Definition

Herpes zoster, commonly known as shingles, is a viral infection caused by the reactivation of the varicella-zoster virus (VZV), which also causes chickenpox. Following the initial infection, VZV stays dormant in the dorsal root or cranial nerve ganglia. Often years later, primarily due to ageing or weakened immunity, the virus reactivates, leading to a painful, unilateral vesicular rash along a specific dermatome.

Description

Herpes zoster is usually classified according to the affected site and associated complications:

• Based on Anatomic Involvement
  • Herpes Zoster Ophthalmicus (HZO) affects the ophthalmic branch of the trigeminal nerve, increasing the risk of vision loss.
  • Herpes Zoster Oticus, also called Ramsay Hunt Syndrome, affects the geniculate ganglion of the facial nerve, causing symptoms like ear pain, vesicles in the ear canal, facial paralysis, and hearing loss.
  • Cranial nerve zoster may affect the trigeminal, facial, or other cranial nerves.
  • The most common types are Cervical, Thoracic, or Lumbar Zoster, which usually appear with a dermatomal rash and pain in the respective areas.
  • Sacral Zoster: May lead to bladder or bowel problems.
• By Complications
  • Simple Herpes Zoster: Rash and pain limited to a dermatome.
  • Herpes Zoster with Postherpetic Neuralgia (PHN): Pain that lasts more than 90 days after the rash first appears.
  • Disseminated Herpes Zoster involves a rash that extends beyond the initial dermatome and is more frequently seen in immunocompromised patients.
  • Neurologic Complications include encephalitis, meningitis, vasculopathy, and myelitis.
  • Ophthalmic and otic complications can lead to vision or hearing impairments.
• By Patient Population
  • Immunocompetent adults typically experience localized disease that is usually self-limiting when treated with antiviral therapy.
  • Immunocompromised patients with severe, prolonged, or widespread disease need intravenous antiviral treatment.

Epidemiology

Incidence/Prevalence

• The overall incidence rate is about 3 to 5 cases per 1,000 person-years in the general population.
• Approximately one in three Americans (30–33%) will experience shingles at some point in their lifetime.
• By age 85, about half of individuals will have experienced an episode.
• Recurrent shingles occur in approximately 4–6% of patients, typically affecting older or immunocompromised individuals.

Age

• Low in youth: approximately 0.86 per 1,000 person-years among individuals aged 19 or younger.
• Significant rise with age: 12.78 per 1,000 person-years in those aged 80 and above.
• For individuals aged 50 and older, the rate is 8.46 per 1,000 person-years, while for those aged 60 and above, it rises to 10.46 per 1,000 person-years.
• Population studies show that 60–68% of cases occur in individuals over age 50, with up to 92% being immunocompetent.

Gender

• Historical data indicate approximately a 28% increased risk in women across all age groups.

Race

• White individuals experience the highest incidence.
• Black Americans have a significantly lower risk of developing shingles, being 25–75% less likely to do so.

Risk factors

• General
  • Age >50 years
    • Mechanism: Declining cell-mediated immunity; highest incidence in ≥60
  • History of varicella (chickenpox)
    • Mechanism: Latent VZV in dorsal root ganglia; prerequisite for reactivation
  • Immunosuppression (e.g., HIV/AIDS, malignancy, transplant)
    • Mechanism: Impaired T-cell surveillance; RR up to 4.5 in transplant patients
  • Psychological stress
    • Mechanism: Cortisol-mediated immune suppression; modest increase in risk
  • Female gender
    • Mechanism: Slightly higher incidence; possibly hormonal or reporting bias
  • Family history of zoster
    • Mechanism: Genetic susceptibility; RR ~2.5
  • Physical trauma (especially near dermatomes)
    • Mechanism: Local nerve irritation may trigger viral reactivation
• Physiological
  • Diabetes mellitus.
    • Mechanism: Impaired innate and adaptive immunity; RR ~1.5–2.0.
  • Chronic kidney disease (CKD).
    • Mechanism: Uremia-related immune dysfunction.
  • Cardiovascular disease (CVD).
    • Mechanism: Chronic inflammation and vascular stress.
  • Chronic obstructive pulmonary disease (COPD).
    • Mechanism: Steroid use and systemic inflammation.
  • Rheumatoid arthritis (RA) / Systemic lupus erythematosus (SLE).
    • Mechanism: Autoimmune dysregulation; often treated with immunosuppressants.
  • Inflammatory bowel disease (IBD).
    • Mechanism: Immunosuppressive therapy and mucosal immune imbalance.
  • Cancer (solid or hematologic).
    • Mechanism: Direct immune compromise and chemotherapy effects.
  • Depression and mental health disorders.
    • Mechanism: Neuroimmune modulation; increased susceptibility.
  • Asthma.
    • Mechanism: Chronic inflammation and corticosteroid exposure.

Etiology

• Primary infection.
  • Herpes zoster results from the varicella-zoster virus (VZV), which also causes varicella (chickenpox).
  • Once the primary infection occurs, often during childhood, the virus remains dormant for life within the sensory dorsal root ganglia, cranial nerve ganglia, and autonomic ganglia.
• Reactivation:
  • Herpes zoster happens when the dormant VZV reactivates, usually many years after the first infection.
  • Reactivation often correlates with decreasing VZV-specific cell-mediated immunity.
• Triggers include the following.
  • Advanced age, associated with immune senescence, is typical among adults over 50 years old.
  • Immunosuppression (due to HIV, cancer, organ transplants, chemotherapy, or corticosteroid use).
  • Stress or trauma impacting the affected dermatome.
  • Chronic conditions such as diabetes and autoimmune diseases.
• Pathophysiology
  • Latency setup:
    • Following primary infection (chickenpox), VZV moves retrogradely along sensory axons to reach the dorsal root ganglia or cranial nerve ganglia.
    • The virus stays inactive, kept in check by the immune system.
  • Reactivation process:
    • A decline in VZV-specific T-cell–mediated immunity permits the virus to replicate in neurons.
    • Virus propagates anterogradely along sensory nerves to reach the skin.
    • This results in inflammation, neuronal damage, and increased viral replication within the affected dermatome.
  • Dermatomal rash and pain:
    • Clinically, patients present with a unilateral vesicular rash confined to a single dermatome.
    • Pain occurs due to neuronal inflammation and damage, which explains its burning and shooting sensations.

History

Patients with herpes zoster frequently report:

• Prodromal Symptoms (2–3 days before rash)
  • Localized burning, tingling, itching, or shooting pain along a specific dermatome.
  • Pain can be intense, often described as sharp, stabbing, or electric shock–like.
• Timeline of Symptoms
  • Pain usually starts before the rash appears, which is a common reason patients seek medical help.
  • A vesicular rash appears in the same dermatome within 1 to 5 days.
  • Patients might seek medical attention once the rash appears or if pain persists, which could lead to postherpetic neuralgia.

Physical findings on examination

• Skin Appearance
  • Unilateral vesicular rash following a dermatomal pattern, most often affecting thoracic or cranial dermatomes.
  • Rash progresses from erythematous macules to papules, then vesicles, pustules, and finally crusts over 7–10 days.
  • In immunocompromised patients, lesions might be extensive or appear on both sides.
• Neurologic Findings
  • Allodynia (pain caused by light touch) or hyperesthesia in the affected dermatome.
  • Reduced or changed sensation in the rash area.
  • Motor weakness may occasionally occur if the virus impacts motor fibers.
• Systemic Findings
  • Mild fever, fatigue, or swollen lymph nodes.
  • In severe cases, especially among immunocompromised individuals, symptoms may include a widespread rash, eye involvement, or neurological issues such as encephalitis, myelitis, or cranial neuropathies.
• Special Situations
  • Herpes zoster ophthalmicus appears as a rash on the forehead, eyelid, or tip of the nose (Hutchinson’s sign), which increases the risk of corneal involvement and possible vision loss.
  • Herpes zoster oticus, also called Ramsay Hunt syndrome, shows vesicles in the ear canal along with facial nerve palsy and hearing loss.

Laboratory Tests

Lab tests are typically unnecessary for classic cases but are used when the diagnosis is unclear or uncertain. complications occur.).

• PCR (Polymerase Chain Reaction) for Varicella-Zoster Virus (VZV)
  • Conducted on skin lesion swabs, vesicle fluid, crusts, or CSF.
  • The gold standard in the U.S. for diagnosing herpes zoster.
• VZV Direct Fluorescent Antibody Test (DFA)
  • Reliable and quick at detecting VZV in lesion scrapings.
• CSF Studies (only if meningitis/encephalitis suspected)
  • CSF VZV PCR is the most accurate test for detecting CNS involvement.
  • CSF cell count, protein, and glucose levels are measured to evaluate inflammation.
• HIV Testing (if indicated)
  • Recommended for young adults experiencing shingles or recurrent episodes, since shingles can indicate immunosuppression.

Diagnostic Tests

Diagnosis is primarily clinical, with imaging reserved for suspected complications.

• Clinical Examination – The Main Method for Diagnosis
  • Unilateral vesicular rash following a dermatomal pattern.
  • Pain often occurs before a rash appears.
• PCR-Based Diagnostic Testing (from skin lesions)
  • Confirms the presence of VZV in patients with atypical, early-stage, or weakened immune systems.
• MRI Imaging (only in complications)
  • Used for suspected Ramsay Hunt syndrome (facial nerve involvement), myelitis, encephalitis, or stroke-like issues from VZV vasculopathy.
• Ophthalmic Examination (for herpes zoster ophthalmicus)
  • Perform a slit-lamp exam to identify corneal involvement, keratitis, and uveitis.

Differential Diagnosis

• Herpes simplex virus (HSV) infection
  • HSV can cause localized, recurring vesicular eruptions.
  • A key characteristic is that HSV lesions typically recur at the same location, such as the perioral or genital areas, rather than following a dermatomal pattern.
• Contact dermatitis
  • Allergic or irritant dermatitis can lead to a vesicular, itchy rash.
  • Often bilateral or not confined to a single dermatome.
  • Tracking new exposures—like soaps, plants, or chemicals—helps in making distinctions.
• Impetigo
  • Typically caused by Staphylococcus aureus, this is a bacterial skin infection.
  • Shows vesicles or pustules that burst, leaving honey-colored crusts.
  • Usually, in children, it is not dermatomal.
• Cellulitis or erysipelas
  • Bacterial skin infections leading to pain, redness, swelling, and warmth.
  • No vesicular phase; borders may be diffuse, as in cellulitis, or sharply defined, like in erysipelas.
• Dermatitis herpetiformis
  • Autoimmune blistering condition associated with celiac disease.
  • Severe, itchy vesicles appear symmetrically on the extensor surfaces.
  • Unlike zoster, it does not appear unilaterally or follow dermatomal patterns.
• Scabies
  • Intensely itchy burrows and vesicles, often seen in web spaces, wrists, and waistline.
  • Usually widespread and affecting both sides, not confined to dermatomes.
• Drug eruptions, including Stevens-Johnson syndrome (SJS)
  • Vesiculobullous drug reactions can resemble shingles.
  • Generally, they affect several sites and can involve mucous membranes.
• Burns or insect bites
  • May appear similar to localized blistering.
  • Distinguished by their exposure history and lack of neuropathic prodromal pain.

General treatment items

• Antiviral Therapy (first-line in U.S. practice).
  • Goal: Decrease viral replication, shorten duration, and lower the risk of postherpetic neuralgia (PHN).
• Oral antivirals (most effective if initiated within 72 hours of rash appearance):
  • Acyclovir 800 mg PO 5×/day for 7–10 days.
  • Valacyclovir 1000 mg PO every 8 hours for 7 days.
  • Famciclovir 500 mg PO every 8 hours for 7 days.
• IV acyclovir (10 mg/kg every 8 hours) for severe, disseminated, or immunocompromised patients.
• Pain Management:
  • Mild–moderate pain: NSAIDs, acetaminophen.
  • Moderate to severe pain: Short-term use of opioids (e.g., oxycodone, hydrocodone).
  • Neuropathic pain agents (acute or PHN): gabapentin, pregabalin, and tricyclic antidepressants (e.g., amitriptyline, nortriptyline).
  • Corticosteroids (adjunctive in select cases).
  • A short tapering course of oral prednisone may be used in immunocompetent patients to reduce acute pain and inflammation.

Surgical Interventions

• Surgical and Interventional Therapies (for refractory cases, especially PHN in the U.S.).
• Not typical for acute zoster but considered when pain persists or is disabling.
• Nerve blocks (local anaesthetic with or without corticosteroid injections into paravertebral, epidural, or sympathetic ganglia).
• Spinal cord stimulation (SCS): Employed in select U.S. pain management centres for refractory postherpetic neuralgia.
• Pulsed radiofrequency ablation: A minimally invasive method for dorsal root ganglion modulation in PHN.

Adjunctive Therapies

• Topical Treatments:
  • Lidocaine 5% patches – FDA-approved for postherpetic neuralgia.
  • Capsaicin 8% patches (Qutenza®) – Used in specialty pain clinics; offers long-lasting relief for PHN.
  • Calamine lotion and cool compresses for symptom relief of rash.
• Other Supportive Measures:
  • Maintain adequate hydration, rest, and skincare to prevent secondary bacterial infections.
  • Loose clothing to reduce irritation.
  • Vaccination (Preventive, but essential in U.S. care).
  • The CDC recommends the recombinant zoster vaccine (Shingrix®) for all adults age 50 and older, and for immunocompromised adults age 19 and older, to prevent herpes zoster and PHN.

Medications indicated with specific doses

Toxoids

• Not Applicable

Immunoglobulins

• Not Applicable

Vasodilators

• Not Applicable

Thrombolytic agents

• Not Applicable

Dietary or Activity restrictions

• Avoid:
  • Refined carbohydrates (e.g., white bread, white rice, pastries)
  • Processed foods (e.g., chips, fast food, sweetened cereals)
  • Alcohol
  • Spicy foods
• Prefer:
  • Anti-inflammatory foods (e.g., leafy greens, berries, fatty fish)
  • Immune-supportive nutrients (e.g., vitamins A, B, C, E, zinc)
• Restrict:
  • Contact sports or skin-to-skin activities
  • Swimming or communal bathing
  • Excessive physical exertion during the acute phase
• Encourage:
  • Light activity (e.g., walking, stretching)
  • Rest and hydration

Disposition

• Most patients with herpes zoster are treated as outpatients using antivirals, pain relievers, and careful monitoring.
• Hospital admission is recommended when there are complications or high-risk features.

Admission Criteria

• Patients might need to be admitted if they have:
  • Severe Disease / Complications
  • Disseminated herpes zoster involves vesicles that extend beyond the primary and neighbouring dermatomes.
  • Visceral involvement includes conditions such as pneumonitis, hepatitis, encephalitis, and meningitis.
  • Severe or persistent pain that cannot be managed effectively on an outpatient basis.
  • Ophthalmic zoster involving the eye (poses a risk to vision).
  • Otic zoster (Ramsay Hunt syndrome) presenting with facial paralysis or vestibulocochlear symptoms.
• High-Risk Populations
  • Immunocompromised patients, such as those with HIV/AIDS, transplant recipients, and individuals undergoing chemotherapy.
  • Pregnant women with zoster pose a potential risk to the fetus, which is rare but requires close monitoring.
  • Elderly or frail patients who cannot sustain oral intake, hydration, or self-care.

Discharge criteria

• Patients are deemed safe to discharge if they satisfy these criteria:
  • The rash is confined to a specific area (not spread) and can be treated with topical or systemic therapies at home.
  • Vital signs are stable, with no signs of systemic toxicity, and pain is well-managed using oral medication.
  • Able to comfortably tolerate oral antivirals and fluids.
  • There are no signs of eye or nervous system issues that need immediate specialist attention.
  • Offering sufficient outpatient support and follow-up, particularly for elderly or immunosuppressed patients.

Monitoring

• Annual Incidence: approximately 1 million cases per year
• Lifetime risk: approximately 30% (about 1 in 3 Americans)
• Primary Surveillance Sources:
  • CDC NNDSS (National Notifiable Diseases Surveillance System)
  • Medicare/Medicaid claims data
  • VA and immunization registries
• Vaccine Monitoring:
  • Zostavax (ZVL): Live attenuated, for age ≥60 (2006), for age ≥50 (2011)
  • Shingrix (RZV): Recombinant, adjuvanted, for those 50 years and older (2017), preferred
  • Coverage (2016): approximately 33% for ZVL in individuals aged 60 and older.
  • Coverage (2023 est.): increased uptake of Shingrix, especially among older adults
• Complications Tracked:
  • Postherpetic Neuralgia (PHN)
  • Ophthalmic Zoster
  • Disseminated Zoster (IC/IS patients)
• Monitoring Tools:
  • VZV PCR: For atypical/disseminated cases
  • Clinical diagnosis: Dermatomal rash with pain
  • Serology: Not routinely recommended
• Documentation Tips:
  • Note rash location and dermatomal pattern.
  • Record pain severity (e.g., VAS score)
  • Flag complications (e.g., PHN, ocular involvement)
  • Include vaccination history (ZVL/RZV)

Patient Education

• Goals: Encourage early identification of complications and the necessity for medical intervention.
• Enhance overall quality of life and emotional health.
• General education: Avoid contact with pregnant women, newborns, and immunocompromised individuals until lesions crust over.
• Early antiviral therapy (acyclovir, valacyclovir, famciclovir) within 72 hours of rash onset reduces severity and complications
• Action Plan for Patients and Families:
  • Use prescribed topical treatments if recommended.
  • Watch for any signs of infection or increasing pain.
  • Encourage adequate rest and hydration.

Complications

• Postherpetic neuralgia (PHN) is persistent nerve pain that lasts three or more months after a rash.
• Herpes zoster ophthalmicus – eye involvement that threatens vision
• Herpes zoster oticus (Ramsay Hunt syndrome) – facial paralysis and hearing loss
• Secondary bacterial skin infection, such as Staphylococcus aureus.
• Encephalitis – brain inflammation that is rare but serious
• Meningitis – Viral Aseptic Presentation
• Myelitis – inflammation of the spinal cord
• Zoster-associated vasculopathy—stroke risk, especially among older adults.
• Motor neuropathy – limb weakness, rare.
• Acute retinal necrosis – risk of vision loss
• Optic neuritis – inflammation of the optic nerve.
• Glaucoma caused by ocular zoster
• Pneumonia is rare in immunocompromised patients.
• Death is rare, typically occurring in disseminated or CNS cases.

Prevention

• Get vaccinated – Shingrix (recombinant zoster vaccine) is the preferred option.
• Recommended for adults aged 50 and older, regardless of their history of chickenpox.
• Two-dose series, spaced 2 to 6 months apart.
• 90% effectiveness in preventing shingles and postherpetic neuralgia.
• Avoid contact with active shingles lesions, especially for immunocompromised or unvaccinated individuals.
• Maintain strong immune health by managing diabetes, reducing stress, and avoiding immunosuppressants when possible.
• Prompt antiviral treatment (acyclovir, valacyclovir, famciclovir) within 72 hours of rash onset decreases complications.
• Educate high-risk groups – elderly, cancer patients, transplant recipients, and HIV-positive individuals.
• Report and monitor outbreaks in healthcare environments.

Prognosis

• Most cases clear up within 3–5 weeks.
• Painful rash usually crusts over within 7–10 days.
• Blisters typically heal completely within 2–4 weeks.
• Early antiviral treatment (within 72 hours) enhances outcomes.
• Postherpetic neuralgia (PHN) can last for 3 months or more in 10–18% of cases.
• There is a risk of recurrence, particularly in immunocompromised or elderly individuals.
• Ocular or CNS involvement can cause long-term deficits.
• Disseminated zoster has a worse prognosis, especially in immunosuppressed patients.
• Vaccination (e.g., Shingrix) decreases incidence and severity.
• Mortality is rare but can occur in severe CNS or disseminated cases.

Associated conditions

• Postherpetic neuralgia (G53.0)
• Herpes zoster ophthalmicus (B02.3)
• Herpes zoster oticus (Ramsay Hunt syndrome) – facial paralysis and hearing loss
• Herpes zoster encephalitis (B02.0)
• Herpes zoster meningitis (B02.1)
• Herpes zoster myelitis – rare involvement of the spinal cord
• Disseminated herpes zoster (B02.7) in immunocompromised patients
• Secondary bacterial skin infection, e.g., Staphylococcus aureus.
• Zoster-associated vasculopathy – stroke risk in older adults
• Zoster-related motor neuropathy – limb weakness
• Acute retinal necrosis – a condition that threatens vision
• Zoster sine herpete – pain without rash

Synonyms

• Shingles
• Zoster
• Zona
• Herpes zoster virus (HZV)
• Varicella-Zoster Virus (VZV) – Causative Agent
• Acute posterior ganglionitis – old term
• Ramsay Hunt Syndrome

ICD-10-CM

• B02 - Zoster [Herpes Zoster] (umbrella code)
• B02.0 - Zoster encephalitis
• B02.1 - Zoster meningitis
• B02.2 - Zoster with other nervous system involvement
• B02.3 - Zoster ocular disease
• B02.7 - Disseminated zoster
• B02.8 - Zoster with other complications
• B02.9 - Zoster without complications

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