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Clumping of Staphylococcus aureus in the peritoneal cavity of mice
Abstract:
Kapral, Frank A. (Philadelphia General Hospital, Philadelphia, Pa.). Clumping of Staphylococcus aureus in the peritoneal cavity of mice. J. Bacteriol. 92:1188-1195. 1966.-Nonencapsulated strains of Staphylococcus aureus inoculated into the peritoneal cavity of mice are promptly clumped by the interaction of fibrinogen with the bound coagulase present on the bacterial surface. Some of the pre-existing leukocytes adhere to the staphylococcal clumps during the 1st hr, but phagocytosis is minimal. During the 2nd hr, there is an influx of neutrophils into the region, and these form a thick layer around the staphylococcal clumps and, apparently, prevent further egress of toxin. Leukocytes in proximity to the organisms undergo degeneration, but cells located externally maintain an effective barrier and, thus, confine the organisms. The encapsulated Smith strain of S. aureus is not clumped under these circumstances, presumably because the capsule prevents the bound coagulase-fibrinogen interaction.
Insights
Nonencapsulated Staphylococcus aureus strains clump in mouse peritoneal cavities due to bound coagulase. Encapsulated strains resist clumping, suggesting capsules impede this crucial bacterial interaction.
Area of Science:
- Microbiology
- Immunology
- Bacterial Pathogenesis
Background:
- Staphylococcus aureus possesses surface-bound coagulase, an enzyme influencing its interaction with host factors.
- Bacterial capsules can modulate host-pathogen interactions and immune evasion strategies.
Purpose of the Study:
- To investigate the in vivo clumping mechanism of Staphylococcus aureus in the mouse peritoneal cavity.
- To determine the role of bacterial surface coagulase and capsule in host immune response.
Main Methods:
- Intraperitoneal inoculation of non-encapsulated and encapsulated Staphylococcus aureus strains into mice.
- Microscopic examination of bacterial clumping and host leukocyte response over time.
Main Results:
- Non-encapsulated S. aureus strains rapidly formed clumps via fibrinogen interaction with bound coagulase.
- Leukocytes, primarily neutrophils, infiltrated and surrounded bacterial clumps, limiting toxin spread.
- Encapsulated S. aureus strains (Smith strain) did not clump, indicating capsule interference with coagulase-fibrinogen binding.
Conclusions:
- Bacterial clumping mediated by bound coagulase is an early host defense mechanism against non-encapsulated S. aureus.
- Bacterial capsules can inhibit this clumping, potentially contributing to virulence by preventing early immune containment.