Action of Sulfapyridine upon Pulmonary Lesion of Experimental Pneumococcal Pneumonia

Abstract

The action of type specific antiserum upon the pulmonary lesion of lobar pneumonia has been described in a previous paper. 1 Pneumonia was produced experimentally in white rats by intrabronchial inoculation of type I pneumococci suspended in mucin. The disease was uniformly fatal in untreated animals, and pneumococci were found to spread through the lung by way of edema fluid at the advancing margin of the lesion. Type specific antiserum penetrated the pneumonic lesion and apparently stopped its spread by agglutinating and immobilizing the invading organisms in the outer edema zone. The fixed pneumococci were then overtaken and were rapidly phagocytized by leucocytes.

Although sulfapyridine has proven beyond any doubt to be effective in the treatment of lobar pneumonia, the mechanism by which recovery is induced is not yet understood. Fully encapsulated living pneumococci are resistant to phagocytosis unless opsonized by specific antibody, 2 , 3 and phagocytosis is the only known method by which the host can destroy these organisms. 4 Since chemotherapy often causes a crisis long before antibodies appear in the blood, 5 and sulfapyridine in the usual dosage is mainly bacteriostatic rather than bactericidal, 6 it is not at all clear how the drug brings about the final destruction of pneumococci in the lung.

Thirty-eight albino rats were treated with sulfapyridine 6 hours after inoculation. The drug was suspended in 10% gum acacia and introduced into the stomach through a blunt cannula. Two hundred and fifty milligrams of sulfapyridine suspended in 4 cc of gum acacia mixture were given as an initial dose, and half of this amount in 2 cc of acacia was administered thereafter every 12 hours. In uninfected rats no toxic effects were noted after 1 week of treatment.