RAI BugWiki

Clostridium perfringens

[notice]Hazard Group 2[/notice]

Clostridium perfringens is an anaerobic rod-shaped, Gram-positive bacterium associated with foods such as rolled meat joints, stews and gravies. This common commensal is rarely pathogenic and is usually limited to the immunocompromised and those with open wounds but can also cause food poisoning with abdominal pain, diarrhoea, vomiting is rare. In very rare cases it has been associated with tissue necrosis, bacteraemia, emphysematous cholecystitis or gas gangrene.

During cooking, vegetative cells of C. perfringens die but they form spores able to survive the unfavourable conditions. If the food is cooled slowly, the spores can germinate into vegetative cells that can then multiply to high numbers. When the highly contaminated food is eaten, although the cells are unable to grow in the gut they form spores and as the cells break to release the spore, a large amount of toxin is released into the gut. Symptoms include watery diarrhoea and abdominal pain that usually resolves itself as the diarrhoea removes the toxin from the body.

There are five types of C. perfringens based on toxin type (A, B, C, D, E). Most C. perfringens food poisoning cases reported in developed countries are caused by type A strains. Type C causes a rare, severe, necrotic enteritis. Less than 5% of all C. perfringens carry the gene responsible for the production of the enterotoxin causing Type A illness (the cpe gene). Only strains carrying this gene in a chromosome (C-cpe) cause foodborne illness. For this reason we shall stick to Type A and cpe positive C. perfringens.

[important]Growth and Control[/important]

Isolates with chromosomal cpe have a competitive advantage over isolates with the same gene located on a plasmid (P-cpe), as they are more resistant to several food preservation procedures (e.g. heat, refrigeration, freezing).

Optimal heat shock occurs around 75°C which will activate germination of any spores in the food. Slow cooling and / or slow reheating provide germinating spores and any surviving vegetative cells with conditions (>10°C to <54°C) allowing multiplication to large numbers, particularly as competitive flora will have been killed.



Minimum 10°C

Maximum 54°C

Optimum 43°C

Some isolates have a very short generation time (<10 min). Enterotoxin is produced only during spore formation but remains intracellular until lysis of the mother cell to release the mature spore. Toxin is not produced in significant amounts during optimum vegetative growth. Toxin production is optimum at 35-40°C.


Optimum 6-7

Range 5.1 to 9.7

Spore formation occurs between pH 5.1 and 9.9 (Li and McClane 2006a).


Optimal under anaerobic conditions.

Small amounts of oxygen, up to a redox potential of +200 mV can be tolerated, but generation and lag times lengthen. The redox potential of many foods, including meat, is sufficient to allow growth to start, after which the atmosphere is made more anaerobic by the organism. Growth rates are similar under carbon dioxide or nitrogen atmospheres.

Minimum Water Activity




Concentrations of C-cpe vegetative cells decline at refrigeration temperatures, with C-cpe isolates surviving longer; D4°C of 11 days compared to 1.8 days for P-cpe isolates (Li and McClane, 2006b). Similarly, the D-20°C was 1.5 days for C-cpe cells compared to 0.6 days for P-cpe isolates.

Spores survive both refrigeration (4°C) and freezing (-20°C) with less than 1-log reduction in spore viability after 6 months at both refrigeration and freezing temperatures.


Sporulation occurs between pH 6 and 8 under gut conditions. The hardy spores show less than a 1.2 log decrease in numbers after 3 months at pH 4 and pH 10.


C. perfringens vegetative cells survive some exposure to oxygen (redox potentials between +200 to +300 mV).



A literature review indicated a mean D70C of 23 seconds with a 95th percentile of 125 seconds (based on 146 data points).

Cooking for 2 minutes at 70°C would achieve a mean (approximate) 6-log reduction in vegetative cells, but would not kill spores. In the same review, a mean D120C of 18 seconds was calculated for spores, with a 95th percentile of 161 seconds (based on 64 data points ).

D-values for different isolates of C. perfringens vary, particularly when present as spores, and C-cpe strains appear more hardy. As spores, the D100C of six C-cpe strains was between 30 and 124 min compared with 0.5-1.9 min for P-cpe strains.

While the enterotoxin is a heat-labile protein and inactivated by heating for 5 min at 60°C, it is not generally produced in food.


Vegetative C-cpe cells inactivated below pH 5 (Bates and Bodnaruk, 2003)

C-cpe spores slow inactivation below pH 5

Enterotoxin not generally produced in food


For the curing of meats hurdle technology is often used. For example, the use of pH (6.2), salt (1%) and sodium nitrite (50μg/ml) act synergistically to inhibit C. perfringens vegetative growth at 15°C.

Disinfectants / Sanitisers

QACs and chlorine sanitisers destroy vegetative C. perfringens cells on surfaces. See here for guidance.

Glutaraldehyde, formaldehyde, chlorine, iodine, acids, alkalis, hydrogen peroxide, peroxy acids, ethylene oxide, ß-propionolactone and ozone are all sporicidal at high concentrations with long contact times – Antibak is far quicker and less toxic – see here for further info.

Phenolics, QACs, alcohols, bisguanides, organic acids and esters have little sporicidal effect. Chlorine disinfectants such as household bleach contain 5.25% sodium hypochlorite (52,500 ppm available chlorine) are not effective against C. perfringens spores.

[important]Clinical Notes[/important]

[warning]Don’t forget to read the disclaimer![/warning]

Incubation: 6-24 hours, usual onset 10-12 hours.

Symptoms: Profuse watery diarrhoea with severe abdominal pain that subsides within 24 hours or less. Diarrhoea is initiated by the enterotoxins causing tissue-damage to intestinal cells. Vomiting and nausea are rare. Severity of illness is lessened by the diarrhoea flushing out both the enterotoxin and sporulating cells from the small intestine. Estimated hospitalisation and fatality rates are 0.3% and 0.05%, respectively.

Condition: Gastroenteritis or C. perfringens enteritis.

Dose: Approximately108 organisms. Large numbers of vegetative cells must be ingested. Assuming a 100g serving, at least 106/g of food is needed to cause illness.

Toxins: Illness is due to foodborne infection with toxin produced in the intestine. Rare cases of intoxication with pre-formed toxin have been reported, resulting in earlier onset of symptoms. In instances where the bacteria have multiplied to such levels that sporulation and toxin production occurs, the food is usually in an advanced state of spoilage. Up to 15% of a sporulating cell’s protein can be enterotoxin.

At Risk Groups: No specific ‘at risk’ groups.

Long Term Effects: Generally none.

Treatment: Not usually given as symptoms resolve naturally (McClane, 2007).

[important]Reservoirs / Sources[/important]

Human: USA, Finnish and Japanese studies indicate that most healthy adults are not routinely colonised by C. perfringens C-cpe type strains but about half of all subjects studied were colonised with non-enterotoxigenic type A vegetative cells and/or spores, including P-cpe strains.

In general, counts in populations of healthy individuals of <103-104/g faeces are considered normal. The organism is more numerous in healthy neonates and the elderly than in adults. Food handlers are not thought to be a source of food contamination as the organism already exists on the at-risk foods. As levels of C. perfringens spores can be elevated in some healthy individuals (e.g. the elderly), detection of toxin in faeces is preferable to culture for diagnosis and outbreak investigation. Analysis for enterotoxin should be carried out within 48 hours of onset due to rapid elimination of toxin from the gut. PCR methods on suspected food samples are also useful because they identify the presence of the C-cpe gene.

Animal: C. perfringens can be found in the contents of virtually all animal intestines. Contamination of carcasses occurs at slaughter. Animal foods are the most common vehicles.

Food: C. perfringens can be found in raw, dehydrated and cooked foods. Type A food poisoning often involves large volumes of food, especially meat and poultry dishes, prepared and cooked (possibly undercooked) in advance then allowed to cool too slowly. Cooking creates an anaerobic atmosphere as oxygen is depleted. Rolled meats, stuffed poultry, pies, thick soups, stews, gravies and curries have been implicated in outbreaks. In the case of rolled meats, any bacteria on the outside of the meat are rolled into the centre where conditions are anaerobic and heat can be slow to penetrate. Undercooking of foods is a major factor for survival of vegetative cells. Heating activates any spores while slow cooling promotes germination and growth.

The most effective way to prevent C. perfringens food poisoning is to prevent its growth in food, i.e. strict controls on cooling and on storage temperatures.

Environment: Spores of C. perfringens are resilient and are widely distributed in soil, dust and vegetation.

Transmission routes: Primarily ingestion of food with high levels of C. perfringens vegetative cells (>106/g).

[important]Plague and Pestilence[/important]

No particular seasonal patterns. Outbreak investigations commonly reveal control point failures including preparation too far in advance (implying temperature abuse), undercooking, inadequate cooling, poor reheating and improper hot holding.

Outbreaks have been associated with inadequate cooling or refrigeration, reheating, improper hot holding.