Definition and epidemiology
Shingles is an acute viral infection caused by reactivation of varicella-zoster virus (VZV), the same virus responsible for chickenpox. After primary infection (chickenpox), VZV remains dormant in sensory ganglia and can reactivate years or decades later, typically when cellular immunity declines.
The lifetime risk is approximately 30%, with an incidence of 3-5 cases per 1,000 person-years in the general population. Incidence increases dramatically with age: approximately 10 cases per 1,000 person-years in those over 60. More than two-thirds of cases occur in adults over 50. There is no significant sex predilection. The condition is slightly more common in immunocompromised individuals and those of European ancestry compared to other ethnic groups.
- Shingles is VZV reactivation; unilateral dermatomal rash that does not cross midline is pathognomonic.
- Start antiviral therapy (valacyclovir, famciclovir, or acyclovir) within 72 hours of rash onset to reduce duration and PHN risk.
- Postherpetic neuralgia (pain >90 days after rash) is the most common complication; risk increases with age.
- Hutchinson sign (vesicles on tip of nose) in herpes zoster ophthalmicus indicates nasociliary involvement and high risk of ocular complications; requires urgent ophthalmology referral.
- Ramsay Hunt syndrome: facial palsy + vesicles in ear canal + hearing loss (geniculate ganglion involvement); treat with antivirals plus corticosteroids.
- Recombinant zoster vaccine (Shingrix) is recommended for adults ≥50 years; over 90% effective in preventing shingles and PHN.
- Immunocompromised patients are at risk for disseminated zoster and visceral involvement; consider IV acyclovir.
- Zoster sine herpete: dermatomal pain without rash; diagnosis confirmed by PCR or rising VZV antibody titers.
Etiology and risk factors
Shingles results from reactivation of latent VZV in dorsal root ganglia or cranial nerve ganglia. Primary VZV infection (chickenpox) typically occurs in childhood, after which the virus establishes lifelong latency in sensory neurons.
Major risk factors:
- Advanced age — most important risk factor; incidence rises sharply after age 50
- Immunosuppression — HIV/AIDS, organ transplantation, immunosuppressive therapy, hematologic malignancies (especially lymphoma)
- Medications — corticosteroids, chemotherapy, TNF-alpha inhibitors, other biologics
- Chronic diseases — diabetes mellitus, chronic kidney disease, COPD
- Psychological stress — may trigger reactivation
- Local trauma or radiation — to dermatomes where VZV is latent
- Female sex — slightly higher risk of postherpetic neuralgia
Prior history of chickenpox (or VZV vaccination) is required; individuals who have never been infected with VZV cannot develop shingles. Shingles is much less contagious than chickenpox; transmission occurs through direct contact with vesicular fluid and can cause chickenpox in susceptible individuals, not shingles.
Pathophysiology
After primary VZV infection, the virus travels along sensory nerves to dorsal root ganglia where it remains dormant. Cellular immunity, particularly VZV-specific T cells, keeps the virus in check. When cell-mediated immunity wanes due to aging, immunosuppression, or other factors, VZV reactivates.
Upon reactivation, the virus replicates in the ganglion and travels antegradely along sensory nerve fibers to the skin, producing inflammation of the nerve and corresponding dermatome. This causes the characteristic prodromal pain followed by vesicular eruption in a dermatomal distribution. The thoracic dermatomes (T3-L2) are most commonly affected, accounting for approximately 50-70% of cases, followed by cranial (10-20%, especially trigeminal) and lumbosacral regions.
The virus causes direct neuronal damage and intense inflammation. Severe cases can result in neuronal destruction, leading to chronic neuropathic pain (postherpetic neuralgia). Viral invasion of blood vessels may cause ischemic necrosis, and in immunocompromised hosts, dissemination can occur.
Clinical features
Shingles typically progresses through distinct phases:
Prodromal phase (1-5 days before rash)
- Dermatomal pain, burning, tingling, or itching
- Malaise, fever, headache
- Pain may be severe and is often mistaken for other conditions (myocardial infarction, pleurisy, acute abdomen) depending on location
Acute eruptive phase
- Erythematous papules progressing to vesicles on an erythematous base ("dew drops on a rose petal")
- Unilateral dermatomal distribution that does not cross the midline (pathognomonic)
- New lesions continue to appear for 3-5 days
- Vesicles become pustular, then crust over within 7-10 days
- Complete healing typically occurs within 2-4 weeks
- Pain often accompanies or precedes the rash
Distribution patterns
- Thoracic dermatomes — most common (50-70%)
- Herpes zoster ophthalmicus (HZO) — involves ophthalmic division of trigeminal nerve (V1); Hutchinson sign (lesions on tip of nose) suggests nasociliary branch involvement and increased risk of ocular complications
- Ramsay Hunt syndrome — facial nerve involvement with vesicles in ear canal, facial paralysis, and sometimes hearing loss
- Sacral dermatomes — may cause urinary retention or constipation
Atypical presentations
- Zoster sine herpete — dermatomal pain without rash
- Disseminated zoster — more than 20 lesions outside primary and adjacent dermatomes; occurs in immunocompromised patients
- Motor involvement — weakness in affected myotome (rare)
Systemic symptoms are generally mild in immunocompetent patients but may be prominent in immunocompromised individuals.
Diagnosis
Diagnosis is typically clinical based on characteristic presentation. Laboratory confirmation is rarely necessary in immunocompetent patients with classic presentation.
Clinical diagnosis
- Unilateral dermatomal vesicular rash
- Preceding or concurrent dermatomal pain
- History of chickenpox or residence in endemic area
- Does not cross midline
Laboratory confirmation (when needed)
Indications: atypical presentations, immunocompromised hosts, disseminated disease, CNS involvement, or legal/epidemiologic purposes.
Preferred tests:
- PCR of vesicular fluid — most sensitive and specific
- Direct fluorescent antibody (DFA) — rapid, good sensitivity
- Viral culture — specific but slow and less sensitive
- Tzanck smear — shows multinucleated giant cells but cannot distinguish VZV from HSV; largely replaced by PCR
Serologic testing (IgM/IgG) is not useful for acute diagnosis because most adults have antibodies from prior chickenpox.
Imaging
Not routinely indicated. MRI may be used if CNS complications (meningitis, encephalitis, myelitis) are suspected.
Differential diagnosis
Herpes simplex virus (HSV) — can appear identical but more commonly recurs in same location, often orolabial or genital; less likely to follow strict dermatomal pattern; PCR distinguishes.
Contact dermatitis — can be unilateral but typically has history of exposure; less painful; no vesicles on erythematous base.
Impetigo — honey-crusted lesions, not vesicular initially; more common in children; not dermatomal.
Dermatitis herpetiformis — intensely pruritic grouped vesicles on extensor surfaces; associated with celiac disease; bilateral and symmetric.
Acute pain before rash emergence:
- Myocardial infarction (thoracic zoster)
- Pleurisy or pneumonia (thoracic)
- Cholecystitis or appendicitis (abdominal dermatomes)
- Renal colic (lumbar)
Erythema multiforme — target lesions, often acral, bilateral.
Drug eruption — usually bilateral and symmetric; history of new medication.
Bacterial cellulitis — unilateral erythema and swelling but does not follow dermatomal pattern; no vesicles.
Burns (chemical or thermal) — history of exposure; distribution corresponds to contact pattern, not dermatome.
Management
Antiviral therapy
Should be initiated within 72 hours of rash onset for maximum benefit. Benefits include reduced duration of viral shedding, faster healing, and decreased risk of postherpetic neuralgia.
First-line oral antivirals (immunocompetent adults):
- Valacyclovir — preferred for convenience
- Famciclovir — alternative
- Acyclovir — effective but requires more frequent dosing
Treat for 7 days. Consider treatment beyond 72 hours if new lesions are still forming, in immunocompromised patients, or with ophthalmic or disseminated involvement.
Indications for IV acyclovir:
- Severe immunosuppression
- Disseminated zoster
- CNS involvement (meningitis, encephalitis, myelitis)
- Herpes zoster ophthalmicus with severe disease
- Inability to tolerate oral medications
Pain management
Acute pain:
- Acetaminophen or NSAIDs for mild pain
- Opioids for moderate to severe pain (short-term)
- Gabapentin or pregabalin — may reduce acute pain and risk of postherpetic neuralgia
- Topical lidocaine — for localized relief
- Wet-to-dry compresses — soothe vesicular lesions
Corticosteroids — not routinely recommended; no proven benefit in preventing postherpetic neuralgia and may increase dissemination risk in immunocompromised patients.
Special situations
Herpes zoster ophthalmicus:
- Urgent ophthalmology consultation
- Oral antivirals
- Topical corticosteroids and cycloplegics (under ophthalmology guidance)
- Monitor for keratitis, uveitis, increased intraocular pressure, retinitis
Ramsay Hunt syndrome:
- Oral antivirals plus corticosteroids
- Eye care if incomplete eye closure
Immunocompromised patients:
- IV acyclovir for severe or disseminated disease
- Longer treatment duration
- Monitor for visceral involvement
Postherpetic neuralgia (PHN)
Pain persisting more than 90 days after rash onset; most common complication.
First-line treatments:
- Gabapentin or pregabalin
- Tricyclic antidepressants (amitriptyline, nortriptyline)
- Topical lidocaine patches
- Topical capsaicin (high-concentration)
Second-line:
- Duloxetine or venlafaxine (SNRIs)
- Opioids — reserved for refractory cases
- Tramadol
Prevention
Vaccination:
- Recombinant zoster vaccine (Shingrix) — preferred; two doses, over 90% efficacy in preventing shingles; recommended for adults 50 and older, including those who have had shingles previously
- Live attenuated zoster vaccine (Zostavax) — less effective; no longer preferred in most countries
Vaccination significantly reduces incidence and severity of shingles and postherpetic neuralgia.
Infection control
- Cover lesions until fully crusted
- Avoid contact with pregnant women (if non-immune), newborns, and immunocompromised individuals
- Healthcare workers should not work with high-risk patients until lesions are crusted
Complications and prognosis
Complications
Postherpetic neuralgia (PHN) — most common; chronic neuropathic pain lasting more than 90 days after rash onset. Risk increases with age (10-15% in those over 60, up to 50% in those over 80 without antiviral treatment). Early antiviral therapy reduces risk.
Ophthalmic complications (HZO):
- Keratitis, uveitis, conjunctivitis
- Acute retinal necrosis
- Optic neuritis
- Increased intraocular pressure and glaucoma
- Permanent vision loss in severe cases
Neurological complications:
- Ramsay Hunt syndrome — facial nerve palsy, vesicles in ear canal, hearing loss
- Meningitis or encephalitis — rare but serious
- Myelitis — transverse myelitis with motor and sensory deficits
- Cranial nerve palsies — any cranial nerve can be affected
- Peripheral motor neuropathy — weakness in affected myotome
- Vasculopathy — VZV-associated stroke (granulomatous arteritis of cerebral vessels)
Cutaneous complications:
- Bacterial superinfection — impetigo, cellulitis, abscess
- Scarring — particularly after severe vesicular eruption or secondary infection
Disseminated zoster — visceral involvement (lungs, liver, CNS); primarily in immunocompromised patients; can be life-threatening.
Other:
- Ramsay Hunt syndrome — approximately 20% do not recover full facial function despite treatment
- Autonomic dysfunction — urinary retention, constipation with sacral involvement
Prognosis
Most immunocompetent patients recover completely within 2-4 weeks. Pain typically resolves as rash heals, though PHN develops in 10-20% of patients over 60. Early antiviral treatment improves outcomes and reduces complication risk.
Recurrence: Approximately 5% of patients experience a second episode. Recurrence is more common in immunocompromised individuals.
Mortality: Rare in immunocompetent hosts; increased risk in immunocompromised patients with disseminated disease or CNS involvement.
Vaccination with recombinant zoster vaccine has dramatically reduced disease burden in vaccinated populations. Patients who develop shingles despite vaccination typically have milder disease and lower risk of PHN.
Practice questions
1. A 68-year-old woman presents with a 2-day history of severe burning pain on the left side of her chest. She describes the pain as constant and says it started 3 days before a rash appeared. On examination, there is a band of erythematous papules and vesicles on an erythematous base extending from the left side of her back around to the anterior chest, stopping at the midline. She has a history of chickenpox as a child. Vital signs are normal. What is the most appropriate initial treatment?
2. A 72-year-old man with a history of chronic lymphocytic leukemia presents with a 3-day history of painful vesicular rash on the right side of his forehead and scalp. On examination, vesicles are present on the right forehead, right upper eyelid, and the tip of his nose. His right eye appears red and he reports blurred vision. What is the most appropriate next step in management?
3. A 55-year-old woman presents with persistent burning pain on her left lateral chest wall. She had a vesicular rash in the same location 5 months ago that was diagnosed as shingles and treated with a 7-day course of valacyclovir. The rash has completely healed but the pain has not improved. She rates the pain as 7/10 and describes it as constant burning with occasional shooting sensations. She has tried over-the-counter acetaminophen without relief. What is the most appropriate treatment?
Frequently asked questions
What causes shingles?
Shingles is caused by reactivation of varicella-zoster virus (VZV), the same virus that causes chickenpox. After initial chickenpox infection (usually in childhood), the virus remains dormant in nerve ganglia and can reactivate years or decades later when immunity declines, typically due to aging, stress, or immunosuppression. The reactivated virus travels along sensory nerves to cause a painful rash in a dermatomal distribution.
What are the first symptoms of shingles?
The first symptoms are typically pain, burning, tingling, or itching in a specific area of skin, usually on one side of the body. This prodromal phase occurs 1-5 days before the rash appears. Some people also experience fever, headache, or fatigue. The pain can be quite severe and is sometimes mistaken for other conditions like heart attack or appendicitis, depending on its location. The characteristic vesicular rash appears after these early symptoms.
How is shingles diagnosed?
Shingles is usually diagnosed clinically based on the characteristic appearance of a painful, unilateral vesicular rash in a dermatomal distribution that does not cross the body's midline. Laboratory confirmation is rarely needed in typical cases but can be done through PCR testing of vesicular fluid, which is the most accurate method. Direct fluorescent antibody testing or viral culture may also be used. Laboratory testing is more important in atypical cases, immunocompromised patients, or when complications are suspected.
Is shingles curable?
Shingles is a self-limited infection that typically resolves on its own within 2-4 weeks, though it is not "cured" in the sense that the virus remains dormant in the body afterward. Antiviral medications like valacyclovir or acyclovir can significantly shorten the duration of the illness, reduce symptom severity, and lower the risk of complications like postherpetic neuralgia when started within 72 hours of rash onset. Most immunocompetent patients recover completely, though some develop chronic pain (postherpetic neuralgia).
Shingles vs chickenpox — what is the difference?
Both are caused by the same virus (VZV) but represent different stages of infection. Chickenpox is the primary infection, usually occurring in childhood, causing widespread itchy vesicles all over the body and is highly contagious through respiratory droplets. Shingles is reactivation of the dormant virus years later, causing a painful vesicular rash in a single dermatome on one side of the body. Shingles is less contagious and spreads only through direct contact with the rash, not through the air.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: B02
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.