Genital Herpes (HSV-2)

Sexual contact with an infected partner is the primary trigger for HSV-2 transmission.

Initial exposure to HSV-2 leads to primary genital infection.

Reactivation can be triggered by stress, illness, or immunosuppression.

Mucosal microabrasions during intercourse facilitate viral entry.

Hormonal changes may influence susceptibility to reactivation.

The incubation period from exposure to symptom onset is typically 2 to 12 days.

Latency in dorsal root ganglia is lifelong with intermittent reactivation.

Recurrent outbreaks often occur within weeks to months after primary infection.

Asymptomatic viral shedding can occur during latency without lesions.

Latency period allows virus to evade immune clearance.

Initial symptoms may be mild or mistaken for other genital conditions such as yeast infection or bacterial vaginosis.

Patients may not seek care due to stigma or lack of awareness.

Asymptomatic viral shedding leads to undiagnosed transmission.

Misinterpretation of lesions as herpes zoster or chancroid delays diagnosis.

Lack of routine HSV testing in genital ulcers contributes to delayed diagnosis.

Painful genital vesicles and ulcers are the hallmark clinical presentation.

Burning, itching, or tingling sensation often precedes lesion appearance (prodrome).

Dysuria and urethral discomfort are common in urethral involvement.

Fever, malaise, and headache may accompany primary infection.

Tender inguinal lymphadenopathy is frequently present during outbreaks.

Patients typically report painful genital vesicles or ulcers preceded by prodromal symptoms like burning or tingling.

Primary infection often presents with fever, malaise, and inguinal lymphadenopathy.

Lesions evolve from vesicles to pustules and then painful ulcers over 7-10 days.

Recurrent episodes are usually milder and shorter in duration than primary infection.

Dysuria and urethritis may accompany lesions in males.

History of prior genital herpes outbreaks indicates recurrent HSV-2 infection.

Previous diagnosis of other sexually transmitted infections increases risk.

Immunosuppressive conditions such as HIV/AIDS worsen disease severity.

Use of immunosuppressive medications may precipitate reactivation.

No protective immunity after primary infection leads to lifelong susceptibility to recurrences.

No direct heritable genetic predisposition is established for HSV-2 infection.

Family members may share similar sexual behavior risk factors.

Rarely, familial immunodeficiency syndromes can increase susceptibility to severe HSV infections.

Vertical transmission risk is increased if mother has active genital HSV-2 at delivery.

No known familial clustering of HSV-2 beyond shared environmental exposures.

Multiple painful vesicles and ulcers on the genitalia, perineum, or perianal area are characteristic.

Erythematous base surrounding the vesicles and ulcers is commonly observed.

Tender inguinal lymphadenopathy may be present due to regional lymph node involvement.

Friable mucosal erosions can be seen in severe cases involving the urethra or cervix.

Dysuria and urethral discharge may be noted if the urethra is involved.

Maintain good genital hygiene to reduce irritation and secondary bacterial infection.

Use of analgesics and topical anesthetics to relieve pain and discomfort during outbreaks.

Avoid sexual contact during active lesions to prevent transmission.