Fatal Enteritis Necroticans (Pigbel) in a Diabetic Adult

Gui, Lizhen; Subramony, Charu; Fratkin, Jonathan; Hughson, Michael D.

doi:10.1038/modpathol.3880491

Cited by 76 publications

(32 citation statements)

References 22 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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“…Type C-associated human disease is most closely associated with Papua New Guinea, where it was once the second leading cause of death in children who were more than 1 year old, which led to a childhood vaccine program that helped to reduce this problem (22). In addition, type C human necrotic enteritis is now seen in developed countries, typically in patients with pancreatic disease (10,18,23,29,37).…”

Section: Vol 74 2006mentioning

confidence: 99%

Dissecting the Contributions of Clostridium perfringens Type C Toxins to Lethality in the Mouse Intravenous Injection Model

Fisher

Fernández‐Miyakawa

Sayeed³

et al. 2006

Infect Immun

127

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The gram-positive anaerobe Clostridium perfringens produces a large arsenal of toxins that are responsible for histotoxic and enteric infections, including enterotoxemias, in humans and domestic animals. C. perfringens type C isolates, which cause rapidly fatal diseases in domestic animals and enteritis necroticans in humans, contain the genes for alpha toxin (plc), perfringolysin O (pfoA), beta toxin (cpb), and sometimes beta2 toxin (cpb2) and/or enterotoxin (cpe). Due to the economic impact of type C-induced diseases, domestic animals are commonly vaccinated with crude type C toxoid (prepared from inactivated culture supernatants) or bacterin/ toxoid vaccines, and it is not clear which toxin(s) present in these vaccines actually elicits the protective immune response. To improve type C vaccines, it would be helpful to assess the contribution of each toxin present in type C supernatants to lethality. To address this issue, we surveyed a large collection of type C isolates to determine their toxin-producing abilities. When late-log-phase vegetative culture supernatants were analyzed by quantitative Western blotting or activity assays, most type C isolates produced at least three lethal toxins, alpha toxin, beta toxin, and perfringolysin O, and several isolates also produced beta2 toxin. In the mouse intravenous injection model, beta toxin was identified as the main lethal factor present in type C late-log-phase culture supernatants. This conclusion was based on monoclonal antibody neutralization studies and regression analyses in which the levels of alpha toxin, beta toxin, perfringolysin O, and beta2 toxin production were compared with lethality. Collectively, our results highlight the importance of beta toxin for type C-induced toxemia.

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“…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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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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Fatal Enteritis Necroticans (Pigbel) in a Diabetic Adult

Cited by 76 publications

References 22 publications

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

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

Dissecting the Contributions of Clostridium perfringens Type C Toxins to Lethality in the Mouse Intravenous Injection Model

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

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