David P. Earle

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

Studies on the Chemotherapy of the Human Malarias. IX. Effect of Pamaquine on the Blood Cells of Man.

Pamaquine (6-methoxy-8-amino [N-diethylaminoisopentyl] quinoline) is recognized to be a potentially dangerous drug. However, a definitive appraisal of its hazard had not been achieved at a time when the further exploration of the antimalarial activity of the 8-aminoquinolines was considered advisable. Pamaquine toxicity can involve the gastro-intestinal tract, the central nervous system, and the circulating blood. Symptoms referable to the gastro-intestinal tract and the central nervous system may be annoying, but there is no evidence that they constitute a hazard to life or persist beyond the termination of therapy. Effects on the blood do constitute a serious hazard and are considered in this paper.

STUDIES ON THE CHEMOTHERAPY OF THE HUMAN MALARIAS. VII. THE ANTIMALARIAL ACTIVITY OF PAMAQUINE

Pamaquine, synthesized in 1926, was introduced in the treatment of malaria as a schizonticide. It was soon found, however, that the great schizonticidal activity which it possessed in cathemerium malaria of canaries did not obtain in the human malarias. It was shown to be relatively ineffective in acute attacks of vivax malaria and to have only minimal activity against the asexual forms of P. falciparum, although it did eradicate the gametocytes in this infection. In addition, the general usefulness of pamaquine was limited by the frequent occurrence of toxic effects with doses in the therapeutic range. Nonetheless, evidence was advanced favoring both a prophylactic (1, 2, 3) and curative action (4) in vivax malaria. The toxicity of the drug and an incomplete understanding of the biology of vivax malaria led the commission on malaria of the Health Organization of the League of Nations (5) to state that its prophylactic action was not practical and to discount the work of Sinton on its curative action (4). The commission recommended that pama-