Abstract
Urogenital infections caused by Neisseria gonorrhoeae are epidemic in many parts of the world. Gonococcal infections of the female reproductive tissues, such as pelvic inflammatory disease, which may be complicated by infertility, chronic pelvic pain and ectopic pregnancy, continue to place the major burden of gonococcal infections on women and their unborn children [1]. Despite intensive efforts at controlling the spread of gonococcal infections by treating symptomatic patients and identifying and treating their sexual contacts, the incidence of gonorrhea and pelvic inflammatory disease has not declined [1]. Because of the continued prevalence of gonococcal infections in general and the tremendous cost of pelvic inflammatory disease in particular (both in monetary terms and in personal tragedy), efforts in laboratories around the world are being channelled toward the development of a safe and effective gonococcal vaccine [2]. Critical to such efforts at preventing gonococcal infections is a basic understanding of the mechanisms by which gonococci infect and damage human fallopian tubes. Immunity elicited by a vaccine, in order to be effective, must interfere with the molecular mechanisms by which gonococci interact with genital mucosa and cause disease.
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Literatur
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Robinson, E.N. et al. (1984). Symposium D. In: 90. Kongreß. Verhandlungen der Deutschen Gesellschaft für Innere Medizin, vol 90. J.F. Bergmann-Verlag, Munich. https://doi.org/10.1007/978-3-642-85457-6_13
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