esting to note that the poisonous substance has apparently been transmitted through the milk of the dam. This may be of importance in regions where cottonseed plays an important part in feeding milch cows supplying milk to infants. The ascitic liquid was of a brownish yellow color, of an oily appearance but not an oily consistency. It gelatinized three minutes after removal, forming a peculiar opalescent streaky solidified mass surrounded by brownish yellow serum. This liquid in the calves was similar to the ascitic liquid in the pigs that died. The ascitic liquid in the pigs that recovered after change of diet was of the consistency as well as appearance of water. The slight amount of coagulum on the peritoneum contained numerous fibroblasts. This seems to show that the ascites is possibly the first to appear and the last to disappear in the cottonseed meal poisoning. The periods at which the pigs died suggest that some of them are more tolerant to the cottonseed than others. The difference in the appearance of the thyroid glands in those animals that died and those that recovered is suggestive. We hope to attempt certain experiments with a view of determining if possible the cause of the relative immunity. The actual cause of the oedema is as yet a mystery. It is possible that the effect of the poisonous material upon the myocardium is responsible for it. This seems to be strengthened by the fact that the last pig to die showed cardiac dilatation. Some authors also state that hypertrophy of the heart" is the lesion in cottonseed poisoning. This hypertrophy was probably a result of the obstruction to the circulation in the lungs. The contention of some biochemists is that oedema is due to increased acidity of the tissues. On account of this Wells and Ewing (3), attempted to determine whether or not there is acidosis in cottonseed injury, with negative results. We hope to perform some experiments with a view of solving some biochemic problems that suggest themselves as a result of the lesions we have encountered in these experiments. Thus far the following conclusions seem to be justifiable. 1. That the lesions in cottonseed injury are generalized oedema. 2. That the initial lesion apparently is ascites. 3. That the poisonous substance may be transmitted to the offspring through the milk. REFERENCES 1. MARCHLEWSKI, L. P. T., Jour. Prakt. Chem., N. F. 1899, LX, 84. 2. WITHERS, W. A. and CARRUTH, F. E., Jour. Agr. Res., 1915, V, 261. 3. WELLS, C. A. and EWING, P. V., Ga. Exp. Sta. Bul. 119, 1916 (Lit.) 4. HAINES, G. Unpublished Experimental Work Performed for a Manufacturing Corporation. DESCRIPTION OF PLATE Healing of hemorrhage. Sinus of lymph node pig 11. x 285. Fig. 3. x 90. Thyroid pig, showing marked perifollicular hyperemia and granular material in the follicles. x 285. x 285. Fig. 6. Lymphoid nodules surrounding a small bronchus pig 11. x 80. THE LESIONS IN NECROBACILLOSIS S. A. GOLDBERG Department of Comparative Pathology and Bacteriology The economic importance of necrobacillosis must be considerable since it affects all of our domestic animals and in these it manifests itself in various forms. While young animals suffer the most, adults are also affected. The causative agent of this disease is B. necrophorus. It is supposed to be a motile organism varying in its morphology from coccoid forms to filaments 100 micra in length. Its natural habitat is the intestine of various animals. It is found in filth and in soil contaminated with manure. It is a strict anaerobe and is not easily cultivated artificially. The production of toxins has not been clearly demonstrated although the sudden death of certain animals, both experimentally and naturally infected, leads to a suspicion of a toxemia. It is the cause of foot rot of sheep and cattle, necrotic dermatitis of various animals, necrotic quittor, lip and leg ulceration of sheep, necrotic stomatitis, diphtheroid of calves, necrotic gastritis, enteritis, anovulvitis and vaginitis. This organism is quite commonly found in sharply circumscribed necrotic areas of livers of practically all of our domesticated animals. It apparently enters the liver by means of the portal vein from the intestine. In some cases the intestinal mucosa shows a catarrhal or diphtheroid inflammation. In most cases, however, such an enteritis is lacking. According to Joest this would indicate that either there was at one time a temporary enteritis, or that the Bacillus necrophorus may enter the portal circulation from an intact or from a very slightly injured mucosa. This, he claims, is quite possible since there are quite regularly found large numbers of these organisms in the intestines of adult cattle and of calves. In calves the organisms may also enter the liver from the umbilical vein both extra and intra uterine. This is evidenced by the observations of Joest, Berndt, and Bang. In adult cattle the necrosis bacillus may also enter the liver from the fore stomach on a foreign body. Macroscopically the necrotic areas in the liver are sharply circumscribed, more or less rounded, of a yellowish brown, grayish yellow or grayish brown color, lighter than the surrounding liver tissue and very often surrounded by a red zone. Where there are a large number of necrotic areas the liver as a whole is enlarged, with rounded edges. The color of the liver may be unchanged or is icteric. We have observed a case in a cow where the liver was adherent at these areas to the diaphragm and the necrosis spread and affected the diaphragm for a depth of 2 millimeters. The liver may be adherent to adjacent organs by fibrin or there may be found a diffuse sero-fibrinous peritonitis. Microscopically in the very early stages we found a thrombosis and widening of the sinusoids, a gradual disappearance of the nuclei of the liver cells and a collection of small round cells (fig. 2). In the thrombosed sinusoids and around this area generally there are numbers of the organisms. In later stages the center is entirely structureless and there are hyperemia, round cells and a few polymorphonuclear leucocytes at the periphery where there are also large numbers of the bacilli. Joest describes also still later stages where the areas are encapsulated by connective tissue. This state we have not encountered. In the intestine and other mucous membranes the necrotic areas may be slightly raised from the surface or even depressed. They usually extend into the deeper tissues involving the submucosa and even the muscular coats. There is often a sharp line of demarcation by a reddened zone similar to that found in the liver. There may also be connective tissue proliferation at the base of the ulcer. Microscopically the glandular cells at first become smaller, their nuclei are shrunken and stain darker than the nuclei of normal cells. Later there is formed a structureless mass with some small round cells and a very little fibrin at the periphery. The organisms are present in large masses around the glands at the periphery of the necrotic areas. In addition to the necrotic pneumonias in pigs and calves we have observed metastasis in lungs of adult cattle, in which the necrotic areas were almost identical with those found in the livers of these animals. In a case of a yearling heifer sent in from Nebraska the lesions were generalized in the liver, lung, spleen and heart. We have encountered a number of cases of necrotic laryngitis in calves and an outbreak of a disease among sheep in which there are progressive necrosis of the ears, listlessness, keeping away from the herd and finally death. This was quite likely due to Bacillus necrophorus. There were recently received for diagnosis specimens of a tongue and stomach of a foal showing lesions resembling those found in calf diphtheroid. (Figs. 1 and 4.) Microscopically, they showed necrosis of the mucosa extending into the submucosa. Sections stained with methylene blue showed rod shaped organisms arranged along the border of the necrotic areas. Gastrophilus equi larvae. were also found attached to the mucosa of the stomach. It may be that these parasites opened an avenue for invasion of the B. necrophorans organisms. Dr. Taylor of Henrietta, N. Y., brought section of the tongue, rumen and mammary gland of a pure bred Guernsey cow. The lesion in the rumen was superficial necrosis over an area of 8 cm. in diameter. This area was raised from the surface for about 3 mm. On section the necrosis extended deeply into the tissue with a considerable amount of connective tissue around it. The lesions in the tongue were almost identical with those shown in fig. 1. There were small round yellowish necrotic nodules in the mammary gland similar to those commonly found in the livers affected with necrobacillosis. Smears from the periphery of the lesions showed the curved filaments of B. necrophorus. Numerous individuals of this herd are constantly or periodically affected with foot rot and necrotic stomatitis. In a herd of cattle near Ithaca, where occasionally we have had cases of generalized necrobacillosis for autopsy, a number of cows show peculiar obscure symptoms which may be due to internal necrobacillosis. REFERENCES FITCH, C. P. 22nd Ann. Rept. U. S. Live Stock San. Assoc., 1918. KITT, TH. Path. Anat. d. Haust., 1911, I. DESCRIPTION OF PLATE Fig. 1. Necrobacillosis tongue foal. x 12. Fig. 2. B. Confluent necrotic areas. C. Normal mucosa of tongue on section. D. Necrotic area on section showing its deep invasion into the tissues and surrounding dark zone. An early lesion of necrobacillosis. Liver, pig. Showing lymphocytic infiltration. Fig. 3. Early lesion of necrobacillosis. Intestine, pig. Fig. 4. A. Superficial coagulation necrosis of mucosa. B. Disintegrating glands surrounded by lymphocytes. The organisms were present in large numbers around the epithelial cells of these glands. Necrotic gastritis. Cardiac portion of stomach, foal. A. Normal mucosa. X 2. B. Necrotic mucosa extending in the larger areas nearly to the serous coat. |