14 J. Glenn Songer Until the recent advent of PCR genotyping, Clostridium perfringens type E was relatively uncommonly reported as a cause of disease, with the first reports of enteric infection of domestic animals occurring in the late 1940s. However, in the past few years, an increasing number of cases of type E-associated disease have been reported in several domestic and wild animal species. Most of these reports were based, however, on isolation of C. perfringens type E from feces or intestinal content of animals with enteric disease, and the role of this microorganism in disease production remains mostly undetermined. Koch postulates have not been fulfilled for C. perfringens type E. Type E is probably the least commonly reported genotype of C. perfringens, but in specific conditions, it may be quite common. C. perfringens type E isolates are defined by their production of alpha (CPA) and iota (ITX) toxins. The role of ITX in disease of animals is poorly understood, although it is usually assumed that the pathogenesis of intestinal diseases produced by C. perfringens type E is mediated by ITX toxin. This toxin has been described in detail in Chapter 5. Briefly, ITX toxin is a guinea pig-dermonecrotic, mouse-lethal toxin which cross-reacts with the ITX-like toxin of Clostridium spiroforme. Antibodies against C. spiroforme or C. perfringens type E neutralize toxins from both species. C. perfringens genotype E isolates associated with hemorrhagic enteritis of neonatal calves produce CPA and ITX and, very frequently, carry sequences for the cpe gene, encoding C. perfringens enterotoxin (CPE), although they are usually unable to produce this toxin. These silent cpe sequences are highly conserved among type E isolates. In most cases, these silent sequences contain multiple nonsense and frameshift mutations and lack the initiation codon, promoters, and ribosome-binding site. Little is known about the pathogenesis of type E infections. In vitro and in vivo models suggest that genotype E is well adapted to take advantage of changes caused by ITX on epithelial cell surfaces. In addition, type E produces metabolites that affect the growth of potential competitors. Enterocyte morphologic changes induced by ITX, associated with the specific increase of type E cell adhesion and the strong intra-specific growth inhibition of other strains, could be competitive traits that improve the fitness of type E isolates in the bovine gut. Further research is required to develop a clearer understanding of the interaction of ITX toxin with host tissues, as well as methods for prevention of these negative consequences. The role of C. perfringens type E in animal disease is poorly understood, although this toxinotype has been associated with enteric disease in several animal species. Very little information is, therefore, currently available about clinical diseases produced by C. perfringens type E. Historically, enterotoxemia of rabbits has been associated with C. perfringens type E. However, it is currently thought that most, if not all, of those cases are caused by C. spiroforme
Infections by Clostridium perfringens type E
Introduction
Etiology
Pathogenesis
Animal disease
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