NOTE ON BACTERIOLOGY AND TREATMENT OF HÆMOGLOBINÆMIA IN THE HORSE.

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

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

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

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

In neither of the horses was the urine sanguineous.

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

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

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

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

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

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

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