prevalent lung plague may be in the countries immediately around. The immemorial immunity of the Western Continent, up to the date of the arrival of the now famous Dunn cow, the continued immunity of Canada and Mexico after the infection of the Eastern United States, and the immunity of the United States since the last infected cattle were destroyed in 1892, are equally conclusive in this respect.

Bacteriology. The history of lung plague forcibly illustrates how harmless microbes of large size, that may be easily discovered, and which existing in the environment, readily find their way into diseased and susceptible parts (in this case into the bronchia), may be held to be the pathogenic cause. Willems and Van Kempen, in 1852, found microbes in the exudate. Lustig in 1885 found four separate microbes in the lesions, 1st, a short, thick, liquefying bacillus to which he attributed the disease; and 2d, 3d, and 4th, three forms of micrococcus. Poels and Nolen, in 1886, demonstrated bacilli of variable size (0.9μ), solitary, in pairs and chains, cultivable in different media, and inoculable by injecting such cultures into the lungs, but the resulting lesions were not marked by the full lung plague exudate. Arloing, in 1887, separated from the exudate the bacillus liquefaciens bovis, a very short, slender bacillus, often in pairs with flagella, motile, staining easily in anilin but not in Gram’s solution, quickly liquefying gelatine as a culture medium and assuming a form that might be taken for micrococci, quickly obscuring peptonized bouillon, and growing on potato. The exudate placed in a thermostat at 95° F. encreases in potency. The bouillon cultures injected under the skin or into the lung, produced characteristic lesions of lung plague.

In the light of the later experiments of Nocard and Roux in 1897–8, it would appear that Arloing’s bouillon cultures were probably complex, containing not only the bacillus liquefaciens bovis, but also, the infinitesimal microbe which is the true cause of the lung plague. In seeding culture media with the exudate taken with all possible precaution against contamination, from the interlobular pulmonary connective tissue, they and others constantly failed to obtain results. Better success attended their efforts with Martin’s culture bouillon for producing diphtheritic toxin. Five pigs’ stomachs are minced, pounded to pulp, mixed as follows: stomach 200 grs., pure muriatic acid 10 grs., water 50° C., 1000 grs., left in a thermostat at 50° C. for 12 hours, (to 24), then heated to 100°C. to destroy the action of the pepsin, then lowered to 80° C., alkalized, filtered from flocculi that formed, heated to 120° C., and filtered. This is then mixed with peptonized meat juice prepared as follows: fresh beef or veal, minced and pulped, 500 grs., and water, 1 litre, are kept for 20 hours at 35° C., the liquid expressed, 5 grs. common salt added, mixed in equal proportions with the peptonized liquid from the pig’s stomach, heated to 70° C. to coagulate albuminoids, filtered, alkalized and sterilized. To this mixture is added ¹⁄₂₅th part of blood serum (sterile) from the rabbit or cow.

This bouillon was inoculated with the pulmonary interlobular exudate, enclosed in collodion capsules, having very thin walls, and inserted aseptically into the abdomen of the rabbit. In 15 days the rabbit was sacrificed, and the capsules enucleated from their envelopes of exudate and cells. The contents showed the slightest possible shade of opacity, but they contained neither cells nor any other definite organism. Under a magnifying power of 2000 diameters the liquid contents were found to be full of brilliantly refrangent points, actively mobile, but so minute that their form could not be made out even when staining was resorted to. The contents of these capsules when inoculated on cattle produced the unequivocal phenomena of lung plague infection in a period of from 8 to 15 days. Other collodion culture cases inoculated from this produced the same cultures in the peritoneum of the rabbit. Collodion cases charged with the uninoculated peptonized bouillon, and placed in the rabbit’s peritoneum remained absolutely clear, with no refrangency nor motility under high powers and with no infectivity when inoculated. The rabbits used for the infective cultures often became emaciated to the last degree and even died, but their tissues proved in no respect infecting to culture media nor when inoculated. The attempt to cultivate the germs in collodion cases in Guinea pigs completely failed.

This ingenious form of culture devised by Metchnikoff for experiments on the more delicate organisms, has been used by Nocard to accustom the tubercle bacillus of mammals to grow in the bird and opens up great possibilities for future investigators. The collodion, being impermeable to leucocytes and bacteria, allows these to grow almost together, only on the opposite sides of the collodion wall, restrains phagocytosis, and protects the microbe against the destruction which would otherwise overtake it.

Modes of transmission. The exhalations from the sick convey the infection to susceptible healthy cattle. Yet even this was denied by one veterinary teacher in Great Britain in the latter half of the 19th century. The transmission of the disease by mediate contagion was denied by those in authority in Great Britain up to the end of the century and this delusion contributed largely to the loss of many millions by the nation. Experiments made at Brown Institution were held to sustain this, but not an atom of evidence was furnished to show that the exposed animals were susceptible ones. Diseased lungs kept for a year at 21° F. proved infecting when inoculated (Laguerriere).

Contagion through the air in the same stable was admitted even by the English sceptics. It may be carried in this way for forty yards, or if dried on dust or light materials to a great distance.

Infection through food soiled by breath or nasal defluxion is a common cause. In our great swill stables during the prevalence of the plague, it was notorious that the disease advanced rapidly along the line of a feeding trough to the sixty or more animals using it, and that the rapidity of the advance was determined largely by the fact that the first animal was at the higher end of the trough. If at the lower end there was no upward current to carry infection to the others. Open pastures where the sick have fed and watering troughs or ponds are common sources of infection. The permanence of infection in and around large cities is largely due to the common pasturage by different herds in succession on the same unfenced lots waiting to be purchased for building. For this reason the plague always extended in summer when the cattle frequented these lots, and diminished in winter when they were strictly confined to stables and yards.

Mingling of different herds on great unfenced areas has been the main cause of the maintenance of the infection from time immemorial in the hills and forests of central Europe and on the boundless Steppes of Europe and Asia. This alone is chargeable with the permanence of the affection, in spite of all efforts for its extinction, in South Africa, Australia, Tasmania and New Zealand.

Contagion carried by attendants, cattle dealers and even dogs, is generally recognized, I have elsewhere quoted the case, in E. Lothian, Scotland, in which the son of the steward, who was cattleman on an infected farm, was the means of infecting first, his father’s cow, and later the whole of the stock on the place; also the case at Quincy, Mass., in which a farmer coming straight from the slaughter of sick cattle, infected his own herd; also the case of Mr. Jewell, of Long Island, who carried the infection from the herds visited, to his own family cow in a thoroughly secluded stable.

Infection through infected and emptied stables, was a common experience in dealing with the lung plague in America. Cows kept alone and only introduced after the predecessor had died habitually contracted the disease, though brought, through the most carefully guarded stockyards, from healthy districts. Stables have continued infecting for a year after having been vacated, (Friedberger and Fröhner).

Infection through manure spread on ground to which susceptible cattle had access was an occasional occurrence.

An active, unrestricted commerce is however the most prolific means of infection in cultivated countries. Slow as the disease progresses, and long as the animal diffuses infection, it soon attacks and kills or immunizes all the susceptible animals in the single herd, and if no other susceptible animal is bought or born into the herd, the germ in due time loses its pathogenic potency and infection is at an end. In this way many centres of infection started in herds on well fenced farms have worn themselves out. But the case was far otherwise in the city dairies and swill stables. The trade demanded that the stalls emptied by deaths should be filled up to consume the swill, or supply the milk route and thus fresh susceptible cattle were constantly exposed in the infected stable. The dairy cows were supplied by dealers who charged exorbitant prices for them and held a chattel mortgage for the amount. They had come through the infected dealer’s stable, and if they did not come up to the milk yield promised, they were either passed on to another dairy or returned to the dealer’s stable carrying back a new load of infection. The wagons used to carry the cows through the city were constantly infected and infecting. The swill stables became the final destination of the surviving cows that had gone dry and thus infection constantly gravitated into them.

In Europe where the great cattle and meat trade with England and the constant demand for cattle to consume the marc of the beet sugar and other factories, cause a continuous draught upon the infected districts the great western centres of enterprise and commerce have found it impossible to exterminate the plague.

In the country districts in England outbreaks were almost exclusively confined to the times when fresh cattle were purchased at one of the great fairs. Hence the late autumn, the period of laying in feeding cattle, witnessed the greatest extensions.

In Ireland, as shown by Ferguson, the whole cattle trade seemed to be arranged as if for the speedy and universal diffusion of infection. Calves, bought by jobbers from all sources, were bunched together with every opportunity for intercommunication and infection. As soon as they were a little further matured, they were assorted in lots and sent to a fair, where they were sold, and found their way to great common pastures, and this process was repeated again and again until they had reached full maturity. On the way to and from each market they were quartered over night in a public yard which had just been vacated by other animals, often diseased, traversed the same roads, and drank and fed from the same troughs which diseased ones had just used.

The introduction of apparently recovered cattle is generally credited with the infection of a fresh herd and Friedberger and Fröhner quote with approval Walley’s assertion that a recovered animal with a sequestrum in the lung can infect a herd into which it is taken. I have failed to produce even local exudate, subcutem or in the lung, from sequestra which were much more recent, but the animals operated on were rendered immune and inspired me to carry out a system of immunization by the use of the sterilized fresh exudate. The actual date of the expiration of virulence in the necrotic lung tissue has never been demonstrated and probably varies in different cases.

The receptivity of different breeds has been discussed and the Holsteins and Shorthorns have been thought to show the greatest susceptibility. These are among the cattle that are most prized, bought and sold, and exposed to infection. The Shorthorn especially has a great development of the circulatory system, including the connective tissue with its great lymph sacs and channels, and the microbe we are dealing with shows a marked preference for the lymph system, in which it finds its appropriate field of development. Susceptibility is greatly encreased by a warm climate or hot season, under which large herds may die without a single exception, the disease running a fatal course in two or three days. In cooler climates 20 per cent. will often escape at first (French Commission Experiments, 1849).

Lesions. If death has taken place early, the lesions are usually essentially pulmonary, though they may implicate the pleuræ and mediastinum. In many cases the lung alone is involved, yet even then the predilection of the microbe for the lymph network of the interlobular tissue is strongly manifested in the serous infiltration of that, rather than of the lung structure proper. This determines the much talked of marbled lung, the pulmonary lobules standing out at first as a more or less deep red brown or black, while the marbling is caused by the yellowish or grayish infiltrated tissue surrounding each pulmonary lobulette which appear set in, as in mosaic on the surface of a section. Sometimes a blood extravasation discolors the interlobular exudate as well, yet it retains its soft liquid appearance which sufficiently distinguishes it from the firmer lung tissue. These yellowish interlobular markings vary much in thickness, but in acute cases this may be up to half an inch or even more. In the lesions of longer standing the interlobular exudate has usually coagulated, or even undergone fibroid organization, so that it compresses and condenses the lobules which it surrounds.

The pulmonary lobules may show the earliest changes of the alveolar and lobular capillaries, with formation of an exudate, and an active proliferation of small round cells in and around the alveoli. Later the exudate coagulates, forming the familiar red hepatization, and this in its turn may pass into the gray, or it may liquefy and undergo absorption and resolution. Other changes are not uncommon. The excess of interlobular exudate will compress the pulmonary lobules so as to reduce their size and expel the blood from their structure, giving them a pale color, or this compression becomes still greater, completely arresting the circulation and inducing lobular gangrene. Thrombi in the afferent and efferent vessels contribute to the necrotic change, and sequestra of varying size, from that of a nut to that of an infant’s head or larger, are formed. The earliest stage of this necrosis is usually infarction of the lung, a definite area of which becomes saturated with dark blood cells so that in contrast with the rest of even the hepatized lung, it is almost as characteristic as the marbling. The further progress of this necrosis is varied. Most commonly the exudate surrounding the necrotic mass becomes organized into white fibrous tissue and forms an investing sac in the interior of which is the dead lung tissue, showing for a time distinctly, the bronchia, blood vessels, lobulettes, and interlobular tissue. This gradually becomes detached and floating in a liquid debris, slowly undergoes solution, and is absorbed, the sac meanwhile closing in on the cavity. A large sequestrum may be a year or sixteen months in undergoing complete solution. In other cases the pulmonary lobulettes undergo an individual softening while the interlobular tissue becomes organized and when cut across, the lung presents a distinct honeycombed appearance. In still other cases a considerable area of both lobulettes and interlobular tissue is necrosed and liquefied, while the exudate, around the bronchial tubes, that supplied it, becomes organized, and on the necropsy the latter are found to constitute a thick branching mass of a very characteristic appearance.

The newly affected lobulettes have a watery or gelatinoid or dropsical appearance and if freely incised give out a large amount of serum and flatten down in doing so. When hepatized the cut surface is granular, and microscopic examination shows the terminal bronchia and alveoli filled with a fibrinous exudate containing great quantities of red blood globules and leucocytes. The distension of the lung is enormous, so that when the entire organ is infiltrated it may weigh from 50 to 100 pounds.

In recent cases the lung may be extensively affected without affecting the pleuræ; in other cases both are early involved. In advanced cases the pleuræ are always implicated. First there is the subpleural infiltration over the affected part of the lung; later the pleural surface has reddened arborescent patches, with a slight solid exudate, and a yellowish (sometimes blood-stained) serum collects in the bottom of the cavity; later still the affected portion of the lung is covered more or less thickly with false membranes, while others cover the organ or the parietal pleura below this level, and hang in shreds or bind the lung to the ribs. In old standing and recovered cases these may be largely represented by dense, white fibrous investments covering the lung or the rib, or establishing permanent adhesions. The amount of pleural effusion may be about two gallons in bad cases, and like the invasion is either unilateral or bilateral. The pericardium is usually more or less involved in pleuritic cases.

The larger bronchia sometimes contain false membranes.

The bronchial, prepectoral and mediastinal lymph glands are often enlarged, congested and infiltrated with an abundant exudate.

Similar infiltration of the lymph glands of the pharynx, mesenteries. sublumbar region and groin are described, together with hypertrophy and congestion of the intestinal follicles, and congestion of the muscles and intermuscular tissue, of the articular and tendinous synovial sacs, and even of the meninges of the brain and cord. I know of no facts to show that these conditions result from anything else than the toxins and the general constitutional disorder. The indications are that the microbes are speedily destroyed in the circulating blood, and intravenous injections and caudal inoculations alike fail to cause the characteristic lesions in the lung, their favorite point of casual election.

Incubation. This usually lasts from 6 to 30 days, being greatly abridged by hot weather and often prolonged in the cold. Delamotte claims to have seen it extend to 5 months, and in one case a calf turned out on Montauk Point, L,. I., from an infected place was noticed ill on the 104th day. Australia, South Africa and Norway were each infected by cattle that had been three months out of their native infected land. I have seen cattle pass three or four months after purchase in an unthrifty condition, yet without cough or other recognized diagnostic symptom and then come down with lung plague. Such doubtless explain the alleged protracted incubations, the system has been invaded, ill health ensues, but the lungs are only slightly affected for a length of time. In other cases one animal in a herd has had a mild attack, which escaped notice, and it was only later that the disease was recognized in a second victim, infected from this first.

The bearing of this on imported animals is evident. An animal imported alone should be kept under surveillance for a month or two after quarantine, while in any considerable herd the disease would certainly manifest itself during the prescribed three months detention.

Symptoms. These vary greatly with the animal and its environment. Other things being equal it may develop more suddenly and violently in the obese Shorthorn, Angus, Hereford, Ayrshire or Dutch, and less so in the spare Brittany or Jersey. In very hot weather the attack is very sudden and severe. A chill from exposure, an attack of bronchitis or pneumonia, the excitement attendant on parturition, on travelling by rail or driving may precipitate and aggravate the seizure. Under some such conditions there may be sudden and extreme hyperthermia, rapid pulse, oppressed breathing, percussion and auscultation evidence of extensive pulmonary consolidation and death in two or three days, while the body is still plump and fat.

Individual susceptibility appears to have influence, the same stable presenting simultaneously cases of acute and fatal type and others that are slow, and insidiously progressive. In newly invaded countries and in bovine families that have not been exposed to the infection for many generations the tendency is to a higher proportion of severe and fatal cases, while in herds native to districts that have been continuously or frequently exposed, mild cases tend to predominate. The more susceptible strains of blood have been killed out, and the surviving strains show a greater power of resistance.

Apart from the predisposing environment the tendency of lung plague is to set in slowly, insidiously, and for a time almost without outward symptom. For a week, fortnight, month or more there may be a slight cough heard only at rare intervals and neither painful nor specially troublesome. Though sometimes hard, it is more commonly small, weak, short and husky, noticed only when the animal rises, drinks cold water, goes out to the cold air, or eats dusty or fibrous fodder, and is usually attended by arching of the back, extension of the head, opening of the mouth and protrusion of the tongue. For weeks there may be no indication of constitutional disorder, appetite, rumination, milking, and other functions appearing to be normal. Driving the animal may unduly accelerate the breathing, and a careful auscultation may detect an unusually loud blowing sound behind the middle of the shoulder, a mucous râle, or a wheeze. In some cases the disease never advances farther, the trouble subsides and the subject is thereafter immune. Cases of this kind occurring as the first in a herd, explain some instances of what are claimed to be specially prolonged incubations.

In the great majority of cases further symptoms appear, hyperthermia sets in, varying in different animals from 103° to 108° F., the animal becomes dull, depressed, loses in appetite, rumination and milking, omits pandiculation on rising, shows stiffness of the hind limbs, sometimes knuckles forward at the fetlocks, wanders apart from the herd, is found lying apart, shows extra thirst, bloats slightly, and shows some constipation. Pulse and breathing are accelerated, auscultation signs are more marked, and on percussion, areas of flatness may indicate lobular consolidation, usually more extended than in ordinary pneumonia with the same grade of constitutional disturbance. The muzzle becomes hot and dry, the roots of the ears and horns hot, and the hair stands erect along the dorsal aspect or in patches over the body. Pinching of the dorsal spines, sternum or intercostal spaces, may cause marked wincing and a deep groan. The eye is dull, lacking in prominence and clearness, and the lids are often partially closed. At this stage improvement sometimes ensues and after inappetence and suppression of milk for one or two days, the patient may take to feeding and milking as before, and apparently recover, though with a large pulmonary sequestrum.

In the continuous and violent cases all the symptoms are aggravated. Fever may run to its extreme height, there is complete anorexia and suspension of rumination, pulse and breathing are rapid, the victim no longer lies down but stands with feet apart, arms and elbows turned out, head extended nearly on a line with the neck, mouth open, tip of the tongue projecting, and each expiration accompanied by a moan, so loud that it may be heard at a distance (often 50 yards). The breath is heavy, feverish, mawkish. The flanks heave violently, the nostrils are widely dilated and discharge muco-purulent, often bloody liquid, strings of fœtid saliva drivel from the open mouth, there may be tympany or even colic, the eyes are sunken, and the conjunctiva and nasal and buccal mucosæ are of a dull brownish and yellowish red. Emaciation advances at a rapid rate, and the constipation may be superseded by a profuse, fœtid diarrhœa which wears out the animal. The skin is dry, scurfy, withered, pale, and clings firmly to the bones, and the interior of the vulva may show the pallor of anæmia. The spine, sternum and intercostals are more than ever tender, and pressure on the tender areas may detect a lack of movement of the lung which is felt on the healthy parts.

On percussion very extensive areas of consolidation are revealed by the dulness and flatness. If pleuritic effusion exists the resulting flatness is extreme below and up to a given horizontal level, the line of which may, however, be elevated at points by consolidation of the lung at such parts. Auscultation may reveal almost any of the abnormal sounds of pneumonia or pleurisy. Absence of respiratory murmur over large areas, with blowing, heart or abdominal sounds in unwonted situations (where the murmur is absent), and abnormally loud murmur where the lungs are still pervious; crepitation around the margins of the consolidated portions; the creaking sound of stretched false membranes, scarcely distinguishable from crepitation; mucous râles; wheezing sounds of various pitches; exceptionally splashing sounds, and if the animal has just risen, the metallic tinkling sound. In other cases the pleural friction sound is prominent.

Abortions are common in pregnant animals.

Course. This varies greatly. In our northern states in winter, many would seem to recover after a few days illness; in summer, many died in a few days with excessive exudate, dyspnœa, and prostration. Others died early from tympany of the rumen. In others still, profuse, fœtid, colliquative scouring led to an early death. In extreme cases there would be a loss of one-third or one-half the weight in a single week. In the less rapidly fatal cases all the symptoms became aggravated, the emaciation progressed, and a liquid pultaceous condition of the bowels continued for two, three, four, or even six weeks, the animal finally dying in a state of marasmus. In such cases the shrunken, pallid skin and mucosæ bespoke an extreme degree of anæmia.

Recoveries may take place from comparatively advanced stages, but they are liable to be slow and imperfect, the animal remaining unthrifty for a length of time. In some of the more favorable cases, when the recovery is less interrupted or retarded, fattening may take place rapidly, so that it would appear as if the loss of a portion of lung, and the lessened consumption of hydrocarbonaceous matter contributed to the deposition of fat.

In some cases the active morbid processes subside, but are not quite arrested and the malady assumes a chronic form, the exudates become organized, causing a sclerotic or fibroid condition of the lung and especially of the interlobular tissue, which compresses and carnifies the lung tissue, or leads to necrotic changes and the formation of sequestra, or again to liquefaction and the formation of vomicæ. Here the proliferation of the germ may go on, though little new tissue is invaded, and the animal may remain infecting for a long period. The patient remains thin, and weak, is easily blown under exercise, has a small, accelerated pulse, little power of digestion or assimilation, shows frequent tympanies, and may have profuse diuresis or diarrhœa. The cough is frequent, often paroxysmal, easily roused, loose, mucous, painful and may be attended by muco-purulent discharge. Such animals are liable to die in the end in marasmus.

In some cases the malady is complicated by other infections, leading to the formation of abscesses in the lungs, pleuræ, chest walls, bronchial glands, joints or elsewhere, or tuberculous deposits may complicate the lung plague, and there may be an early death or a long drawn out decline.

Diagnosis. So many different affections resemble lung plague closely during life, that a certain means of diagnosis is a great desideratum. Yet many points help one to reach a reasonably certain diagnosis:

1. Does lung plague exist in the country? If not the presumption is very strongly against it.

2. Have the suspected animals been recently imported from a lung plague infected country? or have they been in contact with animals recently imported from such a country?

3. Have they been fed on provender imported from such a country?

4. Have they been attended by a man recently from such a country and whose clothes have not been sterilized?

5. Have they been carried on any imperfectly disinfected car or ship which has carried the cattle of such country?

6. Has the affection attacked a considerable proportion of the herd at the same time? A rare thing with lung plague.

7. Has the attack come on slowly and insidiously? Very characteristic of lung plague.

8. Has hyperthermia been marked? Indicative of lung plague.

9. Have a succession of cases occurred at intervals of several days or weeks, irrespective of weather? Suggestive of lung plague.

10. Have the indications of consolidated lung been early and over extensive undivided areas? Like lung plague.

11. Have cases been milder in cold dry weather and more violent in hot and moist? Such is lung plague.

12. Does the same subject present lung lesions of very different ages;—infiltration with tough, elastic lung; red hepatization; gray hepatization; black infarction; sequestra, etc.? Bespeaks lung plague.

13. Do the infiltration and red hepatization show a marbling with very extensive filling and turgidity of the interlobular and subpleural connective tissue, and abundant effusion into the chest? This is the nature of lung plague.

14. Does the lung exudate when inoculated in the tail of a susceptible bovine animal (one that has never had the disease), produce local inflammation and exudation and procure immunity? This characterizes lung plague. Does it fail to cause inoculation swelling, in an animal that had lung plague. Lung plague is still more indicated.

15. If the disease has lasted long enough in a place to determine, has it affected any other than bovine animals, and does inoculation of the lung exudate into any other genus of animal cause the disease? Other genera are immune from lung plague.

Tuberculosis is distinguished by the habitual absence of the high temperature, the numerous circumscribed areas of flatness with wheezing or other abnormal lung sounds, in the midst of a general field giving the normal respiratory murmur, by the enlargement or induration of superficial lymph glands, by the response to the tuberculin test, and by the lung tubercles and diseased lymph glands,—congested, indurated, caseated, calcified—found at the necropsy. Inoculation of other genera causes tuberculosis.

Simple bronchitis is usually connected with climatic change or exposure, tends to affect a number at once, gives the blowing and mucous râles, without indications of extended lung consolidation or pleural effusion, and after death does not furnish lesions of all ages, recent and remote.

Verminous bronchitis, attacks the young only or mainly, and never seriously injures the mature, involves all or nearly all the young in the herd, shows less hyperthermia, and less extensive consolidation, more wheezing in the lungs, and a free expectoration in which the worms (embryos or adults) may be found by careful search.

Simple fibrinous pneumonia is likely to arise from climatic conditions or from exposure, attacks several at once and none later, has less abrupt rise of temperature, less tenderness of the chest walls, less dyspnœa, less obstinate standing, and after death, less interlobular exudate and marbling, and no presentation of old and recent lesions in the same lung.

In the infectious pneumonia occasionally seen in western cattle, the distinction must be made mainly by the less elevated temperature, less dyspnœa, the lack of the early signs of extensive consolidation of the affected lung, and after death, absence of the extensive interlobular infiltration, and in the predominance of the whitish points or mottling indicating the broncho-pneumonia and the cell proliferation in the terminal bronchia and alveoli.

The pulmonary form of hæmorrhagic septicæmia (Wildeseuche) is distinguished by its enzoötic character, in connection with wet lands, its occurrence in the summer season, its association with other forms of localization, in the abdomen, muscular system, etc., its dependence on a cocco-bacillus, easily found in the exudate, and its inoculability on the smaller ruminants, horses, pigs and rodents.

The perforation of lungs and heart by a sharp pointed foreign body from the reticulum, occurs sporadically in one animal which has usually been kept indoors; it shows as a rule less fever, may be preceded by tympany or other gastric trouble, shows a line of consolidation from the reticulum forward, is earlier or later complicated by morbid heart sounds or rhythm, and commonly shows a pitting swelling beneath and beside the sternum.

Pulmonary emphysema is sporadic only, usually devoid of sudden hyperthermia, or constitutional disorder, has a dry paroxysmal cough, wheezing sounds on auscultation, and a drumlike sound on percussion. If associated with bronchitis or pneumonia and attendant fever, the case is more equivocal.

Aspergillosis of the Lung usually advances more slowly, in the comparative absence of sudden hyperthermia, shows more limited areas of consolidation, less dyspnœa, and usually affects smaller animals (birds) as well. At the necropsy the presence of aspergillus in bronchia and lung tissue is conclusive.

The acute pulmonary congestion of heat stroke is sufficiently identified by the conditions under which it occurs, its sudden and rapid progress, the implication of the brain, and its occurrence in other animals similarly exposed.

Such conditions as atelectasis, pulmonary actinomycosis, distomatosis, or echinococcus, the congestion of mercurialism, etc., should be readily recognized by the attendant conditions, analysis or necropsy.

Attempts have been made to diagnose lung plague by securing a reaction, local or general, as the result of injection of the sterilized lung exudate or cultures, but they have proved eminently unreliable. The susceptibility of the serum to change under manipulation, the existence of hyperthermia before the injection, and the disposition to local infiltration under the lung plague poison are apparently insuperable obstacles.

Treatment. No treatment has been devised that would warrant the preservation of the infected animals when the alternative of prevention is available. The question is an economic one, and with a disease that is so insidious, with such a long incubation, with so many occult and chronic cases liable to escape observation and recognition, and with such a constant and prolonged exhalation from the lungs of the virulent material and the certainty almost of the diffusion and preservation of the latter, no more suicidal policy could be adopted than the preservation and treatment of the sick.

If allowed at all, treatment should be conducted in an isolated locality, well secluded from visitors and wandering animals including birds, and under the most intelligent antisepsis. It should proceed on general principles according to the individual manifestations of the disease, and might include serum therapy from immunized animals.

Prevention. For a country like the United States, now happily free from the lung plague infection, the important object is its permanent exclusion. For this the federal quarantine for three months now in force ought to be effective. The only question would be in the case of small importations of one or two animals, which might introduce infection under an apparently prolonged incubation, or with a chronic type of the disease. Small importations of one or two, might be dismissed at the end of three months quarantine under a ticket of leave system, under which they and the herd into which they are taken can be kept track of for three months more. In the larger imported herds the possibility of the escape of infection under a three months quarantine is so infinitesimal that it may be practically ignored.

Similar precautions must be taken against the importation of cattle from a country reputed to be free from the lung plague, but which imports cattle from an infected country without imposing the three months’ quarantine.

The use, for transportation of cattle from one part of an immune country into another, of cars or boats which have been used for transporting cattle in an infected country can only be permitted after the vehicles in question have been thoroughly cleansed and disinfected and attested so by the official experts.

The landing in an uninfected country of hay, fodder, or cattle-food of any kind, or of litter, grain bags, head ropes, manure, or other article coming from an infected country must be prohibited until such article shall have been thoroughly disinfected.

Horns, hoofs, hides, hair and other products introduced into the country must be disinfected. The treatment adopted to exclude anthrax would be amply sufficient for lung plague.

Measures to Extirpate the Infection. Stop all accessions of possibly infected cattle from outside. Proclaim the infected area, prohibiting all entrance and egress of cattle, and all movement of cattle from herd to herd within the area, except under special license, based on the soundness of each herd for six months antecedent. Prohibit absolutely the pasturage of cattle on public highways and unfenced or insufficiently fenced places. Send to instant slaughter cattle found in such places in violation of this rule. Make an accurate census, with individual description of each bovine animal in the infected district, and make a necropsy of each such animal dying at the hands of the butcher or casually. Hold the owner guilty of a misdemeanor with heavy penalty, for every bovine animal that goes amissing in the infected district without official post mortem examination. When an infected animal is found in a herd have the whole herd, marked, appraised slaughtered under official supervision and with necropsy of each animal. If any herd has been losing animals, or had sick animals within a year, buy and kill the whole herd. Indemnify the owners to the amount of at least two thirds or three fourths of the sound market value for all except the advanced and acute cases of the disease, and such animals as have been moved into the State less than three months before. These latter may be sacrificed without indemnity. Disinfect thoroughly all infected premises and things at public expense. Close the fields against all outside cattle for three months. Burn all hay, straw, litter, and grain in the infected buildings or see that they be fed to horses, sheep or pigs apart from where cattle are kept. Burn or disinfect all manure or have it drawn out and plowed under by horses, and the wagons and implements used in doing so thoroughly disinfected. Allow restocking of the disinfected premises from sound districts only, and keep up the strictest supervision and control of the herds for from three to six months.

For private Control in the absence of Government Action. The stockowner in a secluded locality, not bordering on a highway or railway can as a rule secure the immunity of his herd by such measures as the following. Breed all the stock on the farm. If a change of blood is required buy the bull young and keep him strictly by himself for at least four months, allowing him to mingle with other cattle only after he has been thoroughly attested. Allow no animals to go outside for service or any other purpose and afterward return to the herd. Allow none to enter from without for any such purpose. If from any cause cattle must be bought, secure them from healthy herds and transport them in thoroughly disinfected cars, boats and by healthy roads, and never through an infected district. Place them in special premises at least one hundred paces from all other cattle, and under special attendants for three months.

Immunizing through a First Attack. When lung plague was at its worst in Great Britain, Mr. Harvey a dairyman on a large scale in Glasgow practiced the method of buying heifer calves and exposing them in his infected stables until they contracted the disease. He had a loss of 20 per cent. and the surviving 80 per cent. were then turned out on his farm and raised and when they came in milk, were sent into Glasgow as new milch cows immunized from the plague. He thus reduced his losses to the minimum of one fifth of the inexpensive calves, and warded off the heavy losses previously sustained in the valuable milch cows and preserved the still more valuable trade in the milk of healthy animals. The method was a mere temporary makeshift, depending for its success on the permanent maintenance of the lung plague, but so long as there were no well considered government measures for its extinction its permanence was assured in any case, and Mr. Harvey was working no injury to any one, while he was substituting a profitable occupation for a losing one, and supplying his customers with milk from sound cows in place of those that were continually coming down with the plague. Under official measures for the plague-extinction his attempt would have been most reprehensible, but in the absence of such measures it was highly meritorious.

Inoculation in the Tip of the Tail. This is an advance and in some respects an improvement on the Harvey system, as the infection and lesions are localized in the tail, and the mortality is reduced to 2 per cent. In practice a recently attacked animal is selected, and a portion of the lung which is strongly infiltrated but not yet hepatized. This is laid upon a clean scalded plate and incised with a clean scalded knife when an abundance of a clear yellow serum drains out. This is drawn up into a sterilized hypodermic syringe, and the tails having been washed and sterilized, the nozzle is inserted under the skin of each in succession and a drop or two of the liquid discharged subcutem. If despatch is important the washing may be dispensed with and the nozzle wiped and dipped in strong carbolic acid between each two successive insertions.

Various modifications of this procedure have been made. To avoid the inevitable entrance of ærial germs, flamed pipettes have been inserted into a puncture in the turgid lung, made with a flamed knife, the point is then broken and the serum is drawn up to fill the vacuum caused by the heat employed in sterilization. The point is then sealed by melting the glass in the flame of an alcohol lamp, or by melted wax.

Nocard washed the surface of the infiltrated or hepatized lung with boiled water, then with a sterilized knife cut out a deep segment so as to leave a conical cavity and covered this with an awning to keep off dust. The space soon fills with the draining exudate in a very pure condition.

Pasteur inoculated a calf in the dewlap or behind the elbow, where an enormous engorgement forms, involving the whole ventral aspect, and supplying an almost unlimited amount of serum, which may be collected with such precautions against contamination as are indicated above. The product is thus secured at a comparatively cheap rate, and the risk of its diffusion on the air in breathing is lessened enormously.

Another method is to employ the serum from the swellings in the inoculated tails and carry it on indefinitely from tail to tail.

Arloing in his turn employed the cultures in vitro of his pneumo-bacillus, but with the modern evidence that this is not the infective germ, such cultures can not always be implicitly relied on.

In place of the hypodermic syringe, Australians have used a simple thread soaked in the exudate and drawn through beneath the skin. Others have used a small lancet with a groove hollowed out in the middle of the flat surface of the blade on one side, and which carries in the required drop of the serum.

To preserve the exudate for some time against decomposition, it has been kept on ice, or mixed with chloral hydrate or phenic acid (½ its volume), and glycerine (½ its volume) for two or three months.

Injection into the veins practiced by Burdon-Sanderson has the advantage of producing no local lesion whatever and yet securing a fair measure of immunity. It is, however, a much more delicate operation as it entails a possible though remote possibility of producing capillary thrombi, and some danger of infection of the wound in the vein. To avoid this latter, the jugular vein is raised as for phlebotomy, and a short needle is passed into it. A longer and more delicate needle is now passed through this, and the injection of a few drops of the exudate is made through the latter. The small needle is then carefully withdrawn to be followed a few seconds later by the large.

Injection of the Sterilized Exudate Subcutem. In 1881 having found that liquids obtained from old sequestra, produced no local lesions when inoculated subcutem, but secured immunity for the subjects, I inoculated ten susceptible cattle with the fresh pulmonary exudate which had just been heated for 30 minutes to 180° F. No local inflammation nor exudate occurred in any of them, but subsequent inoculations with fresh unsterilized lung plague exudate were resisted in the same way. Six of these immunized cattle were subsequently placed in two infected stables and herds, (Mr. Butts, Brooklyn, N. Y., and Mr. Christopher Slade, White Hall, Baltimore Co., Md.) and retained there for three months without showing the slightest indication of disease. Later I applied the measure on a number of herds with thoroughly satisfactory results. About ten years later a similar resort was had by Arloing and Rossignol with corresponding success.

Two advantages come from this method: 1st, there is no local infection and no marked swelling so that the injection can be made on the side of the neck where the skin is thin, and clean, and the connective tissue abundant, and where there is less risk of extraneous infection than in the too often dirty or filth soaked tail; 2d, as no living germ is introduced there is no possibility of propagating the disease to other neighboring susceptible animals. Two per cent. of loss, of animals inoculated by the Willem’s method is counted on, but with the sterilized virus there is not even a remote probability of loss. Infection cannot occur from the animal injected with the sterilized virus, so that it can be safely applied among cattle that have not been exposed to infection, but which are likely to be in the future, and these injected cattle can be left to mingle with others that have not been injected without a shadow of danger to either.

Conditions permitting and forbidding Immunization. Immunization is permissible or commendable in all cases in which lung plague is already widely spread in a land destitute of fences and in which cattle roam at large, and herd mingles freely with herd. Here the extension of the disease is inevitable and continuous and effective measures for extinction are impossible. It is permissible where the plague is widely spread among cultivated and fenced farms, but where no authoritative measures are in force for its extinction. In such case, with the Willem’s system the inoculated herd should be kept thoroughly secluded in premises or well fenced pastures, apart from any highway, and not adjoining any other cattle pasture.

When on the other hand official measures are in force for the extinction of lung plague, every form of immunization based on the production of the pathogenic germ in the living body of the bovine, or even in vitro, is to be unqualifiedly condemned. The risk of the escape of the infection through subtle, unsuspected channels is too great to allow of its reproduction in any form. By restriction of cattle movement, slaughter and disinfection, extinction of lung plague is easy and certain, but, whatever may be true of an individual herd, no country has ever permanently extinguished lung plague infection, when the virus was systematically multiplied for uses in inoculation.

CATTLE PLAGUE.

Synonyms. Definition: infectious fever of polygastrics, with sudden onset, violent progress, high mortality, congestions of mucosæ, petechiæ, concretions on buccal and vulvar mucosæ and on skin, erosions of gastro-intestinal mucosæ, and pulmonary interlobular emphysema. Historic notes: ancient—China, Hindoostan, Steppes; in middle ages—Europe, Britain; recent—Europe, England (1714 and 1740), Scotland (1770), Central Europe (1796–1816), Southern Europe (1827), Germany (1830–1), Egypt (1841), Britain (1865), France (1870–1), S. Africa (1881), Abyssinia (1890), Japan (1892), The Phillipines (1898–9). Animals susceptible: ruminants, peccary, (swine?). Bacteriology: minute corpuscles in cell nucleus (Semmer, etc.), which are held back by Berkefeld and Chamberland filter. Accessory causes: such as favor preservation, multiplication and diffusion of germ. Susceptibility varies with previous exposure of the race. Immunity after one attack. All liquids and secretions of the sick are virulent; also manure, hay, straw, dust, stables, troughs, cars, boats, loading banks, yards, milk, flesh, fat, sausage cases, hairs, horn, hoofs, wool, bristles, hides, bones, halters, harness, shafts, poles, goads, boots, clothes, feet (animals), wheels, runners, vermin, wild animals. Virulence lost in drying. Manure preserves for weeks. Lost at zero, and at 131° F. Lesions: congestion, petechiæ, hæmorrhages and erosions on fourth stomach, small intestine, rectum, vagina and mouth, emaciation, sunken eyes, diarrhœa, wart-like epidermic elevations, concretions on mouth; conical papillæ dark, like port wine; petechiæ and extravasations in subderma and submucosa; swollen intestinal glands; spleen normal; liver, pale, soft; kidneys swollen, congested, petechiated, softened; lungs with spots of congestion and extravasation and emphysema: petechiæ on heart and pericardium: blood has excess of fibrine and leucocytes, black. Incubation 2 to 9 days. Symptoms; hyperthermia (104° to 108° F.), white epithelial concretions on gums, followed by abrasions, congestion of visible mucosæ, weariness, debility, thirst, constipation followed by diarrhœa, tender loins, drooping head and ears, weeping eyes, grinding teeth, rapid pulse, expiration with arrest and click, suppression of milk, relaxed sphincters. May become aggressive or soporific. Diagnosis: by rapid and deadly progress, and manifest infection; from malignant catarrh by the active spread, numbers attacked, concretions on mouth, and known exposure; from thrush by the high fever, contagion to old as well as young, and severe abdominal symptoms; from aphthous fever by the high temperature, the absence of distinct vesicles on mouth, teats and feet, by the comparative immunity of swine, and by its high mortality; from dysentery, by the early hyperthermia, the concretions in the mouth, by rapid general extension irrespective of filth and crowding, and by the implication of stomachs and small intestines, rather than the large; from gastro-enteritis, due to chemical irritants, by the lack of such manifest cause, and its rapid progress from herd to herd; from anthrax, by its rapid spread beyond an anthrax locality, the buccal and skin concretions and desquamations, by the insusceptibility of horse, dog, and rodent, by the absence of splenic enlargement or incoagulable blood. In sheep: mortality in Steppes, 30 to 50 per cent.; in new countries 90 to 95 per cent. Treatment: to be condemned where its permanence is not accepted. Serum-therapy: blood serum of immunized animal subcutem. Prevention by immunization: mixture of virus and bile; inject with highly immunized and defibrinated blood, and expose to the sick, only admissible where extinction is despaired of. Exclusion: exclude all ruminants and their products which come from suspected lands, or admit on certificate and quarantine, or for slaughter only. Extinctions: Trace and kill all ruminants that come in proximity to every infected animal, or to any place or thing where it has been, disinfect thoroughly the carcasses, products, places and things, register all ruminants around a wide area of possible infection, make necropsy in every case of death, appraise and sacrifice any herd showing the infection. Each seaboard state should provide for instant action by the Federal Government. Question of extinction in the Philippines.

Synonyms. Pestis Bovina, Rinderpest, Magenseuche, Viehpest, Viehseuche, Pockenseuche (German). Pest Bovine, Typhus Contagieuse, Typhus du gros Betail (French). Tifo Bovino (Italian). Dzuma (Polish). Tchouma Reina (Russian). Low peng (belly sickness, China). Pushima (Hind., Burma.).

Definition. A contagious fever of polygastric mammals (bovine, ovine, caprine, cervine, exceptionally porcine), characterized by sudden invasion, rapid advance, hyperthermia, great constitutional disorder, congestion and blood extravasations of the mucosæ generally, but especially of the gastric and intestinal, epithelial and epidermic hypertrophy in the form of white concretions or warty-like masses on the mouth, (vulva), and skin, followed by erosions, by pulmonary, interlobular emphysema, by a catching, arrested inspiration, followed by an expiratory moan, and by an early and very high mortality.

Historic Notes. As the most rapidly developing and deadly of the cattle plagues, this attracted the greatest attention of people in earlier times, and thus its invasions and ravages can be more satisfactorily identified, than those of the tardier and somewhat less deadly lung plague which usually followed in its wake.

Sanctus Severus and Vegetius Renatus indicate its advent into Western Asia on the borders of the Caspian and Black Seas, coincident with the irruption of the Mongols in the first Christian century. It still prevails in China and adjoining countries, including Hindoostan, and since that date the Steppes near the Black and Caspian Seas have been looked on as the perennial home of the plague. Before 376, A. D., the chronicles of epizoötics in Europe suggest anthrax affections which prevailed widely in man and beast, and since that time the special plagues of cattle come into prominence. At this date the Huns began a great onward movement from the region of the Caspian and Black seas into Dacia (Hungary), Northern Italy, Germany and Gaul, and this was the occasion for a general diffusion of Rinderpest over these countries.

After this date cattle plague spread widely on the occasion of any great European war in which the eastern nations were involved or which was so general or continued as to draw upon Eastern Europe for the supply of the commisariat parks. One great epizoötic culminated in 810 after the wars of Charlemagne; one occurred in 820 in connection with invasion of Hungary by the Franco-German army; one in 1223 to 1225 laid waste Central Europe and is said to have reached Great Britain; in 1233–4 it again gained a wide extension following the invasion by hosts of Mongols from Siberia; great extensions are recorded in Italy in 1616 and 1625 during the 30 years’ war; in 1709 Charles XII wintered with his army in the Ukraine and his return was followed by the most disastrous mortality ever seen in Europe and which lasted from 1710 to 1717. This reached England in 1714 and was there stamped out by killing and burning the sick, disinfecting the buildings and closing up the infected pastures. Paulet claims that Europe lost 1,500,000 head of cattle in the first three years of this invasion. It continued more or less prevalent in the eastern countries of Europe, and, following the course of war, entered Italy in 1735, and extended westward. Again in 1740 in connection with the war of the Austrian Succession it extended westward invading the Western Countries from France to Denmark inclusive, and once more extended into England, where it prevailed until 1756 and caused an unprecedented destruction. It was finally stamped out as on the previous invasion. During this invasion Europe lost 3,000,000 head of cattle (Delafond). In 1770 another invasion of Great Britain occurred through the landing of infected Dutch hay at Portsoy, N. B., but this was quickly suppressed by the destruction of every bovine animal in the infected herds, and the thorough disinfection of premises, supplemented by a daily scrutiny of all cattle within a radius of 18 miles. In the second half of the 18th century cattle plague prevailed more or less generally in all Continental Europe, except Norway, Sweden and the Spanish peninsula, into which no cattle were imported, and carried off 200,000,000 head of cattle (Freidberger and Fröhner). In 1796 to 1816 the cattle plague followed the marches and countermarches of the various armies in connection with the French revolution and the Napoleonic wars, causing unheard of losses throughout Europe. In 1827 it spread widely in connection with the war of independence in Greece, and again in 1830–1 a wide extension occurred in connection with the Polish revolution. In 1844 Russia lost 1,000,000 head of cattle. In 1841 a shipment of Roumanian and Anatolian cattle to Alexandria, Egypt, carried the plague and in two years upwards of 350,000 head of Egyptian cattle perished, only a few being left. From this date the great development of manufactures in the Western European nations, and especially in Great Britain, the consequent increasing demand for beef, and the inauguration of rapid transit from Eastern Europe by steamer and rail, introduced an era of the extension of the cattle plague by commerce rather than war, and Röll gives the losses in Austria alone in 1847 to 1864 at 500,000 head. In 1865 a cargo of cattle from Revel on the Baltic, landed the infection at Hull, whence it speedily extended over the entire country, and prevailed for 18 months, but was stamped out by vigorous measures of destruction and disinfection. In all 279,023 head were reported attacked of which 233,629 died or were killed and 40,165 recovered. In 1865 the plague was once more imported into Egypt, this time from the Danubian Principalities. A wide extension took place in the parks of the French and German armies in the war of 1870–1, as many as 43 departments in France having suffered. In 1872 it was imported from Russia into Great Britain but was speedily extirpated, and again in 1877 from Germany when it spread somewhat more widely but was easily suppressed. In 1881 it was introduced into S. Africa in Asiatic cattle during the war in the Transvaal and coming after the long continued prevalence of lung plague it threatened the cattle interests with ruin. In 1890 it reached Abyssinia by cattle sent for the supply of the Italian Army. In 1892 Japan suffered through importation from the main land. The latest extension of cattle plague was in 1898–9 into the Phillipines in the shipments of Asiatic cattle sent for the supply of the American army, and there as elsewhere in unfenced countries it is proving the cause of disastrous losses.

Animals Susceptible. In spite of its name—cattle plague, Rinderpest—this affection is not like lung plague peculiar to bovine animals. Yet bovine animals are by far the most susceptible, by them it is mainly propagated, and upon them comes the greatest mortality. Infection, however, extends to all other ruminants,—sheep, goats, deer, elk, antelopes, gazelles, aurochs, yaks, camels, dromedaries, buffaloes, etc. Swine which show a pouch on the left sac of the stomach show a certain susceptibility, it killed the peccaries in the Jardin des Plants, Paris, and Viseur in France and Pluning in Sumatra, claim to have seen cases in the domestic pig. The horse, dog, rabbit, bird, and man are immune.

Bacteriology. In a disease with such destructive changes in blood and tissues, bacteria are found, almost of necessity, in the seats of the lesions and even in the blood. No constant microörganism has, however, been isolated, cultivated in artificial cultures, and successfully inoculated on other and susceptible animals. Saweljeff isolated sporulating motile bacilli which break up into micrococci and streptococci, with the cultures of these on agar he produced what he believed to be cattle plague. Metchnikoff found a short bacillus with rounded ends, forming cocci and leptothrix-like threads, non-liquefying, and producing cattle plague in calves. Sacharow found a bacillus 0.25μ to 1.5μ long and Tokishige a very small short bacillus the cultures of which produced rinderpest in cattle. It would seem as if here as in the case of lung plague, the experimenters had retained the real but invisible pathogenic agent in what they took for pure cultures. Semmer attributes the disease to fine corpuscles which have so far eluded current methods of staining and cultivation, and that they exist in the number of from one to six in the enlarged cell nucleus. Nicolle and Adel Bey sustain this position, having found that the unseen virulent germ passed through the more open and thinner Berkefeld filter, but failed to traverse the denser Berkefeld and Chamberland porcelain filters even when favored by a somewhat higher temperature. As this filtration usually removes the germ and renders the liquid noninfecting they hold that the real germ is almost certainly intraleucocytic. When in exceptional cases a few pass through the filter it is held to be only such as were free in the liquid, and these are usually so small in number, that inoculation with the filtrate does not kill, nor always produce appreciable symptoms, but only immunity.

Accessory Causes. The essential cause being the germ, accessory causes are of necessity such as contribute to the preservation of that microbe and its introduction into the systems of susceptible animals.

Susceptibility has a powerful influence even in races habitually subject to rinderpest. The highest susceptibility inheres in cattle, and yet the surviving cattle of the Steppe race, which has been exposed to the infection for centuries, mostly recover from the plague, while fresh cattle imported into the Steppes perish almost without exception. Sheep and goats contract the disease but it is more severe and deadly in the latter than in the former animal. Both, however, can carry the infection back to the bovine animal, as can also the whole group of ruminants. The Guinea pig contracts the affection by inoculation and may thus become an indirect means of conveying infection from ox to ox.

Immunity follows a first attack. Calves born of cows that passed through cattle plague during the last months of gestation are usually immune.

Exposure to infection arises in various ways. All of the secretions of the diseased animal are apparently infecting, and the virus possesses great vitality, so that the channels of infection are almost endless. It is carried in the manure, washed on in streams, and drains, dried up on hay, straw, feathers and other light objects, or in dust, and blown about by the winds, left in stables, in feeding and watering troughs, in railroad cars, steamboats, ferry boats, loading banks and yards, it is carried in the fresh milk, flesh, fat, sausage cases, hairs, hoofs, horns, wool and bristles, in hides and bones, in halters and harness, on wagon shafts and poles, on goads, on boots and clothes of men, and the feet of dogs, birds and other animals, on the wheels of vehicles, the runners of sleighs, and by vermin and wild animals. The various infected products, however, soon lose their virulence after drying. Galtier assures us on the basis of the experiments of a Russian Commission, and the experience of France, Belgium, England and other countries that dried or salted hides can be introduced with perfect safety, and that rendered suet, and dried skins, horns, bones and hairs are equally harmless. On stalls, mangers and racks on the other hand, in an obscure and still atmosphere, virulence may be preserved for three months (Müller, Dieckerhoff). Again in litter and manure in the open air, and even in yards and pastures it may retain its vitality for weeks (Chauveau). The infection is destroyed by a temperature of zero, or 131° F. (Semmer).

Whatever determines a movement of animals from an infected locality, determines the extension of the plague, hence war, and commerce, the food demands of a large and encreasing manufacturing population, the inauguration of new routes of rapid transit by steam over land or sea all contribute in their various ways to the extension of rinderpest.

Lesions. The most significant feature of the morbid lesions is their concentration on the fourth stomach, small intestine, rectum, oral cavity and vagina. The respiratory apparatus, eyes, skin, muscles, and nervous system suffer to a lesser extent. If the case has gone on to a fatal result there is usually marked emaciation, the natural openings (mouth, nose, eyes, anus) are soiled with morbid discharges (muco-purulent, feculent) the thighs smeared with offensive liquid fæces, and the skin may be yellowish red, or dark, with a general scurfy condition and distinct eruptions, especially of rounded wart-like epidermic concretions on teats and udder. The eyes are deeply sunken, the conjunctiva of a yellowish red, and the lips and muzzle dry, swollen and it may be eroded.

The buccal mucosa is swollen, fœtid, with marked epithelial desquamation and more or less deep and extended erosions on the upper and lower lips, gums, dental pad of the upper jaw, cheeks, hard palate, and root of the tongue. There may still be some of the characteristic, white, epithelial concretions, or the epithelium may hang in loose semi-detached shreds, or there may be extensive areas of abrasion, in transverse cracks or broad patches, and finally extensive petechiæ. The conical papillæ on the cheeks and dorsum of the tongue are especially liable to dark red petechial discolorations.

The subderma and submucosa are also suffused with these congestions and petechiæ, and like the epidermic layer show a marked increase of all elements and of the cell nuclei.

The congestions, petechiæ, desquamations, erosions, are found on the fauces, pharynx, gullet, nasal mucosa, trachea, and bronchia, to a greater or less extent in different cases. There may be even limited areas of superficial necrosis and even the formation of false membranes. In the diseased epidermis and epithelium, in the necrotic plaques and false membranes there are spores and mycelia of fungi and bacterial growths.

In the rumen, reticulum and manifolds, the mucosa and submucosa usually show limited areas of thickening and punctiform or arborescent congestion with softening and even detachment of the epithelium.

The abomasum is profoundly involved, especially in the vicinity of the pylorus. The folds are of a deep blood red or purple, or blackish, port wine hue, or they may be in part brownish red, or when necrotic, slate colored or mottled. The peptic glands are swollen, elevated and dilated, and patches and spots of softened and loosened epithelium are easily detached leaving a deep red surface with, it may be redder oozing points. Ulcerous sores may show on the summits of the folds. The contents are a viscous, fœtid grayish yellow, or reddish liquid, without solid ingesta.

The small intestines show similar lesions, deep, dark red congestions, most intense on the summits of the folds, softened, loosened, ragged patches of epithelium, erosions, ulcers, circumscribed sloughs, casts of the gut formed by desquamating epithelium, and congested, enlarged, and prominent aguimated and solitary glands are more or less in evidence. The contents are liquid and yellowish, grayish or reddish and fœtid. Microscopically the distension of the glands, (of duodenum, Lieberkuhn and Peyer), the proliferation and softening of the epithelium, the enlargement of the nuclei of these and of the cells of the submucosa, and the profusion of microörganisms are marked features.

In the cæcum and colon the lesions are usually less prominent, though swelling, softening and desquamation of the epithelium often exists, and points and patches of congestion, ecchymosis, and necrosis are not uncommon, particularly in the cæcum, and may extend to the muscular layer.

The terminal portion of the rectum is especially liable to marked congestion and blood extravasation, with more or less desquamation and erosion. The summits of the mucous folds are often of a dark red (port wine) hue, and as this is everted and exposed in defecation or later by the relaxation of the sphincter it becomes a marked lesion even in life.

The spleen is normal in strong contrast with anthrax in which similar gross lesions are often found on the mucosæ and especially the rectum.

The liver is usually rather pale and soft, as in other cases of high fever and centres of necrosis may be present. The gall bladder contains a variable amount of thin bile. The pancreas is nearly or quite normal. The lymph glands generally and especially those of the mesentery and abomasum are congested, enlarged and softened.

The kidneys are congested, often petechiated, swollen and softened, with centres of necrosis. The bladder, vagina and uterus show mucous congestion, and thickening uniformly or in spots with muco-purulent secretion.

The lungs show spots of hyperæmia, extravasation and at times hepatization, but a very characteristic lesion is the interlobular emphysema already referred to as connected with the abdominal pain and the sudden arrest of inspiration. This gives a gross appearance of marbling as in lung plague, only in this case the inflated interlobular tissue is dark colored instead of white as in lung plague, and it collapses at once when incised.

The encephalon, medulla and nerves present more or less hyperæmia and even exudation.

The heart is usually pale except in the spots infiltrated by blood, but it may be mottled with petechiæ and particularly on the endocardium. The pericardial fluid is often red. The blood is at first little altered, but later undergoes marked changes, notably an increase of fibrine (50 per cent.) and a decrease of water (as in Asiatic cholera). There is marked leucocytosis, and distortion of the red globules. Before death it becomes black and incoagulable.

The whole capillary system tends to be relaxed and over-distended (congested).

Incubation. As seen in England the incubation was from four to five days. Four to nine days are claimed by Galtier as the extremes, yet he quotes incubations apparently as short as 12, 24, 36 and 48 hours respectively. A source of fallacy rests in the prevalence of cattle plague in the district and the possibility of infection through unsuspected channels, before the recognized exposure. Something must also be allowed for the greater susceptibility and the larger dose of the poison which would tend to shorten the incubation. Thus the western improved breeds, which suffer a mortality of 80 to 95 per cent. (Refik Bey), and the winter season, when the virus is concentrated in small ill ventilated houses, both tend to shorten the incubation. At the Albert Veterinary College in 1865, Gerlach went direct from the infected stable to the sound one, and in 48 hours several of the cattle in the latter had a manifest rise of temperature. Roloff observed the elevation of temperature in 36 hours after exposure, and Ranpach and Ravitsch as early as 11 hours after the inoculation.

Symptoms. The earliest symptom is abrupt hyperthermia, (104° to 108° F.). This is virtually pathognomonic in a herd or locality in which the disease exists, or in suspected animals presumably coming from an infected region. The temperature usually rises to its height on the third or fourth day, and falls materially when other symptoms are developed. In some instances death supervenes during the high temperature, but in the majority the temperature goes below the normal before death.

Often on the second day, or the third, white epithelial eruptions or concretions appear on the inner sides of the lips, closely resembling the eruption of muguet (thrush) and often showing also on the dental pad of the upper jaw and along the gums of the lower. In connection with the high temperature, which is absent in thrush, this symptom is virtually pathognomic. These concretions are more or less abundant in different cases, sometimes so slight as to be easily overlooked, and in other cases encreasing up to the sixth day, and covering not only the lips, dental pad and gums, but extending back over the hard palate, pharynx and gullet. The concretion is as soft as cream cheese, easily detached and leaves a bright red abrasion (not ulcerated) when removed.

By the fourth day there are dry or staring coat, sometimes rigors, sometimes small, accelerated pulse (60 to 120 per minute), some loss of appetite and impairment of rumination, dry muzzle, a general flush of the mucosæ (mouth, vagina, rectum), and deep blood red discoloration of many of the buccal papillæ. There is weariness or debility, the animal remaining down much of the time, also marked thirst, constipation, the fæces covered with mucus or blood, rapidly advancing emaciation, and marked tenderness of the skin, especially of the loins. The head and ears are drooped, saliva drivels, the mouth has a fœtid odor, the eyes weep, and there may be grinding of the teeth. The skin may be hot and the white and delicate parts (udder, teats) suffused by a deep blush. The milk is decreased at first and finally completely dried up.

As the malady advances the belly becomes tender, the constipation is succeeded by diarrhœa with much attendant rumbling, the fæces are at first watery, greenish and acid, and later highly offensive, yellowish brown or gray, and alkaline. These become encreasingly profuse, fœtid and liquid, assuming perhaps a pea soup or rice water consistency before death. The sphincter, at first firm and quickly responsive, finally undergoes permanent relaxation, with constant exposure of the dark red mucosa.

When the disease is fully established the respirations often become highly characteristic. There is not the sudden catching and shortening of the inspiration as in pleurisy, but a sudden closure of the glottis with an audible clicking sound in the course of the expiration, and, after a perceptible interval of holding of the breath, the expiration is resumed with or without an accompanying moan. This phenomenon is so characteristic as to be largely diagnostic. Whether it is due to abdominal pain roused by the sudden forward movement of the diaphragm, or to nervous disorder alone, it is a valuable symptom always to be looked for. It further explains the interlobular emphysema usually met with in the lungs in this disease.

In the more violent cases death supervenes from the sixth to the ninth day, but in the indigenous breeds of Eastern Europe and Asia, which represent a survival of the fittest, the great majority suffer mild attacks and recover, and even in newly invaded countries, when the invasion has spent itself and the less susceptible are largely attacked, a fair proportion survive for a longer period and even recover.

In these milder, protracted, or surviving cases the skin symptoms are likely to come out prominently. Chief among these and very constant at the height of the disease is an abundant unctuous exudation which dries on, forming a crust, comparable to what is seen on the skin in the fevers of swine. At different points, notably on the teats, udder, inner sides of the thighs, and arms, and on the neck, lips and face generally, are epidermic concretions having a warty-like appearance, and respectively seated on a very slightly swollen and congested point of the dermis. The deeper layers of these epidermic concretions often soften, so that they have been mistaken for vesicles and pustules, and hence the error by which cattle plague was held to be but a malignant form of cowpox. But these concretions are histologically distinct from vesicles; there is no liquid exudate on the papillary layer raising the epidermis in the form of a little sac, but merely an excessive production of the cuticular cells with abnormally large nuclei, as happens generally to cells in active proliferation, and an admixture with those of spores and mycelium of fungi which have no special significance.

Papules, vesicles and pustules may form on the diseased skin and are described by different authors, but they are not characteristic of the disease as are the epidermic proliferations.

In some rare cases nervous symptoms appear, the animal moves unsteadily without proper sense of balance, it may toss its head and horns as if attacking an enemy or it may sink into a somnolent or comatose condition. Wasting advances rapidly, abortion occurs in pregnant females, the weakness becomes extreme, the animal remains constantly down, unable to rise, rests his head on the ground, breathes heavily and stertorously and perishes with or without convulsions.

Diagnosis in Cattle. Individual symptoms of cattle plague may be found in other diseases, but the aggregate symptoms, in a rapidly spreading and fatal affection, and connected with a previous prevalence of the disease in the country or district, or distinct evidence of the introduction of infection should in every case obviate error. The chief diagnostic symptoms are: a sudden, very marked rise of temperature; a congestion or blush of the visible mucosæ generally (mouth, nose, vulva, eyes); the formation of white curd-like epithelial concretions on the inside of the lips, dental pad, or gums of the incisors; the formation of red spots or petechiæ on the mucosæ; later the desquamation of the softened epithelium with the formation of erosions or even ulcers; the wart-like rounded epidermic eruptions on the skin; the great abdominal tenderness with tucking up of the abdomen, and sudden arrest of the expiration with a sharp clicking sound and moan; the fœtid, watery diarrhœa and exposure of the dark red, congested and hæmorrhagic rectal mucosa; the discharge from nose, mouth and eyes; the characteristic fever odor; and the rapid progress of the disease from animal to animal, and to a fatal issue. The rapidly advancing contagion and its fatality in cattle, sheep and goats, together with the immunity of horses, dogs, birds and human beings are important elements in diagnosis.

Malignant Catarrh of Cattle is distinguished by the absence of active contagion, one or two only in a herd being attacked; by the absence of the curd-like concretions on lips, dental pad, and gums; by the involving of the matrix of the frontal horns; by the great congestion, swelling and discharge from the eyes; and by the impossibility or improbability of the cattle plague contagion in the particular locality. In localities where cattle plague actually prevails, it may sometimes be impossible to distinguish at first, and then every precaution should be taken to prevent diffusion of infection in case it should be cattle plague.

Thrush of the mouth, though causing an eruption of the same kind, occurs in sucklings only, is unattended by fever, marked congestion, or severe abdominal symptoms.

Foot and Mouth Disease, though equally contagious, and spreading with the same rapidity, is easily distinguished by the very slight hyperthermia, the vesicular character of the mouth and mammary eruption (the cuticle being raised by an abundant clear straw-colored liquid exudate); by the absence, in nearly all cases, of severe abdominal disorder; by the all but constant vesiculation of the interdigital space, and by its mild and non-fatal issue. Swine contract it as readily as cattle and sheep, and horses, dogs, birds and men by inoculation.

Dysentery is marked by the absence of the early, abrupt hyperthermia, though the temperature may rise gradually to a high point; also of the curd-like concretions on the buccal mucosa; by the earlier onset of the fœtid diarrhœa, and by the indisposition to contagious diffusion apart from the confined, foul, crowded buildings. The lesions are mainly on the large intestines while in cattle plague they are on the small intestines, fourth stomach, mouth, throat and skin.

Gastro-enteritis and Stomatitis from corrosive agents and irritant bacteria, can be traced to a definite local cause, do not extend beyond the herd or animal poisoned, and usually occur where the possibility of cattle plague can be excluded. There is usually an entire absence of the white epithelial concretions, of the blush of the mucosæ generally, and of the wart-like epidermic proliferation.

Anthrax of the alimentary tract and rectum is distinguished by the fact that it is largely an enzoötic disease, not spreading widely by simple contact; that it is easily transmissible to horse, dog and man; that it lacks the buccal epithelial concretions and characteristic desquamations and the warty-like skin products; that it shows marked enlargement and engorgement of the spleen; and that the blood and local lesions contain the large sized, square ended anthrax bacillus.

Diagnosis in Sheep and Goats. This is based on the same phenomena as in cattle; the sudden and exalted hyperthermia, blush or petechiæ of the visible mucosæ, concretions on the lips, gums and skin, epiphora, salivation, prostration, emaciation and diarrhœa. These last symptoms are, however, less marked than in cattle and the mortality and infectiousness are materially reduced. Pneumonic complications are much more common in sheep.

Mortality. Among native cattle in the Steppes the mortality is 30 to 50 per cent. whereas elsewhere it is 90 to 95 per cent. Among sheep in Austria it reached 60 to 66 per cent. Among camels in Asia and Africa the fatality proved as high as among cattle. The Italian buffalo usually recovered after seven days illness.

Treatment. The therapeutic treatment of cattle affected with cattle plague has been eminently unsatisfactory and is so certain to become a means of extension of the disease that it is legally prohibited in all countries, in which the plague has not been allowed to become generally diffused. Where it has become general in an unfenced country in which accordingly its permanence is virtually ensured, it may be employed.

Serum-therapy is advocated by Refik Bey. An animal is hyper-immunized by repeated inoculations. His blood is then withdrawn and the serum obtained from it is injected in a dose of 25cc., subcutem, at a temperature of 104° F. The temperature is taken from the 3d to the 5th day and if it does not at this time rise above normal the treatment is ended. If still above normal a second dose of 25cc. is given. It is claimed that the serum is harmless and may be safely given in a single dose of 50cc. in case it is impossible to keep watch of the animal for five days.

Prevention by Immunization. Semmer attempted this by inoculating cattle with virus which had been weakened by heat or by passing it through the body of a Guinea pig. The results were, however, far from perfect and even in Russia the method failed of any wide acceptance. Koch and Edington in South Africa practised extensive inoculations with a mixture of the virus in bile. Still better results are claimed by Danyoz, Bordet and Theiler in the Transvaal. These treated the animals by injecting 25cc. to 50cc. of highly immunized blood, defibrinated, and while the subjects were thus rendered temporarily insusceptible, they were exposed to infection by contact with diseased animals.

As with serum-therapy, measures of this kind are only permissible in a country in which cattle plague is already generally diffused, and where there are no fences to limit the continued diffusion of the infection. The preservation of the cattle artificially infected until highly immunized, and again of the sick cattle requisite to give the disease to the cattle operated on, and finally of these last through the mild attacks that are to render them immune, affords an endless number of loopholes for the escape of contagion which would forbid the adoption of the method whenever the extinction of the disease is possible. When on the other hand a disease is already spread universally in a country destitute of fenced enclosures, in which herd mingles with herd in the most perfect freedom, and where accordingly extinction is impossible, the method is admissible and even commendable as a means of reducing the otherwise ruinous mortality.

Exclusion and Extinction of Cattle Plague. For countries adjoining lands infected with cattle plague such general measures as the following are imperative: Prohibition of all imports of cattle, sheep and other ruminants, camels and swine from such infected countries, also of the fresh hides and other products of such animals, and of litter, fodder and other things that may have been stored in the buildings with infected cattle or otherwise soiled by them. Prohibition of imports of all cattle or other ruminants from adjacent countries (which may be plague-free), but which animals have been carried in undisinfected cars or boats that had been in previous use for such species of animals drawn from infected countries, or that had been passed through infected countries, yards, buildings, loading banks, chutes, piers, gangways, or other places, or furnished with fodder, halters or appliances from such infected localities. In Eastern Europe the practice is to patrol the frontiers day and night to prevent the smuggling of cattle through from the infected country. Infected animals or herds, that it is sought to pass, are turned back or slaughtered. Sheep from countries that had been previously infected are often admitted on affidavit of the official veterinarian in the country from which they come, that during the three months before they left, there had been no contagious disease of cattle nor sheep in the locality, and on the further condition that they shall be slaughtered at the point of entry, or, if brought by rail, at the nearest slaughter house approached by such railroad after entry. In France, sheep, sent from Russia by sea, in French bottoms, certified as above by the Russian authorities, and accompanied on the voyage by a French veterinarian and certified sound by him, are allowed to circulate freely after three days detention at the port of arrival without evidence of disease.

In the United States the 90 days quarantine of cattle (dated from the time of shipping at the foreign port), and the 15 days for sheep and other ruminants under strict veterinary supervision is safe as regards the importation of cattle plague in live animals. The greatest danger will doubtless come from intercourse with the Phillipines, which were infected with the cattle plague during the recent war. The greatest possible precautions as regards the carriage of cattle on transports or other ships, will be necessary. Not only should no Phillipine cattle be imported, but no vessel, that has carried Phillipine cattle or sheep, should be allowed to take on board home cattle nor other ruminants until it has been thoroughly disinfected.

Cattle or sheep should be rejected when imported on ships which, on the same voyage or a recent one, carried fresh hides or other fresh products of animals, derived from a country in which rinderpest exists.

Hides that are thoroughly dried and salted, those that have been freely exposed for one week to the sun and air, and such as have been treated by active antiseptics, (caustic quicklime, mercuric chloride, lime chloride, formalin, phenic acid, etc.), need be held under no such restriction. The same applies to thoroughly dried, sunned and aired hair, wool, hoofs, horns, bones and sinews. Rendered tallow is equally safe.

Extinction of Cattle Plague in a Country. This should never be called for on the American Continent. The introduction of such a deadly disease, with such a short period of incubation, and such severe symptoms and rapid course, would argue a most reprehensible carelessness, which it is to be hoped will never be shown by the Federal Bureau of Animal Industry. Yet under the stress of a great European war this plague invariably overleaps the barriers successfully maintained in time of peace, and the same has happened to the two great English-speaking powers in connection with the wars in South Africa and the Phillipines respectively and therefore it cannot be said that importation is impossible under any possible circumstances.

In case of a recent importation the infection would be easily controlled. Trace at once to its destination every bovine animal and other ruminant that arrived on the infected vessel, and all that came in contact with them since, or with the gangways, wharfs, streets, highways, yards, houses, fields, cars, loading banks and other places and things that might have been contaminated; stop all cattle and sheep traffic or movement for a large area around each centre of possible infection caused by such cattle; remorselessly kill every head of such animals carried by such vessel, or that came in direct contact with them; bury, burn, boil or dissolve in mineral acids, every animal thus exposed; thoroughly disinfect the importing ship, and every house, place or thing the imported stock came in contact with, together with all the dejections and debris, and even the surface of the graves; make a census of all cattle within the different quarantined areas, and hold the owners or custodians responsible, under a heavy penalty, to report every death and every case of illness; whenever the cattle plague is found in a place dispose of the entire herd as has already been done with the infected imported stock, and in a very few weeks the plague can be completely extirpated. The violence of the individual attack, and the very short period of latency, makes the work incomparably easier than the extinction of lung plague. There is never a long period of uncertainty (incubation), there is virtually never a slight or occult case of the disease, there is no equivocal chronic form of the affection. The attack is made boldly and above board, and can be met successfully if met promptly and energetically. The danger in such cases lies, less in the nature of the disease, than in the army of foolish, even if well meaning, meddlers, who denounce the temporary interference of trade, the payment of indemnities to the cattle owners, the interference with private property, the destruction of valuable thoroughbred herds, the interruption of the dairyman’s business, the cost of disinfection, and a thousand other things, and who too often succeed in hampering and delaying action, until the infection has reached and spread over great unfenced territories thereby getting beyond control, or, short of this, has so established itself as to necessitate the outlay of a hundred thousand for every hundred that would have been demanded at first, and a long continued restriction of trade in place of the very transient interruption required by early, sharp, decisive action.

One of the most important prerequisites is that every state, but especially those on the seaboard and with ports of entry, should enact such laws as would make it possible for the Executive to act at a moment’s notice and to call in the help of the Federal Government to make an early and effective application of the only successful remedy. Most things can wait for the call, assembling and action of a legislature; the infection of cattle plague can not. Such laws are not superfluous. If never called for they still show a wise provision against a terrible, though remote, possibility; if really called for and they are not found ready, the great cattle industry and even the agriculture of the continent may be largely sacrificed by the neglect.

As guardian of the interests of The Philippines the United States is to-day called upon to consider the question of exterminating the disease which our interference brought upon the islands. On the unfenced lands of these islands we have to face on a smaller scale the problem of stamping out the plague which has baffled the wisdom of Europe and Asia. The individual islands may perhaps be taken independently, the cattle collected in small herds under fence, and by the sacrifice of a few the remainder of any herd that shows infection may be immunized, and the premises where they are confined disinfected until finally no more cases occur. But whatever method is adopted the seclusion of all within well fenced areas is the most important consideration. No nation has ever succeeded in extirpating this nor any other important infection in animals when they are allowed to run at large and mingle freely, herd with herd, on unfenced land.

PICTOU CATTLE DISEASE. HEPATIC CIRRHOSIS.

This is a fatal affection of cattle met with in the counties of Pictou and Antigonish, Nova Scotia, which seems to make a slow extension from farm to farm, but does not spread widely after the manner of a disease propagated by contagion alone, apart from other concurrent causes.

Alleged Causes. E. F. Thayer (1880) tells us that the inhabitants traced its origin to the arrival from Scotland, about 1853, of a ship in earth ballast, containing the seeds of the common ragweed of Europe (Ambrosia Artemisiæfolia), alleging that the trouble extended with the extension of this weed. This plant has a strong odor (it is known in Pictou as “Stinking Willie”), and, like other plants shedding an abundance of odoriferous pollen, has been charged with arousing “hay fever,” but though very common in Europe it has never been charged with producing anything like the Pictou cattle disease. The coincidence of the plant and the disease is manifestly a mere accident. Professor Lawson, of Halifax, investigated the flora of the district but was unable to find any poisonous plant to which the mortality could be attributed. D. McEachran tells us that many farms are covered with the ragweed, so that it is abundant in the hay, yet they are absolutely free from the disease.

The idea of a mineral poison must be dismissed in the same way. Pictou lies on the Silurian formation with abundant coal fields, and the chemical analyses made for McEachran were entirely fruitless of results.

Wyatt Johnston investigated the question of communicability by contagion from animal to animal, but he found that neither contact, nor inoculation produced positive results. Nothing positive has come of investigations into the possible microbiology of the disease. In blood from the jugular vein of a cow suffering from the disease, Thayer and McEachran found bacteria, under an object glass magnifying 600 diameters. Wyatt Johnston, “in a series of pretty exhaustive bacteriological examinations, in which all the tissues, including the blood, the spleen, the kidneys, lungs, and the fluids from the lymph glands” were employed, failed to find any constant or characteristic organism.

Attacks are very rare in winter, the disease usually appearing in the warm summer months, from June to August, and after the animals have been some time at pasture. This might lead to the suspicion of bacteria or other microbe on the growing vegetation; or of some insect enemy which, maturing at that season, transfers the poison from animal or other source to animal; or of some poison, vegetable or mineral, which acts injuriously on the liver, and which can only be had in the pasture. This, however, is mere hypothesis.

Liver affections are common in hot, damp seasons, but Pictou and Antigonish do not differ in climate from other counties in Nova Scotia, and much less do the infecting farms from those adjacent.

McEachran compares the disease to what occurs in the human being during famines, from the ingestion of innutritious and unsuitable agents especially deficient in albuminoids. The Pictou farmers, being nearly all fishermen, neglect the farms during the summer season, so that hay is only cut after the seeds have been shed, and when little nutritive matter is left in the stalks. Almost all the cases he saw were on such neglected farms. Wyatt Johnston, however, found it equally prevalent in overfed animals, so that hepatic disorder from either extreme seems to conduce to it. Again, if caused by lack of nutrition in the hay, winter, rather than summer, ought to be the season of attack and prevalence. Starvation and excess may both favor the attack, but the gradual extension from farm to farm, is strongly suggestive of the presence of a specific cause—probably a living organism.

The limitation of the disease to certain farms and even fields, and the cirrhotic condition of the liver remind one of the Schweinsberg disease of horses, and the lupinosis of sheep, in which the poison is evidently the product of cryptogamic or bacterial growth. With the damp, foggy climate of Nova Scotia, it would not be surprising if it should be ultimately shown that the source of the trouble is in a cryptogam which has as yet only invaded a given limited area. The winter immunity would be explainable on this basis. So also would be the statement of Wyatt Johnston that “When it attacks a new farm it affects chiefly animals that have been on the farm for two or three years. By the end of the second year it kills or attacks 10 per cent., and by the end of the third season it has practically involved all the old cattle which have been allowed to remain on the farm.” The hepatic disorder being a progressive one and probably due to the toxic products of fermentations carried on outside the animal body, a few only would show the morbid results at first, while later, with advancing structural changes in the liver, and an increase of the toxins that cause it, the number of sick animals would steadily increase.

Symptoms. The animal is at first dull and sluggish, with drooping head, lusterless eyes, staring coat, normal respiration and temperature, pulse often about 60 per minute, relaxed bowels and marked diminution of the milk secretion. The milk acquires a bitter taste and unpleasant odor. The pulse is usually full and soft, and the eyeballs may bulge visibly out of the sockets. The diarrhœa tends to encrease, the stools becoming liquid and black, yet in exceptional cases the bowels are confined for the first four or five days, or even permanently, appearing to be completely paretic. By the end of a week the abdomen becomes full and pendent with hollow flanks (pot bellied), or even rounded and tense, while manipulation and percussion show an abundant exudation into the peritoneal cavity. The pulse encreases in frequency (80) but the temperature is not elevated unless there is concurrent sepsis (Johnston). Thayer quotes an advanced case with a temperature of 105° F. He also notes obstinate standing, trembling of the muscles of the hind limbs, and complete suppression of appetite and milk secretion.

The disease is essentially chronic, often lasting a number of months. Many cases are doubtless slightly affected before external symptoms are manifested.

Lesions. If the disease has resulted in death there is usually marked emaciation, yet the abdomen is distended by accumulation of a clear yellowish fluid. From six to nine or more gallons may be present. The fat of the omentum, mesentery and sublumbar region has disappeared and the connective tissue is distended by a clear, amber-colored, watery fluid. The liver is the seat of marked changes. In the early stages it is congested and the gall ducts and bladder are filled to repletion with a thick, dark colored bile, which is further present in abundance in the intestines. In these early stages Johnston found cloudy swelling and opacity of the hepatic cells; somewhat later they had undergone distinct fatty degeneration. In the advanced stages, however, in animals that had been ill for two or three months, there was distinct fibrous degeneration, and compression and disappearance of the normal liver cells, in other words, a condition of marked cirrhosis, the result doubtless of the early congestion.

Johnston further notes the distension of the submucosa of the fourth stomach at intervals by a clear, viscid, liquid exudate, so that rounded swellings appear on the surface, and in some instances, after a month’s illness, distinct ulcers are shown upon the mucosa.

The lungs, pleuræ, pericardium and nervous system, are usually normal, unless in case of septic complication when petechiæ and circumscribed blood extravasations may be seen.

Prevention. The Canadian government has gone to great expense in buying and slaughtering the diseased cattle with no very evident good result. McEachran suggested the feeding of oil cake and other albuminoid and oleaginous food to counteract the alleged malnutrition, but Johnston’s cases in over fed animals show that something more is demanded. Another suggestion has been made to the effect that cattle should be exterminated in the affected counties to remove the material necessary for the maintenance of the poison. But, if the poison is produced by a cryptogam growing on the vegetation, as seems not improbable, it would be likely to extend all the same in the absence of cattle. In such a case the true course is to study the nature of the organism, and the phanerogam on which it grows, when it might become possible either to exterminate the flowering plant which acts as a host for the offending organism, or to spray it with an effective fungicide and thus reach the object in another way.

INFECTIVE GASTRO-ENTERITIS AND PNEUMONIA IN THE NEW BORN; WHITE SCOUR.

In treating of this disease in Vol. II, page 141–2, the work of Jensen, Perroncito and Nikolski is quoted, with the remark that “it is premature to specify any particular microbe as the sole cause of the affection.” Since the publication of that volume, Nocard, investigating in Ireland a very prevalent and fatal affection of new born calves, which proved fatal by “white scour” a few days after birth, or by pneumonia one or two weeks later, identified as the pathogenic agent a small, nonmotile, ovoid bacterium, taking the polar aniline stain, bleaching in Gram’s solution, failing to liquefy gelatine, or to form indol or to grow on potato. In other words it shows the general characters of the colon group of bacteria, causative of hæmorrhagic septicæmia, and classed as pasteurellas by Trevisan and Lignieres. This is not found in blood and lesions in all subjects, but is usually present in pure culture in the most acute, fatal cases. Its occasional absence later in the disease is explained, according to Lignieres, by the power possessed by these germs of robbing the healthy tissues of their power of resistance and laying them open to the attacks of other microörganisms which are usually present in abundance, but are harmless to the healthy tissues in the absence of the Pasteurella. As the disease advances, therefore, the primary pathogenic agent (the Pasteurella) is crowded out by the active growth of other bacteria, which accordingly are found in complex cultures and in great variety. In his first observations on the victims of the white scour, Nocard found only these complex cultures, of which no one variety, isolated in pure cultures in vitro, and inoculated, proved capable of causing the disease. Later he found the Pasteurella (cocco-bacillus) in impure cultures from the diseased femoro-tibial joint of one of the subjects of the affection, and the pure cultures obtained from this were virulently infective.

A few drops injected into the peritoneum of a Guinea pig, or veins of a rabbit, killed in six to eighteen hours with the lesions of hæmorrhagic septicæmia which characterize the most acute cases of white scour. The blood and viscera swarmed with the microbe.

A calf one day old had 3cc. of the culture injected into the jugular, the temperature rose in six hours, and in twenty hours the subject lay with sunken eye, retracted abdomen, a temperature of 95° F., and having the bed saturated with a yellowish, fœtid, fæcal liquid. Death took place 30.5 hours after the injection and all the lesions of acute white scour were met with.

A second calf four weeks old, which had already suffered from white scour and recovered, had an injection into the jugular of 10cc. of the same culture. In six hours he suffered a slight rise of temperature, was dull and breathed short, but in twenty hours he was completely recovered, full of life and appetite.

In other casual and experimental cases, Nocard found that when death occurred within one or two days the symptoms and lesions were mainly those of hæmorrhagic septicæmia and white scour, whereas if the calf survived several days, the impaired resistance of the tissues invited the invasion of a variety of other germs from the intestines, and infective inflammation of the lungs, joints and other organs were brought about by such secondary invasions.

An important question is as to the direct source of the primary (Pasteurella) infection. The concentration of the acute cases on the alimentary canal would strongly suggest infection through the food which in this case means the milk. But careful bacteriological examination of the milk of the dam of a calf that had just died of white scour, and of other milk secured with careful precautions from cows in an infected stable, showed that both were clear of the germ. Inoculations and culture experiments were equally fruitless.

This does not exclude the probability of the contamination of the milk, obtained under ordinary conditions, with the germ contained in the floating barn dust, or that which was adherent to the teat and udder.

Another suggestion is that the infection is derived from the infected womb prior to birth, but as Nocard justly says, if this were so, abortions would be much more prevalent, as the rapidly fatal issue of the disease would determine the prompt death of the fœtus and its expulsion. The coincidence of abortion and white scour in a herd is not uncommon, and in such cases intrauterine infection of the fœtus is not improbable, but in the great majority of cases no such coincidence exists.

We are thus thrown back on infection through the raw surface of the ruptured umbilical cord, as the rule in such cases. It may be that this has come from the vagina or vulva, but in the great majority of cases it is manifestly derived from the infecting bowel dejections and the dust caused by their desiccation. The extraordinarily rapid progress and fatal result of the acute disease, and the early abundance of the germ in the blood and liver, suggest that the microbe traverses the umbilical vein to the liver, and finding a congenial home in the blood is quickly distributed through the entire body.

Prevention must be based on the destruction and exclusion of the microbe.

A thorough disinfection of the stable with mercuric chloride has not given us uniformly satisfactory results, even when the building has been kept apparently almost immaculately clean. This argues a renewed infection through the fæces of the cows, yet it is the rule that the removal of the cow to a new or unused stable a few days before calving will usually secure the immunity of the calf. This method is however open to the objection that the removal to such calving stable of a succession of cows coming from infected premises soon introduces the infection and renders it as dangerous as the place they have left. To carry out such a plan therefore a number of new stables or sheds must be provided to be used in succession, as they become one by one contaminated.

Nocard confines his instructions to the antisepsis of parturition and of the offspring:

“Cows ready to calve should be provided with dry and clean bedding until after the birth of the calf.”

“As soon as labor sets in, the vulva, anus and perineum should be cleaned with a tepid solution of lysol in rain water: 20 grammes of lysol to each litre of water. The vagina should also be cleansed by injecting with a large syringe a great quantity of the same solution tepid.”

“As far as possible the calf should be received on a clean cloth or on a thick fresh bedding, not soiled by urine or fæces.”

“The cord should be tied immediately after birth, with a ligature kept in a lysol solution, and the cord amputated below the ligature.”

“The stump of the cord and the umbilicus should be washed with the following solution:

Rain water 1 litre. Iodine crystals 2 grammes. Potassium iodide 2 grammes.”

“The disinfection of the umbilicus and cord should be completed by coating them with

Methylic alcohol 1 litre. Iodine crystals 2 grammes.”

“When the alcohol has evaporated the cord and umbilicus should be covered with a thick layer of iodine collodion (1 per cent.) applied with a brush. When the collodion has dried the calf may be left to the care of the dam.”

This treatment may be changed by substituting other antiseptics, and by prompt separation of the calf from the infected stable and dam. It is also important to disinfect thoroughly and often the cow stable and calf-pen, to remove instantly any calf that may show signs of scouring or general disorder and to purify its pen and leave it unoccupied for some time.

It should be added that the period of danger is in the first few days after birth, and while the umbilicus is still unhealed. If scouring should come on later it is much more amenable to treatment. A seclusion of the calf for one week is usually sufficient to secure its escape.

NOTE ON BACTERIOLOGY AND TREATMENT OF HÆMOGLOBINÆMIA IN THE HORSE.

As supplementary to the article on hæmoglobinæmia (vol. II., page 437) the later bacteriological investigations of Lignieres must be noted. A superb Percheron, after two days of idleness, went to work at 10 P. M., was attacked at 1 A. M. and died at 3 P. M. Inoculations from blood, spleen, liver, kidney, bone marrow, myelon and subarachnoid fluid from the loins to the bulb proved sterile, excepting that made from the subarachnoid liquid on a level with the bulb, which yielded a rich culture of a streptococcus that appeared to the eye as small granules. It proved ærobic and anærobic, stained well with Gram’s (I) solution, coagulated milk, acidified the culture, formed small, round, grayish white colonies on peptonized gelatine, without liquefying, failed to propagate on potatoes, but grew well in serum and bouillon.

Two or three drops proved fatal to mice, producing, when thrown into the peritoneum a highly acute parenchymatous nephritis with bloody urine. Very few microbes were found in the kidney. There was loss of control of the hind limbs and extreme nervous irritability.

Intravenous injection of 300cc. of the culture in a powerful stallion produced hyperthermia, 102° F. on the second day, 104° on the third, 105° on the fourth, on the sixth day he became paraplegic and died on the seventh.

A second horse, which received 150cc., was sick for several days, but without paraplegia, then appeared to recover, but three weeks after he became paraplegic with albuminous urine and died next day.

In neither of the horses was the urine sanguineous.

Carnivora, swine, ruminants and birds proved insusceptible. The guinea pig succumbed to intraperitoneal inoculation, and the rabbit to intravenous.

It is to be noted that hæmoglobinuria was lacking in both experimental equine cases, and though this may be so in mild casual cases, the same is not true of violent and fatal ones. It is, therefore, evident that further research is necessary in this direction.

Accepting the conclusions reached by Lignieres, we are still debarred from entering the affection in the list of animal plagues proper, to be met by official restrictions. The streptococcus may be an essential condition in each case of the disease, or it may be one of several microbes that may act in the causation, yet the microbe in ordinary doses as accidentally introduced, does not prove pathogenic excepting in the presence of concurrent conditions of high feeding and condition, work, interrupted by one or more days of absolute idleness, and the resumption of exercise. The presence of the microbe is not enough to cause the disease in the horse in continuous work, nor in that which is kept in the stable all the time, nor even in the horse that has worked steadily and then stood idle for a day, until he again goes to work. One animal or a few only out of a stable, are attacked, and there is no such active extension from animal to animal in the vicinity that characterizes the plagues proper.

The prevention of the disease, therefore, must be sought along the lines previously laid down and well understood, in the avoidance of sudden plethora, of transient idleness during a period of high condition and steady work, and of gradual restoration to work after such period of rest. Similarly the treatment by rest, depletion, diluents, evacuants, and nerve sedatives is still in order. A new importance, however, attaches to the use of nerve sedatives and antiseptics, as calculated to prove a check on the disorder of the nervous structure and functions and on the active proliferation of the microbe.

The presence of the streptococcus may also contribute, along with the permanent changes in the nerve structure, in predisposing to relapses or second attacks, which are so common unless the animal which has once suffered is subjected to very special care.

As a fruit of the research by Lignieres, W. A. McClanahan, Redding, Ia., essayed internal antisepsis by ½ oz. doses of potassium iodide. In three severe cases relief was obtained in 15 to 20 minutes and an early and complete convalescence followed. In the hands of J. H. Kelly of New Haven, Conn., and T. S. Childs of Saratoga, N. Y., it seemed to prove equally successful, the first meeting with almost invariable success, and the latter reporting a series of 10 successive cases, several of them severe, which all recovered in from 1 to 5 days. The only untoward result was an open knee joint in one subject, the result of bruises sustained before Dr. Childs arrived. His treatment was ½ oz. of the iodide at once, and 1 to 2 drs. every hour or second hour, according to the size of the animal and the severity of the case.

In other hands this medication has been less successful, which may well be explained by the violence of the attacks, and the lack of absorption from the inactive stomach. Unless it passed on to the duodenum, it would be utterly useless, and hence the exhibition by the rectum or subcutem might be tried. The parallelism of the treatment of the two diseases of the plethoric and possibly infected subject,—parturient paresis and hæmoglobinæmia,—is striking, and it does not seem that the iodide treatment should be abandoned because of a few unsuccessful cases. Whether the iodide acts mainly as a microbicide, a chemical antidote to toxins, an eliminant, or a nerve sedative, or in two or more of these modes, is unknown, but it would be rational to expect good results along one or more of these lines. Iodide treatment should supplement, not supersede, the methods formerly in use.

INFECTIVE ULCERATION OF ANUS AND VULVA IN CATTLE.

This curious affection is recorded as having prevailed in the winter of 1897–8 in different localities in Iowa, Missouri, Kansas and Nebraska. In 1900 and 1901 it was again reported in different parts of Iowa.

Causation. No bacteriology of the disease has been given, and its appearance in isolated herds which had no known communication with other herds, and even in the young cattle on a farm to the exclusion of the older ones, seems to suggest an enzoötic origin, perhaps in food or water, or in some toxin determined by a fermentation of organic matter out of the body.

On the Rodkey farm at Blue Rapids, Marshall county, Kan., eight heifers from ten to fourteen months old, suffered, while the seventeen steers of the same age and the milch cows escaped. (Steddom). Near Shelby, Ia., a bull, from a healthy herd, broke into an affected herd and served cows there, and was afterward returned to his own herd and served cows there, but did not communicate the disease. (S. T. Miller). No case is recorded to show that any bull serving affected cows or heifers contracted ulcer or other disease of sheath or penis.

In one herd near Shelby, Ia., nineteen head of cows and heifers suffered, while the four steers in the herd escaped. In another herd of twenty-six head, in the same district, the four cows and eight of the twenty-two steers suffered. It is not, therefore, confined to the females. (S. T. Miller).

In all cases the disease appeared in the cooler months, from October to April inclusive, and while the cattle were secluded in muddy yards.

In different cases they occupied the yards in common with swine which were charged with wounding the vulva, until the general character of the outbreak forbade this conclusion. At Blue Rapids it was sixty-two days after they had been yarded with the hogs before the disease was observed.

In this case the lot was small, poorly drained and very muddy most of the time. Calves and hogs drank from the same troughs until the disease appeared. The water supplied to the calves and hogs was from a well sixteen feet deep. The cows, which escaped, were supplied with water from the Blue River.

Cows, heifers and steers were fed on a ration of shelled corn 6 parts, rye 1 part, oats 1 part, and had an abundance of fodder, consisting of prairie hay and millet in equal parts. They were in good condition, some of them fat, and nearly all dehorned. A second herd had shelled corn, kafir corn and cane, with water from a shallow well, and all (cows and heifers) suffered.

As showing the localized nature of the cause, C. Muller adduces the case near Ottumwa, Ia., in which a herd of 30 calves were attacked, and sold out, the owner filling the same yard a few days later with 30 more bought in the surrounding country, and which he put on the same rations. In about 10 days the disease appeared in the second lot.

On the Rice farm, Blue Rapids, were 60 yearling heifers, bought in Kansas City, and two home cows. In the first week after arrival 5 heifers suffered, in the second week 20, in the third week 40, and in the fourth week all the 60. The two cows mingling with them were only slightly affected.

In the Rodkey farm, Blue Rapids, cases, all of the young cattle (which alone suffered) had been raised on the farm and had not been exposed to outside cattle.

Symptoms. “The ulcer, in almost every case, started as a mere abrasion, the size of a pinhead, usually on the inner surface of the labia, near the border of the inferior commissure, gradually eating its way through until it appeared as a much larger denuded surface on the outside” (C. Miller). S. T. Miller says: “The first noticeable symptom was serous exudate, rapidly forming into a brown scab, under which was very fœtid pus, with extensive inflammation. The affection usually occurred on the lower portion of the lips of the vulva, in heifers and cows, and in steers around the anus or root of the tail. The scabs which formed seemed to spread very rapidly, destroying more and more of the underlying tissue and forming a thicker and thicker scab. The scab, if pulled off, would expose a raw surface which would bleed very readily. In a short time a new scab would be formed.”

Steddom says: “The vulvar lips thickened and continued to discharge for four or five days. In the meantime certain pustules appeared, 0.1 to 2.5 centimeters in diameter. About the fifth day these ruptured and discharged yellowish pus.” The mucous membranes of the vulva and vagina were dry and slightly congested. The ulcers were covered with brown leathery scabs, which adhered tenaciously and when detached left an angry, red, purulent, granular, elevated and pitted surface. In some of the more severe cases, one or both lips of the vulva had sloughed off, and the sore had extended 10 to 15 centimeters on the skin of the escutcheon. The pus from this sore did not corrode the adjacent skin.

The more severe cases showed loss of appetite, constipation, hurried breathing, tucking up of the abdomen, with general dulness and dejection, and great tenderness of the affected skin with stiff, straddling gait.

Pathology. This is very obscure. The primary cause of the sores is not evident, though their occurrence on the anus and vulva only, and especially on the latter would suggest an elective affinity of the poison (microbian or chemical) for these structures and their products. If we assume a pathogenic microbe in the fæces, the question arises as to the cause of the habitual immunity of the steer, and of the margin of the anus in the majority of the affected heifers. The susceptibility of heifers rather than cows may imply a previous exposure and acquired immunity on the part of the mature animal.

Again if we suspect the existence of a necrobiotic agent of organic origin (like ergotin, secalin, sphacelin) we must assume a superadded microbian infection, implanted in the primary sore and rapidly extending it. The prompt recovery under antiseptic treatment shows that no mere chemical poison maintains the destructive process, for it is manifestly the microbicide which puts a prompt limit to the disease, and under such treatment no sphacelating agent in the blood or tissues keeps up the advance of the ulceration or prevents healing.

Treatment. The ulcers healed rapidly under cleanliness and antiseptic applications. The tail, anus, and vulva were washed with tepid water, and then dressed with a solution of creolin (5:100), or carbolic acid (3:100), or mercuric chloride (1:500 or 1000). The ulcers were touched with a pencil of silver nitrate. S. T. Miller followed the sublimate lotion by the subjoined ointment: iodoform 20 grains, eucalyptol 40 minims, phenic acid 20 minims, petrolatum enough to make 2 oz. C. Miller in addition to the carbolic acid lotion applied the common white lotion (zinc sulphate 1 oz., lead acetate 1 oz., water 1 qt.) and used silver nitrate on the ulcers. Four dressings on four successive days were given and in the milder cases healing was completed in 10 or 12 days.

NOTE ON GOOSE SEPTICÆMIA.

As these pages are going through the press, Cooper Curtice’s bulletin on Goose Septicæmia comes to hand.

This affection in 1900 caused a loss of 3,200 geese in July and August to Mr. Cornell, a Rhode Island owner. Mr. Snell lost 500.

Bacteriology. The blood and tissues swarmed with a minute bacillus having the general morphological staining and biological characters of that of chicken cholera and rabbit septicæmia. It differed from these in the failure to infect chickens, whether inoculated or fed to them. It proved deadly to geese, ducks, pigeons, rabbits, mice, and more slowly to Guinea pigs. Geese were infected by inoculation or feeding of the germs, ducks from inoculation only.

Symptoms. The geese were often found dead, and even in those noticed ill, death supervened so early that no very diagnostic symptoms were made out. The affected geese moved tardily and unsteadily, and failed to keep with the remainder of the flock. Some burrowed the head in the dirt and twisted it around, indicating, it was supposed, spasms of the throat. Some were seized with the death agony in a few minutes; in others the illness lasted for hours, and from experimental cases it was concluded that the period from infection to death, in the majority of cases, did not exceed thirty-six hours. Some were believed to merge into a chronic condition, but the owner thought that none recovered. No diarrhœa is noted.

Lesions. The head was the seat of marked venous and capillary congestion, suggesting asphyxia. The bill and throat contained a large quantity of tenacious mucus, which was especially viscid in the nose. Extravasated blood in abundance was present in the gastro-intestinal mucosa and contents, much of it more or less digested. At some points there was abundant mucous exudate; at others the folds were only marked by punctiform petechiæ, or by bloody patches formed by their coalescence. The cæca were usually normal.

The liver showed numerous punctiform extravasations and yellow patches of necrosis extending more or less deeply into the hepatic tissue. Other congestions were seen in individual cases, implicating, in one instance, the heart and pericardium, and in another the lungs. Petechiæ were frequent on the pericardium and other mucosæ. The blood was usually black, tarry, and with little disposition to brighten on exposure to the air.

Diagnosis. It is recognized as an infection of domestic water fowl by its attacking the larger proportion of that class of animals exposed to it. It is supposed that those which escape do so because of immunity due to a previous attack, or by reason of the absence of any wound of the mouth, throat or stomach by which the germ might enter. It is distinguished from fowl (chicken) cholera by the immunity of the chicken in this case. It is differentiated from Klein’s diarrhœal enteritis of fowls, by the fact that neither pigeon nor rabbit is immune. From the duck cholera of Cornil and Loupet, it is diagnosed by the immunity of the chicken only, while the rodents and pigeon suffer.

The germ is manifestly one of the family of bacilli of the colon group, found in the different septicæmias, but sufficiently distinctive from these other forms, in its pathogenesis, to demand a separate place in connection with sanitary work.

Treatment is hopeless from our present point of view.

Prevention is the rational resort. In the case of those raising geese from the egg, it is imperative to abandon, for the season at least, any pastures that may have become contaminated. It would be better still to subject such pastures to cultivated crops for one or two years. The pens should be thoroughly disinfected or abandoned and burned. Mr. Cornell used his infected pens for ducks without evil result. The drainage from infected pastures or pens must be guarded against, no geese nor ducks being allowed on land through which, or on which it passes, and no water receiving such drainage being employed for geese. In the case of feeders or handlers of geese who buy the birds in large numbers from many sources, a subsidiary quarantine should be constantly maintained, by enclosing the birds in as small groups as possible in separate pens, so that infection in one pen will not endanger the whole flock. When infection is shown in a pen, the diseased birds should be at once destroyed and burned, the pen thoroughly disinfected, and the other birds returned, or better, divided up into still smaller lots, so that infection showing in one of these will not endanger the great number taken from the original infected pen. The utmost care should be taken to maintain the most perfect cleanliness in the pens of exposed and suspected geese, and to sprinkle the floors and manure liberally with an antiseptic, such as a solution of sulphuric acid in water (2:100), or of phenic acid (3:100), or of a combination of the two. This will do much to prevent the hatching of flies to act as infection-bearers, and if these can be further excluded by screens the condition will be still more satisfactory. Vermin of all kinds should be excluded and whenever possible, separate feeders and attendants should be furnished for the suspected geese, and those that have not been exposed.

NOTE ON HÆMORRHAGIC SEPTICÆMIA IN CHICKENS AND TURKEYS.

Lucet describes a septicæmia of chickens and turkeys accompanied by dysenteric discharges. The microbe resembles the bacillus gallinarum of Klein (see Vol. II, p. 254), even in the immunity of pigeons and rabbits when injected subcutem. Rabbits, however, suffer when injected intravenously. The probability is that this bacillus is identical with that of Klein. Yet in this whole class of microbes of the colon group, variations, apparently superinduced by environment, appear to result at times in a deadly pathogenesis for different genera, and epizoötics differing from each other.

DISEASES, INFECTIVE OR TOXIC, TREATED IN EARLIER VOLUMES.

=Catarrh; Malignant of Cattle.= Vol. I, p. 105. — =Chronic, Infective, Summer.= Vol. I, p. 104. =Anæmia; Pernicious.= Vol. I, p. 375. =Diphtheria in Calves.= Vol. II, p. 24. =Ulcerative Stomatitis of Swine.= Vol. II, p. 29. =Mycotic Stomatitis; Thrush in Sucklings.= Vol. II, p. 36. =Microbian Tonsilitis in Pigs.= Vol. II, p. 46. =Diphtheria of Pigeons and Chickens.= Vol. II, p. 67. =Dysentery of Cattle.= Vol. II, p. 240. =Infective Catarrhal Enteritis of Birds.= Vol II, p. 254. =Coccidian Enteritis in Cattle.= Vol. 2, p. 258. „ „ =Dog.= Vol. II, p. 261. „ „ =Rabbit.= Vol. II, p. 262. „ „ =Birds.= Vol. II, p. 263. =Cerebro-Spinal Meningitis.= Vol. III, p. 118. =Tubercle and other Infective Diseases of the Vertebræ.= Vol. III, p. 172. =Parturition Fever= (=Paresis=). Vol. III, p. 299. =Infectious Conjunctivitis in Herbivora.= Vol. III, p. 368. =Recurrent Ophthalmia.= Vol. III, p. 404. =Contagious Pustular Dermatitis in the Horse.= Vol. III, p. 505. =Rachitis.= Vol. III, p. 565. =Rarefying Osteitis.= Vol. III, p. 579. =Rheumatism.= Vol. III, p. 528.

INDEX.

Abortion and ergot, 371.

Abortion, contagious, 370.

Abscesses, secondary, their seats, 5.

Acute hæmorrhagic toxæmia, 141.

Adynamic catarrhal fever of the horse, 112.

Adynamic pneumonia, 95.

Agglutination test in diagnosis, 457.

Amœba Meleagridis, 388.

Anæmia in dourine, 524.

Anæmia, pernicious, 585.

Anasarca, 141.

Anasarcous toxæmia, 141.

Anthrax, 195.

Anthrax and protozoan cattle fever, 560.

Anthrax, apoplectic, 202, 206.

Anthrax, bacillus, 200.

Anthrax bacillus, vitality, 201.

Anthrax, causes, 197.

Anthrax, definition, 196.

Anthrax, differential diagnosis, 209.

Anthrax, disinfection, 213.

Anthrax, drainage of land, 220.

Anthrax, emphysematous, 181.

Anthrax, external, 203, 206.

Anthrax, forms of, 202.

Anthrax, fulminant, 202, 206.

Anthrax, geographical distribution, 196.

Anthrax, History, 196.

Anthrax, immunity after first attack, 198.

Anthrax, immunization from, 214.

Anthrax, immunization, modes of, 216.

Anthrax, imports restricted, 220.

Anthrax in birds, 208.

Anthrax, incubation, 205.

Anthrax in dogs, 208.

Anthrax, infection atria, 202.

Anthrax in horse, 207.

Anthrax in man, 221.

Anthrax in man, causes, 221.

Anthrax in man, forms, 222.

Anthrax in man, intestinal, 224.

Anthrax in man, lesions, 223.

Anthrax in man, prevention, 226.

Anthrax in man, pulmonary, 226.

Anthrax in man, treatment, 227.

Anthrax in sheep and goats, 207.

Anthrax in swine, 207.

Anthrax, interdiction of sales, 214.

Anthrax, internal, 203.

Anthrax, isolation, 213.

Anthrax, lesions, 203.

Anthrax, mortality, 211.

Anthrax, movement of herds, 213.

Anthrax œdema, 223, 225.

Anthrax, pathogenesis, 198.

Anthrax, prevention, 11.

Anthrax, prevention in animals, 212.

Anthrax, prognosis, 211.

Anthrax symptoms, 205.

Anthrax, synonyms, 196.

Anthrax toxins, 204.

Anthrax, treatment, 221.

Aphtha epizoötica, 316.

Aphthous fever, 316.

Apiosoma bigeminum, 545.

Apoplectiform septicæmia immunization, 397.

Apoplectiform septicæmia in chickens, 393.

Apoplectiform septicæmia, lesions, 394.

Apoplectiform septicæmia, pathogenesis, 396.

Apoplectiform septicæmia, symptoms, 394.

Argentina, Lombriz in, 65.

Arteritis and pyæmia, 4.

Aseptic fever, 8.

Asthenia in chickens, 392.

Asthenia in chickens, bacterium, 392.

Asthenia in chickens, pathogenesis, 392.

Asthenia in chickens, treatment, 393.

Australian tick fever, 543.

Avian and human bacillus of tubercle, Nocard’s experiment, 413.

Azoturia, bacteriology of, 649.

Azoturia in the horse, 649.

Babesia bigeminum, 545.

Bacilli in distemper, 168.

Bacillus anthracis, 200.

Bacillus anthracis emphysematosa, 183.

Bacillus Chauvæi, 183.

Bacillus choleræ suis, 24, 26.

Bacillus gastromycosis ovis, 510.

Bacillus liquefaciens bovis, 603.

Bacillus mallei, 233.

Bacillus of emphysematous anthrax compared with that of anthrax, 184.

Bacillus of emphysematous anthrax, vitality, 185.

Bacillus of malignant œdema, 11, 12.

Bacillus of Nicolaier, 293.

Bacillus of rouget, 20.

Bacillus of septicæmia hæmorrhagica in cattle, 56.

Bacillus of septicæmia hæmorrhagica in cattle, vitality of, 57.

Bacillus of septicæmia hæmorrhagica in sheep, 65, 70.

Bacillus of swine plague, 47.

Bacillus pestis suis, 47.

Bacillus tetani, 293.

Bacillus tetani, as a saprophyte, 294.

Bacillus tetani, toxins of, 295.

Bacillus tuberculosis, 410.

Bacillus tuberculosis, action of disinfectants on, 415.

Bacillus tuberculosis, biology, 411.

Bacillus tuberculosis, evolutionary forms, 412, 413.

Bacillus tuberculosis in diagnosis, 457.

Bacillus tuberculosis in man and cattle, 466.

Bacillus tuberculosis in man and ox, common features, 470.

Bacillus tuberculosis in salted meat, 414.

Bacillus tuberculosis, morphology, 410.

Bacillus tuberculosis of man rendered pathogenic to bird, 469.

Bacillus tuberculosis of man variable in potency, 468.

Bacillus tuberculosis, staining, 411.

Bacillus tuberculosis, vitality, 413.

Bacterium choleræ gallinaceæ, 159.

Bacterium coli commune, 27.

Bacterium of chicken asthenia, 392.

Bacteriology of septicæmia hæmorrhagica in cattle, 55.

Barbone, 55.

Bench show distemper, 181.

Bilious pneumonia, 95.

Blackhead in turkeys, 388.

Blackleg, 181.

Black quarter, 182, 55.

Black water, 543.

Blautong, 516.

Blitz catarrh, 113.

Blood clots, infective, 4.

Blood, relation to pyæmia of microbes and toxins in, 5.

Blue sickness, 23.

Blue tongue in horse, 516.

Bones, tubercle of, 436.

Boöphilus bovis, 548.

Boöphilus bovis as the cause of Texas fever, 548.

Boöphilus, dressing for, 564.

Boöphilus, its destruction on pastures, 564.

Bovine periodic fever, 543.

Bovine pleuro-pneumonia, 599.

Bovine yellow fever, 543.

Bradsot, 508.

Brain, tubercle of, 436.

Braxy, 508.

Braxy, causes, 509.

Braxy, definition, 508.

Braxy, geographical distribution, 508.

Braxy, its bacteriology, 510.

Braxy, lesions, 511.

Braxy, pathogenesis, 510.

Braxy, prevention, 512.

Braxy, symptoms, 511.

Braxy, treatment, 513.

Breeding paralysis, 519.

Brine poisoning of pigs, 39.

Broken buttock, 533.

Bronchitis, infectious stable, 111.

Brustseuche, 95.

Buffalo disease, 55.

Caderas, mal de, 532.

Calcified tubercle, 431.

Canine distemper, 165.

Canine madness, 260.

Carbuncular fever, 23.

Carceag, 573.

Caseated tubercle, 430.

Catarrhal fever, adynamic, 112.

Catarrh, infectious bronchial, in dog, 181.

Cattle lung plague, 598.

Cattle plague, 623.

Cattle plague, accessory causes, 628.

Cattle plague, bacteriology, 627.

Cattle plague, channels of infection, 628.

Cattle plague, definition, 624.

Cattle plague, gastro-intestinal lesions, 630.

Cattle plague, historic notes, 625.

Cattle plague, immunity, 628.

Cattle plague, lesions, 629.

Cattle plague, pathogenesis, 627.

Cattle plague, susceptibility to, 628.

Cattle, pulmonary tuberculosis in, 431.

Cattle tick, 548.

Cattle, ulcerative infection of the limbs in, 74.

Chancrous epizoötic, 519.

Charbon, 196.

Charbon blanc, 141.

Charbon symptomatique, 182.

Chauveau’s experiments on tuberculosis, 409.

Chicken cholera, 158.

Chicken cholera, accessory causes, 160.

Chicken cholera, bacteriology, 159.

Chicken cholera, diagnosis, 163.

Chicken cholera, distribution, 158.

Chicken cholera, history, 158.

Chicken cholera, immunization from, 164.

Chicken cholera, incubation, 161.

Chicken cholera, lesions, 162.

Chicken cholera, losses from, 159.

Chicken cholera, pathogenesis, 161.

Chicken cholera, prevention, 164.

Chicken cholera, prognosis, 163.

Chicken cholera, symptoms, 161.

Chicken cholera, treatment, 165.

Chicken pasteurellosis, 158.

Chicken typhoid, 158.

Cholera suis, 22.

Cimurro, 166.

Cirrhosis of the liver in cattle, enzoötic, 641.

Clavelee, 347.

Cocco-bacilli in distemper, 169.

Cocco-bacillus of contagious pneumonia of the horse, 99.

Cocotte, 113.

Consumption, 399.

Contagious abortion, 369.

Contagious abortion, accessory causes, 370.

Contagious abortion, acquired immunity, 380.

Contagious abortion bacillus of colon group, 377.

Contagious abortion, bacteriology, 376.

Contagious abortion, Bang’s bacillus, 377.

Contagious abortion, casual infections, 374.

Contagious abortion, definition, 370.

Contagious abortion, exclusion, 385.

Contagious abortion, experimental infections, 375.

Contagious abortion, extinction, 386.

Contagious abortion, immune infecting, 382.

Contagious abortion in mares, 384.

Contagious abortion, lesions, 383.

Contagious abortion, micrococcus, 376.

Contagious abortion, pathogenesis, 370.

Contagious abortion, pathology, 376.

Contagions abortion, prevention, 384.

Contagious abortion, symptoms, 383.

Contagious abortion, synonyms, 370, 372.

Contagious abortion, treatment, 384.

Contagious abortion, varieties, 377.

Contagious pleuro-pneumonia, 599.

Contagious pneumonia and influenza, 133–4.

Contagious pneumonia causes, 96.

Contagious pneumonia, convalescents infecting, 97.

Contagious pneumonia, definition, 95.

Contagious pneumonia, history, 96.

Contagious pneumonia in horse, 97.

Contagious pneumonia in horses, 95.

Contagious pneumonia in the horse, bacteriology of, 98.

Contagious pneumonia in the horse, course, 104.

Contagious pneumonia in the horse, diagnosis, 105.

Contagious pneumonia in the horse, immunization against, 110.

Contagious pneumonia in the horse, incubation, 101.

Contagious pneumonia in the horse, lesions, 100.

Contagious pneumonia in the horse, prevention, 106.

Contagious pneumonia in the horse, prognosis, 105.

Contagious pneumonia in the horse, quarantine for, 109.

Contagious pneumonia in the horse, serum therapy of, 111.

Contagious pneumonia in the horse, symptoms, 101.

Contagious pneumonia in the horse, treatment, 106.

Contagious pneumonia less diffusible than influenza, 97.

Cornstalk disease, 55.

Coronet, gangrene of, 76.

Coryza contagiosa equorum, 78.

Coryza gangrenosa, 141.

Cowpox, 340.

Cowpox, causes, 340.

Cowpox, course, 346.

Cowpox, diagnosis, 345.

Cowpox, prognosis, 346.

Cowpox, symptoms, 344.

Cowpox, treatment, 346.

Curtice’s smear for boöphilus, 564.

Cynolyssa, 260.

De Schweinitz, serum therapy in swine plague, 52.

De Schweinitz, serum treatment in hog cholera, 45.

Destruction of red globules, 553.

Diagnosis of septicæmia hæmorrhagica in cattle, 61.

Diagnosis of swine plague, 50.

Diastashemia, 141.

Dikkopziekte, 513.

Diphtheria in pig, 23.

Diplococcus pneumoniæ Contagiosæ Equi, 98.

Disinfection in hog cholera, 42.

Distemper, forms of, 170.

Distemper in dogs and cats, 165.

Distemper in dogs, causes, 167.

Distemper in dogs, cutaneous symptoms, 173.

Distemper in dogs, definition, 166.

Distemper in dogs, digestive symptoms. 173.

Distemper in dogs, eye symptoms, 172.

Distemper in dogs, history, 166.

Distemper in dogs, immunization, 176.

Distemper in dogs, incubation, 171.

Distemper in dogs, lesions, 174.

Distemper in dogs, microbiology of, 168.

Distemper in dogs, nervous symptoms, 174.

Distemper in dogs, pathogenesis, 166.

Distemper in dogs, prevention, 175.

Distemper in dogs, respiratory symptoms, 171.

Distemper in dogs, symptoms, 171.

Distemper in dogs, synonyms, 166.

Distemper in dogs, treatment, 177.

Distemper in young horses, 78.

Distemper, mortality, 170.

Distemper of bench show, 181.

Distemper, prognosis, 171.

Distemper, virulent products in, 170.

Dog ill, 166.

Dog pox, 361.

Dogs, paludism in, 577.

Dourine, 519.

Dourine, abdominal lesions.

Dourine, causes, 520.

Dourine, changes in blood, 524.

Dourine, definition, 519.

Dourine, diagnosis, 528.

Dourine, extinction of, 531.

Dourine, history, 520.

Dourine, history in America, 520.

Dourine in geldings, 520.

Dourine, its primary home, 520.

Dourine, lesions in dog, 525.

Dourine, lesions in horse, 523.

Dourine, lesions in mare, 525.

Dourine, microbiology, 521.

Dourine, nervous lesions, 523.

Dourine, pathogenesis, 519.

Dourine, prevention, 530.

Dourine, prognosis, 528.

Dourine, symptoms, 525.

Dourine, symptoms in ass and mule, 529.

Dourine, symptoms in dog, 529.

Dourine, symptoms in horse, 525.

Dourine, symptoms in mare, 527.

Dourine, symptoms in rabbits, 530.

Dourine, treatment, 530.

Dropsies in malignant œdema, 13.

Dropsy of connective tissue, 141.

Druse, 78.

Dunpaardziekte, 513.

Eczema epizoötica, 316.

Edematous pneumonia, 95.

Embolism and pyæmia, 4, 6.

Emphysematous anthrax, 181.

Emphysematous anthrax, accessory causes, 185.

Emphysematous anthrax, causes, 183.

Emphysematous anthrax, definition, 182.

Emphysematous anthrax, diagnosis, 187.

Emphysematous anthrax, distribution, 182.

Emphysematous anthrax, immunization, 191.

Emphysematous anthrax, incubation, 186.

Emphysematous anthrax, lesions, 187.

Emphysematous anthrax, pathogenesis, 182.

Emphysematous anthrax, prevention, 189.

Emphysematous anthrax, symptoms, 186.

Emphysematous anthrax, synonyms, 182.

Emphysematous anthrax, treatment, 188.

Emprosthotonos, 299.

Entero-hepatitis, amœba of, 388.

Entero-hepatitis, diagnosis, 390.

Entero-hepatitis, lesions, 389.

Entero-hepatitis, prevention, 391.

Entero-hepatitis, symptoms, 389.

Entero-hepatitis, treatment, 391.

Enzoötic abortion, 370.

Epizoötic, 113

Epizoötic abortion, 370.

Epizoötic catarrh, 113.

Epizoötic cellulitis, 113, 129, 140.

Epizoötic paraplegia, 519.

Epizoötic pleuro-pneumonia, 599.

Equine influenza, 112.

Equine syphilis, 519.

Equinia, 231.

Ergot and abortion, 371.

Erysipelas in swine, 23.

Eye, tubercle of, 436.

Farcy, 231.

Farcy in cattle, 257.

Fermentation fever, 8.

Fibroid tubercle, 431.

Fibrosis in tubercle, 431.

Foot and mouth disease, 316.

Foot and mouth disease, bacteriology, 318.

Foot and mouth disease, causes, 317.

Foot and mouth disease, definition, 316.

Foot and mouth disease, diagnosis 321.

Foot and month disease, geographical distribution, 317.

Foot and mouth disease, history, 317.

Foot and mouth disease, infection of man, 321.

Foot and mouth disease in man, prevention, 323.

Foot and mouth disease, mortality, 320.

Foot and mouth disease, pathogenesis, 316.

Foot and mouth disease, prevention, 324.

Foot and mouth disease, prognosis, 320.

Foot and mouth disease, symptoms, 319.

Foot and mouth disease, symptoms in man, 323.

Foot and mouth disease, treatment, 325.

Foot and mouth disease, treatment in man, 324.

Foot and mouth disease, virulent products, 318.

Fowl cholera, 158.

Gangrene in malignant œdema, 13.

Gangrene of coronet in horse, 76.

Garrapata, 551.

Gastro-conjunctivitis, 113.

Gastro-enteric epizoötic, 113.

Gastro-enteritis, infective, in new born, 645.

Gastro-enteritis of new born, bacteriology, 645.

Gastro-enteritis of new born, prevention, 647.

Gastro-mycosis ovis, 508.

Genital catarrh, infectious in rabbits, 367.

Genital tuberculosis, symptoms, 449.

Genito-urinary tubercle, 435.

Gerlach’s experiments on tuberculosis, 409.

Glanders, 230.

Glanders, acute, symptoms of, 236.

Glanders, causes, 232.

Glanders, chronic, symptoms of, 238.

Glanders, cutaneous, symptoms, 239.

Glanders, definition, 231.

Glanders, diagnosis, 239.

Glanders, forms of, 236.

Glanders, geographical distribution, 231.

Glanders in carnivora, 245.

Glanders, infection atria, 235.

Glanders in frog, 245.

Glanders in man, 246.

Glanders in man, causes, 246.

Glanders in man, lesions, 250.

Glanders in man, symptoms, 248.

Glanders in man, treatment, 256.

Glanders in rodents, 244.

Glanders in sheep and goat, 244.

Glanders in swine, 243.

Glanders, latent or occult, 239.

Glanders, lesions of, 241.

Glanders, pathogenesis, 232.

Glanders, prevention, 251.

Glanders, synonyms, 231.

Glanders, treatment, 254.

Gloss-anthrax, 55, 203, 206.

Glossina morsitans, 595.

Goatpox, 360.

“Going light”, 392.

Goose septicæmia, 654.

Gourme, 77.

Grapes, 399.

“Grease”, 237.

Great white plague, 399.

Hæmaphysalis Leachi, 579.

Hæmaphysalis rosea, 552.

Hæmatoblasts and blood globules in pyæmia, 4.

Hæmoglobinæmia, bacteriology of, 649.

Hæmoglobinæmia in the horse, 649.

Hæmoglobinæmia in the horse, antiseptic treatment, 650.

Hæmoglobinæmia, iodine treatment, 650.

Hæmolysis in influenza, 130.

Hæmorrhagic septicæmia in chickens, 656.

Hæmorrhoidal anthrax, 203, 207.

Heart, tubercle of, 433.

Hepatic cirrhosis of cattle, 641.

Hog cholera, 15, 22.

Hog cholera, accessory causes, 28.

Hog cholera, accessory causes, removal of, 37.

Hog cholera and faulty feeding, 30.

Hog cholera and interstate sanitary work, 44.

Hog cholera and state rights, 44.

Hog cholera bacillus, 24.

Hog cholera bacillus and allied organisms, table of, 26–28.

Hog cholera, definition, 22.

Hog cholera, diagnosis of, 35.

Hog cholera, disinfection, 43.

Hog cholera, disseminated by commerce, 41.

Hog cholera, extinction in herds, 44.

Hog cholera, fulminant, 33.

Hog cholera, gastro-intestinal lesions of, 33.

Hog cholera germ, carried by animals, 40.

Hog cholera germ, carried by flies, 40.

Hog cholera germ, exclusion of, 40.

Hog cholera, history, 23.

Hog cholera, immunization, 42.

Hog cholera, incubation, 33.

Hog cholera losses in U. S., 24.

Hog cholera, market restrictions, 43.

Hog cholera, poisoning mistaken for, 30, 31.

Hog cholera, precautions for owner, 42.

Hog cholera, prevention, 37.

Hog cholera restrictions in England, 43.

Hog cholera, serum treatment, 45.

Hog cholera, spread through markets and butcher shops, 31.

Hog cholera, Swine plague and Rouget, table of differential symptoms, 38.

Hog cholera, symptoms, 33.

Hog cholera, symptoms of acute form, 33.

Hog cholera, symptoms of subacute form, 35.

Hog cholera, synonyms, 23.

Hog cholera, therapeutic treatment, 45.

Hog cholera, Widal test in, 36.

Holzkrankheit, 543.

Horse, gangrene of coronet in, 76.

Horse pox, 337.

Horse pox, symptoms, 338.

Horse pox, treatment, 340.

Horse sickness, 513.

Horse sickness, definition, 514.

Horse sickness, forms of, 516.

Horse sickness, from damp, green fodder, 514.

Horse sickness, geographical distribution, 514.

Horse sickness, immunity, 515, 518.

Horse sickness, lesions, 517.

Horse sickness, pathogenesis, 514.

Horse sickness, penicillium of, 515.

Horse sickness, prevention, 518.

Horse sickness, symptoms, 516.

Hydrophobia, 259.

Hydrophobia, diagnosis, 282.

Hydrophobia, symptoms, 280.

Ictero hæmaturia in sheep, 573.

Immunization against apoplectiform septicæmia, 397.

Immunization against hog cholera, 42.

Immunization against sheeppox, 357.

Immunization against strangles, 92.

Immunization against Texas fever, 567.

Immunization, from anthrax, 214.

Immunization from canine distemper, 177.

Immunization from chicken cholera, 164.

Immunization from septicæmia hæmorrhagica of cattle, 62.

Immunization from swine plague, 51.

Immunization in rabies, 285.

Infarction in pyæmia, 6.

Infections, purulent and septic, 1.

Infectious abortion, 370.

Infectious bronchial catarrh in dogs, 181.

Infectious entero-hepatitis in turkeys, 388.

Infectious genital catarrh in rabbits, 367.

Infectious stable bronchitis, 111.

Infectious stomatitis in lambs and kids, 367.

Infectious stomatitis in lambs, causes, 368.

Infectious stomatitis, lesions, 368.

Infectious stomatitis, mortality, 369.

Infectious stomatitis, pathogenesis, 368.

Infectious stomatitis, prevention, 369.

Infectious stomatitis, streptococcus of, 368.

Infectious stomatitis, symptoms, 368.

Infectious stomatitis, treatment, 369.

Infective blood clots, 4.

Infective myelo-meningitis, 500.

Infective ulceration of anus and vulva in cattle, 651.

Inflammatory œdema, 153.

Influenza, accessory causes, 122.

Influenza, as compared with croupous pneumonia, 133.

Influenza, bacteriology, 120.

Influenza, catarrhal symptoms, 125.

Influenza, cocci and cocco-bacilli, 120.

Influenza, complications in, 129.

Influenza, contagion, 116.

Influenza, diagnosis of, 132.

Influenza, diagnostic symptoms, 124.

Influenza, digestive disorder, 127.

Influenza, equine, 112.

Influenza, exudations, 129.

Influenza, gastro-intestinal lesions in, 130, 131.

Influenza, hæmolysis in, 130.

Influenza, history, 114.

Influenza, immunity, 123

Influenza, incubation, 123.

Influenza, inoculations, 120.

Influenza, lesions, 129.

Influenza, leucocytosis in, 130.

Influenza, mortality, 134.

Influenza, nervous symptoms, 128.

Influenza of 1872–3, 115.

Influenza ophthalmic symptoms, 128.

Influenza phenomena as compared with contagious pneumonia, 133.

Influenza, prevention, 139.

Influenza, prognosis, 134.

Influenza, pulmonary lesions in, 131.

Influenza, quarantine for, 139.

Influenza, rheumatoid symptoms, 129.

Influenza, symptoms, 124.

Influenza, thoracic symptoms, 126.

Influenza, treatment, 135.

Inoculation in diagnosis, 457.

Intestinal anthrax in man, 224.

Ixodic anæmia, 543.

Ixodic toxæmia, 500.

Ixodis Algeriensis, 552.

Ixodis annulata, 552.

Ixodis bovis, 548.

Ixodis Dugesii, 548.

Klebs’ experiments on tuberculosis, 409.

La Grippe, 113.

Lambs and kids, infectious stomatitis in, 367.

Laminitis in influenza, 129.

Lesions in hæmorrhagica septicæmia in sheep, 67.

Lesions in septicæmia hæmorrhagica in cattle, 59.

Lesions of swine plague, 49.

Leucocytosis in influenza, 130.

Leucophlegmasia, 141.

Liver, tubercle of, 434.

Lockjaw, 292.

Lombriz, 63.

Louping-ill, 500.

Lungenseuche, 599.

Lung plague, 56.

Lung plague, abortions in, 613.

Lung plague, absent from lands breeding all their cattle, 600.

Lung plague, acute symptoms, 612.

Lung plague and aspergillus, 616.

Lung plague, and bronchitis, 615.

Lung plague and emphysema, 616.

Lung plague, and fibrinous pneumonia, 616.

Lung plague and foreign body in the heart, 616.

Lung plague and hæmorrhagic septicæmia, 616.

Lung plague and infectious pneumonia, 616.

Lung plague and Oldenburg, 601.

Lung plague and pulmonary congestion, 617.

Lung plague, and tuberculosis, 615.

Lung plague and verminous bronchitis, 616.

Lung plague, auscultation in, 613.

Lung plague, bacteriology, 603.

Lung plague, bronchial exudates, 610.

Lung plague, causes, 602.

Lung plague, chronic form, 614.

Lung plague, complex infection, 614.

Lung plague, contagion through the air, 605.

Lung plague, course, 613.

Lung plague definition, 599.

Lung plague, diagnosis, 614.

Lung plague, duration of infection in sequestra, 607.

Lung plague, exclusion of infected things, 618.

Lung plague, extension into new countries, 600.

Lung plague, extensions in autumn, 607.

Lung plague, granular, hepatised lung, 609.

Lung plague, history, 599.

Lung plague, honey combed lung, 609.

Lung plague, immunity of secluded islands, mountains, etc., 602.

Lung plague, immunizing by a first attack, 619.

Lung plague in Atlantic States, 601.

Lung plague in Australia, 602.

Lung plague in Brooklyn, 601.

Lung plague in cattle, 598.

Lung plague, incubation, 610.

Lung plague in Denmark, 600.

Lung plague, individual receptivity, 611.

Lung plague in England, 600.

Lung plague, infarction of lung, 608.

Lung plague, infection by mingling of herds, 605.

Lung plague, infection through active trade, 606.

Lung plague, infection through attendants, 605.

Lung plague, infection through convalescent, 607.

Lung plague, infection through food, 605.

Lung plague, infection through manure, 606.

Lung plague, infection through pastures, 605.

Lung plague, infection through stables, 606.

Lung plague, infection through unfenced places, 605.

Lung plague, infection through watering troughs, 605.

Lung plague, infiltrated lung, 609.

Lung plague in Holland, 600.

Lung plague in Ireland, 600.

Lung plague, injection of sterilized serum subcutem, 621.

Lung plague in Massachusetts, 601.

Lung plague in Mississippi Valley, 601.

Lung plague in New Jersey, 602.

Lung plague in Norway, 600.

Lung plague, inoculation in tail, 620.

Lung plague, inoculation methods, 620.

Lung plague in Schleswig, 601.

Lung plague, insidious onset, 611.

Lung plague in South Africa, 602.

Lung plague in Sweden, 600.

Lung plague in Tasmania and New Zealand, 602.

Lung plague, intravenous inoculation, 621.

Lung plague, laryngeal lesions, 610.

Lung plague, lesions, 608.

Lung plague, limits of admissible immunization, 622.

Lung plague, marbled lung, 608.

Lung plague, measures to extirpate, 618.

Lung plague microbe, Nocard’s culture of, 604.

Lung plague, micrococci and bacilli in, 603.

Lung plague, modes of transmission, 604.

Lung plague, only by infection, 600.

Lung plague, percussion in, 613.

Lung plague, pericardial exudates, 610.

Lung plague, pleural exudates, 609.

Lung plague, prevention, 618.

Lung plague, private control of, 619.

Lung plague, proclivity of breeds, 611.

Lung plague, quarantine for, 618.

Lung plague, recoveries, 613.

Lung plague, refrangent corpuscles in, 603.

Lung plague, sequestra, 608.

Lung plague, stalactite-like bronchia, 609.

Lung plague, suppression in America, 601.

Lung plague, symptoms, 611.

Lung plague, synonyms, 599.

Lung plague, thoracic glands in, 610.

Lung plague, transient cases, 611.

Lung plague, treatment, 617.

Lung plague, varying receptivity, 607.

Lymphangitis epizoötica, 257.

Lymphangitis farcinoides, 257.

Lymphangitis saccharomycotica, 257.

Lymphangitis saccharomycotica, distribution, 257.

Lymphangitis saccharomycotica, pathogenesis, 257.

Lymphangitis saccharomycotica, symptoms, 258.

Lymphangitis saccharomycotica, treatment, 258.

Lymphangitis ulcerosa, 257.

Lymph glands, tubercle of, 437.

Lyssa, 260.

Lytta, 260.

Magenseuche, 624.

Maladie de bois, 543.

Maladie de jeune age, 166.

Maladie des chiens, 166.

Maladie du coit, 519.

Mal de Caderas, 532.

Mal de tete de contagion, 141.

Malignant carbuncle, 196.

Malignant œdema, 11.

Malignant œdema, abscess from small dose, 14.

Malignant œdema, cause, 11.

Malignant œdema, diagnosis, 14.

Malignant œdema, immunization, 14.

Malignant œdema, infection channels, 12.

Malignant œdema, invasion by the intestine, 13.

Malignant œdema, lesions, 13.

Malignant œdema, pathogenesis, 12.

Malignant œdema, prevention, 14.

Malignant œdema, symptoms, 13.

Malignant œdema, treatment, 14.

Malignant œdema with proteus vulgaris or micrococcus, 13.

Malignant protozoan jaundice in dogs, 577.

Malignant pustule, 196.

Malignant vesicle, 223, 224.

Malleinization, 254.

Mallein test, 240.

Malleus, 231.

Malleus gangrenosa, 141.

Mammary tubercle, 435.

Mammary tuberculosis, symptoms, 449.

Measles in swine, 23.

Mexican fever, 543.

Microbes, modified by environment, 467.

Micrococci in distemper, 169.

Micrococcus prodigiosus in malignant œdema, 13.

Milk sickness, 325.

Milk sickness, contagion, 327.

Milk sickness, geographical distribution, 326.

Milk sickness, incubation, 329.

Milk sickness in man, 331.

Milk sickness, lesions, 331.

Milk sickness, prevention, 332.

Milk sickness, symptoms, 329.

Milk sickness, treatment, 332.

Miltzbrand, 196.

Moor ill, 543.

Morbus maculosus, 141.

Muscles, tubercle of, 436.

Nagana, 594.

Nagana, alike on flesh and vegetable food, 597.

Nagana, anæmia in, 596.

Nagana, animals susceptible, 595.

Nagana, attempts at immunization, 597.

Nagana, elephants and zebras immune, 595.

Nagana, eye lesions, 596.

Nagana, inoculation, 595.

Nagana, lesions, 596.

Nagana, muscular wasting and debility, 596.

Nagana, not prevented by surra, 597.

Nagana, œdema in, 596.

Nagana, pigeons and hens immune, 595.

Nagana, prevention, 597.

Nagana, symptoms of, 596.

Nagana, toxins, 597.

Nagana, virulent products, 595.

Nagana, vitality of virus, 595.

Nervous fever, 113.

Nocard’s culture of lung plague microbe, 604.

Œdema mycosis, 513.

Œdema mycosis, causes, 514.

Œdema mycosis, pathogenesis, 514.

Omphalitis, 5.

Opisthotonos, 299.

Orthrotonos, 299.

Osteomyelitis, 5.

Ovination, 357.

Ovination, technique, 358.

Oxygen, used by horse, ox and pig, 39.

Paludism in cattle, 542.

Paludism in dogs, 577.

Paludism in dogs, anæmia in, 577.

Paludism in dogs, geographical distribution, 577.

Paludism in dogs, hæmolysis in, 577.

Paludism in dogs, lesions, 580.

Paludism in dogs, microbiology, 578.

Paludism in dogs, prevention, 580.

Paludism in dogs, symptoms, 579.

Paludism in dogs, treatment, 580.

Paludism in horses, 580.

Paludism in horses, anæmia in, 583.

Paludism in horse, causes, 582.

Paludism in horses, duration, 583.

Paludism in horses, geographical distribution, 581.

Paludism in horses, hæmolysis, 582.

Paludism in horses, icterus in, 583.

Paludism in horses, immunization, 582.

Paludism in horses, lesions, 583.

Paludism in horses, microbiology, 581.

Paludism in fresh horses, mortality, 582.

Paludism in horses, prevention, 583.

Paludism in horses, remissions, 582.

Paludism in horses, symptoms, 582.

Paludism in horses, treatment, 584.

Paludism in horses, vertigo in, 582.

Paludism in sheep, 573.

Paludism in sheep, duration, 576.

Paludism in sheep, geographical distribution, 573.

Paludism in sheep, lesions, 575.

Paludism in sheep, microbiology, 575.

Paludism in sheep, prevention, 576.

Paludism in sheep, symptoms, 576.

Pancreas, tubercle of, 435.

Paralysis of breeding solipeds, 519.

Paraplegia, infections, of solipeds in Europe, 538.

Paraplegia, infectious of solipeds in Maraja, 533.

Paraplegia of Maraja, causes, 534.

Paraplegia of Maraja, history, 534.

Paraplegia of Maraja, lesions, 536.

Paraplegia of Maraja, mortality, 537.

Paraplegia of Maraja, prevention, 537.

Paraplegia of Maraja, symptoms, 535.

Paraplegia of Maraja, treatment, 537.

Paraplegia of solipeds in Europe, causes, 538.

Paraplegia of solipeds in Europe, diagnosis, 541.

Paraplegia of solipeds in Europe, history, 538.

Paraplegia of solipeds in Europe, lesions, 540.

Paraplegia of solipeds in Europe, prevention, 542.

Paraplegia of solipeds in Europe, prognosis, 541.

Paraplegia of solipeds in Europe, symptoms, 540.

Paraplegia of solipeds in Europe, treatment, 542.

Pasteurellosis ovina, 63.

Pathogenesis of septicæmia hæmorrhagica in cattle, 56.

Peltrot, 347.

Penicillium of horse sickness, 515.

Peripneumonia exudativa, 599.

Peripneumonie, 599.

Pernicious anæmia in horse, 585.

Perroncito, serum treatment in hog cholera, 45.

Pest bovine, 624.

Pestis bovina, 624.

Petechial fever, 141.

Petechial fever, antistreptococcic serum in, 153.

Petechial fever, a sequel to other diseases, 142.

Petechial fever, causes, 142.

Petechial fever, course and duration, 148.

Petechial fever, definition, 141.

Petechial fever, diagnosis, 148.

Petechial fever in cattle, 153.

Petechial fever in cattle, causes, 154.

Petechial fever in cattle, diagnosis, 156.

Petechial fever in cattle, lesions, 154.

Petechial fever in cattle, prevention, 156.

Petechial fever in cattle, symptoms, 155.

Petechial fever in cattle, treatment, 156.

Petechial fever, intratracheal treatment, 152.

Petechial fever, intravenous treatment, 153.

Petechial fever, lesions, 143.

Petechial fever, mortality, 149.

Petechial fever, prognosis, 149.

Petechial fever, symptoms, 145.

Petechial fever, synonyms, 141.

Petechial fever, treatment, 150.

Peters, serum treatment in hog cholera, 45.

Pharyngeal anthrax, 203, 206.

Phillipines, paludism in horses in, 582.

Phlebitis and pyæmia, 4.

Phthisis in cattle, 431.

Picotte, 347.

Pictou cattle disease, 641.

Pictou cattle disease, alleged causes, 641.

Pictou cattle disease, lesions, 641.

Pictou cattle disease, prevention, 644.

Pictou cattle disease, symptoms, 643.

Pigs poisoned by brine, 39.

Pigs poisoned by soaps, 39.

Pig typhoid, 23.

Pining, 399.

Pink eye, 113, 140.

Piroplasma bigeminum, life history, 546.

Pirosoma bigeminum, 545.

Pleuro-pneumonia contagiosa equorum, 95.

Pleurosthotonos, 299.

Pneumo-enteritis in cattle, 55.

Pneumo-enteritis, infectious in sheep, 63, 70.

Pneumo-enteritis in the horse, 112.

Pneumo-enteritis in pig, 23.

Pneumonia contagious, 95.

Pneumonia in new born, infective, 645.

Pneumonia sporadic, 55.

Pneumosarcia, 599.

Pockenseuche, 624.

Poisoning mistaken for hog cholera, 30, 31.

Potchetchoui, 76.

Powdered soaps poison pigs, 39.

Pox, 333.

Prevention of septicæmia hæmorrhagica in cattle, 62.

Prevention of septicæmia hæmorrhagica in sheep, 68, 73.

Prevention of swine plague, 50.

Prognosis of strangles, 90.

Proteus vulgaris in malignant œdema, 13.

Protoplasma bigeminum, 545.

Protozoan cattle fever, 542.

Protozoan cattle fever, anæmia in, 553.

Protozoan cattle fever and anthrax, 560.

Protozoan cattle fever, bile in, 555.

Protozoan cattle fever, causes, 545.

Protozoan cattle fever, course, 559.

Protozoan cattle fever, diagnosis, 560.

Protozoan cattle fever, hæmolysis, 553.

Protozoan cattle fever, history, 543.

Protozoan cattle fever, immunization, 567.

Protozoan cattle fever, incubation, 556.

Protozoan cattle fever, kidney lesions, 555.

Protozoan cattle fever, lesions, 552.

Protozoan cattle fever, liver lesions, 554.

Protozoan cattle fever, microbiology, 545.

Protozoan cattle fever, mortality, 560.

Protozoan cattle fever, spleen lesions, 555.

Protozoan cattle fever, symptoms, 557, 560.

Protozoan ictero hæmaturia in sheep, 573.

Pulmonary murrain, 599.

Pulmonary tubercle in cattle, 431.

Purples, 23.

Purpura hæmorrhagica, 141.

Purulent infections, 1.

Pyæmia, 1.

Pyæmia and septicæmia, distinction, 2.

Pyæmia, causes, 2.

Pyæmia, delay of access, 5.

Pyæmia, lesions of, 6.

Pyæmia, mortality, 7.

Pyæmia, prevention, 7.

Pyæmia, symptoms, 6.

Pyæmia, treatment, 8.

Pyæmic blood, effect of different doses, 3.

Pyroplasma in cattle, 545.

Pyroplasma in dogs, 577.

Pyroplasma in sheep, 573, 575.

Quarter ill, 182.

Quebra bunda, 533.

Quebra bunda definition, 533.

Rabbits, infectious genital catarrh in, 367.

Rabidus canis, 260.

Rabies, 259.

Rabies, cases in ratio with bites, 265.

Rabies, causes, 261.

Rabies, countries immune, 261.

Rabies, definition, 260.

Rabies, diagnosis, 273.

Rabies, diagnosis in man, 282.

Rabies, eradication from a country, 285.

Rabies, furious symptoms, 269.

Rabies, geographical distribution, 261.

Rabies in camel and deer, 278.

Rabies, incubation, 266.

Rabies, lesions, 283.

Rabies, lethargic symptoms, 272.

Rabies, microbe of, 263.

Rabies, morbific agent, 263.

Rabies, orrotherapy in, 284, 289.

Rabies, paralytic symptoms, 271.

Rabies, pathogenesis, 261.

Rabies, premonitory symptoms, 267.

Rabies, prevention, 285.

Rabies, symptoms in birds, 279.

Rabies, symptoms in cats, 275.

Rabies, symptoms in cattle, 276.

Rabies, symptoms in dogs, 267.

Rabies, symptoms in Guinea pig, 279.

Rabies, symptoms in man, 280.

Rabies, symptoms in rabbits, 279.

Rabies, symptoms in sheep and goat, 277.

Rabies, symptoms in solipeds, 275.

Rabies, symptoms in swine, 278.

Rabies, symptoms in wild carnivora, 280.

Rabies, synonyms, 260.

Rabies, the Pasteur treatment, 285.

Rabies, therapeutic treatment, 284.

Rabies, treatment of bites, 286.

Rabies, treatment with sterilized matter from infected brain, 290.

Rabies, viability of microbe, 264.

Rabies, virulent matters, 262.

Rauschbrand, 182.

Rauschbrand bacillus, 183.

Red fever of swine, 17.

Red globules, destruction of, 553.

Red soldier, 23.

Red water, 543.

Red water absent in mild cases of Texas fever, 558.

Relapsing fever in horse, 585.

Resorption fever, 8.

Rheumatic catarrh, 113.

Rhino-adenitis, infections, 77.

Rhipicephalus annulatus microplus, 552.

Rinderpest, 624.

Rinderseuche, 55.

Rot, 584.

Rothlauf, 15, 17.

Rouget, 15, 17.

Rouget, bacillus of, 20.

Rouget, causes, 17.

Rouget, course, 18.

Rouget, definition, 17.

Rouget, immunization, 21.

Rouget, morbid anatomy, 19.

Rouget, mortality, 19.

Rouget, pathogenesis, 21.

Rouget, swine plague and hog cholera, table of differential symptoms, 38.

Rouget, symptoms, 18.

Roumanian hæmoglobinuria, 543.

Sanitary police for strangles, 91.

Sapræmic fever, 9.

Scalma, 111.

Scarlatina in swine, 23.

Schweinepest, 23.

Schweineseuche, 15, 47.

Scrofula, 399.

Scrub-tick of Australia, 552.

Septicæmia, 1, 8.

Septicæmia from toxins, 9.

Septicæmia hæmorrhagica, definition, 55.

Septicæmia hæmorrhagica, history, 55.

Septicæmia hæmorrhagica in cattle, 55.

Septicæmia hæmorrhagica in cattle, abdominal form, 59.

Septicæmia hæmorrhagica in cattle, accessory causes of, 57.

Septicæmia hæmorrhagica in cattle, bacteriology, 56.

Septicæmia hæmorrhagica in cattle, chronic, 59.

Septicæmic hæmorrhagica in cattle, external form, 58.

Septicæmia hæmorrhagica in cattle, immunization, 62.

Septicæmia hæmorrhagica in cattle, in winter and spring, 57.

Septicæmia hæmorrhagica in cattle, lesions of, 59.

Septicæmia hæmorrhagica in cattle, mortality, 62.

Septicæmia hæmorrhagica in cattle, on wet soils, 57.

Septicæmia hæmorrhagica in cattle, pathogenesis of, 56.

Septicæmia hæmorrhagica in cattle, prevention, 62.

Septicæmia hæmorrhagica in cattle, symptoms, 58.

Septicæmia hæmorrhagica in cattle, thoracic form, 58.

Septicæmia hæmorrhagica in horse, 113.

Septicæmia hæmorrhagica in sheep, 63.

Septicæmia hæmorrhagica in sheep, acute, 66, 71.

Septicæmia hæmorrhagica in sheep, bacteriology, 65, 70.

Septicæmia hæmorrhagica in sheep, causes, 64.

Septicæmia hæmorrhagica in sheep, chronic, 67, 72.

Septicæmia hæmorrhagica in sheep, definition, 63.

Septicæmia hæmorrhagica in sheep, diagnosis, 66.

Septicæmia hæmorrhagica in sheep, distribution, 63.

Septicæmia hæmorrhagica in sheep, lesions, 67, 72.

Septicæmia hæmorrhagica in sheep, mortality, 68.

Septicæmia hæmorrhagica in sheep, prevention, 68, 73.

Septicæmia hæmorrhagica in sheep, symptoms, 65.

Septicæmia hæmorrhagica in sheep, synonyms, 63.

Septicæmia hæmorrhagica suis, 47.

Septicæmia hæmorrhagica, synonyms, 55.

Septicæmia hæmorrhagica, treatment, 62.

Septicæmia in chickens and turkeys, 656.

Septicæmia in geese, 654.

Septicæmia in geese, bacteriology, 654.

Septicæmia in geese, diagnosis, 655.

Septicæmia in geese, lesions, 655.

Septicæmia in geese, pathogenesis, 654.

Septicæmia in geese, prevention, 656.

Septicæmia in geese, symptoms, 654.

Septicæmia in geese, treatment, 656.

Septicæmia, lesions, 9.

Septicæmia, mortality, 10.

Septicæmia, prevention, 10.

Septicæmias, 2.

Septicæmia, symptoms, 9.

Septicæmia, treatment, 10.

Septic infections, 1, 8.

Septic intoxication, 8.

Septico-pyæmia, 8.

Serum therapy in hog cholera, 45.

Serum therapy in swine plague, 52.

Sheep, paludism in, 573.

Sheeppox, 347.

Sheeppox, accessory causes, 349.

Sheeppox, causes, 347.

Sheeppox, definition, 347.

Sheeppox, forms, 347.

Sheeppox, geographical distribution, 347.

Sheeppox, incubation, 350.

Sheeppox in goat, 360.

Sheeppox, mortality, 354.

Sheeppox, pathogenesis, 347.

Sheeppox, prevention, 355.

Sheeppox, preventive inoculation, 357.

Sheeppox, prognosis, 354.

Sheeppox, symptoms, 350.

Sheeppox, treatment, 354.

Sheep, ulcerative infection of the limbs in, 74.

Skin, tubercle of, 436.

South African horse sickness, 513.

Southern cattle fever, 543.

Spanish fever, 543.

Spleen, tubercle of, 435.

Splenic apoplexy, 196.

Splenic fever, 196, 545.

Stable pneumonia, 95.

Staupe, 166.

Stomatitis, infectious, in lambs and kids, 367.

Stomatitis, ulcerous, in lambs and kids, 367.

Strangles, 77.

Strangles, abdominal, 87.

Strangles, accessory causes, 80.

Strangles, bacteriology, 78.

Strangles, cutaneous, 88.

Strangles, definition, 78.

Strangles, diagnosis, 89.

Strangles, forms of, 84.

Strangles, fulminant, 89.

Strangles, general symptoms, 84.

Strangles, history, 78.

Strangles, immunization, 92.

Strangles, incubation, 84.

Strangles, infecting products, 80.

Strangles, mild, symptoms, 85.

Strangles, nervous lesions, 89.

Strangles, pathogenesis, 99.

Strangles, pathology, 82.

Strangles, pharyngeal, 86.

Strangles, prevention, 90.

Strangles, pulmonary, 87.

Strangles of genital organs, 89.

Strangles, sanitary police, 91.

Strangles, synonyms, 78.

Strangles, tracheotomy in, 94.

Strangles, treatment, 92.

Streptococcus coryzæ contagiosæ equi, 78.

Streptococcus equi, 78.

Streptococcus equi, its relation to strangles and contagious pneumonia, 79.

Streptococcus infection of limbs in cattle and sheep, 74.

Streptococcus of apoplectiform septicæmia, 394, 395.

Streptococcus of infectious stomatitis, 268.

Streptococcus pneumoniæ contagiosæ equi, 98.

Streptococcus rhino-adenitis, 78.

Surra, 584.

Surra, accessory causes, 586.

Surra, anæmia in, 590.

Surra, avoidance of infected localities, 593.

Surra, carried by crows, 587.

Surra, carried by insects, 586.

Surra, cattle don’t infect horses casually, 593.

Surra, cattle infect rodents, carnivora and apes, 593.

Surra, cause, 585.

Surra, definition, 585.

Surra, destruction of the sick, 594.

Surra, diagnosis, 591.

Surra, disinfectants on manure, 593.

Surra, disinfectants on skin, 593.

Surra, disinfectants on stables, 593.

Surra, disposal of manure and garbage, 593.

Surra, exclusion of flies, 593.

Surra, geographical distribution, 585.

Surra, goats and ducks immune, 593.

Surra, in camels, 592.

Surra, in cattle, 592.

Surra in cattle in India, 592.

Surra in cattle in Phillipines, 592.

Surra, incubation, 589.

Surra, lesions, 588.

Surra, mortality, 592.

Surra, parasite, 585.

Surra, pathology, 588.

Surra, prevention of, 593.

Surra, remissions in, 589.

Surra, sanitary police, 594.

Surra, smudges, 594.

Surra, sterilization of carcasses, 594.

Surra, symptoms of, 589.

Surra, synonyms, 584.

Surra, treatment of, 593.

Surra, trypanosoma, 585.

Swine, complex fevers of, 52.

Swine, erysipelas, 15, 17.

Swine, erysipelas bacillus and allied organisms table, 27.

Swine, erysipelas, immunization, 21.

Swine, erysipelas, lesions, 19.

Swine, erysipelas, symptoms, 18.

Swine, fever, 15, 23.

Swine, fever bacillus and allied organisms table, 26, 28.

Swine fevers, effects of varying doses, 16.

Swine, infectious fevers of, 15.

Swine, plague, 47.

Swine, plague, accessory causes, 48.

Swine, plague, bacillus and allied organisms table, 26, 28.

Swine, plague and hog cholera, duality, 53.

Swine, plague, bacteriology, 47.

Swine, plague, deadly to wild birds and rodents, 49.

Swine, plague, diagnosis, 50.

Swine plague, hog cholera, and Rouget, table of differential symptoms, 38.

Swine plague, immunization, 51.

Swine plague, lesions, 49.

Swine plague, Marseilles, 54.

Swine plague, McFadyean’s, 53.

Swine plague, pathogenesis, 48.

Swine plague, prevention, 50.

Swine plague, serum therapy, 52.

Swine plague, symptoms, 50.

Swine plague, treatment, 52.

Swine pox, 360.

Symptomatic anthrax, 182.

Symptoms of septicæmia hæmorrhagica, cattle, 58.

Symptoms of swine plague, 50.

Tabes, 399.

Tappeiner’s experiments on tuberculosis, 409.

Tetanus, 291.

Tetanus, accessory causes, 298.

Tetanus, antidotal treatment, 309.

Tetanus, antitoxin treatment, 309.

Tetanus bacillus, 293.

Tetanus, brain emulsion for, 312.

Tetanus causes, 293.

Tetanus, course, duration, 312.

Tetanus, definition, 292.

Tetanus, diagnosis, 304.

Tetanus, form of death from, 304.

Tetanus, general symptoms, 298.

Tetanus immunization, 315.

Tetanus, intra cranial injections for, 312.

Tetanus, lesions, 304.

Tetanus, mortality, 303.

Tetanus, orrotherapy, 310.

Tetanus, pathogenesis, 292.

Tetanus, pathology, 293.

Tetanus, prevention, 313.

Tetanus, symptoms in birds, 302.

Tetanus, symptoms in cattle, 301.

Tetanus, symptoms in dogs, 302.

Tetanus, symptoms in horse, 300.

Tetanus, symptoms in sheep and goat, 302.

Tetanus, symptoms in swine, 302.

Tetanus, synonyms, 291.

Tetanus, treatment, 306.

Texas fever, 542.

Texas fever and anthrax, diagnosis, 560.

Texas fever and anthrax, table of distinctions, 561.

Texas fever, course and duration, 559.

Texas fever, cultivating infested pastures, 564.

Texas fever, definition, 543.

Texas fever, federal restrictions, 572.

Texas fever, immunization against, 567.

Texas fever, immunization by blood, 570.

Texas fever, immunization by blood from ticks, 571.

Texas fever, immunization of limited value, 571.

Texas fever, infecting by small number of ticks, 568.

Texas fever, infection by blood of immunized, 569.

Texas fever, infection of sucking calf, 568.

Texas fever, legislation for its extinction, 566.

Texas fever, marketing the beef, 572.

Texas fever, mortality in severe form, 560.

Texas fever pastures, purifying by exclusion of cattle, 564.

Texas fever, prevention, 562.

Texas fever, prevention by dipping or smearing, 563.

Texas fever, prevention by picking off ticks, 562.

Texas fever, purifying infected pastures, 564.

Texas fever, red water absent in mild cases, 558.

Texas fever, susceptibility of cattle on purified pastures, 565.

Texas fever, symptoms of mild form, 560.

Texas fever, treatment, 561.

Texas fever, value of its extinction, 566.

Texas fever, watery blood in, 559.

Therapeutics in hog cholera, 45.

“The trembles,” 325.

Thrombosis and pyæmia, 4.

Ticks, destruction of, in pastures, 564.

Ticks, dressing for, 564.

Ticks in paludism in dogs, 579.

Toxins as cause of septicæmia, 9.

Treatment of septicæmia hæmorrhagica in cattle, 62.

Treatment of strangles, 92.

Treatment of swine plague, 52.

Trembling in sheep, 500.

Trembling in sheep, accessory causes, 504.

Trembling in sheep, bacilli, cocci and penicillium, 503.

Trembling in sheep, bacteriology, 503.

Trembling in sheep, causes, 501.

Trembling in sheep, definition, 500.

Trembling in sheep, diagnosis, 505.

Trembling in sheep, geographical distribution, 500.

Trembling in sheep, lesions, 506.

Trembling in sheep, pathogenesis, 500.

Trembling in sheep, prevention, 506.

Trembling in sheep, sheepticks, 501.

Trembling in sheep, symptoms, 504.

Trembling in sheep, treatment, 507.

Trismus, 292, 299.

Tristeza, 543.

Trypanosoma Brucii, 595, 596.

Trypanosoma equiperdum, 521.

Trypanosoma Evansi, 585.

Trypanosoma in blood during paroxysm of surra, 591.

Trypanosomosis, 585.

Trypanosoma, staining of, 591.

Tsétsé fly, 595.

Tsétsé fly disease, 594.

Tubercle bacillus, 410.

Tubercle bacillus, diminished pathogenesis when from cold blooded host, 482.

Tubercle, calcification, 431.

Tubercle, cardiac and pericardial, 433.

Tubercle, caseation, 430.

Tubercle, fibroid degeneration, 431.

Tubercle, genito-urinary, 435.

Tubercle in lymph glands, 433.

Tubercle, local, 498.

Tubercle of brain and spinal cord, 436.

Tubercle of bones, 436.

Tubercle of bronchial and mediastinal glands, 433.

Tubercle of eye, 436.

Tubercle of lymph glands, 437.

Tubercle of mammæ, 435.

Tubercles of mouth and throat, 434.

Tubercle of muscles, 436.

Tubercle of pancreas, 435.

Tubercle of skin, 436.

Tubercle of spleen, 435.

Tubercle, relative frequency in different parts, 437, 438.

Tubercle, structure of, 429.

Tuberculin, action on parturient cows, 464.

Tuberculin, dose of, 461.

Tuberculin, reaction under, 463.

Tuberculin test, 458.

Tuberculin test, antipyretics during, 426.

Tuberculin test, effect on sound animals, 464.

Tuberculin test, its reliability, 465.

Tuberculin test, later effect on the tuberculous, 464.

Tuberculin test, precautions, 459.

Tuberculin tests, false certificates of, 426.

Tuberculin test, technique, 461.

Tuberculosis, 398.

Tuberculosis, accessory causes, 415.

Tuberculosis and absence of indemnity, 424.

Tuberculosis and increased trade, 421.

Tuberculosis and private testing of herds, 426.

Tuberculosis and sale of tuberculous, 424.

Tuberculosis and sales of sound stock, 424.

Tuberculosis and unrestricted trade, 423.

Tuberculosis, bacilli of bird, horse and rabbit, 413.

Tuberculosis, breeding healthy stock from infected parents, 489.

Tuberculosis, butter, cheese and whey, 497.

Tuberculosis by feeding, 409.

Tuberculosis by inhalation, 409.

Tuberculosis, cerebral, symptoms, 450.

Tuberculosis, culling out the unthrifty and sick, 491.

Tuberculosis, Danish method in Pennsylvania, 492.

Tuberculosis, Danish method of restriction, 491.

Tuberculosis, decrease of in England, 481.

Tuberculosis, definition, 399.

Tuberculosis, diagnosis of, 456.

Tuberculosis, direct infection from man to ox, 474.

Tuberculosis, encrease in infants in England, 481.

Tuberculosis, expense of extinction in cattle, 486.

Tuberculosis, experiments of Adami and Ravenel, 482.

Tuberculosis from common feeding trough, 428.

Tuberculosis from dusty infected stables, 428.

Tuberculosis from feeding hogs after diseased cattle, 428.

Tuberculosis from feeding offal to hogs, 427.

Tuberculosis from infected milk, 427.

Tuberculosis, gastro-intestinal, peritoneal and mesenteric, 434.

Tuberculosis, generalization of, 499.

Tuberculosis, generally applicable measures, 494.

Tuberculosis, genital in the bull, symptoms, 449.

Tuberculosis, geographical distribution, 402.

Tuberculosis, Gerlach’s experiment, 409.

Tuberculosis, glandular symptoms, 450.

Tuberculosis held virulent in early times, 403.

Tuberculosis, hereditary vulnerability, 415.

Tuberculosis, hygiene of meat, 498.

Tuberculosis, hygiene of milk and meat, 495.

Tuberculosis, hygiene of oleomargarine, 497.

Tuberculosis in apes and menagerie animals, lesions, 441.

Tuberculosis in apes and monkeys, 401.

Tuberculosis in birds, 399.

Tuberculosis in birds, symptoms, 456.

Tuberculosis in cattle, 400.

Tuberculosis in chickens, lesions, 441.

Tuberculosis in dog and cat, lesions, 440.

Tuberculosis in dogs and cats, 401.

Tuberculosis in dogs and cats, symptoms, 455.

Tuberculosis, infection from ox to man, 476.

Tuberculosis in fishes, 399.

Tuberculosis in Hebrews and Christians, 481.

Tuberculosis in horse, ass and mule, 400.

Tuberculosis in horse, lesions, 439.

Tuberculosis in horse, symptoms, 453.

Tuberculosis in indoor subjects, 402.

Tuberculosis in man, 402.

Tuberculosis in man with sound cattle, 472.

Tuberculosis in park and menagerie animals, 402.

Tuberculosis in parrot, lesions, 441.

Tuberculosis in pheasants, lesions, 441.

Tuberculosis in reptiles, 399.

Tuberculosis in rodents, 400.

Tuberculosis in sheep and goat, 400.

Tuberculosis in sheep and goat, lesions, 439.

Tuberculosis in sheep and goat, symptoms, 455.

Tuberculosis in swine, 401.

Tuberculosis in swine, lesions, 439.

Tuberculosis in swine, symptoms, 452.

Tuberculosis, its extinction in cattle, 486.

Tuberculosis, lesions, 429.

Tuberculosis, limited susceptibility of ox to germ from man, 482.

Tuberculosis, mammary symptoms, 449.

Tuberculosis of bones and joints, symptoms, 451.

Tuberculosis of liver, 434.

Tuberculosis of lungs in cattle, 431.

Tuberculosis of lungs, symptoms, 445.

Tuberculosis of man and ox coextensive, 470.

Tuberculosis of skin, symptoms, 450.

Tuberculosis of the abdomen, symptoms, 448.

Tuberculosis of the eye, symptoms, 451.

Tuberculosis of the heart, symptoms, 451.

Tuberculosis, pathogenesis, 399.

Tuberculosis, pharyngeal, symptoms, 450.

Tuberculosis, practicability of its extinction in cattle, 487.

Tuberculosis, primary and secondary infection, 442.

Tuberculosis, raising healthy calves from diseased dams on the range, 490.

Tuberculosis, sanitary police measures, 495.

Tuberculosis, sifting process in N. Y. markets, retention of the tuberculous, 493.

Tuberculosis, symptoms in cattle, 445.

Tuberculosis, testing imported stock, 493.

Tuberculosis through insects, 429.

Tuberculosis through vermin, 428.

Tuberculosis, treatment, 483.

Tuberculosis, uterine, symptoms, 449.

Tuberculosis, varying pathogenesis, its value in sanitary police, 483.

Tuberculosis, Villemin’s inoculations, 408.

Tuberculosis, virulence, 403.

Tuberculosis, with bad ventilation, 416.

Tuberculosis with conformation, 418.

Tuberculosis with damp stables, 417.

Tuberculosis with debilitating diseases, 420.

Tuberculosis with early breeding, 419.

Tuberculosis with heavy milking, 418.

Tuberculosis with inbreeding, 419.

Tuberculosis with insufficient nourishment, 418.

Tuberculosis with old age, 420.

Typhoid fever bacillus, 27.

Typhoid fever in the horse, 113.

Typhoid in pig, 23.

Typhose, 113.

Typhus, 141.

Typhus contagieuse, 624.

Typhus des chenils, 166.

Typhus du gros betail, 624.

Typhus in pig, 23.

Ulceration of anus and vulva in cattle, 651.

Ulcerative infection of the limbs in cattle, 74.

Variola, 333.

Variola caninæ, 361.

Variola caprina, 360.

Variola equina, 337.

Variola, history, 334.

Variola, nomenclature, 334.

Variola ovina, 347.

Variola, pathogenesis, 336.

Variola suilla, 360.

Variola vaccinæ, 340.

Variole des chiens, 166.

Variolisation, 357.

Venereal disease of solipeds, 519.

Vesicular exanthema, causes, 362, 365.

Vesicular exanthema, diagnosis, 364.

Vesicular exanthema of horse, 362.

Vesicular exanthema, prevention, 364, 367.

Vesicular exanthema, symptoms, 363, 366.

Vesicular exanthema treatment, 364, 367.

Viehpest, 624.

Villemin’s inoculations of tubercle, 408.

Vulva, infective ulceration of, causes, 651.

Vulva, infective ulceration of, in cattle, 651.

Vulva, infective ulceration of, pathology, 653.

Vulva, infective ulceration of, symptoms, 652.

Vulva, infective ulceration of, treatment, 654.

White scour, 645.

White scour, microbiology, 646.

Widal test in hog cholera, 36.

Wildseuche, 55.

Wood-ill, 543.

Woolsorter’s disease, 196, 226.

Yellow water, 153.

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TRANSCRIBER’S NOTES

Page Changed from Changed to

106 A safer and hardly less A safer and hardly less affective method is to apply effective method is to apply around the around the

123 immune ones, which for a time immune ones, which for a time resist, throw off the desease resist, throw off the disease with with

182 percussion resonance, finally percussion resonance, finally cold, insensible, withered. On cold, insensible, and withered. incision black On incision black

185 to 139° F., and it is sterilized to 139° F., and it is sterilized at a temperature of 212° for at a temperature of 212° F. for twenty twenty

266 In the dog incubation rages In the dog incubation ranges from 15 to 60 days, and perhaps from 15 to 60 days, and perhaps 4 4

603 heated to 100° to destroy the heated to 100° C. to destroy the action of the pepsin, then action of the pepsin, then

● Typos fixed; non-standard spelling and dialect retained. ● Used numbers for footnotes. ● Enclosed italics font in underscores. ● Enclosed bold or blackletter font in =equals=. ● Subscripts are shown using an underscore (_) with curly braces { }, as in H_{2}O.

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