Clostridium difficile typhlitis associated with cecal mucosal hyperplasia in Syrian hamsters. Academic Article uri icon

Overview

abstract

  • A sudden increase in mortality occurred in a closed breeding colony of Syrian hamsters (Mesocricetus auratus). The colony consisted of approximately 40 hamsters, 8 of which were affected. Four adult males died suddenly. One pregnant female and one weanling died after having been observed as depressed for 1 day and 2 weeks respectively. One weanling and one adult male were euthanized. All affected hamsters had signs of diarrhea. At necropsy, hemorrhagic fluid-filled ceca were noted in five of eight animals. Clostridium difficile cytotoxin B was present in high titers [10(-3) to 10(-8)] in cecal contents of six of six animals tested, whereas C. difficile culture yielded positive results in only one of six animals. Histopathologically, findings consistent with Clostridium-induced typhlitis including necrosis, epithelial denudation, vascular congestion, and hemorrhage were present in six of six ceca evaluated. In addition, signs of a more chronic disease process included cecal mucosal hyperplasia in five of six hamsters. A silver stain of cecal hyperplastic mucosa for intracellular organisms including Campylobacter-like organisms was negative in all affected hamsters. Antibiotics had not been administrated to any hamster in this colony, nor had the affected animals been experimentally manipulated. Testing for antibiotic residues in the feed was negative, and C. difficile was not isolated from feed, water, or feces of unaffected hamsters. Thus C. difficile-induced typhlitis should be included in the differential diagnosis of deaths in hamsters which have no clinical histories of prior antibiotic administration or experimental manipulation.(ABSTRACT TRUNCATED AT 250 WORDS)

publication date

  • December 1, 1991

Research

keywords

  • Bacterial Proteins
  • Enterocolitis, Pseudomembranous
  • Mesocricetus

Identity

Scopus Document Identifier

  • 0026347632

PubMed ID

  • 1667196

Additional Document Info

volume

  • 41

issue

  • 6