varicella-zoster virus

VZV establishes lifelong latency in sensory (dorsal root or trigeminal) ganglia after primary infection. Primary infection (chickenpox) presents with a pruritic vesicular rash in different stages of healing ('dew drops on a rose petal'), fever, and malaise, typically in unvaccinated children; complications include pneumonia, encephalitis, and secondary bacterial (Group A Streptococcus) superinfection. Congenital varicella syndrome can occur if maternal infection happens early in pregnancy, causing limb hypoplasia, chorioretinitis, and CNS defects. Reactivation (shingles) occurs with waning cell-mediated immunity (aging, immunosuppression, HIV) and presents as a painful, dermatomal vesicular rash that does not cross the midline; can be complicated by postherpetic neuralgia, ophthalmic zoster (VZV in V1 branch of trigeminal nerve, risk of vision loss), and Ramsay Hunt syndrome (geniculate ganglion involvement causing facial palsy, ear pain, vesicles in ear canal). Diagnosis is usually clinical; PCR of vesicular fluid is the gold standard when needed; Tzanck smear shows multinucleated giant cells but doesn't distinguish HSV from VZV. Treatment includes acyclovir/valacyclovir for moderate-severe cases or immunocompromised patients; VZIG for post-exposure prophylaxis in high-risk individuals. Prevention includes live attenuated varicella vaccine (childhood) and live attenuated or recombinant zoster vaccine (adults >50) to reduce reactivation risk.