Neisseria gonorrhoeae: Antigenic Structure, Genetics and Antigenic Heterogeneity, Pathogenesis, Pathology and Clinical Findings, Diagnostic Flashcards
(10 cards)
Neisseria gonorrhoeae: antigenic structure
Neisseria gonorrhoeae is a gram-negative diplococcus with pili (fimbriae) and outer membrane proteins. The pili allow attachment to mucosal cells and undergo antigenic variation. The outer membrane has porins (Por proteins), Opa proteins for adherence, Rmp proteins (block antibodies), lipooligosaccharide (LOS, similar to endotoxin), and IgA protease that cleaves IgA on mucosal surfaces.
Neisseria gonorrhoeae: genetic variation and heterogeneity
Genetic variation occurs via transformation, conjugation, and antigenic variation. The pili and Opa proteins vary greatly, helping the bacteria evade immune responses. Phase variation allows turning on/off expression of these antigens. This heterogeneity makes vaccine development difficult.
Neisseria gonorrhoeae: pathogenesis
The bacterium attaches to mucosal epithelial cells via pili and Opa proteins, invades them, and triggers an intense neutrophilic response. It produces lipooligosaccharide (LOS), which causes inflammation and tissue damage. It releases IgA protease to evade mucosal immunity. In men, it causes urethritis; in women, cervicitis, salpingitis, and PID. Disseminated gonococcal infection (DGI) can lead to arthritis and skin lesions.
Neisseria gonorrhoeae: pathology
The inflammation caused by N. gonorrhoeae results in purulent exudates and damage to the mucosal surfaces. In women, ascending infection can cause salpingitis, tubo-ovarian abscesses, and infertility. In neonates, eye infection (ophthalmia neonatorum) occurs due to exposure during childbirth.
Neisseria gonorrhoeae: clinical findings
In men: purulent urethral discharge and dysuria. In women: often asymptomatic or mild cervicitis, but can progress to pelvic inflammatory disease (PID), with abdominal pain, fever, and infertility. Disseminated gonococcal infection (DGI): septic arthritis, pustular skin lesions, tenosynovitis. Rectal and pharyngeal infections can occur. Neonates: ophthalmia neonatorum (purulent conjunctivitis).
Neisseria gonorrhoeae: diagnostic tests
Diagnosis includes gram stain of urethral discharge (shows gram-negative diplococci inside neutrophils, useful in men), culture on Thayer-Martin (chocolate agar + antibiotics), and nucleic acid amplification tests (NAATs), which are highly sensitive and specific. NAAT is the preferred test for both symptomatic and asymptomatic cases.
Neisseria gonorrhoeae: immunity
Immunity is incomplete. Reinfection is common due to antigenic variation of pili and Opa proteins. No protective antibodies develop consistently. IgA protease helps evade mucosal immunity. No effective vaccine exists due to antigenic variability.
Neisseria gonorrhoeae: treatment
First-line treatment is a single intramuscular dose of ceftriaxone (a third-generation cephalosporin), often combined with oral doxycycline or azithromycin to cover possible coinfection with Chlamydia trachomatis. Resistance to penicillin, tetracycline, and fluoroquinolones is widespread. Some strains show reduced susceptibility to ceftriaxone, making resistance monitoring critical.
Neisseria gonorrhoeae: epidemiology
It is a sexually transmitted infection with worldwide prevalence. Highest rates occur in young adults. Humans are the only reservoir. Risk factors include unprotected sex, multiple partners, and co-infection with other STIs. Asymptomatic carriers, especially women, contribute to spread.
Neisseria gonorrhoeae: prevention and control
Prevention involves safe sex practices (condom use), early detection and treatment of cases and their contacts, and screening high-risk groups. No vaccine is available. Neonatal eye infection is prevented by prophylactic eye treatment (erythromycin ointment) at birth.
