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Investigating the Alleviating Effects of Bacillus cereus Administration on Colitis through Gut Microbiota Modulation
Published on: July 27, 2022
Liver failure after Bacillus cereus food poisoning, an under-recognized entity: A case report
Olivier Chatelanat1, Mikaël de Lorenzi-Tognon2, Laurent Spahr3
1Department of Gastroenterology and Hepatology, Geneva University Hospitals, Geneva 1205, Switzerland. olivier.chatelanat@gmail.com.
Background:
Bacillus cereus (B. cereus) is known to cause 2 types of foodborne diseases; the diarrheal and emetic syndromes. They are largely underreported due to their usually self-limiting course. Rare and sometimes fatal cases of liver failure, pulmonary hemorrhage and cerebral oedema have been reported mainly in children and young adults. We present here a case of liver failure associated with B. cereus food poisoning in a middle-aged patient.
Case Summary:
A 48-year-old female patient presented to the emergency department for emesis, diarrhea, chills without fever, asthenia and diffuse abdominal cramps that started less than 30 minutes after eating a rice salad. Her past medical history was relevant for cholecystectomy and a cured Hashimoto's disease. She did not take any medication, drugs and declared a consumption of one glass of wine per week. In the emergency department, she was treated with acetaminophen, metoclopramide, ondansetron, and an intravenous normal saline infusion. Blood gas analysis revealed a metabolic acidosis with hyperlactatemia, coagulation revealed a low prothrombin activity [32 %; normal values (N): 70-140] and a low Factor V activity (15%; N: > 70). Transaminases were elevated with hyperbilirubinemia, elevated lipase and rhabdomyolysis. N-acetylcysteine treatment was introduced. Abdominal echography revealed no signs of chronic hepatopathy or hepatomegaly. Day after the admission, psychomotor activity improved, transaminases and lipase started decreasing. Rhabdomyolysis gradually worsened to peak on day 3. Screening tests for liver disease were negative for viral and autoimmune cause of liver failure. Stools cultures were positive for colonies of the B. cereus group which were also identified in the rice salad samples processed whereas blood cultures were negative. The patient's condition improved gradually including her liver function parameters and psychomotor activity which allowed her discharged home on day 9.
Conclusion:
We describe a rare case of hepatocellular dysfunction due to a foodborne B. cereus intoxication in an adult patient. Even if it is uncommon, the severity of liver dysfunction reported and mechanism of the cereulide toxin toxicity on liver suggest that acetaminophen should be avoided in case of a foodborne intoxication and n-acetylcysteine could be a potential therapy helping to prevent hepatocytes necrosis due to the oxidative stress induced by mitochondrial dysfunction.
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