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29 Cards in this Set

  • Front
  • Back
where do arboviruses replicate?
in the vector
what are the 5 families that have arbovirus?
toga (genus alpha, not rubi), flavi (genera flavi and pesti and not hepaci), bunya (genera bunya, phlebo, and nairo but not hantavirus), rhabdo and reo
describe the virion structure of flavi? Toga? Bunya?
env, matrix, icos, no packaged enzymes. Enveloped, matrix, icos, no packaged enzymes. Enveloped, no matrix, variable nucleocapsid structure, has RNA dependent RNA pol.
describe the genomes of flavi, toga, and bunya.
flavi is +ssRNA of 1 molecule, toga is +ssRNA of 1 mol, bunya is ambisense or -ssRNA with 3 molecules
describe the replication of flavi, toga, and bunya.
positive rep strategy, 1st step is tsln to polyprotein, no subgenomic RNAs. Pos ssRNA, 1st step is tsln of the 5' 2/3rds of the genome into polyprotein, has subgenomic RNAs. Negative/ambisense RNA, 1st step is txn of pos sense copy of genome, has subgenomic RNAs and has packaged viral enzymes.
factors influencing epizootic/epidemic outbreaks?
abundance of enzootic and epizootic vectors, competence of enzootic and epizootic vectors, abundance of vertebrate reservoir host, the viral genome, and human behavior
commonalities of arboviruses?
SQ inoculation of virus by vector, humans usually dead end host except dengue and yellow fever. Most are asymptomatic, most symptomatic infections are mild and flulike and biphasic, early is flu like. Later you see other stuff like rash, myositis, and enceph in some viruses. Severity of disease is usually age dependent
for every person that is infected with an arbovirus and is symptomatic, how many are infected with no symptoms?
10s to 1000s, low attack rate
what will make arbovirus infections symptomatic and are most infections symptomatic?
viral dose and human genetics/immune response. Most infections are not symptomatic, there is a very low attack rate
describe st. louis encephalitis virus.
flavivirus, avian reservoir, mosquitoe virus, OH-MS valley, seroprevalence is anout 6% in urban in SE US, attack rates in epidemic attack is less than 1 in 100, 7% fatality in symptomatic ppl age related, 1 in 800 are symptomatic (85:1 in elderly)
describe west nile in the old world.
flaviviurs, avian reservoir, mosq vector, hyperendemic in Africa and mid east meaning most ppl have Ab to WNV, no epidemics bc most are protected, when endemic immunity wanes infection rate goes up, most symptomatic infections go unrecognized bc it is mild febrile illness, can have 60% epidemic attack rates in low immunity areas, CNS infection is RARE
describe WNV in new world
enzootic transmission cycles in birds and mosquitoes, abrupt onset of febrile illness (fever, headache, neck stiffness, vomiting and rash in 50%), progresses to neuro signs (enceph) depressed consciousness, etc, different than old world infections, case fatality is 20 to 30%, note most do not get enceph
describe eastern and western equine enceph.
togavirus, genus alpha virus, avian reservoir, mosq vector, periodic epizootic/epidemic in humans, horses, emus, turkeys. Highest rate of enceph, seizures and sequelae in children. WEE is about 34 cases/yr in ppl, 10% mortality, case to infection ratio 1:50 in children under 5 and 1:1000 in adults, sequelae in ~5% of survivors. EEE average of 7 human cases/yr, ~30 to 70% case fatality rate, case to infection ratio is 1:8 for kids under 10, 1:23 in adults, 35% to 80% have neuro seuquelae
describe the arboviral hemorrhagic fever clinical manifestations
potentially lethal and characterized by flu like sxs, vomiting, mucosal and GI bleeding, edema, hypotension. Begins with flushing, conjunctival injection and petechial hemorrhage. Progresses to frank mucosal hemorrhage, hypotension, shock circulatory collapse. DIC is disseminated intravascular coagulation or death is coming. associated with multisystem organ failure.
describe yellow fever history
flavi first reported in new world and europe in 1600's, outbreaks in port cities until 1900's, last US outbreak in NO in 1905, first filterable human pathogen, causative agent isolated in 1928, first live attenuated virus vaccine,
describe yellow fever epidemiology.
monkeys are reservoir hosts, vector is mosqs, sub saharan africa and south america, endemic from mosq bite from monkey in the forest causes about 200K per year, ~30 to 1000 epidemic cases a year when it goes human to human, range of YFV is expanding, re emergence of vector in SE US
describe yellow fever clinical manifestations.
biphasic, 1st is flu like, then 24 hr remissiom, sx return and worsen. Hepatic induced coagulopathy and hemorrhagic manifestations: black vomit and bloody diarrhea (hematemesis), epistaxis (nasal bleed) and gum bleeding, petechial, ecchymotic or purpuric hemorrhage. systemic manifestations including deepening jaundice and albuminuria: early appearance of jaundice (day 3) has poor prognosis, transaminase elevations reflect degree of hepatic injury. inlate stages get hypotension, shock, metabolic acidosis, acute tubular necrosis, myocardial dysfunction and arrhythmia. late CNS manifestations are confusion, seizure and coma. death in usually 7 to 10 days
describe the epidemiology of rift valley fever virus
bunyavirus genus phlebovirus, subsaharan and north africa, threatens to go to Asia and Europe, affects livestock, epizootic outbreaks in years of heavy rainfall, signalled by abortion storm amongst livestock, during epizzootic pd. Humans can be infected by bite from mosq, contact with blood or body fluids from infected animals, and inhalation of aerosolized virus
describe crimean congo hemorrhagic fever epidemiology.
rodents are reservoir, vectors are ticks, primarily zoonotic, endemic in africa, eastern europe, and asia, severe disease with high mortality rate, during epizootic outbreaks humans can get infected with bite of tick or contact with blood, infected fluid, usually seen in slaughterhouse workers, etc
arboviral hemorrhagivc fever differentials?
place of residence and/or exposure, prior exposure/infection, occurrence and serodiagnosis of similar cases in the community, specefic sxs are typically not diagnosis. Differentials are flu, rubella, rubeola, malaria, scrub typhus, leptospirosis and other arboviral infections causing fever and rash
describe the one vaccine that can be used for a disease in these lectures.
yellow fever 17D vaccine, first live attenuated virus vaccine, one of the safest and most efficacious viral vaccines available, grown in eggs and safety tested in monkeys, 13 million made annually but 11 million used in Brazil… recommended for ppl to traveling endemic areas, contraindicated in pregnant women, infants under 6 mo, and immunosuppressed
describe old world hantavirus.
discovered in korean war, causes hemorrhagic fever with renal syndrome, mice are reservoir hosts,
describe new world hantavirus.
hantavirus pulmonary syndrome (id-ed in SW US in 1993), flu like sxs then more severe respiratory disease (bilateral infiltrates, resp failure, shock and death 2 - 10 days after onset of illness in 50 to 80% of cases) wi 2 wks, newly id-ed hantavirus, sin nombre shown to cause disease, reservoir host and vector is deer mouse, throughout the new world and caused by 10+ different hantaviruses each with different rodent hosts
describe the epidemiology of the sin nombre virus.
responsible for most HPS cases in NA, deer mice t/o western and central US and Canada, most cases in SW US but seen in other states, rare infection, only <1% seroprevalence in endemic areas,
describe the clinical manifestations of hemorrhagic fever with renal syndrome.
2 to 3 wk incubation after hantaan or dobrava virus infection, sudden onset of fever then flushing, edema and lower back pain, increased vascular permeability, hypotensive phase follows with thrombocytopenia and petechial hemorrhage, low grade DIC and shock. oliguria may occur and renal failure accounts for about 50% of fatalaties, mortality rate of 5 to 15%, survivors have phae of diuresis, lasting several months, milder disease seen in seoul and puumula virus types
describe the clinical manifestations of hantavirus pulmonary syndrome.
2 to 3 wk incubation period after sin nombre virus infection, sudden onset of flu like sxs for 4 days, then pulmonary edema, dyspnea, and hypoxemia. See tachypnea, tachycardia, hypotension and crackles or rales on lung exam. Bilateral infiltrates on CXR. infection damages lung microvascular endothelial cells, increased permeability and fluid leakage into lungs. rapid deterioration - throbocytopenia, DIC, hypotension and shock. Death in 50% of cases within 1 to 3 days of hospital admission. Recovery remarkably rapid - lung lesions and shock resolve in 3 to 6 days.
describe filovirus epidemiology.
probably zoonotic, transmitted to humans from host. Reservoir hosts are unidentified. Not known how virus transmitted from natural reservoir to us. Person to person is via close contact with individual or body fluids. Epidemics wane when infected individuals quarantined, can have aerosol transmission for ebola reston but this is not a pathogenic strain
describe the regions where ebola is found.
DRC, gabon, sudan, ivory coast, and uganda, basically around the african rainforest
describe filovirus pathogenesis.
most severe hemorrhagic fevers known, 4 to 10 day incubation then flu like sxs, subsequent signs and sxs include multisystem involvement and: systemic manifestations, GI issues, respiratory manifestations, vascular manifestations (conjunctival injection, hypotension, edema), and neurologic manifestations (headache, confusion, coma)