Since the end of 2002, outbreaks due to a hypervirulent clone have been reported in the United States, Canada, the United Kingdom, France, Belgium, and the Netherlands.21 This has completely changed the epidemiology and clinical impacts of CDAD in adults. In the province of Quebec, Canada, more than 30 hospitals have been struggling with an epidemic of CDAD characterized by a high case-fatality rate (16.7%) and increased risk of recurrence following metronidazole or vancomycin treatment, mostly in patients aged 65 years and older.22–24 These outbreaks have been associated with an emerging toxinotype III ribotype NAP1/027 strain characterized by massive toxins A and B hyperproduction.25 However, little information is available on the impact of NAP1/027 on children. In a retrospective analysis of 200 CDAD cases diagnosed in a university-affiliated pediatric hospital in 2000–2003 (no characterization of strains was performed, but this analysis has taken place in a city plagued by NAP1/027 outbreaks during that period), a majority were outpatients at onset, but 23% needed to be hospitalized for the care of CDAD. Out of 110 patients treated for CDAD, 31% experienced at least 1 recurrence, none required a colectomy and only 2 died.26 The frequent need for hospitalization may reflect the higher virulence of the predominant strain within this pediatric population. In a well-defined population of Canada where NAP1/027 emerged at the end of 2002, the incidence of CDAD increased from 36 per 100,000 in 1991–1992 to 156 per 100,000 in 2003; while the incidence among people aged ≥65 years increased 10-fold, to 866 per 100,000 in 2003, the annual incidence in children remained stable, between 20 and 40 per 100,000.23 This suggests that children are much less prone than the elderly to develop symptomatic infections when exposed to NAP1/027.