IMMUNOLOGICAL STUDIES IN PATIENTS WITH PNEUMOCOCCUS TYPE III PNEUMONIA TREATED WITH SUL-FANILAMIDE AND SERUM

Abstract

Sulfanilamide in concs, of 7 mg. or more per 100 cc. inhibits the growth of large numbers of Type III pneumococci in the blood of non-pneumonic individuals or of patients ill with pneumonia due to this organism when such bloods lack pneumococcidal activity. The drug probably does not influence phagocytosis in these bloods. It usually exerts no bactericidal effect in a conc, of 10 mg.%, but may do so in greater cones. Patients with pneumococcus Type III pneumonia, whose blood is bactericidal for pneumococci of the homologous type during the acute disease and before treatment, usually acquire homologous type-specific agglutinins, mouse protection, and phagocytosis after treatment with either sulfanilamide or serum or both. Blood invasion does not occur after treatment in such cases and if death occurs it is usually due to superinfections or to other conditions not directly related to the Type III pneumococcal infection. In an occasional patient the pneumonia extends in spite of the presence of circulating antibodies and in spite of the absence of bac-teremia throughout the disease. Therapeutic antipneumo-coccus rabbit serums induce pneumococcidal activity in the blood of patients ill with pneumonia due to this type. Antiserum and sulfanilamide used together have a greater bacteriostatic and bactericidal effect than the same amounts of either the serum or the sulfanilamide used separately. The bactericidal-promoting property of the antiserum is usually accompanied by demonstrable phagocytosis. In patients whose blood lacks bactericidal properties, treatment with sulfanilamide probably renders the blood bacteriostatic until heat stable specific antibodies (agglutinins and mouse protection) develop or until a balance of such antibodies is passively introduced. When such heat stable antibodies are acquired, the pneumococcal infection is usually overcome. With antiserums in proper amounts, the infection may be overcome without the additional use of sulfanilamide, especially in patients who are not heavily infected. Death in either event may nevertheless occur, but under such circumstances it is due either to complications or to conditions not related to the Type III pneumococcal infection. Following treatment with sulfanilamide alone, occasional patients with Type III pneumococcus pneumonia recover without developing demonstrable homologous type-specific antibodies. This may occur even if the pneumococcus is recovered from the blood stream.