bunya Flashcards

1
Q

What’s unique about bunyaviridae envelopes?

A

there’s no matrix protein

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2
Q

describe bunyaviridae genomes

A

SEGMENTED, negative sense, ssRNA

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3
Q

bunyaviridae are generally ______ for vertebrate cells

A

cytocidal

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4
Q

what are the four genera of bunyaviridae?

A

arthropod borne:-orthobunyavirus; akabane-phlebovirus; rift valley fever-nairovirus; Nairobi sheep virusnon-arthropod borne:-hantavirus; Hantaan

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5
Q

etiology of Rift Valley Fever virus?

A

phlebovirus, family bunvyaviridae

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6
Q

hosts of Rift Valley Fever?

A

sheep cattle and goatscan infect humans as well

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7
Q

how does rift valley infect humans?

A

percutaneous or aerosol exposure while slaughtering or handling infected fetusAedes mosquito bitesNO HUMAN TO HUMAN TRANSMISSION

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8
Q

rift valley fever occurs throughout _________

A

most of africa

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9
Q

main vectors of rift valley fever?

A

mosquitos(biological):Primary - Aedes sppSecondary - Culex spp, and Anopheles sppbiting flies(mechanical) - culicoides

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10
Q

describe the epizootic-endemic cycle of rift valley fever

A

-flooding of dambos (increased rain)-massive emergence of transovarially infected Aedes –> feed on livestock –> abortion storms(epizootic) –> culex/anopheles infections –> human infections (epidemic)details: The virus is transmitted transovarially (thorugh egg) among floodwater Aedesspp. mosquitoes.  The virus survives for very long periods in mosquito eggs laid at the edges of usually dry depressions, called “dambos”. When the rains come and the dambos flood, the eggs hatch, and infected mosquitoes emerge and infect nearby wild and domestic animals.  These Aedesmosquitoes become very numerous after heavy rains, and infect sheep and cattle.  Large number of these infected sheep and cattle become viremic, allowing many more mosquitoes (inducing secondary mosquito vectors) to become infected.  This amplification, together with mechanical transmission by biting flies, results in infection and disease in a very high proportion of animals and humans at risk

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11
Q

describe the pathogenesis of rift valley fever

A

 Rift Valley fever virus replicates rapidly and reaches very high titer in target tissues.  Virus replicates in liver and other major organs, resulting in widespread cell necrosis.  Extensive hepatocellular necrosis is common in terminally affected sheep.  Encephalitis, hemorrhages in GI tract and enlarged spleen.  Hepatic necrosis, renal failure, and shock, sometimes with hemorrhagic complications, are the primary causes of death.  About 90-100% of pregnant animals abort

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12
Q

clinical signs of rift valley fever?

A

 Sheep:  Mortality in young lambs is high (90%–100%) Young animals surviving the hepatic infection may show encephalomyelitis.  90-100% of pregnant ewes abort.  Cattle:  Less severe than sheep. However, 90-100% of infected pregnant cows abort

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13
Q

rift valley fever Dx?

A

RVF should be suspected when abnormally heavy rains and flooding are followed by widespread occurrence of abortions and mortality among newborn animals characterized by necrotic hepatitis, concurrent with influenza-like disease in people handling animals or their products

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14
Q

rift valley fever control?

A

 Control is based primarily on livestock vaccination, but vector control (via use of mosquito larvicides and insecticides) is also used during outbreaks.  Attenuated-virus Rift Valley fever vaccines produced in mouse brain and in embryonated eggs are effective and inexpensive for use in sheep, but they cause abortions in pregnant ewes.  Inactivated-virus vaccines produced in cell cultures avoid the problem of abortion, but are expensive

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15
Q

Akabane is a ________-transmitted virus that causes ___________________ in ruminants

A

insect; congenital abnormalities of the CNS

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16
Q

what is the etiology/host of akabane?

A

orthobunyaviridae, of family bunyaviridaecongenital dz of cattle, sheep, goats

17
Q

transmission of akabane?

A

Akabane virus is transmitted by biting midges (gnats) of genus Culicoides, as well as by mosquitoes (Aedes and Culex spp)

18
Q

pathogenesis of Akabane in a pregnant animal?

A

 After the bite of an infected mosquito, the virus infects the pregnant ruminant (cow, goat, or sheep). Virus reaches the fetus from the maternal circulation.  The most severe fetal lesions in cattle result from infection at 3–4 months of gestation, and earlier in sheep and goats, when the central nervous system is developing.  Fetal infection results in both encephalomyelitis and polymyositis.  Virus infection of CNS causes destruction of the developing brain and subsequent hydranencephaly.  Arthrogryposis, the other highly characteristic manifestation of fetal infection with Akabane virus, is characterized by muscular atrophy and the abnormal fixation of several limbs

19
Q

4 main conditions to associate with Akabane?

A

polymyositis, hydranencephaly, arthrogryposis, encephalomyelitis

20
Q

clinical signs of akabane?

A

No clinical signs in adults and young animals.  Infection of pregnant cattle or sheep can lead to one of two outcomes:  death of the fetus and abortion,  or birth, sometimes premature, of progeny with congenital defects.  Affected fetuses characteristically have:  Hydranencephaly  Arthrogryposis

21
Q

diagnosis of akabane?

A

 Detection of a specific neutralizing antibody in serum collected from aborted fetuses or from newborn calves, kids, or lambs before ingestion of colostrum.  Virus is difficult or impossible to isolate after calves, kids, or lambs are born, but can be isolated from placenta or aborted fetus

22
Q

control of akabane?

A

Akabane disease should be reported immediately to state or federal authorities upon diagnosis or suspicion of the disease.  An inactivated virus vaccine is available in Japan and Australia