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Infect Immun, February 1998, p. 692-695, Vol. 66, No. 2
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Investigation of the Roles of Toxin-Coregulated Pili and Mannose-Sensitive Hemagglutinin Pili in the Pathogenesis of Vibrio cholerae O139 Infection

Carol O. Tacket,1,* Ronald K. Taylor,2 Genevieve Losonsky,1 Yu Lim,1 James P. Nataro,1 James B. Kaper,1 and Myron M. Levine1

Center for Vaccine Development, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201,1 and Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire 037552

Received 29 May 1997/Returned for modification 23 September 1997/Accepted 26 November 1997

In this study, adult volunteers were fed tcpA and mshA deletion mutants of V. cholerae O139 strain CVD 112 to determine the role of toxin-coregulated pili (TCP) and mannose-sensitive hemagglutinin (MSHA) in intestinal colonization. Eight of 10 volunteers who received CVD 112 or CVD 112 Delta mshA shed the vaccine strains in their stools; the geometric mean peak excretion for both groups was 1.4 × 105 CFU/g of stool. In contrast, only one of nine recipients of CVD 112 Delta tcpA shed vibrios in his stool (P < 0.01); during the first 24 h after inoculation, 3 × 102 CFU/g was recovered from this volunteer. All recipients of CVD 112 and 8 (80%) of the recipients of CVD 112 Delta mshA developed at least a fourfold rise in vibriocidal titer after immunization. In contrast, only one (11%) of the nine recipients of CVD 112 Delta tcpA developed a fourfold rise in vibriocidal titer (P < 0.01). We conclude that TCP are an important colonization factor of V. cholerae O139 and probably of El Tor V. cholerae O1. In contrast, MSHA does not appear to promote intestinal colonization in humans.

* Corresponding author. Mailing address: Center for Vaccine Development, 685 West Baltimore St., Room 480, Baltimore, MD 21201. Phone: (410) 706-5328. Fax: (410) 706-4171. E-mail: ctacket{at}umppa1.ab.umd.edu.




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