ena-STUDY-1-22-02-2017-06:40:21:114-52
Prevalence of Binary Toxin Positive Clostridium difficile in Symptomatic Humans in the Absence of Epidemic Ribotype 027
Virulence of Clostridium difficile is primarily attributed to toxins A and B while the role of binary toxin remains unclear. Binary toxin often occurs simultaneously with toxins A and B and the prevalence of human strains possessing only binary toxin genes (A-B-CDT+) is generally low (< 5%). Conversely, A-B-CDT+ C. difficile appears highly prevalent in Australian neonatal livestock. Zoonotic transmission of C. difficile has been suggested previously and many diagnostics may miss human A-B-CDT+ cases due to the focus on detection of toxin A and/or B. We performed a brief prospective investigation into the prevalence and genetic characteristics of A-B-CDT+ C. difficile in symptomatic humans. All faecal specimens from symptomatic inpatients over 30 days in early 2015 (n = 592) were screened for the toxin B gene or GDH, a non-toxin marker of C. difficile, before enrichment culture. C. difficile ribotypes and presence of toxin genes were determined by PCR. We recovered 43 C. difficile isolates including two A-B-CDT+ isolates. This corresponded to an A-B-CDT+ prevalence of 2/35 (5.7%) isolates possessing at least one toxin, 2/10 (20%) A-B- isolates, 2/3 CDT+ isolates and 1/28 (3.6%) presumed true CDI cases. No link between Australian livestock-associated C. difficile was found. Both A-B-CDT+ isolates were not the dominant A-B-CDT+ strain; PCR ribotype 033, nor did they belong to toxinotype XI. Previous reports infrequently describe A-B-CDT+ C. difficile in human patients and in strain collections but the in situ prevalence of human A-B-CDT+ C. difficile is rarely investigated. This study suggests A-B-CDT+ C. difficile to be more common than previously thought, and at least warrants larger investigations.
Virulence of Clostridium difficile is primarily attributed to toxins A and B while the role of binary toxin remains unclear. Binary toxin often occurs simultaneously with toxins A and B and the prevalence of human strains possessing only binary toxin genes (A-B-CDT+) is generally low (< 5%). Conversely, A-B-CDT+ C. difficile appears highly prevalent in Australian neonatal livestock. Zoonotic transmission of C. difficile has been suggested previously and many diagnostics may miss human A-B-CDT+ cases due to the focus on detection of toxin A and/or B. We performed a brief prospective investigation into the prevalence and genetic characteristics of A-B-CDT+ C. difficile in symptomatic humans. All faecal specimens from symptomatic inpatients over 30 days in early 2015 (n = 592) were screened for the toxin B gene or GDH, a non-toxin marker of C. difficile, before enrichment culture. C. difficile ribotypes and presence of toxin genes were determined by PCR. We recovered 43 C. difficile isolates including two A-B-CDT+ isolates. This corresponded to an A-B-CDT+ prevalence of 2/35 (5.7%) isolates possessing at least one toxin, 2/10 (20%) A-B- isolates, 2/3 CDT+ isolates and 1/28 (3.6%) presumed true CDI cases. No link between Australian livestock-associated C. difficile was found. Both A-B-CDT+ isolates were not the dominant A-B-CDT+ strain; PCR ribotype 033, nor did they belong to toxinotype XI. Previous reports infrequently describe A-B-CDT+ C. difficile in human patients and in strain collections but the in situ prevalence of human A-B-CDT+ C. difficile is rarely investigated. This study suggests A-B-CDT+ C. difficile to be more common than previously thought, and at least warrants larger investigations.