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Chapter 22: Varicella; Epidemiology and Prevention of Vaccine

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Chapter 22: Varicella; Epidemiology and Prevention of Vaccine Varicella Adriana Lopez, MHS; Theresa Harrington, MD, MPH&TM; and Mona Marin, MD Varicella is an acute infectious disease caused by varicella- zoster virus (VZV). Primary varicella infection (chickenpox) Varicella was not reliably distinguished from smallpox until the end of ● Acute infectious disease caused the 19th century. In 1875, Rudolf Steiner demonstrated that by varicella-zoster virus (VZV) chickenpox was caused by an infectious agent by inoculating ● Distinguished from smallpox at volunteers with the vesicular fluid from a patient with acute the end of the 19th century varicella. In 1954, Thomas Weller used cell culture to isolate VZV from vesicular fluid of patients with varicella or zoster. A ● Live, attenuated varicella vaccine developed in 1970s live, attenuated varicella vaccine was developed in Japan in the 1970s. The vaccine virus was developed from virus isolated ● Varicella and MMRV vaccines by Michiaki Takahashi from vesicular fluid from an otherwise licensed for use in the U.S. in healthy child with varicella disease. Varicella vaccine was 1995 and 2005, respectively licensed for general use in Japan and Korea in 1988, and in the United States in 1995 for persons age 12 months or older. In 2005, a combination measles, mumps, rubella, and varicella (MMRV) vaccine was licensed in the United States for persons Varicella-Zoster Virus (VZV) age 12 months through 12 years. ● Herpesvirus (DNA) ● Primary infection results in varicella (chickenpox) Varicella-Zoster Virus ● Reactivation of latent infection VZV is a DNA virus and is a member of the herpesvirus results in herpes zoster group. Like other herpesviruses, VZV persists in the body as a (shingles) latent infection after the primary (first) infection; VZV persists ● Short survival in environment in sensory nerve ganglia. Primary infection with VZV results in varicella. Latent infection can reactivate resulting in herpes zoster (shingles). The virus has a short survival time in the environment. Varicella Pathogenesis ● Enters through respiratory tract Pathogenesis and conjunctiva ● Replication in nasopharynx and VZV enters the host through the respiratory tract and regional lymph nodes conjunctiva. It replicates at the site of entry in the nasopharynx and in regional lymph nodes. A primary viremia occurs 4 to 6 ● Primary viremia 4 to 6 days days after infection and disseminates the virus to other organs, after infection such as the liver, spleen, and sensory ganglia. Further replication ● Multiple organs infected during occurs in the viscera, followed by a secondary viremia, with viral viremia 22 infection of the skin. Virus can be cultured from mononuclear ● Secondary viremia with viral cells of an infected person from 5 days before to 1 to 2 days skin infection after replication after the appearance of the rash. Clinical Features Varicella Clinical Features The incubation period is 14 to 16 days after exposure, with ● Incubation period 14 to 16 days a range of 10 to 21 days. The incubation period may be (range, 10 to 21 days) prolonged (e.g., up to 28 days or more) in those who have ● Prolonged incubation period received postexposure prophylaxis with varicella specific if received postexposure immune globulin. prophylaxis with varicella specific immune globulin 329 Varicella Primary Infection (Varicella) Primary Infection (Varicella) A mild prodrome may precede the onset of a rash. Adults may ● Rash often first sign of disease have 1 to 2 days of fever and malaise prior to rash onset, but in in children; adults may have 1 children the rash is often the first sign of disease. to 2 days of fever and malaise before rash In individuals who have not received varicella vaccine, the ● In unvaccinated individuals, rash is generalized and pruritic and progresses rapidly (within generalized and pruritic rash 24 hours) from macules to papules to vesicular lesions before progresses rapidly crusting. The rash usually appears first on the scalp, face ● Clinical course in healthy or trunk, and then spreads to the extremities; the highest children is mild; adults may concentration of lesions is on the trunk. Lesions also can occur have more severe disease on mucous membranes of the oropharynx, respiratory tract, vagina, conjunctiva, and the cornea. Lesions are usually 1 to ● Recovery usually results in 4 mm in diameter. The vesicles are superficial and delicate lifetime immunity 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 all stages of development at the same time. For example, macular lesions may be observed in the same area of skin as mature vesicles. Healthy children usually have 250 to 500 lesions in 2 to 4 successive crops. The clinical course in healthy children is generally mild, fever (up to 102°F) and other systemic symptoms (e.g., malaise, headache) usually resolve within 2 to 4 days after onset of the rash. Adults may have more severe disease and have a higher incidence of complications. Immunocompromised children may develop a severe progressive form of varicella characterized by high fever, extensive vesicular eruption, and high complication rates. Persons infected with human immunodeficiency virus (HIV) are also at risk for severe, prolonged illness. Recovery from primary varicella infection usually results in lifetime immunity. In otherwise healthy persons, a second occurrence of varicella is uncommon; it is more common in immunocompromised persons. As with other viral diseases, re-exposure to natural (wild) varicella may lead to reinfection that boosts antibody titers without causing clinical illness or 22 detectable viremia. Breakthrough varicella is defined as varicella due to infection with wild-type VZV occurring more than 42 days after varicella vaccination; breakthrough infection can occur after 1 or 2 doses of vaccine. With decreasing incidence of varicella overall and increasing varicella vaccination coverage, more than half of varicella cases reported during the mature phase of the vaccination program are breakthrough varicella cases. Breakthrough varicella is less severe than varicella in unvaccinated persons, 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 330 Varicella typically shorter in duration and has a lower incidence of fever than in unvaccinated persons. However, about 25% to 30% of breakthrough varicella cases in vaccinees who received one dose have clinical features more similar to those in unvaccinated children, and complications with visceral dissemination, hospitalizations, or death, although uncommon, have been reported. Complications Varicella Complications ● Bacterial infection of skin Acute varicella is generally mild and self-limited, but it may be lesions associated with complications. Secondary bacterial infections of skin lesions with Staphylococcus or Streptococcus (primarily ● Pneumonia invasive group A) are the most common cause of hospitalization ● Central nervous system and outpatient medical visits and can lead to death. Pneumonia manifestations following varicella is usually viral but may be bacterial. Primary ● Reye syndrome (rare) viral pneumonia is uncommon among immunocompetent children but is the most common complication in adults. Secondary bacterial pneumonia is more common in children younger than age 1 year. Central nervous system manifestations of varicella range from aseptic meningitis to encephalitis. Encephalitis is an infrequent complication of varicella (1 per 50,000 cases of varicella in unvaccinated children) and may lead to seizures and coma. Diffuse cerebral involvement is more common in adults than in children. Involvement of the cerebellum, with resulting cerebellar ataxia, is the most common central nervous system manifestation (1 per 4,000 cases of varicella in unvaccinated children) and generally has a good outcome. Reye syndrome may follow varicella, although this outcome has become very rare with the recommendation to not use aspirin or other salicylates to reduce fever in children with varicella. Rare complications of varicella include aseptic meningitis, transverse myelitis, Guillain-Barré syndrome, thrombocytopenia, hemorrhagic varicella, purpura fulminans, glomerulonephritis, myocarditis, arthritis, orchitis, uveitis, iritis, and hepatitis. The risk of complications from varicella varies with age. Complications are infrequent among healthy children. 22 They occur much more frequently in persons older than age 15 years and infants younger than age 1 year. In the prevaccine era, approximately 10,500 persons with varicella required hospitalization each year. Hospitalization rates were approximately 1 to 2 per 1,000 cases among healthy children and 14 per 1,000 cases among adults. The fatality rate for varicella was approximately 1 per 100,000 cases among children age 1 through 14 years, 6 per 100,000 cases among persons age 15 through 19 years, and 21 per 100,000 cases among adults. Most deaths occur in immunocompetent children and adults. Since 1995, when the varicella vaccination program was implemented, hospitalizations and deaths from varicella have declined in the United States 93% and 94%, respectively. 331 Varicella Immunocompromised persons have a high risk of disseminated disease (up to 36% in one report). These persons may have multiple organ system involvement, and the disease may become
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