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V McGann

Publications and source records attributed to V McGann.

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Staphylococcus aureus enterotoxin B release (excretion) under controlled conditions of fermentation.

Release of Staphylococcus aureus enterotoxin B (SEB) into the culture medium was initiated during the mid-log phase of growth. A medium consisting of 4% N-Z Amine A (Sheffield), 0.2% dextrose, and 1% yeast extract supported maximum production of SEB. Although pH of the medium during cultivation did not significantly affect the growth curve of the organism, the time required for detectable excretion was affected, as was the final yield. Optimal conditions for SEB production were achieved with pH control at 7.0; alkaline control (pH 8.0) produced only minimal amounts of toxin, whereas acid control (pH 6.0) resulted in 50% reduction in yield. Slightly less SEB was produced when there was no extrinsic pH control, and cultures were buffered only by media constituents and by-products of growth. With pH control at 7.0, deletion of 0.2% dextrose from the medium resulted in 40% reduction in the 8-h yield. There was also a delay in production during early stages of fermentation.

Culture Media↗

Chemotactic activity generated by staphylococcal enterotoxin B.

Staphylococcal enterotoxin B (SEB) has significant toxicity for several mammalian species by both oral and parenteral routes. When highly purified SEB was incubated for 1 hr at 37 C with fresh serum from normal young adult men with little or no antibody activity for SEB, a factor(s) chemotactic for human polymorphonuclear leukocytes (PMN) was formed. Similar experiments using rabbit serum and autologous peritoneal PMN also demonstrated chemotactic activation. All chemotactic activity generated at 37 C was destroyed by heating at 56 C for 30 min. In human studies, precipitating antibody to SEB prevented generation of chemotactic activity by SEB. Based on heat lability and antibody sensitivity, the chemotactic factor(s) generated by SEB differs from that generated by endotoxin, and suggests a mechanism by which the PMN may participate in the pathophysiology of enterotoxemia.

Journal Article↗