Abstract
Clostridium perfringens uses its large arsenal of protein toxins to produce histotoxic, neurologic and intestinal infections in humans and animals. The major toxins involved in diseases are alpha (CPA), beta (CPB), epsilon (ETX), iota (ITX), enterotoxin (CPE), and necrotic B-like (NetB) toxins. CPA is the main virulence factor involved in gas gangrene in humans, whereas its role in animal diseases is limited and controversial. CPB is responsible for necrotizing enteritis and enterotoxemia, mostly in neonatal individuals of many animal species, including humans. ETX is the main toxin involved in enterotoxemia of sheep and goats. ITX has been implicated in cases of enteritis in rabbits and other animal species; however, its specific role in causing disease has not been proved. CPE is responsible for human food-poisoning and non-foodborne C. perfringens-mediated diarrhea. NetB is the cause of necrotic enteritis in chickens. In most cases, host–toxin interaction starts on the plasma membrane of target cells via specific receptors, resulting in the activation of intracellular pathways with a variety of effects, commonly including cell death. In general, the molecular mechanisms of cell death associated with C. perfringens toxins involve features of apoptosis, necrosis and/or necroptosis.
Highlights
The ability of Clostridium perfringens to produce a large repertoire of toxins makes it a serious pathogen of humans and animals, being able to produce histotoxic, enteric and/or enterotoxemic diseases [1,2]
Lytic concentrations of C. perfringens Alpha Toxin (CPA) can result in extensive degradation of plasma membrane and lactate dehydrogenase (LDH) release [22,35], which is characteristic of necrosis [36]
C. perfringens Beta Toxin (CPB) was demonstrated by immunohistochemistry only in endothelial cells within the lamina propria in naturally-occurring cases of necrotic enteritis in piglets [57] and in a human patient [58], as well as in an experimental infection model in pigs associated with early vascular lesions [59]
Summary
The ability of Clostridium perfringens to produce a large repertoire of toxins makes it a serious pathogen of humans and animals, being able to produce histotoxic, enteric and/or enterotoxemic diseases [1,2]. Toxin production varies significantly among C. perfringens strains, which is the basis for a classification system that was traditionally based upon the presence of encoding genes for alpha (CPA), beta (CPB), epsilon (ETX) and iota (ITX) toxins [1]. This typing system, was recently revised to include two additional types, i.e., C. perfringens type F strains producing enterotoxin (CPE). C. perfringens type A has been associated with cases of gas gangrene in animals, the role of CPA in these species has not been established [4]
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