End of Term: Set II

Question 1

Smallpox

Answer 1

poxvirus

pathogenesis: spread via resp droplets from oral lesions. URI w/ growth in mucosa and nodes, viremia affects lungs, liver, spleen; secondary viremia affects skin. S/s: papules, vesicles, pustules, oral lesions. Dried virus in pustule crusts is infectious.
epidemiology: eradicated using live attenuated vaccine and ring vaccination for isolated last cases. Post-exposure vaccination is effective. 1 serotype; all infections are symptomatic.
vaccine: live attenuatedl complications include encephalitis, vaccinia necrosum (spreading necrosis @site of vaccination from T cell immunity defect), eczema vaccinatum, generalized vaccinia (spread of lesions), myo/pericarditis.
diagnosis: cytoplasmic inclusion bodies.
treatment: passive immunization with human vaccinia-Ig for severe complications.

Question 2

Molluscum contageosum

Answer 2

poxvirus

pathogenesis: spread via intimate cutaneous contact (young kids, wrestlers, lovers). 2-8wk incubation. S/s: pearly white papules. Self-limiting over months/years via functional T cell immunity.
diagnosis: poor growth in culture makes difficult. Cytoplasmic inclusion bodies.

Question 3

Rabies

Answer 3

rhabdovirus

pathogenesis: spread via animal bite. Travels to CNS from site, then to salivary gland where replicates; but no viremia. Weeks/months incubation. S/s: fever, anorexia, hydrophobia. CNS symptoms: behavior in animals, neuronal destruction (coma/paralysis), almost always fatal.
epi: 30k ppl treated prophylactically in US annually, prophylactic immunization in prevalent areas or in ppl w/ high exposure (vets). Transmission in US traced to bats.
diagnosis: fluorescent tagging of Negri bodies (inclusions) in nerve cells.
vaccine: killed, given in 5 doses, effective before symptoms begin. Allergic encephalitis no longer a concern.
treatment: passive IgG + active immunization.

Question 4

HIV

Answer 4

lentivirus (retrovirus)

pathogenesis: spread via sex, blood, birth, breast feeding. Gp120 on viral envelope binds host CD4, cellular CXCR4 or CCR5 (chemokine receptor on activated helper T cells and APCs) needed for absorption. Gp41 mediates envelope fusion; Env proteinaceous spike. CD4 cells gradually depleted/cell-mediated immunity suppressed; CTL destruction and apoptosis of affected cells; pyroptosis. S/s: 3 stages, early w/ mono-like symptoms + high viremia, middle (latency) w/ decline in CD4 cells, late: AIDS/immunodeficiency, increased susceptibility to OIs and tumors (KS, B-cell lymphoma, autoimmune thrombocytopenia, chronic lymphadenopathy, dementia/brain disease). HIV-1 infected women progress faster than men w/ same VL.
diagnosis: ELISA for viral antigens, western blot (less sensitive but more specific), PCR.
treatment: HAART, nucleoside analog RT inhibitors, non-nucleoside analog RT inhibitors, protease inhibitors, entry inhibitors, integrase inhibitors, CCR5 inhibitors (maraviroc).