@article{mbs:/content/journal/micro/10.1099/00221287-133-6-1593, author = "Usui, Yukio and Ohshima, Yukio and Yoshida, Kosaku", title = "Platelet Aggregation by Group B Streptococci", journal= "Microbiology", year = "1987", volume = "133", number = "6", pages = "1593-1600", doi = "https://doi.org/10.1099/00221287-133-6-1593", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/00221287-133-6-1593", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", abstract = "Summary: Forty-six strains of group B streptococci (GBS), including various serotypes and nonserotypable strains, were tested for their ability to induce platelet aggregation in human plateletrich plasma; four strains, all belonging to type III, showed a positive reaction. The characteristics of the reaction were investigated in these four positive strains. Aggregation was dependent on the ratio of bacteria to platelets, being maximal at a ratio of 4·3. Platelet aggregation was inhibited by EDTA (100% inhibition at 3·1 mM), indomethacin (100% inhibition at 10 mM), acetylsalicylic acid (93-100% inhibition at 5·0 mM) and quinacrine (100% inhibition at 0·25 mM). Thus the reaction was cation-dependent and required cyclooxygenase activity. Assays for cytosolic lactate dehydrogenase did not indicate platelet lysis. GBS induced the release of [3H]serotonin, which was maximal (68-78%) at 10 min after the reaction was started. Experiments with gel-filtered platelets suggested that GBS-induced platelet aggregation required both fibrinogen and heat-resistant (56°C, 30 min) serum factors. Type-specific antisera prevented the platelet aggregation activity of heat-killed bacteria, but not of live bacteria. Trypsin digestion of the bacterial cells caused an almost complete loss of the platelet aggregation activity.", }