Genotypic and Phenotypic Characterization of Clostridium perfringens and Clostridium difficile in Diarrheic and Healthy Dogs

Marks, Stanley L.; Kather, Elizabeth J.; Kass, Philip H.; Melli, Ann C.

doi:10.1892/0891-6640(2002)016<0533:gapcop>2.3.co;2

Cited by 74 publications

(108 citation statements)

References 45 publications

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“…In addition, all animal and human isolates displayed 39-bp deletions in tcdC, and most (45/47; 96%) were binary toxin positive. Although C. diffi cile is recognized as a cause of disease in several animal species (19)(20)(21)(22), little investigation has been conducted on the potential for interspecies transmission of C. diffi cile to humans. Previous studies have suggested the possibility of C. diffi cile transmission between humans and domestic pets (23,24), but no interspecies transmission has been documented, and few studies have examined the possible link between CDAD in food animals and humans.…”

Section: Discussionmentioning

confidence: 99%

Toxinotype VClostridium difficilein Humans and Food Animals

Jhung

Thompson

Killgore

et al. 2008

Emerg. Infect. Dis.

197

155

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Clostridium diffi cile is a recognized pathogen in neonatal pigs and may contribute to enteritis in calves. Toxinotype V strains have been rare causes of human C. diffi cileassociated disease (CDAD). We examined toxinotype V in human disease, the genetic relationship of animal and human toxinotype V strains, and in vitro toxin production of these strains. From 2001 through 2006, 8 (1.3%) of 620 patient isolates were identifi ed as toxinotype V; before 2001, 7 (<0.02%) of ≈6,000 isolates were identifi ed as toxinotype V. Six (46.2%) of 13 case-patients for whom information was available had community-associated CDAD. Molecular characterization showed a high degree of similarity between human and animal toxinotype V isolates; all contained a 39-bp tcdC deletion and most produced binary toxin. Further study is needed to understand the epidemiology of CDAD caused by toxinotype V C. diffi cile, including the potential of foodborne transmission to humans. R ecent evidence suggests that the epidemiology of Clostridium diffi cile-associated disease (CDAD) is increasing in incidence and severity (1-3). These changes are due, at least in part, to the emergence of a more virulent C. diffi cile strain, designated NAP1 (based on its pulsed-fi eld gel electrophoresis [PFGE] pattern), BI (by restriction endonuclease analysis [REA]), toxinotype III (by PCR characterization of the pathogenicity locus), and 027 (by PCR ribotyping) (4). However, the emergence of BI/NAP1/027 may not be solely responsible for changes in CDAD epidemiology, and the origin of this and other virulent strains is still largely unknown. C. diffi cile has also recently emerged as a pathogen or commensal in food animals such as neonatal pigs and beef and dairy calves (5-7); most of these animal isolates are toxigenic. Although several ribotypes have been identifi ed in calves, the predominant ribotype in both calves and pigs is a toxinotype V strain (8,9). Moreover, recent reports suggest that C. diffi cile strains recognized as causes of human disease may contaminate retail meats (10).To better understand whether food sources could be a source of infection for humans, we investigated recent and past human CDAD caused by toxinotype V C. diffi cile and compared isolates from these cases with those recovered from neonatal pigs and calves. We documented apparent changes in the frequency with which these toxinotype V strains cause human CDAD and compared the molecular characterization and toxin production of these strains with those of recent epidemic (i.e., BI/NAP1/027) and nonepidemic isolates. Materials and Methods Human Case Finding and Defi nitionsCase fi nding was performed by reviewing recent and past human isolates of interest from 2 sources. Cases were defi ned as patients with clinical isolates identifi ed as toxinotype V by analysis of restriction fragment length polymorphisms (RFLPs) of toxin-encoding genes. First, we reviewed 620 C. diffi cile human isolates sent to the Centers for Disease Control and Prevention (CDC) from healthcare facilities and ...

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Section: Discussionmentioning

confidence: 99%

Toxinotype VClostridium difficilein Humans and Food Animals

Jhung

Thompson

Killgore

et al. 2008

Emerg. Infect. Dis.

197

155

View full text Add to dashboard Cite

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“…For example, one study showed the presence of cpe-positive type A isolates and CPE in the small intestines of a goat kid suffering from necrotic enteritis (199). Additionally, fecal CPE and CPE-positive fecal isolates have been associated with canine diarrhea (200), and cpe-positive strains were suggested to cause recurrent diarrhea in dogs. In horses, fecal CPE was detected in ϳ20% of adults with diarrhea and ϳ30% of foals with diarrhea, while no fecal CPE was detected in healthy adult horses or foals (201).…”

Section: Diseases Involving Primarily Plasmid-encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

231

282

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SUMMARY In both humans and animals, Clostridium perfringens is an important cause of histotoxic infections and diseases originating in the intestines, such as enteritis and enterotoxemia. The virulence of this Gram-positive, anaerobic bacterium is heavily dependent upon its prolific toxin-producing ability. Many of the ∼16 toxins produced by C. perfringens are encoded by large plasmids that range in size from ∼45 kb to ∼140 kb. These plasmid-encoded toxins are often closely associated with mobile elements. A C. perfringens strain can carry up to three different toxin plasmids, with a single plasmid carrying up to three distinct toxin genes. Molecular Koch's postulate analyses have established the importance of several plasmid-encoded toxins when C. perfringens disease strains cause enteritis or enterotoxemias. Many toxin plasmids are closely related, suggesting a common evolutionary origin. In particular, most toxin plasmids and some antibiotic resistance plasmids of C. perfringens share an ∼35-kb region containing a Tn 916 -related conjugation locus named tcp (transfer of clostridial plasmids). This tcp locus can mediate highly efficient conjugative transfer of these toxin or resistance plasmids. For example, conjugative transfer of a toxin plasmid from an infecting strain to C. perfringens normal intestinal flora strains may help to amplify and prolong an infection. Therefore, the presence of toxin genes on conjugative plasmids, particularly in association with insertion sequences that may mobilize these toxin genes, likely provides C. perfringens with considerable virulence plasticity and adaptability when it causes diseases originating in the gastrointestinal tract.

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confidence: 99%

“…However, C. perfringens can be cultured from the fecal specimens of more than 80% of diarrheic and nondiarrheic dogs, and CPE can also be detected in up to 14% of nondiarrheic, healthy dogs 11, 1515, 16, 17. In addition, the moderate‐to‐poor sensitivity and specificity of commercial ELISA, which was used in this previous study, have been reported by comparison with the gold standard of cytotoxicity assays 18…”

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confidence: 99%

Endoscopically Visualized Lesions, Histologic Findings, and Bacterial Invasion in the Gastrointestinal Mucosa of Dogs with Acute Hemorrhagic Diarrhea Syndrome

Unterer¹,

Busch²,

Leipig³

et al. 2013

Veterinary Internal Medicne

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BackgroundEtiology of hemorrhagic gastroenteritis (HGE) syndrome in dogs is unknown and histopathologic and microbial investigations have only been performed post mortem.ObjectiveTo identify characteristic intra vitam endoscopic and histologic mucosal lesions, as well as bacterial species, within the mucosa of dogs with HGE.AnimalsTen dogs diagnosed with HGE were included. Eleven dogs with gastroduodenoscopy and different intestinal diseases were used as controls for microbial changes. Dogs pretreated with antibiotics or diagnosed with any disease known to cause bloody diarrhea were excluded from the study.MethodsIn this prospective study, gastrointestinal biopsies were collected from 10 dogs with HGE. Endoscopic and histologic changes were assessed according to WSAVA guidelines. Biopsies from the stomach, duodenum, ileum, and colon were investigated by histology and by immunohistochemistry for the presence of Clostridium spp. and parvovirus. The first duodenal biopsy taken with a sterile forceps was submitted for bacterial culture.ResultsAcute mucosal lesions were only found in the intestines, not in the stomach. Clostridium spp., identified as Clostridium perfringens in 6/9 cases, were detected on the small intestinal mucosa in all dogs with HGE, either by culture or immunohistopathology. In the control group, C. perfringens could only be cultured in one of 11 dogs.Conclusions and Clinical ImportanceThe results of this study demonstrate an apparent association between C. perfringens and the occurrence of acute hemorrhagic diarrhea. The term “HGE,” which implies the involvement of the stomach, should be renamed as “acute hemorrhagic diarrhea syndrome.”

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Genotypic and Phenotypic Characterization of Clostridium perfringens and Clostridium difficile in Diarrheic and Healthy Dogs

Cited by 74 publications

References 45 publications

Toxinotype VClostridium difficilein Humans and Food Animals

Toxinotype VClostridium difficilein Humans and Food Animals

Toxin Plasmids of Clostridium perfringens

Endoscopically Visualized Lesions, Histologic Findings, and Bacterial Invasion in the Gastrointestinal Mucosa of Dogs with Acute Hemorrhagic Diarrhea Syndrome

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