Uncomplicated cases of gonorrhea include an acute urogenital infection that involves the urethra in men and endocervix in women who have reached the reproductive age. In some cases infection can also occur on the female urethra, rectum or pharynx. In girls of the prepubescent stage of development and the post menopausal women, infection presents as virginitis as opposed to as cervicitis. This age dependent difference in the nature of infection is a result of differences in the histology of the endocervical region.
Upon entrance in the urogenital tract, N. gonorrhoeae facilitate adherence to columnar cells hence withstanding the flushing force of urine in the urethral tract as well as the continual cervical mucus shredding. Adherence to the epithelium is aided by the pili and the functionally associated gonococcal lipooligosaccharides; OMP II and opacity proteins (Jersey, 2000). Human membrane co-factor protein (CD46) acts as the receptor for the N. gonorrhoeae pili. Ironically, it is the same human membrane molecule that serves as measles virus host cell receptor.
The opacity proteins (Opa) bind to the host cells’ CD66 glycoproteins which are a subset of the carcinoembryonic family (Apicella et al 1996). Consequently, Opa mediated adherence induces the uptake of the bacterial cells by the neutrophils and the epithelial cells. This mode of entry into the cell have been visualized in tissue culture assays, visualization of N. gonorrhoeae within cervical and urethral cells as well as in the subepithelium of an endometrial tissue that have been excised from a 10 week case in an infected woman(Jerse 2000; Apicella et al 1996).
Polarized epithelial cell intracellular invasion studies suggest that invasion of the subepithelium occurs via the traversal through the epithelial cellular lining. Invasion of the subepithelium promotes the subepithelial space access and hence the entry of the bacteria into the bloodstream hence the disseminated gonococcal infection (DGI). Locally disseminated infection of the locally ascended infection occurs when N. gonorrhoeae ascends from the lower genital tract to higher tissues or organs in the genital tract like epididymitis in men and endometricitis, pelvic peritonitis and salpingitis in female patients.
These manifestations in the female genital tract are collectively referred to as pelvic inflammatory disease (PID). N. gonorrhoeae species selectively adhere to non ciliated secretory fallopian tubes cells. Invasion of the subepithelium occurs via the epithelium and the adjacent cells. Gonococcal cells secret toxic lipooligosaccharides (LOS) that exfoliate ciliated cells hence reducing ciliary activity. Extensive damage to the female reproductive tract may lead to an irreversible case of infertility.
In addition to the primary gonococcal infections, post infection complications may include ectopic pregnancies, chronic pelvic pain, and a life threatening case originating from the fallopian tubes scarring (Jerse 2000). There is no conclusive evidence to explain the mechanisms by which the pathogen ascends the female reproductive tract but avenues like traveling while attached to spermatozoa or reflux of menstrual blood form the major hypotheses to this end.
Locally disseminated gonococcal infections are more prevalent (for instance between 10-20% of patients with gonococcal cervitis). Systematically disseminated gonococcal infections (DGI) have been observed in 0. 5-3. 0% of patients presenting untreated cases of mucosal infections (Jerse 2000). Hematogenous spread of the bacterial infection to the skin and joints causes acute dermatitis and arthritis respectively. In DGI, infection presentation as endocarditis is less prevalent. DGI occurs in most women within seven days after menstruation. N.
gonorrhoeae is equipped with mechanisms of persistence that allow it to avoid or in some cases capitalize on the hot factors it encounters during infection. Most importantly, the bacteria have transcriptional regulation mechanisms of genes to provide an effective response to the stimuli in the mucosal layer. This among other persistence mechanisms enable the bacteria to gain entrance into the human body through nutritionally different micro environments as well as counter the physiological stress induced by a variety of non specific host defenses(Jerse 2000).