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51 Cards in this Set
- Front
- Back
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Human Herpes Viruses
(other kinds are in primates, mammals, birds, fish) |
HSV-1
HSV-2 VSV EBV CMV HHV6 HHV7 HHV8 |
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Human Herpes Virus Characteristics
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Linear, dsDNA
icosahedral Tegument of viral proteins/enzymes Lipid enelope Thermolabile, organic solvent sensitive Replicate in nucleus |
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HSV1 & HSV2
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Two antigenic types 1 & 2
Diseases: acute & recurrent/latent |
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HSV1 Diseases
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gingivostomatitis
fever blisters herpetic whitlow ocular herpes encephalitis genital herpes |
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HSV2 Diseases
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Genital herpes
Neonatal herpes |
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HSV1/2 Habitat
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everywhere, humans are only reservoir
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HSV1/2 transmission
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direct contact with secretions
asymptomatic shedding |
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HSV1/2 Predisposing Factors
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Immunologic Status
Socioeconomic Status |
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HSV1/2 Pathophysiology
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Multinucleated (syncytia) cells
ballooning degeneration of epithelial cells, necrosis,inclusion bodies, inflammatory response, cell-cell spread, infection of ganglia |
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Do HSV1/2 destroy ganglia?
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No, viral genome persists as circular DNA; reactivation leads to recurrent disease
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HSV1/2 recurrence triggered by
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stress, UV light, hormones
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HSV1/HSV2 spreads in presence of
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antibody.
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What contributes to symptoms and resolution of HSV1/2 infection?
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Cell mediated immunity
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Clinical Manifestations of HSV1
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often asymptomatic
50-90% of population is seropositive Primary gingivostomatitis: fever, irritability, painful vesicles on buccal mucosa, tongue, gums, throat, 1-2 weeks recurrent infection caused by prodrome, followed by unilateral vesicles; 1 week duration ocular lesions--corneal scarring 70% mortality of untreated encephalitis |
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HSV2 clinical manifestations
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Primary-->papules-->vesicles/pustules, lymphadenopathy, tenderness, 3-4 week gestation
recurrent infection characterized by prodrome, vesicles on genitalia, 1-2 weeks Neonatal herpes usually HSV2; get it in canal. 60% mortality. Neurologic sequelae; vesicles; internal organ involvement |
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HSV1/2 Diagnosis
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Cell culture with vesicle fluid or secretion
Scraping/Tzank smear ELISA Serology--only for primary infections |
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HSV1/2 Therapy & Prevention
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Acyclovir for encephalitis/neonatal infections
Foscarnet for acyclovir resistant HSV Prevention: avoid contact, C-section for infected mothers |
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Varicella Zoster Virus Characteristics
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Only one antigenic type
Slow replication |
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VZV Diseases
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acute and recurrent/latent
Varicella: chickenpox is acute Herpes zoster: shingles is recurrent form arising from latency |
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VZV Habitat
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everywhere
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VZV Mode of transmission
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Very contagious
respiratory droplets contact with lesions |
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VZV predisposing factors
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immunologic status
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VZV pathophysiology
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ballooning degeneration of cells, syncytia, inclusion bodies, remains cell-associated
Begins in mucosa of respiratory tract, spreads via blood and lymphatics to RE system Secondary viremia gives apparent lesions Latent infection of dorsal root or cranial nerve ganglia virus migrates to skin to form lesions Antibody presence allows spread cell to cell Cell-mediated immunity causes symptoms and resolution |
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Clinical manifestations of chickenpox
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mild, childhood
before age 10 fever, itchy maculopapular rash after 14-21 incubation different crops in various areas vesicles crust over lesions generalized, more prevalent on trunk mucous membrane involvement is typical VZV rare in adults 20% mortality in immunocompromised |
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Clinical manifestations of shingles
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Lesions preceded by pain in affected dermatome
vesicles close together on reddened base multiple attacks not common older people might have post herpetic neuralgia progressive in immunocomprosmised |
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Diagnosis of VZV
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Tzanck smear
Immunological antigen detection |
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Therapy and Prevention of VZV
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Acyclovir in severe cases/immunocompromised
immunoprophylaxis with VZV immune globulin live, attenuated vaccine available |
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Epstein Barr Virus Characteristics
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Limited tropism/host range
Only replicates in lymphoblastoid cells and epithelial cells of oropharynx/cervix |
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Epstein Barr Disease
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acute/chronic
associated with malignancies acute: mononucleosis Cyclic recurrent: like mono B cell lymphoma in immuno compromised African Burkitt's lymphoma Nasopharyngeal carcinoma Hodgkin's disease AIDS associated non-Hodgkin's lymphoma Non-Hodgkin's lymphoma Oral hairy leukoplakia (productive EBV) in immunosuppressed |
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Epstein Barr Habitat
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Everywhere
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Epstein Barr Transmission
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transmitted in saliva;
low contagion potential; asymptomatic shedding |
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Epstein Barr Predisposing Factors
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Immunologic status
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Epstein Barr Pathophysiology
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Epithelial cells of oropharynx
Accesses B cells via C3D receptor Lysis of cells; others activated to produce immunoglobulin and membrane antigen that is a T cell target Atypical lymphocytes (Downey cells) causes symptoms In absence of T cells, B cells immortalized-->chonic infection and lymphoma |
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Clinical manifestations of EBV
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Primary often asymptomatic
90% of adults are seropositive Clinically apparent disease: infectious mononucleosis; young adults, fever, lymphadenopathy, sore throat, fatigue, malaise Time course is variable cyclical recurrent disease possible |
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EBV association with malignancies
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African Burkitt: endemic in malaria belt of africa; limited antigen expression allows evasion of immune system
B cell lymphomas post transplant Nasopharyngeal carcinoma endemic in China AIDS associated non-Hodgkin's Non-Hodgkin's |
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EBV role in malignancy
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EBV infection-->B Cell proliferation, T cell suppression-->cell alterations (chromosome translocation-->oncogene activation)
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EBV Diagnosis
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Atypical lymphocytes
Heterophile antibodies (monospot) cross react with sheep/bovine RBCs Serologic tests for IgM anti VCA, IgG anti-EBNA |
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EBV therapy/prevention
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supportive therapy
prevention difficult due to ubiquitous presence |
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Cytomegalovirus Characteristics
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common
cell-associated |
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Cytomegalovirus Diseases
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Acute & recurrent, latent infections
Congenital: prevalent viral cause of disease Infectious mononucleosis (heterophile negative) Retinitis, encephalitis, pneumonia, colitis, esophagitis in the immunocompromised |
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Habitat of CMV
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everywhere
secretions |
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CMV transmission
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Congenital, oral, sexual, blood transfusion, transplants
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CMV predisposing factors
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immuno status, primary infection during pregnancy
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CMV pathophysiology
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latent infection of lymphocytes and other leukocytes
cytomegaly: cell enlargement cytoplasmic inclusions Infection is immunosuppressive Cell-mediated immunity essential in resolution |
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CMV manifestations
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asymptomatic, 50% adults seropositive
illness resembles mono, but less severe and no heterophile antibody Congenital: microcephaly, intracerebral calcification, HSM, rash, hearing loss, mental deficits disseminated disease in AIDS patients |
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CMV diagnosis
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Cytomegalic cells; intranuclear inclusions in tissues and urine
Antigen detection culture in diploid fibroblasts serology |
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CMV therapy/prevention
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Ganciclovir
Foscarnet Hyperimmune globulin Prevention by using seronegative donors or leukocyte depleted blood condoms |
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HHV6 characteristics
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replicates in lymphoid tissues
cytopathic for T cells found in salivary glands shedding causes spread causes exanthem subitum (roseola) most communicable of herpes viruses (almost all children infected by age 5) Can reactivate in immunosuppression; may contribute to rejection in transplant patients |
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HHV7 characteristics
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resembles HHV6
almost all infected by age 2 mononucleosis syndrome |
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HHV8
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Kaposi's sarcoma associated herpes virus
NOT ubiquitous |
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HHV8 involved in pathogenesis of Kaposi's Sarcoma (KS) which is
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predominant tumor of gay AIDS patients
risk increases with number of partners saliva main means of transmission immunosuppression is cofactor in KS pathogenesis CD19+ B cells are main reservoir persists in latent form in lymphoid tissues Tumors may result from IL-6 dysregulation due to KS infection Rare primary effusion lymphomas (variant of B cell lymphoma) Homologues to human protooncogenes Foscarnet/ganciclovir help prevent KS in AIDS patients |
