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Emergency And Acute Medicine – Genital Herpes
Overview And Definition
Genital herpes is a lifelong, recurrent viral infection caused by herpes simplex virus (HSV). Approximately one in four Americans older than 30 years are seropositive for HSV-2, though most are asymptomatic. The infection is characterized by periods of latency and reactivation, with viral shedding that can occur even in the absence of visible lesions, contributing to ongoing transmission.
Disease Course And Natural History
Primary infection has an incubation period of approximately 2–12 days, with symptoms typically peaking 8–10 days after onset and lesions healing within about three weeks. Primary disease may present with a more severe clinical syndrome and complications such as meningitis, encephalitis, or hepatitis. Importantly, more than half of first recognized episodes are not true primary infections, as earlier asymptomatic exposure is common.
Recurrent infection results from viral reactivation in the dorsal root ganglia. The average patient experiences about four recurrences per year. Recurrences are generally milder, involve fewer lesions, and resolve within 10 days. HSV-1 genital infections recur significantly less often than HSV-2.
Asymptomatic infection is common, with intermittent viral shedding that frequently leads to transmission by individuals without symptoms or lesions.
Etiology And Risk Factors
Most cases (70–90%) of genital herpes are caused by HSV-2, with the remainder caused by HSV-1. Genital HSV-1 infections are increasing in prevalence, likely due to higher rates of oral–genital contact and reduced childhood exposure to HSV-1, leaving more adolescents and adults susceptible. Acquisition of HSV-2 in individuals with prior HSV-1 infection tends to be less symptomatic, whereas acquisition of HSV-1 in those with HSV-2 is uncommon.
Genital herpes is strongly associated with HIV and other sexually transmitted infections. HSV infection increases both susceptibility to HIV and HIV viral shedding during HSV reactivation. Despite extensive research, no effective HSV vaccine is currently available.
Clinical Manifestations
Patients commonly report local pain, itching, or burning. A prodrome of tingling, itching, or pain may occur 1–2 days before lesion eruption and can sometimes mimic radicular pain such as sciatica. Lesions typically begin as macules and papules, progress to vesicles and pustules, and then ulcerate by approximately day five. Skin lesions crust over, whereas mucosal lesions heal without crusting.
Associated manifestations may include herpetic cervicitis, vaginitis, or urethritis, presenting with dysuria, urinary hesitancy or retention, vaginal discharge, or pelvic pain. Systemic symptoms such as fever, malaise, headache, myalgias, photophobia, anorexia, and lymphadenopathy are more common during primary infection.
Physical Examination Findings
Examination may reveal grouped vesicles on an erythematous base involving the vulva, vagina, cervix, perineum, buttocks, penile shaft, or glans. On moist mucosal surfaces, ulcers may predominate. Atypical findings include localized edema, erythema, fissures, or crusts.
Special Populations
Pediatric patients with genital herpes require careful evaluation, as neonatal infection is often disseminated or involves the central nervous system and carries high morbidity and mortality. Congenital HSV infection without vesicles may resemble other congenital infections. Sexual abuse must be considered in children with genital HSV, and evaluation for other sexually transmitted infections is recommended.
Pregnancy is a high-risk context, particularly with primary infection, which is associated with significant neonatal morbidity. Suppressive antiviral therapy after 36 weeks’ gestation reduces lesion recurrence at delivery and lowers cesarean section rates.
Diagnostic Approach
Diagnosis is usually clinical, based on history and examination. Laboratory testing is useful when confirmation is needed or in atypical or severe cases. Viral culture from vesicle fluid or ulcer base is positive in most early lesions but loses sensitivity as lesions heal. PCR testing is more sensitive and is the diagnostic test of choice, especially for central nervous system involvement. Serologic testing detects prior exposure but is not useful for diagnosing acute disease, as it cannot distinguish recent from chronic infection.
Differential Diagnosis
Important considerations include syphilis, chancroid, lymphogranuloma venereum, granuloma inguinale, candidiasis, and Behçet syndrome.
Emergency Management
Treatment reduces symptom severity and duration but does not eradicate latent virus or prevent future recurrences once therapy is stopped.
Episodic therapy for recurrences shortens lesion duration if started during the prodrome or within one day of lesion onset.
Suppressive therapy, recommended for patients with frequent recurrences (six or more per year), reduces recurrence frequency by approximately 75% and decreases viral shedding.
Severe disease, systemic involvement, or infection in immunocompromised patients requires intravenous antiviral therapy. Resistance to acyclovir occurs in a minority of immunocompromised patients, in which case foscarnet may be effective. Women with urinary retention may require bladder catheterization due to sacral nerve involvement.
Pharmacologic Treatment
First-episode, recurrent, suppressive, and HIV-associated genital herpes are treated with oral or intravenous acyclovir, valacyclovir, or famciclovir, with regimen selection based on severity, immune status, and recurrence pattern. Dosing adjustments may be necessary in renal impairment.
Disposition And Counseling
Hospital admission is indicated for patients with central nervous system involvement, disseminated disease, severe pain or urinary retention, or significant immunosuppression. Immunocompetent patients without systemic involvement can be managed as outpatients.
Discharge counseling is essential and should emphasize avoidance of sexual contact during prodrome and active lesions, consistent use of barrier protection even when asymptomatic, and the lifelong nature of infection. Patients should be informed about the likelihood of recurrence and the option of suppressive therapy.
Key Clinical Pearls
Primary genital herpes may be severe and should be treated promptly. Always consider sexual abuse in children presenting with genital HSV. Genital herpes is lifelong, with intermittent asymptomatic shedding that plays a major role in transmission.
Overview And Definition
Genital herpes is a lifelong, recurrent viral infection caused by herpes simplex virus (HSV). Approximately one in four Americans older than 30 years are seropositive for HSV-2, though most are asymptomatic. The infection is characterized by periods of latency and reactivation, with viral shedding that can occur even in the absence of visible lesions, contributing to ongoing transmission.
Disease Course And Natural History
Primary infection has an incubation period of approximately 2–12 days, with symptoms typically peaking 8–10 days after onset and lesions healing within about three weeks. Primary disease may present with a more severe clinical syndrome and complications such as meningitis, encephalitis, or hepatitis. Importantly, more than half of first recognized episodes are not true primary infections, as earlier asymptomatic exposure is common.
Recurrent infection results from viral reactivation in the dorsal root ganglia. The average patient experiences about four recurrences per year. Recurrences are generally milder, involve fewer lesions, and resolve within 10 days. HSV-1 genital infections recur significantly less often than HSV-2.
Asymptomatic infection is common, with intermittent viral shedding that frequently leads to transmission by individuals without symptoms or lesions.
Etiology And Risk Factors
Most cases (70–90%) of genital herpes are caused by HSV-2, with the remainder caused by HSV-1. Genital HSV-1 infections are increasing in prevalence, likely due to higher rates of oral–genital contact and reduced childhood exposure to HSV-1, leaving more adolescents and adults susceptible. Acquisition of HSV-2 in individuals with prior HSV-1 infection tends to be less symptomatic, whereas acquisition of HSV-1 in those with HSV-2 is uncommon.
Genital herpes is strongly associated with HIV and other sexually transmitted infections. HSV infection increases both susceptibility to HIV and HIV viral shedding during HSV reactivation. Despite extensive research, no effective HSV vaccine is currently available.
Clinical Manifestations
Patients commonly report local pain, itching, or burning. A prodrome of tingling, itching, or pain may occur 1–2 days before lesion eruption and can sometimes mimic radicular pain such as sciatica. Lesions typically begin as macules and papules, progress to vesicles and pustules, and then ulcerate by approximately day five. Skin lesions crust over, whereas mucosal lesions heal without crusting.
Associated manifestations may include herpetic cervicitis, vaginitis, or urethritis, presenting with dysuria, urinary hesitancy or retention, vaginal discharge, or pelvic pain. Systemic symptoms such as fever, malaise, headache, myalgias, photophobia, anorexia, and lymphadenopathy are more common during primary infection.
Physical Examination Findings
Examination may reveal grouped vesicles on an erythematous base involving the vulva, vagina, cervix, perineum, buttocks, penile shaft, or glans. On moist mucosal surfaces, ulcers may predominate. Atypical findings include localized edema, erythema, fissures, or crusts.
Special Populations
Pediatric patients with genital herpes require careful evaluation, as neonatal infection is often disseminated or involves the central nervous system and carries high morbidity and mortality. Congenital HSV infection without vesicles may resemble other congenital infections. Sexual abuse must be considered in children with genital HSV, and evaluation for other sexually transmitted infections is recommended.
Pregnancy is a high-risk context, particularly with primary infection, which is associated with significant neonatal morbidity. Suppressive antiviral therapy after 36 weeks’ gestation reduces lesion recurrence at delivery and lowers cesarean section rates.
Diagnostic Approach
Diagnosis is usually clinical, based on history and examination. Laboratory testing is useful when confirmation is needed or in atypical or severe cases. Viral culture from vesicle fluid or ulcer base is positive in most early lesions but loses sensitivity as lesions heal. PCR testing is more sensitive and is the diagnostic test of choice, especially for central nervous system involvement. Serologic testing detects prior exposure but is not useful for diagnosing acute disease, as it cannot distinguish recent from chronic infection.
Differential Diagnosis
Important considerations include syphilis, chancroid, lymphogranuloma venereum, granuloma inguinale, candidiasis, and Behçet syndrome.
Emergency Management
Treatment reduces symptom severity and duration but does not eradicate latent virus or prevent future recurrences once therapy is stopped.
Episodic therapy for recurrences shortens lesion duration if started during the prodrome or within one day of lesion onset.
Suppressive therapy, recommended for patients with frequent recurrences (six or more per year), reduces recurrence frequency by approximately 75% and decreases viral shedding.
Severe disease, systemic involvement, or infection in immunocompromised patients requires intravenous antiviral therapy. Resistance to acyclovir occurs in a minority of immunocompromised patients, in which case foscarnet may be effective. Women with urinary retention may require bladder catheterization due to sacral nerve involvement.
Pharmacologic Treatment
First-episode, recurrent, suppressive, and HIV-associated genital herpes are treated with oral or intravenous acyclovir, valacyclovir, or famciclovir, with regimen selection based on severity, immune status, and recurrence pattern. Dosing adjustments may be necessary in renal impairment.
Disposition And Counseling
Hospital admission is indicated for patients with central nervous system involvement, disseminated disease, severe pain or urinary retention, or significant immunosuppression. Immunocompetent patients without systemic involvement can be managed as outpatients.
Discharge counseling is essential and should emphasize avoidance of sexual contact during prodrome and active lesions, consistent use of barrier protection even when asymptomatic, and the lifelong nature of infection. Patients should be informed about the likelihood of recurrence and the option of suppressive therapy.
Key Clinical Pearls
Primary genital herpes may be severe and should be treated promptly. Always consider sexual abuse in children presenting with genital HSV. Genital herpes is lifelong, with intermittent asymptomatic shedding that plays a major role in transmission.
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