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Category: Food Microbiology
Clostridium perfringens, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555819972/9781555819965.ch19-1.gif /docserver/preview/fulltext/10.1128/9781555819972/9781555819965.ch19-2.gifAbstract:
Significant progress has been made in the last few years towards our understanding of the epidemiology, pathogenicity, and control of foodborne disease, including food poisoning, caused by Clostridium perfringens strains. Despite this, a significant burden of food poisoning illnesses still occurs in the United States every year, with nearly a million cases reported. C. perfringens food poisoning commonly occurs as outbreaks in institutions where food is prepared in large quantities. Prophylactic measures to prevent food poisoning should focus on restricting multiplication of vegetative cells in cooked foods. Cooking at the proper temperature and for the right time, along with rapid cooling after cooking with subsequent refrigeration, is the most effective action to control the multiplication of C. perfringens and thus avoid food poisoning outbreaks. Processors can take advantage of multiple food formulation factors or hurdles in foods (e.g., water activity, pH, and added preservatives) to restrict growth from spores in cooked foods. Predictive models have been developed to estimate growth under conditions that are relevant to food processing operations. Recent advances in molecular techniques have enabled researchers to characterize C. perfringens virulence factors, toxins, sporulation, spore heat resistance, to carry out epidemiologic trace-back of foodborne illness and toxigenic typing methods, etc. Future research efforts should be directed towards efficient tracing of C. perfringens strains of public health significance, multiple hurdles in formulated foods, proper processing of ready-to-eat foods, and consumer awareness of handling of such foods.
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Electron micrograph of thin sections of C. perfringens FD-1041. Arrows indicate a spore and a CPE containing round inclusion body. Magnification, ×40,000. Bar, 0.5 μ. Reproduced with permission from reference 5 .
CpAL regulation of C. perfringens virulence factors ( 13 , 15 , 16 , 18 , 20 – 28 , 36 – 40 ). CpAL is encoded by agrD and agrB, whose products are the AgrD signaling peptide (inset) and a transmembrane protein (AgrB) involved in its processing. The AgrD peptide is sensed by the membrane sensor (VirS), which in turn phosphorylates VirR, the response regulator. Upon CpAL activation, VirR directly upregulates transcription of several toxin genes or a small VR-RNA which ultimately activates expression of plc and colA. Whether VirR upregulates transcription of the CpAL operon is not clear.
Histological damage is induced by C. perfringens lysates. Tissue specimens shown were collected from rabbit ileal loops treated with either concentrated vegetative (FTG) or concentrated sporulating (DS) culture lysates of C. perfringens wild-type, mutant, or complemented strains. Tissue specimens shown were treated with 50-fold-concentrated DS or FTG (as indicated) lysates of wild-type SM101, cpe knockout mutant MRS101, or complemented strain MRS101(pJRC200). Tissue specimens treated with 50-fold-concentrated FTG lysates prepared from either MRS101 or complemented strain MRS101(pJRC200) were indistinguishable from specimens treated with FTG lysates of SM101 (data not shown).
Detection of CPA on C. perfringens biofilms. Strain S13Δplc or S13Δplc/plc was inoculated into a four-well chamber slide containing tryptone glucose yeast extract, followed by incubation for 24 h at 37°C. Bacteria were stained with SYTO9, and CPA was detected using rabbit polyclonal anti-C. perfringens CPA antibodies, followed by goat anti-rabbit immunoglobulin secondary antibodies conjugated to Alexa Fluor 555. Optical middle and top sections were obtained with a confocal microscope. Arrows point to areas of colocalization.
Pathogenesis of C. perfringens type A food poisoning. Vegetative cells of an enterotoxin (CPE)-producing C. perfringens strain multiply rapidly in contaminated food (usually a meat or poultry product) and, after ingestion, sporulate in the small intestine. Sporulated C. perfringens cells then produce CPE, which is released at the completion of sporulation, when the mother cell lyses to release its endospore. CPE then causes morphologic damage to the small intestine, resulting in diarrhea and abdominal cramps. Modified and reproduced with permission from reference 236 .