Enterotoxin synthesis by nonsporulating cultures of Clostridium perfringens

Goldner, S B; Solberg, Myron; Jones, Susan; Post, Laurie S.

doi:10.1128/aem.52.3.407-412.1986

Cited by 32 publications

(9 citation statements)

References 46 publications

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“…An alternative explanation for our results is that enterotoxin was not produced at all in infected patients who did not become ill. This explanation implies that enterotoxin production might not be necessary for sporulation to occur: a possibility suggested recently by Goldner et al (8). Our data cannot distinguish between these two explanations.…”

Section: Discussioncontrasting

confidence: 48%

Characterization of an outbreak of Clostridium perfringens food poisoning by quantitative fecal culture and fecal enterotoxin measurement

et al. 1988

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Published criteria for implicating Clostridium perfringens as the cause of food-poisoning outbreaks include finding a median fecal C. pefringens spore count of > 106/g among specimens from ill persons. We investigated a food-poisoning outbreak with the epidemiologic characteristics of C. perfringens-related disease in a nursing home in which the median fecal spore count for ill patients (2.5 x 107/g) was similar to that for well patients (4.0 x 106/g), making the etiology of the outbreak uncertain. All il and well patients tested had eaten turkey, the implicated food item. C. perfiringens enterotoxin was detected by reverse passive latex agglutination in fecal specimens from six of six ill and none of four well patients who had eaten turkey (P = 0.005), suggesting that this organism had caused the outbreak. This investigation suggests that detection of fecal C. perfringens enterotoxin is a specific way to identify this organism as the causative agent in food-poisoning outbreaks. Clostridium perfringens is a common cause of food-poisoning outbreaks in the United States (2). The illness is characterized by diarrhea and abdominal cramps without fever (1, 2, 21). Symptoms typically begin 7 to 15 h after consumption of food contaminated with high concentrations of the organism and last c24 h (21). Epidemiologic criteria have been established to confirm whether C. perfringens is the etiologic agent in outbreaks, since it is common for C. perfringens spores to be present in small numbers in human fecal specimens and raw food samples (11). These criteria include a median fecal C. perfringens spore count of >106/g in ill persons (1, 11, 21); >105 organisms per g in epidemiologically implicated food items (1, 2, 11, 21); and identification of C. perfringens of the same serotype in most ill persons, but not in well persons (2). Recently, however, there have been several reports that C. perfringens spore counts of >106/g may be found in fecal samples taken from institutionalized well patients at times when no outbreak had occurred (24, 26).

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Section: Discussioncontrasting

confidence: 48%

Characterization of an outbreak of Clostridium perfringens food poisoning by quantitative fecal culture and fecal enterotoxin measurement

et al. 1988

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“…To induce sporulation, each C. perfringens strain was grown in Duncan-Strong broth (29) for 8 h at 37°C without shaking. To determine if heat-resistant endospores were present in C. perfringens cultures, a 1-ml aliquot of vegetative or sporu-lating C. perfringens NCTC 8239 culture was heat shocked at 85°C for 20 min as described previously (7,10). Dilutions of the heat-shocked culture were plated on brain heart infusion agar and incubated for 16 h at 37°C in GasPak jars.…”

Section: Methodsmentioning

confidence: 99%

Cloning, nucleotide sequencing, and expression of the Clostridium perfringens enterotoxin gene in Escherichia coli

1993

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A complete copy of the gene (cpe) encoding Clostidium perfingens enterotoxin (CPE), an important virulence factor involved in C. perfringens food poisoning and other gastrointestinal illnesses, has been cloned, sequenced, and expressed in Escherichia coli. The cpe gene was shown to encode a 319-amino-acid polypeptide with a deduced molecular weight of 35,317. There was no consensus sequence for a typical signal peptide present in the 5' region of cpe. Cell lysates from recombinant cpe-positive E. coli were shown by quantitative immunoblot analysis to contain moderate amounts of CPE, and this recombinant CPE was equal to native CPE in cytotoxicity for mammalian Vero cells. CPE expression in recombinant E. coli appeared to be largely driven from a clostridial promoter. Immunoblot analysis also demonstrated very low levels of CPE in vegetative cell lysates of enterotoxin-positive C. perfringens. However, when the same C. perfringens strain was induced to sporulate, much stronger CPE expression was detected in these sporulating cells than in either vegetative C. perfringens cells or recombinant E. coli. Collectively, these results strongly suggest that sporulation is not essential for cpe expression, but sporulation does facilitate high-level cpe expression. Clostridium perfringens ranks among the most important of the anaerobic bacterial pathogens for humans and domestic animals, causing myonecrosis (gas gangrene), anaerobic cellulitis, septicemia, uterine infections, and gastrointestinal illnesses (28). The virulence of this endospore-forming, gram-positive bacterium results from its prolific ability to produce protein toxins (28). Among the 13 types of toxins known to be produced by this organism is C. perfringens enterotoxin (CPE), which is a single polypeptide of 35 kDa with a unique amino acid sequence (9, 23, 24, 28). CPE causes the symptoms associated with C. perfringens type A food poisoning, which is among the most common human food-borne illnesses (23, 24, 28), and it also appears to be involved in other important human and veterinary gastrointestinal illnesses (2, 5, 24). Recent studies (11, 15, 26, 27, 43) have shown CPE action to involve sequentially (i) specific binding of enterotoxin to a proteinaceous receptor on mammalian membranes, (ii) insertion of CPE into plasma membranes, (iii) formation of a complex between enterotoxin and two mammalian membrane proteins of 70 and 50 kDa, (iv) production of membrane permeability alterations for small molecules such as ions, and (v) induction of secondary effects which culminate in cell death. CPE binding to mammalian receptors is mediated by a 30-amino-acid region at the extreme C terminus of enterotoxin (12, 14). Cytotoxicity also requires sequences in the N-terminal half of the enterotoxin, suggesting the existence of separate binding and cytotoxicity domains on CPE (13). Upon entering the human host, it is common for many bacterial pathogens to undergo global changes in gene expression (30). These changes often include de novo synthesis of virulence factors...

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“…There are reports of CPE synthesis by nonsporulating cultures of C. perfringens (8,9); however, the CPE responsible for illness is generally thought to be synthesized during sporulation (5,11) and has been described as a sporulationspecific gene product (5) and a structural component of the spore coat (7,8).…”

mentioning

confidence: 99%

Synthetic DNA probes for detection of enterotoxigenic Clostridium perfringens strains isolated from outbreaks of food poisoning

et al. 1990

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Four synthetic oligonucleotides encoding different parts of the Clostridium perfringens enterotoxin gene were used to test the enterotoxigenicity of C. perfringens strains isolated from confirmed outbreaks of food poisoning. Of the 245 strains isolated from food and feces originating from 186 separate outbreaks, 145 (59%) gave hybridization reactions with each of the four DNA probes used, while 104 strains did not hybridize with any of the probes. There was no correlation between serotype and the presence of the enterotoxin gene, although the C. perfiringens enterotoxin gene was rarely detected among nontypable strains (17%). Results show that DNA hybridization is a suitable method for the identification of C. perfringens strains which have the potential to produce enterotoxin.

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Enterotoxin synthesis by nonsporulating cultures of Clostridium perfringens

Cited by 32 publications

References 46 publications

Characterization of an outbreak of Clostridium perfringens food poisoning by quantitative fecal culture and fecal enterotoxin measurement

Characterization of an outbreak of Clostridium perfringens food poisoning by quantitative fecal culture and fecal enterotoxin measurement

Cloning, nucleotide sequencing, and expression of the Clostridium perfringens enterotoxin gene in Escherichia coli

Synthetic DNA probes for detection of enterotoxigenic Clostridium perfringens strains isolated from outbreaks of food poisoning

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