⦿ INTRODUCTION ⦿ EPIDEMIOLOGY AND TRANSMISSION ⦿ STRUCTURE ⦿ REPLICATION ⦿ PATHOGENESIS AND CLINICAL SIGNIFICANCE ⦿ LABORATORY DIAGNOSIS ⦿ T R E A TME N T A N D P R E V E N TION CONTENT
⦿ Herpes (Greek: creep or crawl) ⦿ Herpes simplex viruses belong to the ubiquitous Herpesviridae family ⦿ Human herpes simplex virus (HSV) causes contagious infection with a large reservoir in the general population ⦿ Herpesviruses are able to establish lifelong persistent infections in their hosts and undergo periodic reactivation ; incurable ⦿ HSV has a potential for significant complications in the immunocompromised host INTRODUCTION
⦿ HSV-1 is normally associated with orofacial infections and encephalitis ⦿ HSV-2 usually causes genital infections and can be transmitted from infected mothers to neonates ⦿ Both viruses establish latent infections in sensory neurons and, upon reactivation, cause lesions at or near point of entry into the body INTRODUCTION
Biologic properties Examples Subfamil y ( “herpes v iri nae) Growth cycle and cytopathology Latent infectio n s Genus (“ v iru s) Official name (“Human herpes v iru s ”) Common name Alpha Short, cytolytic Neurons Simplex 1 Herpes simplex virus type 1 2 Herpes simplex virus type 2 Varicello 3 Varicella-zoster virus Beta Long, cytomegalic Glands, kidneys Cytomegalo 5 Cytomegalovirus Long, l y m phoproliferati v e L y m phoid tissue Roselo 6 Human herpesvirus 6 7 Human herpesvirus 7 Gamma Variable, lymphoproliferative Lymphoid tissue Lymphocrypto 4 Epstein-Barr virus Rhadino 8 Kaposi's sarcoma- associa t ed herpes v irus CLASSIFICATION OF HSV
⦿ HSV-associated diseases are among the most wide-spread infections affecting nearly 60-95% of human adults ⦿ No animal reservoirs or vectors ⦿ Highest incidence of HSV-1 infection occurs among children 6 months to 3 years of age ⦿ 70–90% of persons thus acquire type 1 antibodies by adulthood ⦿ Primary infection by HSV-2 is more common in young adults EPIDEMIOLOGY
⦿ Transmission of both HSV types is by direct contact with virus-containing secretions or with lesions on mucosal or cutaneous surfaces ⦿ HSV-1 is spread by contact, usually by infected saliva ⦿ HSV-1 primarily infects skin above the waist ⦿ HSV-2 is transmitted sexually or from a maternal genital infection to a newborn ⦿ HSV-2 primarily infects skin below the waist TRANSMISSION
⦿ Virions are spherical, 150-200nm in diameter ⦿ HSV-1 and HSV-2 contains an envelope- derived from the nuclear membrane of the infected cell; contains viral glycoproteins a tegument—an amorphous layer of proteins that surround the capsid an icosahedral capsid Genome (linear, a large double-stranded viral DNA; encoding 70-200 proteins) STRUCTURE
Virus adsorption and penetration Viral DNA replication and nucleocapsid assembly Acquisition of the viral envelope Latency REPLICATION
⦿ HSV causes cytolytic infections ⦿ Pathologic changes are due to necrosis of infected cells together with the inflammatory response Viral cytopathy PATHOGENESIS
⦿ Ballooning of infected cells ⦿ Production of Cowdry type A intranuclear ( Lipschutz ) inclusion bodies ⦿ Margination of chromatin ⦿ Formation of multinucleated giant cells PATHOGENESIS
⦿ HSV-1 Acute gingivostomatitis Recurrent herpes labialis (cold sores) Herpetic whitlow Keratoconjunctivitis Encephalitis ⦿ HSV-2 Genital herpes Neonatal herpes (may be by HSV-1 as well) CLINICAL SIGNIFICANCE
A. Cytopathology: A rapid cytologic method Scrapings obtained from the base of a vesicle is stained with 1% aq. solution of toluidine blue ‘0’ for 15 seconds Presence of multinucleated giant cells or ‘ Tzanck cells ’ = + HSV Intranuclear inclusion bodies with Giemsa-stained smears LABORATORY DIAGNOSIS
B. Isolation and identification: Inoculation of tissue cultures in human diploid fibroblasts is preferred for viral isolation Typical cytopathic changes may be seen in 24-48 hrs C. Polymerase chain reaction D. Serology: Antibodies appear in 4–7 days after infection; reach a peak in 2–4 weeks Rise in Ab titre may be demonstrated by ELISA or complement fixation tests LABORATORY DIAGNOSIS
⦿ Aciclovir, Valaciclovir, Famciclovir ⦿ Asymptomatic shedding is frequent in patients with genital herpes ⦿ Transmission can be reduced by: avoidance of contact with potential virus-shedding lesions safe sexual practice antiviral therapy TREATMENT AND PREVENTION
⦿ Harvey RA, Champe PC, Fischer BD. Lippincott’s Illustrated Reviews: Microbiology. 2 nd edition. 2007. ⦿ Jawetz, Melnick & Adelberg. Medical Microbiology. The McGraw-Hill Companies. 25th edition ⦿ Richard J Whitley, Bernard Roizman. Herpes simplex virus infections. Lancet. 2001; 357: 1513– 18 ⦿ Fatahzadeh M & Schwartz RA. Human herpes simplex virus infections: Epidemiology, pathogenesis, symptomatology, diagnosis and management. JAM ACAD DERMATOL. 2007; 737-763 REFERENCE