Volume 12, Number 6—June 2006
Epidemic Clostridium difficile Strain in Hospital Visitation Dog
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|EID||Lefebvre SL, Arroyo LG, Weese J. Epidemic Clostridium difficile Strain in Hospital Visitation Dog. Emerg Infect Dis. 2006;12(6):1036-1037. https://dx.doi.org/10.3201/eid1206.060115|
|AMA||Lefebvre SL, Arroyo LG, Weese J. Epidemic Clostridium difficile Strain in Hospital Visitation Dog. Emerging Infectious Diseases. 2006;12(6):1036-1037. doi:10.3201/eid1206.060115.|
|APA||Lefebvre, S. L., Arroyo, L. G., & Weese, J. (2006). Epidemic Clostridium difficile Strain in Hospital Visitation Dog. Emerging Infectious Diseases, 12(6), 1036-1037. https://dx.doi.org/10.3201/eid1206.060115.|
To the Editor: Rates of illness and death from Clostridium difficile–associated disease (CDAD) and reports of CDAD in persons without traditional risk factors (1) have been increasing. One particular strain of C. difficile has been implicated in outbreaks of CDAD in hospitals in North America and Europe and appears to be spreading internationally at an alarming rate. This strain is classified as ribotype 027, toxinotype III, and possesses genes encoding toxins A, B, and CDT (binary toxin) as well as a deletion in the tcdC gene, which is believed to increase virulence (2).
We report this toxin-variant strain of C. difficile in a healthy, 4-year-old toy poodle that visits persons in hospitals and long-term care facilities in Ontario on a weekly basis. C. difficile was isolated from a fecal sample collected in the summer of 2004 as part of a cross-sectional study evaluating pathogen carriage by visitation dogs (3). The isolate was subsequently characterized by ribotyping (4) and by polymerase chain reaction (PCR) detection of genes that encode production of toxins A and B (5). Toxin CDT was confirmed by amplifying the portion of the gene (cdtB) that encodes for the receptor-binding component of the toxin, according to a previously reported protocol (6). As a result, the isolate was classified as ribotype 027, toxinotype III (7), and was found to possess all 3 toxin genes. The tcdC gene deletion was also confirmed with PCR (8).
These results indicate that this canine isolate is indistinguishable from the major strain implicated in outbreaks of highly virulent CDAD around the world. According to the infection control practitioner at the hospital the dog visited, CDAD cases were occurring at increased frequency in the facility around the time the dog’s fecal specimen was collected. However, patient diagnosis was made solely through fecal toxin testing, and strains were not characterized. The facility has reported only sporadic cases of CDAD in the past few years.
This is the first report of this human, epidemic strain of C. difficile in a dog. Many C. difficile strains isolated from animals, including dogs, are indistinguishable from strains associated with disease in humans (9). To date, no study, including this one, has shown that interspecies transmission occurs; however, that possibility exists, as is becoming apparent with other pathogens, such as methicillin-resistant Staphylococcus aureus. The recurrent exposure of this dog to human healthcare settings suggests that the animal acquired this strain during visits to the hospital or long-term care facility, either from the healthcare environment or contaminated hands of human contacts. We recommend that future studies evaluating the dissemination of this strain and investigations of the movement of C. difficile into the community consider the role of animals.
We thank Joyce Rousseau for her assistance with culturing and identifying strains of C. difficile.
This work was supported by the Pet Trust Foundation of the Ontario Veterinary College.
- Centers for Disease Control and Prevention. Severe Clostridium difficile–associated disease in populations previously at low risk—four states, 2005. MMWR Morb Mortal Wkly Rep. 2005;54:1201–5.
- Warny M, Pepin J, Fang A, Killgore G, Thompson A, Brazier J, Toxin production by an emerging strain of Clostridium difficile associated with outbreaks of severe disease in North America and Europe. Lancet. 2005;366:1079–84.
- Lefebvre SL, Waltner-Toews D, Peregrine AS, Reid-Smith R, Hodge L, Arroyo LG, Prevalence of zoonotic agents in dogs visiting hospitalized people in Ontario: implications for infection control. J Hosp Infect. Epub 2006 Feb 5.
- Barbut F, Lalande V, Burghoffer B, Thien HV, Grimprel E, Petit JC. Prevalence and genetic characterization of toxin A variant strains of Clostridium difficile among adults and children with diarrhea in France. J Clin Microbiol. 2002;40:2079–83.
- Kato H, Kato N, Watanabe K, Iwai N, Nakamura H, Yamamoto T, Identification of toxin A–negative, toxin B–positive Clostridium difficile by PCR. J Clin Microbiol. 1998;36:2178–82.
- Stubbs S, Rupnik M, Gibert M, Brazier J, Duerden B, Popoff M. Production of actin-specific ADP-ribosyltransferase (binary toxin) by strains of Clostridium difficile. FEMS Microbiol Lett. 2000;186:307–12.
- Rupnik M, Avesani V, Janc M, von Eichel-Streiber C, Delmee M. A novel toxinotyping scheme and correlation of toxinotypes with serogroups of Clostridium difficile isolates. J Clin Microbiol. 1998;36:2240–7.
- Cohen SH, Tang YJ, Silva J Jr. Analysis of the pathogenicity locus in Clostridium difficile strains. J Infect Dis. 2000;181:659–63.
- Arroyo LG, Kruth SA, Willey BM, Staempfli HR, Low DE, Weese JS. PCR ribotyping of Clostridium difficile isolates originating from human and animal sources. J Med Microbiol. 2005;54:163–6.
Please use the form below to submit correspondence to the authors or contact them at the following address:
Sandra L. Lefebvre, Department of Population Medicine, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1, Canada
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