Prodromal phase (2–5 days before rash):

Hyperesthesia or allodynia over the affected area

Malaise, mild fever, headache may occur

Dermatomal phase:

Does not cross midline (except in immunocompromised patients)

Rash progression:

Maculopapular erythematous patches → clear vesicles → pustules → crusts (7–10 days)

Complete healing typically within 2–4 weeks

Scarring may occur in severe or necrotic lesions

Neurological features:

Sensory loss or diminished sensation over the dermatome

Occasional motor weakness when motor fibers involved

Zoster ophthalmicus (V1 involvement):

Conjunctivitis, keratitis, uveitis, episcleritis

Severe photophobia and decreased vision possible

Zoster oticus (Ramsay Hunt Syndrome):

Facial paralysis, ear vesicles, tinnitus, vertigo

Hearing loss in severe cases

Oral involvement:

Vesicles or ulcers on palate, tongue, buccal mucosa

Painful swallowing (odynophagia)

Systemic features (occasionally):

Headache, fatigue, mild fever

Lymphadenopathy corresponding to affected region

Special clinical notes:

Thoracic zoster → chest pain mimicking MI

Lumbar zoster → flank or abdominal pain mimicking renal colic or appendicitis

Post-herpetic neuralgia (PHN):

Persistent neuropathic pain >90 days

Risk ↑ with age >50, severe rash, severe acute pain

Secondary bacterial infection:

Staphylococcus aureus or Streptococcus pyogenes

Causes cellulitis, impetigo, abscess formation

Herpes zoster ophthalmicus (HZO):

Involvement of ophthalmic division (V1) of trigeminal nerve

Herpes zoster oticus (Ramsay Hunt syndrome):

Vesicles in ear canal + facial nerve palsy

Hearing loss, tinnitus, vertigo possible

Motor neuropathy:

Weakness in affected myotome

Rare but may mimic stroke if facial nerve involved

Meningitis / encephalitis:

More common in immunocompromised

Severe headache, altered sensorium, fever

Myelitis:

Segmental spinal cord inflammation → sensory/motor deficit

Disseminated herpes zoster:

>20 widespread vesicles beyond initial dermatome

Risk of visceral involvement (lungs, liver, brain)

Pneumonia:

Especially in immunocompromised or elderly

May progress to respiratory failure in severe cases

Ocular complications:

Keratitis, conjunctivitis, scleritis, optic neuritis

Visceral involvement:

Rare — hepatitis, pancreatitis, gastritis

More common in HIV, cancer, transplant patients

Zoster sine herpete:

Neuropathic pain without rash

Difficult diagnosis—requires VZV PCR or antibodies

Herpes simplex virus (HSV):

Recurrent vesicles, may cross midline, often on lips/genitals

PCR helps differentiate HSV vs VZV

Contact dermatitis:

Pruritic rather than painful

Often bilateral or not dermatomal

History of allergen exposure

Impetigo:

Honey-colored crusts

Usually in children

Not dermatomal; painless

Insect bites:

Grouped itchy papules

Not vesicular in classic dermatome pattern

Cellulitis / Erysipelas:

Diffuse redness, warmth, tenderness

No grouped vesicles

Systemic signs more prominent

Scabies:

Burrows, intense itching

Involves finger webs, flexures

Not dermatomal, polymorphic lesions

Dermatitis herpetiformis:

Intensely itchy grouped vesicles

Symmetrical distribution (extensor surfaces)

Associated with celiac disease

Eczema herpeticum (Kaposi varicelliform eruption):

Widespread painful vesicles in patients with atopic dermatitis

Caused by HSV; may resemble disseminated zoster

Post-herpetic neuralgia (without rash):

Neuropathic pain after previous zoster

No active lesions — “zoster sine herpete”

Acute otitis externa or otitis media:

Ear pain without vesicles

Differentiated from Ramsay Hunt syndrome (zoster oticus) by lack of vesicles and facial palsy

VZV is a DNA virus belonging to the Herpesviridae family, genus Varicellovirus.

After primary infection (varicella/chickenpox), the virus becomes latent in dorsal-root and cranial-nerve sensory ganglia.

Factors that trigger reactivation include older age, HIV infection, malignancies, chemotherapy, radiation, chronic diseases, and high-dose steroids.

Viremia does not occur during zoster; the infection remains localized unless immunocompromised.

Transmission of VZV can occur from a zoster patient to a susceptible person, but it results in varicella (not zoster).

Clinical diagnosis:

Painful dermatomal distribution with typical evolution (macule → vesicle → crust)

Tzanck smear:

Multinucleated giant cells present

PCR (preferred test):

Useful in atypical presentations and immunocompromised patients

Direct fluorescent antibody test (DFA):

Detects VZV antigen from lesion scrapings

Faster than culture; moderately sensitive

Viral culture:

Low sensitivity for VZV

Rarely used now

Serology:

VZV IgM may indicate recent infection but low reliability

IgG helps assess immunity, not useful for acute shingles

CSF analysis (when neurological involvement suspected):

Mild lymphocytic pleocytosis, raised protein

Ophthalmological evaluation (if V1 involvement):

Slit-lamp exam for keratitis, uveitis

Intraocular pressure measurement

Imaging (if complications suspected):

MRI brain/spine → suspected encephalitis, myelitis, radiculopathy

CT orbit → severe orbital involvement or complications

Why does herpes zoster occur only on one side?

The varicella-zoster virus remains dormant in a single dorsal root ganglion or cranial nerve ganglion. When reactivated, it affects the sensory nerve distribution of that ganglion, resulting in a strictly unilateral dermatomal rash.

Why does pain occur even before the rash appears?

During reactivation, the virus causes inflammation of the affected sensory nerve (neuritis). This nerve inflammation leads to burning or shooting pain days before skin lesions appear.

Why is post-herpetic neuralgia more common in older adults?

Age-related decline in cell-mediated immunity leads to more severe nerve inflammation and slower nerve healing. Damaged sensory nerves fire abnormally, causing chronic pain (PHN).

Why do some patients get motor weakness?

If viral inflammation spreads to the ventral (motor) roots, segmental zoster paresis can occur, leading to limb weakness in the same dermatome/myotome.

Why does ophthalmic zoster need urgent treatment?

Involvement of the ophthalmic (V1) branch of the trigeminal nerve can lead to keratitis, uveitis, and vision loss. Prompt antivirals reduce ocular complications.

Why do antivirals help even if started 72 hours later in high-risk patients?

In elderly or immunocompromised patients, viral replication may continue longer. Antivirals still reduce complications such as PHN, ocular damage, or neurological involvement.

Why is zoster infectious only until crusting?

The virus is shed from fresh vesicles. Once all lesions crust over, viral shedding stops and the patient is no longer contagious.

Why does the rash follow a dermatomal pattern?

The virus travels centrifugally along the sensory nerve from the ganglion to the skin, producing lesions confined to that nerve’s dermatome.

Why does stress/reactivation occur years later?

Cell-mediated immunity wanes with age, stress, illnesses, malignancy, HIV, or immunosuppressive therapy — allowing dormant VZV to reactivate.

Why can zoster cause facial paralysis (Ramsay Hunt syndrome)?

If the geniculate ganglion of cranial nerve VII is involved, inflammation affects motor fibers → facial palsy, ear vesicles, and severe otalgia.

Herpes zoster does NOT recur often — but recurrence is possible in immunosuppressed individuals.

A second episode should always raise suspicion for HIV, diabetes, malignancy, or chronic steroid use.

Zoster can occur without a rash — called “zoster sine herpete” — presenting only with dermatomal pain.

If lesions cross the midline, suspect either multiple adjacent ganglia involvement or immunocompromised state.

Lesions are deeper and more painful than varicella; varicella is centripetal while zoster is dermatomal.

Scarring and skin pigmentation changes are more common in darker-skinned individuals after zoster.

Antivirals work best when started early, but elderly and immunocompromised still benefit even after 72 hours.

Steroids DO NOT prevent post-herpetic neuralgia, but they may reduce acute pain when used with antivirals.

Pain out of proportion with mild skin lesions may indicate early PHN — often needs neuropathic pain agents early.

If zoster appears in a young adult with severe pain or multiple dermatomes, screen for underlying immunodeficiency.

Zoster vaccination is recommended even for individuals with prior zoster to reduce recurrence and PHN risk.

Ramsay Hunt syndrome has a worse prognosis for facial nerve recovery than Bell’s palsy.

Herpes zoster can trigger Guillain–Barré syndrome in rare cases due to immune-mediated neuropathy.

Chronic zoster keratitis can occur years after ophthalmic zoster, even after apparent recovery.

Touching zoster lesions does not cause zoster in others; it can cause *chickenpox* in non-immune individuals.

Zoster is NOT transmitted via respiratory droplets — only by direct contact with active lesions.

Atypical presentations (multidermatomal, disseminated) must be treated as medical emergencies.

After primary varicella infection, VZV establishes lifelong latency in dorsal-root, cranial-nerve, and autonomic ganglia.

Triggers include aging, emotional/physical stress, HIV, malignancies, immunosuppressive drugs, and chronic illness.

Once reactivated, VZV replicates inside neuronal cells and travels along the sensory nerve toward the skin.

*Virus spreads centrifugally along the affected dermatome*, causing inflammation of the nerve and skin.

Ganglionic inflammation produces severe neuropathic pain before the rash (prodrome).

Inflammation of affected sensory nerves can lead to neuronal damage.

In immunocompromised individuals, reactivated virus may disseminate hematogenously, causing multi-dermatomal disease or visceral involvement.

• Virus remains dormant after primary varicella infection

• Reactivates when cell-mediated immunity declines (age, stress, illness)

• Neuronal swelling and degeneration

• Lymphocytic infiltration around neurons

• Demyelination of involved sensory nerve fibers

Skin pathology:

• Vesicle formation due to intra-epidermal ballooning degeneration

• Multinucleated giant cells (Tzanck smear positive)

• Viral inclusion bodies within keratinocytes

• Dermal edema with perivascular lymphocytes

Nerve pathology:

• Axonal damage in peripheral nerve

• Segmental demyelination

• Persistent inflammation may predispose to post-herpetic neuralgia

Timeline:

• Reactivation → ganglionitis → viral spread along dermatome → vesicles → crusting

• Nerve inflammation persists long after skin lesions heal

Primary prevention:

Vaccination — the most effective strategy:

Recombinant zoster vaccine (Shingrix)

• Recommended for adults ≥50 years

• 2-dose schedule, 2–6 months apart

• Preferred over live vaccine due to higher efficacy and safety

• Can be given even if patient had zoster previously

• Can be given in immunocompromised individuals

Live attenuated vaccine (Zostavax)

• Used less now

• Not recommended in immunosuppressed persons

Varicella vaccination in childhood:

• Routine varicella vaccination → lower lifetime VZV burden

• Indirectly reduces zoster incidence in adulthood

Avoid triggers that may weaken immunity:

Adequate sleep, nutrition, stress reduction

Good control of chronic conditions (diabetes, CKD, HIV)

Preventing spread to others:

• Avoid close contact with pregnant women, newborns, and immunocompromised persons

• Keep lesions covered until crusted

• Maintain hand hygiene

Occupational health (health-care workers):

• Workers with active lesions should avoid caring for high-risk patients

• Vaccination recommended for non-immune staff

Post-exposure prophylaxis (for high-risk contacts):

Varicella-zoster immune globulin (VZIG)

• Given within 10 days of exposure

• For pregnant, neonates, and severely immunocompromised contacts

When imaging is done (atypical cases, complications, severe pain):

CT Scan:

• Usually normal in uncomplicated zoster

• May show mild soft-tissue swelling in the affected dermatome

• Useful to rule out alternative causes of thoracic or abdominal pain

MRI (most useful in complicated zoster):

• T2 hyperintensity of affected dorsal root or cranial nerve

• Enhancement of dorsal root ganglion (ganglionitis)

• Enhancement of peripheral nerve along affected dermatome

• In cranial involvement (e.g., Ramsay Hunt), MRI may show VII or VIII nerve enhancement

Complicated herpes zoster:

• Myelitis — focal T2 hyperintensity in spinal cord

• Zoster-related motor neuropathy — signal changes in involved motor roots

• Orbital zoster — orbital fat stranding, extraocular muscle edema

Chest radiograph:

• Usually normal

• May show mild asymmetric interstitial infiltrates in rare zoster pneumonitis

Imaging role summary:

• Exclude alternate diagnoses (radiculopathy, tumor, abscess)

• Confirm neuritis when symptoms are severe or atypical

• Assess complications (myelitis, cranial neuropathies)

• Only one VZV serotype is known

• Genetic variability exists but does not create separate serotypes like dengue or influenza

VZV genotypes (not clinically used):

• Several molecular clades (E1, E2, J, M1, M2)

• Geographic distribution varies — e.g., E clades in Europe, J in Japan

• Clinical presentation and severity are similar across clades

Clinical implication:

• All genotypes respond to acyclovir, valacyclovir, famciclovir

• Vaccines protect across all VZV genotypes

General examination:

• Low-grade fever

• Tender regional lymphadenopathy

Skin signs:

Dermatomal distribution does **not cross the midline** (except in immunocompromised).

Rash progression (clinical observation):

• Maculopapular stage → vesicles → pustules → ulcers → crusts

• New vesicles may appear for 3–5 days

Neurological signs:

Decreased sensation in the affected dermatome may occur.

Special signs by location:

• **Ophthalmic zoster (V1):**

– Conjunctival injection

– Keratitis

– Uveitis

– *Hutchinson sign*: vesicles on the tip/side of nose → indicates nasociliary nerve involvement → high risk of ocular complications

• **Otic zoster (Ramsay Hunt Syndrome):**

– Vesicles in external ear canal

– Ipsilateral facial paralysis

– Vertigo or tinnitus

• **Oral zoster:**

– Vesicular lesions on palate or buccal mucosa following trigeminal branches

The disease primarily affects older adults and immunocompromised individuals and can lead to post-herpetic neuralgia, a chronic pain syndrome.

Prodromal symptoms (appear 2–3 days before rash):

• Fever, malaise, headache

• Burning, tingling, or stabbing pain along a dermatome

Acute symptoms (rash phase):

Rash progresses: macules → papules → vesicles → pustules → crusting by 7–10 days.

Allodynia (pain from light touch) is common.

Dermatome involvement:

• Thoracic (most common)

• Trigeminal (especially ophthalmic division – V1)

• Cervical and lumbar dermatomes less commonly

Systemic symptoms:

• Mild fever

• Fatigue

• Headache

• Lymphadenopathy

Atypical forms:

• *Zoster sine herpete* — radicular pain without rash

• Multi-dermatomal rash (more common in immunocompromised)

Goals of treatment:

Antiviral therapy (start ideally within 72 hours of rash onset):

Acyclovir 800 mg five times daily × 7–10 days

Valacyclovir 1 g three times daily × 7 days

Famciclovir 500 mg three times daily × 7 days

Start even after 72 hours if: new vesicles, severe pain, elderly, immunocompromised

Analgesia:

Paracetamol / NSAIDs for mild pain

Neuropathic pain agents if required:

Gabapentin or pregabalin

TCAs (amitriptyline) in low doses if neuropathic features present

Corticosteroids:

Used only with antivirals

Prednisone 60 mg/day taper over 3 weeks

Avoid in diabetics, uncontrolled hypertension, severe immunosuppression

Care of skin lesions:

Keep area clean and dry

Cool compresses for relief

Calamine lotion may reduce discomfort

Avoid rupturing vesicles; prevent bacterial superinfection

Management of post-herpetic neuralgia (PHN):

Topical lidocaine 5% patches

Capsaicin 8% patch for selected cases

Tramadol only if severe refractory pain

Special situations:

Herpes Zoster Ophthalmicus → URGENT ophthalmology referral

Facial nerve palsy (Ramsay Hunt) → antivirals + steroids early

Immunocompromised patients → IV acyclovir 10 mg/kg every 8 hrs

Disseminated zoster → hospital admission + IV antivirals

Vaccination (prevention, but relevant in treatment section):

*Recombinant zoster vaccine (Shingrix)* recommended for adults ≥50 yrs

Given even if past zoster infection occurred