![]() ![]() Confirmation of the clinical suspicion of gonorrhea is established by detection of N. Populations that engage in anogenital sexual intercourse and/ or insertive oral sex will require screening for gonorrhea from the anus and pharynx in addition to urogenital screening. gonorrhoeae infection's diagnosis is made by direct detection of the gonococcal pathogen in urogenital, anorectal, pharyngeal, or conjunctival swab specimens or first-catch urine. ĭiagnostic laboratory assays are essential to confirm the clinical suspicion of gonorrhea. gonorrhoeae manifest systemically as fever/septicemia, tenosynovitis, arthritis, and vasculitis. If left untreated, gonorrheal infection of the rectum can proceed to manifest with rectal pain, bleeding, discharge, and proctitis. Like cervicitis, gonococcal infection of the pharynx, the rectum, and the female urethra often present asymptomatically or with subtle symptoms. Male urogenital gonococcal complications include orchitis, epididymitis, penile lymphangitis, penile edema, and post-infectious urethral strictures. The prevalence of rectal and pharyngeal gonococcal infections has been increasing among populations of men who have sex with men. The most common clinical manifestations of gonococcal disease in males include penile purulent discharge, dysuria, and testicular discomfort. Īlthough many females, more than 50%, will not manifest symptoms of their gonococcal cervix infections, most males, more than 90%, will manifest urogenital gonorrhea symptomatically. Gonococcal infections complicating pregnancy can lead to adverse pregnancy outcomes such as low birth weight newborns and transmission to newborns resulting in oropharyngeal or conjunctival infections. Pelvic inflammatory disease can manifest with pelvic pain, infertility, and increase the risk of ectopic pregnancy. If cervicitis goes undetected and untreated, ascending gonococcal infection can result in upper reproductive tract involvement such as salpingitis and pelvic inflammatory disease. Gonorrheal infection of the Bartholin’s glands adjacent to the vaginal introitus manifests as labial soft tissue swelling, abscess formation, and pain. When female patients with gonococcal urogenital infections have symptoms, they may complain of vaginal discharge, dysuria, or pelvic pain. gonorrhoeae most commonly infects the cervix, resulting in cervicitis. gonorrhoeae has evolved multiple mechanisms to combat the innate and adaptive immunity systems of their host organisms’ immune defenses. Gonococci are classified as either serum-sensitive or serum-resistant based upon their sensitivity to killing by complement activation serum-resistant strains have the potential to cause disseminated infection. ![]() Neisseria gonorrhoeae induces localized infection at the anatomic site of inoculation, typically urethra, cervix, pharynx, or anus in adults and the eye conjunctiva or the pharynx of newborns, but dissemination can occur. Ruffling then allows gonococci to enter host cells in large vacuoles called macropinosomes and subsequently multiply within infected cells. This causes extensive rearrangement of the host cell actin, resulting in large projections called ruffles. This communication is initiated by the binding of pili to the CR3. Invasion of cervical epithelium involves bacterial cells interacting with host cell complement receptors type 3 (CR3). LOS attaches to sperm cells and likely leads to transmission from males to uninfected sexual partners. Other surface proteins involved in cellular attachment include Opa, opacity-associated proteins, and LOS, lipooligosaccharide. ![]() Pili also provide motility and protection. Their ability to lengthen and retract allows the bacteria to attach from a distance and move closer to the epithelial cells, promoting cellular invasion. Hair-like appendages, pili cover the bacterial surface. gonorrhoeae utilize pili to initiate adhesion to epithelial cells. Gonorrhea has multiple surface proteins that facilitate adhesion. ![]() gonorrhoeae infection starts with the adhesion of gonococci to epithelial cells, followed by local cellular invasion. ![]()
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