The 131st Annual Meeting (November 15-19, 2003) of APHA

Abstract #69736

John. E Bos, MPH¹, Lauri Smithee, MES, MS¹, Ron F Distefano, DO², Bruce McClane, PhD³, Mike McDermott, BS⁴, and Mike Crutcher, MD, MPH¹. (1) Communicable Disease Division, Oklahoma State Dept of Health, 1000 NE 10th St, Oklahoma City, OK 73117-1299, 405-271-4060, johneb@health.state.ok.us, (2) Oklahma Office of the Chief Medical Examiner, 1115 W 17th St, Tulsa, OK 74107, (3) School of Medicine, University of Pittsburgh, E 1240 BSTWR, Pittsburgh, PA 15261, (4) Public Health Laboratory, Oklahoma State Dept of Health, 1000 NE 10th St, Oklahoma City, OK 73117-1299

Background: Clostridium perfringens type A (C. perfringens) is a major cause of foodborne disease outbreaks in the US. On November 24, 2001, a rural Oklahoma hospital reported three cases, two fatal, of severe acute gastroenteritis. Reported cases resided in a facility for the mentally ill. We investigated to determine the cause and source of disease. Methods: We conducted chart reviews of severe cases, environmental inspections, and a retrospective cohort study. Autopsies of the deceased were performed, and specimens were submitted for testing. Testing for the presence and production of C. perfringens enterotoxin (CPE) included the Oxoid CPE detection kit, Western blot, and multiplex PCR. Results: We identified 7 cases (3 confirmed, 4 probable) among 20 residents and staff with illness consistent with C. perfringens following consumption of high risk foods. Three severe cases developed bowel necrosis, resulting in 2 deaths. CPE was detected in stool specimens from all confirmed cases. C. perfringens isolates from these specimens were confirmed to carry the toxin producing genes and the ability to produce CPE. Each severe case received daily, multi-drug therapy for mental illness and presented with evidence of constipation and fecal impactions. Conclusion: Evidence suggests adverse effects of medications used to treat mental illness exacerbated a typically mild foodborne disease. Drug induced fecal impactions prevented the usual expedient passage of CPE through the colon. We believe the severe necrosis resulted from prolonged exposure of CPE to intestinal tissue.

Learning Objectives:

At the conclusion of this session, the participant will be able to:
• recognize the potential for severe disease from C. perfringens type A foodborne disease;
• discuss the necessity for close monitoring of the adverse effects of psychotropic drugs; and
• identify the difficulties of investigating a foodborne disease outbreaks among a mentally ill cohort.

Keywords: Epidemiology, Outbreaks

Presenting author's disclosure statement:
I do not have any significant financial interest/arrangement or affiliation with any organization/institution whose products or services are being discussed in this session.