The Pathogenesis of Enteritis Necroticans

Lawrence, Gregory J.

doi:10.1016/b978-012595020-6/50014-0

Cited by 27 publications

(54 citation statements)

References 15 publications

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“…In the 1960s to 1970s, type C-induced enteritis necroticans (known locally as pigbel) was very common in Papua New Guinea (PNG), causing Ͼ50% of the deaths occurring in children between 5 and 10 years of age (189,190). The disease is clinically characterized by abdominal pain that develops 1 to 5 days after eating a high-protein meal.…”

Section: Diseases Involving Primarily Plasmid-encoded Toxinsmentioning

confidence: 99%

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Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

231

282

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SUMMARY In both humans and animals, Clostridium perfringens is an important cause of histotoxic infections and diseases originating in the intestines, such as enteritis and enterotoxemia. The virulence of this Gram-positive, anaerobic bacterium is heavily dependent upon its prolific toxin-producing ability. Many of the ∼16 toxins produced by C. perfringens are encoded by large plasmids that range in size from ∼45 kb to ∼140 kb. These plasmid-encoded toxins are often closely associated with mobile elements. A C. perfringens strain can carry up to three different toxin plasmids, with a single plasmid carrying up to three distinct toxin genes. Molecular Koch's postulate analyses have established the importance of several plasmid-encoded toxins when C. perfringens disease strains cause enteritis or enterotoxemias. Many toxin plasmids are closely related, suggesting a common evolutionary origin. In particular, most toxin plasmids and some antibiotic resistance plasmids of C. perfringens share an ∼35-kb region containing a Tn 916 -related conjugation locus named tcp (transfer of clostridial plasmids). This tcp locus can mediate highly efficient conjugative transfer of these toxin or resistance plasmids. For example, conjugative transfer of a toxin plasmid from an infecting strain to C. perfringens normal intestinal flora strains may help to amplify and prolong an infection. Therefore, the presence of toxin genes on conjugative plasmids, particularly in association with insertion sequences that may mobilize these toxin genes, likely provides C. perfringens with considerable virulence plasticity and adaptability when it causes diseases originating in the gastrointestinal tract.

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Section: Diseases Involving Primarily Plasmid-encoded Toxinsmentioning

confidence: 99%

“…C. perfringens type C isolates cause food-borne enteritis necroticans, which currently occurs sporadically throughout much of Southeast Asia and less commonly elsewhere (92,189,190).…”

Section: Diseases Involving Primarily Plasmid-encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

231

282

View full text Add to dashboard Cite

show abstract

“…EN has a 40% lethality rate and was first described in post-World War II Germany, where it was known as Darmbrand (Db) (16,17). However, EN is historically most associated with Papua New Guinea, where it is locally known as Pig-Bel.…”

mentioning

confidence: 99%

“…Type C strains, which by definition must produce beta toxin but sometimes also produce CPE, cause enteritis necroticans (EN) (13)(14)(15)(16)(17). EN has a 40% lethality rate and was first described in post-World War II Germany, where it was known as Darmbrand (Db) (16,17).…”

mentioning

confidence: 99%

Contributions of NanI Sialidase to Caco-2 Cell Adherence by Clostridium perfringens Type A and C Strains Causing Human Intestinal Disease

McClane

2014

Infect Immun

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Previous studies showed that Clostridium perfringens type D animal disease strain CN3718 uses NanI sialidase for adhering to enterocyte-like Caco-2 cells. The current study analyzed whether NanI is similarly important when type A and C human intestinal disease strains attach to Caco-2 cells. A PCR survey determined that the nanI gene was absent from typical type A food poisoning (FP) strains carrying a chromosomal enterotoxin (CPE) gene or the genetically related type C Darmbrand (Db) strains. However, the nanI gene was present in type A strains from healthy humans, type A strains causing CPE-associated antibioticassociated diarrhea (AAD) or sporadic diarrhea (SD), and type C Pig-Bel strains. Consistent with NanI sialidase being the major C. perfringens sialidase when produced, FP and Db strains had little supernatant sialidase activity compared to other type A or C human intestinal strains. All type A and C human intestinal strains bound to Caco-2 cells, but NanI-producing strains had higher attachment levels. When produced, NanI can contribute to host cell attachment of human intestinal disease strains, since a nanI null mutant constructed in type A SD strain F4969 had lower Caco-2 cell adhesion than wild-type F4969 or a complemented strain. Further supporting a role for NanI in host cell attachment, sialidase inhibitors reduced F4969 adhesion to Caco-2 cells. Collectively, these results suggest that NanI may contribute to the intestinal attachment and colonization needed for the chronic diarrhea of CPE-associated AAD and SD, but this sialidase appears to be dispensable for the acute pathogenesis of type A FP or type C enteritis necroticans.

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“…6 Type C disease also occurs occasionally in adult animals and human beings ingesting significant amounts of food with trypsin inhibitors, such as sweet potato and soy bean, and also in patients with pancreatic disease. 4,5,8 Infection by C. perfringens type C occurs worldwide and affects several animal species. 18 The pathology of the disease has been described with some detail in foals and piglets.…”

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confidence: 99%

The pathology of enterotoxemia by Clostridium perfringens type C in calves

et al. 2013

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The pathology of Clostridium perfringens type C infection has been described with detail only in foals and piglets. The current report describes the diagnostic workup and detailed pathology of 3 cases of C. perfringens type C infection in calves. A 2-day-old Jersey calf and fresh and fixed tissues from a 4-week-old Angus calf and from a 1-week-old Jersey calf were received at the California Animal Health and Food Safety Laboratory System with a history of digestive disease and death. The gross changes in the gastrointestinal tract of 1 calf consisted of multifocal subserosal hemorrhages of the rumen, diffuse congestion and multifocal hemorrhages of the small intestinal mucosa, and dilated cecum with bloody liquid contents. In a second calf, a large segment of small intestine was hemorrhagic. The small intestine of the third calf was dilated and filled with abundant yellow fluid content. Microscopically, all 3 calves had diffuse coagulation necrosis of the intestinal mucosa. Clostridium perfringens type A was isolated from the intestinal content of 2 calves. In addition, enzyme-linked immunosorbent assay for Bovine rotavirus was positive on colonic content of 1 calf. Small numbers of cryptosporidia were seen in smears of colonic content of 2 calves, and Salmonella sp. group E was detected in the small intestinal content of another calf. Clostridium perfringens beta toxin was detected in the intestinal content of the 3 animals. A diagnosis of C. perfringens type C infection was confirmed based on pathological findings and detection of beta toxin in the intestinal content of the 3 animals.

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The Pathogenesis of Enteritis Necroticans

Cited by 27 publications

References 15 publications

Toxin Plasmids of Clostridium perfringens

Toxin Plasmids of Clostridium perfringens

Contributions of NanI Sialidase to Caco-2 Cell Adherence by Clostridium perfringens Type A and C Strains Causing Human Intestinal Disease

The pathology of enterotoxemia by Clostridium perfringens type C in calves

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