Comparative pathogenesis of enteric clostridial infections in humans and animals

Abstract

Several enteric clostridial diseases can affect humans and animals. Of these, the enteric infections caused by Clostridium perfringens and Clostridium difficile are amongst the most prevalent and they are reviewed here. C. perfringens type A strains encoding alpha toxin (CPA) are frequently associated with enteric disease of many animal mammalian species, but their role in these diseased mammals remains to be clarified. C. perfringens type B encoding CPA, beta (CPB) and epsilon (ETX) toxins causes necro-hemorrhagic enteritis, mostly in sheep, and these strains have been recently suggested to be involved in multiple sclerosis in humans, although evidence of this involvement is lacking. C. perfringens type C strains encode CPA and CPB and cause necrotizing enteritis in humans and animals, while CPA and ETX producing type D strains of C. perfringens produce enterotoxemia in sheep, goats and cattle, but are not known to cause spontaneous disease in humans. The role of C. perfringens type E in animal or human disease remains poorly defined. The newly revised toxinotype F encodes CPA and enterotoxin (CPE), the latter being responsible for food poisoning in humans, and the less prevalent antibiotic associated and sporadic diarrhea. The role of these strains in animal disease has not been fully described and remains controversial. Another newly created toxinotype, G, encodes CPA and necrotic enteritis toxin B-like (NetB), and is responsible for avian necrotic enteritis, but has not been associated with human disease. C. difficile produces colitis and/or enterocolitis in humans and multiple animal species. The main virulence factors of this microorganism are toxins A, B and an ADP-ribosyltransferase (CDT). Other clostridia causing enteric diseases in humans and/or animals are Clostridium spiroforme, Clostridium piliforme, Clostridium colinum, Clostridium sordellii, Clostridium chauvoei, Clostridium septicum, Clostridium botulinum, Clostridium butyricum and Clostridium neonatale. The zoonotic transmission of some, but not all these clostridsial species, has been demonstrated.

Molecular Characterization of Clostridium perfringens Strains Isolated in Italy

“…In this case, CPE is a typing toxin because its association with the cpa toxin genes has been demonstrated to be responsible for enterotoxigenic infections in humans [ 7 , 8 ] and animals [ 9 ]. The new type G produces the CPA toxin and the NetB toxin and is responsible for necrotic enteritis in poultry [ 10 ].…”

“…CPB is a thermolabile, trypsine sensitive toxin and it is biological active only in the presence of trypsin inhibitors [ 10 ]. CPB is produced by type B and C of C. perfringens and is considered to be responsible for fatal hemorrhagic dysentery in sheep (type B) and the fatal intestinal necrosis (e.g., pig-bel disease) seen in type C infections in several animal species (e.g., piglets) and humans [ 13 ].…”

Evidence That VirS Is a Receptor for the Signaling Peptide of the Clostridium perfringens Agr-like Quorum Sensing System

“…The Gram-positive, anaerobic bacterium Clostridium perfringens is a major cause of histotoxic and intestinal infections in humans and other animals ( 1 – 3 ). C. perfringens infections such as gas gangrene, enteritis, and enterotoxemia are mediated in large part by the ability of this bacterium to produce more than 20 different toxins ( 4 , 5 ).…”

“…Of importance for the current study, type B isolates must carry genes encoding CPA, CPB, and ETX toxins, while type C isolates must carry only genes encoding CPA and CPB toxins. Each C. perfringens type is associated with particular diseases, e.g., type B and C strains cause necrotizing enteritis and enterotoxemia ( 1 – 3 , 5 ).…”

Clostridial diseases in farm animals: 1. Enterotoxaemias and other alimentary tract infections

“…The identification of antibodies against ε toxin of C perfringens type D in people has been suggested to indicate its involvement in the pathogenesis of multiple sclerosis; however, the evidence for this association is lacking (Uzal and others 2018).…”