Experimental Human Gonococcal Urethritis: 250 Neisseria gonorrhoeae MS11mkC Are Infective

Neisseria gonorrhoeae MS11mkA (mkA) expressesone 3.6-kDa lipooligosaccharide (LOS). Variant MS11mkC (mkC), expressing four larger LOSs, occurs in vitro among mkA at a frequency of 10−3. Infectivity of these variants was compared in 2 groups of volunteers inoculated with ∼40,000 piliated, Opa− gonoco...

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Published inThe Journal of infectious diseases Vol. 172; no. 1; pp. 180 - 185
Main Authors Schneider, Herman, Cross, Alan S., Kuschner, Robert A., Taylor, David N., Sadoff, Jerald C., Boslego, John W., Deal, Carolyn D.
Format Journal Article
LanguageEnglish
Published Chicago, IL The University of Chicago Press 01.07.1995
University of Chicago Press
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ISSN0022-1899
1537-6613
DOI10.1093/infdis/172.1.180

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Summary:Neisseria gonorrhoeae MS11mkA (mkA) expressesone 3.6-kDa lipooligosaccharide (LOS). Variant MS11mkC (mkC), expressing four larger LOSs, occurs in vitro among mkA at a frequency of 10−3. Infectivity of these variants was compared in 2 groups of volunteers inoculated with ∼40,000 piliated, Opa− gonococci of either strain. The mkC variant infected 5 of 5 while mkA infected only 2 (40%) of 5. Gonococci recovered from the mkA infections showed a transition toward the mkC LOS phenotype. The mkA inoculum contained ∼40 mkC gonococci. These data confirmed earlier studies and suggested that small numbers of mkC gonococci would be infective. This hypothesis was tested in three more experiments. In two, volunteers were inoculated with 250 or 1250 mkC, infecting 3 of 7 in each group, and in the third, 1600 mkC infected 2 of 6, resulting in a total of 8 of 20 infected by ⩾ 1600 mkC. Gonococci shed by infected volunteers maintained the mkC LOS phenotype but shifted from Opa− to Opa+. Thus, LOS and opacity protein, as well as pilus, are gonococcal virulence factors.
Bibliography:Present affiliation: Sexually Transmitted Diseases Branch, Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
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Reprints or correspondence: Dr. Herman Schneider, Dept. of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, DC 20307-5100.
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ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/172.1.180