varicella -zoster virus

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Varicella -zoster virus. Varicella -zoster virus. Varicella-zoster virus (VZV) causes primary, latent, and recurrentinfections. The primary infection is manifested as varicella ( chickenpox ) and results in establishment of a lifelong latent infection of sensory ganglion neurons. - PowerPoint PPT Presentation

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  • Varicella-zoster virusVaricella-zoster virus (VZV) causes primary, latent, and recurrentinfections.

    The primary infection is manifested as varicella (chickenpox) and results in establishment of a lifelong latent infection of sensory ganglion neurons. Reactivation of the latent infection causes herpes zoster (shingles).

    Although often a mild illness of childhood, chickenpox can cause substantial morbidity and mortality in otherwise healthy children; it increases morbidity and mortality in immunocompetent infants, adolescents,adults, as well as in immunocompromised persons.

    it predisposes to severe group A streptococcus and Staphylococcus aureus infections

    Primary clinical disease can be prevented by immunization with live-attenuated VZV vaccine (varicella vaccine). Herpes zoster vaccine (zoster vaccine), higher potency, is recommended for persons 60 yr of age to boost their immunity; painful postherpetic neuralgia.

  • ETIOLOGYVZV is a neurotropic human herpesvirus with similarities to herpes simplex virus, which is also -herpesvirus. These viruses are enveloped with double-stranded DNA genomes that encodemore than 70 proteins, including proteins that are targets of cellular and humoral immunity.

  • EPIDEMIOLOGYMost children were infected by 15 yr of age, withfewer than 5% of adults remaining susceptible. This pattern of infection at younger ages is characteristic in all countries intemperate climates. In tropical areas, varicella occurs among older persons, with many cases occurring among adults.Varicella is a more serious disease in young infants, adults, and immunocompromised persons, in whom there are higher rates of complications and deaths than in healthy children.Patients with varicella are contagious 24-48 hr before the rash is evident and until vesicles are crusted, usually 3-7 days after onset of rash. Susceptible persons may also acquire varicella after close, direct contact with adults or children who have herpes zoster.predominantly in children in upper elementary school rather than in the preschool years.Herpes zoster is due to the reactivation of latent VZV.Herpes zoster is uncommon to children and very rare in healthy children
  • PATHOGENESIS

    VZV is transmitted in oropharyngeal secretions and in the fluid of skin lesions either by airborne spread or through direct contact. Primary infection (varicella) results from inoculation of the virus onto the mucosa of the upper respiratory tract and tonsillar lymphoid tissue. During the early part of the 10- to 21-day incubation period, virus replicates in the local lymphoid tissue, and then a brief subclinical viremia spreads the virus to the reticuloendothelial system. Widespread cutaneous lesionsoccur during a second viremic phase that lasts 3-7 days. VZV is also transported back to the mucosa of the upper respiratory tract and oropharynx during the late incubation period, permitting spread to susceptible contacts 1-2 days before the appearance of rash. Virus is transported in a retrograde manner through sensory axons to the dorsal root ganglia throughout the spinal cord, where the virus establishes latent infection in the neurons and satellite cells associated with these axons. Subsequent reactivation of latent virus causes herpes zoster, a vesicular rash that usually is dermatomalin distribution. During herpes zoster, necrotic changes may be produced in the associated ganglia. The skin lesions of varicella and herpes zoster have identical histopathology, and infectious VZV is present in both.Suppression of cell-mediated immunity to VZV correlates with an increased risk for VZV reactivation as herpes zoster.

  • CLINICAL MANIFESTATIONVaricella is an acute febrile rash illness that was common in children in the USA before the universal childhood vaccination program. It has variable severity but is usually self limited. It may be associated with severe complications, including staphylococcal and streptococcal superinfection, pneumonia, encephalitis, bleeding disorders, congenital infection, and life-threatening perinatalinfection. Herpes zoster, uncommon in children, causes localized cutaneous symptoms but may disseminate in immunocompromised patients.

  • Varicella

    The illness usually begins 14-16 days after exposure, although the incubation period can range from 10 to 21 days.Prodromal symptoms may be present, particularly in older children and adults. Fever, malaise, anorexia, headache, and occasionally mild abdominal pain may occur 24-48 hours beforethe rash appears. Temperature elevation is usually moderate, usually 100-102F, but may be as high as 106F; fever and other systemic symptoms usually resolve within 2-4 days after the onset of the rash.Varicella lesions often appear first on the scalp, face, or trunk.The distribution of the rash is predominantly central or centripetal, in contrast to that in smallpox, which is more prominent on the face and distal extremities.

  • Ulcerative lesions involving the mucosa of oropharynx and vagina are also common; many children have vesicular lesions on the eyelids and conjunctivae, but corneal involvement and serious ocular disease are rare. The average number of varicella lesions is about 300, but healthy children may have fewer than 10 to more than 1,500 lesionsThe differential diagnosis of varicella includes vesicular rashes caused by other infectious agents, such as herpes simplex virus, enterovirus, monkey pox, rickettsial pox, and S. aureus; drug reactions; disseminated herpes zoster; contact dermatitis; and insect bitesSevere varicella was the most common illness confused with smallpox before the eradication of smallpox.

  • Varicella in Vaccinated Individuals (Breakthrough Varicella)

    Breakthrough disease is varicella that occurs in a person vaccinated >42 days before rash onset and is caused by wild-type VZV

    In the early stages of the varicella vaccination program, rash occurring within the 1st 2 weeks after vaccination was most commonly wild-type VZV, reflecting exposure to varicella before vaccination could provide protection.

    Rash occurring 14-42 days after vaccination was due to either wild or vaccine strains, reflecting breakthrough varicella or vaccine-associated rash, respectively.

  • As varicella disease continues to decline, rashes in the interval 0-42 days after vaccination will be less commonly caused by wild-type VZV. The rash in breakthrough disease is frequently atypical and predominantly maculopapular, vesicles are seen less commonly, and the illness is most commonly mild with
  • Progressive Varicella

    Progressive varicella, with visceral organ involvement, coagulopathy, severe hemorrhage, and continued vesicular lesion development, is a severe complication of primary VZV infection.

    Severe abdominal pain, which may reflect involvement of mesenteric lymph nodes or the liver, or the appearance of hemorrhagic vesicles in otherwise healthy adolescents and adults, immunocompromised children, pregnant women, and newborns, may herald severe disease.

    Although rare in healthy children, the risk for progressive varicella is highest in children with congenital cellular immune deficiency disorders and those with malignancyvaricella-related deaths usually occur within 3 days after the diagnosis of varicella pneumonia

    Unusual clinical findings of varicella, including lesions that develop a unique hyperkeratotic appearance and continued new lesion formation for weeks or months, have been described in children with untreated,late stage HIV infection.

  • Neonatal Varicella

    Mortality is particularly high in neonates born to susceptible mothers who contracted varicella around the time of delivery.Infants whose mothers demonstrate varicella in the period from 5 days prior to delivery to 2 days afterward are at high risk for severe varicella. The infant acquires the infection transplacentally as a result of maternal viremia, which may occur up to 48 hr prior to onset of maternal rash. The infants rash usually occurs toward the end of the 1st week to the early part of the 2nd week of life (although it may be as soon as 2 days). Because the mother has not yet developed a significant antibody response, the infant receives a large dose of virus without the moderating effect of maternal anti-VZV antibody. If the mother demonstrates varicella >5 days prior to delivery, she still may pass virus to the soon-to-be-born child, but infection is attenuated because of transmission of maternal VZV-specific antibody across the placenta.This moderating effect of maternal antibody is present if delivery occurs after 30 wk of gestation, when maternal immunoglobulin G (IgG) is able to cross the placenta.

  • The recommendations for human varicella zoster immune globulin (VariZIG) reflect the differing risks to the exposed infant. Newborns whose mothers demonstrate varicella 5 days before to 2 days after delivery should receive 1 vial of VariZIG as soon as possible.

    If VariZIG is not available, intravenous immune globulin (IGIV) may provide some protection, althoughvaricella-specific antibody titers may vary from lot to lot. Becauseperinatally acquired varicella may be life threatening, the infantshould be treated with acyclovir (10 mg/kg every 8 hr IV) whenlesions develop Infants with neonatal varicella who receive prompt antiviral therapy have an excellent prognosis.

  • Congenital Varicella Syndrome

    When pregnant women do contract varicella early in pregnancy, experts estimate that as many as 25% of the fetuses may become infected. Fortunately, clinically apparent disease in the infant is uncommon: the congenital varicella syndrome occurs in approximately 0.4% of infants born to women who have varicella during pregnancy before 13 wk of gestation and approximately 2% of infants

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