Aetiology
Urethritis is an inflammatory condition that may result from either infection (the main focus of this topic) or trauma. Infectious causes are sexually transmitted and divided into either gonococcal (GU) or non-gonococcal (NGU) urethritis. The classic cause of acute infectious urethritis is Neisseria gonorrhoeae. Urethritis owing to any other cause is referred to collectively as NGU. Unprotected vaginal, anal, and insertive oral sex have all been associated with urethritis.[9]N gonorrhoeae and Chlamydia trachomatis may be transmitted to neonates by infectious exudates in the birth canal. Infants with N gonorrhoeae may develop ophthalmia neonatorum, rhinitis, vaginitis, urethritis, or sepsis. Infants exposed to C trachomatis may develop ophthalmia neonatorum or pneumonia.[1]
Causative organism of GU[1]
N gonorrhoeae.
Common causes of NGU[1][12][13]
C trachomatis (15% to 50%)
Mycoplasma genitalium (6% to 20%)
Trichomonas vaginalis
Yeasts
Herpes simplex virus
Adenovirus
Other bacteria such as streptococci, mycobacteria, or anaerobes.
Post-traumatic urethritis may develop in patients after intermittent catheterisation, instrumentation, or foreign body insertion or with vigorous urethral stripping (compression). Latex catheters have an increased risk of causing urethritis than silicone catheters.[14] This topic addresses only the infectious causes of urethritis.
Pathophysiology
In general, the bacteria causing urethritis have tropism for human mucosa and must attach to the cell to cause infection. For example, gonococci use pili, opacity (Opa) proteins, and lipooligosaccharide to attach to the host cell.[15]Neisseria gonorrhoeae can elude the immune system by changing the outer membrane antigens through genomic plasticity related to DNA mutation or recombination with related species.[16] Resistance to antibiotics in gonococci develops due to spontaneous mutation and/or gene acquisition, which is effectively selected due to antibiotic pressure.[17] Tissue damage in gonococcal infections is caused by activation of the host’s innate immune response and the resulting direct toxic effects of endotoxins and cytokines at the sites of colonisation.[15]
Chlamydia trachomatis preferentially infects mucosal surfaces and epithelial cells. Because C trachomatis cannot synthesise adenosine triphosphate, it is an obligate intracellular pathogen.[18] Infection leads to an acute inflammatory reaction with lymphocytic infiltration of the mucosa and submucosa. More severe disease results primarily from the immunopathological response.[19] For example, complications such as salpingitis, chronic NGU, and reactive arthritis are thought to be owing to the production of antibodies against a heat-shock protein (hsp60) that cross-reacts with human homologues.[20]
Urethritis, if untreated, may also result in epididymitis, orchitis, prostatitis, proctitis, cervicitis, iritis, pneumonia, urethral strictures, ectopic pregnancy, infertility, and pelvic inflammatory disease. Disseminated disease may occur (gonococcal urethritis only).
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