Genital herpes

Clinical presentation and disease forms

The acute period of a typical form lasts 8–10 days. Patients report pain, itching, burning, and heaviness in the lower abdomen; dysuria is possible. Secondary infection leads to purulent discharge. Systemic manifestations include low-grade fever, lymphadenopathy, and headache. Neuropsychiatric disorders are characteristic: drowsiness, irritability, and decreased performance. The frequency of relapses depends on immunobiological resistance and varies from monthly to once every 2–3 years.

In 40–75% of cases, an atypical form occurs. It presents without classic herpes rashes, affecting internal genital organs (mimicking non-specific inflammation). It is accompanied by itching, leukorrhea unresponsive to antibiotic therapy, and recurrent cervical erosions. This is a frequent cause of infertility and recurrent pregnancy loss.

Diagnostic workup

The basis of diagnosis is the anamnesis and physical examination. The typical form is easily recognized by vesicular rash. In differential diagnosis, it is important to distinguish ruptured herpes vesicles from a syphilitic hard chancre (firm, painless, with smooth edges).

Clinical diagnostics of atypical forms is extremely challenging and requires highly sensitive laboratory methods. The material used is discharge from the urethra, vagina, cervical canal, or vesicles.

• “Gold standard”: virus cultivation on a chicken embryo cell culture.
• Detection of DNA and antigens: PCR, ELISA, immunofluorescence assay.

Important: simple detection of antibodies in the blood is not an accurate criterion. It only confirms the fact of HSV infection, but does not prove genital localization.

Genital herpes and pregnancy

Transmission of the virus to the child occurs predominantly intranatally (85%), less frequently during pregnancy (5%, especially in the third trimester) or in the postnatal period (10%). Risk factors include maternal somatic diseases and fetoplacental insufficiency.

Intrauterine infection threatens pregnancy loss and severe malformations: microcephaly, hydrocephaly, agenesis of the corpus callosum, and chorioretinitis. In 80% of newborns with viral dissemination, herpetic encephalitis develops, and generalization with involvement of internal organs is possible.

To prevent fetal infection, antiviral drugs are used (administration in the first trimester is undesirable). If herpetic lesions are present on the genitalia prior to delivery, delivery by Caesarean section is indicated.

Principles of treatment

All antiherpetic drugs act virustatically—they suppress replication but do not completely eliminate the virus. The first-line drug is acyclovir.

• Localized forms: combination therapy (topical + systemic) for a course of 7–10 days. Oral regimens include acyclovir (400 mg 3 times daily), famciclovir, or valacyclovir.
• Severe course and visceral lesions: intravenous administration of acyclovir (up to 14–21 days). When clinical resistance is suspected, a reserve drug is used — foscarnet sodium.
• Suppressive therapy: continuous administration of medications to block virus reactivation in patients with frequent relapses. For example, taking valacyclovir for 12 months reduces the risk of virus transmission to a seronegative partner.

The comprehensive approach is supplemented by specific (vaccine, γ-globulin) and nonspecific immunotherapy, as well as interferon preparations.

Class and exam questions

What else to study on this topic

• Herpetic encephalitis and intensive care
• Suppressive therapy in frequently recurring herpes
• Neonatal herpetic infection and malformations
• Comprehensive immunotherapy and interferon system correction
• Features of herpes therapy in the context of HIV infection

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.