VARICELLA ZOSTER VIRUS.pptx micro biology and cloning features of vericella

Micro biology

1. VARICELLA ZOSTER VIRUS

2. Varicella -Zoster virus (VZV) belongs to herpes viridae group, is a significant pathogenic virus that is known to cause mucocutaneous conditions in oropharyngeal mucosa and skin. PATHOGENESIS AND LATENCY VZV causes both primary and recurrent infections and remains latent in neurons present in the sensory ganglia. Incubation period is approximately 2 weeks ( 7-23 days). VZV responsible for two major clinical infections namely primary type is chickenpox and the recurrent type is herpes zoster or shingles.

3. CHICKENPOX- CLINICAL MANIFESTATION Chickenpox usually begins with prodormal symptoms such as headache, rhinitis and anorexia. It is followed by maculopapular rash that are intensively pruritic or vesicular eruptions of the skin and low-grade fever. The evolution of the rashes are so rapid and the stages are macule , papule, vesicle,pustule and scab. The eruptions are noted on the trunk and spread to involve the face and extremities, ie.centripetal in distribution. Chickenpox spread from nasopharyngeal secretions or by coming in direct contact with skin lesions of the infected patients. Oral lesions are characterised by small blister-like manifestations that involves various areas of oral mucosa and that resembles vesicles of primary HSV infection. Complications of chickenpox includes encephalitis, pneumonitis, Reye’s syndrome and Guillian-Barre syndrome .

4. HERPES ZOSTER INFECTION-CLINICAL MANIFESTATION Following the primary infection of varicella -zoster , virus becomes reactivated from the latency at dorsal root of cranial nerve ganglia. Herpes zoster is an acute infectious viral condition which is extremely painful and is associated with vesicular eruptions of the skin or mucus membrane in areas supplies by the affected sensory nerves. Ramsay Hunt syndrome is a rare form of zoster affecting the facial nerve characterised by unilateral vesicles of oral mucosa and external ear. In immunocompromised patients,HZ may cause large local lesions or disseminated infection and alveolar bone necrosis with exfoliation of teeth have been reported.

5. LABORATORY DIAGNOSIS Cytopathology : Giemsa staining of the scrapings from the ulcer base ( Tzanck smear) reveals cytopathological changes similar to that of HSV infection, such as formation of multinucleated giant cells. Virus isolation : Virus isolation in various cell lines can also produce HSV-like cytopathic effects such as diffuse rounding and ballooning of infected cells. VZV-specific methods : Specific antigen detection by direct immunofluorescence staining and PCR detecting VZV-specific genes.

6. TREATMENT Acyclovir is the drug of choice. It can prevent the complications of chickenpox and can also halt the progression of zoster in adults. PREVENTION VACCINE Live attenuated vaccine using Oka strain of VZV is available. It is given to children after 1 year of age; 2 doses, first dose is given at 12-15 months and second at 4-6years. In seronegative adults; 2 doses given at 1-month gap. Transmission of the vaccine virus can occasionally cause mild rashes in the recipient. Protectivity : The vaccine is > 80% effective in preventing chickenpox in children but less so in adults (70%). However, ii is 95% effective in preventing severe disease.

7. VZIG (VARLCELLA-ZOSTER IMMUNOGLOBULIN It is recommended for post exposure prophylaxis . It is given within 96 hours (preferably 72hours) of exposure. It is also indicated for neonates born to mothers suffering from chickenpox if the onset of chickenpox in mother is between < 5days before delivery till 48 hours after delivery. VZIG is not indicated for the neonate, if the mother has zoster.