herpes simplex

HSV-1 and HSV-2 are enveloped dsDNA viruses that infect mucocutaneous surfaces, establishing latency in sensory neurons (HSV-1 typically in the trigeminal ganglion, HSV-2 in the sacral ganglia). Primary infection may be asymptomatic or present with painful grouped vesicles on an erythematous base that ulcerate; gingivostomatitis is common in children with HSV-1. Reactivation is triggered by stress, UV light, immunosuppression, or fever, causing recurrent 'cold sores' (HSV-1) or genital lesions (HSV-2). Diagnosis is via Tzanck smear (multinucleated giant cells - nonspecific), viral culture, PCR (gold standard), or direct fluorescent antibody. Histopathology shows characteristic Cowdry type A intranuclear inclusions. Key complications include herpetic whitlow (finger infection, common in healthcare workers), herpes gladiatorum (wrestlers), eczema herpeticum (disseminated infection in atopic dermatitis patients - can be life-threatening), and herpes keratitis (leading cause of infectious blindness, presents with dendritic corneal ulcers). HSV encephalitis, most commonly caused by HSV-1, characteristically affects the temporal lobes, presenting with fever, altered mental status, and seizures; CSF shows RBCs (hemorrhagic necrosis) and PCR is diagnostic; treatment is IV acyclovir. Neonatal herpes, usually acquired from HSV-2 during vaginal delivery, can cause severe disseminated disease, encephalitis, or skin/eye/mouth involvement - cesarean section is recommended if active genital lesions are present at delivery. Treatment includes acyclovir, valacyclovir, or famciclovir (guanosine analogs requiring viral thymidine kinase for activation, then inhibit viral DNA polymerase). Latency and lack of a cure mean recurrences are common but treatment reduces severity/duration and can be used prophylactically to reduce transmission.