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Chapter: Microbiology and Immunology: Virology, Virus: Herpesviruses

Clinical Syndromes - Varicella Zoster Virus

Varicella zoster virus causes following two distinct clinical syndromes: (a) varicella (chickenpox) and (b) herpes zoster (shingles).

Clinical Syndromes

Varicella zoster virus causes following two distinct clinical syndromes: (a) varicella (chickenpox) and (b) herpes zoster (shingles).

 Varicella (chickenpox)

Varicella is one of the five childhood exanthemata along with measles, rubella, rubeola, and fifth disease. Chickenpox is a benign illness of the childhood, which is characterized by an exanthematous varicella rash that occurs following infection with VZV.

Incubation period is about 2 weeks. The condition is nor-mally asymptomatic. In symptomatic cases, the condition man-ifests as fever and maculopapular rash that progresses within a few hours to thin-walled vesicle on an erythematous base. This vesicle, which is the hallmark of chickenpox, is characteristi-cally surrounded by a red ring. The vesicle, which measures approximately 2–4 mm in diameter, becomes a pustule within 12 hours and begins to ulcerate, after which scabs appear. Successive crops of vesicles appear over 2–5 days and as a result at any given time all stages of the lesions are seen on the skin.

Primary infection in adults is generally more severe than in children. The vesicles heal more slowly; secondary bacterial infections and scarring are more common. The accompanying fever is more prolonged and higher. Interstitial pneumonia, Guillain–Barre syndrome, and Reye’s syndrome may occur in some of the patients.

In pregnancy, VZV tends to cause more serious disease if the mother has not been infected during the childhood. The virus crosses the placenta and causes congenital infection in the fetus. Congenital malformation with hypoplasia of limbs, cho-rioretinitis, and scarring of skin are seen in the fetus infected during pregnancy.

 Herpes zoster

Herpes zoster is a recurrence of latent varicella infection acquired many years earlier. This occurs due to reactivation of the VZV, which has remained latent in one or more sensory gan-glia following primary varicella many years earlier. The viruses travel down along the sensory nerve to produce painful vesicles in the areas of the skin (dermatome) innervated by the nerves from the affected ganglia. Severe pain in the area innervated by the nerve preceding the appearance of chickenpox-like lesion is the hallmark of the disease. The rashes are usually restricted to a dermatome. For example, if thoracic nerve supplies are affected, rashes appear most commonly on the chest walls. The rashes are distributed on the scalp and forehead when the ophthalmic nerve of trigeminal ganglion is affected. In more than 50% of the cases, the eye is affected, leading to corneal ulceration, anterior uveitis, and stromal keratitis.

The accompanying pain and herpetic neuralgia is very much severe for up to a few weeks and occurs in about half of the patients over 60 years of age. The pain may persist for months, which may even require surgical ablation of the ganglion.

Zoster of the seventh nerve ganglion may cause Bell’s palsy and Ramsay Hunt syndrome. This is caused by reactivation of virus involving the facial and auditory nerves. Vesicular lesions may develop on the pinna, tragus, in the auditory canal, and on the tympanic membrane. The patient may have nystagmus, vertigo, or facial nerve palsy resembling Bell’s palsy.

Postherpetic neuralgia is a chronic pain syndrome caused by VZV. The condition is characterized by persistence of recurrent pain lasting 30 or more days after the acute infection. This con-dition occurs in more than 30% of patients, in the older people aged 65 years and above.

Herpes zoster ophthalmicus is the most serious and devastating form of acute herpes zoster (Color Photo 57). The condition occurs due to reactivation of the fifth cranial (tri-geminal) nerve. This condition may appear weeks to months after resolution of other symptoms. Postherpetic neuralgia and long-term sequelae are common in this condition.

Varicella zoster virus infection in immunocompromised patients: The virus causes more lesions, and a progressiveand life-threatening disease in immunocompromised patients and in neonates. The defective CMI in these patients facilitates rapid dissemination of the virus to the brain, lungs, and liver, thereby causing a fatal infection. The condition may occur fol-lowing primary infection by varicella or by reactivation of latent disease.

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