Bunyaviridae Flashcards
What’s unique about bunyaviridae envelopes?
there’s no matrix protein
describe bunyaviridae genomes
SEGMENTED, negative sense, ssRNA
bunyaviridae are generally ______ for vertebrate cells
cytocidal
what are the four genera of bunyaviridae?
arthropod borne:
- orthobunyavirus; akabane
- phlebovirus; rift valley fever
- nairovirus; Nairobi sheep virus
non-arthropod borne:
-hantavirus; Hantaan
etiology of Rift Valley Fever virus?
phlebovirus, family bunvyaviridae
hosts of Rift Valley Fever?
sheep cattle and goats
can infect humans as well
how does rift valley infect humans?
percutaneous or aerosol exposure while slaughtering or handling infected fetus
Aedes mosquito bites
NO HUMAN TO HUMAN TRANSMISSION
rift valley fever occurs throughout _________
most of africa
main vectors of rift valley fever?
mosquitos(biological):
Primary - Aedes spp
Secondary - Culex spp, and Anopheles spp
biting flies(mechanical) - culicoides
describe the epizootic-endemic cycle of rift valley fever
- 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 Aedes
spp. 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
describe the pathogenesis of rift valley fever
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
clinical signs of rift valley fever?
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
rift valley fever Dx?
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
rift valley fever control?
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
Akabane is a ________-transmitted virus that causes ___________________ in ruminants
insect; congenital abnormalities of the CNS
what is the etiology/host of akabane?
orthobunyaviridae, of family bunyaviridae
congenital dz of cattle, sheep, goats
transmission of akabane?
Akabane virus is transmitted by biting midges (gnats) of genus Culicoides, as well as by mosquitoes (Aedes and Culex spp)
pathogenesis of Akabane in a pregnant animal?
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
4 main conditions to associate with Akabane?
polymyositis, hydranencephaly, arthrogryposis, encephalomyelitis
clinical signs of akabane?
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
diagnosis of akabane?
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
control of akabane?
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
tell me about the Schmallenberg
Etiology: Belongs to genus Orthobunyavirus
Host:Cattle, Sheep, Goats
Distribution: European countries
Transmission:Insect vector transmission, Culicoides spp
Clinical signs:
Malformed animals (Arthrogryposis/ Hydranencephaly) and stillbirths
Adults (cattle): Diarrhea, Abortion, reduced milk production
