Preventing Foodborne Illness: Clostridium perfringens

EDIS ◽  
2017 ◽  
Vol 2017 (3) ◽  
Author(s):  
Keith R. Schneider ◽  
Renee M. Goodrich Schneider ◽  
Ploy Kurdmongkoltham ◽  
Bruna Bertoldi
Keyword(s):  
Clostridium Perfringens ◽  
Food Poisoning ◽  
Common Type ◽  
Foodborne Illness ◽  
Vegetative Cells ◽  
The Us ◽  
Contaminated Food ◽  
Us Fda ◽  
Enteritis Necroticans

The bacterium Clostridium perfringens causes of one of the most common type of foodborne gastroenteritis, often referred to as perfringens food poisoning, in the US (FDA 2012). It is associated with consuming contaminated food that contains great numbers of vegetative cells and spores that will produce toxin inside the intestine. There are two forms of disease caused by C. perfringens: gastroenteritis and enteritis necroticans. The latter disease, also known as pig-bel disease, is not common in the US. It is often associated with contaminated pork (FDA 2012) and can be very severe. 

Growth and Sporulation Potential of Clostridium perfringens in Aerobic and Vacuum-Packaged Cooked Beef

1994 ◽  
Vol 57 (5) ◽  
pp. 393-398 ◽  
Author(s):  
V. K. JUNEJA ◽  
B. S. MARMER ◽  
A. J. MILLER
Keyword(s):  
Clostridium Perfringens ◽  
Food Poisoning ◽  
Ground Beef ◽  
Viable Count ◽  
Anaerobic Conditions ◽  
Vegetative Cells ◽  
Aerobic Conditions ◽  
C Storage ◽  
Meat Samples ◽  
Aerobic And Anaerobic

Growth of Clostridium perfringens in aerobic-and anaerobic-(vacuum) packaged cooked ground beef was investigated. Autoclaved ground beef was inoculated with ~3.0-log10 CFU/g of C. perfringens, packaged and stored at various temperatures. Vegetative cells and heat-resistant spores were enumerated by plating unheated and heated (75°C for 20 min) meat samples on tryptose-sulfite-cycloserine agar. Clostridium perfringens grew to >7 logs within 12 h at 28, 37 and 42°C under anaerobic atmosphere and at 37 and 42°C under aerobic conditions. At 28°C under aerobic conditions, growth was relatively slow and total viable count increased to >6 logs within 36 h. Similarly, growth at 15°C in air was both slower and less than under vacuum. Regardless of packaging, the organism either declined or did not grow at 4, 8 and 12°C. Spores were not found at <12°C. Spores were detected as early as 8 h at 42°C under anaerobic conditions, but in general, the type of atmosphere had little influence on sporulation at ≥28°C. Temperature abuse (28°C storage) of refrigerated products for 6 h will not permit C. perfringens growth. However, cyclic and static temperature abuse of such products for relatively long periods may lead to high and dangerous numbers of organisms. Reheating such products to an internal temperature of 65°C before consumption would prevent food poisoning since the vegetative cells were killed.

scholarly journals Clostridium perfringens – epidemiological importance and diagnostics

2019 ◽  
Vol 75 (01) ◽  
pp. 6161-2019
Author(s):  
NINA KOZIEŁ ◽  
ELŻBIETA KUKIER ◽  
KRZYSZTOF KWIATEK
Keyword(s):  
Clostridium Perfringens ◽  
Extracellular Enzymes ◽  
Food Poisoning ◽  
Immunocompromised Host ◽  
Necrotic Enteritis ◽  
Virulence Determinants ◽  
Gastrointestinal Infections ◽  
Food Borne ◽  
Disease Diagnostics ◽  
Enteritis Necroticans

Clostridium perfringens is one of the most widespread anaerobic spore forming bacteria found in the environment. The toxotype A of the species inhabits the gastrointestinal tract of birds and mammals exhibiting pathogenic properties in the immunocompromised host. The virulence determinants of C. perfringens are toxins and extracellular enzymes which cause gas gangrene, enteritis necroticans, food poisoning, and non-food borne gastrointestinal infections in humans. The young animals suffer from enterotoxaemia, dysentery and necrotic enteritis due to the anaerobic spore forming bacilli. This article reviews the epidemiological significance of C. perfringens and its disease diagnostics, taking into account all known to date virulence determinants of the microorganism.

scholarly journals Comparative Effects of Osmotic, Sodium Nitrite-Induced, and pH-Induced Stress on Growth and Survival of Clostridium perfringens Type A Isolates Carrying Chromosomal or Plasmid-Borne Enterotoxin Genes

2006 ◽  
Vol 72 (12) ◽  
pp. 7620-7625 ◽  
Author(s):  
Jihong Li ◽  
Bruce A. McClane
Keyword(s):  
Clostridium Perfringens ◽  
Food Poisoning ◽  
Type A ◽  
Food Preservation ◽  
Vegetative Cells ◽  
Growth And Survival ◽  
Resistance Phenotype ◽  
Enhanced Resistance ◽  
Enterotoxin Genes ◽  
High And Low Temperatures

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.

USE OF TIME-TEMPERATURE EVALUATIONS IN DETECTING THE RESPONSIBLE VEHICLE AND CONTRIBUTING FACTORS OF FOODBORNE DISEASE OUTBREAKS1

1971 ◽  
Vol 34 (12) ◽  
pp. 576-582 ◽  
Author(s):  
Frank L. Bryan ◽  
Thomas W. McKinley ◽  
Byron Mixon
Keyword(s):  
Clostridium Perfringens ◽  
Bacterial Growth ◽  
Room Temperature ◽  
Foodborne Illness ◽  
Boiling Water ◽  
Foodborne Disease ◽  
Contributing Factors ◽  
Vegetative Cells ◽  
Use Of Time ◽  
Cooked Meat

An investigation of an outbreak of Clostridium perfringens foodborne illness indicated that turkey or dressing prepared in a school kitchen was responsible. When turkey was again prepared in the kitchen, a bacteriological survey and a time-temperature evaluation were made of the thawing, cooking, chilling, and reheating to which the turkey, stock, or dressing were subjected. During thawing of 22-lb. turkeys in plastic wrappers and in paper bags at room temperature for 18 hr, neither internal nor surface temperatures reached a level at which C. perfringens could grow. Cooking the turkeys in a steamer or in a pot of boiling water raised internal temperatures to a level lethal to vegetative cells. The stock (in gallon jars and a large rectangular pan) and deboned meat (in similar pan) were stored overnight in a reach-in refrigerator. During storage the temperature of both were within a range so that C. perfringens spores could germinate and its vegetative cells multiply for 7–9 hr. The stock was later used in dressing, which when baked, reached internal temperatures known to destroy vegetative cells of C. perfringens. Meat and gravy, when reheated, did not reach such levels. Clostridium perfringens, Staphylocoocus aureus, and Salmonella were isolated from raw turkey; C. perfringens was isolated from cooked meat, stock, and kitchen equipment. Nine recommendations for heat destruction of vegetative cells, inhibition of bacterial growth during storage, and cleaning and sanitizing equipment are made. These recommendations will help prevent foodborne illness whenever turkey and dressing are prepared.

scholarly journals Comparative Experiments To Examine the Effects of Heating on Vegetative Cells and Spores of Clostridium perfringens Isolates Carrying Plasmid Genes versus Chromosomal Enterotoxin Genes

2000 ◽  
Vol 66 (8) ◽  
pp. 3234-3240 ◽  
Author(s):  
Mahfuzur R. Sarker ◽  
Robert P. Shivers ◽  
Shauna G. Sparks ◽  
Vijay K. Juneja ◽  
Bruce A. McClane
Keyword(s):  
Clostridium Perfringens ◽  
Gastrointestinal Disease ◽  
Food Poisoning ◽  
Meat Products ◽  
Gastrointestinal Diseases ◽  
Vegetative Cells ◽  
Food Borne ◽  
Enterotoxin Genes ◽  
Plasmid Genes ◽  
High Degree

ABSTRACT Clostridium perfringens enterotoxin (CPE) is an important virulence factor for both C. perfringens type A food poisoning and several non-food-borne human gastrointestinal diseases. Recent studies have indicated that C. perfringensisolates associated with food poisoning carry a chromosomalcpe gene, while non-food-borne human gastrointestinal disease isolates carry a plasmid cpe gene. However, no explanation has been provided for the strong associations between certain cpe genotypes and particular CPE-associated diseases. Since C. perfringens food poisoning usually involves cooked meat products, we hypothesized that chromosomalcpe isolates are so strongly associated with food poisoning because (i) they are more heat resistant than plasmid cpeisolates, (ii) heating induces loss of the cpe plasmid, or (iii) heating induces migration of the plasmid cpe gene to the chromosome. When we tested these hypotheses, vegetative cells of chromosomal cpe isolates were found to exhibit, on average approximately twofold-higher decimal reduction values (Dvalues) at 55°C than vegetative cells of plasmid cpeisolates exhibited. Furthermore, the spores of chromosomalcpe isolates had, on average, approximately 60-fold-higherD values at 100°C than the spores of plasmidcpe isolates had. Southern hybridization and CPE Western blot analyses demonstrated that all survivors of heating retained theircpe gene in its original plasmid or chromosomal location and could still express CPE. These results suggest that chromosomalcpe isolates are strongly associated with food poisoning, at least in part, because their cells and spores possess a high degree of heat resistance, which should enhance their survival in incompletely cooked or inadequately warmed foods.

scholarly journals Further Comparison of Temperature Effects on Growth and Survival of Clostridium perfringens Type A Isolates Carrying a Chromosomal or Plasmid-Borne Enterotoxin Gene

2006 ◽  
Vol 72 (7) ◽  
pp. 4561-4568 ◽  
Author(s):  
Jihong Li ◽  
Bruce A. McClane
Keyword(s):  
Clostridium Perfringens ◽  
Food Poisoning ◽  
Type A ◽  
Storage Conditions ◽  
Enterotoxin Gene ◽  
Vegetative Cells ◽  
Growth And Survival ◽  
Low Temperature Storage ◽  
D Values ◽  
Better Than

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.

Regulatory decisions from the US FDA

2001 ◽  
Vol &NA; (1272) ◽  
pp. 22
Author(s):  
&NA;
Keyword(s):  
The Us ◽  
Us Fda ◽  
Regulatory Decisions

scholarly journals A Putative Amidase Endolysin Encoded by Clostridium perfringens St13 Exhibits Specific Lytic Activity and Synergizes with the Muramidase Endolysin Psm

Antibiotics ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 245
Author(s):  
Hiroshi Sekiya ◽  
Maho Okada ◽  
Eiji Tamai ◽  
Toshi Shimamoto ◽  
Tadashi Shimamoto ◽  
...  
Keyword(s):  
Cell Wall ◽  
Clostridium Perfringens ◽  
Antimicrobial Agents ◽  
Catalytic Domain ◽  
Food Poisoning ◽  
Binding Activity ◽  
Lytic Activity ◽  
Intestinal Bacterium ◽  
Terminal Domain ◽  
Cell Wall Binding

Clostridium perfringens is an often-harmful intestinal bacterium that causes various diseases ranging from food poisoning to life-threatening fulminant disease. Potential treatments include phage-derived endolysins, a promising family of alternative antimicrobial agents. We surveyed the genome of the C. perfringens st13 strain and identified an endolysin gene, psa, in the phage remnant region. Psa has an N-terminal catalytic domain that is homologous to the amidase_2 domain, and a C-terminal domain of unknown function. psa and gene derivatives encoding various Psa subdomains were cloned and expressed in Escherichia coli as N-terminal histidine-tagged proteins. Purified His-tagged full-length Psa protein (Psa-his) showed C. perfringens-specific lytic activity in turbidity reduction assays. In addition, we demonstrated that the uncharacterized C-terminal domain has cell wall-binding activity. Furthermore, cell wall-binding measurements showed that Psa binding was highly specific to C. perfringens. These results indicated that Psa is an amidase endolysin that specifically lyses C. perfringens; the enzyme’s specificity is highly dependent on the binding of the C-terminal domain. Moreover, Psa was shown to have a synergistic effect with another C. perfringens-specific endolysin, Psm, which is a muramidase that cleaves peptidoglycan at a site distinct from that targeted by Psa. The combination of Psa and Psm may be effective in the treatment and prevention of C. perfringens infections.

scholarly journals Innovative and Highly Sensitive Detection of Clostridium perfringens Enterotoxin Based on Receptor Interaction and Monoclonal Antibodies

Toxins ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 266
Author(s):  
Thea Neumann ◽  
Maren Krüger ◽  
Jasmin Weisemann ◽  
Stefan Mahrhold ◽  
Daniel Stern ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Clostridium Perfringens ◽  
Food Poisoning ◽  
Receptor Interaction ◽  
Clostridium Perfringens Enterotoxin ◽  
Fast Detection ◽  
Highly Sensitive ◽  
Basic And Applied Research ◽  
Highly Sensitive Detection

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.

scholarly journals Ravulizumab: a novel C5 inhibitor for the treatment of paroxysmal nocturnal hemoglobinuria

2019 ◽  
Vol 10 ◽  
pp. 204062071987472 ◽  
Author(s):  
Robert M. Stern ◽  
Nathan T. Connell
Keyword(s):  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Bone Marrow Failure ◽  
Phase Iii ◽  
The European Union ◽  
Regulatory Review ◽  
Dosing Schedule ◽  
The Us ◽  
United States Food ◽  
States Food ◽  
Us Fda

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare stem cell disorder characterized by hemolytic anemia, bone marrow failure, and thrombosis. Until recently, the complement inhibitor, eculizumab, was the only United States Food and Drug Administration (US FDA)-approved therapy for the treatment of PNH. Although effective, eculizumab requires a frequent dosing schedule that can be burdensome for some patients and increases the risk of breakthrough intravascular hemolysis. Ravulizumab, an eculizumab-like monoclonal antibody engineered to have a longer half-life, is intended to provide the same benefits as eculizumab but with a more convenient and effective dosing schedule. In two recently published phase III non-inferiority trials, ravulizumab was found to be non-inferior to eculizumab both in efficacy and safety for the treatment of patients with PNH. Based on these results, ravulizumab was approved by the US FDA on 21 December 2018 and is currently under regulatory review in both the European Union and Japan.

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