Initial infection with the varicella-zoster virus results in a widespread vesicular eruption known as varicella or chickenpox. Reactivation of the same virus results in a more localized infection known as herpes zoster or “shingles.”
Varicella clinical evidence of infection begins with a prodrome of fever and malaise 10-14 days after exposure to the virus. Shortly thereafter, vesicles begin to develop on the central portions of the trunk and face. These vesicles are 3-5 mm in diameter and are surrounded by a thin ring of erythema. The vesicles are randomly distributed, and clustering does not occur. As individual vesicles resolve, new ones appear in a centrifugal pattern, such that vesicles develop on the arms and legs 2-3 days after the trunk lesions have first appeared. A few vesicles may be found in the mouth, but mucosal involvement is not prominent. Vesicles are also almost always present in the scalp. Pruritus is often severe in children, but this is less prominent in adults. As the individual vesicles age, the fluid within them becomes cloudy, and the roof begins to sag, causing an umbilicated appearance. By the end of the first week the early vesicles have become crusted; eventually, all of the lesions heal with little or no scarring. Diagnosis is based on the epidemiology and clinical appearance of the disease. Confirmation of a clinical diagnosis may be obtained through Tzanck smears or by viral culture .
Viral reactivation ( reinfection) in an individual previously exposed to the varicella-zoster virus results in the development of herpes zoster (shingles). In this disease, small vesicles 3-5 mm in diameter occur in clustered patterns. Each cluster consists of 5-20 vesicles; numerous clusters are found in a linear distribution along a single dermatome. The eruption occurs unilaterally with little or no crossover at the midline.
Any dermatome can be involved, but in children and young adults the thoracic dermatomes are most commonly infected. In older adults the first branch of the trigeminal nerve (scalp and upper face) is frequently involved. Individual vesicles have a narrow ring of erythema around them. Where the clustering of vesicles is tight, the erythema becomes confluent, and the vesicles appear to arise from an underlying erythematous base.
The fluid within the vesicles is initially clear, although a small amount of hemorrhage may be noted in some of the blisters. Vesicular fluid becomes somewhat cloudy as the vesicles age. Because of blister roof fragility the vesicles often rupture, resulting in clusters of irregularly shaped erosions.
In adults, pain generally precedes the appearance of the vesicles (sometimes by as much as a week or more) and may continue, long after the vesicles have resolved, as postherpetic neuralgia. In childhood zoster, pain is not usually a significant factor.
New crops of vesicles continue to occur along the dermatome for several days, but by the end of the first week, new vesicles have stopped forming, and resolution of the earliest vesicles has begun.
Atypical Clinical Manifestations
Disseminated herpes zoster can occur in individuals who have depressed cell-mediated immune responsiveness. In such patients, lesions begin along a dermatome, but shortly thereafter, vesicles also begin to appear in other widely disseminated areas. The scattered lesions occurring outside of the dermatome are identical in appearance with those seen in chickenpox. Disseminated zoster is particularly likely to occur in individuals with advanced Hodgkin’s disease.
Patients with facial zoster sometimes develop an accompanying eye infection. This seems particularly likely to occur if the tip of the nose (representing nasociliary nerve infection) is involved.
Patients with varicella or disseminated zoster occasionally develop systemic infection, most usually in the form of pneumonia or encephalitis. Motor nerve infection with accompanying paralysis is even less commonly seen.
Diagnosis of varicella and herpes zoster can almost always be made on the basis of history and physical examination. However, it should be noted that herpes simplex infection can sometimes cause a dermatomal vesicular eruption. In fact, about 10% of zosteriform eruptions of the groin and legs appear to be due to HSV infection. Laboratory confirmation is possible with Tzanck smears and viral cultures .
Course and Prognosis
Varicella (chickenpox) infections resolve spontaneously within 7-14 days. Contagion is unlikely after the first week. Healing generally takes place without scarring, but a few small pits may be left at the site of secondarily infected vesicles. after resolution of varicella, inactive viral DNA remains indefinitely in a latent form within the sensory ganglia. Subsequent reactivation of the virus results in the appearance of herpes zoster. Reinfection from an external source is believed by some to also cause the appearance of zoster, but this must be a very rare event.
The lesions of herpes zoster resolve spontaneously in 10-14 days in children but may remain active for 14-21 days in adults. Scarring following resolution of zoster rarely occurs in children but is occasionally found in adults. Neuralgia neither precedes nor follows zoster in children. Pain before, during, and after infection in older adults can, however, be extraordinarily severe.
Most patients will experience only a single episode of zoster, but approximately 5% of patients will develop one or more recurrences.
The varicella-zoster virus, Herpesvirus varicellae, is a DNA virus of the herpesvirus group. Initial exposure to this virus occurs via droplet spread and results in a viremia with subsequent skin and mucous membrane infection. Viral replication takes place in the nuclei of epithelial cells and continues until the process is halted by development of cell-mediated immunologic response. The antibody formation that occurs seems to be important in preventing internal, systemic dissemination of the disease but apparently plays little or no role in the control of skin lesions. Interferon and other T-cell-mediated responses, on the other hand, are responsible for controlling the severity and spread of the infection within the skin. When the lesions of varicella heal, viral DNA remains in the sensory ganglia indefinitely in an inactive, latent phase.
The virus may be reactivated under a variety of circumstances. Reactivation occurs in the form of zoster. The trigger that sets off reactivation is not known, although depression of cell-mediated immune responsiveness and the occurrence of trauma to a latently infected ganglia or nerve root may play some role. Nerve destruction is greater in zoster than in herpes simplex, and this is presumably the reason for the clinical problem of preherpetic and postherpetic neuralgia.
Acyclovir has recently been approved for the treatment of zoster, and several studies have demonstrated that varicella can be effectively treated also. Certainly, immunosuppressed patients with either zoster or varicella should be treated with acyclovir, but the desirability of treatment in normal, healthy individuals is currently controversial. The treatment of varicella in children does not interfere with the development of a standard antibody response. For this reason, treated children are unlikely to be at greater than normal risk for the development of varicella-zoster complications later in life. It is also apparent that even very early use of acyclovir in zoster has little or no effect on the likelihood that postherpetic neuralgia will occur. The dose of acyclovir for zoster is 800 mg (an 800-mg capsule is now available) 5 times/day for 7-10 days. Immunosuppressed patients may require intravenous therapy in order to obtain and maintain sufficiently high blood levels of the drug.
On a day-to-day basis, most treatment for varicella and zoster is, simply, symptomatic. The itching of chickenpox can be treated will either topical antipruritic agents or with the administration of antihistamines . Soaks and systemically administered analgesics may be necessary to alleviate the discomfort of herpes zoster occurring in older adults. Postherpetic neuralgia is extraordinarily difficult to treat. Intracutaneously injected triamcinolone, oral administration of tricyclic antidepressants, transcutaneous electrical stimulation of nerves, and surgical sectioning of affected nerves are possible approaches for those unrelieved by analgesics.