Midterm 2: ENTO 210
175 Cards in this Set
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What is an emerging disease
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a disease that has appeared in a population for the first time, or that may have existed previously but is rapidly increasing in incidence or geographic range.
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what is a re-emerging or resurging disease
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have been around for decades or centuries but have come back in a different form, different intensity or a different location.
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Neglected tropical diseases have high prevalence among which population
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the rural poor; 1 billion people
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what type of diseases hit in high prevalence in the rural poor
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non emerging, ancient diseases. As well as chronic diseases that cause disability or disfigurement
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How prevalent are the diseases in the rural poor
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high disease burden, but low mortality. 530,000
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which are the two arboviruses
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hemorrhagic, and encephalitic viruses.
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how many animals viruses are suspected to be transmitted by arthropods
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501
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how many arthropod transmited animal viruses have been documented to cause illness in humans
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134
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with the exception of what two diseases are humans always the dead-end hosts
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Dengue and Yellow Fever
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To which family does the dengue virus belong to
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flaviviradae
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to what genus does dengue belong to
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flavivirus
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how many viruses does the family Flaviviridae include
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70
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of the 70 flaviviridae viruses, how many are mosquito borne
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40
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Besides dengue, what are other known flaviviruses
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West Nile, Japanese Encephalitis, and Yellow fever.
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how does serotype immunity work in dengue
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infection with one serotype produces immunity for remainder of life against that serotype; very limited cross-immunity: around 2 months to a year
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do all four dengue serotypes produce the same disease?
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yes
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What is the WHO definition of dengue hemorrhagic fever (1975)
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Fever (bladder problems, constant headaches, severe dizziness and loss of appetite), Hemorrhagic tendency, low platelet count, Evidence of plasma leakage.
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which mosquito species transmits dengue
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Aedes aegypti
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how long is the incubation of aedes aegypti
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3-14 days
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how long is the febrile period of aedes aegypti
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5-7 days
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how long is covalescence in aedes aegypti
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3 weeks
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what percent of dengue patients are asymptomatic
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50 percent
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what is the most common manifestation of dengue
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undifferentiated fever
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what are the symptoms of classic dengue fever
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fever, headache, muscle, and joint pain, nausea/ vomiting, rash.
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What are the symptoms of dengue shock syndrome (DSS)
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dangerously low blood pressure, patient goes into shock, death.
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what are some characteristics of aedes aegypti
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well adapted to contemporary urban life; tires, containers, cans, flowerpots, tree holes; nervous feeders, multiple hosts
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what is the primary preferred habitat of aedes aegypti adults
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homes where they can feed on human blood
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when and how was there an attempt to control Aedes aegypti
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In the Americas, 1970's with DDT
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Aedes albopictus transmits what 5 diseases
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dengue, yellow fever, eastern equine encephalitis, La Crosse virus, and West Nile virus.
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why is Aedes albopictus a preferred vector to Aedes aegypti
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it is a less efficient vector of dengue
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why is Aedes albopictus a less effective vector for dengue
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it is a more generalist feeder
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What is the transmission cycle of dengue
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dengue came from the forrest but is currently maintained in human populations; may still exist in jungled but plays no role in epidemics
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what vectors Yellow Fever
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aedes aegypti
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where did yellow fever originate
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africa
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when did yellow fever spread to the New World
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during the 14th adn 15th centuries via slave trade; though the freezing killed them , the migrating slaves reintroduced it
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how long is the intrinsic incubation period of yellow fever
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3-6 days
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what is the inapparent/ apparent ration in children for yellow fever
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1/2
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what is the inapparent/ apparent ratio in adults for yellow fever
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1/22
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what are the mild yellow fever symtoms
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fever, nausea, headache, slow heart rate. Nose bleeding in particular.
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what are some of the toxic phase symptoms for yellow fever
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liver damage with Jaundice, Internal bleeding with black vomit, seizures, bloody nose and gums, red eyes.
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What is the Sylvatic cycle
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mosquitoes to primates to mosquitoes in jungle
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what is the rural cycle
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primates to mosquitoes to humans in the rural tropics
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what is the urban cycle
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rural tropics, to suburban, to urban. Humans carry between cities, not mosquitoes.
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What cycle is yellow fever maintained in, or resivoired
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zylvatic cycle; by primates
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who brings yellow fever from the sylvatic to urban and rural cycles
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people entering the jungle
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where does the rural cycle tak eplace
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edge of forrest where more than just one species of mosquitoes is involved
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what species is primairly responsible for transmission in urban cycles
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aedes aegypti
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how is the american yellow fever cycle different than the african one
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there is no intermediate rural cycle, only sylvatic and urban. Humans take it between the two
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what percent of west nile is asymptomatic
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80 percent
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how many of the 20 percent symptomatic west nile patients develop severe symtpoms
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1/50
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what are the three types of west nile
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west nile encephalitis, west nile mninghitis, and west nile meningoencephalitis
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what is a bridge vector
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a vector repsonsible for transmitting disease from animals to humans; a generalist feeder
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what three species get west nile
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birds, humans, and horses; mosquitoe is the bridge vector
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what mosquitoes transmits west nile
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62 species; culex pipens (northern house mosquitoe) and culex quinquefasciatus (southern house mosquitoe) are the most ocmmon. (also c.salinarius, c. restauns, and c tarsalis)
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Where does eastern equine encephalitis happen
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easter usa in swampy regions; rural agricultural areas
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what is the inapparent to apparent ration of eee
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low; high proportion of infected horses and people become ill, but only 4-5 percent develope eee.
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whate are the symptoms of eee
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fever; chills, malais, myalgia arthralgia (muscle and joint pain)
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what is the fatality rate for acute necrotizing encephalitis
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33 percent
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where is acute necrotizing encephalitis prevalent
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children under 15 or adults over 50
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what are the causes of death of acute necrotizing encephalitis
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coma, death, stupor, convulsions, and myocarditis along with lung failure
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what species vectors eeev
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Aedes taeniorhyctus (and Ae. solicitans)
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what is the resivoir for eee
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birds
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what are the dead end hosts for eee
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game birds, horses, humans
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Where is weev found
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western, rural human populations
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what is the inapparent/apparent ration for weev
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high, mostly asymptomatic
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symptoms for weev
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mild; headache and fever
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percent of weev patients that get severe encephalitis
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13 percent
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symptoms of weev severe encehpalitis
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fever, drowsiness, nausea, confusion, coma, seizures
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what percent of weev is fatal
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3 percent of the 13 percent with severe sypmtoms
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what populations does weev kill and is there treatment
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children and elderly, only supportive treatment, no cure.
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slev was first recognized in what year
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1933 in snt lous
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what family of viruses is slev
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flaviviridae
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how many reported cases and deaths of slev were in st louis
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1095 cases, and 201 deaths
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where is slev found
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southern canada to argentina (america)
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how many slev cases have been reported since 64
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4651
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what is the resivoir host for slev
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birds
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what are the vectors for slev
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culex nigripalpus in california. culex tarsalis in midwest, culex pipiens everywhere else
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lacev is transmited by what mosquitoe species
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aedes triseriatus
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where does lacev occure
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wooded areas where resivoir hosts are found: rodents, chipmunks, squirrles
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what are lacev's resivoirs
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rodents, chipmunks, squirrels
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what are lacev's symptoms
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mild: fever; severe: coma, death (encephalitis)
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who is mostly affected by lacev
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children under 16
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what percent of lacev is fatal
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less than one percent of severe cases
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what family of viruses is lacev
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bunyaviridae
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how many neuroinvasive cases of lacev occure each year
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80-100
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jev is vectored by what
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culex species
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where is jev reservoired
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swine and wild birds
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when was the major epidemic of jev; how many cases
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1924 in japan, 6125 cases, half the fatalitites
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how many current cases of jev
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30-50k
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what are jev's symptoms
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Mild: fever and headache; acute: paralisis, seizures, coma, death
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who does jev affect
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children under 15
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mortality rate of jev
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30 percent of acute cases
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is there treatment for jev
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yes, a vaccine
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what family of viruses is jev
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flaviriridae
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what superfamily are filarial worms in
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filariodea
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what family are filarial worms in
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onchocericidae
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how many genre of filarial worms
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34
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which 4 filarial worms are of medical importance to humans
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wuchereia, brugia, onchocerca, and loa
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what causes lyphatic filiariasis
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wuchereri bancrofti, brugia malayi, and brugia timori
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what percent of cases of lymphatic filiariris are caused by brugia
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9 percent
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what vectors wucherei bancrofti
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culex, aedes anopheles; primairly culex quinquefaciatus
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wucheria bancrofti life cycle
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bite>lymphatic system>blood and lymph>mosquitoe>larva develop in mosqutioe>bite again (larvae enter, microphilaria leave)
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Lymphatic filariasis phase 1 involves what
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no symtoms, microfilaria in blood, people are resivoir
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lyphatic filiariasis pahse 2 involves what
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acute inflamatory lymphatic disease (adenolymphangitis); secondary bacterial infections, no microfilaria
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Lymphatic filariasis phase 3 involves what
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blockage of lymph channels; Chyluria (lymph in urine) Lymphoedema (big feet); hydrocoel (big balls)
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what blocks channes in elephantitis (LF)
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adult worms carcases
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is elephantitis fatal
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no
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what causes river blindness
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ochocera volvulus
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onchocera volvulus life cycle
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larva enter (fly bite)>subcutaneous>nodule forms>re-emerge on skin>leave as microfilaria to flies> larval cycles> back in host through bite
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what vectors ochocera volvulus (river blindness)
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family simuliidae, blackflie
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which species of black fly is of most importance for river blindness
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simulium damnosum (95 percent of transmission )
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what do simuliidae larva feed on
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organid debree in flowing water
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where do simuliddae live
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flowing water, sedentary in sumberged rocks and crabs
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What is the first stage of river blindness
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nodules (below waist in africa, above waist in america), caused by L3 larvae
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how long do onchoceriasis worms need to mature in skin
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1 year
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how long can onchoceriais worms live
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up to 15 years
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What is the second stage of river blindess
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microfilaria cause elastic fiber scaring, loss of pigmentation, itching, sleeplessnes.
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what are some results of onchoceriasis secondary symtoms
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social outcast, suicide, lizard skin, leopard skin
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Tertiary river blindess symptoms
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microfilariae reach the eyes, they damage the eye when they die in it; irreversable
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how many people suvver onchoceriasis blindness
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240k people
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where is river blindness found in
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older than 40, some adolescents
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Onchocera volvulus i west african savana
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common blindness
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onchocera volvulus in west africa forest
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rare blindness
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onchocera voluvulus in east africa
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skin problems, rare blindness
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are different strains of ochocera found in savana vs forrest
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yes
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why don't bednets and irs work on simmullidae control
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adults are daytime feeders
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what works best against sumullidae for control
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repellents; incectisiding rivers
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how many km of river were treated between 1986 and 1991
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50km
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how is river blindness treated
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Ivermectin (mectizan) (DEC too dangerous)
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what does Ivermectin (mectizan) do
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prevents adult females from producing microfialriae in one dose with few side effects
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what are the 2 medically important genre of trypanosomatidae
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trypanosoma and leismania
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what type of organisms are trypanosomatidae
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protozoans
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what is african trypanosomiasis
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sleeping sickness
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what is amercian trypanosomiases
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chagas disease
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what vectors trypanosoma
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tsetse fly (africa) kissing bug (america)
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what vectors leishmania
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sandflies
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trypanosoma brucei life cycle
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epimastigote>trypomastigone (in vector)> infects humans>lymph chanels and blood> trypomastigote>vector>epimastigoe
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uniqueness of tryanosoma bruci
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cyclodeveopmental in humans; develomental in vectors
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where are epimastigotes of trypanosoma found
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in vector
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where do trypomastigotes develop comletely
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humans
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what are the 3 subspecies of trypanosoma brucei
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T. brucei brucei (animals) T. brucei gambinse (wet africa, chronic sleeping sickness), and T. brucei rhodesiense (east africa, acute sleeping sickness)
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where is acute sleeping sickness found and what causes it
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East africa, T. brucei rhodesinse
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Where is chronic sleeping sickness found and what causes it
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West africa, T. brucei gambinse
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stage 1 chronic trypanosomiasis
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west africa, 5-15 days after bite, lesion forms
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stage 2 chronic trypanomiasis
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1-3 weeks after bite; periodic fever, fatigue, joint pain; lasts 3 months. Can Cause Organ Damage
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what is winterbom's sign
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lesions caused by trypanosomiasis (chronic)
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stage 3 chronic tripanosomiasis
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meningoencephalitic stage; takes several years to happen; agresivness, fatigue, coma, death.
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Acute trypanosomiasis
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caused by t. brucei rhodesinse; death in less than 12 months, not years.
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west vs east HAT
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forrest vs savana; gambiense vs rhodenise; chronic vs acute; slow vs fast death.
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tsetse fly family and genus
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glossinidae; glossina
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where are tse tse found
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south saharan africa
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2 glossina species
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g. mortistans, g. Palpalis
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glossina mortisans found in
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east africa woodland savanna, feeds on cattle
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glossina palpalis found in
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west africa rivers and forrest; feeds on humans
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how do tsetse flies reproduce
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single, 3rd instar larvae at a time; 8-10 days development.
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glosina control
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disease screeenings, killing wildlife and insectiside (east africa), TRAPS, sterilized insects (zanzibar)
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where were steralized tsetse released
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zanszibar
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where were kiling of wildlife used to control tsetse flie
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east afric
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what causes chagas disease
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trypanosoma cruzi
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what is T cruzi's life cycle
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epimastigote to trypomastigote in vector; trypomastigote to amastigote in humans
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what is the vector development of T cruzi
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picks up trypomastigote> epimastiote> trypomastigote again>back in human
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what is human development of T cruzi
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trypomastigote to amastigote back to trypomastigote and into vector
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where do amastigotes develop
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inside the muscle and nurao cells; they distroy them
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unique about T cruzi cycle
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cyclodevelopmental in humans
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where is T cruzi found
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latin american coasts
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Acute T chagas symptoms
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ring of romania (eye), mostly in children; fever, vomit, and diarhea; heart tissue scarring, 80 percent o fcardiac nerves lost
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how long before acute T chagas kills
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3-4 weeks in 5 percent of cases
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Chronic T chagas symptoms
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30 percent of acute survivors; after years of asymptomatic enfection (10-30 years); cns and pns; nerves contoling esophagus and colon destroyed: megacolon, megaesohpagus; death from crhonic heart failure
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what vectors t cruzi
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heteroptera>reduvvidae>triatominae
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what are the two highly domesticated species of triatominae
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triatoma infestans; trhodinus prolixus
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Triatomidae resivoirs
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opossums, rats, squirrels, skinks, iguanas, bats, birds
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infestans and R. prolixus resivoirs
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domestic: donkeys, cattle, horses, etc.DOGS and HUMANS
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Triatomidae control
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IRS, House plastering, bloodbank screening, prenatal screening
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1991 southern cone initiative
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chile argentina, boivia, brazil, paraguay, uruguay
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number of infected army recruites
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1.9, down from 10 percent in 65
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