Downloaded 14 times
More Related Content
Similar to Epstein barr virus (ebv) and varicella
More from Nur Izzatul Najwa
Epstein barr virus (ebv) and varicella
- 1. EPSTEIN BARR VIRUS(EBV) AND VARICELLA ZOSTER NUR IZZATUL NAJWA BINTI SHARUPUDDIN 082015100036
- 2. LEARNING OUTCOMES : Allof students are able to : • Describe the morphology of virus • Understand the clinical manifestations of virus • Describe the pathogenesis of virus • List the mode of transmission of virus • Know the complications of virus • List the laboratory diagnosis of virus Epstein-Barr virus (EBV) and Varicella Zoster virus
- 3. INTRODUCTION • First discoveredby Epstein and Barr who isolated the virus from Burkitt’s lymphoma • Has affinity for lymphoid tissue • EBV infects B lymphocytes which have receptors ( CD21 molecules) specific for it • 80% - 90% children acquire EBV infections by the age of three years and once infected, it stays for life
- 4. MORPHOLOGY • Double- strandedlinear DNA • Enveloped • Icosohedral symmetry
- 5. CLINICAL MANIFESTATION • Infectiousmononucleosis (IM) or Glandular fever ▫ Acute self limiting disease of children ▫ Charaterised by fever, sore throat, lymphadenopathy and presence of abnormal lymphocyes in peripheral blood ▫ Incubation period : 4 to 7 weeks ▫ Presence of Downey cell
- 6. • Infection toimmunocompromised host ▫ Cause progressive lymphoproliferative disease in immunodeficient children, transplant recipient and aids patient • EBV- associated malignancies ▫ Burkitt’s lymphoma ▫ Nasopharyngeal lymphoma ▫ B-cell lymphoma
- 7. PATHOGENESIS OF EBVINFECTION MALIGNANCY Mutation and t (8:14) Sustained B- cell proliferation Activates NF-kB and JAK/STAT pathways Virus codes for latent membrane protein 1 (LMP1) Promotes cell cycle Activation of cyclin D EBNA 2 gene
- 9. MODE OF TRANSMISSION •Person to person spread by: Close contact with infected person Crowded living conditions with asymptomatic shedders Kissing Contact with infected oral secretion SALIVA
- 10. COMPLICATIONS • Hepatitis • Meningoencephalitis •Pneumonitis • Splenic rupture • B cell lymphoma • Nasopharyngeal lymphoma • Burkitt’s lymphoma
- 11. LABORATORY DIAGNOSIS WHITE BLOODCELL COUNT • Mild increase Total Leukocyte Count (TLC) • Atypical lymphocytes ▫ Larger ▫ Abundant blue cytoplasm – Duck skirting ▫ Oval, folded nucleus PAUL BUNNEL TEST • Presence of heterophile antibodies - IgM
- 14. INTRODUCTION • Family ofherpes virus • Virus causes two diseases: varicella (chickenpox) and herpes zoster (shingles) • Varicella is the primary infection in a non- immune individual • Herpes zoster is reactivation of the latent virus when immunity falls to ineffective level
- 15. MORPHOLOGY • Double- strandedlinear DNA • Enveloped • Icosohedral symmetry
- 16. CLINICAL MANIFESTATION • VARICELLAOR CHICKEN POX ▫ An acute vesicular exanthem occuring in non- immune person especially children ▫ Begins as infection of the nasopharynx ▫ Viraemia accompanied by onset of fever, malaise and anorexia ▫ Maculopapular rash, usually upper trunk and face ▫ Formation of vesicles ->rupture ->heals with formation of scabs
- 18. • HERPES ZOSTEROR SHINGLES ▫ A recurrent, painful, vesicular eruption caused by reactivation of dormant of VZV ▫ Condition is infectious and spreads in children ▫ Pathogenesis : Virus during latent period resides in dorsal root spinal ganglia or in cranial nerve ganglia On reactivation, virus spreads from ganglia to the sensory and peripheral nerve Burning, painful skin lesion develop in specific skin dermatome
- 21. MODE OF TRANSMISSION •Varicella ▫ Aerosolized respiratory secretion ▫ Contact with ruptured vesicles • Zoster ▫ Reactivation from dorsal root ganglion
- 22. LABORATORY DIAGNOSTIC • Fewdrops on tops of rose petals ; a red base with fluid filled vesicle • Multinucleated giant cells
- 24.
- 25. REFERENCE • TEXTBOOK OFPATHOLOGY, HARSH MOHAN, 7TH EDITION • CLINICAL MICROBIOLOGY MADE RIDICULOUSLY SIMPLE, 4TH EDITION • TEXTBOOK OF MICROBIOLOGY, PROF CP BAVEJA, 4TH EDITION