VARICELLA- INFECTIOUS VIRAL DISEASE .pptx

Pediatrics

1. VARICELLA By- Dr. Yoshi Chawla Pediatric Resident Petals Newborn and Children hospital Raipur

2. Varicella- zoster virus (VZV) causes primary, latent, and reactivation infections. The primary infection manifests as varicella (chickenpox) and results in establishment of a lifelong latent infection of sensory ganglionic neurons . Reactivation of the latent infection causes herpes zoster (shingles ). Varicella predisposes to severe group A streptococcus and staphylococcus infections .

3. Etiology VZV is a neurotropic human herpesvirus with similarities to herpes simplex virus. VZV enveloped viruses contain double- stranded DNA genomes that encode 71 proteins, including proteins that are targets of cellular and humoral immunity .

4. Primary varicella is highly transmissible. Within households, transmission of VZV to susceptible individuals occurs at a rate of 65–86 %. Persons with varicella may be contagious 24- 48 hours before the rash is evident and until vesicles are crusted, usually 4- 7 days after onset of rash, consistent with evidence that VZV is spread by aerosolization of virus in cutaneous lesions; spread from oropharyngeal secretions may occur but to a much lesser extent.

5. Herpes zoster is caused by the reactivation of latent VZV. It is not common in childhood and shows no seasonal variation in incidence . The lifetime risk for herpes zoster for individuals with a history of varicella is at least 30%, with 75% of cases occurring after 45 years of age. The attenuated VZV in the varicella vaccine can establish latent infection and reactivate as herpes zoster . It is usually manifested by a vesicular rash that is unilateral and dermatomal in distribution .

6. Pathogenesis 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 spreads to T lymphocytes, causing a viremia that delivers the virus to skin where innate immunity controls VZV replication for several days. After innate immunity is overcome in skin, widespread cutaneous lesions develop as the incubation period ends.

7. Clinical manifestation It has variable severity but is usually self- limited. It may be associated with severe complications, including bacterial superinfection , especially with staphylococci and group A streptococci, pneumonia , encephalitis, bleeding disorders, congenital infection, and life- threatening perinatal infection. Herpes zoster is not common in children and typically causes localized cutaneous symptoms, but may disseminate in immunocompromised patients.

8. Varicella in Unvaccinated Individual T he illness usually begins 14- 16 days after exposure, although the incubation period can range from 10- 21 days . Fever, mal aise , anorexia, headache, and occasionally mild abdominal pain may occur 24- 48 hours before the rash appears. Temperature elevation is usually 37.8–38.9°C (100–102°F) but may be as high as 41.1°C (106°F ). Varicella lesions often appear first on the scalp, face, or trunk. The initial exanthem consists of intensely pruritic erythematous macules that evolve through the papular stage to form clear, fluid- filled vesicles. Clouding and umbilication of the lesions begin in 24- 48 hours.

9. The distribution of the rash is predominantly central or centripetal, with the greatest concentration on the trunk and proximally on the extremities . T he differential diagnosis of varicella includes vesicular rashes caused by other infectious agents, such as herpes simplex virus, entero virus, monkey pox ( mpox ), rickettsial pox, and Staphylococcus aureus ; drug reactions; disseminated herpes zoster; contact dermatitis; and insect bites (especially for breakthrough varicella.

10. Varicelliform Rashes in Vaccinated Individuals Breakthrough varicella is disease caused by wild- type virus in a vaccinated person, occurring after 42 days past vaccination. One dose of varicella vaccine is 98% effective in preventing moderate and severe varicella and is 82% effective in preventing all disease after exposure to wild- type VZV. Breakthrough cases have been reported among two- dose vaccinees ; however, recipients of two doses of varicella vaccine are less likely to have breakthrough disease than those who received one dose.

11. Neonatal Varicella Neonatal Varicella Mortality is particularly high in neonates born to susceptible moth ers who contract varicella around the time of delivery. Infants whose mothers demonstrate varicella in the period from 5 days before deliv ery to 2 days afterward are at high risk for severe varicella. Newborns whose mothers develop varicella during the period of 5 days before to 2 days after delivery should receive VZIG as soon as possible after birth. Although neonatal varicella may occur in about half of these infants despite administration of VZIG, it is milder than in the absence of VZIG administration.

12. Because perinatally acquired varicella may be life threatening, the infant should usually be treated with acyclovir (10-15 mg/kg every 8 hours IV) when lesions develop. Infants with neonatal varicella who receive prompt antiviral therapy have an excellent prognosis

13. Congenital Varicella Syndrome The congenital varicella syndrome occurs in approximately 0.4% of infants born to women who have varicella during pregnancy before 13 weeks of gestation and in approximately 2% of infants born to women with varicella between 13 and 20 weeks of gestation. The congenital varicella syndrome is characterized by cicatricial skin scarring in a zoster- like distribu tion ; limb hypoplasia; and abnormalities of the neurologic system (e.g., microcephaly, cortical atrophy, seizures, and intellectual disability), eye (e.g., chorioretinitis , microphthalmia , and cataracts), renal system (e.g., hydroureter and hydronephrosis ), and autonomic nervous system (e.g., neurogenic bladder, swallowing dysfunction, and aspiration pneumonia).

14. The diagnosis of VZV fetopathy is based mainly on the history of gestational varicella combined with the presence of characteristic abnormalities in the newborn infant. A persistently positive VZV IgG antibody titer at 12- 18 months of age is a reliable indicator of prenatal infection in the asymptomatic child, as is the development of zoster in the first year of life without evidence of postnatal infection.

15. COMPLICATIONS The complications of VZV infection (varicella or zoster) occur more commonly in immunocompromised patients. Mild thrombocytopenia occurs in 1–2% of children with varicella and may be associated with petechiae . Purpura , hemorrhagic vesicles, hematu ria , and gastrointestinal bleeding are rare complications that may have serious consequences. Other complications of varicella, some of them rare, include acute cerebellar ataxia, encephalitis, pneumonia, nephri tis, nephrotic syndrome, hemolytic - uremic syndrome, arthritis, myo carditis , pericarditis, pancreatitis, orchitis , and acute retinal necrosis.

16. Pneumonia Varicella pneumonia (viral, due to VZV) is a severe complication that accounts for most of the increased morbidity and mortality from varicella in adults and other high- risk populations. Progressive Varicella – It occurs with visceral organ involvement, coagulopathy, severe hemorrhage , and continued vesicular lesion development after 7 days, is a severe complication of primary VZV infection.

17. DIAGNOSIS Varicella and herpes zoster are usually diagnosed primarily by their clinical appearance. Laboratory evaluation has not been considered necessary for diagnosis or management . VZV can be identified quickly by either PCR amplification testing (vesicular fluid, crusts) or direct fluorescence assay of cells from cutaneous lesions (vesicular fluid). In the absence of vesicles or scabs, scrapings of maculopapular lesions can be collected for PCR or direct fluorescence assay testing.

18. VZV IgG antibodies can be detected by several methods, and a fourfold or greater rise in IgG antibodies is confirmatory of acute infection. Clinicians should use clinical judgment to decide on the best course of therapy.

19. TREATMENT Antiviral treatment with acyclovir or valacyclovir modifies the course of both varicella and herpes zoster. Foscarnet and cidofovir may be useful for the treatment of acyclovir- resistant VZV infections. Varicella- Oral therapy with acyclovir (20 mg/kg/dose; maximum: 800 mg/dose) given as four doses/day for 5 days can be used to treat uncomplicated varicella. Valacyclovir or famciclovir may be given to older children who can swallow tablets.

20. Patients receiving these antivirals should be well hydrated, and for prolonged use, renal function and white blood cell counts (especially neutrophils) should be monitored frequently. Intravenous therapy is indicated for severe disease and for vari cella in immunocompromised patients (even if begun more than 72 hours after onset of rash). Any patient who has signs of disseminated VZV, including pneumonia, severe hepatitis, thrombocytopenia, or encephalitis, should receive immediate treatment. Intravenous acyclovir therapy (10 mg/kg or 500 mg/m2 every 8 hours) initiated within 72 hours of development of initial symptoms decreases the likelihood of progressive varicella and visceral dissemination in high- risk patients.

21. Herpes Zoster- Antiviral drugs are effective for treatment of herpes zoster. In healthy adults, acyclovir (800 mg 5 times a day PO for 5- 7 days), famciclovir (500 mg tid PO for 7 days), and valacyclovir (1,000 mg tid PO for 7 days) reduce the duration of the illness but do not prevent development of postherpetic neuralgia.

22. PROGNOSIS Primary varicella in unvaccinated persons has a mortality rate of 2- 3 per 100,000 cases, with the lowest case fatality rates among children 1- 9 years of age (∼1 deaths/100,000 cases). Compared with these age groups, infants have a 4 times greater risk of dying and adults have a 25 times greater risk of dying. The most common complications among people who died from varicella were pneumonia, central nervous system complications, secondary infections, and hemorrhagic conditions. T

23. PREVENTION VZV transmission is difficult to prevent, especially from persons with varicella, because a person with varicella may be contagious for 24- 48 hours before the rash is apparent. Infection control practices, including caring for patients with varicella in isolation rooms with filtered air systems, are essential. All healthcare workers should have evidence of varicella immunity.

24. Vaccine Varicella is a vaccine- preventable disease. Varicella vaccine contains live, attenuated VZV (Oka strain) and is indicated for subcutane ous or intramuscular administration . Varicella vaccine is recommended for routine administration as a two- dose regimen to healthy children at ages 12- 15 months and 4- 6 years. Administration of the second dose earlier than 4- 6 years of age is acceptable, but it must be at least 3 months after the first dose.

25. Vaccine- Associated Adverse Events Varicella vaccine is safe and well tolerated . A mild vaccine- associated varicelliform rash was reported in approximately 1–5% of healthy vaccinees , consisting of 6- 10 papular - vesicular, erythem atous lesions with peak occurrence 8- 21 days after vaccination. Serious adverse reactions confirmed to be caused by the vaccine strain are rare and include pneumonia, hepatitis, meningitis, recurrent herpes zoster, severe rash, and seven deaths (all deaths occurred in persons with immunocompromising conditions)

26. Postexposure Prophylaxis Vaccine given to healthy children within 3 and up to 5 days after exposure (as soon as possible is preferred) is effective in preventing or modifying varicella . High- titer anti- VZV immune globulin as postexposure prophy laxis is recommended for immunocompromised children, pregnant women, and newborns exposed to varicella. Newborns whose mothers have varicella 5 days before to 2 days after delivery should receive VariZIG (0.5 vial for those weighing ≤2 kg and 1 vial for those weighing >2 kg).

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