Quiz 4: Set II Flashcards
Mumps
paramyxovirus
pathogenesis: resp. droplet transmission, 18-21d incubation. Systemic viremia, 1 serotype, related to influenza. Multiplies @resp epithelium and local nodes, infects salivary glands/organs, excrete in saliva. 70% infxns asymptomatic; s/s: prodromal fever, malaise, anorexia. Parotid swelling, orchiditis, can affect panc/ovary/meninges (aseptic meningitis). Lifelong immunity via IgG.
diagnosis: hemagglutination
vaccine: MMR, live attenuated, 2x.
treatment: none
Measles
paramyxovirus
pathogenesis: resp droplets, 14d incubation, most contagious. Infects resp epithelium, local nodes and conjunctiva. almost never asymptomatic. Excrete from resp tract, tears and urine. multinucleated giant cells @lymph and mucosa due to viral fusion protein. Infection suppresses cell-mediated immunity, can lead to 2ndary infection. S/s: prodromal fever, cold-like, Koplik spots, photophobia. Rash post-incubation. Pneumonia in 1/20, otitis media, acue encephalitis.
epi: outbreak every 3 winters pre-vaccine, needs large/concentrated population for continuous transmission. 5-25% mortality rate in developing countries, can become SSPE in ppl. with previous uncomplicated measles.
diagnosis: hemagglutination, multi-nucleated giant cells in lymph.
vaccine: MMR 2x live atten.
treatment: none
rubella
togavirus (not arbovirus though)
pathogenesis: spread via resp. aerosols; aka german measles. Local multiplication at respiratory epithelium–>viremia, less contagious than measles. 18d incubation period–>3 day exanthem (rash) w/ fever and lymphadenopathy. Shedding from RT +/- 1 week from rash. Sometimes subclinical, more severe in adults; can cause transient arthritis. Produces lifelong immunity. Congenital rubella syndrome: primary infection in mom during 1st trimester–> via placenta, causes congenital cataracts, heart defects, deafness, intellectual disability. Risk of abnormality decreases later in pregnancy. Fetus sheds virus during gestation/2 years in urine. Fetal IgM, neonatal IgG.
epi: Herd immunity from school children immunization protects non-immune pregnant women (individual immunity needs to last into child-bearing years). Vaccinate seronegative women before conceiving. CRS is major problem in developing countries.
vaccine: MMR (live attenuated)
EEEV
Togavirus
pathogenesis: direct transmission via blood (vector, mosquito). 7 day incubation period. Most deadly arbovirus encephalitis in US. 75% cases fatal, many subclinical. Mostly affects children.
epi: Focal outbreaks in summer at swampy/wetlands, mostly affects children and horses; both dead-end hosts. Virus maintained in nature by mosquito/bird cycle. Control outbreak w/ mosquito control.
No treatment.
Parvovirus B-19
Parvovirus
pathogenesis: airborne transmission (inhalation) or transplacental. 14d incubation. Asymptomatic or fever/malaise–>slapped cheek (erythema infectiosum, 5th disease, usually transient, caused by immune complex deposition in capillaries) and transient arthritis. Can have keratitis at eye. Tropism for erythrocyte precursors–>inhibits RBC production (transient aplastic crisis), which can be problem for RBC deficient/compromised pts (i.e. sickle cell anemia). IC/IS: prolonged anemia. Primary infection in mom at any point during pregnancy can cause fetal death, sometimes associated w/ hydrops fetalis (fetal edema).
Epi: 90% of adults are seropositive.
treatment: passive immunization of human gamma globulin for pts w/ prolonged anemia.
HPV
papovavirus
pathogenesis: transmitted via direct contact, sexual contact, or perinatal transfer. Causes benign papillomas (facial and genital); can progress to cervical carcinoma and head/neck cancer in 15-20 years. Infects epithelial cells of skin and MM–>benign outgrowth of wart, sometimes dysplasia. Condylomas=most common urogenital manifestation; 16 & 18 are highest risk serotypes. Oncogenes E6 and E7 for transformation (inactivate p53 and Rb).
epi: Most common STD. >60 serotypes, 1/3 of college women have in cervix, 80-90% of cervical carcinoma have integrated HPV genome. Cofactors like smoking can increase CC risk.
diagnosis: appearance, PAP smear, PCR.
vaccine: gardasil prevents against 16, 18, 6, 11.
treatment: Imiquimod topical cream, works against TLR7 and IFNa.
Adenovirus
adenovirus
not associated w/ tumors in humans but can in other species. Keratoconjunctivitis (pink eye) and infant gastroenteritis/diarrhea.
HSV-1
herpes virus
pathogenesis: transmit via saliva and lesion fluid. infection ascends nerve to sensory ganglia & remains latent; reactivates/takes neural p’way to skin. 1-2wk incubation, 1st infection typically subclinical (bilateral if symptoms). Reactivation: increased viral replication, virions cause cold sores (vesicular lesions, shed); cell mediated immunity leads to symptoms/resolves infxn. Most common cause of non-epidemic encephalitis (high mortality, neuro sequelae. S/s high fever, confusion, lymphocytes in CSF, unilateral lesions in temporal lobes.) Can cause ocular disease (keratoconjunctivitis, can cause permanent damage). Most comm
epi: Kids, HC workers and IS are most vulnerable; 80% seroprevalence in adults.
diagnosis: diagnose w/ PCR.
vaccine: none.
treatment: acyclovir, penciclovir, AA. Triflurodine for keratitis.
VZV
herpes virus
pathogenesis: aerosol/lesion spread. 2-3wk incubation, multiplies in respiratory tract w/ viremia. S/s: prodromal fever and malaise–>rash (small, itchy, diff. stage spots). Congenital varicella syndrome if mom has 1st-2nd trimester infxn–> affected limb atrophy/scarring. Latent in DRG. Lifelong immunity to varicella but can reactivate as zoster/shingles: unilateral dermatomal lesions and pain that can persist as post-herpetic neuralgia. Zoster risk increases after 50 b/c declining cell-mediated immunity. IS patients have risk of disseminated zoster due to spread via viremia.
epi: Winter/spring epidemics every few years. Common in 4-10 yo non-vaccinated. Can survive in small populations.
diagnosis: clinical or by IgM.
vaccine: live attenuated, routine peds use, needs booster. Result is declining WT virus, no natural boosting of latent infected ppl- possible reactivation risk. Zostavax for older ppl (decrease risk of zoster)
treatment: usually palliative, passive IgG from donors for IC; acyclovir.
Cytomegalovirus
herpes virus
pathogenesis: transmission via close contact, excrete in nasopharyngeal fluid, semen, urine, vaginal secretions. Large infected cells w. nuclear inclusion bodies (owl’s eye). Usually asymptomatic if healthy, can cause recurrent pneumonia, retinitis, or mono-nucleosis-like infxn. Latent in leukocytes, evades immune response. Most common cause of congenital abnormality if mom has primary infxn during 1st trimester (placental transfer). S/s: microcephalic intellectual disability, intracerebral calcification, neuro-sensory deafness, jaundice, spleno/hepatomegaly, anemia. Infant makes anti-CMV IgM.
epi: 40% chance of breastmilk transmission; problem in organ transplants.
diagnosis: owls eye inclusion bodies.
vaccine: experimental live vaccine.
treatment: congenital–>treat w/ ganciclovir or foscarnet. Vitravene for ocular use.
EB Virus
herpesvirus
pathogenesis: spread via saliva. 4-6wk incubation, often asymptomatic. Transforms B cells (active division). major cause of infectious mononucleosis, s/s: fever, sore throat, lymphadenopathy. Blood contains high CD8 to combat infect B cells. Associated w/ Burkitt’s lymphoma: transformed B cells dont require integration of viral genes; proliferate at germinal centers. Overexpress c-myc oncogen. Tumor when T cell responsive is insufficient. Multifocal malignant B-cell lymphomas @jaw/abdomen, starry cell appearance.
Also nasopharyngeal carcinoma (Asia), 30% of hodgkin’s lymphoma, 50% of lymphoma in immunosuppressed, and oral hairy leucoplakia in IC (i.e. AIDS pts). Post-transplant disease.
epi: >90% seropositivity. Malaria/ cofactor/immunosuppression/HIV =higher risk. Burkitt’s lymphoma: equatorial African kids (esp boys), rainfall and hot temps.
diagnosis: detect short-term increase in heterophile Ab (induced by EB virus antigen, x-reactive w/ sheep RBC).
vaccine: none.
treatment: none.
JC virus
papovavirus
pathogenesis: slow virus, years-long incubation–>death, have genetic predisposition, re-emerge from latency during immune suppression. Becomes progressive multifocal leukoencephalopathy (demyelinating), leading to blindness, dementia, coma and death.
epi: immunocompromised at risk for reactivation.
SSPE
paramyxovirus (measles)
pathogenesis: 4-17y delayed intellectual deterioration, psych disturbances, paralysis and blindness.
diagnosis: inclusion bodies, high Ab titers for measles, viral antigen in CNS.
vaccine:
treatment:
CJD/variant CJD
PrP (prion, infectious protein)
pathogenesis: spongiform encephalopathies affecting CNS, slowly fatal.
CJD: most common, transmitted to primates, spontaneous mutation; some iatrogenic from corneal transplant.
Variant CJD: related to bovine spongiform encephalopathy.
HTLV-1
oncovirus (retrovirus), no oncogene. Closely related to HTLV-2.
pathogenesis: spread via sexual contact, blood, breast milk (horizontal transmission). viral Tax protein (TF) induces IL-2 and receptor for autocrine transformation loop. Usually asymptomatic, 0.1% develop ATL (adult T-cell leukemia) after 10-30yr latency.
epi: Endemic in S. Japan, central Africa and Caribbean.
