Evaluation of the Cepheid Xpert C. difficile/
            <i>Epi</i>
            and Meridian Bioscience
            <i>illumi</i>
            gene C. difficile Assays for Detecting Clostridium difficile Ribotype 033 Strains

Androga, Grace O.; McGovern, Alan M.; Elliott, Briony; Chang, Barbara J.; Perkins, Timothy T.; Foster, Niki F.; Riley, Thomas V.

doi:10.1128/jcm.03297-14

Cited by 18 publications

(16 citation statements)

References 16 publications

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“…RT 033 predominated in diarrhoeic calves in Germany (57%, 103/181) [13] but was present in lower proportions in another European study [17]. The prevalence and clinical burden of these two LCT -, CDT + RTs is likely to be underestimated: current molecular diagnostic assays (which rely on amplification of tcdA/B) fail to detect RT 033 [30].…”

Section: Discussionmentioning

confidence: 99%

Contamination of Australian newborn calf carcasses at slaughter with Clostridium difficile

Knight

Putsathit

Elliott

et al. 2016

Clinical Microbiology and Infection

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In North America and Europe, reports of a genetic overlap between toxigenic strains of Clostridium difficile isolated from humans, livestock and retail meat suggest that food-borne transmission may be occurring. We investigated the prevalence, concentration and genetic diversity of C. difficile on the carcasses (n = 300) and in the faeces (n = 30) of neonatal veal calves at three abattoirs in Australia in 2013. Selective culture (both direct and enrichment) was performed, and all isolates were characterized by PCR for the toxin genes tcdA, tcdB and cdtA/B and by PCR ribotyping. Prevalence of C. difficile was 25.3% (76/300) on carcasses and 60.0% (18/30) in faeces. Multiple PCR ribotypes (RT) were detected, with four binary toxin-positive RTs accounting for 70.3% (71/101) of isolates; 127 (A(+), B(+), CDT(+), 32.7%), 288 (A(-), B(-), CDT(+), 28.7%), 033 (A(-), B(-), CDT(+), 6.9%) and 126 (A(+), B(+), CDT(+), 2.0%). Viable counts of a subset of samples revealed detectable numbers of C. difficile in 66.7% (10/15) of faecal samples (range 2.0 × 10(3) to 2.3 × 10(6) CFU/mL, median count 2.5 × 10(4) CFU/mL) and in 16.7% (25/150) of carcase samples (range 3 to 33 CFU/cm(2), median count 7 CFU/cm(2)). These data further confirm that Australian neonatal veal calf carcasses are contaminated with potentially significant strains of C. difficile at slaughter.

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Section: Discussionmentioning

confidence: 99%

Contamination of Australian newborn calf carcasses at slaughter with Clostridium difficile

Knight

Putsathit

Elliott

et al. 2016

Clinical Microbiology and Infection

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“…Additionally, the prevalence and clinical burden of these two LCT-negative, CDT-positive RTs are likely to be underestimated. A recent study by Androga et al (106) found that current molecular diagnostic assays (which rely on amplification of the toxin A and B genes) fail to detect C. difficile RT033.…”

Section: Phylogenetics and Molecular Epidemiologymentioning

confidence: 99%

Diversity and Evolution in the Genome of Clostridium difficile

et al. 2015

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SUMMARY Clostridium difficile infection (CDI) is the leading cause of antimicrobial and health care-associated diarrhea in humans, presenting a significant burden to global health care systems. In the last 2 decades, PCR- and sequence-based techniques, particularly whole-genome sequencing (WGS), have significantly furthered our knowledge of the genetic diversity, evolution, epidemiology, and pathogenicity of this once enigmatic pathogen. C. difficile is taxonomically distinct from many other well-known clostridia, with a diverse population structure comprising hundreds of strain types spread across at least 6 phylogenetic clades. The C. difficile species is defined by a large diverse pangenome with extreme levels of evolutionary plasticity that has been shaped over long time periods by gene flux and recombination, often between divergent lineages. These evolutionary events are in response to environmental and anthropogenic activities and have led to the rapid emergence and worldwide dissemination of virulent clonal lineages. Moreover, genome analysis of large clinically relevant data sets has improved our understanding of CDI outbreaks, transmission, and recurrence. The epidemiology of CDI has changed dramatically over the last 15 years, and CDI may have a foodborne or zoonotic etiology. The WGS era promises to continue to redefine our view of this significant pathogen.

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“…26 The Illumigene assays fail to detect several tcdA-negative ribotypes, particularly RT 033. 27 Currently, almost all assays focus on tcdB detection, but if a tcdB-variant strain was to proliferate, these assays could fail to identify them. With shifts in circulating strains, validation of assays is required in diagnostic laboratories.…”

Section: Issues With Naatsmentioning

confidence: 99%