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Varicella

Varicella, or chickenpox, is a highly contagious viral infection that, during epidemics, affects the majority of urban children before puberty. The incidence peaks sharply in March, April, and May in temperate climates. Transmission occurs via airborne droplets or vesicular fluid. Patients are contagious from 2 days before onset of the rash until all lesions have crusted. The systemic symptoms, extent of eruption, and complications are greater in adults; thus some parents intentionally expose their young children. Patients with defective, cell-mediated immunity or those using immunosuppressive drugs, especially systemic corticosteroids, have a prolonged course with more extensive eruptions and a greater incidence of complications. An attack of chickenpox usually confers lifelong immunity. After it has produced chickenpox, varicella-zoster virus (VZV) becomes latent in ganglia along the entire neuraxis. Unlike HSV, however, VZV cannot be cultured from human ganglia. Varicella vaccine is effective and approved for use in children and adults.

CLINICAL COURSE.

The incubation period averages 14 days, with a range of 9 to 21 days; in the immunosuppressed host, the incubation period can be shorter. The prodromal symptoms in children are absent or consist of low fever, headache, and malaise, which appear directly before or with the onset of the eruption. Symptoms are more severe in adults. Fever, chills, malaise, and backache occur 2 to 3 days before the eruption.

ERUPTIVE PHASE.

Lesions of different stages are present at the same time in any given body area. New lesion formation ceases by day 4 and most crusting occurs by day 6; the process lasts longer in the immunosuppressed patient. The lesion starts as a 2- to 4-mm red papule that develops an irregular outline (rose petal) as a thin-walled clear vesicle appears on the surface (dewdrop) (Figure 12-43). This lesion, "dewdrop on a rose petal," is highly characteristic. The vesicle becomes umbilicated and cloudy and breaks in 8 to 12 hours to form a crust as the red base disappears. Fresh crops of additional lesions undergoing the same process occur in all areas at irregular intervals during the following 3 to 5 days, giving the characteristic picture of intermingled papules, vesicles, pustules, and crusts (see Figures 12-44 and 45). Moderate to intense pruritus is usually present during the vesicular stage. The degree of temperature elevation parallels the extent and severity of the eruption and varies from 101° to 105° F. The temperature returns to normal when the vesicles have disappeared. Crusts fall off in 7 days (with a range of 5 to 20 days) and heal without scarring. Secondary infection or excoriation extends the process into the dermis, producing a craterlike, pockmark scar. Vesicles often form in the oral cavity and vagina and rupture quickly to form multiple, aphthaelike ulcers.

The rash begins on the trunk (centripetal distribution) (Figure 12-44) and spreads to the face (Figure 12-45) and extremities (centrifugal spread). The extent of involvement varies considerably. Some children have so few lesions that the disease goes unnoticed. Older children and adults have a more extensive eruption involving all areas, sometimes with lesions too numerous to count.

DIFFERENTIAL DIAGNOSIS.

The differential diagnosis includes drug eruptions, smallpox, other viral exanthemas, scabies, erythema multiforme, and insect bites.

COMPLICATIONS

Skin infection.

The most common complication in children is bacterial skin infection. Secondary infection should be suspected when the vesiculopustules develop large, moist, denuded areas, and particularly when the lesions become painful.

Neurologic complications.

The most common extracutaneous complication is central nervous system involvement. Encephalitis and Reye's syndrome are complications of chickenpox. ³⁸ There are two forms of encephalitis. The cerebellar form seen in children is self-limited and complete recovery occurs. There is ataxia with nystagmus, headache, nausea, vomiting, and nuchal rigidity. Adult patients with encephalitis have altered sensorium, seizures, and focal neurologic signs with a mortality rate of up to 35%. ³⁹ Reye's syndrome is an acute, noninflammatory encephalopathy associated with hepatitis or fatty metamorphosis of the liver; 20% to 30% of Reye's syndrome cases are preceded by varicella. The fatality rate is 20%. Salicylates used during the varicella infection may increase the risk of the development of Reye's syndrome.

Pneumonia.

Varicella pneumonia occurs in 1:400 cases. Pneumonia is rare in normal children, but it is the most common serious complication in normal adults. Viral pneumonia develops 1 to 6 days after onset of the rash. In most cases it is asymptomatic and can be detected only with a chest x-ray examination. Cough, dyspnea, fever, and chest pain can occur. The mortality rate for adult varicella pneumonia is 10% of immunocompetent patients and 30% of immunocompromised patients.

Other.

Hepatitis is the most common complication in immunosuppressed patients. Mild degrees of thrombocytopenia can accompany routine cases.

Chickenpox in the immunocompromised patient

Patients with cancer or patients who are taking immunosuppressive drugs, particularly systemic and intranasal corticosteroids, have extensive eruptions and more complications. The mortality rate for immunosuppressed children or children with leukemia is 7% to 14%. Adults with malignancy and varicella have a mortality rate as high as 50% (Figure 12-46). Hemorrhagic chickenpox, also called malignant chickenpox, is a serious complication, in which the lesions are numerous and often bullous and bleeding occurs in the skin at the base of the lesion. ⁴⁰ The bullae turn dark brown and then black as blood accumulates in the blister fluid. Patients are usually toxic, have high fever and delirium, and may develop convulsions and coma. They frequently bleed from the gastrointestinal tract and mucous membranes. Pneumonia with hemoptysis commonly occurs. The mortality rate was 71% in one series. ⁴¹

Chickenpox and HIV infection

Many children with HIV infection who acquire varicella have an uncomplicated clinical course and have a significant antibody response to VZV. ⁴² Some, however, have chronic, recurrent, or persistent varicella. ^43, ⁴⁴ Varicella in adult HIV-infected patients is a potentially severe infection, but these patients respond well to acyclovir therapy. Immune status to varicella does not correlate with the declining CD4 ⁺ counts and is well preserved, even in patients with fewer than 200 CD4 ⁺ cells/mm ³. ⁴⁵

Chickenpox during pregnancy

Varicella during pregnancy poses a risk for both the mother and the unborn child. In a study of 43 pregnant women, 4 developed symptomatic pneumonia and 1 died of the infection. ⁴⁶ Smoking is a possible risk factor. Pregnant women with pneumonitis, who received high-dose intravenous acyclovir, ranging from 10 to 18 mg/kg every 8 hours, showed rapid improvement. Lower dosages may not be effective. ⁴⁷

Congenital and neonatal chickenpox

Maternal varicella

FIRST TRIMESTER.

Infection with the VZV during pregnancy can produce an embryopathy characterized by limb hypoplasia, chorioretinitis, cortical atrophy, and cutaneous scars (congenital varicella syndrome). ⁴⁶ The risk is greatest when infection occurs during the first 20 weeks of pregnancy. The absolute risk of embryopathy after maternal varicella infection in the first 20 weeks of pregnancy is approximately 2%. ^48, ⁴⁹

SECOND TRIMESTER.

Maternal varicella in the middle months of pregnancy may result in undetected fetal chickenpox. The newborn child who has already had chickenpox is at risk for developing herpes zoster (shingles). This may explain why some infants and children develop herpes zoster without the expected history of chickenpox.

NEAR BIRTH.

The time of onset of maternal lesions correlates directly with the frequency and severity of neonatal disease (Figure 12-47). If the mother has varicella 2 to 3 weeks before delivery, the fetus may be infected in utero and be born with or develop lesions 1 to 4 days after birth. Transplacental maternal antibody protects the infant and the course is usually benign. The risk of infection and complications is greatest when the maternal onset of varicella is from 5 days before to 2 days after delivery. When maternal infection appears more than 5 days before delivery, maternal antibody can develop and transfer via the placenta. Maternal infection that develops more than 2 days after delivery is associated with onset of disease in a newborn approximately 2 weeks later, at which point the immune system is better able to respond to the infection.

There is a high incidence of disseminated varicella in the infant when the mother's eruption appears 1 to 4 days before delivery or the child's eruption appears 5 to 10 days after birth. When the maternal rash appears within 5 days before delivery, approximately one third of infants become infected. After 5 days, transmission occurs in approximately 18%. ⁵⁰ When the rash appears in infants between 5 and 10 days old, the mortality rate may be as high as 20%. ⁵¹ In this situation, the virus is either acquired transplacentally or from contact with maternal lesions during birth; there is insufficient time to receive adequate maternal antibody. The infant is immunologically incapable of controlling the infection and is at great risk of developing a disseminated disease. These infants should be given zoster immune globulin (ZIG), varicella-zoster immune globulin (VZIG), or gamma globulin if ZIG or VZIG is not available.

LABORATORY DIAGNOSIS

Culture.

In questionable cases, virus can be cultured from vesicular fluid. Culture is not easily obtained because VZV is a labile virus that is cultured much less readily than HSV.

Serologic testing.

The main value of serologic testing is the assessment of the immune status of immunocompromised patients, such as children with neoplastic diseases, who are at risk of developing severe disease with VZV infection. There are qualitative and quantitative tests that measure IgG and IgM antibodies. The presence of IgM antibodies or a fourfold or greater rise in paired sera IgG titer indicates recent infection. The presence of IgG indicates past exposure and immunity.

Tzanck smear.

Cytologic smear (Tzanck smear), as described for the diagnosis of herpes simplex (Figure 11-18), is a valuable tool for rapid diagnosis. The test does not differentiate herpes simplex from varicella. Scrape the base of an early lesion and stain with hematoxylin-and-eosin, Giemsa, Wright's, toluidine blue, or Papanicolaou. Multinucleated giant cells and epithelial cells containing eosinophilic intranuclear inclusions are seen.

A chest x-ray examination should be obtained if respiratory symptoms develop. The white blood cell count is variably elevated, but it is necessary to obtain a count only if the disease progresses.

Varicella vaccine

The live attenuated varicella vaccine was approved for use in the United States in 1995 and is recommended for all susceptible persons 12 months of age or older. One dose is given for healthy children 12 to 18 months of age, and two doses, in a 4- to 8-week interval, is given to susceptible persons older than 13 years. The vaccine is highly effective; it prevented chickenpox in 85% of immunized children, with 97% protection against moderately severe and severe disease. A documented history of vaccination is sufficient to predict a level of immunity to VZV that will prevent severe cases of chickenpox in healthy children. ⁵²

Studies show that protection against varicella seems to last at least 6 years. ⁵³ The incidence of zoster in children with leukemia is no greater than that in children who have had natural varicella infection. ⁵⁴ The live attenuated vaccine should not be given to patients with HIV infection or to other immunosuppressed patients.

Treatment

Bland antipruritic lotions (e.g., Sarna Anti-Itch [camphor and menthol over-the-counter]), cool wet compresses, tepid baths, and antipyretics (excluding aspirin because of its association with Reye's syndrome) provide symptomatic relief. Antihistamines (e.g., hydroxyzine) may help control excoriation. Oral antibiotics active against Streptococcus and Staphylococcus are indicated for secondarily infected lesions.

ACYCLOVIR AND VIDARABINE

Children and adolescents.

Oral acyclovir therapy initiated within 24 hours of illness for otherwise healthy children with varicella typically results in a 1-day reduction in fever and an approximately 15% to 30% reduction in the severity of cutaneous and systemic signs and symptoms. Therapy has not been shown to reduce the rate of acute complications, pruritus, spread of infection, or duration of absence from school.

The American Academy of Pediatrics Committee on Infectious Diseases published recommendations for the use of oral acyclovir in otherwise healthy children with varicella. Recommendations are that (1) oral acyclovir therapy is not routinely recommended for the treatment of uncomplicated varicella in otherwise healthy children and that (2) for certain groups at increased risk of severe varicella or its complications, oral acyclovir therapy for varicella should be considered if it can be initiated within the first 24 hours after the onset of rash. These groups include otherwise healthy, nonpregnant individuals 13 years of age or older, ⁵⁵ children older than 12 months with a chronic cutaneous or pulmonary disorder, and those receiving long-term salicylate therapy, although in the latter instance a reduced risk for Reye's syndrome has not been shown to result from oral acyclovir therapy or from milder illness with varicella.

Adults.

Early therapy with oral acyclovir (800 mg 5 times per day for 7 d) decreases the time to cutaneous healing of adult varicella, decreases the duration of fever, and lessens symptoms. Initiation of therapy after the first day of illness is of no value in uncomplicated cases of adult varicella. ⁵⁶

Immunocompromised patients.

Studies show that immunosuppressed patients treated with acyclovir had decreased morbidity from visceral dissemination; there was a modest effect on the cutaneous disease (see Table 12-2). ^57, ⁵⁸ Acyclovir (500 mg/m ² intravenous every 8 hours for 7 to 10 days) is the drug of choice for treatment of varicella in immunocompromised patients.

A continuous infusion of acyclovir may be beneficial for severe, life-threatening VZV infections that are resistant to treatment with the conventional regimen, and perhaps even acyclovir-resistant herpesvirus infections. A continuous infusion of acyclovir at a rate of 2 mg/kg body weight/hr (2250 mg/day) was effective in one report. ⁵⁹

The recommended dose for vidarabine is 10 mg/kg/day intravenously for 5 to 10 days, the risk of neurotoxicity limits its use.

Acyclovir-resistant strains of VZV have been reported in AIDS patients. Foscarnet is a potentially effective with acyclovir-resistant VZV strains.

VARICELLA-ZOSTER IMMUNE GLOBULIN.

VZIG, a more readily available preparation than ZIG, has been used to modify the course of varicella. It is indicated for immunosuppressed patients and certain nonimmunosuppressed patients. VZIG must be administered as early as possible after the presumed exposure but may be effective when given as late as 96 hours after exposure. VZIG is not known to be useful in treating clinical varicella or zoster or in preventing disseminated zoster. The duration of protection is estimated to be 3 weeks. Patients exposed again more than 3 weeks after a dose of VZIG should receive another full dose. VZIG is given intramuscularly. ⁶⁰

GAMMAGLOBULIN.

Intravenous gammaglobulin may be an acceptable substitute if VZIG is not available. ⁶¹

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