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Infection and Immunity, June 2001, p. 4180-4184, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.4180-4184.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Haemophilus ducreyi Lipooligosaccharide Mutant Defective in Expression of beta -1,4-Glucosyltransferase Is Virulent in Humans

Royden S. Young,1 Melanie J. Filiatrault,2,3 Kate R. Fortney,1 Antoinette F. Hood,1,4,5 Barry P. Katz,1 Robert S. Munson Jr.,6 Anthony A. Campagnari,2,3,7 and Stanley M. Spinola1,4,8,*

Departments of Medicine,1 Microbiology and Immunology,8 Pathology and Laboratory Medicine,4 and Dermatology,5 School of Medicine, Indiana University, Indianapolis, Indiana 46202; Departments of Medicine7 and Microbiology2 and Center for Microbial Pathogenesis,3 University of Buffalo, Buffalo, New York 14214; and Children's Research Institute and Departments of Pediatrics and Microbiology, The Ohio State University, Columbus, Ohio 43205-26966

Received 6 February 2001/Returned for modification 1 March 2001/Accepted 15 March 2001

The lipooligosaccharide (LOS) of Haemophilus ducreyi contains a major glycoform that is immunochemically identical to paragloboside, a glycosphingolipid precursor of major human blood group antigens. We recently identified the gene responsible for the glucosyltransferase activity and constructed an isogenic mutant (35000glu-) deficient in this activity. 35000glu- makes an LOS that consists only of the heptose trisaccharide core and 2-keto-deoxyoctulosonic acid (KDO). For this study, the mutant was reconstructed in the 35000HP (human passaged [HP]) background. Five human subjects were inoculated with 35000HP and 35000HPglu- in a dose-response trial. The pustule formation rates were 40% (95% confidence interval [CI], 13.7 to 72.6%) at 10 sites for 35000HP and 46.7% (95% CI, 24.8 to 69.9%) at 15 sites for 35000HPglu-. The histopathology and recovery rates of H. ducreyi from surface cultures and biopsies obtained from mutant and parent sites were similar. These results indicate that the expression of glycoforms with sugar moieties extending beyond the heptose trisaccharide core is not required for pustule formation by H. ducreyi in humans.

* Corresponding author. Mailing address: Department of Medicine, 435 Emerson Hall, Indiana University, 545 Barnhill Dr. Indianapolis, IN 46202-5124. Phone: (317) 274-1427. Fax: (317) 274-1587. E-mail: sspinola{at}iupui.edu.

Infection and Immunity, June 2001, p. 4180-4184, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.4180-4184.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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