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Equine colitis X associated with infection by Clostridium difficile NAP1/027.

Abstract: A 14-year-old Quarter Horse with a 48-hr history of colic was euthanized after failure to respond to treatment. At necropsy, cecal and colonic mucosae were congested throughout, and there was segmental edema and significant thickening of the intestinal wall. Excessive numbers of mononuclear cells were found in mucosal lamina propria. Submucosal hemorrhage was diffuse and extensive, and Clostridium difficile toxins A and B were detected. Large numbers of C. difficile were isolated, and genetic characterization revealed them to be North American pulsed-field gel electrophoresis type 1, polymerase chain reaction ribotype 027, and toxinotype III. Genes for the binary toxin were present, and toxin negative-regulator tcdC contained an 18-bp deletion. This genotype comprises the current human "epidemic strain," which is associated with human C. difficile-associated disease of greater than historical severity. The diagnosis was peracute typhlocolitis, with lesions and history typical of those attributed to colitis X.
Publication Date: 2009-05-02 PubMed ID: 19407094DOI: 10.1177/104063870902100314Google Scholar: Lookup
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Summary

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This research article presents the case of a 14-year-old Quarter Horse which developed severe colitis linked to infection by a specific strain of Clostridium difficile (C. difficile). This strain is similar to one known for causing severe disease in humans.

Background

  • The study revolves around a 14-year-old Quarter Horse that fell ill over two days, showing symptoms of colic—an extremely painful digestive disorder. Despite treatment, the horse did not respond and was later euthanized (put to sleep to prevent further suffering).
  • Postmortem examinations showed multiple symptoms, including congestion of cecal and colonic mucosae, edema, substantial thickening of the intestinal wall, excessive mononuclear cells in the mucosal lamina propria, and extensive submucosal hemorrhage.

Findings

  • The researchers identified the presence of toxins A and B from Clostridium difficile in the horse’s system, suggesting that this bacterium was responsible for the illness.
  • Using genetic analysis, the researchers isolated large numbers of C. difficile and identified them to be a very specific kind: North American pulsed-field gel electrophoresis type 1, polymerase chain reaction ribotype 027, and toxinotype III.
  • This strain of bacteria was found to possess the genes necessary to produce a binary toxin, and also contained a particular deletion in the tcdC gene—anegative-regulator of toxin production. This genetic characteristic could have contributed to the severity of the infection.

Implications

  • This strain of bacterial infection has been recognized as the ‘epidemic strain’ in human medicine due to its association with severe Clostridium difficile-associated disease. Hence, the findings suggest the horse had developed a severe, acute form of typhlocolitis, commonly referred to as colitis X.
  • The study raises concerns about potential cross-species infections, as this severe C. difficile strain appears to be harmful to horses as well as humans.
  • More research is needed to understand the prevalence of this strain in equine populations, its potential transmission routes, and suitable prevention or treatment strategies.

Cite This Article

APA
Songer JG, Trinh HT, Dial SM, Brazier JS, Glock RD. (2009). Equine colitis X associated with infection by Clostridium difficile NAP1/027. J Vet Diagn Invest, 21(3), 377-380. https://doi.org/10.1177/104063870902100314

Publication

ISSN: 1040-6387
NlmUniqueID: 9011490
Country: United States
Language: English
Volume: 21
Issue: 3
Pages: 377-380

Researcher Affiliations

Songer, J Glenn
  • Department of Veterinary Science and Microbiology, 1117 East Lowell Street, The University of Arizona, Tucson, AZ 85721, USA. gsonger@u.arizona.edu
Trinh, H T
    Dial, Sharon M
      Brazier, Jon S
        Glock, Robert D

          MeSH Terms

          • Animals
          • Clostridioides difficile / classification
          • Clostridium Infections / microbiology
          • Clostridium Infections / pathology
          • Clostridium Infections / veterinary
          • Colitis / microbiology
          • Colitis / pathology
          • Colitis / veterinary
          • Enteritis / microbiology
          • Enteritis / veterinary
          • Horse Diseases / microbiology
          • Horse Diseases / pathology
          • Horses

          Citations

          This article has been cited 6 times.
          1. Uchida-Fujii E, Niwa H, Senoh M, Kato H, Kinoshita Y, Mita H, Ueno T. Clostridioides difficile infection in thoroughbred horses in Japan from 2010 to 2021. Sci Rep 2023 Aug 11;13(1):13099.
            doi: 10.1038/s41598-023-40157-xpubmed: 37567893google scholar: lookup
          2. Hain-Saunders NMR, Knight DR, Bruce M, Riley TV. Clostridioides difficile infection and One Health: an equine perspective. Environ Microbiol 2022 Mar;24(3):985-997.
            doi: 10.1111/1462-2920.15898pubmed: 35001483google scholar: lookup
          3. Uzal FA, Diab SS. Gastritis, Enteritis, and Colitis in Horses. Vet Clin North Am Equine Pract 2015 Aug;31(2):337-58.
            doi: 10.1016/j.cveq.2015.04.006pubmed: 26048413google scholar: lookup
          4. Gerding DN, Johnson S, Rupnik M, Aktories K. Clostridium difficile binary toxin CDT: mechanism, epidemiology, and potential clinical importance. Gut Microbes 2014 Jan-Feb;5(1):15-27.
            doi: 10.4161/gmic.26854pubmed: 24253566google scholar: lookup
          5. Freeman J, Bauer MP, Baines SD, Corver J, Fawley WN, Goorhuis B, Kuijper EJ, Wilcox MH. The changing epidemiology of Clostridium difficile infections. Clin Microbiol Rev 2010 Jul;23(3):529-49.
            doi: 10.1128/CMR.00082-09pubmed: 20610822google scholar: lookup
          6. Clements AC, Magalhães RJ, Tatem AJ, Paterson DL, Riley TV. Clostridium difficile PCR ribotype 027: assessing the risks of further worldwide spread. Lancet Infect Dis 2010 Jun;10(6):395-404.
            doi: 10.1016/S1473-3099(10)70080-3pubmed: 20510280google scholar: lookup