Genital Herpes

Key points

  • Organism: herpes simplex virus type 1 or 2 (HSV-1, HSV-2), both now common causes of genital infection.
  • Presentation: painful grouped vesicles that ulcerate, with dysuria, local lymphadenopathy and systemic symptoms in a first episode.
  • Natural history: the virus establishes lifelong latency in dorsal root ganglia; recurrences are usually milder and shorter than the first episode.
  • Diagnosis: viral PCR (or culture) from a swab of the base of an unroofed vesicle or ulcer.
  • Management: aciclovir (or valaciclovir/famciclovir) for first episodes and severe recurrences; supportive care and analgesia throughout.
  • Recurrence prevention: suppressive aciclovir considered for frequent recurrences (typically ≥6 per year).
  • Pregnancy: the timing of acquisition, not just presence of infection, determines neonatal risk and delivery mode.
  • Psychosocial impact: often disproportionate to the physical severity; explanation and reassurance are a core part of management.

Introduction

Genital herpes is caused by herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2), double-stranded DNA viruses that establish lifelong latent infection in sensory nerve ganglia after primary mucocutaneous infection.1 Historically HSV-1 was associated with oral disease ('cold sores') and HSV-2 with genital disease, but HSV-1 is now a leading cause of first-episode genital herpes in many countries, largely reflecting oral-genital contact.

It is one of the most common STIs in the UK, and its impact extends beyond the physical symptoms: the diagnosis carries substantial psychological weight because of its incurable, lifelong and potentially recurrent nature, which makes clear explanation and destigmatising counselling as important as antiviral treatment.2

Virology and natural history

After initial mucocutaneous inoculation, the virus replicates locally, causing the primary episode (if symptomatic), then travels retrogradely along sensory neurones to establish latency in the dorsal root ganglia - the sacral ganglia for genital infection. Periodic reactivation causes recurrent episodes, and can also cause asymptomatic viral shedding, which is an important, under-recognised source of onward transmission.1

HSV-2 recurs in the genital area more frequently than HSV-1, which is one clinically useful distinction to make at diagnosis, since it affects counselling about expected recurrence frequency, even though management of an individual episode is identical for both types.

Clinical features

First episode

A primary episode is often the most severe, particularly in someone with no pre-existing HSV antibodies of either type. Painful, grouped vesicles appear on the genitals, perineum or perianal area, which rapidly rupture to form shallow, tender ulcers. Associated features include marked dysuria (sometimes severe enough to cause urinary retention, particularly in women), tender inguinal lymphadenopathy, and systemic symptoms such as fever, myalgia and headache, reflecting viraemia.1

Photograph of multiple grouped vesicular and ulcerated lesions on the vulva in genital herpes.
Grouped vesicles and shallow ulcers of genital herpes.SOA-AIDS Amsterdam, CC BY-SA 3.0, via Wikimedia Commons

Recurrent episodes

Recurrences are usually shorter, milder and more localised than the first episode, often preceded by a prodrome of tingling, itching or burning at the site hours before lesions appear. Systemic symptoms are uncommon in recurrences. Frequency varies widely between individuals and tends to decrease over time.

Asymptomatic shedding

The virus can be shed from genital skin and mucosa without any visible lesion or symptom, which explains why transmission commonly occurs between partners with no active outbreak at the time, and why consistent condom use reduces but does not eliminate transmission risk.2

Differential diagnosis

  • Syphilis (primary chancre): typically a single painless ulcer, not grouped painful vesicles
  • Chancroid: painful ulcer(s), but ragged rather than vesicular in origin, and rare in the UK
  • Behçet's disease: recurrent oral and genital ulceration with additional systemic features
  • Fixed drug eruption: recurs at the same site after a specific drug exposure
  • Candidiasis or contact dermatitis: cause vulval soreness and fissuring, but not discrete vesicles/ulcers

Investigations

Viral PCR (or, less commonly now, viral culture) from a swab taken from the base of a deroofed vesicle or from an ulcer is the investigation of choice, and can also type the virus as HSV-1 or HSV-2, which is useful prognostically.3 Swabbing should be done as early as possible in the episode, since viral yield falls as lesions heal.

Type-specific HSV serology (detecting antibodies to HSV-1 or HSV-2 glycoproteins) has a limited role - it cannot diagnose an acute episode, since antibodies take time to develop, but can occasionally help in specific situations such as investigating a partner's status or an atypical presentation.

As with other STIs, a diagnosis of genital herpes should prompt a full sexual history and screen for other infections.

Management

First episode: oral aciclovir 400 mg three times daily for 5 days (or valaciclovir/famciclovir as alternatives), started as early as possible - ideally within 5 days of onset or while new lesions are still forming.4 Supportive measures include saline bathing, topical anaesthetic gel (e.g. lidocaine) for severe dysuria, adequate analgesia, and advice to pass urine in a bath or shower if micturition is very painful.

Recurrent episodes are often mild enough not to need antivirals, but a short course of aciclovir started at the first sign of prodrome can shorten the episode if started promptly.

Suppressive therapy with daily aciclovir is considered for patients with frequent recurrences (commonly defined as six or more per year) or where recurrences cause significant distress or disruption, and reduces both the frequency of episodes and the amount of asymptomatic viral shedding.4

Genital herpes in pregnancy

The key factor determining neonatal risk is the timing of maternal acquisition relative to delivery, not simply the presence of infection.5 A primary infection acquired in the third trimester, particularly close to delivery, carries the highest risk of neonatal herpes, because the mother has not yet developed protective antibodies to pass to the fetus, and viral shedding at the time of delivery is likely.

Recurrent genital herpes in a woman with pre-existing HSV antibodies carries a much lower neonatal transmission risk, because passively transferred maternal antibody protects the infant. Management is tailored accordingly: primary infection in the third trimester is generally an indication for caesarean section, while women with recurrent disease can usually be supported to deliver vaginally, sometimes with suppressive aciclovir from 36 weeks to reduce the risk of an outbreak at term.

Complications

Urinary retention can complicate a severe first episode, particularly in women, due to pain and local oedema, and may require temporary catheterisation. Secondary bacterial infection of ulcers can occur. Rarely, HSV can cause aseptic meningitis (more common with HSV-2) or, very rarely, disseminated infection in the immunosuppressed. Neonatal herpes, acquired at delivery, is a severe and sometimes fatal or disabling condition, which is why the pregnancy-specific management above matters so much.5

Red flags

Prognosis

Genital herpes is a lifelong infection with no cure, but the natural history is generally favourable: recurrences become less frequent and less severe over time for most people, and antiviral treatment plus good counselling allow the great majority of patients to manage the condition with minimal disruption to their lives and relationships. The main ongoing risks are to sexual partners, who should be informed, and to a fetus if infection is acquired or reactivates around the time of delivery.

References

  1. BASHH. UK national guideline for the management of genital herpes. 2014. Available here
  2. UK Health Security Agency. Sexually transmitted infections and screening in England, annual report. Available here
  3. Gupta R, Warren T, Wald A. Genital herpes. The Lancet. 2007. Available here
  4. NICE Clinical Knowledge Summaries (CKS). Herpes simplex - genital. Available here
  5. Royal College of Obstetricians and Gynaecologists. Management of genital herpes in pregnancy. Green-top Guideline No. 30. 2014. Available here

This article is written for revision and education. It is not clinical guidance and must not be used to make decisions about the care of a patient. Always check current NICE guidance and local protocols.

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