As supplementary to the article on hæmoglobinæmia (vol. II., page 437) the later bacteriological investigations of Lignieres must be noted. A superb Percheron, after two days of idleness, went to work at 10 P. M., was attacked at 1 A. M. and died at 3 P. M. Inoculations from blood, spleen, liver, kidney, bone marrow, myelon and subarachnoid fluid from the loins to the bulb proved sterile, excepting that made from the subarachnoid liquid on a level with the bulb, which yielded a rich culture of a streptococcus that appeared to the eye as small granules. It proved ærobic and anærobic, stained well with Gram’s (I) solution, coagulated milk, acidified the culture, formed small, round, grayish white colonies on peptonized gelatine, without liquefying, failed to propagate on potatoes, but grew well in serum and bouillon.
Two or three drops proved fatal to mice, producing, when thrown into the peritoneum a highly acute parenchymatous nephritis with bloody urine. Very few microbes were found in the kidney. There was loss of control of the hind limbs and extreme nervous irritability.
Intravenous injection of 300cc. of the culture in a powerful stallion produced hyperthermia, 102° F. on the second day, 104° on the third, 105° on the fourth, on the sixth day he became paraplegic and died on the seventh.
A second horse, which received 150cc., was sick for several days, but without paraplegia, then appeared to recover, but three weeks after he became paraplegic with albuminous urine and died next day.
In neither of the horses was the urine sanguineous.
Carnivora, swine, ruminants and birds proved insusceptible. The guinea pig succumbed to intraperitoneal inoculation, and the rabbit to intravenous.
It is to be noted that hæmoglobinuria was lacking in both experimental equine cases, and though this may be so in mild casual cases, the same is not true of violent and fatal ones. It is, therefore, evident that further research is necessary in this direction.
Accepting the conclusions reached by Lignieres, we are still debarred from entering the affection in the list of animal plagues proper, to be met by official restrictions. The streptococcus may be an essential condition in each case of the disease, or it may be one of several microbes that may act in the causation, yet the microbe in ordinary doses as accidentally introduced, does not prove pathogenic excepting in the presence of concurrent conditions of high feeding and condition, work, interrupted by one or more days of absolute idleness, and the resumption of exercise. The presence of the microbe is not enough to cause the disease in the horse in continuous work, nor in that which is kept in the stable all the time, nor even in the horse that has worked steadily and then stood idle for a day, until he again goes to work. One animal or a few only out of a stable, are attacked, and there is no such active extension from animal to animal in the vicinity that characterizes the plagues proper.
The prevention of the disease, therefore, must be sought along the lines previously laid down and well understood, in the avoidance of sudden plethora, of transient idleness during a period of high condition and steady work, and of gradual restoration to work after such period of rest. Similarly the treatment by rest, depletion, diluents, evacuants, and nerve sedatives is still in order. A new importance, however, attaches to the use of nerve sedatives and antiseptics, as calculated to prove a check on the disorder of the nervous structure and functions and on the active proliferation of the microbe.
The presence of the streptococcus may also contribute, along with the permanent changes in the nerve structure, in predisposing to relapses or second attacks, which are so common unless the animal which has once suffered is subjected to very special care.
As a fruit of the research by Lignieres, W. A. McClanahan, Redding, Ia., essayed internal antisepsis by ½ oz. doses of potassium iodide. In three severe cases relief was obtained in 15 to 20 minutes and an early and complete convalescence followed. In the hands of J. H. Kelly of New Haven, Conn., and T. S. Childs of Saratoga, N. Y., it seemed to prove equally successful, the first meeting with almost invariable success, and the latter reporting a series of 10 successive cases, several of them severe, which all recovered in from 1 to 5 days. The only untoward result was an open knee joint in one subject, the result of bruises sustained before Dr. Childs arrived. His treatment was ½ oz. of the iodide at once, and 1 to 2 drs. every hour or second hour, according to the size of the animal and the severity of the case.
In other hands this medication has been less successful, which may well be explained by the violence of the attacks, and the lack of absorption from the inactive stomach. Unless it passed on to the duodenum, it would be utterly useless, and hence the exhibition by the rectum or subcutem might be tried. The parallelism of the treatment of the two diseases of the plethoric and possibly infected subject,—parturient paresis and hæmoglobinæmia,—is striking, and it does not seem that the iodide treatment should be abandoned because of a few unsuccessful cases. Whether the iodide acts mainly as a microbicide, a chemical antidote to toxins, an eliminant, or a nerve sedative, or in two or more of these modes, is unknown, but it would be rational to expect good results along one or more of these lines. Iodide treatment should supplement, not supersede, the methods formerly in use.
This curious affection is recorded as having prevailed in the winter of 1897–8 in different localities in Iowa, Missouri, Kansas and Nebraska. In 1900 and 1901 it was again reported in different parts of Iowa.
Causation. No bacteriology of the disease has been given, and its appearance in isolated herds which had no known communication with other herds, and even in the young cattle on a farm to the exclusion of the older ones, seems to suggest an enzoötic origin, perhaps in food or water, or in some toxin determined by a fermentation of organic matter out of the body.
On the Rodkey farm at Blue Rapids, Marshall county, Kan., eight heifers from ten to fourteen months old, suffered, while the seventeen steers of the same age and the milch cows escaped. (Steddom). Near Shelby, Ia., a bull, from a healthy herd, broke into an affected herd and served cows there, and was afterward returned to his own herd and served cows there, but did not communicate the disease. (S. T. Miller). No case is recorded to show that any bull serving affected cows or heifers contracted ulcer or other disease of sheath or penis.
In one herd near Shelby, Ia., nineteen head of cows and heifers suffered, while the four steers in the herd escaped. In another herd of twenty-six head, in the same district, the four cows and eight of the twenty-two steers suffered. It is not, therefore, confined to the females. (S. T. Miller).
In all cases the disease appeared in the cooler months, from October to April inclusive, and while the cattle were secluded in muddy yards.
In different cases they occupied the yards in common with swine which were charged with wounding the vulva, until the general character of the outbreak forbade this conclusion. At Blue Rapids it was sixty-two days after they had been yarded with the hogs before the disease was observed.
In this case the lot was small, poorly drained and very muddy most of the time. Calves and hogs drank from the same troughs until the disease appeared. The water supplied to the calves and hogs was from a well sixteen feet deep. The cows, which escaped, were supplied with water from the Blue River.
Cows, heifers and steers were fed on a ration of shelled corn 6 parts, rye 1 part, oats 1 part, and had an abundance of fodder, consisting of prairie hay and millet in equal parts. They were in good condition, some of them fat, and nearly all dehorned. A second herd had shelled corn, kafir corn and cane, with water from a shallow well, and all (cows and heifers) suffered.
As showing the localized nature of the cause, C. Muller adduces the case near Ottumwa, Ia., in which a herd of 30 calves were attacked, and sold out, the owner filling the same yard a few days later with 30 more bought in the surrounding country, and which he put on the same rations. In about 10 days the disease appeared in the second lot.
On the Rice farm, Blue Rapids, were 60 yearling heifers, bought in Kansas City, and two home cows. In the first week after arrival 5 heifers suffered, in the second week 20, in the third week 40, and in the fourth week all the 60. The two cows mingling with them were only slightly affected.
In the Rodkey farm, Blue Rapids, cases, all of the young cattle (which alone suffered) had been raised on the farm and had not been exposed to outside cattle.
Symptoms. “The ulcer, in almost every case, started as a mere abrasion, the size of a pinhead, usually on the inner surface of the labia, near the border of the inferior commissure, gradually eating its way through until it appeared as a much larger denuded surface on the outside” (C. Miller). S. T. Miller says: “The first noticeable symptom was serous exudate, rapidly forming into a brown scab, under which was very fœtid pus, with extensive inflammation. The affection usually occurred on the lower portion of the lips of the vulva, in heifers and cows, and in steers around the anus or root of the tail. The scabs which formed seemed to spread very rapidly, destroying more and more of the underlying tissue and forming a thicker and thicker scab. The scab, if pulled off, would expose a raw surface which would bleed very readily. In a short time a new scab would be formed.”
Steddom says: “The vulvar lips thickened and continued to discharge for four or five days. In the meantime certain pustules appeared, 0.1 to 2.5 centimeters in diameter. About the fifth day these ruptured and discharged yellowish pus.” The mucous membranes of the vulva and vagina were dry and slightly congested. The ulcers were covered with brown leathery scabs, which adhered tenaciously and when detached left an angry, red, purulent, granular, elevated and pitted surface. In some of the more severe cases, one or both lips of the vulva had sloughed off, and the sore had extended 10 to 15 centimeters on the skin of the escutcheon. The pus from this sore did not corrode the adjacent skin.
The more severe cases showed loss of appetite, constipation, hurried breathing, tucking up of the abdomen, with general dulness and dejection, and great tenderness of the affected skin with stiff, straddling gait.
Pathology. This is very obscure. The primary cause of the sores is not evident, though their occurrence on the anus and vulva only, and especially on the latter would suggest an elective affinity of the poison (microbian or chemical) for these structures and their products. If we assume a pathogenic microbe in the fæces, the question arises as to the cause of the habitual immunity of the steer, and of the margin of the anus in the majority of the affected heifers. The susceptibility of heifers rather than cows may imply a previous exposure and acquired immunity on the part of the mature animal.
Again if we suspect the existence of a necrobiotic agent of organic origin (like ergotin, secalin, sphacelin) we must assume a superadded microbian infection, implanted in the primary sore and rapidly extending it. The prompt recovery under antiseptic treatment shows that no mere chemical poison maintains the destructive process, for it is manifestly the microbicide which puts a prompt limit to the disease, and under such treatment no sphacelating agent in the blood or tissues keeps up the advance of the ulceration or prevents healing.
Treatment. The ulcers healed rapidly under cleanliness and antiseptic applications. The tail, anus, and vulva were washed with tepid water, and then dressed with a solution of creolin (5:100), or carbolic acid (3:100), or mercuric chloride (1:500 or 1000). The ulcers were touched with a pencil of silver nitrate. S. T. Miller followed the sublimate lotion by the subjoined ointment: iodoform 20 grains, eucalyptol 40 minims, phenic acid 20 minims, petrolatum enough to make 2 oz. C. Miller in addition to the carbolic acid lotion applied the common white lotion (zinc sulphate 1 oz., lead acetate 1 oz., water 1 qt.) and used silver nitrate on the ulcers. Four dressings on four successive days were given and in the milder cases healing was completed in 10 or 12 days.
As these pages are going through the press, Cooper Curtice’s bulletin on Goose Septicæmia comes to hand.
This affection in 1900 caused a loss of 3,200 geese in July and August to Mr. Cornell, a Rhode Island owner. Mr. Snell lost 500.
Bacteriology. The blood and tissues swarmed with a minute bacillus having the general morphological staining and biological characters of that of chicken cholera and rabbit septicæmia. It differed from these in the failure to infect chickens, whether inoculated or fed to them. It proved deadly to geese, ducks, pigeons, rabbits, mice, and more slowly to Guinea pigs. Geese were infected by inoculation or feeding of the germs, ducks from inoculation only.
Symptoms. The geese were often found dead, and even in those noticed ill, death supervened so early that no very diagnostic symptoms were made out. The affected geese moved tardily and unsteadily, and failed to keep with the remainder of the flock. Some burrowed the head in the dirt and twisted it around, indicating, it was supposed, spasms of the throat. Some were seized with the death agony in a few minutes; in others the illness lasted for hours, and from experimental cases it was concluded that the period from infection to death, in the majority of cases, did not exceed thirty-six hours. Some were believed to merge into a chronic condition, but the owner thought that none recovered. No diarrhœa is noted.
Lesions. The head was the seat of marked venous and capillary congestion, suggesting asphyxia. The bill and throat contained a large quantity of tenacious mucus, which was especially viscid in the nose. Extravasated blood in abundance was present in the gastro-intestinal mucosa and contents, much of it more or less digested. At some points there was abundant mucous exudate; at others the folds were only marked by punctiform petechiæ, or by bloody patches formed by their coalescence. The cæca were usually normal.
The liver showed numerous punctiform extravasations and yellow patches of necrosis extending more or less deeply into the hepatic tissue. Other congestions were seen in individual cases, implicating, in one instance, the heart and pericardium, and in another the lungs. Petechiæ were frequent on the pericardium and other mucosæ. The blood was usually black, tarry, and with little disposition to brighten on exposure to the air.
Diagnosis. It is recognized as an infection of domestic water fowl by its attacking the larger proportion of that class of animals exposed to it. It is supposed that those which escape do so because of immunity due to a previous attack, or by reason of the absence of any wound of the mouth, throat or stomach by which the germ might enter. It is distinguished from fowl (chicken) cholera by the immunity of the chicken in this case. It is differentiated from Klein’s diarrhœal enteritis of fowls, by the fact that neither pigeon nor rabbit is immune. From the duck cholera of Cornil and Loupet, it is diagnosed by the immunity of the chicken only, while the rodents and pigeon suffer.
The germ is manifestly one of the family of bacilli of the colon group, found in the different septicæmias, but sufficiently distinctive from these other forms, in its pathogenesis, to demand a separate place in connection with sanitary work.
Treatment is hopeless from our present point of view.
Prevention is the rational resort. In the case of those raising geese from the egg, it is imperative to abandon, for the season at least, any pastures that may have become contaminated. It would be better still to subject such pastures to cultivated crops for one or two years. The pens should be thoroughly disinfected or abandoned and burned. Mr. Cornell used his infected pens for ducks without evil result. The drainage from infected pastures or pens must be guarded against, no geese nor ducks being allowed on land through which, or on which it passes, and no water receiving such drainage being employed for geese. In the case of feeders or handlers of geese who buy the birds in large numbers from many sources, a subsidiary quarantine should be constantly maintained, by enclosing the birds in as small groups as possible in separate pens, so that infection in one pen will not endanger the whole flock. When infection is shown in a pen, the diseased birds should be at once destroyed and burned, the pen thoroughly disinfected, and the other birds returned, or better, divided up into still smaller lots, so that infection showing in one of these will not endanger the great number taken from the original infected pen. The utmost care should be taken to maintain the most perfect cleanliness in the pens of exposed and suspected geese, and to sprinkle the floors and manure liberally with an antiseptic, such as a solution of sulphuric acid in water (2:100), or of phenic acid (3:100), or of a combination of the two. This will do much to prevent the hatching of flies to act as infection-bearers, and if these can be further excluded by screens the condition will be still more satisfactory. Vermin of all kinds should be excluded and whenever possible, separate feeders and attendants should be furnished for the suspected geese, and those that have not been exposed.
Lucet describes a septicæmia of chickens and turkeys accompanied by dysenteric discharges. The microbe resembles the bacillus gallinarum of Klein (see Vol. II, p. 254), even in the immunity of pigeons and rabbits when injected subcutem. Rabbits, however, suffer when injected intravenously. The probability is that this bacillus is identical with that of Klein. Yet in this whole class of microbes of the colon group, variations, apparently superinduced by environment, appear to result at times in a deadly pathogenesis for different genera, and epizoötics differing from each other.