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