Bacillus cereus

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Bacillus cereus
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B. cereus colonies on a sheep-blood agar plate
Scientific classification
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B. cereus
Binomial name
Bacillus cereus
Frankland & Frankland 1887

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Bacillus cereus is an endemic[where?], soil-dwelling, Gram-positive, rod-shaped, motile, beta hemolytic bacterium. Some strains are harmful to humans and cause foodborne illness, while other strains can be beneficial as probiotics for animals.[1] It is the cause of "fried rice syndrome", as the bacteria are classically contracted from fried rice dishes that have been sitting at room temperature for hours (such as at a buffet).[2] B. cereus bacteria are facultative anaerobes, and like other members of the genus Bacillus, can produce protective endospores. Its virulence factors include cereolysin and phospholipase C.

It was from this species that two new enzymes, named AlkC and AlkD, which are involved in DNA repair, were discovered in 2006.[3]

Ecology

B. cereus competes with other microorganisms such as Salmonella and Campylobacter in the gut, so its presence reduces the numbers of those microorganisms. In food animals such as chickens,[4] rabbits[5] and pigs,[6] some harmless strains of B. cereus are used as a probiotic feed additive to reduce Salmonella in the intestines and cecum. This improves the animals' growth as well as food safety for humans who eat their meat.

Some strains of B. cereus produce cereins, bacteriocins active against different B. cereus strains or other Gram-positive bacteria.[7]

Reproduction

At 30 °C (86 °F), a population of B. cereus can double in as little as 20 minutes or as long as 3 hours, depending on the food product.[8]

Food Minutes to double, 30 °C (86 °F) Hours to multiply by 1,000,000
Milk 20-36 6.6 - 12
Cooked rice 26-31 8.6 - 10.3
Infant formula 56 18.6

Pathogenesis

B. cereus is responsible for a minority of foodborne illnesses (2–5%), causing severe nausea, vomiting, and diarrhea.[9] Bacillus foodborne illnesses occur due to survival of the bacterial endospores when food is improperly cooked.[10] Cooking temperatures less than or equal to 100 °C (212 °F) allow some B. cereus spores to survive.[11] This problem is compounded when food is then improperly refrigerated, allowing the endospores to germinate.[12] Cooked foods not meant for either immediate consumption or rapid cooling and refrigeration should be kept at temperatures below 10 °C or above 50 °C (50 °F and 122 °F).[11] Germination and growth generally occur between 10 °C and 50 °C,[11] though some strains are psychrotrophic.[13] Bacterial growth results in production of enterotoxins, one of which is highly resistant to heat and acids (pH levels between 2 and 11);[14] ingestion leads to two types of illness, diarrheal and emetic (vomiting) syndrome.[15]

  • The diarrheal type is associated with a wide range of foods, has an 8.0- to 16-hour incubation time, and is associated with diarrhea and gastrointestinal pain. Also known as the 'long-incubation' form of B. cereus food poisoning, it might be difficult to differentiate from poisoning caused by Clostridium perfringens.[14] Enterotoxin can be inactivated after heating at 56 °C (133 °F) for 5 minutes however it is unclear whether its presence in food causes the symptom since it degrades in stomach enzymes; its subsequent production by surviving B. cereus spores within the small intestine may be the cause of illness.[16]
  • The 'emetic' form is commonly caused by rice cooked for a time and temperature insufficient to kill any spores present, then improperly refrigerated. It can produce a toxin, cereulide, which is not inactivated by later reheating. This form leads to nausea and vomiting one to five hours after consumption. It can be difficult to distinguish from other short-term bacterial foodborne intoxications such as by Staphylococcus aureus.[14] Emetic toxin can withstand 121 °C (250 °F) for 90 minutes.[16]

The diarrhetic syndromes observed in patients are thought to stem from the three toxins: hemolysin BL (Hbl), nonhemolytic enterotoxin (Nhe) and cytotoxin K (CytK).[17] The nhe/hbl/cytK genes are located on the chromosome of the bacteria. Transcription of these genes is controlled by PlcR. These genes occur in the taxonomically related B. thuringiensis and B. anthracis, as well. These enterotoxins are all produced in the small intestine of the host, thus thwarting digestion by host endogenous enzymes. The Hbl and Nhe toxins are pore-forming toxins closely related to ClyA of E. coli. The proteins exhibit a conformation known as "beta-barrel" that can insert into cellular membranes due to a hydrophobic exterior, thus creating pores with hydrophilic interiors. The effect is loss of cellular membrane potential and eventually cell death. CytK is a pore-forming protein more related to other hemolysins.

The timing of the toxin production was previously thought to be possibly responsible for the two different courses of disease, but in fact the emetic syndrome is caused by a toxin, cereulide, found only in emetic strains and is not part of the "standard toolbox" of B. cereus. Cereulide is a cyclic polypeptide containing three repeats of four amino acids: D-oxy-Leu—D-Ala—L-oxy-Val—L-Val (similar to valinomycin produced by Streptomyces griseus) produced by nonribosomal peptide synthesis. Cereulide is believed to bind to 5-hydroxytryptamine 3 (5-HT3) serotonin receptors, activating them and leading to increased afferent vagus nerve stimulation.[18] It was shown independently by two research groups to be encoded on multiple plasmids: pCERE01[19] or pBCE4810.[20] Plasmid pBCE4810 shares homology with the Bacillus anthracis virulence plasmid pXO1, which encodes the anthrax toxin. Periodontal isolates of B. cereus also possess distinct pXO1-like plasmids. Like most of cyclic peptides containing nonproteogenic amino acids, cereulid is resistant to heat, proteolysis, and acid conditions.[21]

B. cereus is also known to cause difficult-to-eradicate chronic skin infections, though less aggressive than necrotizing fasciitis. B. cereus can also cause keratitis.[22]

Diagnosis

In case of foodborne illness, the diagnosis of B. cereus can be confirmed by the isolation of more than 105 B. cereus organisms per gram from epidemiologically implicated food, but such testing is often not done because the illness is relatively harmless and usually self-limiting.[23]

Prognosis

Most emetic patients recover within six to 24 hours,[15] but in some cases, the toxin can be fatal.[24][25][26][27][28] In 2014, 23 neonates receiving total parenteral nutrition contaminated with B. cereus developed septicaemia, with three of the infants later dying as a result of infection. [29][30]

References

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  23. Bacillus cereus Food Poisoning Associated with Fried Rice at Two Child Day Care Centers from Morbidity and Mortality Weekly Report from Centers for Disease Control and Prevention. 18 March 1994 / Vol. 43 / No. 10 U.S.
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  29. Lipid Phase only of Parenteral Nutrition - potential contamination with Bacillus cereus Medical safety alert - GOV.UK
  30. Third baby dies from contaminated 'Total Parenteral Nutrition' drip feed | Health News | Lifestyle | The Independent

External links