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Summary Table

Domain	Details
Risk Factors	Age >50 years, immunosuppression (HIV/AIDS, organ transplant recipients, chronic corticosteroid use, malignancy), history of primary varicella (chickenpox)
Etiology	Reactivation of latent Varicella-Zoster Virus (VZV) residing in dorsal root ganglia or cranial nerve ganglia
Patient Presentation	Prodromal burning/tingling pain in a dermatomal distribution, followed 2 to 3 days later by a vesicular rash that does not cross the midline
Classic Physical Exam	Grouped vesicles on an erythematous base, strictly unilateral and dermatomal; thoracic dermatomes (T3 to L3) are the most commonly involved
Key Diagnostic Results	Primarily a clinical diagnosis; PCR of vesicular fluid is the most accurate confirmatory test; Tzanck smear shows multinucleated giant cells (nondiagnostic, cannot distinguish from HSV)
Management	Oral antivirals (valacyclovir, acyclovir, famciclovir) initiated within 72 hours of rash onset; analgesics for acute pain; gabapentin or pregabalin for postherpetic neuralgia
Keywords	"Dermatomal," "does not cross midline," "burning pain before rash," "grouped vesicles on erythematous base," "reactivation," "dorsal root ganglion"

1. Pathophysiology

Herpes zoster results from the reactivation of latent VZV that has been dormant in the sensory (dorsal root) ganglia since the primary varicella infection, which may have occurred decades earlier. VZV establishes lifelong latency within neuronal cell bodies after retrograde axonal transport from the skin during the initial infection. The virus is kept in check by cell-mediated immunity (predominantly T-cell surveillance), and any decline in this immune function allows the virus to reactivate.

Once reactivated, VZV replicates within the ganglion and travels anterogradely along the sensory nerve back to the skin, producing inflammation and necrosis of the nerve (ganglionitis and neuritis) and subsequently the characteristic vesicular eruption in the corresponding dermatome. This explains the prodromal pain: the neural inflammation begins before the virus reaches the skin, so patients experience dermatomal burning, itching, or lancinating pain for 1 to 5 days before any visible rash appears. This prodromal phase is a frequent source of diagnostic confusion.

The rash follows a strict dermatomal pattern because VZV reactivates from a single ganglion and tracks along its associated sensory nerve. The vesicles do not cross the midline because each dorsal root ganglion innervates only one side of the body. Involvement of two or more noncontiguous dermatomes or disseminated disease (defined as >20 lesions outside the primary dermatome) should raise concern for severe immunocompromise, such as advanced HIV or hematologic malignancy.

The development of postherpetic neuralgia (PHN), the most common complication, is attributed to persistent neuronal damage and aberrant nerve repair after the acute infection. Inflammatory destruction of the nerve fibers leads to central and peripheral sensitization, resulting in chronic neuropathic pain that can persist months to years after the rash resolves.

2. Classification and Clinical Manifestation

Classification	Dermatome	Key Clinical Features
Thoracic zoster	T3 to L3 (most common overall)	Unilateral band-like vesicular rash along an intercostal nerve; the classic "textbook" presentation
Herpes zoster ophthalmicus (HZO)	Ophthalmic division of CN V (V1)	Vesicles on the forehead, upper eyelid, and nose tip; Hutchinson sign (vesicles on the tip or side of the nose, indicating nasociliary nerve involvement) predicts ocular complications (keratitis, uveitis, secondary glaucoma)
Herpes zoster oticus (Ramsay Hunt syndrome)	Geniculate ganglion of CN VII	Triad of ipsilateral facial nerve palsy, ear pain, and vesicles in the external ear canal or auricle; may also cause sensorineural hearing loss, tinnitus, and vertigo
Sacral zoster	S2 to S4	Can cause urinary retention or bowel dysfunction due to involvement of sacral autonomic fibers
Disseminated zoster	Multidermatomal / widespread	>20 vesicles outside the primary and adjacent dermatomes; strongly associated with immunosuppression; resembles primary varicella; risk of visceral involvement (pneumonitis, hepatitis, encephalitis)
Zoster sine herpete	Any dermatome	Dermatomal pain without any rash; diagnosed by VZV PCR or serology; a recognized cause of unexplained radicular pain

Complications

Complication	Mechanism / Notes
Postherpetic neuralgia (PHN)	Pain persisting >90 days after rash onset; risk increases with age (>60 years), severity of acute pain, and severity of rash
Bacterial superinfection	Secondary infection of open vesicles, most commonly by Staphylococcus aureus or Streptococcus pyogenes
Ocular complications	Keratitis, anterior uveitis, secondary glaucoma, retinal necrosis (in HZO)
Motor neuropathy	Segmental motor weakness in the affected myotome; rare but recognized
CNS complications	VZV encephalitis, meningitis, myelitis, or vasculopathy (granulomatous arteritis causing stroke)

3. Diagnostic Workup

Test	Role	Key Findings
Clinical diagnosis	Best initial approach	Prodromal dermatomal pain followed by grouped vesicles on an erythematous base, unilateral, not crossing midline
PCR of vesicular fluid	Most accurate (confirmatory) test	Detects VZV DNA; highly sensitive and can distinguish VZV from HSV
Direct fluorescent antibody (DFA)	Rapid confirmation	Detects VZV antigens in vesicle scrapings; less sensitive than PCR but faster than culture
Tzanck smear	Supportive but nondiagnostic	Shows multinucleated giant cells and acantholytic cells; cannot differentiate VZV from HSV
Viral culture	Low sensitivity	VZV grows slowly and poorly in culture; largely replaced by PCR
VZV IgM / IgG serology	Limited clinical utility	May support diagnosis in zoster sine herpete or atypical presentations

Herpes zoster is overwhelmingly a clinical diagnosis. The combination of prodromal dermatomal pain followed by a unilateral vesicular eruption confined to a single dermatome is considered sufficient for diagnosis in the vast majority of cases. Laboratory confirmation is reserved for atypical presentations, immunocompromised patients with unusual rash morphology, and suspected zoster sine herpete (pain without rash).

When laboratory confirmation is needed, PCR of vesicular fluid is the test of choice. It is the most sensitive and allows definitive identification of VZV as opposed to HSV, which is important because HSV can occasionally present in a zosteriform pattern. The Tzanck smear, while rapid and inexpensive, should be understood as a nondiagnostic test: it confirms a herpesvirus infection but cannot tell you which one. Exam questions that present a Tzanck smear with multinucleated giant cells are testing whether you know this limitation.

For herpes zoster ophthalmicus, an urgent ophthalmologic examination (slit-lamp exam) is indicated regardless of whether ocular symptoms are present, particularly when the Hutchinson sign is positive. For Ramsay Hunt syndrome, audiometry should be performed to evaluate for sensorineural hearing loss.

4. Management & Treatment

Setting	Treatment	Dose and Duration
Antiviral therapy (immunocompetent)	Valacyclovir (preferred)	1000 mg PO three times daily for 7 days
	Famciclovir (alternative)	500 mg PO three times daily for 7 days
	Acyclovir (alternative)	800 mg PO five times daily for 7 days
Antiviral therapy (immunocompromised or disseminated)	IV Acyclovir	10 mg/kg IV every 8 hours for 7 to 10 days; transition to oral once lesions begin to crust
Acute pain management	NSAIDs, acetaminophen	First-line for mild to moderate pain
Acute pain management	Opioids (short course)	For severe acute pain unresponsive to first-line agents
Postherpetic neuralgia (PHN)	Gabapentin	Start 300 mg/day, titrate to 1800 to 3600 mg/day in divided doses
	Pregabalin	150 to 300 mg/day in 2 to 3 divided doses
	Tricyclic antidepressants (e.g., amitriptyline, nortriptyline)	25 to 150 mg at bedtime
	Topical lidocaine 5% patch	Applied to the affected area; up to 3 patches for 12 hours on, 12 hours off
	Topical capsaicin 8% patch	Single application for 60 minutes; can be repeated every 3 months
Prevention	Recombinant zoster vaccine (Shingrix)	Two doses IM, 2 to 6 months apart; recommended for adults aged 50 and older, and immunocompromised adults aged 19 and older

The cornerstone of acute treatment is antiviral therapy initiated within 72 hours of rash onset. This 72-hour window is one of the most frequently tested concepts. Antivirals reduce the duration of viral shedding, accelerate lesion healing, and most importantly, reduce the risk and severity of postherpetic neuralgia. Valacyclovir is generally preferred over acyclovir for immunocompetent patients due to its superior bioavailability and simpler dosing schedule (three times daily versus five times daily).

However, antivirals may still be started after 72 hours in the following situations: new vesicles are still appearing, the patient is immunocompromised, or ophthalmic (HZO) or otologic (Ramsay Hunt) involvement is present. This nuance is important because exam questions may present a patient at 4 days into the rash who still has new vesicle formation, testing whether you know that ongoing active disease is an indication to treat.

For immunocompromised patients or those with disseminated zoster, IV acyclovir is the treatment of choice. These patients are at risk for visceral dissemination (pneumonitis, hepatitis, encephalitis) and require inpatient management with contact and airborne isolation precautions (the vesicular fluid contains live virus, and disseminated disease can be transmitted via the airborne route, unlike localized zoster which only requires contact precautions).

Corticosteroids (e.g., prednisone 60 mg/day tapered over 21 days) may be used as adjunctive therapy alongside antivirals in patients over 50 years with moderate to severe pain, to reduce acute pain and improve quality of life. However, corticosteroids do not prevent PHN and should not be used in immunocompromised patients.

For established postherpetic neuralgia, first-line pharmacotherapy includes gabapentin, pregabalin, or a tricyclic antidepressant (nortriptyline or amitriptyline). Topical lidocaine patches are an option for patients who prefer localized therapy or cannot tolerate systemic agents. Opioids are reserved as second or third-line options.

Shingrix (recombinant, adjuvanted zoster vaccine) has replaced the older live-attenuated Zostavax. It is recommended for immunocompetent adults aged 50 and older regardless of prior varicella or zoster history, and for immunocompromised adults aged 19 and older. It is given as a two-dose intramuscular series separated by 2 to 6 months. Because Shingrix is a recombinant (non-live) vaccine, it is safe in immunocompromised patients.

5. Differential Diagnosis & Distractors

Differential	Why It Looks Similar	Key Discriminator
Herpes simplex virus (HSV)	Grouped vesicles on an erythematous base; Tzanck smear shows multinucleated giant cells in both	HSV lesions are typically clustered at mucocutaneous junctions (perioral, genital) and tend to recur at the same site; they are NOT dermatomal. Zoster follows a dermatomal band. PCR distinguishes VZV from HSV definitively
Contact dermatitis	Can produce vesicular, pruritic eruptions	Contact dermatitis follows the pattern of allergen exposure (e.g., linear streaks from plant exposure), is typically bilateral, crosses the midline, and lacks prodromal neuralgic pain
Dermatitis herpetiformis	Name contains "herpetiformis," vesicular skin lesions	Bilateral, symmetric distribution on extensor surfaces (elbows, knees, buttocks); intensely pruritic; associated with celiac disease; biopsy shows granular IgA deposits at the dermal papillae
Cellulitis	Erythema and pain over a skin region	Diffuse spreading erythema without vesicles; does not follow a dermatome; associated with warmth, edema, and systemic signs of infection (fever, leukocytosis)
Bullous pemphigoid	Tense blisters on the skin	Widespread, bilateral, tense bullae on normal or erythematous skin; affects elderly patients; not dermatomal; biopsy shows linear IgG and C3 at the basement membrane zone
Zosteriform HSV	HSV can occasionally reactivate in a dermatomal pattern mimicking zoster	Recurrences tend to be in the same limited area, often smaller in extent than true zoster; VZV PCR is negative, HSV PCR is positive
Prodromal zoster vs. MI / cholecystitis / renal colic	Prodromal chest or abdominal pain without rash can mimic visceral disease	If a vignette describes acute dermatomal chest or flank pain in an older adult and the standard cardiac/abdominal workup is negative, the "next step" is to re-examine the skin in 2 to 3 days for emerging vesicles

6. Traps & High-Yield Pearls

The most common way students get herpes zoster questions wrong is by failing to recognize the prodromal phase. A vignette describing an older or immunocompromised patient with localized burning or lancinating pain in a band-like distribution, with a normal skin exam at the time of presentation, is designed to test whether you can identify pre-eruptive zoster. Students frequently anchor on cardiac, biliary, or musculoskeletal diagnoses and miss the diagnosis entirely.

A second major trap involves the 72-hour treatment window. Questions will present a patient at various time points after rash onset to test whether you know the indications to treat beyond 72 hours: new vesicle formation, immunosuppression, or ophthalmic/otologic involvement. The wrong answer is to withhold antivirals simply because the patient presents on day 4 or 5.

The Hutchinson sign (vesicles on the nose tip) is a classic exam pearl: its presence in a patient with forehead vesicles mandates ophthalmologic evaluation because it signals nasociliary nerve involvement and a high risk of keratitis and other ocular complications. Students who treat this as routine thoracic zoster and fail to order an ophthalmic exam will lose the point.

Be aware that the Tzanck smear is a distractor test. It confirms herpesvirus but cannot distinguish between VZV and HSV. If the question asks for the most accurate test, the answer is always PCR. If the question asks what the Tzanck smear shows, the answer is multinucleated giant cells, but you must pair that with the knowledge that this finding is shared by HSV.

Finally, know the isolation precautions. Localized herpes zoster requires contact precautions only (covering the rash). Disseminated zoster or zoster in an immunocompromised host requires both contact AND airborne precautions because the virus can become aerosolized. This distinction is a recurring infection control question.

The core competency being tested across herpes zoster questions is threefold: recognizing the dermatomal pattern (including prodromal and atypical presentations), applying the 72-hour antiviral initiation rule with its exceptions, and identifying high-risk variants (HZO, Ramsay Hunt, disseminated disease) that require escalated management.

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