Shingles (Herpes Zoster): Causes, Symptoms, and Prevention

Shingles is reactivation of latent varicella-zoster virus (VZV) from dorsal root or cranial nerve ganglia after primary chickenpox infection.

Pathogenesis

• VZV enters sensory neurons during varicella → establishes latency in ganglia.
• Decades later, VZV-specific cell-mediated immunity wanes → reactivation → viral replication → anterograde transport down nerve → dermatomal rash.

Risk Factors

• Age >50 (incidence rises sharply; 50% by 85).
• Immunosuppression (HIV, transplant, chemo, biologics, steroids).
• Chronic diseases (COPD, CKD, diabetes, autoimmune).
• Psychological stress, trauma.
• Female sex (slightly higher).

Clinical Phases

1. Prodrome (1–5 days): Pain, burning, itching, paresthesia in dermatome; malaise, headache.
2. Acute Eruptive: Clustered vesicles on erythematous base, unilateral, dermatomal (thoracic > trigeminal > lumbar). Crust in 7–10 days.
3. Postherpetic Neuralgia (PHN): Pain >90 days after rash onset; 10–18% of cases, higher with age.

Transmission

• VZV in vesicle fluid → direct contact → varicella in susceptible (never vaccinated/had chickenpox).
• Not airborne like primary varicella.
• Contagious until all lesions crusted.
• Cover lesions; avoid pregnant, immunocompromised, infants.

Prevention: Vaccination

• Shingrix (RZV): Recombinant subunit + adjuvant. 2 doses 2–6 months apart. >90% efficacy; recommended ≥50 (immunocompetent) and ≥19 (immunocompromised).
• Zostavax (ZVL): Live attenuated. No longer sold in US (2020); less effective.

Treatment

• Antivirals (valacyclovir 1g TID × 7d, famciclovir, acyclovir) — start <72h from rash onset.
• Pain control: gabapentinoids, TCAs, opioids if severe.
• Corticosteroids (adjunct for severe acute pain).

Early antiviral therapy reduces severity, duration, and PHN risk.