TY - JOUR
AU - Bryant, Amy E.
AB - S160 Pathogenesis of Clostridium perfringens Infection: Mechanisms and Mediators of Shock Dennis L. Stevens and Amy E. Bryant From the Infectious Diseases Section, Veterans Affairs Medical Center, Boise, Idaho; and the University of Washington School of Medicine, Seattle, Washington Shock, a common complication of gas gangrene caused by Clostridium perfringens, is related to the elaboration of a- and u-toxins in vivo. This study compared the relative potencies of u- and a- toxins in a rabbit model and determined the role of endogenous mediators of toxin-induced shock. a-Toxin decreased cardiac index, mean arterial pressure, and heart rate and caused death in 83% of animals. u-Toxin did not alter these parameters and caused death in only 25% of animals. a-Toxin also inhibited ex vivo cardiac contractility in a dose-dependent manner. Finally, both a- and u-toxins were potent inducers of endothelial cell – derived platelet activating factor. a-Toxin, but not u-toxin, also stimulated production of tumor necrosis factor by peripheral blood mononuclear cells. Thus, the fulminant nature of shock in patients with gas gangrene caused by C. perfringens is the sum of a-toxin’s direct effects on myocardial contractility and both toxins’ ability to induce production of potent endogenous mediators. Clostridium perfringens is 
TI - Pathogenesis of Clostridium perfringens Infection: Mechanisms and Mediators of Shock
JF - Clinical Infectious Diseases
DO - 10.1086/516249
DA - 1997-09-01
UR - https://www.deepdyve.com/lp/oxford-university-press/pathogenesis-of-clostridium-perfringens-infection-mechanisms-and-p5CV0QL0LM
SP - S160
EP - S164
VL - 25
IS - Supplement_2
DP - DeepDyve
ER -