Dermatology · PANCE / PANRE

Herpes Zoster (Shingles)

Reactivation of latent VZV in a dorsal root ganglion → painful unilateral dermatomal vesicular eruption.

Also known as: herpes zoster, shingles, zoster, postherpetic neuralgia, zoster ophthalmicus

Overview

Reactivation of varicella-zoster virus (VZV) latent in dorsal root or cranial nerve ganglia, producing a painful unilateral vesicular eruption confined to one or two adjacent dermatomes.

Epidemiology

Lifetime risk ~30% in the US; incidence rises sharply after age 50. ~1 million US cases annually. Increased severity, duration, and risk of postherpetic neuralgia (PHN) with age and immunosuppression.

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Question 1Infectious DiseaseMedium
A 35-year-old immunocompetent man presents with a painful vesicular rash in the T5-T6 dermatomal distribution on his left chest that does not cross the midline. He reports significant burning pain that started 3 days before the rash appeared. Which of the following is the most likely diagnosis?
  • AHerpes simplex
  • BBullous impetigo
  • CHerpes zoster
  • DCellulitis
  • EContact dermatitis
Reveal answer & full explanation
Correct answer: C — Herpes zoster
  • AHerpes simplex
  • BBullous impetigo
  • CHerpes zoster✓
  • DCellulitis
  • EContact dermatitis

Why Herpes zoster is correct

  • Herpes zoster is varicella-zoster virus (VZV) reactivation from a dorsal root or cranial nerve ganglion after primary varicella.
  • Classic features are a painful, grouped vesicular rash in a single dermatome that does not cross the midline.
  • A prodrome of burning or neuritic pain typically precedes the rash by 2-3 days, exactly as described here.
  • Antiviral therapy started within 72 hours of rash onset (valacyclovir 1000 mg TID or famciclovir 500 mg TID for 7 days) shortens the course and reduces complications.
  • Postherpetic neuralgia (pain persisting more than 3 months) is the most common complication; risk rises with age and immunosuppression and is treated with gabapentin, pregabalin, TCAs, or lidocaine patches.

Why the others are wrong

  • Contact dermatitis — Produces symmetric, non-dermatomal eczematous patches at sites of allergen contact; confused-with because both cause vesicles, but it never respects a single dermatome or the midline.
  • Bullous impetigo — Superficial staphylococcal infection with flaccid bullae and honey-colored crusting; confused-with vesicular disease, but it is not dermatomal and lacks the neuritic prodrome.
  • Cellulitis — Poorly demarcated warm erythema without vesicles; right-concept-wrong-setting, as it is a spreading dermal infection rather than a banded vesicular eruption.
  • Herpes simplex — also causes grouped vesicles on an erythematous base, sometimes after a tingling or burning prodrome, but recurrences favor the lips or genitals, involve a small patch, and return to the same site; a band of vesicles along a thoracic dermatome after 3 days of neuritic pain is VZV reactivation (confused-with the other herpesvirus vesicular eruption).

Additional high-yield points

  • Systemic corticosteroids are NOT routine therapy for herpes zoster; they may modestly reduce acute pain but do NOT reduce the risk of postherpetic neuralgia and are not recommended for prophylaxis against it.
  • The recombinant zoster vaccine (RZV/Shingrix), 2 doses 2-6 months apart, is recommended for all immunocompetent adults 50 and older, and is also recommended for immunocompromised adults beginning at age 19.
  • RZV is preferred and can be given to immunocompromised patients because it is non-live (recombinant), with efficacy over 90% in immunocompetent adults.
Question 2DermatologyMedium
A 72-year-old has a painful dermatomal vesicular rash on the right chest. Which of the following complications is most likely?
  • ABacterial superinfection of the vesicles
  • BPneumonitis from varicella-zoster virus
  • CSegmental motor paresis of truncal muscles
  • DPostherpetic neuralgia in the dermatome
  • EDisseminated zoster across multiple dermatomes
Reveal answer & full explanation
Correct answer: D — Postherpetic neuralgia in the dermatome
  • ABacterial superinfection of the vesicles
  • BPneumonitis from varicella-zoster virus
  • CSegmental motor paresis of truncal muscles
  • DPostherpetic neuralgia in the dermatome✓
  • EDisseminated zoster across multiple dermatomes

Why Postherpetic neuralgia in the dermatome is correct

  • Herpes zoster results from varicella-zoster reactivation in a sensory ganglion, here the thoracic dermatome.
  • Postherpetic neuralgia in the dermatome is the most common complication overall and its risk rises sharply with older age, as in this 72-year-old.
  • Early antiviral therapy reduces acute pain and speeds healing, but it has not been shown to reliably reduce the incidence of postherpetic neuralgia; recombinant zoster vaccination is the proven way to prevent it.

Why the others are wrong

  • Bacterial superinfection of the vesicles — Secondary Staphylococcus aureus or group A streptococcal infection of the lesions can occur, but it is much less common than postherpetic neuralgia in an older adult.
  • Segmental motor paresis of truncal muscles — Motor involvement of the matching myotome is an uncommon zoster complication that affects only a small minority of patients and usually recovers, so it is far less likely than postherpetic neuralgia.
  • Disseminated zoster across multiple dermatomes — Dissemination mainly occurs in immunocompromised hosts and is far less common than postherpetic neuralgia in an otherwise healthy older adult.
  • Pneumonitis from varicella-zoster virus — pneumonia is the classic serious complication of primary varicella in adults, and a chest rash can make lung involvement seem likely, but in zoster, VZV pneumonitis occurs mainly with visceral dissemination in immunocompromised hosts and is far less likely than postherpetic neuralgia in a 72-year-old.

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Risk factors

  • Age >50 (declining cell-mediated immunity)
  • Immunosuppression: HIV, malignancy (especially hematologic), transplant, chemotherapy, biologics, chronic corticosteroids
  • Stress, trauma
  • Female sex (slightly higher risk)
  • Family history of zoster

Pathophysiology

Primary varicella infection establishes lifelong latency in sensory ganglia. Decline in VZV-specific cell-mediated immunity allows reactivation → viral replication in ganglion → axonal transport down sensory nerve → cutaneous vesicular eruption in dermatomal distribution. Neural damage produces acute neuritis and, in some, chronic postherpetic neuralgia.

Clinical presentation

Symptoms

  • Prodromal pain, burning, paresthesia in dermatomal distribution 1-5 days (occasionally weeks) before rash
  • Acute neuritic pain — sharp, burning, lancinating, allodynia
  • Malaise, low-grade fever, headache
  • Pruritus, tingling in affected area

Signs / physical exam

  • Unilateral grouped vesicles on erythematous base in a dermatomal distribution — does NOT cross midline (except small overlap)
  • Most common dermatomes: thoracic (T3-L2), trigeminal (especially V1 — ophthalmic), cervical, lumbar
  • Lesions progress: erythematous macules/papules → vesicles → pustules → crusts over 7-10 days; complete healing 2-4 weeks (longer in elderly)
  • Zoster ophthalmicus (V1): involvement of forehead, upper eyelid, tip of nose (Hutchinson sign = nasociliary nerve = high risk of ocular involvement)
  • Ramsay Hunt syndrome (CN VII + VIII): facial palsy + vesicles in ear canal/auricle + vertigo + hearing loss + ageusia
  • Disseminated zoster: >20 lesions outside primary dermatome, especially in immunocompromised
  • Zoster sine herpete: dermatomal pain without rash — diagnosis of exclusion, PCR confirms

Classic findings

Painful unilateral vesicular rash respecting the midline in a dermatomal distribution.

Differential diagnosis

  • Herpes simplex (zosteriform HSV) — Recurrent vesicles in fixed location, not strictly dermatomal; PCR/culture differentiates
  • Contact dermatitis — Geometric/linear borders match contactant; pruritus dominant; no prodromal pain
  • Cellulitis — Diffuse warmth, erythema, no vesicles or dermatomal distribution
  • Impetigo — Honey-colored crusts, not dermatomal
  • Bullous pemphigoid — Tense bullae on urticarial base, widespread, older adult; DIF positive
  • Cardiac ischemia or appendicitis (prodromal pain) — Pain without rash in early prodrome can mimic visceral disease; rash emerges 1-5 days later

Diagnostic workup

Diagnostic criteria

Clinical: prodromal pain + unilateral dermatomal vesicular rash; PCR confirms in atypical cases.

Labs

  • Clinical diagnosis sufficient in most cases
  • PCR of vesicle fluid (most sensitive and specific; preferred when confirmation needed)
  • Direct fluorescent antibody (DFA) — rapid
  • Tzanck smear shows multinucleated giant cells (does not distinguish HSV from VZV)
  • Viral culture (low yield)
  • HIV testing in young adults with zoster
  • Workup for underlying malignancy not routinely indicated in immunocompetent adults but consider in disseminated or recurrent disease

Imaging

  • Slit-lamp examination by ophthalmology for any V1 involvement
  • MRI brain if encephalitis, myelitis, or stroke (varicella vasculopathy) suspected

Diagnostic algorithm

ScenarioKey Management Step
Standard zoster <72 hValacyclovir 1 g TID × 7 d + analgesia
Hutchinson sign / V1 involvementAntiviral + urgent ophthalmology
Ramsay Hunt (CN VII)Antiviral + prednisone taper + ENT/audiology
Immunocompromised / disseminatedIV acyclovir + airborne/contact isolation
Postherpetic neuralgiaGabapentin/pregabalin, lidocaine patch, TCA
PreventionRecombinant zoster vaccine (Shingrix) 2 doses, age ≥50
Herpes zoster scenario-based management.

Treatment

First-line

  • Antiviral therapy within 72 hours of rash onset (still beneficial if vesicles still forming or in immunocompromised): valacyclovir 1 g PO TID × 7 days, OR famciclovir 500 mg PO TID × 7 days, OR acyclovir 800 mg PO 5x/day × 7-10 days (valacyclovir/famciclovir preferred due to better bioavailability and dosing)
  • Renal dose adjustment for all antivirals
  • Pain control: acetaminophen, NSAIDs for mild; gabapentin or pregabalin titrated up for moderate-severe neuritic pain; opioids short-term if needed (codeine, tramadol, oxycodone)
  • Tricyclic antidepressants (nortriptyline, amitriptyline) as adjuncts for acute neuritic pain (evidence that they prevent PHN is insufficient)
  • Local: cool compresses, calamine lotion, topical lidocaine 5% patch (after lesions crust)
  • Vaccination: recombinant zoster vaccine (Shingrix) — 2 doses 2-6 months apart, age ≥50, including those with prior zoster (wait until acute episode resolves)

Zoster ophthalmicus

  • Same antiviral as above PLUS urgent ophthalmology referral within 24 hours
  • IV acyclovir if sight-threatening keratitis, iritis, retinal involvement
  • Topical antivirals and steroids only under ophthalmology direction

Ramsay Hunt syndrome

  • Antiviral + oral corticosteroid (prednisone 60 mg/day tapered over 1-2 weeks) — improves facial nerve recovery
  • ENT referral; audiometry

Disseminated / immunocompromised

  • IV acyclovir 10 mg/kg q8h until clinical improvement, then PO antiviral to complete 14 days
  • Airborne + contact isolation (disseminated disease can transmit varicella to non-immune contacts)

Postherpetic neuralgia

  • First-line: gabapentin or pregabalin titrated to effect; TCAs (nortriptyline preferred in older adults); topical lidocaine 5% patch; topical capsaicin 8% patch
  • Second-line: SNRIs (duloxetine, venlafaxine)
  • Third-line: opioids, intrathecal corticosteroids, nerve blocks

Second-line / adjunct

  • Systemic corticosteroids — controversial for typical zoster; may speed acute pain resolution but do not prevent PHN; useful in Ramsay Hunt and severe cases
  • Recombinant zoster vaccine (Shingrix) recommended for immunocompromised adults ≥19 years per CDC ACIP 2022

Complications

  • Postherpetic neuralgia (PHN) — pain persisting >90 days after rash onset; affects 10-18% of all zoster patients, ~30% of those >80 years; antivirals speed healing and reduce acute pain, but evidence that they reduce PHN incidence is weak (Cochrane 2014: oral acyclovir does not; data for valacyclovir/famciclovir are insufficient); recombinant zoster vaccination prevents both zoster and PHN
  • Bacterial superinfection of skin lesions
  • Zoster ophthalmicus: keratitis, uveitis, scleritis, acute retinal necrosis, secondary glaucoma, vision loss
  • Ramsay Hunt syndrome: facial palsy (worse prognosis than Bell's palsy), hearing loss, vertigo
  • CNS: meningoencephalitis, myelitis, varicella vasculopathy → stroke
  • Disseminated visceral zoster (pneumonitis, hepatitis) in immunocompromised
  • Motor zoster (segmental muscle weakness)
  • Transmission of varicella to non-immune contacts (especially neonates, pregnant women, immunocompromised) from active lesions

PANCE pearls

  • Hutchinson sign (vesicles on tip of nose) predicts ocular involvement in zoster ophthalmicus — urgent ophthalmology referral.
  • Antiviral therapy is most effective if started within 72 hours of rash onset, but still consider in ongoing vesicle formation, ocular involvement, immunocompromised, or severe pain.
  • Recombinant zoster vaccine (Shingrix) is preferred over the older live attenuated vaccine (no longer marketed in the US) and is recommended for all adults ≥50 and immunocompromised adults ≥19.
  • Zoster in a young adult should prompt HIV testing.
  • Gabapentin/pregabalin are used for acute neuritic pain and treat established PHN, but they have not been shown to prevent PHN when started during acute zoster; recombinant zoster vaccination is the proven way to prevent PHN.

References

  • CDC ACIP 2022 — Use of Recombinant Zoster Vaccine in Immunocompromised Adults Aged ≥19 Years (Anderson et al., MMWR 2022)
  • AAFP 2017 — Herpes Zoster and Postherpetic Neuralgia: Prevention and Management (Saguil et al., Am Fam Physician 2017)
  • Cochrane 2014 — Antiviral Treatment for Preventing Postherpetic Neuralgia (Chen et al., Cochrane Database Syst Rev 2014)

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