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Herpes Simplex Virus Infections

Herpes Simplex Virus Infections

Herpes Simplex Virus Infections

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HSV Basics - Viral Villains Unveiled

  • Family: Herpesviridae (Subfamily: Alphaherpesvirinae).
  • Types & Primary Tropism:
    • HSV-1 (HHV-1): Typically orofacial; latency in trigeminal ganglia.
    • HSV-2 (HHV-2): Typically genital; latency in sacral ganglia (S2-S5).
    • Note: Significant site crossover occurs.
  • Structure: Enveloped, icosahedral capsid, linear double-stranded DNA genome.
  • Transmission: Direct contact with active lesions, mucosal surfaces, or infected secretions (saliva, genital fluids). Vertical transmission possible during childbirth.
  • Lifecycle Hallmark:
    • Primary infection → Local replication → Retrograde axonal transport to sensory ganglia → Lifelong Latency → Reactivation (triggers: stress, UV light, fever, immunosuppression) → Anterograde transport → Recurrent mucocutaneous lesions. Herpes Simplex Virus Virion Structure

⭐ HSV establishes lifelong latency within sensory nerve ganglia, specifically the trigeminal ganglion for HSV-1 and sacral ganglia for HSV-2. This is a key characteristic enabling recurrent infections.

Clinical Picture - Rash Decisions

  • Primary Orolabial (HSV-1):
    • Gingivostomatitis: Painful vesicles, erosions on oral mucosa, gingiva, lips. Fever, malaise. Children (6m - 5y).
  • Recurrent Orolabial (HSV-1):
    • Herpes labialis ("cold sore"): Grouped vesicles on vermilion border. Prodrome: tingling, burning.
  • Primary Genital (HSV-2 > HSV-1):
    • Painful vesicles, pustules, erosions on genitalia. Systemic: fever, myalgia, lymphadenopathy.
  • Recurrent Genital:
    • Milder, shorter, localized. Prodrome common.
  • Lesion Morphology:
    • Grouped vesicles on erythematous base ("dew drops on rose petal").
    • Vesicle → pustule → ulcer → crust. Herpes Simplex: Grouped Vesicles on Erythematous Base
  • Specific Sites/Forms:
    • Herpetic Whitlow: Painful HSV on fingers/toes. Healthcare workers.
    • Eczema Herpeticum: Widespread HSV in eczema. Severe, life-threatening.
    • Herpes Gladiatorum: Wrestlers, contact sports.
    • Erythema Multiforme: Post-HSV; target lesions.

⭐ Tzanck smear: Multinucleated giant cells, ballooning keratinocytes.

Diagnosis & DDx - Spotting the Suspect

Clinical suspicion: Grouped vesicles on erythematous base.

  • Lab Confirmation:
    • Tzanck Smear: Multinucleated giant cells (MNGCs). (📌 Tzanck: All Nuclei Clubbed)
    • Viral Culture: Gold standard, but slow.
    • PCR: Rapid, highest sensitivity & specificity. Test of choice.
    • DFA: Detects viral antigens.
    • Serology (IgM/IgG): For primary infection, typing. Tzanck smear: multinucleated giant cells in HSV infection
  • Key DDx:
    • Herpes Zoster: Dermatomal.
    • Aphthous Stomatitis: Oral, no vesicles.
    • Hand, Foot, Mouth Disease: Typical distribution.
    • Impetigo: Honey-colored crusts.
    • Erythema Multiforme: Target lesions (often HSV-triggered).

⭐ Tzanck smear showing multinucleated giant cells is a classic, rapid diagnostic clue for HSV/VZV infections.

Treatment & Prevention - Calming the Chaos

  • Antiviral Therapy (Cornerstone):

    • Acyclovir: Oral (Primary: 200mg 5x/day, 7-10d; Recurrent: 800mg TDS, 2d or 200mg 5x/day, 5d), IV, topical.
    • Valacyclovir: (Episodic: 500mg-1g BD, 3-5d) - ↑ bioavailability.
    • Famciclovir: (Episodic: 125-250mg BD/TDS, 5d).
    • Mechanism: Inhibit viral DNA polymerase.
    • Duration: Episodic (2-10 days based on drug/severity); Suppressive (long-term).
  • Indications: Genital/Orolabial herpes, Keratitis, Neonatal HSV, Encephalitis.

  • Supportive Care: Analgesia, hygiene.

  • Resistant HSV: Foscarnet, Cidofovir (immunocompromised).

  • Prevention:

    • Avoid triggers (stress, UV).
    • Barrier methods (condoms).
    • Suppressive therapy for >6 recurrences/year.
    • C-section if active genital lesions at term.
    • Patient education on asymptomatic shedding.

⭐ Acyclovir requires dose adjustment in renal impairment; it's a common exam question.

High‑Yield Points - ⚡ Biggest Takeaways

  • HSV-1 typically causes orolabial herpes; HSV-2 primarily causes genital herpes.
  • Primary infection often more severe; herpetic gingivostomatitis (HSV-1) is common in children.
  • Virus establishes latency in sensory nerve ganglia, leading to recurrent outbreaks.
  • Tzanck smear shows multinucleated giant cells & Cowdry A inclusions; PCR is gold standard.
  • Acyclovir is the first-line antiviral treatment.
  • Key complications: Eczema herpeticum (Kaposi's varicelliform eruption), herpes keratitis, herpes encephalitis.

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