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. 1983 Jul;18(1):121–127. doi: 10.1128/jcm.18.1.121-127.1983

Gonococcal sensitivity to fecal lipids can be mediated by an Mtr-independent mechanism.

L McFarland, T A Mietzner, J S Knapp, E Sandstrom, K K Holmes, S A Morse
PMCID: PMC270754  PMID: 6411761

Abstract

Various factors affect the sensitivity of Neisseria gonorrhoeae to physiological levels of hydrophobic molecules. A total of 98 N. gonorrhoeae strains from rectal, cervical, and urethral cultures of homosexual men and heterosexual men and women were examined for their sensitivities to fecal lipids. Isolates were characterized according to cell envelope phenotype, auxotype, and protein I serogroup. Although cell envelope phenotype was an important factor in the resistance of this organism to fecal lipids (Mtr phenotype greater than wild type greater than Env phenotype), other factors were also of importance. AHU- strains (strains having a requirement for arginine, hypoxanthine, and uracil) uniformly exhibited a wild-type envelope phenotype but were as sensitive to fecal lipids as were Env strains. The protein I serogroup was not a factor in determining the sensitivity of wild-type envelope phenotype non-AHU- strains to fecal lipids. However, sexual preference and site of isolation were important factors. Wild-type envelope phenotype (non-AHU-) strains from homosexual men and heterosexual women were more resistant to fecal lipids than were similar isolates from heterosexual men. When these strains were compared by isolation site, it was observed that rectal isolates from homosexual men and heterosexual women were more resistant than were cervical isolates from heterosexual women or urethral isolates from heterosexual men. Urethral isolates from homosexual men were also more resistant to fecal lipids than were urethral isolates from heterosexual men. These data suggest that the host environment can select for increased resistance to hydrophobic molecules by an Mtr-independent mechanism. The basis for this Mtr-independent resistance is presently unknown, but it is likely that it involves an alteration of the target site(s) for fecal lipid inhibition.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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