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The acute diarrhoeal disease cholera is caused by the aquatic pathogen Vibrio cholerae upon ingestion of contaminated food or water by the human host. The mechanisms by which V. cholerae is able to persist and survive in the host and aquatic environments have been studied for years; however, little is known about the factors involved in the adaptation or response of V. cholerae transitioning between these two environments. The transition from bacillary to coccoid morphology is thought to be one mechanism of survival that V. cholerae uses in response to environmental stress. Coccoid morphology has been observed for V. cholerae while in a viable but non-culturable (VBNC) state, during times of nutrient limitation, and in the water-diluted stool of cholera-infected patients. In this study we sought conditions to study the coccoid morphology of V. cholerae, and found that coccoid-shaped cells can express and produce the virulence factor toxin co-regulated pilus (TCP) and are able to colonize the infant mouse to the same extent as bacillus-shaped cells. This study suggests that TCP may be one factor that V. cholerae utilizes for adaptation and survival during the transition between the host and the aquatic environment.

Nutrient-dependent, rapid transition of Vibrio cholerae to coccoid morphology and expression of the toxin co-regulated pilus in this form