Question
Describe the etiology, pathogenesis, lab diagnosis and immunization of chicken pox.
Answer
Etiology: Varicella-zoster virus (VZV), a member of the Herpesviridae family (subfamily Alphaherpesvirinae), a double-stranded DNA virus.
Pathogenesis: primary infection occurs via inhalation of infected respiratory droplets/aerosols or direct contact with vesicle fluid. The virus initially replicates in the nasopharyngeal/respiratory mucosa and regional lymph nodes, followed by a primary viraemia that seeds the reticuloendothelial system (liver, spleen), and then a secondary viraemia that disseminates the virus to the skin, producing the characteristic generalized vesicular rash appearing in successive crops (giving lesions at different stages of evolution simultaneously — macule → papule → vesicle → pustule → crust — the classical “polymorphic” rash, described as a “dew drop on a rose petal” appearance). After the primary infection resolves, the virus establishes lifelong latency in the dorsal root ganglia, and can later reactivate (particularly with waning cell-mediated immunity, e.g., in elderly or immunocompromised individuals) to cause herpes zoster (shingles), a localized, dermatomal vesicular eruption.
Laboratory diagnosis:
- Tzanck smear — scraping from the base of a vesicle, showing multinucleated giant cells with intranuclear inclusions (rapid, though not specific for VZV vs HSV).
- Direct Fluorescent Antibody (DFA) test — on vesicle fluid/scraping, rapid and specific for VZV antigen.
- PCR — the most sensitive and specific method, detecting VZV DNA from vesicle fluid, CSF (in cases of VZV encephalitis/CNS involvement), or other clinical samples.
- Virus isolation in cell culture — possible but slow and technically demanding, not routinely used.
- Serology — IgM antibody indicates recent/acute infection; IgG indicates past infection/immunity, useful for assessing immune status (e.g., in healthcare workers or before immunosuppressive therapy).
Immunization: Live attenuated Varicella vaccine (Oka strain), given as a two-dose schedule (typically at 12–15 months, with a second dose at 4–6 years); reduces the incidence and severity of primary varicella and, by lowering the wild-type viral exposure burden, has some impact on later herpes zoster risk. A separate recombinant zoster (subunit) vaccine exists specifically for prevention of herpes zoster/shingles in older adults, distinct from the primary childhood varicella vaccine. Both are contraindicated (for the live varicella vaccine) or used cautiously in pregnancy and significant immunosuppression.