The cadA gene of Vibrio cholerae is induced during infection and plays a role in acid tolerance

Vibrio cholerae is a facultative pathogen of humans that must survive expos ure to inorganic and organic acids in the stomach and small intestine. To l earn more about the mechanisms by which this pathogen colonizes the intesti nal tract, we used a recombinase gene fusion reporter to identify transcrip ts induced during infection in an adult rabbit model of cholera. One of the genes identified was cadA, which encodes an inducible lysine decarboxylase . CadA was also induced during infections of the suckling and adult mouse i ntestines, and in vitro under conditions of low pH and high lysine concentr ation. We show that V. cholerae is capable of mounting an acid tolerance re sponse (ATR) to both inorganic and organic acid challenges. Mutational anal yses revealed a significant role for cadA, but not for speF, which encodes an ornithine decarboxylase, in both inorganic and organic ATR. Potential ro les for toxR, toxT and rpoS in ATR were examined, and it was found that tox R plays a ToxT-independent role in mediating organic ATR, whereas rpoS play ed no detectable role in either ATR. Transcriptional analysis showed that t he toxR defect in ATR is not caused by decreased cadA transcription. Despit e induction of cadA in these animal models, competition assays revealed tha t neither cadA nor speF alone or together were required for colonization of suckling or adult mice. However, acid-adapted wild-type V. cholerae exhibi ted a major competitive advantage over unadapted cells during colonization of suckling mice.