Varicella Zoster Virus : Clinical Features, Complications, Laboratory Diagnosis and Medical Management
VZV is a DNA virus and is a member of the herpesvirus group. Like other herpesviruses, VZV has the capacity to persist in the body after the primary (first) infection as a latent infection. VZV persists in sensory nerve ganglia. Primary infection with VZV results in chickenpox. Herpes zoster (shingles) is the result of reactivation of latent VZV infection. The virus is believed to have a short survival time in the environment.
Pathogenesis
VZV enters through the respiratory tract and conjunctiva. The virus is believed to replicate at the site of entry in the nasopharynx and in regional lymph nodes. A primary viremia occurs 4 to 6 days after infection and disseminates the virus to other organs, such as the liver, spleen, and sensory ganglia. Further replication occurs in the viscera, followed by a secondary viremia, with viral infection of the skin. Virus can be cultured from mononuclear cells of an infected person from 5 days before to 1 or 2 days after the appearance of the rash.
Clinical Features
The incubation period is 14 to 16 days after exposure, with a range of 10 to 21 days. The incubation period may be prolonged in immunocompromised patients and those who have received postexposure treatment with a varicella antibody–containing product.
Primary Infection (Chickenpox)
A mild prodrome may precede the onset of a rash. Adults may have 1 to 2 days of fever and malaise prior to rash onset, but in children the rash is often the first sign of disease.
In individuals who have not been vaccinated with varicella vaccine, the rash is generalized and pruritic and progresses rapidly from macules to papules to vesicular lesions before crusting. The rash usually appears first on the head, then on the trunk, and then the extremities; the highest concentration of lesions is on the trunk. Lesions also can occur on mucous membranes of the oropharynx, respiratory tract, vagina, conjunctiva, and the cornea. Lesions are usually 1 to 4 mm in diameter. The vesicles are superficial and delicate and contain clear fluid on an erythematous base. Vesicles may rupture or become purulent before they dry and crust. Successive crops appear over several days, with lesions present in several stages of development. For example, macular lesions may be observed in the same area of skin as mature vesicles. Healthy children usually have 200 to 500 lesions in 2 to 4 successive crops.
Breakthrough varicella is defined as a case of varicella due to infection with wild-type VZV occurring more than 42 days after varicella vaccination. With decreasing incidence of varicella overall and increasing varicella vaccination coverage, more than half of varicella cases reported in the varicella active surveillance sites in 2010 were breakthrough varicella. In clinical trials, breakthrough varicella was substantially less severe with the median number of skin lesions commonly less than 50; vesicular lesions are less common and the lesions are commonly papules that do not progress to vesicles. Varicella in vaccinated persons is typically shorter in duration and has a lower incidence of fever than in unvaccinated persons. Breakthrough varicella has been reported in both one- and two-dose vaccine recipients.
The clinical course in healthy children is generally mild, with malaise, pruritus (itching), and temperature up to 102°F for 2 to 3 days. Adults may have more severe disease and have a higher incidence of complications. Respiratory and gastrointestinal symptoms are absent. Children with lymphoma and leukemia may develop a severe progressive form of varicella characterized by high fever, extensive vesicular eruption, and high complication rates. Children infected with human immunodeficiency virus (HIV) also may have severe, prolonged illness.
Recovery from primary varicella infection usually results in lifetime immunity. In otherwise healthy persons, a second occurrence of chickenpox is not common, but it can happen, particularly in immunocompromised persons. As with other viral diseases, reexposure to natural (wild) varicella may lead to reinfection that boosts antibody titers without causing clinical illness or detectable viremia.
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Recurrent Disease (Herpes Zoster)
Herpes zoster, or shingles, occurs when latent VZV reactivates and causes recurrent disease. The immunologic mechanism that controls latency of VZV is not well understood. However, factors associated with recurrent disease include aging, immunosuppression, intrauterine exposure to VZV, and having had varicella at a young age (younger than 18 months). In immunocompromised persons, zoster may disseminate, causing generalized skin lesions and central nervous system, pulmonary, and hepatic involvement.
The vesicular eruption of zoster generally occurs unilaterally in the distribution of a sensory nerve. Most often, this involves the trunk or the fifth cranial nerve. Two to four days prior to the eruption, there may be pain and paresthesia in the involved area. There are few systemic symptoms.
Complications
Varicella
Acute varicella is generally mild and self-limited, but it may be associated with complications. Secondary bacterial infections of skin lesions with Staphylococcus or Streptococcus are the most common cause of hospitalization and outpatient medical visits. Secondary infection with invasive group A streptococci may cause serious illness and lead to hospitalization or death. Pneumonia following varicella is usually viral but may be bacterial. Secondary bacterial pneumonia is more common in children younger than 1 year of age.
Central nervous system manifestations of varicella range from aseptic meningitis to encephalitis. Involvement of the cerebellum, with resulting cerebellar ataxia, is the most common central nervous system manifestation and generally has a good outcome. Encephalitis is an infrequent complication of varicella (estimated 1.8 per 10,000 cases) and may lead to seizures and coma. Diffuse cerebral involvement is more common in adults than in children. Reye syndrome is an unusual complication of varicella and influenza and occurs almost exclusively in children who take aspirin during the acute illness. The etiology of Reye syndrome is unknown. There has been a dramatic decrease in the incidence of Reye syndrome, presumably related to decreased use of aspirin by children.
Rare complications of varicella include aseptic meningitis, transverse myelitis, Guillain-Barré syndrome, thrombocyte penia, hemorrhagic varicella, purpura fulminans, glomerulonephritis, myocarditis, arthritis, orchitis, uveitis, iritis, and hepatitis.
In the prevaccine era, approximately 11,000 persons with varicella required hospitalization each year. Hospitalization rates were approximately 2 to 3 per 1,000 cases among healthy children and 8 per 1,000 cases among adults. Death occurred in approximately 1 in 60,000 cases. From 1990 through 1996, an average of 103 deaths from varicella were reported each year. Most deaths occur in immunocompetent children and adults. Since 1996, hospitalizations and deaths from varicella have declined more than 70% and 88% respectively.
Laboratory Diagnosis
Laboratory testing, whenever possible, or epidemiological linkage to a typical case or laboratory-confirmed case should be sought to confirm – or rule out – varicella.
Varicella zoster virus polymerase chain reaction (PCR) is the method of choice for diagnosis of varicella. VZV may also be isolated in tissue culture, although this is less sensitive and requires several days to obtain a result. The most frequent source of VZV isolation is vesicular fluid. Laboratory techniques allow differentiation of wild-type and vaccine strains of VZV.
Rapid varicella virus identification techniques are indicated for a case with severe or unusual disease to initiate specific antiviral therapy. VZV PCR is the method of choice for rapid clinical diagnosis.
Real-time PCR methods are widely available and are the most sensitive and specific method of the available tests. Results are available within several hours. If real-time PCR is unavailable, the direct fluorescent antibody (DFA) method can be used, although it is less sensitive than PCR and requires more meticulous specimen collection and handling.
Specimens are best collected by unroofing a vesicle, preferably a fresh fluid-filled vesicle, and then rubbing the base of a skin lesion with a polyester swab. Crusts from lesions are also excellent specimens for PCR. Because viral proteins persist after cessation of viral replication, PCR and DFA may be positive when viral cultures are negative. Additional information concerning virus isolation and strain differentiation can be found at http://www.cdc.gov/ chickenpox/lab-testing/index.html. A variety of serologic tests for varicella antibody are available commercially including a latex agglutination assay (LA) and a number of enzyme-linked immunosorbent assays (ELISA) that can be used to assess disease-induced immunity. Currently available ELISA methods are not sufficiently sensitive to reliably detect seroconversion to vaccine, but are robust enough to screen persons for VZV susceptibility.
ELISA is sensitive and specific, simple to perform, and widely available commercially. A commercially available LA is sensitive, simple, and rapid to perform. LA is somewhat more sensitive than commercial ELISAs, although it can result in false-positive results, leading to failure to identify persons without evidence of varicella immunity. This latter concern can be minimized by performing LA as a dilution series. Either of these tests would be useful for screening for varicella immunity.
Epidemiology
Occurrence
Varicella and herpes zoster occur worldwide. Some data suggest that in tropical areas varicella infection occurs more commonly among adults than children. The reason(s) for this difference in age distribution are not known with certainty.
Reservoir
Varicella is a human disease. No animal or insect source or vector is known to exist.
Transmission
Infection with VZV occurs through the respiratory tract. The most common mode of transmission of VZV is believed to be person to person from infected respiratory tract secretions. Transmission may also occur by respiratory contact with airborne droplets or by direct contact or inhalation of aerosols from vesicular fluid of skin lesions of acute varicella or zoster.
Temporal Pattern
In temperate areas, varicella has a distinct seasonal fluctuation, with the highest incidence occurring in winter and early spring. In the United States, incidence is highest between March and May and lowest between September and November. Less seasonality is reported in tropical areas. Herpes zoster has no seasonal variation and occurs throughout the year.
Communicability
The period of communicability extends from 1 to 2 days before the onset of rash until lesions have formed crusts. Vaccinated persons with varicella may develop lesions that do not crust (macules and papules only). Isolation guidance for these persons is to exclude until no new lesions appear within a 24-hour period. Immunocompromised patients with varicella are probably contagious during the entire period new lesions are appearing. The virus has not been isolated from crusted lesions.
Varicella is highly contagious. It is less contagious than measles, but more so than mumps and rubella. Secondary attack rates among susceptible household contacts of persons with varicella are as high as 90% (that is, 9 of 10 susceptible household contacts of persons with varicella will become infected).
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