Clostridium difficile infection (CDI) is responsible for 250,000 infections and 14,000 deaths annually. High rates of treatment failure, recurrent infections, and potential for antibiotic resistance are all evidence that new and effective treatments for CDI are needed. A potential treatment for CDI is Auranofin, which disrupts the selenoproteins used for anaerobic metabolism in C. difficile. The aim of this study is to assess the potential of Auranofin as a treatment for CDI.

The effect of Auranofin on C. difficile growth was tested on CD01 (ribotype UKI-001) which is the most commonly isolated ribotype in Australia. Growth assays using optical density and viable cell counts showed that Auranofin inhibits the growth of C. difficile at concentration of 50µM when compared to the control (p<0.0001). No viable cells were recovered from the Auranofin treated cultures, indicating that Auranofin is bactericidal against C. difficile. Sporulation assays indicate that Auranofin also inhibits sporulation, with no viable spores recovered from the Auranofin treated cultures. Cell cytotoxicity assays showed that Auranofin treated cultures had less cytotoxic activity against vero cells than the no treatment control (p<0.0001) but is not significantly different to the ethanol control.

Growth assays comparing Auranofin to Metronidazole, one of the current treatments for CDI, were also performed. These assays indicated that there is no significant difference between the two treatments when it comes to inhibiting C. difficile growth, cell viability or sporulation.

The bactericidal activity, pharmacokinetics and prevention of sporulation make Auranofin a good candidate for a CDI treatment. Auranofin may also be narrow spectrum, with just 14% of bacteria utilising selenoproteins.  Further experiments will test Auranofin in a CDI and recurrent CDI mouse model. The aims of these experiments will focus on treatment of disease, prevention of recurrent disease, disease severity and effects on the intestinal microbiota.