SF VJ33 Cornell University Library SF 959.D6W33 Dourine in Canada, 1 904-1 SM-Histor^^^ 3 1924 000 260 855 CORNELL UNIVERSITY. THE ' ' ' THE GIFT OF V^/53 ROSWELL P. FLOWER FOR THE USE OF THE N. Y. STATE VETERINARY COLLEGE r897 8394-1 /^. DOMINION OF CANADA DEPARTMENT OF AGRICULTURE HEALTH OF ANIMALS BRANCH DOURINE IN CANADA 1904-1920 HISTORY, RESEARCH AND SUPPRESSION BY E. A. WATSON, V.S., (Capt. C.A.V.C.) CHIEF ANIMAL PATHOLOGIST OTTAWA THOMAS MULVEY PRINTER TO THE KING'S MOST EXCELLENT MAJBSTT 1920 Cornell University Library The original of this book is in the Cornell University Library. There are no known copyright restrictions in the United States on the use of the text. http://www.archive.org/details/cu31924000260855 DOMINION OF CANADA DEPARTMENT OF AGRICULTURE HEALTH OF ANIMALS BRANCH DOURINE IN CANADA 1904-1920 HISTORY, RESEARCH AND SUPPRESSION BY E. A. WATSON, V.S., (Capt. C.A.V.C.) CHIEF ANIMAL PATHOLOGIST OTTAWA THOMAS MULVEY PRINTER TO THE KING'S MOST EXCELLENT MAJESTY 1920 INTRODUCTION. Canadian experience with dourine extends over a period of fifteen years and covers the study and suppression of a rare and serious disease hitherto untnown in Canada. Although the disease is one of the oldest recorded in veterinary literature and has been known to the Arabs and in certain countries of Asia and Africa for centuries, it is only within the past twenty-five years that the nature of it has come to be recognized and understood. The blood parasite Trypanosoma equiperdum, seen for the firsit time by Eouget, in 1894, was for a long time contested by leading veterin- arians of Europe as being the specific cause of dourine, and the question was still in dispute ten years later when the disease made its first appearance in Canada. It was then recognized by Inspector Burnett (1904), and immediately afterwards by Dr. Rutherford, then Veterinary Director General, who, as a result of his investiga- tion and in the absence of positive proof, held to his conclusions and adopted a policy the wisdom of which was borne out by subsequent events. The long search for the specific cause of the disease and its discovery; the experimental work patiently and labouriously pursued year after year; the determination of specific serum methods of diagnosis, by the aid of which the disease was eventually suppressed; and the difficulties met with and overcome both by the veterinary inspectors in charge of the field work and by the pathologists in the laboratory — furnish an example of persistent and unrelenting effort and success achieved in an important problem of veterinary research and sanitary science. This report includes a review and summary of papers and records published in the Annual Eeports of the Veterinary Director General for the years 1904 to 1919, a. general description of the disease, and a number of appendices. It is presented by permission of Dr. F. Torrance who for the past seven years has directed the work of suppressing dourine and has brought it to success. 9340— IJ CONTENTS. Page Introduction "^ History, Research, and Suppression, a review and summary «> Durine Statistics ' •' The Natural Disease 10 Diagnosis. — Appendix No. 1 1-^ The Complement Fixation Test. — Appendix No. 2 16 Experimental Dourine. — Appendix No. 3 35 Trypanosoma equipprdum. — Appendix No. 4 39 Regulations relating to Maladie du Coit (Dourine). — Appendix No. 5 40 References. — Appendix No. 6 41 Explanation of Plates 42 Explanation of Charts 45 Plates--! to IX. History Charts — I to III. Temperature Charts— I, la, lb, Ic; II, Ila, lib; III; IV; IX and X. HISTORY, RESEARCH AND SUPPRESSION. Review and Summary. The disease was first observed in the province of Alberta, in the Lethbridge district, in the early spring of the year 1904. From the inquiries made in the neighbourhood it appeared probable that the disease had been introduced several years previously. Though the origin was never exactly located there is good reason for attributing it to animals brought in from the Western United' States in which, among range animals, the disease was known to exist from time to time. In March, 1904, Inspector Burnett, Chief Veterinary Officer of the Eoyal North West Mounited Police, reported the existence of dourine (Maladie du Coit) in a stallion and several mares, located near Lethbridge, Alberta. Dr. Eutherford. Veter- inary Director General, Dr. Hargrave, of Medicine Hat, Dr. Davison, of the United States Bureau of Animal Industry, and other veterinarians examined the affected animals and agreed upon the diagnosis. A quarantine station of 1,800 acres of fenced land was thereupon established near Lethbridge, where all suspected animals were gathered in and held under observation. Under the Animal Contagious Diseases Act, 1903, regulations relating to this disease were formulated and brought into force (Appendix No. 5). Pro- vision was also made for the slaughter of infected animals and the payment of reason- able compensation to the owners. The quarantined animals were re-examined after an interval of several months and when it was expected that acute or well-marked symptoms of the disease would have developed. Dr. Butherford reported that instead of finding an aggravation of symptoms and a progressive state of disease, a surprise was encountered in that no well-marked case was presented, that many of the affedted animals had improved in a marked degree, and that there was not among them any one case sufficiently pronounced to warrant .an order for its destruction. Doubts began to arise as to whether the disease was actually dourine or some other. Many examinations of blood and of the body fluids obtained from affected animals were made in the field, and specimens were sent to various laboratories, but without revealing any trace of the presence of the parasite or any definite information as to the nature of the disease. Dr. Rutherford drew attention to the fact that dourine as an indigenous disease in Asia and in Africa had become more irregular and uncer- tain in its course and manifestations in Europe and in America, and, probably, still further modified under the peculiar climatic conditions of the northwest provinces of Canada. The decision was made not to immediately adopt a policy of slaughter, but to hold the suspected animals for a further period in quarantine until more satisfactory evidence was obtainable, and also for the purpose of acquiring as much information as possible as to the behaviour of the disease in this country. In May, 1905, the animals were again examined by Dr. Eutherford and accompany- ing veterinary officers. In some cases the disease was found to have made progress, in others there was little change from conditions noted on previous occasions. One hundred and sixteen horses were destroyed; a considerable number held over for further observation. Special officers were detailed to deal with the disease and were authorized to order the slaughter of any clearly marked cases coming under their notice. In September, 1906, it was decided to slaughter all the animals at the quarantine station excepting a few which had been under observation for upwards of twelve months and appeared to be healthy. It was then arranged to utilize ihe existing 5 quarantine station for experimental work in connection with dourine, and 'Dr. Hadwen, an inspector at Nelson, B.C., was transferred to Lethbridge and placed in charge, with a number of condemned animals at his disposal. Three infected animals were sent to the Biological Laboratory, Ottawa, for study and experiments. Investigations were continued in the field and in the laboratories during the winter of 1905-06 and the following summer. The disease was found to exist in various parts of southern Alberta, and by October 31, 1906, 412 animals had been destroyed. At the Lethbridge quarantine station breeding experiments were conducted with the object of ascertaining Avhether apparently recovered mares would bear healthy offspring or would remain sterile. Diseased and healthy stallions were employed in these experiments. Several slightly affected mares were spayed in the hope that such cases could be spared destruction and usefully employed for work purposes only. The search for the dourine parasite Trypanosoma equiperduni was kept up continuously both at Lethbridge and at Ottawa. Microscopical examinations were made of great numbers of specimens; dogs and other laboratory animals were inoculated with blood and material obtained from diseased tissues, but all were negative in result and every attempt to detect the parasite met with failure. At the Biological Laboratory, Ottawa, Higgins and Watson, had made a cytological study of the blood of dourined horses comparatively with the blood of normal horses and in certain diseases. It was found that the leucocyte formula in dourine differed from that in normal horses and in the other diseases studied, and was ^ of some diagnostic value. A pathogenic trypanosome, Tr. gainbie.nse, was maintained and studied in a series of laboratory animals, mainly with the idea of acquiring a knowl- edge of the habits and characteristics of a blood-haunting protozoan parasite closely allied to that of dourine. In October, 1906, Watson took over 'the investigation of dourine and removed to Lethbridge. In JSTovember and December of that year he discovered trypanosomes in the blood of native " cotton-tail " rabbits and in a species of northern deer-mouse caught on the quarantine grounds at Lethbridge. These findings created much interest at the time, being the first record of trypanosomes found in mammalian blood in Canada. The important discovery of Tr. equiperdum was made in February, 1907, by Watson, in a dourined mare in which tlie disease had been recognized by Inspector Gallivan. The reproduction of the disease by inoculations of this parasite into healthy horses, and the recovery of the parasites from the typical lesions produced, removed all doubt as to whether the dourine of America was a trypanosome disease or not, and clearly established its identity with the dourine of Asia and Africa and of European countries. However, in Africa and Asia, where the disease exists in its most severe lorm, no great difSculty seems to have been encountered in detecting the parasite or in diagnosing the disease by its clinical manifestations. In Europe, on the contrary-, the search for the trypanosome was for many years unsuccessful, the course of the disease was found to be irregular and uncertain, and diagnosis, as a rule, had to be based upon clinical symptotms, which, as often as not, were too vague and elusive to permit of satisfactory conclusions. In America it was already evident that the disease occurred in a still more insidious form and that frequently in the early stages of infection, which might continue for very lengthy periods, neither a characteristic symptom nor a warning sign of the disease was presented. Further, and far from being an invariably fatal disease, many infected mares retained or recovered apparent health, though suspected of being capable of transmitting the disease to the covering stallion. The better bred and especially the pure-bred imported animals of high commercial value were usually the most severely affected and the first to succumb. Prairie-bred animals of the native pony and broncho types were best able to resist or tolerate dourine infection and to lend themselves as carriers of it, and in the absence of any reliable means of recognizing them as such, constituted a frequent and dangerous source of infection. At this time large herds of horses lived and bred on the open ranges where natural conditions all favoured the spread of the disease. The horse industry was thus faced with a serious menace and the Veterinary Department with the formidahle task of overcoming it. The prospect of eradication in face of the apparently insurmountable difficulties in diagnosis did not look encour- aging. It was decided to carry on research, to study the disease from its various aspects and, if possibe, devise a specific or accurate method of diagnosis which would enable the department to deal with dourine in ,an efficient and satisfactory manner and to finally suppress it in its entirety. During the next five years, 1907-12, cases of dourine were discovered in a number of the breeding districts in the provinces of Alberta and Saskatchewan and reported on by Inspectors Gallivan and W. L. Hawke. The procedure when an animal was found affected was to secure the fullest possible history of the case, to trace all animals which had been in contact by breeding and to quarantine sick animals for an indefinite period, forbidding them to be bred, sold or removed without a special license. Periodical examinations were made by the inspectors in charge, and as soon as a clear case of disease had developed the animal was destroyed. But it hap]>ened quite commonly that no definite symptoms could be detected until well on into the second year of the disease, and that in consequence horse-breeding among such groups of animals, often several hundred in numbers, had to be prohibited for two and sometimes three years in succession. Even then there was no certainty that some latent carrier did not remain undetected. In fact, as became known later on, in any large outbreak of dourine and especially among prairie-'bred animals, it is practically certain that such carriers do remain and can only be detected by specific methods of diagnosis. Although no bettor measures of control could be devised under the existing circumstances, the prolonged quarantine for observation purposes, the periodic examination by the veterinary inspectors and the maintenance of large breeding establishments or herds of brood mares which must not be used for breeding purposes, proved costly, onerous and unsatisfactory. These five years (1907-12), saw a great amount of research and experimental work accomplished at the Quarantine and Hesearch Laboratory, Lethbridge. Besides the original trypanosome strain several others were obtained from difi'erent sources of dourine outbreaks. Parallel series of experiments were made with the different strains in a close study of the pathogenecity, life-history and variations in the virulence of Tr. lequiperdum. The strains were main- tained in horses; the evolution of the disease in its various phases was followed from year to year and many observations and experiments were made upon the survivors. Mares which had spontaneously recovered, some from a natural and others from an experimental infection, were successfully bred and raised healthy offspring year after year. It was found that these mares resisted reinfection and that the serum of such animals had immunizing properties. The experimental treatment of dourine was investigated both from a preventive and a curative point of view, immunizing sera and special drugs recommended in other trypanosome diseases, e.g., atoxyl and arse- nophenylglycin, were employed and reported upon. The chief objective, that of deter- mining a precise method of diagnosis, was always kept in view, and to that end the study of the serum properties of dourined animals was a continuous one. Serum reactions and serum methods of diagnosis were worked out and included a serum- globulin test, a trypanosome agglutination test and a precipitin test. Of these, the agglutination test was the more satisfactory but did not meet all requirements. The winter of 1911-12 was spent by Watson in a study of trypanosome diseases in European laboratories. A German strain of dourine (Beschalseuche) and an African strain were obtained from the Imperial Health Institute, Berlin, and brought to Canada for comparative work. Good progress in the serum diagnosis of dourine was made during the year 1912. The Complement-fixation or Complement-deviation test,* after several modifications and improvements in technique had been made, was found to provide a specific, precise and uniform method of testing. As a means of diagnosis it answered all requirements and came into general use during the year 1913. Towards *See Appendix No. 2, pag:s 16, for explanation and description of the Complement-fixation test (for dourine. the end of that year a recurrence of the disease was reported in the southern districts of Alherta. The field investigations showed it to be of very wide extent and to cover the old centres of infection of the first known outbreaks occurring six to eight years pre- viously. On one company's ranch 2,718 horses were involved, including a number ol imported stallions and mares and several hundred animals of high grades and "^^lue. Blood was collected from every animal and sent to the laboratory. As a result of the first test over 400 animals were pronounced infected. Some scepticism was at first evinced by the owners as animals, apparently in perfect health, were condemned on the strength of a positive serum rea.ction. But as many of these animals began to show symptoms and when several had died, all opposition vanished and the owners were will- ing enough to have the animals slaughtered and compensated for, and to fully co-operate in stamping out the disease. The Complement-fixation test has since been employed wherever the disease has made an appearance in this country. It has proved of inestimable value as the ma,in factor in the diagnosis and suppression of the disease, enabling an early and definite decision to be made — ^just as soon as blood can be collected and sent to the laboratory. Instead of holding suspected animals in quarantine for indefinite periods extending into years it has sufficed to apply the test and, after a short interval and to eliminate any doubtful reactors a retest. It was most fortunate that this test was available when the recurrence and wide extent of the disease became known in the years 1913 to 1916. During this period every effort was made to cover the whole field of the disease, and it was then that the heaviesit toll was paid in slaughter and in compensation. The large Indian reservations situated within the infected area of southern Alberta were for long suspected of harbouring dourine. It was rarely possible to detect a case among tflie native ponies themselves but cases were frequently found among the better grades of animals of the neighbouring ranchers which from time to time strayed on to the Indian ranges. A serum test of these Indian herds indicated many cases of hidden infection and of dourine carriers. This was not surprising as the constant inter- mingling of herds, the Indian habit of letting young stallions go uncastrated until three or four years of age, and promiscuous breeding had given every facility for the scattering of infection. To drain out this remaining source the herds were gathered up and tested repeatedly at intervals of six months to one year, and the animals whose serum reacted positively in the complement fiLxation test were destroyed. In connection with the serum-diagnosis of dourine over 40,000 laboratory tests were made during the period 1912-20. Since the disease first came under departmental action aiid up to present date (1904 to 1920), 1,933 horses have been destroyed. The figures year by year are to be found in the table of dourine statistics given below. At the present day dourine appears to have been totally suppressed in Canada. If further outbreaks should occur or the disease be reintroduced it should never have an opportunity of gaining much headway now that there are the means of detectin"- it either in its initial or active stages or in its latent and hidden forms, and thus dealing with it promptly and efficiently. Finally, the testing of all stallions imported into the country and stallions that are travelled through the country for breeding purposes would prevent the reintroduc- tion of the disease and afford an adequate protection to the horse industry. DOURINB STATISTICS (ll9i0'4'-.2») . Year. Horses destroyed. Value. Compensation 1904-05 292 120 167 49 28 37 40 18 18 •471 394 228 48 16 5 2 $ 24,045 00 10,210 00 15,505 00 5,175 00 3,760 00 5,130 00 4,960 00 2,610 00 3,145 00 73,115 00 48,931 00 26,085 00 4,924 00 2,011 00 392 00 105 00 $ 16,029 94 1905-06 6,806 48 1906-07 10,336 44 1907-08 . .... 3,449 92 1908-09 2,506 54 1909-10 3,419 98 1910-11 -. 3,306 60 1911:-12 1,739 99 1912-13 2,096 00 1913-14 48,743 33 1914-15 32,080 66 1915-16 17,389 65 1916-17 3,222 63 1917-18 1,340 66 1918-19 261 33 1919-20 70 00 1,933 230,103 00 152,800 15 Note. — During the present year commencing April 1st, up to the time of going to press, November, 19i2i0', not a single case of dourine has been reported. The final test of the last remaining herd under suspicion — about one thousand mares and stallions running upon an Indian (Reservation—has been concluded, all the reactions being negative. DOURINE. THE NATURAL DISEASE. As it occurs in Canada dourine infection is diredtly communicable from the diseased to the healthy animal by either the horse or the ass through the act of sexual union and in no other way. It is caused by a protozoan parasite named Trypanosoma equiperdum and is the only known disease of trypanosomian origin that occM's m Canada. Natural dourine is very rarely, if ever, observed in an acute form. Start- ing from an infective coitus, at some point in the genital organs the disease takes an irregular 'and uncertain course but is essentially chronic and intermittent. Determining factors in its evolution are (1) the degree of virulence of the try- panosome strain, (2) the degree of resistance or of susceptibility of difierent breeds of horses, and (3) physical and functional conditions and disturbances dependent upon climate and seasonal changes, breeding, exhausting work, and stabling or living a natural life on the open ranges or pastures. As to virulence, Laveran and Mesnil have well stated that "the trypanosome of dourine constitutes one of the best examples of variations in the virulence of the same species following its origin and genealogy." The higher breeds of horses show the greater susceptibility. In the thoroughbred the disease is apt to make quick progress and manifest itself mainly in derangements of the central nervous system. In the heavier and sluggish breeds, such as the "Clydesdale," the disease is more halting and is marked mainly by oedemas and disturbances of the circulatory system. Native pony breeds are the most resistant and frequently serve as carriers and reservoirs of the virus for a duration of years. Donkeys are also well able to tolerate infection and to become dangerous carriers. Climatic changes and extremes/ of temperature may cause either an arrest or an advance in the progress of the disease, cold retarding and heat favouring it. Thus, in Canada it often lies dormant through the winter months, becoming suddenly and increasingly active during the first hot spell of weather in June or July. Under natural conditions on the open range or at pasture more resistance is shown to it than in stable-kept animals. Breeding, heavy work and physical exhaustion favour the disease, especially in the stallion. Mares that have become impregnated at the time of the infective coitus occasionally abort, but more often they carry their young to full term. It has been noted again and again that pregnant infected mares have remained apparently healthy up to the time of parturition and that shortly after and about the time of the first oestrum have changed to a state of obvious disease and rapid breakdown in which marked symptoms of dourine were presented. In short, while all horses are more or less susceptible to dourine, the disease itself, like most chronic infections, is susceptive to various modifications and interruptions. Infection. — Although infection is passed from the diseased to the healthy during the act of copulation, and in that manner alone, it does not follow that transmission is always effected at such time of contact. A stallion, for example, may infect all the mares he covers during one week and none during the next. The contact of two mucous surfaces, the diseased and the healthy, provided the dourine parasite is present at the time, is the only necessary condition for transmission. The trypano- some is quite capable of passing through an intact and mucous membrane and no wound or abrasion is needed for the virus to gain an entry to the tissues. But there are periods in the course of the disease when the parasite is absent from the genital 10 11 ■mucosa and lies dormant in the tissues. These may be called "non-infective"; periods and may have a duration of weeks or of months; they are most apt to occur in the later stages and, consequently, animals in the earlier sitages of infection are usually the most active propagators, vyhile those which enjoy a temporary or partial immunity become the carriers. Period of Incviation. — The interval from the time of the infective coitus to the first appearance of symptoms or of visible changes varies and averages between two weeks and three months. It may be even longer and sometimes it happens that no symptoms can be recognized until the first winter has passed and the second spring or summer arrives. From an immunological viewpoint and as a period of sensitization, the incubation interval is less than one month, for specific serum reactions can be obtained within that time and usually in from ten to twenty days after infection. Evolution of the Disease. — Commencing as a local infection dourine habitually takes a chronic, intermittent and irregular course both in its local and general evolu- tion. With trypanosome strains of low virulence and in animals of strong resistance the infection may be arrested locally and held in check for an indefinite period and, in some cases appears to terminate there. In other cases, and such are in the majority, infection is both local and general, that is to say, it predominates locally, in the genital organs, throughout the course of the disease but, from time to time, finds its way to distant organs and tissues. In a third type of case the opposite holds good, that is, the genital organs acquire a partial or temporary immunity while the disease is progressing in other directions, and especially in its attack upon the central / nervous system. In most accounts of dourine the evolution of the disease is divided into three - well-defined periods or stages to which certain symptoms are ascribed, thus: (1) Primary — oedema, tumefactions and changes in the genital organs; (2) Secondary — plaques and skin eruptions; (3) Tertiary — paralyses, anaemia and cachexia. This arrangement is convenient for descriptive purposes but is arbitrary and rather apt to mislead an inexperienced observer of the disease in his conclusions or diagnosis based upon the clinical history and evidence. Actually, the disease operates in a succession of attacks, each attack being followed by a period of tolerance or teinporary immunity of very uncertain duration. One attack may follow another so closely that symptoms overlap or are never altogether absent. On the other hand, the attacks may be so far apart that in the long intervals between them there is no visible sign of tlie disease. Unless such an interval has continued for at least two years without any relapse it would be hazardous to assume that the animal had permanently recovered. As for the grouping and sequence of symptoms it should be remembered that symptoms of all three groups may be coexistent; or, that symptoms of one group may appear simultaneously with those of another, and that " primary " symptoms, or those categorized as such, may reappear after the first, second, third or any later attack, and, similarly, that those of the " secondary " or " tertiary " groups may recur repeatedly and irrespectively of the order or sequence indicated. In short, the disease is marked by stages of exacerbation, tolerance and relapse, . any of which may be of short or of long duration. -They may occur but once or may - be repeated over and over again before the final stage either of recovery or of decline. The symptoms most frequently noted are fever, tumefactions and local oedemas of the genital parts and mammary glands, oedematous eruptions of the skin, knuckling of joints, and inco-ordinate movement, especially in the hind limbs, facial .paralyses, ocular lesions, anaemia and emaciation. The one true pathognomic symptom is the oedematous patch or " plaque " ; but, unfortunately, it is a rare symptom and can only be observed in a comparatively few cases. In the earlier stages of infection fugitive oedemas of the genital organs and paroxysms of fever are the rule, thus : — In a stallion the first symptom is a slight oedema of the sheath, often accom- panied by a slight swelling of the glans penis. The mucous membrane at the urethral 12 exit may show a bulging, infiltrated appearance and may even protrude from the opening. These first oedemas tend to disappear within a few days. After an interval, usuaUy fifteen to twenty days, the oedema returns and is apt to be more pronounced. It may involve a portion of the scrotum and fluctuates as a cold ^and painless sweUmg. As a rule there are well marked stages of augmentation and diminution with varying intervals between. The oedema advances in a succession of waves and during each recess an increasing extent of permanently thickened and indurated tissues can be noted. The penis may be in a state of paraphymosis, temporary or more or less permanent. In stallions of the heavy sluggish breeds the oedema may extend over the whole of the floor of the abdomen and reach along the chest wall to the brisket, dominating the clinical picture throughout the disease. In the lighter breeds, and especially in the more active and highly-strung running horses, this symptom may be slight and quite transient. In a mare, the first symptom is a patch of slightly swollen mucous membrane of the vulva or vagina and is closely followed by tumefactions of the vulva. Sometimes only one labium is involved, giving a distorted appearance to the vulva. The oedema vanishes and returns, the intervals becoming more and more irregular. The outer black skin of the vulva, and sometimes of the anus, may show irregular shaped patches of depigmentation. The patches usually extend outwards from the inner borders of the labia, at first appearing pink and then becoming white. They are of uncertain duration; in some cases they persist or remain as permanent leucodermic patches, in others they return to a normal appearance within six months to one year. At this stage the vaginal mucosa may show raised and thickened, semi-transparent patches of a glassy or straw-coloured appearance or somewhat mottled. Folds of swollen membrane may protrude into the vulva opening; the clitoris is often swollen and erect. Frequently there are spasmodic attempts to urinate, prolonged periods of oestrum and increased sexual desires. At such times there is an excess of vaginal mucous mixed with a serous exudate and occasionally tinged with blood. In the later stages of disease, and especially when an infected pregnant mare has aborted or foaled, there may be a chronic vesico-uterine discharge. In some mares the genital symptoms may be so slight as to escape observation. After infection has existed for six months or longer, and when it may be impossible to detect any abnormal condition of the vagina or vulva, it is not uncommon to find a slight oedema of the udder or of the skin and underlying tissues just anterior to the udder. Less comimonly there may be noted an oedema about the anus, or one or more patches between the vulva and the udder, or upon the inner surfaces of the thighs. Such symptoms, slight and vague as they may seem to be, are important, for it is in these serosities that the trypanosomes of dourine are most likely to be found by patient searching. The true "plaque," or "dollar spot," differs somewhat in appearance from the oedematous patches already mentioned. The " plaque " has been aptly described as a thin disc of metal slipped under the skin. As such it may appear ujKin any part of the body surface, but seems to favour the sides covering the ribs. In Canada this characteristic symptom of dourine can rarely be observed. In many animals held under continuous veterinary observation, and in which this symptom was especially watched for month after month, in winter and in summer, a plaque was never known to have occurred. Others have exhibited plaques in the first, second and in the third years of the disease. In the most of cases the plaque has occurred singly and at wide intervals of time ; less often, two, or even three, plaques were observed at the one time ; and, in some rare cases, a rapid succession or " crop " of plaques during one brief period in the course of the disease. The average duration of a single plaque is four to five days. Rarely does the eruption and absorption of the swelling occupy less than three days or more than ten days. The average size is one and a half to two inches in diameter, and one-half inch in thickness or elevation. The site of a plaque, especially in animals with a smooth and glossy coat, is often made conspicuous by the staring or bristling appearance of the hair at that point. During the eruptive stage of the swelling and in the serous fluid the trypanosome of dourine can always be found. 13 Fever, distinctly of tlie intermittent or remittent type, may occur during any stage of the disease. It is more regular and pronounced during the early stages and before any marked tolerance or immunity has been acquired. A typical paroxysm has an average duration of five to six days, the maximum temperature, usually 104 to 105° r., being reached about the third or fourth day. The intermission ranges between twenty-one and twenty-eight days. These febrile paroxysms are closely associated with trjrpanosome cycles of development. A renewal of genital symptoms, the eruption of plaques, or a recurrence of oedema on some part of the animal body can usually bo detected during or just preceding the rise in temperature. As the disease advances the febrile conditions become more variable and inconstant. In the later stages a subfebrile temperature of about 102° F. may continue for weeks or months. Very little depression or constitutional disturbance accompanies the fever, even during the severer paroxysims, and the appetite is maintained throughout. The nervous system,^ is subject to severe disorders and disturbance, indicated by ineo-ordinate locomotory action and paraplegic conditions affecting the hind limbs, lips, nostrils, ear and throat. The animal shows a wabbling gait and sways from side to side. There is knuckling over at the fetlock joints, and, in unshod animals, the toes of the hind hoofs wear down from dragging and shuffling the feet. The animal is prone to trip over small obstacles and there is frequently a spasmodic contraction and relaxation of the muscles of the hind legs. Facial paralysis is nearly always unilateral. The ear, upper eyelid, nositril and underlip of one side of the head may be affected at the same time or only one of these appendages. The nervous symptoms are not as fugitive in character as the symptoms of the other groups. They tend to persist or to become aggravated independently of other symptoans, and, as a rule, are the more pronounced in the absence of other symptoms. Ocular symptoms are not constant and occur in only a small percentage of cases. They comprise photophobia, lachrymation, keratitis, corneal opacities and changes in the interior of the eye. Stallions seem more prone to ocular troubles than do mares. It is of interest to note that on more than one occasion a corneal opacity was the first symptom observed in animals that came under suspicion of dourine infection. The- duration of the disease averages between one and two years. Earely is it under six months; sometimes it extends to three years and occasionally to five years. As a rule, if an animal survives the third year of infection a permanent recovery of health follows. In such cases specific infection and immunity reactions are obtained with the complement-fixation test for an indefinite period and even up to 10 years. Termination and Mortality. — ^In cases advancing towards a fatal termination the decline is usually slow and gradual. The appetite remains good almost to the end and often appears excessive. There is a progressive anaemia and emaciation; the animal has a most dejected appearance and continues a miserable existence until finally, from exhaustion and paraplegia, it is down and unable to rise, and, unless destroyed, suffers a lingering death. ' In stallions the disease would appear to be fatal without exception; but in mares the evolution of the disease is slower and more irregular and uncertain in its result. Certainly, a large number of mares would make a natural recovery. The mortality depends upon the factors of virulence of the pathogenic agent and upon the resistance of the breed of animal infected. In the prairie-bred, native animal, the mortality is low; in pure-'bred, imported animals it is high. Among the naturally infected animals, representative of different types and breeds, at the dourine research station, the mortality has not exceeded 50 per cent. Pathological Anathmy.—T'he end stages of dourine are usually marked by a progressive emaciation and anaemia and in many cases, and more particularly in stallions, by oedematous swellings extending along the lower surf aces of the body. The oedema is sometimes of enormous extent and the swollen tissues in the r^ion of the scrotum and under the abdomen may be up to eight inches and more in thickness. 14 At the autopsy one finds more or less gelatinous exudation under the skin. In the stallion the scrotum, sheath and testicular coverings are thickened and infiltrated; and in siome cases the testicles ,are embedded in a tough mass df new sclerdtic tissue in which they are scarcely recognizable. In the mare the vulva, _ vaginal mucosa, uterus, bladder and mammary glands may show thickening and gelatinous infiltration. The lymphatic glandte, particularly the abdominal, are hypertrophied and softened and sometimes hemorrhagic. Further changes similar in character to those foundl in other chronic, wasting disease and anaemia may be noted, viz., gelatinous infiltration, serous transudation from the pleura, peritoneum and pericardium, and fibrinous deposits, adhesions and new growth on the liver, spleen, diaphragm and thoracic organs. Cystitis, pyelitis, nephritis, and bone marrow changes may also be noted. The spleen is not enlarged and may be under weight. The liver may be engorged with blood. The principal changes are to be found in the nervous system, and are most marked in the lumbar and sacral regions of the spinal cord. In animals in which paralytic conditions in the hind limbs have been severe and of long duration the cord shows softened, pulpy and discoloured areas. Histological examination shows a degeneration of the nerve fibres of the posterior columns, and a cellular infiltration, degeneration and 'atrophy in the extraspinal nerve trunks, particularly of the hind limbs. In accordance with these findings Marek names the disease Polyneuritis infeciiosa. 15 APPENDIX No. 1. DIAGN'OiSIS. Symptomatic diagnosis.— TlYie type of oedema affecting the genital organs, the eruption of the characteristic "plaque" and the peculiar nervous symptoms and inco-ordinate locomotion in connection with the hind limhs may sufSce for a diagnosis. ^ But in the early srtages of 'the disease and in latent cases it is diificult or impossible to detect any such symptoms or to recognize them with any certainty. The history of the case or cases suspected and the examination of the contact animals is important and not to be overlooked. Where it may be impossible to come to a conclusion in the case of a single animal, the symptoms presented in a group of animals may clear away all doubt. If it is found that only stallions .and brood mares are affected there are hut two covering diseases to consider, namely, dourine and coital exanthema. The latter is the disease most commonly confused with dourine owing to a misconception of the relative importance of ulcers and depigmented spots in these diseases. In coital exanthema the ulcers, preceded by vesicles and followed frequently by depigmented spots are characteristic lesions and the basis of a sympto- matic diagnosis; in dourine they are not and have very little importance. It has been said and repeated in many descriptions of these diseases that the depigmentation in the former is transient and in the latter permanent. I have found the opposite conditions to prevail. With regard to ulceration of the genital organs in horses it is extremely doubtful if such lesions ever occur as a direct result .of dourine or lany other trypanosome infection. I have never observed an ulcer in any case of experimental infection in horses. Ulcers have occasionally been noted in naturally infected mares, usually in aged animals, and in s'tallions, and also in normal mares and stallions. In appearance the lesions are quite similar in the dourined and in the healthy animals. In mares they are usually situated near the edges of the vulva and in stallions on the inverted portion of the penile sheath. Microscopical examination of deep scrapings frequently show spirochaetae infection. Detection of the paraisite. — In the naturally infected animal the trypanosome appears and multiplies in the serosities of local oedemas. It is futile to search for it in the blood. As soon as a plaque is signalled or an oedematous patch in the region of the vulva, anus or mammary gland is noted, the search should commence. The skin over the patch should be washed, shaved and dried. Two or three punctures are then made with a fine needle and if a clear or only faintly tinged serum exudes on pressure wet cover-glass preparations and stained smears are examined. A very long and thorough search should be made before pronouncing a negative result. Sometimes there are one or several trypanosomes present in each microscopic field but this is a rare finding. Sometimes only one or two organisms are to be found in the whole of the specimen examined. The object in puncturing the swelling with a fine needle is to avoid the blood vessels; the more the serous fluid becomes diluted with blood the less the chance of detecting the trypanosome. As a rule the parasites are present in the serous contents of the oedema only for a few days though the swelling itself may persist for several days after parasites have disappeared from it. It may accordingly be necessary to examine a number of oedemas before the parasite can be detected. In searching for the parasite in the vaginal tract the most oedematous looking patch of mucous membrane is slightly scarified and specimens of the exuding fluids are prepared for examination. A previous irrigation of the vagina with warm salt solution secures fresher specimens, richer in trypanosomes and facilitates the search. 16 The trypanosome is very rarely to he found in the massive oedema that spreads along the under surface of the abdomen nor in the oedema of the scrotum. In horses the parasites are always few in numbers and for long periods in the disease lie inactive so that detection is usually a very difficult matter, and diagnosis by microscopical examination is possible only in rare cases. Serum diagnosis.— The serum of dourine infected animals possesses certain specific properties which can be determined by (1) the complement-fixation test, (2) the agglutination test, and (3) the precipitin test. Of these, the first named is recog- nized as a delicate, safe and satisfactory method of diagnosis. The full technique and description is given further on (Appendix No. 2) together with some observations on the incubation period and longevity of dourine indicated by the serum reaction in the complement fixation test. The agglutination and precipitin tests^. * are useful aids to diagnosis but less satisfactory than the complement fixation method especially when large numbers of animals are involved. 1 Winkler & Wyschelessky, Berlin, Tierarstl, Woch., Dec. 21, WU. 2 Watson, Proc. Amer. Vet. Med. Assoc, 1912. APPENDIX No. 2. DOTJEINE AMD THE OOMPLEMENT-'FIXATIOISr TEST. The full description and detailed technique of the complement-fixation test method of diagnosis was published in 1915 in "Parasitology," and is reprinted in this appendix. Among the animals experimentally and naturally infected with dourine are some which have survived the whole period of these investigations, 1905 to 1920, some which showed tolerance and relative immunity for many years, some which succumbed to the disease and some which died from other causes (charts I, II and' III). The sera of many of these animals were used as controls in the 40,000 serum tests made during the period 1912 to 1919, the records of these re-actions furnishing some remarkable data, summarized below in table No. I. All the animals there listed (table No. I) excepting the last two, Nos. 180 and 182, were infected five to seven years before the complement-fixation test was available, so that the reactions for that period cannot be given. However, Nos. 180 and 182 were tested at intervals of a few weeks from the first to the fourth and fifth years and constantly gave positive reactions. Further, all other horses which succumbed to dourine in from one to five years, not included in this table but which were serum- tested at frequent intervals, gave constant positive reactions up to the time of death. Normal horses and horses in different stages of swamp-fever infection, used year after year as "negative controls," never gave a positive reaction. It may therefore be concluded that in dourine a positive reaction to the complement-fixation test is given in all cases up to the time of death from the disease and up to the fifth year after infection in cases that recover, and continued in some such cases up to the seventh, ninth, eleventh and thirteenth year. In experimental dourine of the horse and donkey the incubation period is de- termined by the complement-fixation test as ten to eleven days (table No II") 17 TABLE No. I. — Showing the serum reaction (to dourine) in the Complement-fixation test for a number of years after infection. Horse No. 2 (Chart No . I) 10 ( " " 1) 13 ( " " 1) 17 ( " " 1) 24 ( " " 1) 29 ( " " 11) 7f ( " " 11) 26 ( " " 111) 48 ( " " 111) 52 ( " " 111) 66 ( " " 111) 67 ( " " 111) 69 ( " " 111) 70 ( " " 111) 71 ( " " 111) 75 ( " " 111) 82 ( " " 111) 180 ( " " 111) 182 ( " " 111) Complement-fixation Test. Positive. Negative. 9th and 10th year. 5th to 11th year.. 5th and 6th year. 7th to 13th year. . 7th year. 7th and 8th year. . 9th and 10th year. 1st to 4th year 1st to 5th year 9th year onwards. 8th year onwards. 6th year onwards 9th " 6th " 7th " 7th year onwards 7th " 7th " 7th " TABLE No. II.— Showing the incubation period of dourine as determined by the Complement-fixation Test. Horse No. 190 (Tabl'e No. Ill) 1st positive reaction, 11th day after inoculation. 130 ( " ' No. Ill) " " 10th " Donkey 183 (Table No. Ill) 10th DOmilNE A!N, -51 — ■^■g 2 g.-s a k &3 qj X ca s. ja .23 en m c ■ rH o m m OQ 1 ' "■ ^ . >» >, r^ :^: 1 1 '0 S CD 'to yn ^ ,a ja - i ." oj 0) 0) a 'oj -*^ -*J +^ M >^ r5- "^ V 01 u ll 1 SI i "ft a d A S 5 ^ .0 •a + + + ++ + + + ++I 1 1 + + +' ++' 1 1 1 1 fH + + + ++ v: >. '^ 1 6 I 6 1 1 1 1 |i 6 10 cq .-H.^ (M cq >-H c ■e l-jj '■*» a 1 a CO a 3 » '0 ^ 2 ^ 0) -*J -*^ t to m rfi C3 § 9 ^ 5 c 1 -*j 5 s 1 CO 1 u all a^ ft " aT3 a> m 1 li s _U -f3 ^ww o« 1 Co s 5^ u P C3>A u ■^ ■» m -4^ CQ 1 « ^ (A H H Ph m 1=1 +3 c3 03 ^1 bH T3 03 Fh -M u m ?:» ^ CO nt, . CO u ca ? i>i>i>i >. >. >> >i rfcSc3(d 03 rt rt rf T3t3x3T) -Ct T3 T3 'd »0CT)O^ iC CD -^ i>. '^(MO^iOO -^ tiO 00 T-H > a S'. 5 = :: :: s Inoculation of trypanosomes after passage. June 12, 1912 Feb. 14, 1913 June 12, 1912 Feb. 14, 1913 (intravenous) Mar. 30, 1915 (intravaginal) Feb., 23 1917 (subcutaneous) June 7, 1915 (subcutaneous) Duration of disease and recovery. (See Chart II) 5i years H years 4} years SJ years Inoculation of trypanosomes before passage. Feb. 17, 1907 Aug. 16, 1908 Aug. 26, 1908 Jan. 8, 1909 a a 1 s S fS 1 o *o a o CO a ,o % 'c § T— ( CO O CC M .9 O "o t CO OO i o 39 APPENDIX No. 4. TETPAlSTOiSOMA EQUIPERDUM. The microscopical appearance of the trypanosome of dourine is very similar to that of other pathogenic trypanosomes of the Bruoei type. In morphology, vitality and general biological features, there is little to distinguish it from the trypanosomes of surra, nagana, mal de caderas and sleeping sickness of man. Very common features of the dourine trypanosome are (1) the presence of a vacuole bordering upon the centrosome and (2) the blunted, cut-off or fish-mouth appearance of the posterior extremity. Tr. equiperdum does not require any insect intermediary carrier ,or host and completes its life cycle in the body of its natural host — the horse — and is directly communicable from one horse to another. Tr. equiperdum is the only known pathogenic trypanosome of tropical or sub- tropical origin that is maintained by natural means in the temperate zones and in countries far removed from tropical conditions. In its natural host, naturally infected, Tr. equiperdum does not live as a true blood parasite but rather as a tissue parasite, selecting special organs, mucous mem- branes and the skin for its development and life cycle. In these respects the try- panosome of dourine differs from the trypanosomes of surra, nagana and the other trypanosome diseases. The appearance, development, multiplication, conglomeration or agglutination, phagocytosis and intracellular digestion of Tr. equiperdum takes place in a single oedematous patch or plaque, and the whole phenomenon can be traced within, and usually occupies, 3 days. The following is an example: — In a young mare, experimentally infected with a trypanosome strain (he fore pass- age through laboratory animals), three- to four-day periods of fever recurred at twenty-four to twenty-eight day intervals and, at the same time or preceding the rise iu temperature by one to two days, an oedematous swelling of the labium pudendi. Examinations of the fluid contents of the patch were made on the first sign of tume- faction or oedema and continued at intervals of a few hours throughout the stages of eruption and absorption. The procedure at each examination was to make a fine needle puncture and with the drop of serous fluid exuding make two dry smears and one wet coverglass-celled preparation. The latter was examined immediately, the former being stained by the Giemsa method. In the first specimens thus obtained the trypanosome could be located only with great difficulty being so few in number. In the subsequent specimens increasing numbers' and multiplication forms were noted up to the thirty-sixth hour. At the 40th hour conglomerations of trypanosomes and attachment to the phagocytes were noted. At the forty-fourth hour nearly all the trypauot( mes were injested by the macrophage cells and in various stages of digestion and disintegration. At the forty-eighth hour no trypanosomes could be identified as such, though in some of the macrophage cells fragmenting parasitic nuclei could be made out. On the third day the swelling diminished in size, was further reduced on the fourth and was quite absorbed by the end of the fifth day. No trypanosomes could be seen in the specimens taken on these days. ■Similar observations were made on a number of occasions and in different horses. In one case in which depigmentation of the skin of the labia pudendi was taking place, it was noted that simultaneously with the macrophagic injestion of the parasites numbers of these phagocytic celk were crowded with blackish granular pigment. In smear preparations many of these swollen cells ruptured and let escape masses of black granules. 40 Agglutination and phagocytosis of the trypanosomes cannot be observed in all casee and, in fact, only in the minority. The later history of these ca«es shows that the infection was well tolerated and the inference is that agglutination and phago- eytosie is an indication of increasing resistance and of the process of immunity. Little is known of the nature and properties of trypanosome toxines: In the acute, generalized infections of small laboratory animals, and in which only one trypanosome cycle is represented, death apparently results from the sudden release and rapid absorption of toxin at the time of maximal trypanosome multiplication and commencing disintegration. In the chronic, intermittent disease in the Ln-ger animals commencing in a local infection, the trypanosome repeats its cycle again and again and the toxic action on the nervous system appears to be progressive and cumulative. Attempts to cultivate Tr. equiperdum on artificial culture media and to isolate a toxin have not succeeded in the hands of the writer. APPENDIX No. 5. REGUIATIONS RELATING TO MAT.ADIE DU COIT. By Order in Govmcil dated 28nd July, 1911, m virtue of the Animal Contagious Diseases Act, B.S.Q., 1906. 1. No animal which is affected, or suspected of being affected with iMaladie du Ooit shall be permitted to run at large or to come in contact with any animal which is not so affected, and no such animal shall, in any case, be used for breeding pur- poses. 2. Any inspector may declare to be an infected place within the meaning of " The Animal Contagious Diseases Act," any common, field, stable, or other place or premises where animals are found which are affected or suspected of being affected with Maladie du Coit. 3. No horse, ass or mule shall be removed out of any place so declared to be an infected place without a license signed by an inspector. 4. The Veterinary Director General may from time to time order the slaughter, castration or other disposition of animals affected with Maladie du Coit. 5. Inspectors are hereby authorized to inspect any animals affected with Maladij du Colt, or suspected of being so affected or which have been in contact with animals so affected, or suspected of being so affected or which have been in any way what- ever exposed to the infection of Maladie du Coit, and may order any such animals to be collected, detained, isolated, castrated, or otherwise dealt with as may to them appear advisable. 6. The expenses of, and incidental to the collection of, isolation, seizure, castra- tion, or otherwise dealing with animals for the purposes of these regulations, shall be borne by the owners of the animals, and no indemnity shall be allowed to the 'owner in case of damage arising out of or resulting from such actions, except as herein- after provided. 7. No entire horse, ass or mule nor any ridgling more than one year old shall be permitted to run at large on unfenced lands in the province of Alberta or in that por- tion of the province of Saskatchewan lying west of the third principal meridian. 8. Any entire horse, ass or mule or any ridgling more than one year old found running at large within the area defined above may be seized and held on the order 41 of any duly authorized veterinary inspector of the Department of Agriculture, who shall forthwith whenever possible notify the owner of the said animal of such seizure, and the said animal, if not claimed within thirty days of such seizure, may be cas- trated, and no indemnity shall be allowed to the owner in case of damage arising out of or resulting from said castration, seizure or detention. &. Animals affected with Maladie du Coit, may on an order signed by a duly appointed veterinary inspector acting under special instructions from the Veterinary Director General, be forthwith slaughtered, and the carcases disposed of as in such order provided, and compensation may. be paid to the owners of such animals if and when the Act so provides. 10. Before an order is made for the payment of compensation in any of the cases aforesaid there must be produced to the Minister of Agriculture a satisfactory report, order for slaughter, and certification of valuation and slaughter, all signed bv an inspector. APPENDIX No. 6. REFERENCES : TOREANCEj F. Burnett, J. F. Watsok, E. A. Rutherford, J. G. — Ann. Rep. Vet. Dir. Gen., Canada, 1904-1912. — ^HiGGixs, 'C. H., and "Watson, E. A. — iSpecial Report on Dourine, Dept. Agric, Canada, Nov. 1907. -Ami. Rep. Vet. Dir. Gen., Canada, 1913-1918. _ .< U u u « " ]^,9.Q4_ _ " " ■' " " ■' 1909-1915. (• Dourine Experiments'., 'Note on the life history of Tr. equiperdum', 1909; 'An Experimental Study of Dourine'., ' On the Diagnosis of Dourine '., 1910 ; ' The later history of 20 survivors of Dourine ', 1912 ; ' Field Investigations of Dourine'., 'The Transmission of Dourine to Laboratory Animals '., 1913; ' The 'Serum Test for Dourine', 1914.) ' Dourine, its pathogenecity and. . .a test of the efficacy of druj; treatment. . . ', Jour, Comp. Path. & Ther., 1911. ' The Serum Reactions and Serum Diagnosis of Dourine ' Proc- Amer. Vet. Med. Assoc, Aug., 1913. 'Dourine and the Complement Fixation Test', Parasitology, Vol. VIII, 1915. p. 156. aii(j Hadwen, S., — ' Trypanosomes found in Canadian Mammals ' Parasitology, Vol. V, 1912. Gallivan, M. V. — ' Dourine '., Ann. Rep. V.D.G., 1914. Appendix No. 10. Hawke VV. L. —'An Outbreak of Dourine', Ann. Rep. V.D.G., 1914. Appendix No. 20. 9340—4 42 EXPLANATION OF PLATES. Plates I, II and III— Natural infection of Stallion No. 35, showing' eye lesions, fluctuating oedema, progressive emaciation and final stages of the disease. Plate IV— Stallion, No. 38, naturally infected with Dourine (1905-1907). Plate 7— Experimental infection of mare No. 66, showing a ring-shaped or hollow-centre "plaque," the ninth to appear, in the tenth month inoculation. Figure 1. Fig. 2. — Natural infection of mare No. 42, showing facial paralysis. Fig. 3. — Paraplegia in a iiiiturally infected mare. Plate VI— Figs. 1, 2 and 3. — Experimental infection in young fillies, showing typical oedem- atous patches of the anus (fig. 1), of the labia pudendi (fig. 2), and of the skin between the buttocks. (Fig. 3). Figs. 4 and 5. — Natural infection of mare No. 159, showing depigmental skin of the vulva and anus and the transient character of such depigmentation. Fig. 5 shows the condition ten months later than fig. 4. At the time these photographs were taken (figs. 1-5), trypanosomes were present in the oedematous fluids, in eacli case. Plate VII— Trypanosoma equiperditm in the oedematous fluid of a swollen labium pudendi, showing the development, multiplication, agglutination, phagocytosis and digestion of the parisites — all taking place within the space of 48 hours. Plate VIII— Trypanosnma-equiperdum. Plate IX— Trypanosoma rquiprrdain—the. flagellated micru-orgaaism causing Dourine, as seen in the vaginal mucous fluid (figs. 1-8) and in the oedematous fluid from swollen patches of the vaginal membranes (figs. 10-18) ; taken from a naturally infected mare (animal No. 36). 43 EXPLANATION OF CHAKT8. IIISTOEY— CHAKTS Nos. I, II, AND III. These charts epitomize the history of forty-two cases of dourine in horses, twenty- two being naturally infected and twenty experimentally inoculated. The chief points of interest and conclusions are: — The fatality in stallions. 'The tolerance and recovery in mares and the relative immunity obtained to reinfection by natural means. Tolerance and acquired immunity to inoculations of a natural strain of dourine (horse) is broken by inoculations of a laboratory strain (rats and guineapigsO and death follows. In some of these mares tha period of observation is fifteen years, in others twelve, ten, and a lesser number of years. Mares spontaneously cured of the disease have shown their usefulness for work purposes and for breeding. No case of natural trans- mission to the offspring has been observed. The four healthy stallions kept for breed- ing these naturally cured mares escaped infection. Specific serum properties, as shown by the complement-fixation test, are retained in some cases for many years after recovery and cure; in others these properties are lost in about five years (see Appendix 2). History Chart No. II shows the origin and genealogy of a strain of dourine in horses, and the exalted virulence obtained by serial passage through foals, and is supplemented by: Temperature Charts Nos. I, la, lb, Ic; II, Ila, lib; III; IV; IX andX. Plate I. Plate II. Plate 111. Plati: V. *S is- rwrn. FIS. 1. Fig, 3. Plate VI. Plate VII. Trypanosom.a equiperduyn. 'LATR VTJT. I'l.ATF. IX V^^^=^^ f- '4 HISTORY-CHART No. 1. Eealtu ok Animals Braxch. — Veterinary Eesearch Laboratory, Lethuridge, Alberta. 1905 1906 1907 1908 1900 1910 1911 1912 1913 1914 1913 1916 1917 191S 1919 Stallion (SI) Natural infection. Oedema Destroyed Stallion (33) Natural infection. Oedema, anaemia, emaciat paraly on, sis, death (July 24) StaWon (72) Natural infection. Oedema. Cachexia, death (Oct. 24) Marf (.') Natural infection. Tolerant. Covered by Stl. 31. Normal. Covered bj Stl. 72. Normal. Bred to healthy stallion. Foaled Foaled. C.F. ++ C,F, +++ Foaled, Failing health. Death (Jan. 25). Complement Ijxation — positive. Man i i 1 Natural infection. Tolerant. 3 coverings by Stls. 31 and 33. Normal. 3 coverings by Stl. 72. Normal. fEmpI Normal, eyed as a w Normal, ork mare) Normal. Inoculated with try- panosomes from mare 165. C.F. +-h+ Oedema, trypano- some periods. C.F. ++ + Failing health. C,F, ++ + Death (Mar, 15), Complement Fixation- positive Mar. (19) Natural infection Tolerant. coverings by Stls. 31 and 33. Normal. 3 coverings by Stl. 72. (Emplo yed as fast driving ma re for 6 year s, and as a brood mare C.F. - C.F, - Died foaling. Complement Fixation- negative. Mnn C) Natural infection. Tolerant Inoc. of tr.\-pano- somes from mare 36. Normal. Normal. Inoc. of trypano- somes from foal 6f. Normal. Normal. Accident- ally hurt. Destroyed M<„r 19) Natural infection. Tolerant. 7 coverings by Stls. 31 and 33. Normal. Inoc. of trypano- somes from mare 3r). llecurring oedema of vaginal mucosa. Normal. (Death from colic.) Marr US) Natural infection. Tolerant, 1 cover ine by Stl. 31. Normal. Bred to healthy stallion. NoriMui. Foaled . Inoc. of trvpano- somes from Foal 12f. A period of high fever after inoculation. Normal. (Employe Norma 1- d as a work C.F. -^++ marc.) C.F, +++ Foaled, C,F, + + + Foaled. C.F. -^-f-h Foaled C.F. ++ + C.F. +-i-H Foaled. C.F. -h++ Complement Fixation- posit ivf. Marc (i:) Natural infection. Tolerant. 1 covering .Stl. 33. Twice inoculated, trypano- somes from mares 9 and 29. Normal. Twice inoculated, trypano- somes from foals If, 7f. Normal. (T'^mployed Normal. as a work Normal, mare.) Foaled. C,F, + C,F. + Died foalins. Complement Fixation — positive. Mnn I/.-') Natural infection. Tolerant, f) varies removed. (Normal h ealth anfl co ndition mai ntained.) Inoc. of trypano- somes from mare 165. Oedema. C.F. -I- + + No symp- toms from March to December. C,F, ++ + Inoc, of trypano- somes from inf, rat. Death, Complement Fixation- positive . Feb.. 3 1914.— Inoc. of trj-panosomes from an infected rat. May. 10 I914.--Death. Mtirt [.v;-! Natural infection. (Apparentl y recovered. ^'ery good condition. No sympto ms.) Inoc. of trypaon- somes from mare 165. No reaction. C.F. -\-+-\- Inoc. of trypano- somes from inf. rat. Death. May 5. — Inoc. of trypano- somes from an infected rat Aug.. 4 1913.— Death. Complement fixation— positi\'e. Mare {.!',) Natural infection. Tolerant . 7 coverings bv Stls. 31 and 33. Normal. Foaled . Slight Oedema. Normal. Foaled. Normal, Foaled. C.F. - Foaled . C,F, - C,F, - . Foaled. C.F. - Foaled. Foaled-, Complement Fixation — negative Mare [I'') Natural infection. Vaginal discharge, emaciation paraplegia. Slow improve- ment. Inco- ordination. Further improve- (General ineo-or lealth and dinationof h chronic sym condition go nd limbs re ptom.) od, though mains as a C.F. +++ Inoc. of trypano- somes from a rat,. Death. Complement Fixation- positive. May, 5 1913.— Inoc. of trypanosomes from an infected rat. Sept., 29 1913.— Death. HISTORY-CHART No. 2, Health of Amjials Branch. — Victerixahy Research Laboratory, Lethbridge, Alberta. S'.-'i.il i^cneration and passago. 1 it T/y)iant>s„rrirs rfjnipordum 1906 1907 1908 1909 1910 1911 1912 1913 1914 1915 1916 1917 1918 1919 ]>t. .Slallion f;.;.'!. N'aturai infection. Oedema, keratitis, anaemia emaciati paraplegi on, Death. h. I'nrI Marc iSC). Natural in faction. Oc at dcma vagin axie paraplt plaquew. al m.m,, gia. Paralysi s. Deat ?,i-i\. Foal (39). Experimenta inoculation, trypano- somes from mare 36. Oed- ema, para- lysis D oath. :;r.l Marc (41). Kxperimental inoculation, trypano- somes from mare 36 . Slight oedema vagina! mm. 29 plaques. Normal. Normal. Normal. * *June 12, 1912. Inoc. dourine trypanosomes from guinea- pig - November 4, 1912, Death. (See Table IN.) .Jrd. Foal (29). Kxperlrnenta inoculation, trypano- Slight oedema vaginal mm. H plaque.s. Xorniai. Normal. Raised healthy foal. Normal. C.F. +-h C.F. ++ Foaled. C.F. + C.F. + - Foaled. C.F. - + C,F. - + C.F. - + Foaled. Complement Fixation,— Weak Homes from mare 36. ■ii\i. ..Frlh: (60). Kxperimental inoculation, trypano- somes from foal 29. Re oe lab curring dema of iia pudendi. Normal. Normal. Norm;ii. C.F. - C.F. - Foaled . C.F. - Foaled . Complement Fixation.— nega- tive. }ih. Foal Cif). Experimental inocu lation . try pano- somcs from foal 29. '.See Tempe Charts I, (See Tcmpe Charts rature la, lb, Ic.) rature II, iia,iri..j fe oc edema, ver paroxys ular and par mptoms nis. aplegic Recovering. Absence of symptoms. *Feb. 14, 1913. Inoc. dourino trypanosomes from an in- fected rat. Mar. 15, 1913. Death. (S.-l- Table IV.) ■IiIj, Foal {.if}. Ivxperirnental inoculation, trypano- somes from foal 29. He oe fe 3 pa curring dcma l.p., ver paroxyh plaques, raplegic «y Ills. mptoms No symptoms. Apparent recovery. ' *June 12, 1912. Inoc. dourine trypanosomes from an in- fected guineapig. Sept. 10, 1912. Death. (See Table IV. ) '>ih. Foal (I/). Experimental inoculation trj pano- some.s from foal of. (See Tempo ra ra ture Cha rtnij rtlV.) Recurring oedema; fever paroxysms Slight paraplegic symptoms. Apparent recovery. ' *June 12, 1912. Inoc. dourine trypanosomes from an in- fected guineapig. 4 Sept., 1912. Death. (Seo Table I v.) (Ifh. Foal (6/). Experimental inoculation, trypano- somes from foal If. (See Tempe ture Cha Kecurrin ma, remi fever, de g oede- ttent bility D eath. 7fh. Foal (7/). Experimental inoculation, trypano- somes from foal 6f. Recur ma, re fever. ring oede- mittent urticaria No s\'mpt Apparent after 3 inje araenophe oms, recovery, ctions of nylglycin. C.F. - C.F. - Foaled . Foa led . Complement Fixation, — nega- tive. sti.. Foal (Hf). Experimental inoculation, trypano- .sftmes from foal 7f. Fev Dea 41 Fe De 51 F D 5 er. th. days. 'Jtli. /''/^a/(ll/j. Experimental inoculation, trypano- somes from foal 8f. See Tempe rature Cha rt IX.) ver. ath. days. H)th. Foal (12/J. Experimental inoculation, trypano- wonies from foal llf. Sc^ Tempo 1 rature Cha rtX 9ver. -ath. I days. HISTORY-CHART No. 3. Health of Animals Branch.— Veterinary Research Laboratory^ Lethbridge, Alberta. 1906 1007 1 IOCS 10O9 1010 1911 1912 lOKl 1!]14 101.5 1916 1917 I9I8 1919 Mar. (>1(x)l from stallion 33. Nov. 21 to Dec 3, 190G. 1 Absence of definite symptoms. 1 plaque (Aug. 22) Trypano- somes detected. Normal. Fouled. Fouled C.F, - Foaled. C.F. - Foaled. Ill hcaltli. Died. Complement* Fixation, - nega- tive. mental transfusion of 600 c.c of blood from mare 36. Apl. 24, 1907. Intermit'nt paraplegic symptoms Normal. Normal. (An exoell ent riding horse.) i:>U'd. irom influenza. mental inoculations of try- panosomes from mares 2S Mnd 41 and from foal 7f. Apl. 21, 1908— May 21. 1909 Oedema of lab. pudend 8 plaques. Trypanoso 1 plaque, mes present Normal. (Made a good saddle mare for 4 years.) C.F. +++ III health. Paralysis. Death (16 Sept.) Complement Fixation,— posit- ive. Relapse of dourine and death after 4 years of toler- ance and normal health. mental inoculations of try- panosomes from mares 29, 41 and 82. Feb. 3. Aug. 27*08 Oedematos swellings under abdomen. Normal. Foaled. C.F. - Foaled. C.F. - Foaled . Foaled . Destroyed (Dec.) Complement Fixation,— nega- tive. Man (69) (3 yr. old). 1 cxperi- inental inoculation of try- panosomes from mare 29. Aug. 27, 1908. Recun'in of labia rich in tryp g oedema pudendi, anosomes . Normal, recovery. (Made a g cod saddle mare fur 4 C.F. - years.) C.F. - Foaled . Foaled . Foaled. Complement Fixation,— nega tive. Man- (70) (2 yr. old). 2 experi- mental inoculations of try- panoHomes from mares 29 and 41. Oct. 4, 1907. Recurring rich in try oedemas, panoaomes. Normal, recovery. Foaled . Foaled . C.F. - Foaled . C.F. - Foaled . Foaled , Foaled . Complement Fixation,— nega- tive. Mare (71) (3 yr. old). Experi- mental inoculation of 100 c.c. i. Absence of definite symptoms . Normal. Foaled . Foaled , C.F. - C.F. - Normal. Complement Fixation,— nega- tive. Murr CH) (5 yr. old). Experi- mental inoculations after re- covery from a natural infec- tion from stallion 35. Tolerant. Slight oedema of vaginal mucosa. Normal. Inoc. of trypano- somes from foal 3f. Normal. Inoc. of trypano- somes from foal l.f Normal. (Employ ed us a fast driving ma C.F. - re or 5 yea C.F. - r».) C.F. - Foaled. F'oaled , Died in foaling. Complenjent Fi.xation,— nega- tive. Immunity acquired. Marr (53) (5 yr. old). Natural infection by stallion 35. Tolerant. Slight oedema and paraplegic symptoms. Normal. (Employe d as a sadd Ic mare for 10 years C.F. - C.F. - Complement Fix;^tion,— nega- tive . (DecO Mar< (75) (7 yr. old). Natural infection . OedemaH mucosa an pudendi, trypano of vaginal d of labia rich in ^omes. Normal, recovery. (Normal h \iii\t\x maint lined.) C.F. +-^ C.F. + + Destroyed . Complement Fixation,— posi- tive- Marr (SB) (7 yr. old). Natural infection . Recurring mucosa, la under abd frcqu oedema of )ia pudendi 5men. Tryp ^ntly detec vaginal and inosomes ted. Normal, recovery. (Normal health.) C.F. + + C.F. + + Destroyed. Complement Fixation,— posi- tive. Mare (180) (5 yr. old). Natural ini'ection (1913) by stallion 182. C.F. -t-++ Plaques. Inco- ordination. C. F. + + Foaled. (Mule) C.F. +++ C.F. +++ Fair Paraplegic condition, symptoms. Emaciation. Died. Complement Fixation,— posi tive. Marr (181) (4 yr. old). Natural infection (1913) by stallion 182. 1 C.F. -l-h-f Paraplegic > C.F. + + + ymptoms. Died. (Aug. 15) i Complement FLxation,— po.-i- tive. Stolhon (183) (3yr.old). Natural infection (1913). i ■ 1 i PlaQuow an t Trypan c pics c C.F. ++ + oedema, somes nt C.F. + + + Castrated, C.F. +++ Worked. C.F. + + + Failing health. C.F. + + + Decline and deatli. Coinplftnent Fixation, -posi- tive. Chart I. Sxperlmental Dourlne. (E. A. Watson.) ISOS Uth August September October No vEMBER December (Age 6/nMsj Horse-foal, Day stJ,i's^'?>? ^ .Si's; '5 JlVie !4;5^^V^ * ..I"!'.!*, «>!»», « .^ !y f ? vvi!» s i. k t ■* » « J ??S!*»?i?!«««i?l<*«M!i5'*vN.,»*.*^«f**>*??s!*!t«9'«^«:?Ji*!'!e'J:!Mi?is 105 104 103 102 101 100 99 98 97 ^it:F,i,.u:::;i4._,::._It::i:::::::::::;::::::::: 1 (Ko.3.f.) / _|.|.ii c. ± J— - -^ v^u- J_ -, i '' A^e G wet^As ' f§! 1 „ 1,,, 1% ._ V" r,!^ JiiT_j::::::m:::j::::::::::::::::::i:::::/? 4 T._ jw -M . Treated J:|'_. _...,____/ l_^j I^._^ A t- - i/t 1 I ^ iHi!^ d \ ..--yjB-- '^ i ' J^ ,,i..,{, Ik iLi /" \il ' 4--r'T-T'""^--^^4^4^T-r^K'MWi ■ WvnM^ T '^n^^v< %/ 1 L X 1 i i : J i ..1 ::f,tf :i::i:::jT::::'T:! n:::::::iT;:^:::::::::::::: ill! _J_ ' J_ 1^ t ..__^ TrypanoE Atoxyl - dose - Day after Inoc oroes _l r Tl ^ QT - T . ( r , Li ■em. T\ ^„_ "" r»-r'-i-"j 1 -F'dr T r i _ . _ _li .^ jl ._j_, . ._ j "t "t XT P j_ 11 if^'iT 1 utfJhra 1 1 1 ^'^f L.l, "r piderc^ rjT:, rr ultn sA •,'» s to ^ tti s:^ ". 1 » s *. "v* <» «;v «.!"!»•> »> k;«<»^ - |-| ■! ' "P "! -il■^^">;»^ '"X!* « 5; ^ 'o*,")i»,S,to ^^ !^ §^[o, ");»ito:to> ^.^ § ^,.^"1 *-;Vijto >'.9|^^ -^ Nflj ♦AMtoV ^ft^ vJN,n*,to,to:x^ Continued:- 19 OS Mth January Februahy March Apl.-Mot^ Day \\;'»'~^S?'v?'5;'?!^'^^?*^^i!!fe'iSlte!5i5fe : "^-' 106 105 104 103 102 101 100 93 98 97 I J iX' i IJ ^ M ! f 1 j 1 i 1 1 ' \\ \v '"tltXiirx"""" 4_iiXr'^"'" T _| [ Ur 1 j_ jii i! jyvj !|_|| W • T 'T yYF \'^ 1 r 1 T ^P •\ '•■\ if HA^ Mil \\\\\ i Xi ' /x 1 1 X X 'ij' '^ 'lU ' ! 1 ! h ' if i i\Aj ! i 1 III ! i 1 ^i 1 i l||l f, Til: S js i i'' T"" [ \ SIVj i ^' ■■''-' J 1 K j i K ; ii i i 1 1 M j ' 1 1/ ' I 1 ' 5 ' , is^ Mr illiiRAil ii/i h'VaR L ^f ' ' 1 .'iI aA" 'Ja^ 'i '"'ii»A''ir '■ m ii/ 'i" "l^ri?"^" m3^ WW /%vV\^'^ta |r|- ' Yi ' , : ' i ! ! 1 ' ; I ' 1 1 ! 1 1 ! ! i M 1 1 J i 1 ! ! ; ! ! ! 1 1 ;' ' C^'§r !ui ixxx:xiiLXX-""""----t--X44-V-" ' tl^t'"' I 4 " J — i^ XI X i 1 ■" 1 &M\ Tiypanosoroes ^- --B--^-i-r¥^- s ' '^ ![?""" /itorvl - doze - bus Donovan's sol. o.cm. ",""":: ::::ss:"+:r ._:::t::5:,::. 3__.,5._| L_L !X_i X._L 5^p?:f:: .. .1 f J_ __^._IT-.5L .F.|.. JjS_._, „ 1 „.S_ 1 An.L»j_.T+t:.___ ,it„_ ri i r__ r f^i, s iv^reV na jyef-yiife>>i C'?re6/'o-iJ>irb( fei/tthsi i T Day after inoc Jltn_ £f ||. '|^,»i|f ^1 fe *^'^!°*:^^ N ^* Vi V >^:*;C^ 1 ^ fs.>-)» h to >^,^:^'^,^'N "> * S.to ^ ^:ci ^^;^J.-'.*:^ to;^ ^|0, ^,N!o»")»>i,to^;^[ch^:\N;"i>toto>v;;c^^^ - v, -J ■-, cK^a^.^Iw"! » to,to!^j%l l " * ! Experimental Station (Health of Aninals)I,ethl)ridgo,Alta, Canada Chart 1. a. Horse, Bo.- 3.'f. 'coi'tHnuea T- i §os>" Mth, APRtL Experimental Dourine« (E. A, Watson.) /►jsKS^SIf:* ?!^ *S!« i>fe'j!'S!^:is^|«j^!: Atoiyl - dose Day riftor inocultn JUNE JULY Hth ArsenophenylglydJF Day after inooultn July August M yg of onimal- /i/eaf a2mf-hs} SEPTEMBER OCTOBER Experimental Station (Health of Animals )Lethbridge,Alta, Canada Hor i 106 se, No. 3. f. Experimental DourltlB. (E. A, ■(fetson.) hfinuec/- I909 I9l6 October November ^ December ^z igeofan;ma/-/^^rx) JANUARY i^^its^k'iiHi, 5!'5] ^I'SVii ^*^'^ ■•;» -> »^!» -^ 'O «'S ^ 51 7 t5i« ¥'9^V5iS'iti5 i i i . 1 ! i i J M h M i i i 1 1 i 1 i 1 1 i i 1 i 4 -jl riX'Tj" irt 11IT ■■ 105 104 l'!Mij!':iiliiil ilMMji!! i ' T _._„_X- xxxxxT^iXx'x1X44xr_Trrx:ii:r 1 MiliMlH" Hi lliMitill 1 ,__^^ , -"""X,, ^..^._.._X__.__.iXJ^^... 103 102 101 100 99 98 97 i rnx'ijTn \ \ i iMi x , i \ u X U t li*. I m^^Mim^^H^^ ^ + T-Xt __ ifn y_v%?-MM\A^ " \ '' \\\ \ "Y\ ix^XT" ' " X"W+~'Vr~ 4 iX 1 XI , r r i r X ^ ■ ix ' Trypanos Day after Inoc ones 1 \ r r~ n Mjaehei-i/Wei/M 7f7tfW ? c4c Aiie.St ^if^/rf ii'nproi>epie^ - '- ' * i 1 ' ! ! ' ii i i ', ! '-- 1 U p Jij 1 J 1 i i I ! ; . 4._F D 11. ..[.__ altn §i|:v ». 1 ♦ >) to \ ^^ - »q*i'2j5 !^a5iS£ '"!&Vj!:i5i?Ji^ J51!i*^i*i'' '^^•'^^^P'X^'^'bj'^^^J: 1910 Mth January Februarv March April May Day kv^V« V J^V. s . . *i. » <'HH^\^%U^tidMk « V s 4,s *.!«=,? v» 5 »* $ ^ in tili.P^QTuT'UXif 1 ilxXJ-U'! IJX 105 105 1 J __ _ ,, "Tr-"^ - - I X ij 1 1 1 . Atoryl - dose - gta Day 97 rtrr rrypanosqrpes^|_[_i^ i Mtll At Mnophe nyl gl ycln July August ta^e of animal • /year * 2 mfhi) SEPTEMBEP y?t I? t W;E?.'>''^*' "^ *!^ i* > '_ ?*> °^ ?*«^^5ij;M^?H5V^v Day after inocultnjo, !«i'5SSiWs^ Octo ber wiW*9?W^ - ^rit^/ft Ocular- pheiioiiii viii • «w£T»)'t:n-.ithi'oASi '^^i^i'^:*''^'^*",^.^(R.' S^ c^a*^ !j);°l!§lj»i ^jitirkea t^e/yrJs'sra^ &^e^era/ i/)hea/^f^. y.5Hff ^ tvedA Experimental Station (Health of Anlmal5)Lethbridge,Alta, Canada Chart Lb. Horse, Fo. 3. f. Expcrlnental Dourlne. (E. A. ^fetson.) Co/jfinuec/:- 1969 ISlO nth October November December (Age ofonimal* ItyrsJ January 106, II r ^J T i ilTilJl TTTljiT ?a§,^'<<.|''^^»^^>?*«5'?5'?'^«'9S^5SJ5«!i^'8^i?'^'NW»'v,e^«'«'Sv?^?!;5';:¥?S^ •^;'Ji iMI! ii ! iM ii -^ : j llT ! T! III i T T r - M 1 NT 111 104 r n t t Tip T Ti r i TE 1 jT^ -^ ^^^ Vu 103 I J^ 1 Jl 1 I i J i i L ') ■ii""" i It X 1 iH-"'"!!"'" pr^i io2^_Tjjj_m TT 1 ji _w^irn]irr . A lL nV» '^ ^ Mv -/--^A^^ ^^AfV -t^^i^/v-L^^/^Ar-^ 99 , ' ^^ i III; r -^^ \-'^ ^---P -,,^ ^ -^_f.4-^- ,-p ^1^ — - 98 i IT ^ ' 111 ^ i t T 1 IJTT IL 11 T Tm " ill " It T 1 1 n ^ T j IT 1 ! 11 Trypaaos Day after inoc oraes i i i i 1. ' L 4 ' 4_ '1 _L_j 1 ' -J -^V '--IT^'T' i Jj K i. 1 i LiHfe iihohaeor^sfh 7A/ // iprovefri^jyr h jefferb/ iheo/^/t ah{!^ *'•' ♦■'^\>K^'».;^^ nS>s''0|>'^j<^^;v n:'*i'».j'^»oX|^;oi ■-oIk^ 1910 Mtt January Februarv March April ^ lAY Day ^ -t *«.?.iiS'«-, . s I. ^ *c,l«'» •. ? X \ v^'* ? «'<'s;V«'S!'«;«k^''.:.'s'v.y (Tt^ji'^ - -p^-j - -^ y - -— ji - }-n-|r -i i TI j- ft 1 i 1 ill ri r ^^'v, 106 1 J Tit n 1 1 1 lost Tt 1 il ft T^itr IT !r|_■YT|JTri1TT!TilT' !«-- ^ . T _T ILrf T^ II III Jl 1 llj' I Hi 'ii 1 103 T 7rj i 1 : J r "'" 1 T T '"T I'lr^ iH li 102 T X |1|T 1 1 1 ^u+i IT ^^^■'■^ r^nii ^'i 'i "z >Ay\yvUftfflv^^ iJ^KfeS %)lrli Hii 99 1 ' -j_ -i^jj^L*.-hFWfcA.\,jmw ryj|yj|f)(||^||| J. , , yMuyyW tW 98 1 III 1 Li ' I'i " ; 97 .4 t 1.4^._ 1 ... i.„.h mi 4 Iiypanos Day after looc oroes [ _L 1 ' ' 1 I ' t, i L i ' ■■■■'' ! ! ' "'" 1 r^ irUed facia/ crrta}. J. ! j 1 1 1 M'*' ■-T jltn §|i^'x'>»«^>^:§^~itSfo;K^JtM,.,»j*,yix,if=,l^v«,»f,»i,j.o;o V^<6X<<) Experimental Station (Health of Animals jLethbridge.Alta, Canada Chart I.e. Experimental Dourlne. (E. A. Watson.) 010 - - -. nth MAV JUNE OuLV August Day:bAMfn?v??S)?^??,<'^«5W;Je**««xv->»',».A«^f»>^^^ 106 Ml i ll_ iiii 105 i i J I ! 1 1 j i i 1 i 1 104 ^ lA ' i i • M3 Jll ■ - , ! 1 1 1 1 W2 1T^ + -4 4^1 r\ T \\ Ji' 1 ! J, ,11,1 i 'fc|i|j ICO MM/Wl^ii^^ nWW/IW^^llvbllliM m w^SjmvmmmtX WiH 99 ' rT tV V y • ' y 'Vyy' V ' jfr m ; , r ', 't-,^*P'^^ |||/fV 98 i~ lU 1x1 ± ^ I J i 1 ! i i 1 1 9' ,,1 r"l""Tr"T^Tr i Trypanos Day after Inoc OrBBS _ _ _ . - - .j--.. 1.. ^ . ..^ . .. ^ _| 4^ tTT"f -rh -i- -+r rp ^ , , ■ i " H -^ - r-i ,5 - ... .-, ..--.,.. .--.._. , ... i^ra^£ier,eror/,eii»h&corfcmon\ , ! ultn S,gNt.1»S»*,««lSs>.S*H,»\»^^ SNS%v,»k»^fNi,^»S«i\«l»|N»^*f,*Vj»«|v^.^»»,»^*«»^x^.,^l{V^V>;\*«|,VM,,,»v>^X>o,|>,N.,»v>4V,««,i:,\v^iV*,X, ^ 1 ■ —" ~ '- ^^ vxb. August. September October February March Day^i'*^ «fev^n»VAV<.>x^^:?!: x^>?f5!S*??*>ii*«'«,*'«T»^^^|v.x«,vVVVJ«**^*«>V»'«<**««^i| 106 ■1+4.+.. T If ^ "'^ T , 1 I , 1 . 1" T TI 1 - +^11 104 In""" I'TT- 103 T , friT T 1 1 102 _, ^.... ; X X X -T 101 MjL jjhA/jyijHJij ,-, + ^ CI /i 100 flW m Wmim -- irf^ r-/h'rt--'i;'*»='v = t5--^r'""S; = "N"^=;-r. ^^I^LfL .^( ui^^i^^^y ^^vfvyycvp- - . i^-»^^i <_>.ii...Yx^j 98 ' iivi,i'mj'\'n^i,^vrto^'1_ \ j 97 T Trypanosc mes ^_ .-. ^ i 'mr ecO 'Hon; 7<> •:,'!, hc yf. ymjafoiHs ! 1 ! i 1 1 1 fai ■ At 1 i.i ii» ' Day after Inooultn |SB|NMi-i-i-i-iHi^'";^*">>:S^r''^V,^*i'^SNN-i-|-iS-'-!-lv-;--;-i-:-t-i-|-!-i- -:-•- ■S^"'^ Experimental Station (Health of ADinalslLethbridge.Alta. Canada 1] ChBrt 11. Szperlmental Dourlne. (E. A. Watson. ) lay after Inooultnjg \t'?»!voj^ji\!^ \ :««rV* Experimental Station (Health of AnimalsjLethbridge.Alta, CanaiJa Expcr ir:'jrL'tal Eciirli- : . chj)'t Ila. Horse No. 5.f. f (Untreated) Continuec/- 1 9 O 9 MlhijUNE 1 " JULV '' " ' _ ' AyjOijST Cogt- Is/ear) SEPTEMBER _ j 9? I I , i ! i I ; ; i ! ! Gfahds en/or^in^ Ur;_.;.>"-i.^-^i^'':\.:.,......,.;..;i Oedema -\y'<'^"'~'-y' C'of^t/'r'ued _ . _._ .,. [.!thi September October November :.:.,..:....:..,.:,^--V.;^USSIl;::.:.-,f^-t-.i.::i!-!i.-i:i-: 99 98 97 Trypanosoroes December I)ay'f*?.«^««WS;«'?^.vV'''«\bX^*,$y;vVfW^m'^!i\ Day after Inooultn Parbplefqic ifitif^ Foiling hea/fhS'citridif ion 1 1 M-t- ^ -i-ijtiUTT I riji ! riiTij'.ij.jTi i i.i'i \\y i i M t M . . Ezperimontal Station (Health oi Anir.al; jLethbridf'i.Alta, Canada. Chart lib Horaa, Ho.- S-f. £xperlmental Dourlne. (E. A. Watson.) Trypanosoraes Day after^ Inocultn Mth Bay after inocultn_ 0'3^&*' Nf^J»is^'o^^|^JO,^^■^;^j■1>j'^>,'>^l•^:<^'|:^j^j'lh^>,^l]v^^:^^|:^.^|.^^ April May June JULV $!vi^'^^V^^^>'^^^S;:;e^'^^:V^.^'^y^>W*kt^'*^$\\^.^'J'?.'?V I — --TIT iiLi:,,:r 1 .| i 1 1 f { .J..U/l...!L. 'ii ■ 1- r- ■-» ' - ; - I- . -■■ ■ ■ M i M i M i 1 M I i 1 M »^||^jc^ll')'♦;stt>*<^'|^■•i^'l♦^'*^>^i*;'^:g^^!''^•J^ Experimental Station (Health of Aninalsjtsthbridge.Alt.i. C'.natla (Si-f Histo'-y-Cliart Xo. 2.) T c^,^t in. Horse. No. f 1. Inoca/a^ec/ w/Y/t T. e qu/perdu m jounne. ( + ■ present \ \ _ . absent ] 102 101 100 99 9a 97 Oec/ema '>f^ent/v/s\ ^ Dat/ aft//sease II 90S --^=^^ ,.= v.i-ii Jui,j9o«.Au9 SpKOcfNm December l>vj , # I I i I " 105 1 I i rj3 1§ (E. A. Watson. February 106 105 104 103 102 101 100 99 9B 97_ January. 1909 1 Ml!''' ! li 1 1 i . ' ' a' ',■!•, . • ■ '',■;,.":,'■■; .-v:- ~ -. :\ -. - ■ ConHnuedf I90Q V«^ 2 >. 1 » Vo 1, , , I ^ ,, , , m >, ^ t, I V ^"i^^'j, ^ j^^:,5 ^-^ I-*!! March x,,.;i 'i';?v-vi»>'i.!\t>|;|x^i»l;|f;^|;;»y?'<^i Oedema o/qemh/s\ \-X-.- lA '^HVwy^/^A^/r^ Day of disease ^*^|*jXD=4i^\a,"-)«wtx%o,|\\ n v'i^tei'^ioi^ ^ "(S Day 106 105 104 103 .102 101 100 99 98 97 I'rypano somes' ConHnued :■ [ 900^ June July Aucus ?«'l?'^*#'*'*«'«<-*»***VvV ysMP^H Bay after Inoeultn^JiiWx Vv§\\ »s >.'« -14- '.-J-, Mth bay 106 lOS 104 103 102 101 100 99 98 97 Trypanoso mas c\^\'9»''^*^to\j^ Conftnuecf:- I909 SEPTEnBER Oct ober ' I i ' gg ljS^\* rrt 0. >- SEPTErlBER %'iiK,'i,'fe\'%'(^l* ^1?.; i Vw m ^Ayi Li lv^^>AAAvHi vW I** *» November ?'\t'f December f£««*^;*fM_«^ Bay after iaocu Uiij£ligiB» K:^!^k'i|*KKM«Kl"N^ »N*K!«WiKK^ Expartaental Station (Health of Aiitoal5)L«thbri(lge,Alta, Canada Hor«e,Ho. I.-f. - Erperlmental Dourlae. ^ j (E.A.Watson.) Chart Til civtfThuedl- I909- lO Uth December January February March ApI Davf^JE^*if§^^^VllSt\^,Ol*^^(v^?^|^**L«!?U»i5«4,**!M?U'^^«^b^^|!«^*^V^W\H?^Y 106 l_ll__ T ^li __I^_T 105 T - ,|l -r+ ^ 104 t --/I ifS ' 103 , ,'P, 1 L .-L-Jl -V. -- _- _ ._-- .-)- 102 W U T ._, ^ _|y4/ JP- - U -^ rr 1 --- '^:,s.^-f^Mpff~--M^^ 98 _ - - -J ^.. 97 . T Trypanos 35ay after inoc oraes _ _, _ r J_ ^_J 1 Hii.fctaJ'i'i \e-'i?U?i.!oAs 1 1 -L-- ^A- . T-.- . - . -p uUnj«^te>^t^S^'»'>»>>*>>'*=iS^'''>»*'*'-^«i(^"''*S"°*>»j!L§^''"'**'*ba!i§^'':i?-C*''*'^§''''''*'"'?^^ ■ Mth APRIL CAV JUNE JULV Day «)iisii»xi4i<>«x^jNl?S?^^nU?ii?*'***H'5"'«V'' '^***'"'^^*^^*'*''*''''**^*^*''^''*''^^^''''^'''*^*'^''*^ 106 _,_--.--_ - . , - - - 105 1 _ _ _ _ ^_ ^ ___■__ _- _ 104 1 1 i/U], L 103'""t""~" /fffl , T.I 102 "" M H "1 -\W^^^ ~-\ ^ A^ "1 1 i^' -'K^/jr+SffiS iilm^im^mw&^^rm^^^mmi IH^mili ^l°'--^^^vi^^] — y^3(|fvy"'yy*'\| V^ ^^i * »*yv — * V^^yy |f' vv^yyvyyi v y yifiy^ 98 J "'" " ^ 97 ■___._----- ---I - J--- - -- - Trypanos Day f^fter inooi oraes ,_ _ _, _i_ 1 ' [ iltn ?»*l*^*<^l&^^">»S'o>^*0|^^^»>♦Slo>^*o,^^^>l».^i'oj>^■^>0|j§^ ^■^*'»to>•»i^J^y^♦JV,^,^^'^v^,,»|^,,s>^l^^»,tl^^lvl»^»B|||v^,'♦^)la>>■»l>,g^^ ^♦ii«x»iii|N«i (See History-Chart No. 2.) Horse No. £6. /nocufafec/ wif'h + ■ present ] — = absen/- Dot/ ofDfsease ^" 195^ Mtb 106 105 104 103 Experimental Dourlna. (E. A. Watson.) ^th ^February. March. April May. 100 99 9S 97 '." .:'/,■ ':inoF :-;■ "^c Injections of ^ Arsenophenyl glycine Treated by (a- 0.05 g.per kg. b- 0.06 5j»l^i» ^ t*^ 5>i^?;f^')?_^5§§S,^*4^j*!?.i?^ivA^»is;>>^ S*^'54,sWw?^ Contin ued: June I Mil!! i G tOffd s eh/^^inif, /jjcki/ii ocu/o:r Viffrr f 101 'Mmm&%^ ^euei?^^ r^t cjat fch 'k3[~ July August fAnima/'iueoro/d) September l~n~r^"r"rT~rr"r— T-rT-rT.-r"i-T_--7:r^:.i-ri.-.-' ' [ i -^ -r r ■■ r - Day of Disease ''^\^^yy\;^ N-^*'^'='>.^5,| v;^,,^^VJ^JX^%^:^^ sj'V,-, U.'S'b'\% t^^^,'v;'^*,*-.|'QX;%Sr^|--JN;nq.S'c'x'(C>'!i;2 ^ ^^'^*,V, ic-^V^C^^ ^ 'v-, -^ -- t^'«;<>i|^|N'0'>-Sb\'%|ci;^''^V'^r»)^ \^90$._Continuedj-~_~^ ----- . -- - ... _ , — [ \^ !_SEPTEMeER r ■■ ;- ■:-l t.er_ inocy itn l|j^i^V© .■r;paiic'.?-j'.-.': | Afsenop g/ycin ■*■ Trypurrbfou, ~j" ■*■ Saafum ^rsvnaf-e L Say after iiiocultn_|g['0|^^i^Li Experimental Dourino. lE. A, Wfitson.) C)-J3rt IV" conhnuec/ I9IO '>i March April MAY June July .. ,$^S-,^*-i»'sfe''>i. ti^^,?!r*|?«V? « ■J S!?'^ ^!^^^« ^:^:\,i!»i 5i?':*!:!S:^■??^i5'S'^«*'J?«;^^^'^^«'•>»SS^''»«?■V^:?;^i!!f>^'?:l^'*ftS^!!^i;^S^^^:'^'»:S til.!' ■ ^ t- 44-* t ■" '■ "- ■■ Ijay after inocultn i^'^.^^^'*.!^*^,^*'^^^'**'!^*^,'^*'^'*^*^!^^'^'*"'^**^*^! ^N'n»-'^'o*''o<^5^,«p i'.th July ^i'^>;'^iVi'K,'o>^'c^«'*^''^*^,'«*^**i$^^'^*'^^*^^*i2^<^'^*i Day \y'il?'^^*!?W^§!?W*'*i?'*'5!^l^i!^ AUGUST September , October^ ?l«MS^!!0i ^ii8« Day after inocultn_ Experimental Station (Health of Aii.iniii.l5)Lfjthbriage Alta Canada T. Experimental Dourlne. (E. A. Watson.) Cf^rt IX. Horse -fool No n.f. Lay after Inocultn T Chart X Af senophenylglyoln" Day after inocultn Experimental Station (Health of Animals )I,ethbridge,Alta, Canada