Enteritis necroticans ‘pigbel’ in a Japanese diabetic adult

Matsuda, Tomomichi; Okada, Yuji; Inagi, Eiji; Tanabe, Yasushi; Shimizu, Yozo; Nagashima, Kazuo; Sakùrai, Jun; Nagahama, Masahiro; Tanaka, Shinya

doi:10.1111/j.1440-1827.2007.02149.x

Cited by 40 publications

(36 citation statements)

References 12 publications

(24 reference statements)

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“…Although less common, this disease also occurs in diabetic patients from developed countries. Persons suffering from enteritis necroticans often survive less than 48 h after the first appearance of symptoms (9,16,21,26). Histologically, the disease is characterized by necrotic enteritis and the presence of numerous bacteria in the intestinal lumen (29).…”

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confidence: 99%

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Effects of Clostridium perfringens Beta-Toxin on the Rabbit Small Intestine and Colon

et al. 2008

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Clostridium perfringens type B and type C isolates, which produce beta-toxin (CPB), cause fatal diseases originating in the intestines of humans or livestock. Our previous studies demonstrated that CPB is necessary for type C isolate CN3685 to cause bloody necrotic enteritis in a rabbit ileal loop model and also showed that purified CPB, in the presence of trypsin inhibitor (TI), can reproduce type C pathology in rabbit ileal loops. We report here a more complete characterization of the effects of purified CPB in the rabbit small and large intestines. One microgram of purified CPB, in the presence of TI, was found to be sufficient to cause significant accumulation of hemorrhagic luminal fluid in duodenal, jejunal, or ileal loops treated for 6 h with purified CPB, while no damage was observed in corresponding loops receiving CPB (no TI) or TI alone. In contrast to the CPB sensitivity of the small intestine, the colon was not affected by 6 h of treatment with even 90 g of purified CPB whether or not TI was present. Time course studies showed that purified CPB begins to induce small intestinal damage within 1 h, at which time the duodenum is less damaged than the jejunum or ileum. These observations help to explain why type B and C infections primarily involve the small intestine, establish CPB as a very potent and fast-acting toxin in the small intestines, and confirm a key role for intestinal trypsin as an innate intestinal defense mechanism against CPB-producing C. perfringens isolates.

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“…Histologically, the disease is characterized by necrotic enteritis and the presence of numerous bacteria in the intestinal lumen (29). Immunohistochemistry studies using anti-CPB antibodies showed the presence of CPB on the necrotic intestinal epithelium of humans suffering from type C infection (9).…”

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confidence: 99%

Effects of Clostridium perfringens Beta-Toxin on the Rabbit Small Intestine and Colon

et al. 2008

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“…Today, this disease still occurs sporadically in malnourished people in many developing countries (17). EN cases also occur occasionally in developed countries, particularly in people with pancreatic disease (18,19).…”

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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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“…EN is characterized by its sudden onset with abdominal cramps, shock, bloody diarrhea, acute inflammation, and pronounced necrosis of intestinal mucosa (27,31). Necrosis of the intestinal epithelium always coincides with the presence of Gram-positive rods characteristic of C. perfringens attached to the surface of the necrotic mucosa that, when visualized by microscopy, appear to form biofilm-like structures (28,29). CPB, the most important toxin for developing EN (32)(33)(34), has been detected on the apical side of intestinal cells underneath those attached bacteria, indicating that in situ production of CPB is important for pathogenesis (29).…”

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confidence: 99%

“…perfringens type C is the etiologic agent of human enteritis necroticans (also called pigbel, darmbrand, or "gangrene of the bowel"), which originates in the intestine (2). Enteritis necroticans (EN) is particularly aggressive in diabetics and immunocompromised patients from developed countries (they survive less than 48 h after the first appearance of symptoms) (25)(26)(27)(28)(29)(30). EN is characterized by its sudden onset with abdominal cramps, shock, bloody diarrhea, acute inflammation, and pronounced necrosis of intestinal mucosa (27,31).…”

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The CpAL Quorum Sensing System Regulates Production of Hemolysins CPA and PFO To Build Clostridium perfringens Biofilms

2015

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Mexico bClostridium perfringens strains produce severe diseases, including myonecrosis and enteritis necroticans, in humans and animals. Diseases are mediated by the production of potent toxins that often damage the site of infection, e.g., skin epithelium during myonecrosis. In planktonic cultures, the regulation of important toxins, such as CPA, CPB, and PFO, is controlled by the C. perfringens Agr-like (CpAL) quorum sensing (QS) system. Strains also encode a functional LuxS/AI-2 system. Although C. perfringens strains form biofilm-like structures, the regulation of biofilm formation is poorly understood. Therefore, our studies investigated the role of CpAL and LuxS/AI-2 QS systems and of QS-regulated factors in controlling the formation of biofilms. We first demonstrate that biofilm production by reference strains differs depending on the culture medium. Increased biomass correlated with the presence of extracellular DNA in the supernatant, which was released by lysis of a fraction of the biofilm population and planktonic cells. Whereas ⌬agrB mutant strains were not able to produce biofilms, a ⌬luxS mutant produced wild-type levels. The transcript levels of CpAL-regulated cpa and pfoA genes, but not cpb, were upregulated in biofilms compared to planktonic cultures. Accordingly, ⌬cpa and ⌬pfoA mutants, in type A (S13) or type C (CN3685) backgrounds, were unable to produce biofilms, whereas CN3685⌬cpb made wild-type levels. Biofilm formation was restored in complemented ⌬cpa/cpa and ⌬pfoA/ pfoA strains. Confocal microscopy studies further detected CPA partially colocalizing with eDNA on the biofilm structure. Thus, CpAL regulates biofilm formation in C. perfringens by increasing levels of certain toxins required to build biofilms.

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Enteritis necroticans ‘pigbel’ in a Japanese diabetic adult

Cited by 40 publications

References 12 publications

Effects of Clostridium perfringens Beta-Toxin on the Rabbit Small Intestine and Colon

Effects of Clostridium perfringens Beta-Toxin on the Rabbit Small Intestine and Colon

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

The CpAL Quorum Sensing System Regulates Production of Hemolysins CPA and PFO To Build Clostridium perfringens Biofilms

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