Enteritis Necroticans due to Clostridium Welchii Type F

Zeissler, Johannes; Rassfeld-Sternberg, Luise; Oakley, C. L.; Dieckmann, C.; Hain, E

doi:10.1136/bmj.1.4597.267

Cited by 159 publications

(37 citation statements)

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“…After World War II, type C strains caused enteritis necroticans outbreaks (termed Darmbrand) in malnourished people in Northern Germany (191). A recent study showed that these Darmbrand strains carry and express both plasmid-borne cpb and cpe genes (40), although multilocus sequence typing (MLST) analyses conducted during that work also indicated that Darmbrand strains are otherwise genetically related to type A food poisoning strains carrying a chromosomal cpe gene.…”

Section: Diseases Involving Primarily Plasmid-encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

226

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%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

226

282

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“…EN is also occasionally observed in developed countries, mainly in people with pancreatic disease (9). Historically, EN (known locally as Darmbrand) affected many malnourished people in northern Germany after World War II (10,11). Prior to vaccination campaigns conducted during the 1970s and 1980s, EN (known locally as pigbel) was also the most common cause of death in children greater than 1 year old in the Papua New Guinea (PNG) highlands (6,7).…”

mentioning

confidence: 99%

Synergistic Effects of Clostridium perfringens Enterotoxin and Beta Toxin in Rabbit Small Intestinal Loops

Gurjar

Theoret

et al. 2014

Infect Immun

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The ability of Clostridium perfringens type C to cause human enteritis necroticans (EN) is attributed to beta toxin (CPB). However, many EN strains also express C. perfringens enterotoxin (CPE), suggesting that CPE could be another contributor to EN. Supporting this possibility, lysate supernatants from modified Duncan-Strong sporulation (MDS) medium cultures of three CPE-positive type C EN strains caused enteropathogenic effects in rabbit small intestinal loops, which is significant since CPE is produced only during sporulation and since C. perfringens can sporulate in the intestines. Consequently, CPE and CPB contributions to the enteropathogenic effects of MDS lysate supernatants of CPE-positive type C EN strain CN3758 were evaluated using isogenic cpb and cpe null mutants. While supernatants of wild-type CN3758 MDS lysates induced significant hemorrhagic lesions and luminal fluid accumulation, MDS lysate supernatants of the cpb and cpe mutants caused neither significant damage nor fluid accumulation. This attenuation was attributable to inactivating these toxin genes since complementing the cpe mutant or reversing the cpb mutation restored the enteropathogenic effects of MDS lysate supernatants. Confirming that both CPB and CPE are needed for the enteropathogenic effects of CN3758 MDS lysate supernatants, purified CPB and CPE at the same concentrations found in CN3758 MDS lysates also acted together synergistically in rabbit small intestinal loops; however, only higher doses of either purified toxin independently caused enteropathogenic effects. These findings provide the first evidence for potential synergistic toxin interactions during C. perfringens intestinal infections and support a possible role for CPE, as well as CPB, in some EN cases.

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“…Necrotic enteritis in man was first recognized in Germany in 1949 (26). At that time, the outbreaks were considered to arise from a new heat-resistant type of C. perfringens, type F. But now it is well known that the C. perfringens type F is a variety of heat-resistant strains of type C (19,20).…”

mentioning

confidence: 99%

“…Skjelkvale and Duncan (15,16) reported that C. perfringens type C strains isolated from enteritis necroticans in New Guinea produced high levels of enterotoxin which was shown to be serologically and biologically identical to the enterotoxin of C. perfringens type A. The beta toxin of C. perfringens type C is presumed to be primarily responsible for severe symptoms such as sudden onset, marked loss of intestinal mucosa, and inflammation of the intestinal wall with the loss of considerable quantities of blood to the lumen of the intestine in necrotic enteritis (26). In order to investigate the enteropathogenic activity of C. perfringens type C, the response of ligated rabbit ileal loops to the living cells, beta-and delta-toxigenic culture filtrates, was examined.…”

mentioning

confidence: 99%

Response of Ligated Rabbit Ileal Loop to Clostridium perfringens Type C Strains and Their Toxic Filtrates

Yamagishi

Gyobu

Sakamoto

et al. 1987

Microbiology and Immunology

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The vegetative cells and toxic filtrates of Clostridium perfringens type C strains were injected into ligated rabbit ileal loops and the responses were observed. Out of 12 strains examined, 2 strains showed positive reaction in this test, when the vegetative cells were injected. One of these 2 strains was an enterotoxigenic and beta-toxigenic and the other was beta-and delta-toxigenic but not enterotoxigenic. Culture filtrates containing beta or delta toxin also showed fluid accumulation in the rabbit ileal loop. Histological findings of loops injected with culture filtrates containing beta toxin showed separated and effaced villi, hemorrhage in the mucosa, engorged vessels, inflammatory cell infiltration, and hyperplasia of the lymphoid tissue.

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Enteritis Necroticans due to Clostridium Welchii Type F

Cited by 159 publications

References 0 publications

Toxin Plasmids of Clostridium perfringens

Toxin Plasmids of Clostridium perfringens

Synergistic Effects of Clostridium perfringens Enterotoxin and Beta Toxin in Rabbit Small Intestinal Loops

Response of Ligated Rabbit Ileal Loop to Clostridium perfringens Type C Strains and Their Toxic Filtrates

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