1) The emetic toxin, referred to as cereulide, has a ring structure which consists of 4 amino and/or oxy acids (Granum & Lund, 1997). The cereulide toxin is most likely to cause serious illness, and is resistant to heat, pH, and proteolysis, but is not considered antigenic (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
2) Hemolysin BL, nonhemolytic enterotoxin, and cytotoxin K are 3 enterotoxins that have been identified as causing diarrheal type outbreaks in Bacillus cereus poisoning (Stenfors Arnesen et al, 2008). These toxins are produced in the small intestine of the host and thought to work synergistically, causing fluid accumulation, membrane destabilization, and cytotoxicity (Stenfors Arnesen et al, 2008; Granum & Lund, 1997).

1) DIARRHEAL SYNDROME is most frequently associated with meat products, soups, vegetables, puddings/sauces, and milk/milk products (Stenfors Arnesen et al, 2008; Granum & Lund, 1997). In Brazil, it was associated with roasted commercial coffee (Chaves et al, 2012).
2) EMETIC SYNDROME is associated with fried and cooked rice, pasta, pastry, and noodles (Delbrassinne et al, 2015; Stenfors Arnesen et al, 2008; Granum & Lund, 1997). In the United States, fried rice is the leading cause of bacillus cereus emetic type food poisoning (Center for Food Safety and Applied Nutrition (CFSAN), 2009). Bacillus cereus is frequently found in uncooked rice and heat resistant spores may survive cooking. If the rice is allowed to be held at room temperature a heat-stable toxin can be produced (Terranova & Blake, 1978).

1) ROASTED COFFEE: In a study investigating the occurrence of Bacillus species in roasted commercial coffee in Brazil, B. cereus was detected in 17 out of 30 (56.7%) coffee samples from 10 different brands. Analysis showed that genes encoding enterotoxins were widely distributed among the B. cereus strains detected in the samples. Nonhemolytic enterotoxin (NHE) was detected in 19 (76%) strains and hemolysin BL (HBL ) enterotoxin in 16 (64%) strains. Diarrheal symptoms have been associated with the presence of enterotoxins and enterotoxins NHE and HBL specifically have been linked to virulence in cases of food poisoning. Factors that may have contributed to the presence of B. cereus in the coffee samples included the addition of sugar and storage in thermic containers, contamination during packaging, and low roasting temperatures (Chaves et al, 2012).

a) Bacillus cereus forms 2 types of foodborne illness.
b) EMETIC SYNDROME: Nausea, vomiting, and general malaise. Rare reports of liver damage leading to death have occurred.
c) DIARRHEAL SYNDROME: Abdominal pain and watery diarrhea. Nausea may also occur. Liver damage is a rare event.

a) Infections with Bacillus cereus are self-limiting and do not exhibit chronic complications.

a) Bacillus cereus emetic-type outbreaks are most commonly caused by starch-rich foods (eg, fried or cooked rice, pasta, pastries, or noodles) and diarrheal-type outbreaks are caused by proteinaceous foods (ie, meat products, milk or milk products), soups, vegetables, puddings, and sauces.

a) EMETIC SYNDROME: 0.5 to 6 hours after ingestion.
b) DIARRHEAL SYNDROME: 6 to 15 hours after ingestion.

a) EMETIC SYNDROME: 6 to 24 hours.
b) DIARRHEAL SYNDROME: 12 to 24 hours (rarely infection can last several days).

a) EMESIS SYNDROME: Onset: 0.5 to 6 hours. Duration: 6 to 24 hours.
b) DIARRHEAL SYNDROME: Onset: 8 to 16 hours (rarely up to 24 hours). Duration: 12 to 24 hours (rarely several days).

a) CASE REPORT: A 7-year-old girl developed pulmonary hemorrhage and diffuse bleeding associated with fulminant hepatic failure and coagulopathy, and died 13 hours after eating a food contaminated with Bacillus cereus (Dierick et al, 2005).

a) SUMMARY: B. cereus forms 2 types of foodborne illness: an emetic syndrome (nausea, vomiting, and malaise) which resembles Staphylococcus aureus with an incubation of 0.5 to 6 hours or a diarrheal syndrome (abdominal pain, watery diarrhea, and occasionally nausea) with an incubation period of 6 to 15 hours and resembles Clostridium perfringens (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Stenfors Arnesen et al, 2008).
b) INCIDENCE: In general, B. cereus foodborne illness is under reported worldwide. In the Netherlands between 1993 and 1998, B. cereus was responsible for 12% of foodborne disease outbreaks when an organism was identified (Stenfors Arnesen et al, 2008).

a) Cereulide is a cyclic peptide toxin that causes an emetic syndrome and appears to be resistant to acid conditions, proteolysis and heat and, thus not easily destroyed by gastric acid, proteolytic enzymes and reheating of food (Stenfors Arnesen et al, 2008; Dierick et al, 2005; CDC, 1994; Granum & Lund, 1997). The toxin causing emetic effects is produced while the B. cereus multiplies in foods (Granum & Lund, 1997).
b) CASE SERIES: In a B. cereus food poisoning outbreak at 2 daycare centers, nausea (71%) was the most common symptom reported, along with abdominal cramps/pain (36%), and diarrhea (14%). The incubation period was approximately 2 hours with a median resolution of symptoms at 4 hours (range 1.5 to 22 hours) (CDC, 1994).
c) CASE REPORT/FATALITY: A healthy 20-year-old man experienced an episode of severe vomiting followed by diarrhea and died approximately 10 hours after eating a meal contaminated with B. cereus. After arriving home from school, he reheated and ate a meal of spaghetti with tomato sauce that had been left at room temperature for 5 days. Approximately 30 minutes later he reported a headache, abdominal pain, and nausea, which was followed by severe vomiting persisting for several hours. He went to sleep at midnight after 2 episodes of watery diarrhea and was found dead at 11:00 am the next morning. The determined time of death was 4:00 am. Autopsy was delayed for 5 days rendering results inconclusive; however, 2 of 5 postmortem fecal swabs were positive for B. cereus (strains: ISP321, ISP322). Upon further analysis, high (9.5 x 10(7) CFU/g) counts of B. cereus (strain ISP303) were isolated in the leftover pasta but no B. cereus was isolated in the tomato sauce. According to polymerase chain reaction test results, all 3 B. cereus isolates were emetic strains (Naranjo et al, 2011).
d) CASE SERIES/PEDIATRIC: Vomiting occurred in 20 of 22 children (ages from 10 months to 1.5 years) within 30 minutes after consuming a cooked rice, cucumber, and chicory meal suspected to be contaminated with B. cereus. All of the children recovered within a few hours. Analysis of the leftovers detected B. cereus counts greater than 15,000,000 colony-forming units/g and cereulide toxin ranging from 3.1 to 4.2 mcg/g (Delbrassinne et al, 2015).

a) SUMMARY: Hemolysin BL, nonhemolytic enterotoxin, and cytotoxin K are the 3 protein enterotoxins that cause a diarrheal type illness from B. cereus food poisoning (Stenfors Arnesen et al, 2008; CDC, 1994; Granum & Lund, 1997). The diarrheal toxin is produced in the small intestine of the host and thought to work synergistically, causing fluid accumulation, membrane destabilization, and cytotoxicity (Stenfors Arnesen et al, 2008; Granum & Lund, 1997).
b) CASE SERIES: In an outbreak reported at 2 daycare centers, diarrhea was reported by 14% of adults and children exposed . The average incubation period was 2 hours. All symptoms resolved at a median time of 4 hours (range 1.5 to 22 hours) after onset (CDC, 1994).
c) CASE REPORT/FATALITY: A healthy 20-year-old man experienced an episode of severe vomiting followed by diarrhea and died approximately 10 hours after eating a meal contaminated with B. cereus. After arriving home from school, he reheated and ate a meal of spaghetti with tomato sauce that had been left at room temperature for 5 days. Approximately 30 minutes later he reported a headache, abdominal pain, and nausea, which was followed by severe vomiting persisting for several hours. He went to sleep at midnight after 2 episodes of watery diarrhea and was found dead at 11:00 am the next morning. The determined time of death was 4:00 am. Autopsy was delayed for 5 days rendering results inconclusive; however, 2 of 5 postmortem fecal swabs were positive for B. cereus (strains: ISP321, ISP322). Upon further analysis, high (9.5 x 10(7) CFU/g) counts of B. cereus (strain ISP303) were isolated in the leftover pasta but no B. cereus was isolated in the tomato sauce. According to polymerase chain reaction test results, all 3 B. cereus isolates were emetic strains (Naranjo et al, 2011).

a) CASE REPORT: A 9-year-old girl developed fulminant hepatitis 18 hours after eating pasta with a sauce that was prepared 48 hours before ingestion. Two hours after eating, the girl experienced severe abdominal pain, emesis, and nonbloody diarrhea without fever. Six hours after ingestion the girl developed tonic-clonic seizures lasting 30 minutes. On arrival to the hospital, the girl was bradycardic, hypotensive, and without spontaneous breathing. She had severe hypoglycemia (blood glucose 1 mmol/L) and her liver enzymes revealed an AST of 14,622 units/L, an ALT of 9018 units/L, and a prothrombin time of 26%. The girl was started on vasopressor and antibiotic therapy for 48 hours. She was weaned once symptoms resolved and normalized all function approximately 1 week after hospitalization. A positive identification of Bacillus cereus was made from cultures of the leftover food(Posfay-Barbe et al, 2008).
b) CASE REPORTS/FAMILY OUTBREAK: An outbreak of Bacillus cereus food poisoning occurred in a family of 5 siblings, in which the youngest sibling (a 7-year-old girl) died 13 hours after eating the implicated food. Initial laboratory tests indicated severe metabolic acidosis and liver failure. At autopsy, extensive liver coagulation necrosis was observed. A 9-year-old boy also developed fulminant hepatic failure (peak AST and ALT 12,254 units/L and 8,656 units/L, respectively), but he responded to aggressive therapy and recovered completely (Dierick et al, 2005).
c) CASE REPORT: Fulminant liver failure developed in a 17-year-old boy following food contaminated with Bacillus cereus emetic toxin. Death occurred within 24 hours of hospitalization. At autopsy B. cereus was cultured from the liver and bile which caused hepatic mitochondrial fatty-acid oxidation. Of note, the patient's father had eaten the same meal, but consumed less food and developed reversible hepatic injury (Mahler et al, 1997).
d) CASE REPORT: A 15-year-old boy presented with evidence of fulminant liver failure. Approximately 30 hours prior to admission, the patient experienced acute abdominal pain and vomiting, with blood observed in his vomit the next day. Initial laboratory data, at ICU admission, revealed elevated liver enzymes (ALT 4823 international units/L and AST 3729 international units/L), serum bilirubin of 42 mcmol/L, a creatine kinase concentration of 12, 592 international units/L, lactic acidosis (pH 7.41, bicarbonate 20 mmol/L, and lactate 5.4 mmol/L) a prothrombin ratio of 21%, a factor V of 23%, and a factor II of 34%. A thoracoabdominal CT scan indicated non-specific hepatomegaly. Over the next several hours, the patient became comatose and an emergent liver transplantation was scheduled. Profuse nonbloody diarrhea and fever developed within 2 days post-admission; stool was sent for analysis. Blood cultures were positive for Klebsiella pneumoniae and Enterobacter cloacae, attributed to intestinal translocation, and the patient was started on IV antibiotic therapy. Following antibiotic therapy, the patient improved neurologically, with resolution of his hepatic abnormalities. History from the patient indicated that he had consumed pasta 4 hours prior to onset of symptoms. The pasta had been cooked 4 days before consumption and had been refrigerated, but appeared to have an abnormal taste and smell. Stool cultures were positive for Bacillus cereus, suggesting that the patient's hepatotoxicity was due to a foodborne illness (Saleh et al, 2012).
e) CASE REPORT: A 13-month-old boy presented with vomiting, abdominal pain, and somnolence approximately 6 hours after ingesting a 2-day-old rice meal that had been refrigerated. The child's vomiting began approximately 2 hours after ingestion of the meal. At admission, laboratory analysis revealed lactic acidosis and an elevated INR, but liver enzymes were normal. Four hours after admission, the patient was transferred to another healthcare facility, presenting with somnolence (Glasgow Coma Scale of 6), tachycardia (170 beats/min), hypotension (79/21 mmHg), and tachypnea (30 breaths/min). Laboratory data revealed liver failure (peak ALT 20,223 units/L and peak AST 38,811 units/L 20 and 25 hours after first admission, respectively), severe rhabdomyolysis, hyperammonemia, and renal failure with severe hyperkalemia. Despite treatment with continuous veno-venous hemodialysis and plasmapheresis, the patient's hyperammonemia and hyperkalemia could not be controlled, and he underwent emergent hepatectomy and liver transplantation approximately 30 hours following admission. Following transplantation, the patient's liver and kidney function normalized. There was no evidence of brain dysfunction, and the patient was discharged for rehabilitation as a quadriplegic and continued on mechanical ventilation. Testing of a rice grain from the child's vomit, 2 weeks following admission, determined the presence of Bacillus cereus positive for cereulide production. At the 1-year post-transplantation follow-up, the patient was breathing on his own, with continued normal liver and kidney function. He was still unable to walk; however, there was no evidence of mental deficits (Tschiedel et al, 2015).

a) CASE REPORT: Acute renal failure with severe hyperkalemia (peak serum creatinine and potassium concentrations of 95 mcmol/L and 7.6 mmol/L, respectively), severe rhabdomyolysis, and acute liver failure developed in a 13-month-old boy following ingestion of a rice meal subsequently determined to contain Bacillus cereus that was positive for cereulide. Following emergent hepatectomy and liver transplantation as well as continuous venovenous hemodialysis, the patient's condition gradually improved with normalization of potassium concentration and kidney function (Tschiedel et al, 2015).

a) CASE REPORT: A 7-year-old girl developed severe pulmonary hemorrhage and diffuse bleeding associated with coagulopathy and fulminant hepatic failure, and died 13 hours after eating a food contaminated with B. cereus, despite aggressive care (Dierick et al, 2005).

a) RABBIT STUDIES: Animal studies indicated that the B. cereus enterotoxin can affect the capillaries of blood vessels locally and systemically (Singh et al, 1992). The enterotoxin was able to produce vascular permeability at the injection site and hemorrhage in the ligated ileal loops of the rabbits (Stenfors Arnesen et al, 2008).

a) CASE REPORT: An adult exposed to Bacillus cereus contaminated food developed rhabdomyolysis (CK 1920 units/L) along with elevated liver enzymes; laboratory values were within normal limits 2 weeks after the ingestion (Mahler et al, 1997).
b) CASE REPORT: A 15-year-old boy developed rhabdomyolysis (CK 12,592 International Units/L) and fulminant liver failure following consumption of pasta suspected to be contaminated with Bacillus cereus. The patient recovered with IV antibiotic therapy (Saleh et al, 2012).
c) CASE REPORT: A 13-month-old boy developed severe rhabdomyolysis (peak CK 389,355 Units/L) as well as kidney failure with hyperkalemia and fulminant liver failure, after ingesting a 2-day-old rice meal contaminated with Bacillus cereus that had been refrigerated. The patient gradually recovered with normalization of liver and kidney function following emergent hepatectomy and liver transplantation as well as continuous venovenous hemodialysis (Tschiedel et al, 2015).

a) Bacillus cereus may mimic other forms of food poisoning. Diagnosis can be confirmed by detecting 10(6) organisms/g of food (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Haddad et al, 1998).
b) Vomitus and stool cultures have not generally been useful as aids in diagnosis of food poisoning from Bacillus cereus due to the short course of illness.