Monday, February 25, 2013

CLINICAL MANIFESTATIONS OF HERPES ZOSTER



VZV reactivation is rare in childhood. When it occurs, it causes vesicular lesions clustered unilaterally in the dermatomal distribution of one or more adjacent sensory nerves, which are preceded or accompanied by localized pain, hyperesthesias, pruritus, and low-grade fever.

The rash is mild, with new lesions appearing for a few days, symptoms of acute neuritis are minimal, and complete resolution usually occurs within 1–2 wk. Immunocompromised children have more severe dermatomal disease and may experience viremia, causing pneumonia, hepatitis, encephalitis, and disseminated intravascular coagulopathy. Severely immunocompromised children, particularly those with HIV infection, may have unusual, chronic, or relapsing cutaneous disease, retinitis, or central nervous system disease without rash. Transverse myelitis with transient paralysis is a rare complication of herpes zoster. In contrast to adults, postherpetic neuralgia is very unusual in children.
  

 
The rash in herpes Zoster

LABORATORY FINDINGS AND DIAGNOSIS.

Laboratory evaluation is not necessary for appropriate management of healthy children with varicella or herpes zoster. Abnormal laboratory values are common during varicella. Leukopenia is typical during the first 72 hr; it is followed by a relative and absolute lymphocytosis. Liver function tests are also often moderately elevated. Patients with neurologic complications of varicella or uncomplicated herpes zoster have a mild lymphocytic pleocytosis and a slight to moderate increase in protein; the cerebrospinal fluid glucose is usually normal. Rapid laboratory diagnosis of VZV is often important in high-risk patients and can be accomplished by direct immunohistochemical staining of cells from cutaneous lesions. Multinucleated giant cells can be detected with nonspecific stains, but false-negative results are common, and these methods do not differentiate VZV and HSV infections. The definitive diagnosis of VZV infection requires the recovery of infectious virus using tissue culture. VZV immunoglobulin G (IgG) antibodies can be detected by several methods, but serologic diagnosis is retrospective; testing for VZV IgM antibodies is not useful for clinical diagnosis because commercially available methods are unreliable. VZV IgG antibody tests are valuable to determine the immune status of individuals whose clinical history of varicella is unknown or equivocal.

TREATMENT.

Acyclovir—9-[(2-hydroxyethoxy) methyl] guanine—is the drug of choice for varicella and herpes zoster when specific therapy is indicated. Any patient who has signs of disseminated VZV including pneumonia, hepatitis, thrombocytopenia, or encephalitis should receive immediate treatment with intravenous acyclovir. Acyclovir therapy given within 72 hr prevents progressive varicella and visceral dissemination in high-risk patients; the dosage is 500 mg/m2 every 8 hr, administered intravenously for 7 days or until no new lesions have appeared for 48 hr. Delaying antiviral treatment until prolonged new lesion formation is evident is not an option because visceral dissemination occurs during the same time period. Recent large, placebo-controlled clinical studies have shown that oral acyclovir diminishes the clinical symptoms of varicella in otherwise healthy children, adolescents, and adults when it is administered within 24 hr after the appearance of the initial cutaneous lesions. Drug efficacy was established for all groups, but the clinical benefit may be considered more significant in older children and in secondary household cases. Acyclovir therapy does not interfere with the induction of VZV immunity.

Acyclovir is also effective for treatment of herpes zoster in healthy and immunocompromised patients. Patients at high risk for disseminated disease should receive 500 mg/m2 or 10 mg/kg every 8 hr intravenously. Onset of VZV reactivation reduces the duration of new lesion formation to only about 3 days. Oral acyclovir is an option for immunocompromised patients who are considered at low risk for visceral dissemination. Antiviral drug resistance is rare but has occurred in children with HIV infection; foscarnet is the only drug now available for the treatment of acyclovir-resistant VZV infections.

PREVENTION.

VZV transmission is difficult to prevent because the infection is contagious for 24–48 hr before the rash appears. Infection control practices, including caring for infected patients in isolation rooms with filtered air systems, are essential in hospitals that treat immunocompromised children. Susceptible health care workers who have had a close exposure to varicella should not care for high-risk patients during the incubation period.

Varicella-zoster immune globulin (VZIG) prophylaxis is recommended for immunocompromised children, pregnant women, and newborn infants exposed to maternal varicella. VZIG is distributed by the American Red Cross Blood Services; the dosage is one vial per 10 kg intramuscularly given within 96 hr or, if possible, within 48 hr after exposure. Adults should be tested for VZV IgG antibodies before VZIG administration because many adults with no clinical history of varicella are immune. Because VZIG prophylaxis does not eliminate the possibility of progressive disease, patients should be monitored and treated with acyclovir if necessary. Immunocompromised patients who have received high-dose intravenous immune globulin (100–400 mg/kg) for other indications within 2–3 wk before the exposure can be expected to have serum antibodies to VZV. Close contact between a susceptible high-risk patient and a patient with herpes zoster is also an indication for VZIG prophylaxis. Passive antibody prophylaxis does not reduce the risk of herpes zoster or alter the clinical course of varicella or herpes zoster when given after the onset of symptoms.

Acyclovir should not be given as prophylaxis against varicella. Acyclovir prophylaxis for herpes zoster is not essential because the prompt initiation of acyclovir for the treatment of recurrent VZV infections is very effective in reducing morbidity and mortality among immunocompromised patients. Prolonged low-dose administration of acyclovir should be avoided to minimize the emergence of drug-resistant VZV.

The live, attenuated varicella vaccine, made from the Oka strain, is the first human herpesvirus vaccine. The live, attenuated varicella vaccine (Oka-Merck strain) has been given to more than 8,500 healthy children and adults in clinical trials in the United States. The vaccine induced seroconversion rates of more than 95%, with complete protection against disease in 85–95% of exposures. Persistence of humoral and cell-mediated immunity has been documented in 94–100% of vaccine recipients monitored for 1–6 yr. The Oka-Merck varicella vaccine can be given to children with acute leukemia in remission, with careful attention to the status of their underlying disease and immunosuppressive therapy regimens.


1 comment:

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