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MeSH Review

Food Poisoning

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Disease relevance of Food Poisoning


High impact information on Food Poisoning

  • Food poisoning following consumption of clenbuterol-treated veal in Italy [6].
  • 9. It is presumed to be the enterotoxin responsible for the diarrheal-type B. cereus food poisoning syndrome and it may also be the pyogenic and pyrogenic factor in nongastrointestinal B. cereus infections of man and animals [7].
  • Clostridium perfringens is a source of food poisoning in humans and animals because of production of a potent enterotoxin (CPE) [8].
  • A passive bacteriocin typing system was developed for use as an epidemiologic tool to study outbreaks of food poisoning caused by Clostridium perfringens type A. The 90 strains tested were from England, the United States, India, Japan, France, and Canada. Forty of 74 strains produced bacteriocin when irradiated with ultraviolet light for 40-90 sec [9].
  • Results of this study clearly indicate that SEH was also present in the raw material of reconstituted milk, indicating that the food poisoning was caused by multiple staphylococcal enterotoxins [10].

Chemical compound and disease context of Food Poisoning


Biological context of Food Poisoning

  • These findings with North American isolates provide important new evidence that, regardless of geographic origin or date of isolation, plasmid cpe isolates cause most CPE-associated AAD cases and chromosomal cpe isolates cause most C. perfringens type A food poisoning cases [16].
  • The transcriptional activity of the cytK promoter region in a food-poisoning strain was studied using a reporter gene and compared with that in the reference B. cereus strain ATCC 14579 [17].
  • Haemolysin BL (HBL), a three-component enterotoxic/necrotizing/vascular permeability toxin, is a likely virulence factor of Bacillus cereus diarrhoeal food poisoning and necrotic infections [18].
  • Proper disinfection is necessary to control this type of food poisoning, as it is now clear that only kitchen strains of C. perfringens are able to produce the large amounts of enterotoxin necessary to cause food poisoning (Granum, 1990; Cornillot et al., 1995) [19].
  • These results have verified the general notion that C. perfringens food poisoning should be categorized as a true "intravital intoxication". The reversed passive hemagglutination test detected enterotoxin directly in most fecal samples [20].

Anatomical context of Food Poisoning

  • The excretion in the feces of Clostridium perfringens producing enterotoxin by 48 patients in 3 cases of food poisoning was studied during the illness and 1 and 3 months after the onset [21].

Gene context of Food Poisoning


Analytical, diagnostic and therapeutic context of Food Poisoning

  • By using counterimmunoelectrophoresis (CIEP), Clostridium perfringens enterotoxin was successfully demonstrated in fecal samples collected within 1 day of attack from sick individuals involved in a bacteriologically and epidemiologically proven outbreak of C. perfringens food poisoning [26].
  • The detailed structural elements revealed by the sequence analysis are presented and used to develop a new perspective on the molecular basis of enterotoxin production in this important food-poisoning bacterium [27].
  • PCR identification of the plasmid-borne enterotoxin gene (cpe) in Clostridium perfringens strains isolated from food poisoning outbreaks [28].
  • New tools such as agglutination test with antispore serum, precipitin-in-gel test with anti-enterotoxin serum, active and passive bacteriocin, bacteriophage and biotyping have been developed using standard strains and isolates of c. perfringens type A from foods, food poisoning and others [29].
  • Bacteriocin typing, plasmid profiling and ribotyping were used to type 34 food and patient Clostridium perfringens isolates from 10 food poisoning cases, respectively, outbreaks [30].


  1. Enterotoxin plasmid from Clostridium perfringens is conjugative. Brynestad, S., Sarker, M.R., McClane, B.A., Granum, P.E., Rood, J.I. Infect. Immun. (2001) [Pubmed]
  2. Enterotoxic activity of hemolysin BL from Bacillus cereus. Beecher, D.J., Schoeni, J.L., Wong, A.C. Infect. Immun. (1995) [Pubmed]
  3. Antimicrobial susceptibility of Salmonella isolated from cattle, swine and poultry (2001-2002): report from the Japanese Veterinary Antimicrobial Resistance Monitoring Program. Esaki, H., Morioka, A., Ishihara, K., Kojima, A., Shiroki, S., Tamura, Y., Takahashi, T. J. Antimicrob. Chemother. (2004) [Pubmed]
  4. Isolation of histamine-producing Lactobacillus buchneri from Swiss cheese implicated in a food poisoning outbreak. Sumner, S.S., Speckhard, M.W., Somers, E.B., Taylor, S.L. Appl. Environ. Microbiol. (1985) [Pubmed]
  5. Comparative description of Pseudomonas cocovenenans (van Damme, Johannes, Cox, and Berends 1960) NCIB 9450T and strains isolated from cases of food poisoning caused by consumption of fermented corn flour in China. Zhao, N.X., Ma, M.S., Zhang, Y.P., Xu, D.C. Int. J. Syst. Bacteriol. (1990) [Pubmed]
  6. Food poisoning following consumption of clenbuterol-treated veal in Italy. Brambilla, G., Loizzo, A., Fontana, L., Strozzi, M., Guarino, A., Soprano, V. JAMA (1997) [Pubmed]
  7. Properties and production characteristics of vomiting, diarrheal, and necrotizing toxins of Bacillus cereus. Turnbull, P.C., Kramer, J.M., Jørgensen, K., Gilbert, R.J., Melling, J. Am. J. Clin. Nutr. (1979) [Pubmed]
  8. Expression from the Clostridium perfringens cpe promoter in C. perfringens and Bacillus subtilis. Melville, S.B., Labbe, R., Sonenshein, A.L. Infect. Immun. (1994) [Pubmed]
  9. Passive bacteriocin typing of strains of Clostridium perfringens type A causing food poisoning for epidemiologic studies. Satija, K.C., Narayan, K.G. J. Infect. Dis. (1980) [Pubmed]
  10. Mass outbreak of food poisoning disease caused by small amounts of staphylococcal enterotoxins A and H. Ikeda, T., Tamate, N., Yamaguchi, K., Makino, S. Appl. Environ. Microbiol. (2005) [Pubmed]
  11. Inhibition of electrical activity in mouse pancreatic beta-cells by the ATP/ADP translocase inhibitor, bongkrekic acid. Kiranadi, B., Bangham, J.A., Smith, P.A. FEBS Lett. (1991) [Pubmed]
  12. Molecular epidemiology of ampicillin-resistant clinical isolates of Salmonella enteritidis. Vatopoulos, A.C., Mainas, E., Balis, E., Threlfall, E.J., Kanelopoulou, M., Kalapothalki, V., Malamou-Lada, H., Legakis, N.J. J. Clin. Microbiol. (1994) [Pubmed]
  13. Domoic acid: a dementia-inducing excitotoxic food poison with kainic acid receptor specificity. Stewart, G.R., Zorumski, C.F., Price, M.T., Olney, J.W. Exp. Neurol. (1990) [Pubmed]
  14. Molecular analysis confirms food source and simultaneous involvement of two distinct but related subgroups of Salmonella typhimurium bacteriophage type 10 in major interprovincial Salmonella outbreak. Bezanson, G.S., Khakhria, R., Duck, D., Lior, H. Appl. Environ. Microbiol. (1985) [Pubmed]
  15. Nondetectable concentrations of human placental Ah receptors are associated with potent induction of microsomal benzo[a]pyrene hydroxylase in individuals exposed to polychlorinated biphenyls, quaterphenyls, and dibenzofurans. Wong, T.K., Sloop, T., Lucier, G.W. Toxicol. Appl. Pharmacol. (1986) [Pubmed]
  16. Genotyping of enterotoxigenic Clostridium perfringens fecal isolates associated with antibiotic-associated diarrhea and food poisoning in North America. Sparks, S.G., Carman, R.J., Sarker, M.R., McClane, B.A. J. Clin. Microbiol. (2001) [Pubmed]
  17. Comparison of cytotoxin cytK promoters from Bacillus cereus strain ATCC 14579 and from a B. cereus food-poisoning strain. Brillard, J., Lereclus, D. Microbiology (Reading, Engl.) (2004) [Pubmed]
  18. Tripartite haemolysin BL: isolation and characterization of two distinct homologous sets of components from a single Bacillus cereus isolate. Beecher, D.J., Wong, A.C. Microbiology (Reading, Engl.) (2000) [Pubmed]
  19. What problems does the food industry have with the spore-forming pathogens Bacillus cereus and Clostridium perfringens? Andersson, A., Ronner, U., Granum, P.E. Int. J. Food Microbiol. (1995) [Pubmed]
  20. Experimental diarrhea in cynomolgus monkeys by oral administration with Clostridium perfringens type A viable cells or enterotoxin. Uemura, T., Sakaguchi, G., Ito, T., Okazawa, K., Sakai, S. Jpn. J. Med. Sci. Biol. (1975) [Pubmed]
  21. Excretion of enterotoxin-producing Clostridium perfringens in feces by patients during and after diarrhea. Saito, M. Kansenshogaku Zasshi (1991) [Pubmed]
  22. Plasmid-mediated histamine biosynthesis in the bacterial fish pathogen Vibrio anguillarum. Barancin, C.E., Smoot, J.C., Findlay, R.H., Actis, L.A. Plasmid (1998) [Pubmed]
  23. Superantigen-induced transcriptional activation of the human TNF gene promoter in T cells. Krämer, B., Machleidt, T., Wiegmann, K., Krönke, M. J. Inflamm. (1995) [Pubmed]
  24. Bacillus cereus phage typing as an epidemiological tool in outbreaks of food poisoning. Ahmed, R., Sankar-Mistry, P., Jackson, S., Ackermann, H.W., Kasatiya, S.S. J. Clin. Microbiol. (1995) [Pubmed]
  25. TPN or intravenous food poisoning? Schloerb, P.R. Nutrition (Burbank, Los Angeles County, Calif.) (2001) [Pubmed]
  26. Detection of Clostridium perfringens enterotoxin in human fecal samples and anti-enterotoxin in sera. Naik, H.S., Duncan, C.L. J. Clin. Microbiol. (1978) [Pubmed]
  27. A complex array of Hpr consensus DNA recognition sequences proximal to the enterotoxin gene in Clostridium perfringens type A. Brynestad, S., Iwanejko, L.A., Stewart, G.S., Granum, P.E. Microbiology (Reading, Engl.) (1994) [Pubmed]
  28. PCR identification of the plasmid-borne enterotoxin gene (cpe) in Clostridium perfringens strains isolated from food poisoning outbreaks. Nakamura, M., Kato, A., Tanaka, D., Gyobu, Y., Higaki, S., Karasawa, T., Yamagishi, T. Int. J. Med. Microbiol. (2004) [Pubmed]
  29. Food borne infection with Clostridium perfringens type A. Narayan, K.G. International journal of zoonoses. (1982) [Pubmed]
  30. Strain differentiation of Clostridium perfringens by bacteriocin typing, plasmid profiling and ribotyping. Schalch, B., Eisgruber, H., Schau, H.P., Wiedmann, M., Stolle, A. Zentralblatt Veterinarmedizin Reihe B (1998) [Pubmed]
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