The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Original Article
PreviousPrevious
Volume 336:1142-1148 April 17, 1997 Number 16
NextNext

Fulminant Liver Failure in Association with the Emetic Toxin of Bacillus cereus
Hellmut Mahler, Ph.D., Aurelio Pasi, M.D., John M. Kramer, B.Sc., Petra Schulte, Grad.Eng., Anne C. Scoging, B.Sc., Walter Bär, M.D., and Stephan Krähenbühl, M.D., Pharm.D.

 Sign up for free e-toc
 

This Article
-Full Text
- PDF

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation
ABSTRACT

Background A 17-year-old boy and his father had acute gastroenteritis after eating spaghetti and pesto that had been prepared four days earlier. Within two days, fulminant liver failure and rhabdomyolysis developed in the boy and he died. The father had hyperbilirubinemia and rhabdomyolysis but recovered. We investigated the cause of these illnesses.

Methods Bacteria were isolated and characterized by conventional methods, and bacterial toxins were quantified by immunoassays and cell-culture techniques. The effect of the isolated toxin on the rates of oxidation of various substrates was analyzed in rat-liver mitochondria.

Results Autopsy of the boy's liver revealed diffuse microvesicular steatosis and midzonal necrosis that suggested impaired {beta}-oxidation of liver mitochondria due to a mitochondrial toxin. There was no evidence of ingestion of heavy metals, halogenated compounds, hepatotoxic drugs, or staphylococcal enterotoxin. However, high concentrations of Bacillus cereus emetic toxin were found both in the residue from the pan used to reheat the food and in the boy's liver and bile. B. cereus was cultured from the intestinal contents and the pan residue. The emetic toxin isolated from the B. cereus cultures was found to be a mitochondrial toxin.

Conclusions Fulminant liver failure developed after the ingestion of food contaminated with the B. cereus emetic toxin. The toxin inhibits hepatic mitochondrial fatty-acid oxidation, indicating that it caused liver failure in this patient.


Source Information

From Endorphin Research Laboratories, Group of Medical Toxicology, Institute of Legal Medicine, University of Zurich, Zurich, Switzerland (H.M., A.P., P.S., W.B.); the Institute of Legal Medicine, Heinrich Heine University of Düsseldorf, Düsseldorf, Germany (H.M.); the Food Hygiene Laboratory, Central Public Health Laboratory, London (J.M.K., A.C.S.); and the Division of Clinical Pharmacology and Toxicology, Department of Internal Medicine, University Hospital of Zurich, Zurich, Switzerland (S.K.).

Address reprint requests to Dr. Pasi at the Institute of Legal Medicine, University of Zurich, CH-8057 Zurich, Switzerland.

Full Text of this Article


This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.