Elizabeth L. Jost

THE ASSOCIATION OF TYPE SPECIFIC HEMOLYTIC STREPTOCOCCI WITH ACUTE GLOMERULONEPHRITIS : AT THE PRESBYTERIAN AND BABIES HOSPITALS, NEW YORK, N. Y., IN THE YEARS 1936-1942

The mechanism by which acute glomerulonephritis develops is unknown, but there is general agreement that an infection initiates the process. This infection commonly occurs in the upper respiratory tract but classical instances of acute glomerulonephritis have followed infections of the skin, subcutaneous tissues, lungs and peritoneal cavity. An antecedent hemolytic streptococcal pharyngitis has not been excluded in all these instances. Clinical, bacteriological and immunological evidence indicates that the hemolytic streptococcus is the precipitating agent in the great majority of the infections that precede acute glomerulonephritis (1-7). It should be noted, however, that acute glomerulonephritis has followed pneumococcic pneumonia (8), subacute bacterial endocarditis (9), and gastrointestinal infections due to various enteric organisms (1). Recently Rammelkamp, Weaver, and Dingle (10) presented evidence indicating that the attack rate of acute glomerulonephritis following Group A hemolytic streptococcus infections varied considerably. In contrast, the incidence of acute rheumatic fever following such infections appeared to be relatively constant. Rammelkamp and his associates postulated that this difference in attack rate was due to the episodic appearance of certain strains of hemolytic streptococci which were more nephritogenic than others. Their collected data

ON THE PERMANENCE OF RECOVERY IN ACUTE GLOMERULONEPHRITIS

Although there is common agreement and occasionfal mention of the fact that nephritis once healed does not recur, there has been little evidence presented in the literature to substantiate this impression. Longcope (1) reports 4 cases out of a series of 24 with healed acute nephritis in whombeta hemolytic streptococci were found subsequently. Two of these, in a single throat culture each, revealed beta hemolytic streptococci, and, in a third patient, beta hemolytic streptococci were cultured repeatedly from chronically infected tonsils. Active invasion of tissue by the streptococcus, as measured by the antistreptolysin titer, was not reported. The fourth patient suffered a severe bronchitis caused by the beta hemolytic streptococcus. In none of these patients was there evidence of an exacerbation or recurrence of nephritis. Boyle et al. (2) mention the cases of 2 boys, each of whomthey state had two distinct attacks of nephritis, each followed by complete recovery. Detailed data on the courses and urinary findings in these 2 patients were not given. In the present study, a group of patients was observed during an attack of acute glomerulonephritis, after recovery, and during a subsequent infection. The infection at the onset of the acute glomerulonephritis and the subsequent infection were proved bacteriologically and immunologically to be caused by the hemolytic streptococcus. It was hoped that such a study might throw light on the alleged permanence of recovery in this disease. The present paper offers bacteriological, immunological, and clinical data on two groups of patients. The case histories have been divided into 2 groups which are described in the following protocols and are presented in Tables I and II respectively. The 8 cases of Group I include all those observed over an approximately four-year period, from 1933 to 1937. The two individuals in Group II are selected on the basis of their unique manifestations.

Precipitins Against Fractions of Streptococci in Hemolytic Streptococcus Disease, Glomerular Nephritis, Rheumatoid Arthritis, and S. Viridans Endocarditis

The sera of 310 patients have been studied for precipitins against 2 protein fractions of S hemolyticus, the nucleoprotein of S. viridans and the group specific carbohydrate of S. hemolyticus. The S. hemolyticus fractions were freshly prepared. The S. viridans protein first used∗ was 5 years old. Later tests with a sample newly isolated from the same strain gave identical results. A description of the precipitin test and the antigens used has been presented in a previous communication. 1 Sera from the following groups of cases have been studied: 1. A control group of 39 healthy nurses during the fall season.† 2. A control group of 16 healthy medical students and nurses during the spring season. 3. A control disease group .of 17 cases with temperatures of 102° or over. These patients were not affected with hemolytic streptococcus disease. All these sera were obtained during the spring season. 4. A control disease group of 100 cases during the spring season. None of these patients was known to have rheumatic fever, rheumatoid arthritis, sub-acute S. viridans endocarditis, proven hemolytic streptococcus disease, glomerular nephritis or peptic ulcer. 5. Twenty-three cases of proven sub-acute S. viridans endocarditis. 1 6. Thirty-six cases of rheumatoid arthritis.‡ 7. Sixteen cases of proven hemolytic streptococcus disease. 8. Fourteen cases of acute glomerular nephritis. 9. Sixteen cases of sub-acute glomerular nephritis. 10. Seven cases of healed glomerular nephritis. 11. Five cases of healed glomerular nephritis during hemolytic streptococcus infection. 12. Twenty-one cases of peptic ulcer with symptoms.

Observations on the Filtrability of B. Tuberculosis.

A series of 21 guinea pigs was inoculated with the Berkefeld filtrates of tuberculous material. Of 12 animals autopsied so far, acid-fast bacilli have been identified in the direct smears from the lung, inguinal and tracheo-bronchial glands of 3 of the animals. Prolonged search was necessary to demonstrate the organisms which, however, occurred usually in large clumps when found. No definite evidence of tuberculosis was found by histological methods, except in the lungs of two of the positive animals. These showed small punctate areas of granulomatous, endotheloid hyperplasia, not specific for tuberculosis. The lesions did not differ materially from those found in the lungs of one out of twelve control animals examined. Exhaustive search of the smears of the lymph glands and lungs of 12 uninoculated animals did not disclose the presence of any acid-fast bacilli. Cultures and inoculation experiments from positive animals yielded negative results. These results as a whole appear in accord with those of the French school, who believe they have demonstrated the filtrability of this organism. Lacking as they do cultivability, or the power of producing classical tuberculosis, we feel that the nature of the acid-fast organism in the smears is uncertain as yet. On the other hand, one of the animals inoculated with the filtrate under different conditions than the rest died between the 6th and 7th month of classical tuberculosis. The lesions involving the abdominal lymph glands, lungs and liver were widespread and unmistakable. Acid-fast bacilli were readily found and on injection again produced classical tuberculosis. A control animal inoculated with the same filtrate as the test animal but under the usual conditions died in five weeks of pneumonia but showed no eviaence of tuberculosis. Attempts to repeat this rather noteworthy result are under way.