Community-Acquired Clostridium difficile Infection, Queensland, Australia

in the case-patient’s family or the community. On the basis of a matching surname, case-patient E was determined to be a member of the same family as case-patients P20, P26, and likely C. Soft tissue infection was documented in all 5 casepatients, supporting the original observation that ST2371 is associated with disease. Evidence of familial transmission in the original outbreak is further supported by transmission between case-patients P20, P26, C, and E. Furthermore, 2 case-patients infected during the original outbreak, P22/A and P14/B, continued to experience disease signs and symptoms for >15 months after their initial diagnosis. Our data highlight the role of hospitals as reservoirs of MRSA and subsequent failure to track the entry and spread of MRSA in the community. MRSA decolonization was advised in all cases in the original outbreak, but this process clearly proved ineffective for case-patients A and B. Potential explanations include not implementing or completing the course of decolonization; failed decolonization; or limiting decolonization to only some members of an affected family. Although the outbreak in the hospital ward was resolved, the lack of a systematic surveillance program to monitor the incidence of noninvasive MRSA infections among the case-patients’ contacts and the community allowed this novel lineage to continue to cause disease in a group of linked persons. Considering recommendations to move from universal to targeted MRSA screening in hospitals in England (6), more active surveillance of any identified case-patients or carriers of MRSA in the community may be warranted.