ANALYTICAL CLINICAL STUDIES
Detection of A/B toxin and isolation of Clostridium difficile and Clostridium perfringens from foals
Article first published online: 3 MAR 2013
© 2013 EVJ Ltd
Equine Veterinary Journal
Volume 45, Issue 6, pages 671–675, November 2013
How to Cite
Silva, R. O. S., Ribeiro, M. G., Palhares, M. S., Borges, A. S., Maranhão, R. P. A., Silva, M. X., Lucas, T. M., Olivo, G. and Lobato, F. C. F. (2013), Detection of A/B toxin and isolation of Clostridium difficile and Clostridium perfringens from foals. Equine Veterinary Journal, 45: 671–675. doi: 10.1111/evj.12046
- Issue published online: 14 OCT 2013
- Article first published online: 3 MAR 2013
- Accepted manuscript online: 11 JAN 2013 08:18AM EST
- Manuscript Accepted: 29 DEC 2012
- Manuscript Received: 21 JUL 2012
- nosocomial diarrhoea;
- A/B toxins
Reasons for performing the study
Toxin detection and screening could contribute to knowledge of the transmission patterns, risk factors and epidemiology of Clostridium difficile and Clostridium perfringens.
To isolate C. difficile and C. perfringens and to detect A/B toxins in faecal samples from diarrhoeic and nondiarrhoeic foals.
Cross-sectional observational study.
A total of 153 samples from foals were collected: 139 samples from farms and 14 samples from diarrhoeic foals admitted to a veterinary hospital. The A/B toxins were detected by cytotoxicity assay. All suspected colonies of C. perfringens were subjected to polymerase chain reaction for detection of the major toxin genes (α, β, ε and ι) and for detection of β2-, NetB- and enterotoxin-encoding genes. Furthermore, C. difficile and C. perfringens isolates were evaluated for in vitro antimicrobial susceptibility.
Seven of 153 (4.6%) samples, all from diarrhoeic foals, were positive for C. difficile A/B toxin. Of these, 5 of 14 (35.7%) were from hospitalised foals, and only 2 of 63 (3.2%) diarrhoeic foal samples were from farms (P = 0.002). Clostridium perfringens was isolated from 31 (20.3%) foals, of which 21 of 76 (27.6%) were diarrhoeic and 10 of 76 (13.2%) were nondiarrhoeic, demonstrating a difference between these 2 groups (P = 0.045). Only 4 strains were positive for the β2-encoding gene (cpb2). All C. difficile and C. perfringens isolates were susceptible to metronidazole and vancomycin.
The present report highlights the need for laboratory diagnostics to differentiate C. difficile-associated infection in foals from other causes of diarrhoea to facilitate adequate antimicrobial therapy.
More studies are needed to clarify the role of C. perfringens as a primary agent of diarrhoea in foals.