Gonorrhoea

Introduction

Gonorrhoea is caused by Neisseria gonorrhoeae, a Gram-negative diplococcus that infects columnar and transitional epithelium of the urethra, endocervix, rectum, pharynx and conjunctiva.¹ It is the second most commonly diagnosed bacterial STI in the UK after chlamydia, and diagnosis rates have risen substantially over the past decade, particularly in urban centres and among men who have sex with men.²

The organism's defining clinical challenge is antimicrobial resistance. N. gonorrhoeae has sequentially acquired resistance to sulphonamides, penicillin, tetracyclines, fluoroquinolones and, increasingly, azithromycin, which is why treatment guidance changes more frequently than for most other STIs and why culture with sensitivity testing - not just NAAT - is central to management.³

Transmission and pathophysiology

Transmission occurs through direct mucosal contact during vaginal, anal or oral sex, and vertically from mother to neonate during delivery, causing ophthalmia neonatorum. The organism attaches to epithelial cells via pili and outer membrane proteins, triggering a marked local neutrophilic inflammatory response, which accounts for the classically purulent discharge - in contrast to the milder, often mucoid discharge of chlamydia.

The incubation period is short, typically 2-7 days, and symptoms in men tend to appear more reliably and more quickly than in chlamydia, though asymptomatic infection is still common, especially at rectal and pharyngeal sites and in women.¹

Clinical features

In men

The classic presentation is a profuse, purulent urethral discharge with dysuria, developing rapidly after exposure. Untreated infection can ascend to cause epididymo-orchitis, presenting with unilateral testicular pain and swelling.

In women

Presentation is often milder or absent - up to half of women with gonorrhoea have no symptoms. When present, symptoms include increased or purulent vaginal discharge, dysuria, and intermenstrual bleeding. Ascending infection causes pelvic inflammatory disease (PID).

Extragenital sites

Rectal infection is usually asymptomatic but can cause proctitis with discharge and discomfort. Pharyngeal infection is almost always asymptomatic and acts as a reservoir for onward transmission and for the emergence of resistance, since antibiotic concentrations achieved in pharyngeal tissue are lower than at genital sites.

Disseminated gonococcal infection

Rarely, gonococcal bacteraemia produces disseminated gonococcal infection (DGI), classically causing a triad of tenosynovitis, dermatitis (a sparse, painless pustular or vesicular rash, often on the hands and feet) and migratory polyarthralgia, which can progress to a purulent septic arthritis, most often affecting the knee.¹ DGI should be considered in any patient presenting with an unexplained acute arthritis or rash of this pattern, particularly if there is a compatible sexual history.

Differential diagnosis

• Chlamydia: frequently co-infects; milder discharge
• Trichomonas vaginalis: frothy, malodorous discharge with vulval irritation
• Non-gonococcal urethritis: negative gonorrhoea and chlamydia testing
• Bacterial vaginosis or candidiasis: non-sexually transmitted causes of discharge in women
• Reactive arthritis: can mimic DGI but lacks the pustular rash and positive culture

Investigations

NAAT is used for screening at genital, rectal and pharyngeal sites as indicated by the sexual history, with high sensitivity. Crucially, any positive NAAT result should prompt culture from the same site before treatment, since culture allows antimicrobial susceptibility testing - essential given the trajectory of resistance in this organism.³

Microscopy of a Gram-stained urethral smear showing Gram-negative intracellular diplococci within polymorphonuclear leukocytes is highly sensitive and specific in symptomatic men and can support same-day presumptive diagnosis, though it is less reliable in women and at rectal or pharyngeal sites.

As with chlamydia, a positive result should prompt a full STI screen and partner notification for the preceding 3 months (or the last partner if longer).

Management

First-line: ceftriaxone 1 g by intramuscular injection as a single dose.⁴ This should be given as monotherapy where the organism's susceptibility is unknown, reflecting a shift away from previous dual therapy with azithromycin, which is now reserved for specific resistance patterns or allergy given concerns about driving azithromycin resistance.

Treatment should ideally be guided by, or at least followed up with, culture and sensitivity results, since local and national resistance patterns evolve; current BASHH guidance should always be checked rather than relied upon from memory.³

Partner notification covers the preceding 3 months, with partners tested and treated. Sexual abstinence is advised until the patient and partner(s) have completed treatment and had a negative test of cure.

Complications

In women, ascending infection causes PID with the same downstream risks of tubal infertility, chronic pelvic pain and ectopic pregnancy as chlamydia, and can also cause Fitz-Hugh-Curtis syndrome (perihepatitis from peritoneal spread, causing right upper quadrant pain). In men, epididymo-orchitis and, rarely, urethral stricture from repeated infection. Disseminated infection (see above) is a recognised but uncommon complication. Vertical transmission causes ophthalmia neonatorum, a sight-threatening neonatal conjunctivitis requiring urgent treatment.

Red flags

Prognosis

Uncomplicated gonorrhoea treated with an effective antibiotic resolves rapidly. The principal threat to good outcomes at both an individual and population level is antimicrobial resistance: an organism resistant to available first-line agents would leave few remaining treatment options, which is why surveillance, culture-based confirmation and mandatory test of cure remain central to management even though they add complexity compared with chlamydia.