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Hypersusceptibility of penicillin-treated group B streptococci to bactericidal activity of human polymorphonuclear
Abstract:
Pretreatment of serotype Ib group B streptococci with benzylpenicillin, other beta-lactam antibiotics, or vancomycin increased the susceptibility of these bacteria to the bactericidal activity of a mixture of human polymorphonuclear leukocytes and normal human serum. Increased susceptibility of the bacteria to killing by phagocytes was elicited even by exposure to subinhibitory levels of the beta-lactam antibiotics. Inhibitors of protein synthesis did not induce such susceptibility. We investigated the possible biochemical basis of penicillin-induced susceptibility to phagocytosis. Penicillin treatment induced the release of substantial quantities of group B streptococcal surface components into the growth medium (lipoteichoic acid, lipid, and capsular polysaccharide). Labeling of the live streptococci with 3H-labeled penicillin was used to evaluate the effect of exposure to subinhibitory concentrations of this antibiotic on the penicillin-binding proteins. Our results suggested that beta-lactam antibiotics and components of the immune system may act in concert to eliminate invading bacteria.
Insights
Pretreating group B streptococci with beta-lactam antibiotics enhances their susceptibility to immune system killing mechanisms. This finding suggests a synergistic approach for combating bacterial infections.
Area of Science:
- Microbiology
- Immunology
- Pharmacology
Background:
- Group B streptococci (GBS) are a significant cause of invasive bacterial infections.
- The effectiveness of antibiotics and host immune responses against GBS can be variable.
Purpose of the Study:
- To investigate how antibiotic pretreatment affects GBS susceptibility to immune-mediated killing.
- To explore the biochemical mechanisms underlying antibiotic-induced changes in bacterial susceptibility.
Main Methods:
- Exposure of serotype Ib GBS to various antibiotics (benzylpenicillin, other beta-lactams, vancomycin) at different concentrations.
- Assessment of bacterial killing by human polymorphonuclear leukocytes and normal human serum.
- Analysis of bacterial surface component release and penicillin-binding proteins following antibiotic exposure.
Main Results:
- Benzylpenicillin, other beta-lactam antibiotics, and vancomycin increased GBS susceptibility to phagocyte and serum killing.
- Even subinhibitory concentrations of beta-lactam antibiotics induced increased susceptibility.
- Penicillin treatment led to the release of GBS surface components like lipoteichoic acid and capsular polysaccharide.
- Inhibitors of protein synthesis did not confer similar susceptibility.
Conclusions:
- Beta-lactam antibiotics can prime GBS for enhanced clearance by the host immune system.
- Antibiotic treatment may disrupt bacterial cell wall integrity, exposing components that facilitate immune recognition and killing.
- Combined antibiotic and immune system action may represent a potent strategy for eradicating GBS infections.