Enteritis Necroticans With Midgut Necrosis Caused by Clostridium perfringens

Clarke, Leon E.; Diekmann-Guiroy, Bernadette; McNamee, William; Java, Domingo J.; Weiss, Stephen M.

doi:10.1001/archsurg.1994.01420290103015

Cited by 49 publications

(14 citation statements)

References 10 publications

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“…perfringens type C food poisoning (necrotic enteritis) in humans has only been reported on very rare occasions in the industrialized world during the recent decades. These rare cases are almost exclusively in diabetic people (Severin et al, 1984;Watson et al, 1991;Clarke et al, 1994;Petrillo et al, 2000;Gui et al, 2002). The symptoms start with abdominal pain and bloody diarrhoea, and are followed rapidly by necrosis of the small intestine, caused mainly by the beta toxin, with contributions of additional toxins from C. perfringens type C (Jolivet-Reynaud et al, 1986).…”

Section: Nature and Form Of The Feedmentioning

confidence: 99%

Clostridium perfringensin poultry: an emerging threat for animal and public health

et al. 2004

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The incidence of Clostridium perfringens-associated necrotic enteritis in poultry has increased in countries that stopped using antibiotic growth promoters. Necrotic enteritis and the subclinical form of C. perfringens infection in poultry are caused by C. perfringens type A, producing the alpha toxin, and to a lesser extent type C, producing both alpha toxin and beta toxin. Some strains of C. perfringens type A produce an enterotoxin at the moment of sporulation and are responsible for foodborne disease in humans. The mechanisms of colonization of the avian small intestinal tract and the factors involved in toxin production are largely unknown. It is generally accepted, however, that predisposing factors are required for these bacteria to colonize and cause disease in poultry. The best known predisposing factor is mucosal damage, caused by coccidiosis. Diets with high levels of indigestible, water-soluble non-starch polysaccharides, known to increase the viscosity of the intestinal contents, also predispose to necrotic enteritis. Standardized models are being developed for the reproduction of colonization of poultry by C. perfringens and the C. perfringens-associated necrotic enteritis. One such model is a combined infection with Eimeria species and C. perfringens. Few tools and strategies are available for prevention and control of C. perfringens in poultry. Vaccination against the pathogen and the use of probiotic and prebiotic products has been suggested, but are not available for practical use in the field at the present time. The most cost-effective control will probably be achieved by balancing the composition of the feed.

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Section: Nature and Form Of The Feedmentioning

confidence: 99%

Clostridium perfringensin poultry: an emerging threat for animal and public health

et al. 2004

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“…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). 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).…”

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confidence: 99%

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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“…Since 1984, two cases of C. perfringens, Type C enteritis necroticans have been reported in the United States, two in England, and one in Australia (Table 1: [11][12][13][14][15]. Three of these five patients had Type 1 or Type 2 diabetes mellitus (11)(12)(13)15).…”

Section: Discussionmentioning

confidence: 99%

“…Three of these five patients had Type 1 or Type 2 diabetes mellitus (11)(12)(13)15). One of the nondiabetics was a vegetarian who consumed large amounts of sweet potatoes, soybeans, and peanut sauce, all of which contain trypsin inhibitors that were thought to have predisposed the patient to the disease (14).…”

Section: Discussionmentioning

confidence: 99%

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Fatal Enteritis Necroticans (Pigbel) in a Diabetic Adult

et al. 2002

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Enteritis necroticans is a segmental necrotizing infection of the jejunum and ileum caused by Clostridium perfringens, Type C. The disease occurs sporadically in parts of Asia, Africa, and the South Pacific, where it primarily affects children with severe protein malnutrition. The disease is extremely rare in developed countries, where it has been seen primarily in diabetics. Two cases have previously been reported in the United States, one in a child with poorly controlled Type 1 diabetes. A 66-yearold woman with a 12-year history of Type 2 diabetes mellitus developed severe abdominal pain and bloody diarrhea after eating a meal of turkey sausage. She died unattended at home. An autopsy showed peritonitis and segmental necrosis of the jejunum and ileum. Microscopic examination showed Gram-positive club-shaped bacilli consistent with Clostridia coating a necrotic mucosa. Products of cpa and cpb genes of C. perfringens, Type C were identified in the necrotic jejunum by polymerase chain reaction amplification.

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Enteritis Necroticans With Midgut Necrosis Caused by Clostridium perfringens

Cited by 49 publications

References 10 publications

Clostridium perfringensin poultry: an emerging threat for animal and public health

Clostridium perfringensin poultry: an emerging threat for animal and public health

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

Fatal Enteritis Necroticans (Pigbel) in a Diabetic Adult

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