Clostridium difficile infection (CDI) is an opportunistic infection of the colon caused by a Gram-positive, spore-forming bacillus. CDI occurs in humans and animals with compromised gut flora, and human infection costs over $4.8 billion USD annually in the USA alone. Symptoms range from mild diarrhoea to life-threatening pseudomembranous colitis. Virulence of C. difficile is classically attributed to toxins A and B, while the role of binary toxin (CDT) remains unclear.
Strains that do not produce toxins A and B but do produce CDT (A−B−CDT+) are highly prevalent in symptomatic Australian livestock, however, this does not seem to be mirrored in humans. In contrast, strains that do produce toxins A and/or B are often shared between humans and animals. As most human diagnostics focus on the detection of toxins A and/or B, human A−B−CDT+ CDI cases are likely underreported. We investigated the prevalence of A−B−CDT+ strains that could be shared between humans and animals.
For 30 days in early 2015, we looked for A−B−CDT+ CDI in human faecal samples submitted for routine C. difficile testing by screening for a toxin-independent marker of C. difficile. All isolates were further characterised by PCR detection of toxin genes and PCR ribotyping. From 600 unique samples, we recovered 51 C. difficile isolates of various toxin profiles. Of these, 2 isolates were A−B−CDT+, equating to a prevalence of 15% amongst A−B− isolates and 50% of all CDT+ isolates. No link between Australian livestock A−B−CDT+C. difficile was found.
Previous studies are rare, but have reported the prevalence of human A−B−CDT+C. difficile to be only 0.5% amongst A−B− isolates collected over 2 years in France (Eckert et al., 2014). While our sample size was low, the presence of these strains in symptomatic patients over such a brief period suggests human A−B−CDT+ CDI may be more common than previously thought and larger investigations are warranted.