Clumping of Staphylococcus aureus in the peritoneal cavity of mice.
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.
D000818:Animals; D001773:Blood Cells; D003030:Coagulase / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D008297:Male; D051379:Mice; D009504:Neutrophils; D010529:Peritoneal Cavity; D010538:Peritonitis / Q000209:etiology*; D010587:Phagocytosis; D013210:Staphylococcus; D014118:Toxins, Biological
D003030:Coagulase; D014118:Toxins, Biological; D005340:Fibrinogen