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Infection and Immunity, April 2000, p. 1967-1974, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Mutations in the Extracellular Protein Secretion Pathway Genes (eps) Interfere with Rugose Polysaccharide Production in and Motility of Vibrio cholerae

Afsar Ali,1 Judith A. Johnson,2,3 Augusto A. Franco,4 Daniel J. Metzger,5 Terry D. Connell,5 J. Glenn Morris Jr.,1,3 and Shanmuga Sozhamannan1,3,*

Division of Hospital Epidemiology, Department of Medicine,1 Department of Pathology,2 and Center for Vaccine Development, Division of Geographic Medicine, Department of Medicine,4 School of Medicine, University of Maryland at Baltimore, and Veterans Affairs Maryland Health Care System,3 Baltimore, Maryland 21201, and Center for Microbial Pathogenesis and Department of Microbiology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York 142145

Received 6 October 1999/Returned for modification 29 November 1999/Accepted 4 January 2000

Vibrio cholerae is the causal organism of the diarrheal disease cholera. The rugose variant of V. cholerae is associated with the secretion of an exopolysaccharide. The rugose polysaccharide has been shown to confer increased resistance to a variety of agents, such as chlorine, bioacids, and oxidative and osmotic stresses. It also promotes biofilm formation, thereby increasing the survival of the bacteria in the aquatic environments. Here we show that the extracellular protein secretion system (gene designated eps) is involved directly or indirectly in the production of rugose polysaccharide. A TnphoA insertion in epsD gene of the eps operon abolished the production of rugose polysaccharide, reduced the secretion of cholera toxin and hemolysin, and resulted in a nonmotile phenotype. We have constructed defined mutations of the epsD and epsE genes that affected these phenotypes and complemented these defects by plasmid clones of the respective wild-type genes. These results suggest a major role for the eps system in pathogenesis and environmental survival of V. cholerae.

* Corresponding author. Mailing address: Division of Hospital Epidemiology, Department of Medicine, University of Maryland School of Medicine, 934-MSTF, 10 S. Pine St., Baltimore, MD 21201. Phone: (410) 706-5157. Fax (410) 706-4581. mail: ssozhama{at}medicine.umaryland.edu.

Infection and Immunity, April 2000, p. 1967-1974, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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