Porin expression is stable for any given strain of N. Many of the major virulence factors undergo phase and/or antigenic variation ( 227), including the pilus ( 56, 73), opacity-associated (Opa) outer membrane proteins ( 139, 229), and lipooligosaccharide (LOS) ( 32, 53, 211, 270). This human adaptability and the repeated phase and antigenic change displayed by the gonococcus have hampered vaccine development. A repertoire of virulence factors have been identified and allow this bacterium to successfully adapt to variable microenvironments within its sole human host.
Studies reveal that the gonococcus can enter human cells ( 257), but only recently has it been shown that the organism is intracellular during human infection ( 5). Disseminated disease, although uncommon, can cause arthritis-dermatitis syndrome, endocarditis, and/or meningitis. gonorrhoeae infection of these distinctly different epithelial cell surfaces leads to a spectrum of clinical manifestations of disease (reviewed in references 58, 109, and 229). Although the urethra and the uterine cervix serve as the initial sites for gonococcal infection in men and women, respectively, infections of the conjunctiva, pharynx, and rectal mucosa are also reported. gonorrhoeae is an exclusive human pathogen that primarily infects the urogenital epithelia. gonorrhoeae is the etiological agent in 40% of all reported cases ( 241). One in 10 women suffers from PID ( 8), of which N. Ascending gonococcal infection occurs in up to 45% of infected women ( 26, 109, 134, 229) and can result in pelvic inflammatory disease (PID), which can cause permanent fallopian tube scarring and blockage, with subsequent infertility and ectopic pregnancies. gonorrhoeae disease is a specific problem in women because of the asymptomatic nature commonly associated with gonococcal cervicitis and the subsequent spread to the upper genital tract ( 26, 58, 59, 134, 229). In addition, susceptibility to chronic complications associated with N. The gonococcus-induced increase in the local expression of viral RNA, in conjunction with the acute inflammatory response generated with gonococcal disease and the subsequent loss of mucosal integrity, is associated with the increased susceptibility to HIV type 1 ( 42). Teenagers and young adults are at high risk for infection, which is unsettling in view of the increased risk associated with gonorrhea for infection with human immunodeficiency virus (HIV) type 1 ( 264). The highest incidence of disease and disease sequelae occurs in less well developed countries however, greater than 300,000 cases are reported to the Centers for Disease Control and Prevention in the United States each year ( 41). Today, gonococcal infection remains a major global health problem, as more than sixty million cases are reported annually worldwide ( 78).
15:1-15:19), making gonorrhea one of the oldest recorded human diseases. Reference to the contagious nature of gonococcal infection dates back to biblical times (Lev. Neisseria gonorrhoeae, the gonococcus, is a gram-negative diplococcus which causes the sexually transmitted disease gonorrhea. A model of gonococcal pathogenesis is presented in the context of the male and female human urogenital tracts. Gonococcal engagement of complement receptor 3 on the cervical epithelia results in membrane ruffling and does not promote inflammation. This is in part the result of the ability of the gonococcus to subvert the alternative pathway of complement present in the lower female genital tract. In contrast, gonococcal infection of the lower female genital tract is typically asymptomatic. Gonococci invade the nonciliated epithelia, and the ciliated cells are subjected to the cytotoxic effects of tumor necrosis factor alpha induced by gonococcal peptidoglycan and lipooligosaccharide. Similarly, gonococcal infection of the upper female genital tract also results in inflammation. Gonococcal interaction with the urethral epithelia cell triggers cytokine release, which promotes neutrophil influx and an inflammatory response. An intimate association occurs between the gonococcus and the urethral epithelium and is mediated by the asialoglycoprotein receptor.
The clinical presentations of disease are also strikingly different upon comparison of gonococcal urethritis to gonococcal cervicitis. The molecular mechanisms used by the gonococcus to initiate infection exhibit gender specificity.
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