Like the herpes simplex viruses, varicella-zoster virus (VZV) is an enveloped, dou-ble-standed, DNA virus of the herpesvirus family. VZV causes two distinct clinical syndromes. Primary exposure to VZV results in varicella (chickenpox), a usually benign, highly contagious infection of children. Reactivation of latent VZV results in herpes zoster (shingles), an illness most commonly seen in adults over the age of 45 yr.
VZV is spread from person to person by direct contact, as an aerosol from skin lesions, or in respiratory tract secretions. Virus enters through the mucosa of the upper respiratory tract or the conjunctiva. Transmission to susceptible hosts occurs from 2 d before appearance of the rash until the lesions crust. Of the 4 million cases of varicella per year, 33% occur in preschool children (1-4 yr of age) and 44% occur in school-age children (5-9 yr of age). The secondary attack rate is 90% among susceptible individuals in the same household. These secondary varicella cases within the family are usually more severe than the primary cases, likely because of the greater intensity of exposure. Only 5% of varicella infections are subclinical (i.e., without rash).
A history of varicella infection is a reliable marker for immunity, with a positive history 97-99% predictive of serologic immunity. Seventy-three to ninety-three percent of individuals with a negative history of varicella are also seropositive.
Nosocomial transmission of varicella is a serious and expensive healthcare problem. After exposure to varicella, susceptible employees can serve as vectors with transmission to patients. Varicella has been reported in hospital employees without direct contact with patients having active lesions but exposed to air from the patient's room (38).
Herpes zoster is more common in adults and the immunocompromised, 75% of cases occurring in those over the age of 45 yr. Immunocompetent children, adolescents, and young adults can develop herpes zoster, so a single episode in these individuals should not suggest underlying immunodeficiency. Herpes zoster may result in varicella in a susceptible host but exposure to someone with varicella does not cause herpes zoster.
Varicella in children is a self-limited disease of 4-5 d duration consisting of fever, malaise, and a generalized, pruritic, vesicular rash that starts on the face and scalp and then spreads to the trunk and later to the extremities. The average incubation period is 14-16 d but varies between 10 and 21 d. Successive crops of vesicular lesions appear over 2-4 d. If the vesicles do not rupture, they become purulent and then crust over. Complications from varicella include bacterial superinfection, especially P-hemolytic Group A streptococci, pneumonia, meningoencephalitis, cerebellar ataxia, and hepatitis. Reyes syndrome associated with aspirin use during VZV infection is now uncommon (39). Adolescent and adults are more likely to have severe disease and are at greater risk of varicella pneumonia and death.
Although perinatal infection is uncommon because most mothers are immune, intrauterine VZV infection may result in fetal varicella syndrome (low birth weight, cutaneous scarring, limb hypoplasia, microencephaly, cortical atrophy, chorioretinitis) if the infection occurs during the first half of the pregnancy. The incidence of fetal varicella syndrome with VZV infection in wk 1-12 is 0.4% and in wk 13-20, 2% (40,41). Varicella infection of the mother 5 d before to 2 d after delivery may result in severe varicella in 17-30% of newborns with a 31% risk of death if untreated. Passive immunization with varicella immune globulin (VZIG) is effective in reducing mortality.
After primary infection, latent VZV persists within the sensory dorsal root ganglia. Herpes zoster presents as a unilateral vesicular rash distributed over one to three der-matomal segments. The rash usually crusts within 10 d and completely heals within a month. When the trigeminal nerve is involved, especially the ophthalmic branch, care must be taken because the eye may become involved and lead to dendritic keratitis, anterior uveitis, iridocyclitis, and panophthalmitis. The most common complication of herpes zoster is pain. Postherpetic neuralgia more often affects people over 50 yr of age and can be severe, lasting for weeks to months. In an immunocompromised host, reactivation of VZV may result in a disseminated infection with a generalized eruption and CNS, pulmonary, hepatic, and pancreatic involvement.
As the rash of varicella is so characteristic, the diagnosis is not difficult to make. The unilateral, dermatomal eruption of herpes zoster is also easy to recognize, although herpes simplex infection can mimic herpes zoster. Patients with herpes zoster may present with pain prior to the appearance of rash, making the diagnosis more difficult.
Several drugs are now available for the treatment of VZV infections. Acyclovir, when given within 24 h of the appearance of the varicella rash, decreases the number of days new lesions appear, duration of fever, and the severity of cutaneous and systemic signs and symptoms. Acyclovir does not, however, decrease transmission or reduce absence from school and is not recommended for the routine treatment of healthy children (42). Because varicella is a more severe disease in adolescents, adults, and immunocompromised children, treatment with acyclovir is recommended (43,44). Prophylaxis with acyclovir can prevent secondary cases among close contacts. In a placebo-controlled trial, 16% of ACV-treated patients developed varicella compared with 100% of controls (45). Treatment must begin early because in the immunocompetent host, viral replication, which acyclovir inhibits, is no longer detectable 72 h after the rash appears.
Because therapeutic levels after oral administration are unreliable, intravenous acy-clovir is recommended for severe VZV infections. Adequate hydration must be maintained during intravenous acyclovir administration to prevent ACV precipitation in the renal tubules resulting in acute renal failure.
Acyclovir is also useful in the treatment of herpes zoster. If given within 72 h of the appearance of rash, it will accelerate the rate of healing, reduce severity of disease, and diminish the incidence and severity of postherpetic neuralgia. Acyclovir is especially useful in treating people over the age of 50 who have a greater incidence of postherpetic neuralgia (46). Although steroids do not protect against postherpetic neuralgia, adding steroids to acyclovir helps decrease the duration of acute pain and the return to daily living (47).
Valacyclovir, a prodrug of acyclovir with better absorption and higher serum levels, can also be used (48). Famciclovir, a prodrug of penciclovir, is effective in treating varicella and herpes zoster (49). The advantages of valacyclovir and famciclovir is convenience. Both are dosed three times a day instead of five times per day as reqvired with acyclovir, leading to better patient adherence. Famciclovir and valacyclovir may decrease the duration of postherpetic neuralgia but not its incidence in elderly patients (see Table 7 for dosing recommendations).
Resistance to these three drugs is uncommon, but when resistance is present foscar-net, which acts by directly inhibiting the viral DNA polymerase, may be useful. The major toxicities of foscarnet are renal dysfunction and electrolyte imbalance.
VZIG provides the most benefit when administered as soon as possible, but if given within 96 h of exposure to someone with VZV disease, it may prevent or ameliorate varicella infection (50). Protection lasts for 3 wk with a single dose of VZIG.
A live attenuated VZV vaccine has been developed and proven effective in preventing VZV infection. Unlike wild-type VZV, the vaccine strain causes a subclinical infection, leading to immunity that is 70-90% effective in preventing the symptoms of varicella. Transmission of the vaccine strain to others is rare but it is advisable for the vaccinee to avoid close contact with those at risk for severe complications of varicella. With the limited follow-up available, herpes zoster rates appear lower in vaccinees than those infected with wild-type VZV. The vaccine is also effective in preventing or modifying varicella infection if given within 3 d of exposure to VZV.
Treatment of Varicella-Zoster Virus
Treatment of Varicella-Zoster Virus
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