STUDIES ON THE MECHANISM OF RECOVERY IN PNEUMOCOCCAL PNEUMONIA : II. THE EFFECT OF SULFONAMIDE THERAPY UPON THE
1Department of Medicine, Johns Hopkins University School of Medicine, Johns Hopkins Hospital, Baltimore, and the Department of Bacteriology and Immunology, Harvard Medical School, Boston.
Abstract:
Experimental pneumococcal pneumonia was produced in albino rats by intrabronchial inoculation of Type I pneumococci suspended in mucin. The resulting pneumonia was uniformly fatal in untreated rats. Eighty per cent of the animals so infected and treated with sulfonamide drugs 6 hours after inoculation survived the pneumonia. At the end of 1 week the surviving animals were sacrificed, and examination of the lungs showed sharply demarcated localized pulmonary lesions containing no pneumococci. Microscopic study of the lungs of treated animals sacrificed at 6, 18, 42, 66, 96, and 168 hours after the start of treatment revealed the following sequence of events. During the first 18 hours the drug apparently had little effect upon the pneumonic lesion, but at the end of 18 hours pneumococci in the edema zone began to show striking changes in their morphology, indicating bacteriostesis. Forty-two hours after the start of treatment the edema zone had disappeared, the pneumonia had ceased to spread, and the pneumococci at the margin of the lesion had been overtaken by leucocytes. Careful examination of the exudate in the periphery of the lesion revealed definite phagocytosis of pneumococci. By the 4th day no pneumococci could be found in the stained sections, and after 1 week there remained only macrophages in the rapidly clearing alveoli. In order to demonstrate the phagocytic reaction more clearly the effect of sulfonamide drugs was studied in pneumonic rats previously rendered leucopenic by exposure to x-ray. The pneumonia in these animals was relatively acellular, and the few macrophages present in each alveolus could be seen to have phagocyted large numbers of pneumococci after 18 to 42 hours of treatment. The macrophages not only phagocyted the pneumococci but ultimately destroyed them, the pneumonic lesion later going on to complete resolution. The fact that this phagocytic reaction was observed in the lungs of animals with bacteremia suggests that the phagocytosis is independent of circulating type-specific opsonins.
Insights
Sulfonamide drugs effectively treated experimental pneumococcal pneumonia in rats, leading to resolution of lung lesions. This treatment promoted phagocytosis of pneumococci by leukocytes and macrophages, clearing the infection.
Area of Science:
- Bacteriology
- Pharmacology
- Pathology
Background:
- Experimental pneumococcal pneumonia was induced in rats using intrabronchial inoculation of Type I pneumococci.
- Untreated rats invariably succumbed to the induced pneumonia, establishing a model for therapeutic intervention.
Purpose of the Study:
- To evaluate the efficacy of sulfonamide drugs in treating experimental pneumococcal pneumonia.
- To elucidate the pathological and cellular mechanisms underlying sulfonamide treatment in pneumonia.
Main Methods:
- Rats were inoculated with pneumococci and treated with sulfonamides 6 hours post-infection.
- Lung tissues were examined microscopically at various time points after treatment initiation.
- Phagocytic responses were assessed in leucopenic rats to clarify the role of macrophages.
Main Results:
- Sulfonamide treatment resulted in an 80% survival rate in infected rats.
- Microscopic analysis revealed the disappearance of pneumococci and resolution of pulmonary lesions within 1 week.
- Evidence of bacteriostasis, leukocyte infiltration, and significant phagocytosis of pneumococci by macrophages was observed.
Conclusions:
- Sulfonamide drugs are highly effective in treating experimental pneumococcal pneumonia.
- The mechanism of action involves bacteriostasis and enhanced phagocytosis by leukocytes and macrophages, independent of circulating opsonins.
- Complete resolution of pneumonia lesions occurs through macrophage-mediated destruction of pneumococci.
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