Varicella-Zoster Virus (VZV) Clinical Presentation

Updated: Feb 12, 2018
  • Author: Wayne E Anderson, DO, FAHS, FAAN; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Pain and paresthesia are typically the first symptoms. Until the characteristic vesicular rash erupts, diagnosis may be difficult.

A prodromal period during which symptoms may vary is common. Pain occurs in 41% of patients, itching in 27%, and paresthesias in 12%.

During the acute illness, 90% of patients experience pain, 20% describe helplessness and depression, and 12% experience flulike symptoms.



Herpes zoster (shingles)

The most common presentation is the shingles vesicular rash, which most commonly affects a thoracic dermatome.

After a prodromal illness of pain and paresthesias, erythematous macules and papules develop and progress to vesicles within 24 hours. The vesicles eventually crust and resolve.

Pain and sensory loss are the usual symptoms, but motor weakness also occurs and is frequently missed on examination. Motor weakness results when the viral activity extends beyond the sensory root to involve the motor root. Cases of actual monoplegia due to varicella-zoster virus (VZV) brachial plexus neuritis have been reported.

Typical zoster in the vicinity of right popliteal Typical zoster in the vicinity of right popliteal fossa in a vertebral nerve L4 distribution.
Human herpesvirus (HHV) type 3. Intraoral herpes z Human herpesvirus (HHV) type 3. Intraoral herpes zoster closely resembles recurrent HHV-1 infection, but the lesions generally follow a dermatome and stop sharply at the midline, as shown here. However, the rules for common sites of occurrence of HHV-1 and HHV-3 often do not apply to patients who are immunocompromised. Courtesy of Sheldon Mintz, DDS.

Zoster multiplex

Shingles may appear in multiple dermatomes, both contiguous and noncontiguous, on either side of the body.

They are more common in individuals who are immunocompromised.

Terminology depends on the number of involved dermatomes and on whether the condition is unilateral or bilateral. For example, zoster duplex unilateralis refers to the involvement of 2 unilateral dermatomes. Cases of zoster simultaneously occurring in 7 noncontiguous dermatomes have been reported.

Zoster sine herpete

VZV infection may reactivate without causing cutaneous vesicles. These patients have severe dermatomal pain, possible motor weakness and possible hypesthesia, but no visible rash or vesicles.

Studies show that VZV infection may present as acute peripheral facial palsy in 8-25% of patients who have no cutaneous vesicles. This is more common in immunosuppressed patients who use acyclovir (or other agents) as zoster prophylaxis. [1]


VZV infection may also cause central nervous system deficits.

Although deficits are more common in immunocompromised individuals, such presentations do occur in the general population.

In one report, the condition began as a typical shingles rash, but spinal cord involvement became apparent 3 weeks after the onset of the initial rash.

The manifestations are usually bilateral. The physical findings may progress.

The underlying pathology typically progresses for 3 or more weeks. Progression for 6 months in immunocompromised individuals has been reported.

With intravenous acyclovir treatment, most cases fully resolve. Recurrence is rare but has been reported.

Zoster encephalitis is also rare but is reported in otherwise healthy individuals. Due to the effectiveness of 2-dose vaccinations, fewer cases of VZV encephalitis occur, [3] yet most cases in vaccinated individuals are due to wild type from the vaccine strain. [4]

Ramsay-Hunt syndrome

This syndrome occurs when the geniculate ganglion is involved.

The clinical presentation includes a peripheral facial palsy, pain in the ear and face, and vesicles in the external ear canal.

Additional auditory and vestibular symptoms may be present. The vesicles are not present in all cases.

Keratitis (herpes ophthalmicus)

This is caused by reactivation of VZV infection in the ophthalmic division of the trigeminal nerve.

The presentation may include conjunctivitis or corneal ulcers. Complications include blindness.

The vesicles do not have to be present.

Rarely, in cases of herpes ophthalmicus, the virus migrates along the intracranial branches of the trigeminal nerve, causing thrombotic cerebrovasculopathy with severe headache and hemiplegia.



Immunosuppression increases the risk of both typical shingles and atypical presentations, such as myelitis, encephalitis, disseminated disease, and visceral involvement.