It's so easy to avoid this ya'll. I believe it's starch products. A family got super sick after eating some pasta salad that was left out.
Bacillus cereus is a well-known cause of food-borne illness, but infection with this organism is not commonly reported because of its usually mild symptoms. A fatal case due to liver failure after the consumption of pasta salad is described and ...
pmc.ncbi.nlm.nih.gov
Fatal Family Outbreak of Bacillus cereus-Associated Food Poisoning
In August 2003, five children of a family became sick after eating pasta salad. The pasta salad was prepared on a Friday and taken to a picnic on the following Saturday; the remainders had been stored in the fridge until the following Monday evening, when they were served for supper to the children. Because the pasta salad had an unusual smell, three children (B14, G10, and G9) ate only a small quantity. At 6 h after the meal the youngest girl (G7), 7 years old, started vomiting. She complained of respiratory distress and was taken to the emergency department of a local hospital. Upon arrival, her brothers and sisters started vomiting as well. Because the clinical condition of two children (G7 and B9) deteriorated rapidly, they were intubated and mechanically ventilated. All children were transported to the University Hospital in Leuven. During transfer, G7 had severe pulmonary hemorrhage and needed continuous resuscitation. Upon arrival she was moribund with coma, diffuse bleeding, and severe muscle cramps. She died within 20 min, at 13 h after the meal. On autopsy
Bacillus cereus was detected in her gut content but also in the spleen, probably by postmortem translocation of the bacterium. A postmortem liver biopsy showed microvascular and extensive coagulation necrosis. Her initial laboratory values showed severe metabolic acidosis and liver failure. All four other children were affected, although to different degrees (Table
1). The 9-year-old boy (B9) was transferred to the pediatric intensive care unit, where mechanical ventilation and invasive hemodynamic monitoring were continued. After fluid resuscitation, his blood lactate levels gradually went down. Basic treatment for liver failure consisted of vitamin K supplementation, oral and rectal lactulose, oral neomycin, and high-dose acetylcysteine. At 24 h after the start of the treatment his aspartate transaminase and alanine transaminase levels peaked at 12,254 U/liter and 8,656 U/liter, respectively; his prothrombin time went down to 21.5%. Thereafter, the hepatic function recovered. He gradually recovered consciousness, and he was successfully extubated. Two sisters (G9 and G10) were treated with fluid resuscitation and bicarbonate substitution. Both gradually recovered. The 14-year-old brother (B14) was kept under observation. Subsequent blood samples showed no deterioration of hepatic function. The surviving children could leave the hospital within 8 days.