Varicella zoster virus infections

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varicella zoster virus infection,Chickenpox ppt. Dr. Bhagat Baghel Assist. Professor BRKM MC Jagdalpur, Chattisgarh INDIA

Transcript of Varicella zoster virus infections

Varicella-Zoster Virus Infections

Chickenpox

• Varicella-zoster virus (VZV) causes primary, latent, and recurrent infections.

• The primary infection is manifested as varicella (chickenpox)

• morbidity and mortality • it predisposes to severe group A streptococcus

and Staphylococcus aureus infections

Etiology

• VZV is a neurotropic human herpesvirus• virus is enveloped with double-stranded DNA

genomes • encode more than 70 proteins

• transmission of VZV to susceptible individuals occurs at a rate of 65-86%

• contagious 24-48 hr before the rash is evident and until vesicles are crusted

• Varicella vaccine is introduced in 1995

Herpes zoster • reactivation of latent VZV. • uncommon in childhood• Zoster is not caused by exposure to a patient

with varicella • The lifetime risk for herpes zoster for

individuals with a history of varicella is 10-20%• 75% of cases occurring after 45 yr of age. • Herpes zoster is very rare in healthy children

<10 yr of age

• Herpes zoster in children tends to be milder than disease in adults

• It occurs more frequently & disease is more severe if- – Children is on immunosuppressive therapy– HIV infected children.

Pathogenesis

• VZV is transmitted in – by airborne spread - oropharyngeal secretion– through direct contact - fluid of skin lesions

• Primary infection (varicella) results from - • inoculation of the virus onto the mucosa of the URT and

tonsillar lymphoid tissue. • virus replicates in the local lymphoid tissue

• brief subclinical viremia(First) • spreads the virus to the reticuloendothelial system

• Widespread cutaneous lesions occur (during a second viremic).

• VZV is also transported back to the mucosa of the upper

respiratory tract and oropharynx

• Virus is transported in a retrograde manner through sensory axons

dorsal root ganglia throughout the spinal cord

virus establishes latent infection in the neurons and satellite cells

Subsequent reactivation of latent virus

herpes zoster

– vesicular rash that usually is dermatomal in distribution. –necrotic changes may be produced in the

associated ganglia. – The skin lesions of varicella and herpes

zoster have identical histopathology– infectious VZV is present in both.

Clinical Manifestation

• Varicella (Chicken pox)• Varicella Zoster• Breakthrough varicella• Progressive varicella• Neonatal varicella• Congenital varicella syndrome

Varicella(Chickenpox)

• incubation period is 10 -21 days. • Subclinical varicella is rare• Prodromal symptoms– Fever– malaise– anorexia– headache– mild abdominal pain

• Varicella lesions – appear first on the scalp, face, or trunk. – The initial exanthem consists of intensely pruritic– erythematous macules– papular stage– fluid-filled vesicles. – Clouding and umbilication of the lesions begin in

24-48 hr.

• simultaneous presence of lesions in various stages of evolution is characteristic of varicella

• The distribution of the rash is predominantly central or centripetal

• The number of varicella lesions 10 to 1,500 • Ulcerative lesions involving the mucosa of

oropharynx and vagina

• vesicular lesions on the eyelids and conjunctivae

• The exanthem may be much more extensive in children with skin disorders

• Hypopigmentation or hyperpigmentation of lesion sites persists for days to weeks.

differential diagnosis

• vesicular rashes caused by other infectious agents :- – enterovirus – monkey pox – rickettsial pox– S. aureus– drug reactions – disseminated herpes zoster– contact dermatitis– insect bites

Varicella in Vaccinated Individuals (“Breakthrough Varicella”)

• One dose of varicella vaccine is >97% effective in preventing severe varicella

• 85% effective in preventing all disease after exposure to wild-type VZV.

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

• rash occurring < 14 days after vaccination was most commonly wild-type VZV

• Rash occurring 14-42 days after vaccination was due to either – Wild-type VZV-------- breakthrough varicella – vaccine strains---------vaccine-associated rash

• The Breakthrough varicella rashes are – atypical – predominantly maculopapular– vesicles are seen less commonly– illness is most commonly mild with <50 lesions – shorter duration of rash – Less contagious– Complications are less– little or no fever

Progressive Varicella

• Progressive varicella, is a severe complication of primary VZV infection.

• visceral organ involvement• coagulopathy• severe hemorrhage • Continued new vesicular lesion development • Severe abdominal pain

• appearance of hemorrhagic vesicles• the risk for progressive varicella – congenital cellular immune deficiency disorders – Malignancy– organ transplantation– Pt. is on steroid therapy

• Unusual clinical findings– develop a unique hyperkeratotic appearance – continued new lesion formation for weeks or

months

Neonatal Varicella

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

• The infant's rash usually occurs toward the end of the 1st week to the early part of the 2nd week of life

• maternal immunoglobulin G (IgG) is able to cross the placenta if delivery occurs after 30 wk of gestation

• Newborns whose mothers demonstrate varicella 5 days before to 2 days after delivery should receive 1 vial of VariZIG as soon as possible.

• All premature infants born <28 wk gestation to a mother with active varicella at delivery (even if the maternal rash has been present for >1 wk) should receive VariZIG

• intravenous immune globulin (IGIV) may provide some protection

• the infant should be treated with acyclovir (10 mg/kg every 8 hr IV) when lesions develop.

• prognosis is good if pt. receive prompt antiviral therapy

Congenital Varicella Syndrome

• Risk of infection (No disease)– Early part of pregnency- 25%

• Risk of CVS– Before 13 wks of gestation – 0.4%– In between 13 – 20 wks - 2%

skin cicatricial skin scarring

Limb limb hypoplasia

Neurologic microcephaly, cortical atrophy, seizures, and mental retardation

Eye chorioretinitis, microphthalmia, and cataracts

Renal hydroureter and hydronephrosis

autonomic nervous system

neurogenic bladder, swallowing dysfunction, and aspiration pneumonia

• The diagnosis of VZV fetopathy is based mainly on the – history of gestational varicella – presence of characteristic abnormalities in the

newborn infant– viral DNA may be detected in tissue samples by PCR. – VZV-specific IgM antibody is detectable in the cord

blood– Chorionic villus sampling

Herpes Zoster

• manifests as vesicular lesions clustered within 1 or 2 adjacent dermatomes

• rash is mild, with new lesions appearing for a few days

• symptoms of acute neuritis are minimal• postherpetic neuralgia is very unusual in

children. • Transverse myelitis with transient paralysis is a

rare complication of herpes zoster

Herpes zoster involving the lumbar dermatome.

• Immunocompromised children –more severe herpes zoster– postherpetic neuralgia is common. –disseminated cutaneous disease – visceral dissemination with pneumonia,

hepatitis encephalitis, and DIC– retinitis.

Diagnosis of varicella

• Laboratory evaluation has not been considered necessary

• Leukopenia• relative and absolute lymphocytosis. • liver function tests are mildly elevated• CSF in CNS complication– mild lymphocytic pleocytosis – moderate increase in protein content

• Rapid laboratory diagnosis– direct fluorescence assay– rapid culture with specific immunofluorescence

staining– PCR amplification testing– multinucleated giant cells can be detected with

nonspecific stains Tzanck smear• VZV IgG antibodies:- Rise > 4 fold• Testing for VZV IgM antibodies is not useful

Treatment in Varicella

• Acyclovir therapy is not recommended routinely for treatment of uncomplicated varicella in the otherwise healthy child– the marginal benefit– the cost of the drug – low risk for complications of varicella.

• Oral acyclovir in children >12 mo of age with – chronic cutaneous

or – pulmonary disorders– Pt. Is on corticosteroid therapy– individuals receiving long-term salicylate therapy

• Nonpregnant individuals > 13 years of age

Intravenous Acyclovir therapy

• Varicella with severe disease– pneumonia– severe hepatitis– thrombocytopenia – encephalitis

• varicella in immunocompromised patients• Dose:- IV acyclovir (500 mg/m2 every 8 hr IV) continued for 7–

10 days• Other molecules

– famciclovir – Valacyclovir

• Acyclovir-resistant VZV:- intravenous foscarnet

Treatment in Herpes Zoster

• uncomplicated HZ - antiviral agent may not always be necessary

• herpes zoster in immunocompromised – Acyclovir (500 mg/m2 or 10 mg/kg every 8 hr IV).

• Use of corticosteroids in the treatment of herpes zoster in children is not recommended.

Complications • more common in immunocompromised

patients• In healthy child, mild varicella hepatitis is

relatively common• Mild thrombocytopenia occurs in 1-2%

Bacterial Infections

• Secondary bacterial infections of the skin– group A streptococci and S. aureus– occur in up to 5% of children– impetigo – cellulitis– lymphadenitis– subcutaneous abscesses.

• manifestation of secondary bacterial infection – erythema of the base of a new vesicle. – Recrudescence of fever 3-4 days after the initial

exanthem

• Other invasive complications– varicella gangrenosa– bacterial sepsis– pneumonia– arthritis– osteomyelitis – cellulitis – necrotizing fasciitis– toxic shock syndrome

Encephalitis and Cerebellar Ataxia

• morbidity from CNS complications is highest among patients < 5 yr

• Nuchal rigidity• altered consciousness• seizures• gait disturbance • nystagmus, and slurred speech• Neurologic symptoms usually begin 2-6 days after the

onset of the rash. • Clinical recovery is rapid and is usually complete

Pneumonia

• Respiratory symptoms, which may include – cough– dyspnea – cyanosis – pleuritic chest pain – hemoptysis

EVIDENCE OF IMMUNITY TO VARICELLA

Evidence of immunity to varicella consists of any of the following:

1. Documentation of age-appropriate vaccination

with a varicella vaccine:

• Preschool-aged children (i.e., aged >12 mo): 1 dose • School-aged children, adolescents, and adults: 2

doses

2. Laboratory evidence of immunity or laboratory confirmation of disease

3. Diagnosis or verification of a history of varicella disease by a health-care provider

4. Diagnosis or verification of a history of herpes zoster by a health-care provider

Postexposure Prophylaxis

1) Vaccine:- given to healthy children within 3-5 days after exposure

2) High-titer anti-VZV immune globulin is recommended - immunocompromised children- pregnant women- newborns exposed to varicella

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