Genital Herpes

Relationship to HSV Virology

Caused by HSV. General virology (serotypes, latency mechanism, primary→dormancy→recurrence pattern) = see Herpes Simplex/VZV topic (Section 05). THIS topic = genital-specific clinical/STI focus.

Serotype/Site — Shifting Picture

HSV-2: historically DOMINANT cause genital herpes, still dominant for RECURRENT disease (better adapted to sacral ganglia). HSV-1 genital: RISING substantially (oro-genital contact) — now large/growing share of FIRST-EPISODE genital herpes in some settings. BUT recurs LESS often than HSV-2 genital (HSV-1 better adapted to trigeminal “home,” not sacral). Serotype (type-specific testing) = prognostic info for expected recurrence frequency → useful counseling.

Clinical Manifestations

First-episode PRIMARY (no prior HSV-1/HSV-2 Ab at all): MOST SEVERE. Multiple painful bilateral vesicles/ulcers, fever, malaise, myalgia, tender inguinal LAD. SYSTEMIC illness. 2-4wk resolution.

First-episode NON-PRIMARY (genital HSV-2 with prior HSV-1 Ab, or vice versa): MILDER (partial cross-reactive immunity).

Recurrent: MILDER STILL, localized. Cluster at/near original site. Prodrome (tingling/burning) hours before lesions. ~1wk resolution.

Asymptomatic viral shedding: mucosal shedding, NO visible lesion, between outbreaks. DOMINANT transmission mechanism (most transmission = neither partner aware of active lesion). COUNSELING IMPLICATION: “no visible sore = no risk” is INACCURATE. Safer-sex counseling must account for background shedding risk, not just visible-outbreak periods.

Complications

Neonatal HSV (see HSV/VZV topic for detail): vaginal delivery, actively shedding maternal tract. Risk DRAMATICALLY HIGHER with FIRST-EPISODE maternal infection NEAR TERM (no protective Ab passed yet) vs longstanding recurrent infection. → Obstetric management: active lesions/recent first episode at term = C-SECTION. Longstanding recurrent, no active lesion at labor = vaginal delivery OK.

HIV interaction: genital HSV ulceration = cofactor BOTH directions — ↑susceptibility to acquiring HIV (mucosal breach) + ↑infectiousness if HIV+ (↑local HIV shedding at ulcer). Important overlapping-epidemic relationship.

Laboratory Diagnosis

PCR (vesicle fluid/ulcer swab) = PREFERRED, more sensitive than culture, types HSV-1 vs HSV-2 directly. Viral culture: available, LESS sensitive esp. healing/crusting lesion (declining shedding). Type-specific serology (glycoprotein G difference): confirms Dx without active lesion; identifies UNRECOGNIZED infection in asymptomatic partner (substantial proportion HSV-2+ report no recognized outbreak ever) — matters for serodiscordant couple counseling.

Treatment

Acyclovir/valacyclovir/famciclovir: ↓symptom duration/severity, first-episode+recurrent. Does NOT eradicate latent infection — explicit patient point, no cure.

Episodic therapy: short course at first recurrence sign, shortens outbreak. Suppressive therapy: daily use, ≥6 episodes/yr typical threshold. ↓recurrence frequency + ↓asymptomatic shedding + ↓transmission risk to partner (benefit beyond own symptom control).

Counseling/Prevention

Lifelong incurable, ongoing transmission risk even between outbreaks → counseling = CENTRAL to management, not afterthought. Covers: natural history (recurrence declines over years), asymptomatic shedding risk, condom use (reduces, doesn’t eliminate — HSV sheds from uncovered skin), partner disclosure.

Relationship to HSV Virology

Genital herpes is caused by herpes simplex virus, and its underlying virology — the two serotypes, the latency mechanism in sensory ganglia, and the general pattern of primary infection followed by ganglion-seated dormancy and recurrence — is common to both oral and genital disease and is covered in full under Herpes Simplex and Varicella-Zoster Virus Infections. This topic focuses specifically on genital disease’s clinical picture, diagnostic approach, and management as a sexually transmitted infection in its own right, since genital herpes carries distinct epidemiological and counselling considerations that oral HSV does not.

Serotype and Site: A Shifting Picture

HSV-2 has historically caused the large majority of genital herpes and remains the dominant cause of recurrent genital disease, since it is genuinely better adapted to establish latency in the sacral ganglia serving the genital dermatome. However, HSV-1 genital infection is now rising substantially in many populations, reflecting changing sexual practices (oro-genital contact readily transmits oral HSV-1 to the genital tract), to the point that HSV-1 now accounts for a large and growing share of first-episode genital herpes in some settings — though HSV-1 genital infection, once established, tends to recur less frequently than HSV-2 genital infection, since HSV-1 remains somewhat better adapted to its “home” trigeminal ganglion than to a sacral one. This matters clinically because serotype (obtained by type-specific testing) carries real prognostic information about expected recurrence frequency, which is directly useful for patient counselling.

Clinical Manifestations

First-episode primary infection (in a person with no pre-existing HSV-1 or HSV-2 antibody at all) is typically the most severe presentation: multiple, painful genital vesicles/ulcers, often bilateral, with fever, malaise, myalgia, and tender inguinal lymphadenopathy — a systemic illness, not merely a local one, taking 2–4 weeks to fully resolve. First-episode non-primary infection (genital HSV-2 acquired by someone with pre-existing HSV-1 antibody, or vice versa) tends to be milder, since partial cross-reactive immunity blunts the presentation. Recurrent genital herpes is typically milder still and more localized — a cluster of vesicles/ulcers at or near the original site, often preceded by a prodrome of local tingling or burning hours before lesions appear, resolving within about a week.

Asymptomatic viral shedding — genital HSV shedding from mucosa with no visible lesion at all — occurs intermittently between recognized outbreaks and is now understood to be the dominant mechanism by which genital herpes actually spreads between partners, since most transmission events occur when neither partner is aware an active lesion is present. This has real, direct counselling implications: advising a patient that “no visible sore means no risk” is genuinely inaccurate, and safer-sex counselling for genital herpes has to account for this ongoing background transmission risk rather than framing risk as confined to visible-outbreak periods alone.

Complications

Neonatal HSV, acquired predominantly through vaginal delivery via an actively shedding maternal genital tract, is covered in detail under Herpes Simplex and Varicella-Zoster Virus Infections, but is worth restating here since it is the single most serious consequence of genital HSV specifically: the risk is dramatically higher with a first-episode maternal infection near term (since the mother has not yet developed protective antibody to pass to the neonate) than with a longstanding recurrent infection — a distinction that directly changes obstetric management, with active lesions or a recent first episode at term generally prompting caesarean delivery, while a history of longstanding recurrent disease with no active lesion at labour onset does not.

HIV interaction: genital herpes ulceration is a well-established cofactor for HIV transmission in both directions — increasing susceptibility to acquiring HIV (via the mucosal breach) and increasing infectiousness in an HIV-positive person with genital HSV (via increased local HIV viral shedding at the ulcer site) — a genuinely important overlapping-epidemic relationship in populations where both infections circulate.

Laboratory Diagnosis

PCR of vesicle fluid or an ulcer swab is now the preferred direct diagnostic method, more sensitive than viral culture and able to type the virus (HSV-1 vs HSV-2) directly from the specimen. Viral culture remains available but is less sensitive, particularly once a lesion has begun healing/crusting, when viral shedding has already declined. Type-specific serology (distinguishing HSV-1 from HSV-2 antibody, based on differences in the viral glycoprotein G) has a genuine, specific role distinct from lesion-based testing: it can confirm the diagnosis in a patient with a suggestive history but no active lesion available for direct testing, and — since a substantial proportion of HSV-2-seropositive individuals report no recognized symptomatic outbreak ever — serology can also identify unrecognized infection in an asymptomatic partner, which matters directly for counselling serodiscordant couples about transmission risk.

Treatment

Antiviral therapy (acyclovir, valacyclovir, or famciclovir) reduces symptom duration and severity for both first-episode and recurrent disease, and does not eradicate latent infection — a point worth making explicit to patients, since none of these drugs cure genital herpes or prevent future recurrence on their own. Episodic therapy (a short antiviral course started at the first sign of a recurrence) shortens individual outbreaks. Suppressive therapy (daily antiviral use, typically considered for patients with frequent recurrences, generally ≥6 episodes/year) reduces recurrence frequency and, genuinely importantly, reduces asymptomatic viral shedding and onward transmission risk to a sexual partner — a benefit that extends beyond the treated patient’s own symptom control.

Counselling and Prevention

Because genital herpes is a lifelong, incurable infection with a real ongoing transmission risk even between recognized outbreaks, counselling is a genuinely central part of management, not an afterthought: explaining the natural history (recurrence frequency typically declines over years), the asymptomatic-shedding transmission risk described above, condom use (which reduces but does not eliminate transmission risk, since HSV can shed from skin areas a condom doesn’t cover), and disclosure to sexual partners are all standard components of care alongside antiviral prescribing.