Host-parasite relationships in experimental pneumonia due to pneumococcus type III
Abstract:
Experimental pneumonia was produced with a highly virulent strain of type III pneumococcus which synthesizes, during rapid growth, large amounts of capsular polysaccharide. The type III pneumonia differed from that caused by pneumococcus I in that (a) death occurred more promptly in the type III infection, (b) the local pulmonary lesion became more heavily infected, and (c) frank suppuration was common even after otherwise effective chemotherapy. The greater pathogenicity of the type III organism was shown by special histologic techniques to be due primarily to its capsular slime layer which interferes with surface phagocytosis. Capsular polysaccharide shed from the organism during growth was also demonstrated in high concentration in certain parts of the pneumonic lesion. Removal of the excess polysaccharide from the alveoli resulted from (a) lymphatic drainage to regional lymph nodes and (b) phagocytosis, particularly by macrophages. The possible relationship of the free carbohydrate to the malignancy and the characteristically viscous exudate of type III pneumonia was discussed. The lung abscesses which resulted from type III infection were observed to occur in those areas in which the maximum number of organisms had accumulated. Evidence was obtained that suppuration was due, not to necrotoxic products peculiar to the type III pneumococcus, but rather to the survival of large numbers of bacteria in the tissues, brought about primarily by the antiphagocytic effect of the slime layer. When pneumonia was produced with an intermediate type III mutant lacking the protective slime layer, back mutation to the mucoid parent occurred during the course of the infection, and the mucoid form eventually predominated in the lung as a result of selective phagocytosis of the intermediate organisms. Similar mutation to the maximally virulent type III form was noted with a transformed intermediate type III strain grown from single cell preparations.
Insights
Type III pneumococcus causes severe pneumonia due to its capsular slime layer, which hinders phagocytosis and leads to rapid, fatal infections. This slime layer promotes bacterial survival and abscess formation, even with chemotherapy.
Area of Science:
- Microbiology
- Pathology
- Immunology
Background:
- Pneumonia is a significant cause of morbidity and mortality.
- Streptococcus pneumoniae is a common bacterial pathogen causing pneumonia.
- Virulence factors of S. pneumoniae strains vary, impacting disease severity.
Purpose of the Study:
- To investigate the pathogenicity of a highly virulent type III pneumococcus strain in experimental pneumonia.
- To elucidate the role of capsular polysaccharide in type III pneumococcus virulence.
- To understand the mechanisms of suppuration and abscess formation in type III pneumonia.
Main Methods:
- Induction of experimental pneumonia in a suitable animal model using a virulent type III pneumococcus strain.
- Histologic examination to assess local pulmonary lesions and bacterial distribution.
- Evaluation of phagocytosis, particularly by macrophages, and lymphatic drainage.
- Analysis of bacterial mutation and survival in the context of chemotherapy.
Main Results:
- Type III pneumococcus caused more rapid and severe pneumonia compared to type I, with increased local infection and suppuration.
- The capsular slime layer of type III pneumococcus was identified as the primary virulence factor, inhibiting surface phagocytosis.
- High concentrations of capsular polysaccharide were found in lesions, contributing to viscous exudate and abscess formation.
- Chemotherapy was less effective due to bacterial survival facilitated by the antiphagocytic slime layer.
- Mutations to the mucoid, highly virulent type III form occurred during infection, especially in intermediate strains lacking the slime layer.
Conclusions:
- The capsular slime layer of type III pneumococcus is crucial for its high pathogenicity by preventing phagocytosis.
- Suppuration and abscesses result from bacterial survival, not necrotoxic products, due to the antiphagocytic slime layer.
- The viscous exudate and malignancy of type III pneumonia are linked to the abundant capsular polysaccharide.
- Bacterial mutation and selective phagocytosis play significant roles in the predominance of virulent type III strains during infection.
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