Genital herpes

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Genital herpes is caused by herpes simplex virus type 1 or 2. Virus enters genital or sacral sensory endings after mucocutaneous contact, travels to dorsal-root ganglia and establishes lifelong latency with intermittent reactivation.

HSV-1 increasingly causes first genital episodes and tends to recur less often genitally than HSV-2. Clinical appearance cannot reliably distinguish type, syphilis, mpox or traumatic ulceration, so lesion NAAT is important.

The first recognised episode is not always newly acquired; previously unrecognised infection can reactivate years later. Counselling should avoid unsupported conclusions about relationship timing or source.

Antivirals shorten symptoms and shedding but do not eradicate latency. Episodic treatment is started at prodrome, while daily suppression reduces recurrences and transmission and is selected according to frequency, distress, pregnancy and immune status.

Key points

Primary genital herpes may cause multiple painful vesicles or shallow ulcers, dysuria, tender nodes, fever and profound malaise.
Recurrent disease is usually shorter and milder, often preceded by tingling or burning in a similar dermatomal area.
Swab the base of a fresh vesicle or ulcer for HSV-1 and HSV-2 NAAT; blood serology does not confirm the cause of an active ulcer.
Start oral antiviral treatment within five days of a first episode or while new lesions are still appearing; do not wait for the swab result.
Give aciclovir 400 mg orally three times daily for five days for an uncomplicated first episode, extending when healing is incomplete.
Use saline bathing, regular analgesia, topical lidocaine and measures that reduce urinary pain alongside antivirals.
Transmission can occur during asymptomatic shedding; avoid sex during prodrome or lesions and discuss condoms and disclosure without stigma.
Pregnancy timing and whether infection is new or recurrent determine delivery and neonatal management.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

HSV-1 genital acquisition

Orogenital or genital contact transmits HSV-1, which increasingly causes first episodes and generally recurs less often genitally.

HSV-2 genital acquisition

Genital skin or mucosal contact transmits HSV-2 during lesions or asymptomatic shedding from an infected partner.

Perinatal exposure

Neonatal infection occurs mainly during birth through an infected genital tract, especially after recent maternal acquisition.

Autoinoculation and direct contact

Virus can rarely transfer to eye, finger or damaged skin during active lesions without careful hand hygiene.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Epithelial replication
HSV enters microscopic breaks, replicates within epithelial cells and produces grouped vesicles that evolve into painful erosions.
2
Sensory neuroinvasion
Virus travels retrogradely along sensory axons to sacral dorsal-root ganglia, where lifelong latent genomes persist between clinically apparent recurrences.
3
Reactivation
Latent virus periodically returns along sensory nerves to genital skin, causing recurrent lesions or asymptomatic shedding that can transmit infection.
4
Host inflammatory injury
Local immune responses create pain and ulceration, while impaired cellular immunity permits extensive chronic or disseminated disease.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

First clinical episode

Clusters of painful vesicles, erosions or ulcers with bilateral tender nodes, dysuria, fever and malaise suggest primary or first recognised herpes.

Recurrent episode

Localized tingling, burning and a small group of lesions returning at a familiar site indicates reactivation.

Herpetic cervicitis

Pelvic discomfort, bleeding and friable ulcerative cervical lesions can accompany a first episode and mimic bacterial cervicitis.

Sacral radiculitisRed flag

Urinary retention, constipation, perineal sensory change or leg symptoms during herpes suggests autonomic and nerve-root involvement.

Disseminated infectionRed flag

Widespread vesicles with hepatitis, pneumonitis, encephalopathy or sepsis is rare but life threatening in pregnancy or immunosuppression.

Neonatal herpesRed flag

A neonate with vesicles, conjunctivitis, poor feeding, fever, hypothermia, seizures or unexplained liver injury needs emergency treatment.

Red flags requiring action

Severe pain with inability to pass urine may require admission, analgesia and temporary catheterisation.
Headache, photophobia, neck stiffness, altered behaviour, weakness or sacral sensory symptoms suggests HSV neurological involvement.
Widespread lesions, hepatitis, pneumonitis or shock can occur in pregnancy or major immunosuppression.
Any suspected neonatal herpes with vesicles, lethargy, poor feeding, seizures or sepsis requires immediate intravenous aciclovir.
A first genital episode late in pregnancy has high neonatal-transmission risk and needs same-day specialist maternity planning.
Persistent, hypertrophic or treatment-resistant ulcers in advanced HIV require culture, resistance and alternative-diagnosis assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Lesion HSV NAATFirst step
Why
Confirm herpes and distinguish HSV-1 from HSV-2 using material from a fresh vesicle or ulcer base.
Interpretation and limitations
Sensitivity falls as lesions crust and heal; a negative late swab does not exclude clinically likely recurrent herpes.
02
Syphilis serology and lesion testing
Why
Exclude a concurrent or alternative infectious ulcer diagnosis.
Interpretation and limitations
Early primary syphilis serology can be negative, so repeat after the window period and use direct testing where available.
03
HIV and wider STI screen
Why
Identify coinfection, prevention needs and immune status affecting severity.
Interpretation and limitations
Offer site-specific chlamydia and gonorrhoea tests and hepatitis assessment according to exposure; repeat HIV after the appropriate window.
04
Pregnancy assessment
Why
Establish gestation, timing of acquisition and fetal or labour concerns.
Interpretation and limitations
First acquisition in the third trimester creates much greater transmission risk than established recurrent infection.
05
CSF HSV PCR
Why
Confirm meningitis or encephalitis when neurological symptoms occur.
Interpretation and limitations
Obtain after urgent assessment, but do not delay intravenous aciclovir for suspected encephalitis while awaiting lumbar puncture or results.
06
Renal function
Why
Guide aciclovir dose and hydration in severe disease, older adults or kidney impairment.
Interpretation and limitations
Renal accumulation can cause crystal nephropathy and neurotoxicity; adjust dose and avoid dehydration.
07
Culture and susceptibility
Why
Investigate persistent lesions despite adherent antiviral treatment in profound immunosuppression.
Interpretation and limitations
Resistance is uncommon in immunocompetent adults but requires specialist testing and alternative therapy when proven.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Primary syphilis

A classically painless indurated chancre and treponemal tests contrast with grouped painful herpetic vesicles, although appearances overlap.

Mpox

Deep firm umbilicated lesions, systemic symptoms and exposure pattern can resemble severe genital herpes and require specific PCR.

Aphthous ulceration

Reactive or idiopathic sharply demarcated ulcers occur without HSV detection, may follow systemic illness and often accompany oral aphthae or inflammatory disease.

Contact or traumatic erosion

Friction, irritant products and dermatitis disrupt genital epithelium without a viral prodrome; exposure history and surrounding dermatitis provide diagnostic clues.

Behçet disease

Recurrent oral and genital ulcers with ocular, skin, neurological or vascular inflammation suggest Behçet disease and require rheumatology or specialist multidisciplinary assessment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01FIRSTTreat the first episode promptlyFirst stepPainful genital vesicles or ulcers began within five days or new lesions continue to appear.

1Swab a fresh lesion for typed HSV NAAT and obtain syphilis, HIV and site-specific STI testing.
2Start aciclovir 400 mg orally three times daily for five days without waiting for the result.
3Provide regular analgesia, saline bathing, topical lidocaine and advice to pass urine in water when severe dysuria occurs.
4Review healing near day five and extend antiviral therapy if new lesions continue or ulcers remain substantially unhealed.

02SEVEREAdmit complicated herpesThere is urinary retention, neurological disease, dissemination, inability to take tablets or major immune compromise.

1Assess bladder, neurological, hepatic and cardiorespiratory function and obtain renal profile, blood and lesion specimens.
2Give intravenous aciclovir 10 mg/kg every eight hours with renal adjustment and hydration under specialist care.
3Catheterise urinary retention when required and investigate meningitis, encephalitis, hepatitis or bacterial superinfection.
4Step down to oral treatment only after clear clinical improvement and a specialist-defined total duration.

03RECURRENTChoose episodic or suppressive careTyped or strongly established genital herpes recurs and affects symptoms, relationships or quality of life.

1For episodic care, provide aciclovir 800 mg orally three times daily for two days to start during prodrome.
2For frequent or distressing recurrence, use aciclovir 400 mg orally twice daily as suppressive therapy.
3Review suppression after six to 12 months, allowing a break when appropriate to reassess natural recurrence frequency.
4Discuss asymptomatic shedding, condoms, avoiding sex during prodrome and shared decision-making about partner disclosure.

04PREGNANCYPrevent neonatal transmissionGenital herpes is first diagnosed or recurs during pregnancy or lesions are present near labour.

1Contact the specialist maternity and sexual-health team the same day and establish whether infection is primary, non-primary or recurrent.
2Use pregnancy-approved aciclovir treatment and plan suppressive therapy from the gestation specified by current national guidance.
3Consider caesarean birth when a first episode occurs within six weeks of expected delivery because shedding and transmission risk are high.
4Create a neonatal observation, sampling and aciclovir plan before birth and avoid invasive fetal monitoring when active lesions are present.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Shortens lesion duration, pain and viral shedding during an uncomplicated first clinical episode.

Aciclovir for first episode

Give 400 mg orally three times daily for five days, starting within five days of onset or while new lesions continue to appear.

Adjust for renal impairment, maintain hydration and extend the course when lesions are still appearing or substantially unhealed.

Aborts or shortens a recurrence when the patient keeps treatment available for rapid self-initiation.

Aciclovir episodic recurrence

Give 800 mg orally three times daily for two days, begun during prodrome or immediately when recurrent lesions appear.

Confirm the recurrent pattern, adjust in renal impairment and reassess atypical, severe or non-healing ulcers rather than repeating courses.

Reduces recurrence frequency, asymptomatic shedding and transmission risk while taken.

Aciclovir suppressive therapy

Give 400 mg orally twice daily for continuous suppression, with review after six to 12 months.

It does not eliminate transmission or latency; monitor renal context and revisit the need, adherence and psychological impact.

Achieves reliable systemic exposure when organ-threatening infection or impaired oral absorption is present.

Intravenous aciclovir

Give 10 mg/kg intravenously every eight hours for severe, disseminated, neurological or neonatal-risk disease, with renal adjustment and specialist duration.

Infuse with adequate hydration, monitor creatinine and neurological status and adjust using ideal or adjusted weight according to local protocol.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Aseptic meningitis

HSV-2 can inflame meninges, causing severe headache, photophobia, neck stiffness and a lymphocytic CSF pattern, sometimes during a first genital episode.

Sacral radiculitis

Sacral nerve-root inflammation causes urinary retention, constipation, perineal sensory change and occasional lower-limb weakness, sometimes requiring temporary bladder catheterisation.

Disseminated herpes

Pregnancy or severe immunosuppression permits visceral spread with hepatitis, pneumonitis, encephalitis and multiorgan failure, creating a life-threatening emergency.

Neonatal herpes

Neonatal skin, eye and mouth disease can progress to encephalitis or disseminated infection with high mortality and long-term neurological disability.

Psychosexual distress

Stigma, fear of transmission and unpredictable recurrences can impair relationships, sexual confidence and wellbeing even when physical disease is medically controllable.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review first episodes at about five days for healing, urinary function, pain control and need to extend therapy.
Monitor renal function and hydration during intravenous therapy or when oral dosing occurs with kidney impairment.
Reassess neurological symptoms, retention, hepatitis or dissemination urgently rather than waiting for lesions to resolve.
During suppression record recurrence frequency, adherence, adverse effects, sexual wellbeing and preference for continued therapy.
In pregnancy document viral type, acquisition timing, suppressive plan, mode of birth and neonatal management.
Repeat syphilis or HIV testing after relevant window periods when initial ulcer screening is negative.
Provide a rapid route back for new pregnancy, severe pain, inability to void, widespread lesions or neonatal symptoms.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

First episode is not first acquisition

Previously silent infection may reactivate, so lesion onset cannot reliably date transmission or identify a particular partner.

Type predicts recurrence

Genital HSV-2 generally reactivates and sheds more frequently than genital HSV-1, informing prognosis after typed NAAT.

Late swabs lose sensitivity

Fresh vesicle fluid and ulcer base yield more virus than a dry, crusted or almost healed lesion.

Antivirals do not eradicate latency

Clinical response does not remove virus from sensory ganglia, so recurrence and asymptomatic shedding remain possible.

Retention can be neurological

Severe dysuria is common, but a full bladder with sacral symptoms suggests autonomic radiculitis requiring admission.

Pregnancy risk is timing dependent

New infection near delivery leaves little time for maternal antibodies, making neonatal risk far higher than recurrent disease.

11Common pitfallsFrequent interpretation and management errors.

01
Do not use blood HSV serology to attribute an active genital ulcer.
02
Do not delay first-episode antivirals while awaiting lesion PCR.
03
Do not assume a first recognised outbreak proves recent partner transmission.
04
Do not miss syphilis, mpox or non-infective ulceration in atypical lesions.
05
Do not manage urinary retention or neurological symptoms as routine outpatient herpes.
06
Do not make a delivery plan for late-pregnancy acquisition without specialist maternity input.