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Background  Cholera toxin (CT) and toxin-co-regulated pili (TCP) are the major virulence factors of Vibrio cholerae O1 and O139 strains that contribute to the pathogenesis of disease during devastating cholera pandemics. However, CT and TCP negative  V. cholerae  strains are still able to cause severe diarrheal disease in humans through mechanisms that are not well understood.    Methodology/Principal Findings  To determine the role of other virulence factors in  V. cholerae  pathogenesis, we used a CT and TCP independent infection model in the nematode  Caenorhabditis elegans  and identified the hemolysin A ( hlyA ) gene as a factor responsible for animal death and developmental delay. We demonstrated a correlation between the severity of infection in the nematode and the level of hemolytic activity in the  V. cholerae  biotypes. At the cellular level,  V. cholerae  infection induces formation of vacuoles in the intestinal cells in a  hlyA  dependent manner, consistent with the previous  in vitro  observations.    Conclusions/Significance  Our data strongly suggest that HlyA is a virulence factor in  C. elegans  infection leading to lethality and developmental delay presumably through intestinal cytopathic changes.

Vibrio cholerae Hemolysin Is Required for Lethality, Developmental Delay, and Intestinal Vacuolation in Caenorhabditis elegans