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Pathology 2 - Second Year BHMS

Contents

Pathology 2 - Second Year BHMS

Contents

CoursesBHMSPathology 2 - Second Year BHMSHERPES VIRUS – VARICELLA-ZOSTER

HERPES VIRUS – VARICELLA-ZOSTER

Content

Q. What is Varicella‑zoster virus (VZV)?
A.

  • DNA virus, family Herpesviridae, subfamily Alphaherpesvirinae.
  • Causes two clinical entities: chicken‑pox (varicella) and shingles (herpes zoster).

Q. How is VZV transmitted?
A.

  • Inhalation of respiratory droplets from vesicular fluid or nasopharyngeal secretions.
  • Direct contact with skin lesions.

Q. What are the main types/clinical forms of VZV infection?
A.

  • Primary infection → varicella (chicken‑pox).
  • Reactivation of latent virus → herpes zoster (shingles).

Q. Pathogenesis of Varicella (primary infection) – step‑wise
A.

  1. → Virus enters via nasal or oral mucosa.
  2. → Replicates in nasopharyngeal epithelium and regional lymph nodes.
  3. → Primary viremia spreads virus to liver, spleen, and skin.
  4. → Secondary viremia carries virus to dermal capillaries.
  5. → Virus infects epidermal keratinocytes → vesicle formation.
  6. → Cell‑mediated immunity (CMI) limits spread; antibodies appear after 7‑10 days.

Memory trick: “Nose‑Lymph‑Blood‑Skin – N‑L‑B‑S – the VZV travel route.”

Q. Clinical features of chicken‑pox (varicella)
A.

  • Incubation 10‑21 days.
  • Prodrome: low‑grade fever, malaise, headache, loss of appetite.
  • Rash: maculopapular → vesicular → pustular → crusted; centripetal distribution, more on trunk and face; lesions at different stages together.
  • Pruritus common.
  • Lesions become umbilicated, clear fluid, later crust.

Q. Common complications of chicken‑pox (exam focus)
A.

  • Bacterial superinfection of lesions → impetigo, cellulitis, scar formation.
  • Pneumonia (especially in adults, smokers, immunocompromised).
  • Encephalitis (rare, high mortality).
  • Hepatitis, myocarditis.
  • Reye’s syndrome (if aspirin given).
  • Hemorrhagic varicella in immunosuppressed.

Q. Pathogenesis of Herpes Zoster (shingles) – step‑wise
A.

  1. → After primary infection, VZV establishes latency in dorsal root ganglion (DRG) sensory neurons.
  2. → Decline in cell‑mediated immunity (age >50 yr, HIV, steroids, malignancy) → viral reactivation.
  3. → Replication within the neuron → anterograde transport along sensory nerve to skin.
  4. → Inflammation of the nerve → neuropathic pain (pre‑eruptive).
  5. → Virus infects epidermis in the dermatome → vesicular rash limited to that dermatome (usually unilateral).

Memory rhyme: “Latent ganglion → immunity drops → virus hops → nerve stops → rash pops.”

Q. Clinical picture of herpes zoster
A.

  • Prodrome: burning, tingling, itching in a band‑like distribution (1‑5 days).
  • Eruption: grouped vesicles on erythematous base, confined to a single dermatome; may involve face (V1) → Hutchinson’s sign.
  • Post‑herpetic neuralgia (PHN) – pain persisting >1 month, common in elderly.
  • Complications: bacterial superinfection, ocular involvement (keratitis, uveitis), motor neuropathy, Ramsay‑Hunt syndrome (facial nerve palsy).

Q. Laboratory diagnosis of VZV infection
A.

  • Direct fluorescent antibody (DFA) or Tzanck smear from vesicle fluid – shows multinucleated giant cells (not specific).
  • Viral culture – Vero or human embryonic lung cells; takes 5‑7 days, low sensitivity.
  • Serology: IgM positive in acute infection; rising IgG titre in convalescence.
  • PCR (most sensitive) – detects VZV DNA in vesicular fluid, CSF, blood; useful for atypical or disseminated disease.
  • In neonates or immunocompromised: quantitative PCR for viral load.

Q. Management of varicella (primary infection)
A.

  • Healthy children: symptomatic treatment – antipyretics, calamine lotion, antihistamines for itching.
  • High‑risk groups (adolescents, adults, immunocompromised, pregnant): oral acyclovir 20 mg/kg q8h (or valacyclovir) within 24 h of rash onset.
  • Intravenous acyclovir for severe disease, pneumonia, encephalitis, or immunosuppressed.

Q. Management of herpes zoster
A.

  • Antiviral therapy (acyclovir 800 mg q5h, valacyclovir 1 g TID, or famciclovir 500 mg TID) started within 72 h of rash.
  • Analgesics: NSAIDs, opioids, gabapentin/pregabalin for neuropathic pain.
  • Corticosteroids (optional) in selected cases to reduce acute pain and PHN.
  • Ophthalmology referral if V1 involvement.

Q. Prevention strategies (exam point)
A.

  • Live attenuated varicella vaccine (2 doses at 12‑15 months and 4‑6 years) – prevents primary infection, reduces complications.
  • Recombinant zoster vaccine (Shingrix) – >90 % efficacy in >50 yr, given in two doses, safe in immunocompromised.
  • Post‑exposure prophylaxis: varicella vaccine within 3‑5 days of exposure or VZIG for high‑risk contacts.

Q. Important exam‑type MCQ pointers
A.

  • VZV latency site = dorsal root ganglion.
  • Primary viremia → secondary viremia → skin lesions.
  • PHN risk ↑ with age >60, severe acute pain, rash on trunk.
  • Reye’s syndrome association = aspirin use in varicella.