Chapter V: Diseases of the Blood (1)

SEPTICÆMIA OF NEW-BORN ANIMALS.

The above title is given to that exceedingly fatal disease commonly known as “white scour,” etc., the mortality in which often rises to 95 per cent.

The disease was studied by Poels in Holland in 1889, Dèle in Belgium in 1891, Perroncito in Italy, Galtier in the centre of France in 1891–92, and quite recently by Nocard in Ireland in 1901.

It occurs throughout all the breeding districts of France, and in some parts causes enormous losses, the mortality comprising two-thirds or even three-fourths of all new-born calves. In certain breeding establishments in Normandy all the new-born animals without exception die unless special precautions are adopted.

In foals, septicæmia of the new-born is very rare, because horse-breeding establishments are much better cared for, and breeding mares are segregated. In byres, on the other hand, the greatest promiscuity exists. The disease is equally uncommon in lambs, although it makes numerous victims in folds which have once been attacked. It is, however, quite common in young pigs.

=Symptoms.= The development and course of the disease are in certain respects characteristic.

The disease usually appears within two or three days after birth, and only in rare cases after the second week. Calves which at birth appeared vigorous and in good health are found dull on the second day; after the second or third meal they suffer from diarrhœa, and from that time refuse all nourishment, lie down as though exhausted, and sometimes die very rapidly.

Some even perish in ten to twelve hours without showing diarrhœa; although apparently well at night, they are found dead or dying the next morning. This is the peracute form.

Most frequently the young creatures suffer for two or three days, sometimes a week. Appetite is partly preserved; at first the diarrhœa resembles that due to inability to digest milk, but the fæces soon become greyish or blackish and very fœtid. The hair of the tail, quarters and hocks is soiled and matted, the skin irritable and reddish; the patients lose strength, appear unsteady on their limbs, and develop rapid respiration and tumultuous action of the heart.

They take little food, become weaker by degrees, and die in a condition of exhaustion.

Fever, well marked at first, frequently diminishes, and the temperature may remain normal for several days, falling to 97° Fahr., or even 95° Fahr., twenty-four hours before death.

This is the commonest form of the disease. It lasts three to five days, and is always grave.

Cattle-men recognise the disease chiefly by the diarrhœa and loss of appetite.

Lastly, a third and rarer form occurs during which appetite is maintained in spite of the diarrhœa. The animals remain thin, develop poorly, but survive for a month, six weeks or two months. The diarrhœa diminishes or disappears, but its disappearance is followed by complications such as broncho-pneumonia, pleuro-pneumonia, endocarditis, acute arthritis, etc., a fact which led Prof. Galtier to give the disease the name of “septic pleuro-pneumonia in calves.” These complications, again, are extremely grave, and generally prove fatal after a period of varying length. They are due to local development of microorganisms of the kind which produce septicæmia, and similar to those described under the name of broncho-pneumonia of intestinal origin in sucking calves.

They differ, however, as regards their cause, from the primary affection, and may be due to very varied organisms, the commonest being those of suppuration. These organisms, in fact, are alien to the primary disease, and obtain entrance from without, very probably by the tracheobronchial tract.

In young pigs septicæmia assumes the same forms as in the calf. In lambs the chronic form seems more frequent than the peracute and the ordinary forms.

=Causation.= The septicæmia of calves, and possibly of all new-born animals, of whatever species, is produced by a microbe which flourishes in the manure and litter of stables, and which Nocard included in the group of Pasteurella. It can be found in the blood from the moment the first external symptoms appear until the time of death. During the last hours, however, the bacterium _Coli communis_ also invades the circulation in many instances, and if cultures are not made until some hours after death, the colon bacillus and bacteria of putrefaction are more particularly discovered.

The microbe of calf septicæmia can be readily cultivated in jelly or in ordinary liquid media. Injected into the veins of experimental animals, it reproduces the clinical symptoms, and causes death more or less rapidly, according to the dose injected.

The virulence of cultures grown in defibrinated calf’s blood seems more intense, and Moussu has been able to reproduce the clinical form of the disease by applying to the umbilical cord of a new-born animal a pledget of cotton wool saturated with such a culture, and covering it with a dressing. The germs of the disease are spread throughout the byres through the medium of fæces. When the umbilical cord has become dry, that is, after the third day, the application of virulent cultures to the stump no longer causes infection.

=Pathogeny.= The pathogeny of this septicæmia of calves and of new-born animals is easy to explain.

At birth the young animals fall on the litter, and the umbilical cord becomes contaminated. The infective agent, finding an excellent culture medium in the tissues of the cord, at once begins to develop, increases in enormous numbers, steadily ascends along the cord, and sets up septicæmia. It grows in the gelatinous Wharton’s jelly and in the fibrinous plug closing the arteries and umbilical vein, and soon enters the true circulation. Septicæmia is then fully established, general disturbance sets in, and with it the diarrhœa by which it is externally indicated.

It is important to remember, however, that infection occurs most readily through the medium of the cord, and during the first few days after birth: it may occasionally be brought about towards the eighth or tenth day, when the shrivelled portion of the cord falls; in this case its entrance is effected through the little umbilical wound.

=Lesions.= The lesions are sometimes so obscure that the practitioner may hesitate to deliver an opinion.

In acute cases, where death occurs in two or three days, or even in ten to twelve hours, post-mortem examination reveals only increased vascularity of the serous membranes—the peritoneum, pleura, pericardium, etc.; and it may be almost impossible to discover anything abnormal in the cord, for although the clots closing the arteries and veins are infected, they are neither separated from the walls of the vessels nor broken up.

On the surface of the urachus, at the base of the bladder, and in the depths of the peritoneal folds supporting the allantoid arteries (sometimes also the hepatic vein), unequivocal signs of local ascending infection may, however, almost always be found, together with intense injection of the capillaries, little hæmorrhagic spots, and commencing formation of false membranes, etc.

The infection extends also by the lymphatic vessels contained in these peritoneal folds, and finally attains the sublumbar region.

When the disease develops less rapidly the peritoneal cavity contains a certain quantity of blood-stained serosity, as do the pleuræ and pericardium, whilst vascular engorgement of the serous membranes is extremely marked. The intestine shows traces of congestion and inflammation throughout its length, and its contents contain the specific organism in very large numbers.

Finally, in the chronic forms, the serous membranes and the intestine seem only slightly attacked, possibly because the lesions have undergone retrogressive changes. The striking features are the secondary lesions, such as those of pneumonia, broncho-pneumonia, pericarditis, and abscess formation in the lung.

Nocard gives the following description of the lesions found during his investigation of “white scour” of calves in Ireland (_Veterinarian_, April, 1902, p. 171; see also Prof. Mettam’s paper, _Veterinarian_, June, 1902, p. 307):—“The lesions found on autopsy vary according to whether the evolution of the disease has been rapid or slow. One lesion, however, is never absent—that of the navel and the navel vessels. In all the calves attacked we found a large umbilicus with hardened coats enclosing a clot easily broken down, sometimes soft and purulent. In every case, also, we observed blood suffusions, often very extensive, along the course of the umbilical vessels and of the urachus, invading often the posterior third of the bladder. In cases where the evolution had been rapid we found the lesions of true hæmorrhagic septicæmia. All the viscera were congested to excess; their surface was studded with petechiæ, ecchymoses, or subserous blood suffusions. The capillary network of the peritoneum, pleura, and pericardium appeared strongly injected. This lesion was especially marked on the epiploon. The intestine was the seat of intense congestion, especially at the level of the ‘floating colon.’

“The mucous membrane was thickened, gorged with blood, and friable; the solitary glands, thick and protruding, were sometimes transformed into a kind of bloody magma, or they were ulcerated, as in anthrax; the contents of the bowel were mixed with a large quantity of blood. The mucous membrane of the fourth stomach was altered nearly to the same degree; it was studded with interstitial hæmorrhages, especially above the level of the open edge of its folds. The mesenteric glands—especially those of the colon—were enormous, gorged with blood, reddish, and often hæmorrhagic. The mucous membrane of the bladder was often covered with petechiæ, the urine which it contained was clear and limpid, but always rich in albumen. [In one sample which was analysed, the urine contained more than 4 grammes of albumen to the litre.] The lungs were gorged with blood, like the intestines; sometimes they were manifestly œdematous, but generally their tissue was still supple, elastic, permeable, and without apparent lesion.

“In the subacute forms the lesions are much less marked. The mucous membrane of the intestine is less congested; sometimes œdema of the submucous tissue exists. The mucous membrane of the fourth stomach is often punctuated with brownish-red patches, traces of the capillary hæmorrhages which were produced at the onset of the disease. The mesenteric glands are swollen, gorged with serum, but not hæmorrhagic; the liver is large and of a yellowish tint; the spleen is little altered; the urine always contains albumen; the lungs are seldom quite sound; they usually contain here and there small diffuse centres of catarrhal pneumonia, of nodular bronchial pneumonia, or simply of atelectasis.

“These lesions are more constant and more dense if the animals have resisted the disease for some time; they then constitute the transition stage between the simple collapse at the beginning of the disease and the suppurating lesion of lung disease. The joint lesions when they exist are very interesting. At the beginning all the periarticular tissues are infiltrated with a yellowish gelatinous serosity. The synovial membrane is covered with vascular aborisations of an extreme richness, which extend on to the articular cartilages. The synovial capsules are distended by a considerable quantity of thick synovia of a deep yellow or brownish tint, holding in suspension flakes of fibrous exudate more or less dense and abundant. When the lesion is older the synovia is replaced by a thick fibrous exudate, which fills sacculations, and extends between the articular surfaces. In this case the lesion appears identical with that of the arthritis seen in pleuro-pneumonia of sucking calves.”

=Diagnosis.= The diagnosis presents no difficulty, for the development and acute course of the disease (the majority of patients die within a week of birth) leave little room for doubt.

This disease is easily distinguished from dysentery in new-born animals, which appears at birth, as also from simple diarrhœic enteritis; in the latter disease the symptoms are delayed, sometimes occurring only when the animals are weaned; moreover, the disease is never so grave as that now under consideration.

Should, however, the post-mortem appearances seem indecisive, the diagnosis can be based simply on the high mortality.

=Prognosis.= The prognosis is extremely grave. About 95 per cent. of the animals attacked die, and among those which survive many show thoracic complications, that render them useless.

=Treatment.= Treatment of animals already affected is useless, and, moreover, too costly. Drugs administered through the digestive apparatus to a large extent miss their mark, because the digestive symptoms are secondary, primary infection having occurred through the circulation. The administration of purgatives and internal antiseptics can, therefore, only prove illusory.

On the other hand, prophylactic treatment is of the greatest value; all that is necessary is to prevent the umbilical cord from becoming infected.

The great mortality, which causes such severe loss to breeders, is simply due to want of proper care of new-born animals. Even in carefully kept byres the mortality may be high, for the specific agent develops in litter contaminated with fæcal matter, by lying on which young animals become fatally infected.

To check or prevent this septicæmia in breeding establishments, it is merely necessary to take the same precaution as is taken in dealing with young children, _i.e._, to apply an aseptic or antiseptic dressing to the stump of the cord after ligation. As soon as the young animal has been dried by the mother or by artificial means, a carefully boiled ligature is applied to the cord at a distance of about 1 inch from the umbilical ring. The portion of the cord below the ligature is snipped off, the remaining part is carefully washed with boiled water or boric solution, and is surrounded with a mass of iodoform wool, kept in place by a bandage passed over the back.

The cord will shrivel a little less rapidly than it would if exposed to the air, but will be protected from all infection. The young animal should be separated from the mother to prevent her from displacing the dressing by licking the parts.

In a few days all danger is at an end. This method is very simple, and can be carried out even by the breeder and in an infected byre. Nocard recommends the use of umbilical dressings containing collodion, and the practitioner can choose whichever method he pleases.

In grave outbreaks involving large establishments, the byres should be rigorously disinfected, and it is sometimes well to segregate cows about to calve in a special byre, from which the calves are not allowed to pass until the umbilicus is cicatrised.

TAKOSIS: A CONTAGIOUS DISEASE OF GOATS.[4]

Footnote 4:

Annual Report, U.S.A. Bureau of Animal Industry, 1902, p. 354 (Mohler
and Washburn).

This disease has been seen in Angora goats brought from Texas into Pennsylvania, U.S.A.

=Symptoms.= The disease presents many of the symptoms usually accompanying a parasitic invasion, and is characterised by great emaciation and weakness, with symptoms of diarrhœa and pneumonia. In the early stages of the affection there is usually little to indicate that anything is seriously amiss with the animal. The first observable symptom manifested is the listless and languid appearance of the animal, evidenced by its lagging behind the flock, and is usually accompanied by a drooping of the ears and a drowsy appearance of the eyes. The pulse is slow and feeble, and the temperature is elevated slightly at first, but becomes subnormal a few days before death. The highest temperature observed in the natural disease was 104·1°, and the lowest, in a prostrated animal a few hours before death, registered 99·7° Fahr. Snuffling of the nose, as in a case of coryza, with occasional coughing is sometimes in evidence.

As the disease advances the animal moves about in a desultory manner, with back arched, neck drawn down toward the sternum, and with a staggering gait. Rumination is seldom impaired. The appetite, while not so vigorous, is still present, though capricious, and the affected animal shows plainly that the ravages of the disease are rapidly overcoming the restorative elements derived from the food. The fleece is usually of good growth, and presents a surprisingly thrifty appearance when the condition of the animal is taken into consideration. All the exposed mucous membranes appear pale, and the respirations are accelerated and laboured. The goats finally become so weak that they are readily knocked down and trampled upon by their fellows. If picked up they may move off slowly and eat a little, but within a few hours are down again, and in this way linger for several days, shrinking to about half their natural weight, and occasionally bleating or groaning, with head bent around on the side or drawn down to the sternum. A fluid discharge from the bowels of a very offensive odour is usually observed in the last few days of life, but this symptom is not constant.

=Course and Susceptibility.= This disease may assume a subacute or chronic type, usually the latter. The animal dies of inanition in from eight days to six or eight weeks. Several owners have reported deaths after only two or three days of illness, but the goats doubtless had been affected for a longer period, although not noticed on account of their mingling in the flock. Many of the animals live for weeks, but gradually become weaker and more debilitated, finally dying in a comatose condition. In no instance has the natural recovery of an animal after once the symptoms of takosis were noticed been observed or heard of.

The younger goats seem to be the most susceptible to the disease, although the old animals are by no means immune.

=Pathological Anatomy.= As already indicated, the general appearance of the carcase simulates that produced by a wasting disease. The visible mucous membranes are pale and anæmic, while the fleece, which appears somewhat dry and lustreless, furnishes a shroud for the extremely emaciated condition, that becomes plainly perceptible on skinning. The same anæmic condition of the subcutaneous and muscular tissues is observed on eviscerating the carcases. The lungs in most cases are the seat of a peculiar diversified inflammation, never of a remarkable extent. The external appearance of these organs is at times mottled, caused by a few congested areas, several patches of an iron-grey colour similar to areas of pneumonia during the process of absorption, and normal tissue. On section through the reddened patches, a frothy mucus may exude from the bronchioles, and in one case numerous punctiform hæmorrhages were observed on the sides of the incision. This tissue, while not so buoyant as a normal portion would be, nevertheless floats when placed in water.

The heart in all cases is pale and dull, its tissue soft and flabby, while inflamed areas, more or less penetrating, are present at times on the epicardium about the auricular appendages, and at other times on the endocardium, especially that lining the ventricles. These hæmorrhagic patches consist of either pure extravasated blood or blood mixed with serum, which gives them a more diffuse appearance and a gelatinous consistence. The pericardium is slightly thickened, and usually contains a small increase of fluid tinged with blood. The liver usually appears normal, although the gall bladder is frequently distended with pale-yellow watery bile. The kidneys are anæmic and softened. The cortex appears slightly thicker and paler than normal, and contrasts strongly with the darker pyramids. The capsule strips off easily from the parenchyma of the organ. In one instance several pale areas simulating anæmic infarcts were observed under the capsule extending into the cortex, which probably resulted from the compression of the capillaries by the swollen parenchymatous cells. The presence of albumin in the urine was detected by the nitric-acid test. The spleen appears atrophied and indurated, and on section the fibrous tissue far exceeds the splenic pulp. Attachments by fibrous adhesions may fix the spleen to the diaphragm or the neighbouring organs. The intestines may contain normal fæcal matter or semi-fluid fæces of a disagreeable odour. The surface of the mucous membrane is at times covered with a slimy mucus or plastic exudate, and the appearance is that of a chronic catarrh associated with necrosis of the mucosa.

=Bacteriology.= Examination of cultures and slides showed the presence of a micrococcus, usually arranged in the form of a diplococcus, which was found in pure cultures from the heart’s blood, spleen, kidneys, and pericardial fluid, and essentially so in the tubes inoculated from the other organs.

The specific organism of takosis appears in fresh bouillon cultures as a spherical or oval micrococcus with a diameter of 0·8 to 1 µ. In these cultures it is single or in chains of two, three, or four elements, but most frequently in pairs, as diplococci, with a diameter transverse to the axis of the chain greater than the longitudinal diameter.

=Treatment: Prophylaxis.= Sudden climatic changes should be avoided as far as possible, and when shipments of goats for breeding purposes are to be made which necessitate their transportation over considerable distances the changes should be made during the months of summer or late spring, and not in the fall or winter, when the contrast of temperature will be so much greater.

Angora goats should be provided with stables that are thoroughly dry, erected upon ground that has perfect natural drainage.

As a third measure of prevention may be mentioned careful feeding.

The segregation or isolation of all affected animals as soon as they evince any symptoms of the disease will be found a most valuable means of protection for those that remain unaffected, and a strict quarantine over all of the diseased members of the flock should be maintained so long as the disease remains upon the premises.

=Medicinal treatment= has proved unsatisfactory in many of the cases of takosis to which it has been applied. The best results have been derived from the administration of calomel in 0.1 gram doses twice daily for two days, followed by arsenic, iron, and quinine, as follows:

Arsenious acid 1·40 grams.
Iron, reduced 12·00 „
Quinine sulphate 6·00 „

Mix and make into twenty powders, giving one to each adult goat morning and evening at the conclusion of the administration of calomel. After an interval of two days this treatment is repeated. In case the diarrhœa persists, the sulphate of iron has been substituted for the reduced iron, with beneficial effects.

=Conclusions.= After preliminary investigation, the following conclusions have been reached:—

(1.) The disease described as takosis has appeared in many parts of America, but particularly in the Northern States, where it has caused great loss to many breeders of Angora goats.

(2.) It is a progressive, debilitative, contagious disease, characterised by great emaciation and weakness, with symptoms of diarrhœa and pneumonia, and causes a mortality of 100 per cent. of those affected and from 30 to 85 per cent. of the whole flock.

(3.) From the carcases of numerous animals that have succumbed a new organism, _Micrococcus caprinus_, has been recovered in purity, and is presumably the etiological factor.

(4.) This micrococcus possesses pathogenic properties for goats, chickens, rabbits, guinea-pigs, and white mice, but not for sheep, dogs, or rats.

(5.) Medicinal treatment was attempted with varying success, while the immunising experiments thus far conducted (although too few to permit of any conclusive statement or accurate estimate as to their protective value) have shown highly encouraging results. When accompanied with measures of isolation and disinfection, the treatment may prove of great assistance in the suppression and eradication of the disease in an infected flock.

BLOOD POISONING (MALIGNANT ŒDEMA) IN SHEEP AND LAMBS IN NEW ZEALAND.

This disease, which occurs during the operations of shearing sheep and of castrating and docking lambs, is the cause of considerable loss annually to sheep breeders in several districts of New Zealand. In 1893 J. A. Gilruth, Chief Veterinarian for New Zealand, issued a leaflet dealing with the disease and the preventive measures to be adopted. Generally the first thing that draws the owner’s attention seriously to the condition of his flock is the discovery, in from thirty-six to forty-eight hours after docking or shearing, of a few dead sheep lying in various parts of the paddocks. Next morning he finds a few more dead, and so on for three or four days, when, as a rule, the mortality ceases.

=Symptoms.= In the early stages of this disease the animal seems listless, disinclined to move about, and, if the sun is shining strongly, prefers to lie in the shade. If forced to move, the hind legs are drawn forward with a peculiar stiff, dragging motion, as if there were no joints. There are slight muscular tremors all over the body, which become spasmodic as the disease progresses. If the flock be driven about much, the diseased animal soon shows signs of great fatigue, ultimately dropping to the ground thoroughly exhausted. The breathing is fast and painful, being maintained more by a series of spasmodic jerks than by any regular act. The pulse is quick and weak; the temperature is very high, registering 106° to 108° Fahr., showing acute fever; the eyes close, and the whole face is expressive of pain. Gradually the spasms cease and coma sets in, resulting in death. The scrotum and surrounding skin right along the floor of the abdomen and between the hind legs become swollen and black. This gangrenous tissue, when present before death, can be peeled off without pain to the animal. On post-mortem examination various conditions are met with. The animals are generally found to be among the best of the flock and in fairly good condition. The scrotal and perineal regions in lambs (between hind legs and below tail) are always, or almost always, gangrenous, this condition extending along to the floor of the chest, and sometimes implicating the tail. Many of the muscles, generally those of the shoulders, haunches, and loins, are dark in colour and infiltrated with a black, watery fluid. The intestines are generally healthy, though sometimes the peritoneum is inflamed. The spleen and liver are in the usual condition after death, due to febrile disturbance. In the chest, either the pleuræ (coverings of the lungs) or pericardium (covering of the heart) are often inflamed, with occasionally a fibrinous exudation, causing surfaces to adhere.

=Cause.= In Gilruth’s report for 1900 he demonstrated the cause of blood poisoning to be a microbe known as the malignant œdema bacillus (_Vibrion septique_ of Pasteur). This organism, which is found in many dirty yards, swampy soils, etc., on gaining entrance to the system of almost any animal by means of a wound, rapidly increases in numbers, producing gangrene, or death, of the part affected first, and ultimately the death of the animal.

=Curative treatment= is practically useless.

=Preventive measures.= Destruction of the carcases of animals which have succumbed to this disease by efficient burial or by fire. Disinfection of surface soil of yards, etc., by quick-lime. Cleansing of floors and walls of sheds with strong hot lime wash containing crude carbolic acid in the proportion of 1 to 50. Disinfection of flesh cuts made by the shears or the docking or castrating knife. Boiling of docking and tailing knives before use. Observance of antiseptic applications even when temporary yards are employed. Sheep and lambs after operation to be kept in a paddock free from swampy patches.

PIROPLASMOSIS.

Under the title piroplasmosis is included a group of diseases caused by hæmosporidia, and found in animals of the bovine and ovine species. These affections are far from having the same importance in temperate as they have in tropical countries; nevertheless, it is very important to be able to recognise them.

BOVINE PIROPLASMOSIS.

Bovine piroplasmosis has been described under different names, such as hæmoglobinæmia, hæmoglobinuria, Texas fever (U.S.A.), tick fever (Australia), tristeza (Argentine Republic), African coast fever, East Coast fever, redwater, Rhodesian fever (Cape), and bovine malaria.

It was first described by Babès in 1888, in animals inhabiting the Danube Valley, and was termed by him bacterial hæmoglobinuria of the ox. Afterwards it was well described by Smith and Kilborne (in 1889) under the title of Texas fever. It was rediscovered in Finland by Krogius and Van Hellens in 1894; in Sardinia by San Felice and Loi; in Australia in 1895 by Pound; and it has been the object of remarkable investigations by Koch in South Africa (1898–1904).

Nicolle and Adil-Bey (1899) state that it exists in a latent form in European Turkey and Asiatic Turkey; and Lignières (1900), after a series of researches in Argentina, suggests the final solution of the questions which it raises.

=Symptoms.= Babès describes it as an acute febrile disease, clinically distinguished by the passage of blood-stained urine. The urine is coloured by dissolved hæmoglobin; red blood corpuscles are not found. Smith and Kilborne, and afterwards Stiles, described two forms: an acute, rapidly fatal form, in which the _Piroplasma bigeminum_ is found in the blood of the general circulation, in the spleen and kidneys; and a chronic form, in which, notwithstanding the absence of clinical signs, the parasites may be discovered in the blood under the form of diplococci.

Lignières describes a grave and a benignant form. The grave form is indicated by dulness, loss of appetite, and considerable fever. In twenty-four hours the temperature rises to 104° or 105° Fahr., and the pulse to 100 or 120 per minute, while the respiration is greatly accelerated.

The urine is of a light-red or brownish-red colour, resembling coffee-grounds, but it contains no blood corpuscles. The animals die in from three to eight days with symptoms of asphyxia; but this termination is not inevitable, and recovery may occur spontaneously. Improvement is indicated by a fall in temperature, disappearance of the blood-stained urine, and a return of appetite, together with marked thirst.

Drs. Smith and Kilborne describe the symptoms as follows:—“The beast when first observed to be amiss appears to be dull and sluggish, with a disinclination to move, and hence it is generally found apart from the rest of the herd. The hair stands erect like that of an animal on a cold day (a staring coat), the ears hang, and the eyes have a dull and lustreless appearance. In some cases the animals cease to feed, or ruminate, in others they continue to nibble at the herbage until nearly the last, but in a languid, indifferent manner, indicating that they have little relish for their food, and they fall off very rapidly in condition. There is generally a dribbling of saliva from the mouth, the muzzle may appear quite moist during the early stages of the disease, but it invariably becomes dry and crusty as the disease advances. Later on the animal manifests a strong reluctance to move, and when compelled to do so, it walks with a dragging, straddling gait, as if weak across the loins. In severe cases, when the sick beast is left undisturbed, it will remain almost constantly in one place, standing with its head depressed and ears hanging in a drowsy semi-comatose condition, looking the very picture of complete nervous prostration. Other animals will lie down the greater part of the time and scarcely move, and when dead the limbs will be found in their natural position, and the head doubled round on the shoulder as if asleep. On making a post-mortem examination of some of these cases the carcase was found to be pale and bloodless, as if the animal had been bled to death.

“In other acute cases a twitching and quivering of the muscles will be observed, especially of those situated in the flank and behind the shoulder. The pulse and breathing are much quickened, and the animal will stand and grind its teeth and curl up its upper lip, indicating great uneasiness and pain. The fæces during the early stages of the disease are very often soft, with a tendency to diarrhœa, more especially in transport oxen on the road, but they invariably become hard as the disease advances; but whether hard or soft, they have generally a brownish tinge, and often mixed more or less with blood and mucus. In some severe cases which recover, the favourable crisis is often ushered in by a salutary diarrhœa.”

In the benign form the animal for the space of about a week shows indifference to its surroundings, loses its appetite, wastes, and, less frequently, has slight feverish symptoms, without discoloration of the urine. The only reason for the belief that this trifling disturbance is due to piroplasmosis is furnished by examination of the blood, in which the parasites may be found in very small numbers in certain blood corpuscles.

Calves seldom take the disease except in the benign form.

=Lesions.= At first glance the lesions appear to resemble those of anthrax, but may be differentiated from them in many details.

The skin is covered with ticks or shows traces of their punctures.

The myocardium appears as if boiled, the spleen is invariably hypertrophied and two or three times as large as in the normal state.

The kidneys are violet in colour and congested, and the adipose layer surrounding the kidney is infiltrated with a yellowish serosity. The urine may present a variety of tints, derived from hæmoglobin. The liver is often engorged with blood and the gall bladder always distended.

When convalescence sets in, icterus appears; but it is a special kind of icterus, depending on changes in the hæmoglobin—in fact, a hæmaphæic icterus. Histological examination of the blood furnishes the explanation of the disease by revealing the presence of the parasite.

=Pathogeny.= The parasite is the _Piroplasma bigeminum_, which is easily demonstrated by drying the blood, fixing it and staining with very weak methylene blue. The blood is light in colour and pale, and the serum is tinted by the dissolved hæmoglobin. The blood corpuscles diminish in number with extreme rapidity while the parasites are developing, and in twenty-four or forty-eight hours may fall from some six millions and a half, the normal number, to one million or even to two or three hundred thousand red blood corpuscles per cubic millimètre.

This destruction is due to the action of the piroplasmata, as may be shown by staining with a ·5 per cent. methylene blue or carbolised thionine. These parasites usually assume a simple pyriform shape, and two or three may be found in one blood corpuscle. The number of parasites and infected blood corpuscles is generally in direct ratio to the intensity of the infection. These parasites are found throughout the blood, but principally in that of the spleen, kidneys, and mesenteric veins. They are only abundant whilst the temperature is rising or at the moment when it reaches its highest point, and they often disappear before death or convalescence.

The pyriform shape is only temporary, and corresponds to the acute phase of the disease, but the parasite assumes the round form as soon as convalescence sets in. This round form gives birth to one, two or three spherical spores, which are set free in the plasma after the destruction of the maternal protoplasm, and are able after transference to a fresh red blood corpuscle to again assume the pyriform shape peculiar to the grave forms of disease.

The parasite can only be cultivated in defibrinated blood from a hæmoglobinuric subject, and the cultures do not always yield more than reproductions of the round form, the pear-shaped form only being produced with red blood corpuscles in the living animal body.

Regarding the method of growth of the piroplasma in the body and in cultures, Lignières believes that the parasite may produce two forms of spores differing in their nature. One, the active spore, has little resisting power. It soon degenerates outside the animal body, forms rapidly at the expense of one of the pear-shaped parasites, and may immediately reinfect another red blood corpuscle. The other, called the passive spore, is very resistant, and retains its vitality for a long time outside the body, being produced at the expense of spherical parasites already withdrawn and incapable of producing the disease.

The form of piroplasmosis at present under consideration is peculiar to the ox, and none of the other domestic animals or experimental subjects can be inoculated with it.

Subcutaneous or intravenous inoculation of the ox with 5 to 10 cubic centimètres always gives positive results when made with blood or active products, such as the pear-shaped parasites or active spores, but is ineffectual when the parasites have already begun to retract in order to form passive spores.

Calves seldom contract more than the benign form of the disease, and do not die.

In the grave form following experimental infection the temperature begins to rise between the third and sixth day, and corresponds with a marked increase in the number of parasites to be found within the red blood corpuscles. The urine at first becomes albuminous, then hæmoglobinuric, whilst the red blood corpuscles diminish in number to a very marked extent, falling from about six or seven millions to one million, or even a few hundred thousands, in the course of a few days. The temperature, which may previously have risen to above 105° Fahr., suddenly falls, indicating the approach of death.

If an immediate autopsy is made, the spleen is always found to be enlarged, the intestinal mucous membrane reddish in tint or blood-stained, and the serous membranes, particularly the endocardium, covered with petechiæ.

Few or no parasites can be discovered except in the blood from the cardiac muscle and the kidneys.

The grave form may end in recovery. This end is indicated by the temperature remaining normal after defervescence, the appearance of hæmaphæic icterus of an obstinate character, and the progressive return of appetite.

The disease is usually transmitted by adult and larval ticks carrying the parasite from infected animals. Lignières has proved that this transmission occurs through the medium of passive spores, which, though themselves incapable of producing the disease, become active and infective in consequence of the local irritation produced by the poisonous saliva of the ticks.

The pathogeny of Texas fever may be shortly summed up as follows:—Animals suffering from the disease carry in their blood a protozoan organism called the _Piroplasma bigeminum_, analogous to the parasite of human malaria; once introduced into the blood, this organism remains there in an active condition throughout the animal’s life; it is transferred to susceptible cattle either within or without the infected district by the Southern (U.S.) cattle tick _Boophilus annulatus_; Southern cattle, although carrying the protozoa, are harmless unless infested by this particular tick: the mature ticks and their eggs contain the protozoa, and the mystery of certain grounds over which infected animals have passed being first dangerous, then harmless, and again dangerous depends on—(_a_) the infestation of the ground with mature infected ticks; (_b_) the destruction or death of the mature ticks; and (_c_) the hatching out of new (infected) ticks from the eggs laid on the ground by the mature female ticks.

Dr. Salmon states that in Texas a successful method of protection is in practice based on the observations that young cattle do not suffer so severely as adults, and that the disease always assumes a milder form in winter. Young animals introduced during the winter are inoculated with virulent blood. They contract a mild form of disease, and afterwards resist. In this way the losses, which previously amounted to 90 per cent. of all freshly introduced stock, have been reduced to about 10 per cent.

A remarkable and very interesting observation (if absolutely reliable) deserves to be mentioned, viz., that the ticks develop regularly in the natural prairie, but do not develop in parts artificially sown with grass such as lucern, and that when contaminated or diseased animals are transferred to artificial meadows they do not convey the disease to other animals already there; the latter are proof against it.

=Diagnosis.= The disease is so typical that it cannot be mistaken for anthrax. In anthrax the urine is never hæmoglobinuric and very rarely hæmaturic, and the fæces are sometimes blood-stained, a symptom never present in piroplasmosis. Anthrax can be transmitted to experimental animals, but piroplasmosis cannot.

=Prognosis.= The prognosis is generally grave.

=Treatment.= Van Hellens recommends the use of quinine in large doses. He give 5 drachms in one dose, and repeats it for the next two, three, or four days.

Lignières says that he has never obtained the slightest success with quinine, though it is true he has never given higher doses than 2½ drachms.

Attempts have been made to confer immunity by injecting animals with serum from others which have recovered. Vaccination with the blood of patients arrived at the period of convalescence has also been tried. The results, however, have not been very satisfactory.

Lignières has formulated an efficient method of vaccination, of which he has not yet published the full details, but which appeared by reason of its simplicity likely to render great service. Nevertheless, his most recent reports seem to show that vaccination is not always efficacious, and that in the Argentine Republic alone several varieties of the disease exist, two being caused by allied but different parasites. The vaccine used against one variety is powerless against the other. The problem of vaccination would therefore appear to be much more complex than in the case where one form only occurs in any particular country.

The immunity arising from attacks of piroplasmosis is in direct ratio to the gravity of the disease, and according to Lignières’ views this acquired immunity is due to the secretion by the piroplasma of a substance which is toxic for the red blood corpuscles. This toxic substance provokes, as in other diseases, an organic antitoxic reaction.

BOVINE PIROPLASMOSIS IN FRANCE.

Until recent years it did not seem that piroplasmosis occurred in France. It had been detected in Algeria, although its existence had not been conclusively proved. Mathis claims to have met with it in the department of the Loire in 1896 and in the Ain in consequence of the importation of Algerian cattle, but its ravages were comparatively trifling.

Having good reason to suspect that certain morbid conditions, known as _mal de Brou_, might be due to piroplasmosis, Lignières endeavoured to verify his theory, and discovered that sometimes, but not often, this disease was mistaken in France for anthrax and _mal de Brou_. Piroplasmosis in France appears less grave than in America, and is rarely fatal.

As regards its =symptoms=, it usually develops suddenly with fever, loss of appetite, acceleration of the pulse and respiratory movements, suppression of the milk secretion, and the passage of red hæmoglobinuric urine. In exceptional cases death may occur in from three to five days.

On post-mortem examination a varying number of ticks (_Ixodes hexagonus_) are found on the skin, the spleen is always increased in size, and the kidneys are black and hæmorrhagic.

The disease transmitted by ticks, as in Texas fever, seems due to the presence of a round parasite, different from the well-known _Piroplasma bigeminum_.

The elucidation of this disease, which occurs towards the northern frontier of France in the neighbourhood of Maubeuge, calls for further investigation. It never appears to be very fatal, and it attacks more especially animals imported into the infected region. A method of vaccination identical with that used by Lignières against one of the forms of the American disease may perhaps in the future prove available against the disease in France. Until then the best =treatment= would appear to consist in free subcutaneous injection of saline solution and the administration of evacuants, sulphate of quinine, and laxatives.

OVINE PIROPLASMOSIS.

=Causation.= The existence in France of this disease has not yet been clearly established, for in the only communication on the subject (by Leblanc in 1899) the writer seems to have confused the toxic hæmoglobinuria produced by feeding on decomposed beet pulp with the parasitic hæmoglobinuria due to piroplasmosis.

In Italy ovine piroplasmosis was described by Bonomo in 1896 under the title of parasitic icteric hæmaturia of sheep. It is said to be due to a parasite of the red blood corpuscles (_Amœba sporidium polyphagum_), the said parasite being of oval form, very refractile, always occupying an outer position near the free margin of the corpuscle, and sometimes floating freely in the plasma.

According to Babès, who described it under the name of _gurceac du mouton_, the same disease appears to occur in the islands and low parts of the Danube valley.

=Symptoms.= The development of this parasite produces in the patient loss of appetite and high fever, accompanied by the passage of dark coloured hæmoglobinuric urine. Icterus is frequently present. The animals rapidly become exhausted, collapse and die.

On post-mortem examination carried out immediately after death the spleen is found to be large, the pulp being like wine lees. The liver is soft and yellowish; the kidneys are soft and black.

The disease is said not to be transmissible by direct transfusion (?).

It would appear that this disease has also been seen in Turkey by Nicolle and Laveran, near Constantinople, in 1899. The parasites (_Piroplasma oris_) are round or slightly elongated and occur near the periphery of the red blood corpuscles. It is to be hoped in the interest of breeders in localities where this disease rages that Lignières’ method of vaccination against bovine piroplasmosis may prove reliable and equally applicable in the case of sheep.

DISEASES PRODUCED BY TRYPANOSOMATA.[5]

Footnote 5:

An interesting article and a series of figures on the “Evolution of
the _Trypanosoma Evansi_” were published in the _Jour. of Comp. Path.
and Therap._ for September, 1904, p. 210. The same number also
contained articles on several piroplasmic diseases.

In 1904 Professor Koch delivered an address, from which the following is a summary, to the Berlin Medical Society regarding his experiences and observations on diseases produced by trypanosomata in Africa:—

A wide field of study has recently been opened by the discovery of various pathological protozoa. Three discoveries especially have directed attention to these special disease organisms—

(1.) Laveran’s discoveries regarding malaria. Ross has shown that the malaria parasites are carried by mosquitoes (_Anopheles claviger_).

(2.) The discovery of the protozoa of Texas fever by Smith. In this case ticks (_Rhipicephalus_ (_boophilus_) _annulatus_) convey the disease.

(3.) The discovery of the trypanosoma of the tsetse disease, which is conveyed by a stinging fly (_Glossina morsitans_).

These discoveries were followed by numerous others indicating protozoa as causes of disease.

The trypanosomata are morphologically distinguished by the existence of a flagellum. When fresh blood is examined it is scarcely possible to overlook the protozoa in the preparation, for attention is at once attracted by the energetic way in which the red blood corpuscles are continually being displaced. The peculiar form of the protozoa, however, can only be detected in stained preparations. Romanowsky’s staining method is probably the best. Trypanosomata stained by this method show a fish-shaped body, the front end of which carries a flagellum. The body of the trypanosoma is coloured blue. At the anterior end may be seen a red-stained nucleus; at the opposite end a much smaller red spot, which has been termed the nucleolus, but is more properly described as the centrosome. From the centrosome a red thread extends along the outer margin of the body as far as the front extremity, where it becomes continuous with the flagellum.

The trypanosomata increase by longitudinal fission. The centrosome and then the nucleus divide, and finally a second flagellum is formed. Sometimes the young trypanosomata remain connected, producing the so-called “rosettes.”

The disturbance produced by trypanosomata seldom becomes acute, but often continues for years. The only sign of disease consists in ill-defined fever with long intermissions. The destruction of the red blood corpuscles causes anæmia, the animals or men become weak and waste away, œdema and sometimes erythema occur at varying points in the body, and occasionally the lymphatic glands become swollen.

The classical land of the tsetse disease is in the neighbourhood of the Zambesi. There it was seen and very well described by Livingstone; but, unfortunately, further investigations have shown that tsetse disease extends over the whole of Africa.

Whilst the trypanosomata of rats can only be conveyed to the one species, those of tsetse disease thrive in all mammals, particularly in the horse, mule, ox, dog, rat, and mouse.

The tsetse organism has been shown to kill both horses and mules, but to be less dangerous for oxen. A certain relative immunity exists in some races. As regards the ass, observers are not agreed; Koch failed to infect it. Sheep and goats are also but slightly susceptible. The conveyance of trypanosomata from the blood to uninfected animals occurs through the medium of a stinging fly (the _Glossina morsitans_).

Surra is endemic in the Philippines, Java, and the island of Mauritius. Koch regards the trypanosomata of surra as strictly analogous with the parasites of tsetse disease. Horses (and, in India, elephants) especially suffer from surra. Although the _Glossina morsitans_ does not occur in India, other stinging flies replace it and convey the disease.

Another variety of trypanosomiasis is _mal de caderas_, seen in South America, particularly in Argentina and Brazil. It affects horses. According to Koch, the parasites of _mal de caderas_ exactly resemble the tsetse and surra parasites. Other observers, however, declare that the _mal de caderas_ parasites are distinguished from those before mentioned by their particularly small centrosome. _Mal de caderas_ affects not only horses, but all the other animals which suffer from tsetse.

Another variety of trypanosoma, the trypanosoma Theileri, is especially striking on account of its size. It is only found in oxen, and exhibits a very slight degree of virulence.

Koch divides trypanosomata into two great groups.

The grouping is based on three important peculiarities: firstly, the morphology of the parasite; secondly, its virulence; and, thirdly, its relation to the host.

The first group only exists in one species of animal. They have become so completely accustomed to this method of life that they cannot exist under other circumstances. Their virulence is slight but constant. This group comprises the trypanosoma of rats and the trypanosoma Theileri.

The second group (to which all other trypanosomata belong) shows great variation in virulence and in form. These trypanosomata are not peculiar to any one species, but may affect dogs, rats, horses, etc. Their morphological peculiarities also vary according to the animals in which they are found. Thus, the tsetse parasites when cultivated in the bodies of dogs and rats become much smaller than usual, and the centrosome appears near the end; when cultivated in horses the end appears pointed, and the centrosome lies near the centre; in the pig the parasites lose their peculiar short flagellum. Their virulence also varies within wide limits.

It has been found possible, as in the case of bacteria, to modify the virulence of trypanosomata by successive passages through different animals. By inoculating dogs with comparatively innocuous trypanosomata and conveying the disease from dog to dog the virulence is markedly increased. On the other hand, parasites which prove very virulent for oxen become much less active for these animals after passages through rats and dogs. This apparently trifling discovery laid the foundation for protective inoculation experiments. Parasites of the second group can also exist in the bodies of almost all mammals.

Koch is of opinion that the parasites of surra in India and of tsetse disease in Africa are absolutely identical. Laveran, on the other hand, states that he has protected animals against tsetse, and that they have nevertheless suffered from surra.

That this in no way disproves the identity of the two parasites is shown by other experiments.

Koch, whilst in Dar-es-Salaam, made some interesting experiments for the purpose of discovering a method of protective inoculation. He had found that the virulence of the ox parasites could be modified. He therefore inoculated oxen first with these weakened parasites and afterwards with others of high virulence. All the control animals died while those treated as above remained alive.

Veterinary Surgeon Schmidt kept these animals under observation, and reinoculated them from time to time with highly virulent material, notwithstanding which they were still perfectly well six years after the first inoculation.

In practising this method, however, the trypanosomata used for the first inoculation must not be unduly weakened. The method would have appeared fully successful were it not for the fact that the protected and apparently quite vigorous animals still suffered from the presence of parasites in the blood. To extend its use, therefore, meant that one would not suppress, but would spread the disease. The effect would be to produce herds harbouring the parasite, which herds, though exhibiting no signs of illness, would nevertheless in a sense be propagating the active cause. Further observation has also shown that the protection so conferred is only relative. Dogs can always be infected with the blood of such animals. It has long been known in Africa that antelopes and buffaloes harbour trypanosomata in their blood without showing external signs of disease.

Another method of protection must therefore be sought, such as destroying the various stinging flies; but this offers little hope of success. Koch admits that he sees no method of dealing with them. The other method is directed against the parasite, and here he seems more hopeful. The disease can be rooted out by killing all diseased animals suspected of disease. The line of procedure is indicated by the experience gained in Mauritius and Java. When surra broke out in Mauritius almost all the oxen died in two years. In Java the nature of the disease was early recognised, and all suspected animals were at once slaughtered or isolated until slaughtered; in this way the disease was soon stamped out.

LOUPING-ILL.

The close analogy between the convulsive form of the disease described as “trembling” (which disease is well known in France) and the condition known in Britain as louping-ill lead us to give here a short account of the latter condition. For a great part of what follows we are indebted to articles by Meek and Greig Smith, published in the _Veterinarian_, Vol. LXIX, Nos. 820 and 840.