Quiz 3: Set II Flashcards
Poliovirus
enterovirus (picornavirus)
epi: summer spike, children females, fecal oral spread w/ viremia. 0.1-1% paralytic rate in older groups. Rarely fatal.
pathogenesis: 2-3 week incubation, invades small intestine, multiplies in lymph node/tonsils, invades CNS via viremia, shed in feces from start. S/S: 99% of cases asymptomatic/subclinical (fever, stiff neck); paralytic can be spinal (attacks motor neurons, withered leg, foot, etc.) or bulbar (attacks respiratory centers)
vaccine: IPV (Salk): killed, stable, 3 serotypes, safe for all, no reversion or spread, needs boosters.
OPV (Sabin): live attenuated, labile, can spread/revert but causes viremia/better protection (sIgA)
treatment: passive->active immunization is best.
Coxsackie virus
enterovirus (picornavirus)
epi: seasonal spike, stable, rarely fatal, stable in environment (daycare problem), large titers shed in feces.
pathogenesis:
A: mucosal surface/skin rash, colds, herpangina (tongue and OP sores) hand foot/mouth, aseptic meningitis, paralytic disease.
B: viscerotropic: neonatal myocarditis, epidemic pleurodynia (devils grip), orchitis (balls)
diagnosis: isolation/cell culture, rising Ab titers, PCR for RNA in CSF.
no vaccine or therapy
Echovirus
enterovirus (picornavirus)
epi: fecal oral, stable in environment, problem in daycare, 32 serotypes.
pathogenesis: similar to polio. S/S: rash, leading cause of aseptic meningitis.
diagnosis: serum titration
no vaccine or treatment
Rhinovirus
enterovirus (picornavirus)
epi: >100 serotypes. airborne transmission; poor growth at body temperature and low pH. >80 antigenic types.
pathogenesis: similar to polio. Most common cause of colds.
diagnosis: trachea organ culture.
no vaccine/treatment
Hepatitis A
hepatovirus (picornavirus)
epi: 0.1% mortality; fecal-oral spread; poor sanitation, some sexual behavior (anal-oral). Epidemics at outdoor summer events with inadequate sanitation facilities; undercooked/raw shellfish contaminated w/ sewage; infected food handler; within family. Infection when older is more dangerous, low sanitation standard areas–>little overt disease because of passive->active - high seropositivity in DC’s.
pathogenesis: 30 day incubation, fecal excretion and viremia precede symptoms. Grows in liver cells. S/S: anorexia, nausea, fever, jaundice** and abnormal liver fxn like aspartate aminotransferase. Acute infection only, acute hepatitis from liver cell death.
diagnosis: liver function, serological (anti-HAV-IgG/M comparison)
vaccine: killed- passive immunity, given to all kids/travelers to endemic spots.
treatment: IM injection of IgG
Rotaviruses
Reovirus
epi: peaks in winter, endemic worldwide, death in poorest countries mostly children <2. Very infectious, fecal-oral, infects livestock. Difficult to control w/ standard hygiene.
pathogenesis: causes vomiting and diarrhea, most common diarrhea in infants, dehydration causes death.
vaccine: live attenuated Rotarix/RotaTeq, safe/effective.
treatment: rehydration therapy
Influenza viruses
orthomyxovirus
epi: P2P via droplets. A causes minor epidemics every 2-3, major/pandemic every 10-30 years. B causes minor epidemics every 3-6 years. Pandemics have high mortality due to antigenic shift (x-species genetic reassortment of HA, sometimes NA); minor epidemics from antigenic drift (minor variation in existing H-antigen RNA). Deaths mostly in young and elderly.
pathogenesis: infects upper and often lower RT, destroys ciliated epithelium but no viremia. Systemic symptoms from toxic site components. Can be secondary to bacterial pneumonia b/c of destroyed/nonfunctional macrophages (fatal=staph, common=pneumococcus). S/S: fever, chills, aches from cytokines.
diagnosis: virus isolation in embryonated eggs or tissue culture; HI assay to compare acute/convalescent sera; rapid fluorescent Ab w/ throat swab specimen
vaccine: killed trivalent 2A/B gets annual update but doesnt induce IgA efficiently. Quadravalent live attenuated intranasal effective in kids.
treatment:
neuraminidase inhibitors (tamiflu and relenza), need to admin early, decrease symptomatic period by 1-2 days.
adamantanes: older anti-flu have lots of ressitance but are effective against H1N1; inhibits uncoating/ attachment.
Parainfluenza viruses
paramyxovirus
epi: airborne, no major antigenic shifts; most common cause of croup; peak incidence @2 yo, no lifelong immunity.
pathogenesis: causes hemagglutination. S/S: fever, croup, severe LRI, dyspnea, stridor.
diagnose w/ hemagglutination assay
treatment: glucocorticoids for severe group.
Respiratory syncytial virus
paramyxovirus
epi: no major antigenic shifts, severe febrile LRI on initial infection.
pathogenesis: No hemagglutination, most frequent LRI cause in infants; cause of significant infection in elderly. S/S: fever, LRI.
treatment: aerosol ribovirin in high risk/severe patients; passive mAb immunization for high risk infants prevents severe pneumonia.
Measles virus
paramyxovirus
epi: local epidemics every 3rd winter prior to vaccine; needs large population to survive. Cell-mediated important for clearing. 5-25% mortality in developign countries, SSPE can result from uncomplicated infection <17 years prior and at early age. Long incubation period, most contagious disease known; almost never subclinical.
pathogenesis: systemic viremia, starts 3 days before symptoms. primary infection in RT, multiplies in nodes/epith/conjunctiva.
S/S: prodromal fever/ cold/ spots/ conjunctivitis and photophobia. Severe hemorrhagic rash in fatal cases. Encephalitis, pneumonia, otitis media. Lifelong immunity from infection; IgG neutralizes.
diagnosis: hemagglutination, multi-nucleated giant cells in lymph from viral-induced fusion. Inclusion bodies seen in SSPE, high Ab titers.
vaccine: live attenuated MMR, given 2x.
treatment: vitamin A reduces mortality, not antiviral.
Mumps virus
paramyxovirus
epi: airborne. 30% infections are subclinical, no
pathogenesis: primary infection of respiratory epithelium/nodes; grows in parotid gland, excreted in saliva. S/S: prodromal fever/malaise followed by swelling of parotids. Can cause orchitis, aseptic meningitis.
diagnosis: hemagglutination
vaccine: MMR (live attenuated)
SARS-associated coronavirus
coronavirus
epi: 2-10 day incubation. airborne spread; causes SARS–severity increases with age; case-fatality 9%. Worldwide spread stopped w/ quarantine.
pathogenesis: LRI. S/S: dry cough, dyspnea, secondary pneumonia is common.
Adenoviruses
adenoviruses (DNA virus)
epi: diseases include pink eye and enteric adenoviruses. Fecal-oral or aerosol.
pathogenesis: severe respiratory diseases, epidemic keratoconjunctivitis (pink eye, can directly infect); enteric: gastroenteritis in infants, diarrhea. 3-10 day incubation. Persists in adenoids/tonsils. 51 serotypes.
Hepatitis B
hepadnavirus
epi: parenteral blood transfer (high incidence in IV drug users), sexual transmission (unsafe MSM), perinatal infection of neonates (90%). Rarely becomes chronic disease; cause primary liver carcinoma. Responsible for 500k cancer deaths annually. HBeAg corresponds w/ infectious virions and progression to hepatic carcinoma in chronically infected patients.
pathogenesis: 70 day incubation, insidious onset. CD8 recognize HBV pepties on MHC I and kill hepatocytes; tumors have integrated HepB DNA. S/S: anorexia, nausea, fever, jaundice, prodromal rash/arthritis.
diagnosis: Test for HBsAg (surface antigen), HBcAg (core); PCR.
vaccine: subunit right after birth
treatment: Alpha-IFN for chronic infection or Iamivudine (RT inhibitor). passive anti-HBV Abs for neonates of infected mothers.
Hepatitis C
Hepacivirus (flavivirus)
epi: STD, needle-sharing, blood transfusion, perinatal infection. Can become hepatocellular carcinoma. 75% chronically infected; 20% develop cirrhosis or carcinoma >10 years post-infection.
pathogenesis: long incubation (60 days). CD8 kill hepatocytes when recognize HCV peptides on MHC I, no integration into genome. S/S: anorexia, nausea, fever, jaundice, prodromal rash/arthritis.
diagnosis: serological test and PCR
vaccine: none
treatment: IFN and iravirin; telaprevir and boceprevir inhibit essential HCV protease.
