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[Intestinal flora of patients with suspected antibiotic associated diarrhea (AAD). I. Clostridium perfringens]

H Pituch1, G Martirosian, P Obuch-Woszczatyński

  • 1Katedra i Zakład Mikrobiologii Lekarskiej AM w Warszawie.

Medycyna Doswiadczalna I Mikrobiologia
|April 5, 2001
PubMed

Insights

Clostridium difficile toxin A was detected in 35 patients with antibiotic-associated diarrhea (AAD). Clostridium perfringens enterotoxin genes were not found, suggesting C. difficile as a primary cause of AAD in this cohort.

Area of Science:

  • Microbiology
  • Gastroenterology
  • Infectious Diseases

Background:

  • Antibiotic-associated diarrhea (AAD) is a common complication of antibiotic use.
  • Clostridium difficile and Clostridium perfringens are known bacterial causes of gastrointestinal infections.
  • Accurate diagnosis of AAD requires identification of specific causative agents and toxins.

Purpose of the Study:

  • To investigate the prevalence of Clostridium difficile toxin A and Clostridium perfringens enterotoxin in patients with suspected AAD.
  • To compare the diagnostic utility of immunoenzymatic assays and PCR for detecting these pathogens.
  • To determine the etiological role of C. difficile and C. perfringens in AAD cases.

Main Methods:

  • Stool samples from 158 patients with suspected AAD were analyzed.
  • Immunoenzymatic assays and PCR were used to detect Clostridium difficile toxin A.
  • PCR with specific primers (ent 1 and ent 2) was employed to detect the Clostridium perfringens enterotoxin gene (cpe).
  • Bacterial cultures were performed to isolate C. difficile and C. perfringens strains.

Main Results:

  • Clostridium difficile toxin A was detected in 35 stool samples (22%).
  • C. difficile strains were cultured from 48 cases (30%), with 21 isolates (13%) confirmed positive for toxin A.
  • The Clostridium perfringens enterotoxin gene (cpe) was not detected in any stool samples or isolated strains.
  • C. difficile and C. perfringens were co-isolated from 4 patients.
  • Clostridium perfringens strains with thermoresistant spores were identified in two AAD patients.

Conclusions:

  • Clostridium difficile toxin A appears to be a significant causative agent of AAD in the studied population.
  • The absence of detectable Clostridium perfringens enterotoxin genes suggests it played a minimal role in these AAD cases.
  • Further investigation into the role of C. perfringens, particularly non-toxigenic strains or other toxins, in AAD may be warranted.

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