scholarly journals The Clostridium perfringens enterotoxin gene is on a transposable element in type A human food poisoning strains

Microbiology ◽  
1997 ◽  
Vol 143 (7) ◽  
pp. 2109-2115 ◽  
Author(s):  
S. Brynestad ◽  
B. Synstad ◽  
P. E. Granum
2002 ◽  
Vol 70 (8) ◽  
pp. 4261-4272 ◽  
Author(s):  
Kazuaki Miyamoto ◽  
Ganes Chakrabarti ◽  
Yosiharu Morino ◽  
Bruce A. McClane

ABSTRACT Clostridium perfringens type A isolates causing food poisoning have a chromosomal enterotoxin gene (cpe), while C. perfringens type A isolates responsible for non-food-borne human gastrointestinal diseases carry a plasmid cpe gene. In the present study, the plasmid cpe locus of the type A non-food-borne-disease isolate F4969 was sequenced to design primers and probes for comparative PCR and Southern blot studies of the cpe locus in other type A isolates. Those analyses determined that the region upstream of the plasmid cpe gene is highly conserved among type A isolates carrying a cpe plasmid. The organization of the type A plasmid cpe locus was also found to be unique, as it contains IS1469 sequences located similarly to those in the chromosomal cpe locus but lacks the IS1470 sequences found upstream of IS1469 in the chromosomal cpe locus. Instead of those upstream IS1470 sequences, a partial open reading frame potentially encoding cytosine methylase (dcm) was identified upstream of IS1469 in the plasmid cpe locus of all type A isolates tested. Similar dcm sequences were also detected in several cpe-negative C. perfringens isolates carrying plasmids but not in type A isolates carrying a chromosomal cpe gene. Contrary to previous reports, sequences homologous to IS1470, rather than IS1151, were found downstream of the plasmid cpe gene in most type A isolates tested. Those IS1470-like sequences reside in about the same position but are oppositely oriented and defective relative to the IS1470 sequences found downstream of the chromosomal cpe gene. Collectively, these and previous results suggest that the cpe plasmid of many type A isolates originated from integration of a cpe-containing genetic element near the dcm sequences of a C. perfringens plasmid. The similarity of the plasmid cpe locus in many type A isolates is consistent with horizontal transfer of a common cpe plasmid among C. perfringens type A strains.


1998 ◽  
Vol 61 (2) ◽  
pp. 240-243 ◽  
Author(s):  
J. RIDELL ◽  
J. BJÖRKROTH ◽  
H. EISGRŰBER ◽  
B. SCHALCH ◽  
A. STOLLE ◽  
...  

The prevalence of the enterotoxin gene in a well-characterized collection of 71 Clostridium perfringens strains from 36 separate food-poisoning cases or outbreaks was analyzed with the polymerase chain reaction (PCR). The clonality of 39 strains originating from 14 outbreaks where at least two isolates were available was studied with pulsed-field gel electrophoresis (PFGE) using SmaI and ApaI restriction endonucleases. The cpe gene PCR assay was found to correlate well with Clostridium perfringens enterotoxin (CPE) production in vitro with reverse passive latex agglutination. Of the C. perfringens food and clinical food-poisoning isolates 24 (86%) and 38 (88%) were cpe-positive, respectively. Different PFGE patterns indicated that multiple cpe-positive clones are frequently present within one outbreak. The existence of cpe-positive and negative isolates with identical or nearly identical PFGE patterns in a single outbreak suggests that the cpe gene may be in a movable genetic element.


Planta Medica ◽  
2020 ◽  
Vol 86 (03) ◽  
pp. 198-204 ◽  
Author(s):  
Takeshi Kawahara ◽  
Kotomi Fujii ◽  
Kouki Nakajima ◽  
Rikuri Fujii ◽  
Shuichiro Inagaki ◽  
...  

AbstractThe physiological functions of the leaves of Japanese big-leaf magnolia (Magnolia obovata) against enterotoxins produced by foodborne pathogens remain unclear. In this study, we evaluated the protective effects of M. obovata leaf extract (MLE) against the cytotoxicity of Clostridium perfringens enterotoxin (CPE), which causes the symptoms of C. perfringens type A food poisoning. The protective effects of MLE against CPE-induced cytotoxicity were evaluated in human intestinal epithelial Caco-2 cells. Pre-treatment with MLE significantly suppressed the cytotoxicity induced by CPE in undifferentiated and differentiated human intestinal Caco-2 cells at a pH range of 4.0 – 7.0. This CPE-suppressive effect was due to a hydrophilic sugar-containing compound without phenolic and protein structures but not the hydrophobic biologically active neolignans, honokiol and magnolol. MLE had a protective effect against cytotoxicity caused by type A C. perfringens. Our results provide novel insight regarding the usage of M. obovata in managing food poisoning.


2006 ◽  
Vol 72 (7) ◽  
pp. 4561-4568 ◽  
Author(s):  
Jihong Li ◽  
Bruce A. McClane

ABSTRACT Clostridium perfringens type A isolates can carry the enterotoxin gene (cpe) on either their chromosome or a plasmid, but food poisoning isolates usually have a chromosomal cpe gene. This linkage between chromosomal cpe isolates and food poisoning has previously been attributed, at least in part, to better high-temperature survival of chromosomal cpe isolates than of plasmid cpe isolates. In the current study we assessed whether vegetative cells and spores of chromosomal cpe isolates also survive better than vegetative cells and spores of plasmid cpe isolates survive when the vegetative cells and spores are subjected to low temperatures. Vegetative cells of chromosomal cpe isolates exhibited about eightfold-higher decimal reduction values (D values) at 4°C and threefold-higher D values at −20°C than vegetative cells of plasmid cpe isolates exhibited. After 6 months of incubation at 4°C and −20°C, the average log reductions in viability for spores of plasmid cpe isolates were about fourfold and about threefold greater, respectively, than the average log reductions in viability for spores from chromosomal cpe isolates. C. perfringens type A isolates carrying a chromosomal cpe gene also grew significantly faster than plasmid cpe isolates grew at 25°C, 37°C, or 43°C. In addition, chromosomal cpe isolates grew at higher maximum and lower minimum temperatures than plasmid cpe isolates grew. Collectively, these results suggest that chromosomal cpe isolates are commonly involved in food poisoning because of their greater resistance to low (as well as high) temperatures for both survival and growth. They also indicate the importance of proper low-temperature storage conditions, as well as heating, for prevention of C. perfringens type A food poisoning.


Toxins ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 266
Author(s):  
Thea Neumann ◽  
Maren Krüger ◽  
Jasmin Weisemann ◽  
Stefan Mahrhold ◽  
Daniel Stern ◽  
...  

Clostridium perfringens enterotoxin (CPE) regularly causes food poisoning and antibiotic-associated diarrhea; therefore, reliable toxin detection is crucial. To this aim, we explored stationary and mobile strategies to detect CPE either exclusively by monoclonal antibodies (mAbs) or, alternatively, by toxin-enrichment via the cellular receptor of CPE, claudin-4, and mAb detection. Among the newly generated mAbs, we identified nine CPE-specific mAbs targeting five distinct epitopes, among them mAbs recognizing CPE bound to claudin-4 or neutralizing CPE activity in vitro. In surface plasmon resonance experiments, all mAbs and claudin-4 revealed excellent affinities towards CPE, ranging from 0.05 to 2.3 nM. Integrated into sandwich enzyme-linked immunosorbent assays (ELISAs), the most sensitive mAb/mAb and claudin-4/mAb combinations achieved similar detection limits of 0.3 pg/mL and 1.0 pg/mL, respectively, specifically detecting recombinant CPE from spiked feces and native CPE from 30 different C. perfringens culture supernatants. The implementation of mAb- and receptor-based ELISAs into a mobile detection platform enabled the fast detection of CPE, which will be helpful in clinical laboratories to diagnose diarrhea of assumed bacterial origin. In conclusion, we successfully employed an endogenous receptor and novel high affinity mAbs for highly sensitive and specific CPE-detection. These tools will be useful for both basic and applied research.


1969 ◽  
Vol 15 (7) ◽  
pp. 765-770 ◽  
Author(s):  
Charles L. Duncan ◽  
Dorothy H. Strong

Diarrhea, the principal symptom of human food poisoning caused by Clostridium perfringens, was experimentally produced in rabbits by intraluminal injection of C. perfringens, but not by oral challenge. The ability to induce diarrhea was dependent not only on the strain but also on the method of preparation of cells for challenge and the number of cells in the challenge. Good correlation was obtained between the ability of the strains to produce fluid accumulation in rabbit ileal loops and overt diarrhea after injection into the normal ileum.


1970 ◽  
Vol 16 (5) ◽  
pp. 331-338 ◽  
Author(s):  
A. H. W. Hauschild ◽  
L. Niilo ◽  
W. J. Dorward

The possible involvement of the following factors in Clostridium perfringens type A enteritis was investigated: cellular constituents of C. perfringens, extracellular components, gas generated by growing cultures, and organic acid production. Lambs were used as experimental animals, and all materials were administered by the intraduodenal route.Vegetative cells (1.5 to 5 × 109) administered along with fresh medium caused diarrhea while 100 times the number of cells in spent medium or saline had no effect. Sporulating cells in saline, and their extracts, caused profuse diarrhea. Supernatant fluids from both vegetative and sporulating cultures concentrated by dialysis against polyethylene glycol had no effect, but diarrhea was produced by supernatant fluids from vegetative cultures concentrated by rotary evaporation, and by the gas generated during growth. The effect of the gas was simulated with hydrogen. The pH of the fluid in the small intestine remained constant during C. perfringens enteritis.It was concluded (i) that the factor responsible for experimental enteritis in lambs resulting from infection of the small intestine with vegetative cells of C. perfringens is produced in situ, and (ii) that of the various factors tested, a heat-sensitive, nondialyzable component of sporulating cells is most likely identical with the main enteropathogenic factor in C. perfringens enteritis.


2006 ◽  
Vol 72 (12) ◽  
pp. 7620-7625 ◽  
Author(s):  
Jihong Li ◽  
Bruce A. McClane

ABSTRACT About 1 to 2% of Clostridium perfringens isolates carry the enterotoxin gene (cpe) necessary for causing C. perfringens type A food poisoning. While the cpe gene can be either chromosomal or plasmid borne, food poisoning isolates usually carry a chromosomal cpe gene. Previous studies have linked this association between chromosomal cpe isolates (i.e., C-cpe isolates) and food poisoning, at least in part, to both the spores and vegetative cells of C-cpe isolates being particularly resistant to high and low temperatures. The current study now reveals that the resistance phenotype of C-cpe isolates extends beyond temperature resistance to also include, for both vegetative cells and spores, enhanced resistance to osmotic stress (from NaCl) and nitrites. However, by omitting one outlier isolate, no significant differences in pH sensitivity were detected between the spores or vegetative cells of C-cpe isolates versus isolates carrying a plasmid-borne cpe gene. These results indicate that both vegetative cells and spores of C-cpe isolates are unusually resistant to several food preservation approaches in addition to temperature extremes. The broad-spectrum nature of the C-cpe resistance phenotype suggests these bacteria may employ multiple mechanisms to persist and grow in foods prior to their transmission to humans.


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