Aggregation of platelets in the mesenteric microcirculation of the rat induced by α- toxin (phospholipase C) of Clostridium perfringens

Potential Role of Phospholipases in Virulence and Fungal Pathogenesis

“…PLC (synonyms: alpha-toxin, lecithinase), which is one of the most active bacterial phospholipases, is 1 of at least 12 different soluble antigens referred to as toxins, produced by Clostridium perfringens, that may be involved in pathogenesis. The findings that clostridial PLC was a potent toxin (109,110,123) with hemolytic (162,195), lethal (196), dermonecrotic (115), vascular permeabilization (186), and platelet-aggregating (134,185) properties attracted a large number of investigators to study this secreted protein, making it the most extensively studied bacterial toxin. Thus, it is not surprising that extensive reviews have been written about this enzyme (67,79,194), its application to the study of cell membranes (3,5,48,126,159,229), and its role in virulence (183).…”

Effects of Fusobacterium necrophorum on the mesenteric microcirculation of guinea pigs

“…Its platelet-aggregating activity which induces thrombosis is recognized to be an initial, important step in the pathogenesis of necrosis (Ohsaka et al 1978). Previously, we observed the aggregation of bovine platelets in vitro by hemagglutinating F. necrophorum (Kanoe and Yamanaka 1988).…”

“…Alpha toxin of Clostridium perfringens is known to produce thrombi in mesenteric microcirculation of laboratory animals (Ohsaka et al 1978). Its platelet-aggregating activity which induces thrombosis is recognized to be an initial, important step in the pathogenesis of necrosis (Ohsaka et al 1978).…”

Clostridial toxins in the pathogenesis of gas gangrene

“…Topical application of PLC to the mesentery of rats revealed platelet thrombi in adjacent vessels that occluded mesenteric blood flow, leading the investigators to conclude that thrombosis was likely an early step in the pathogenesis of necrosis due to PLC [63]. Similarly, we have demonstrated that intramuscular injection of C. perfringens PLC induced a rapid (less than 2 min) and irreversible decline in skeletal muscle perfusion that occurred concomitantly with the formation of intravascular aggregates of activated platelets, leukocytes, and [2] or adjuvant plus the C-domain of C. perfringens PLC and then infected intramuscularly with 3.75 × 10 8 washed, log phase C. perfringens ATCC 13124 in the right thigh.…”