C. difficile infections caused by the (hyper-)virulent Type 027 (NAP1/REA B1) and Type 078 (NAP7/REA BK) are associated with an increased morbidity and severity of disease compared to other types [1, 3] . This increase is suggested to be linked to toxin hyper production [3, 22, 28] . A potential mechanism by which this could occur is through inactivation of a negative regulator of the toxin gene transcription. TcdC has been identified as a negative regulator of toxin production [12] .