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VIROLOGY FINAL > Flaviviridae > Flashcards

Flaviviridae Flashcards

1
Q

what genera of flaviviridae are important for veterinarians?

A

pestivirus, and to a lesser extent pegivirus

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2
Q

what are some conditions caused by flaviviruses?

A

pesti - bovine viral diarrhea, classical swine fever(hog cholera)

pegi -some horse stuff (theiler’s dz) and some primate/rodent/bat stuff

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3
Q

flaviviridae replication occurs in __________

A

the cytoplasm.

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4
Q

flaviviridae have what kind of RNA?

A

linear, positive sense ssRNA

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5
Q

what are the biotypes of bovine viral diarrhea virus?

A
  • non-cytopathogenic (ncp)

- cytopathogenic(cp)

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6
Q

what is the main difference between ncp and cp BVDV? (think protein)

A
  • ncp has uncleaved NS2-3 protein; does not induce apoptosis

- cp has non-structural protein NS3, from cleaving NS2-3; induces apoptosis

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7
Q

how does cp BVDV arise?

A

mutation of ncp BVDV in persistent infected calves

insertion of sequences into NS2-3 gene into the BVDV genome, leading to an additional protease cleavage site in the viral polyprotein–> cleavage of NS2-3 –> release of NS3

also point mutations

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8
Q

which of the two BVDV types is most common? What does it cause?

A

NCP- leads to congenital, reproductive, enteric disorders

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9
Q

how is ncp BVDV transmitted?

A

cross placenta –> invade fetus –> PI calves

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10
Q

what does cp BVDV lead to?

A

mucosal dz, in cattle persistently infected with ncp biotype

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11
Q

apoptosis is associated with what BVDV biotype?

A

cp (NS3 protein)

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12
Q

what are the two genotypes of BVDV? which is more common? which produces cp and ncp?

A

BVDV-1 and 2.
1 is more frequently detected.
Both produce cp and ncp biotypes

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13
Q

what usually occurs with BVDV infection of a non-pregnant adult cow?

A

mild infection, scours, milk production drop, reduced WBCs

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14
Q

what things happen with BVDV infection in a pregnant cow, depending on how far along the pregnancy is when infected?

A
  • early (1 mo.); embryo death
  • month 2-4; PI calves
  • month 5-9… abortion(middle), deformities, or normal calves(late)
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15
Q

describe how a PI calf (BVDV) comes to be, and what the two possible outcomes are.

A

cow is infected with ncp BVDV 40-120 days into gestation, transplacental infection, fetus does not recognize as foreign. immunotolerant calf (PI) born. decreased weight gain, chronic ill thrift, and continuous shedding of virus.

1) PI calf survives and sheds. develops Ab to heterologous cp and ncp virus. OR
2) superinfected with cp virus which is antigenically homologous to the persistent ncp strain and/or the ncp strain mutates to cp… results in mucosal dz

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16
Q

why are PI calves so significant in BVDV?

A

because they are the primary source of the virus

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17
Q

what are the outcomes of BVDV in immunocompetent, non-pregnant cattle?

A
  • subclinical dz, diarrhea in calves (<6 wk), peracute bvdv diarrhea
  • thrombocytopenia and hemorrhagic syndrome (adults and veal calves)
  • immunosuppression
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18
Q

outcomes of BVDV in immunocompetent, pregnant cattle?

A
  • conception failure, embryonic mortality, abortion, fetal mummification, stillbirths
  • congenital defects in birthed calves
  • stunted, weak calves
  • PI calves
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19
Q

what are some of the congenital defects that BVDV results in?

A
  • cerebellar hypoplasia
  • stargazing
  • hydranencephaly, porencephaly
  • arthrogryposis (stiff joints)
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20
Q

clinical signs/lesions of acute mucosal dz?

A
  • severe diarrhea, runny nose, dull coat
  • ulcerated nose and mouth, ulcerations in gum, dental pad, tongue
  • esophageal erosions, rumen ulceration, hemorrhage in abomasum
  • intestine mucosal and peyer’s patch necrosis, SI hemorrhages
  • some animals have ulceration of hoof coronary band
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21
Q

clinical signs of chronic mucosal dz?

A

-diarrhea, inappetence, emaciation, rough hair, bloat

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22
Q

what is the etiology of CSF (classical swine fever aka hog cholera)

A

pestivirus, of the family flaviviridae

antigenically related to BVDV

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23
Q

how do you distinguish between classical swine fever and African swine fever?

A

clinically indistinguishable

24
Q

how many antigenic variants of CSF are there, and who are the hosts?

A

one variant, infects pigs (domestic and wild)

25
Q

how does OIE classify classical swine fever?

A

List A disease

26
Q

t/f - hog cholera is endemic in the US

A

false; it has been eradicated from the US

27
Q

where is hog cholera endemic?

A

most countries of South America, and far East Asia, except Japan and Korea.

28
Q

main modes of transmission of CSF virus?

A
  • direct contact, fecal oral, aerosol
  • fomites
  • veterinarians and farm workers
  • feeding scraps containing uncooked, infected pig meat
29
Q

Infected pigs shed CSF virus in the ____________

A

feces, urine, saliva, nasal discharge

30
Q

t/f - CSF virus is sensitive to freezing

A

false

virus lasts for years in frozen infected meat

31
Q

in CSF, early immunosuppression leads to the reduction of these cells

A

CD1, CD4, and CD8 thymocytes

32
Q

CSF results in a ______-lymphocyte deficiency due to destruction of __________

A

B

germinal centers of lymphoid tissues

33
Q

in CSF pathogenesis, what cytokine affects lymph nodes? what is the result?

A

infected lnn. see the release of TNF-alpha, resulting in lymphocyte apoptosis

34
Q

how do macrophages play a role in CSF pathogenesis?

A

activation of macrophages leads to inflammatory cytokine release

35
Q

how does CSF affect the vasculature?

A

degeneration of vascular epithelium; thrombosis and hemorrhages

36
Q

what are some important clinical signs and lesions of acute and per acute CSF?

A
  • cyanosis of ears
  • blotchy, purplish discoloration of skin
  • diarrhea
  • hemorrhage in urinary bladder
  • “turkey egg” kidneys; spotty
37
Q

what is associated with the reproductive form of CSF?

A

abortion, stillbirth, mummified fetus

38
Q

what nervous sign is seen with CSF?

A

goose stepping gait

39
Q

what is necessary for control of CSF?

A

quarantine farms, slaughter and proper carcass disposal(incineration)

40
Q

what is the number one easiest and important thing to do to avoid CSF spread?

A

avoid feeding uncooked meat products or garbage to pigs

41
Q

what is the etiology of West Nile Virus? WNV

A

genus flavivirus, family flaviviridae

42
Q

where is WNV considered endemic?

A

Africa, Asia, Australia, Middle East, Europe, USA

43
Q

describe the WNV transmission cycle

A

mosquito takes blood meal from infected bird(reservoir) –> virus replicates in mosquito –> mosquito bites human or horse, transmitting virus

44
Q

what are the modes of transmission of WNV from human to human?

A
  • transfusion
  • organ transplant
  • intrauterine exposure
  • breast feeding
  • lab accidents
45
Q

what are the lineages of WNV, which ones are implicated in human dz, and what is the most commonly distributed in human dz?

A

At least 7 lineages.
1 & 2 are implicated in human dz.
sublineage 1a is the most widely distributed.

46
Q

What are the clinical forms of WNV in humans?

A
  • West nile neuroinvasive dz (WNND)
  • west nile virus encephalitis (WNE)
  • west nile meningitis (WNM)
  • west nile meningoencephalitis
  • west nile poliomyelitis (WNP)
  • cutaneous manifestations (rashes)
  • non-neuro complications (myocarditis, hepatitis, nephritis)
  • West nile fever (flu-like symptoms)
47
Q

t/f - very few cases of WNV in humans are asymptomatic.

A

False

a high number of cases are either asymptomatic, or fail to attract medical attention due to mild symptoms.

48
Q

WNV clinical signs in horses?

A

mostly asymptomatic
~8% develop neuro signs
encephalomyelitis with ataxia are the primary clinical signs

49
Q

what is Louping Ill?

A

tick-borne, zoonotic, viral dz important in sheep and red grouse.

50
Q

what is the etiology of louping ill?

A

genus flavivirus, family flaviviridae

51
Q

there are at least _____ subtypes of louping ill

A

4

52
Q

where is Louping Ill distributed, and what is the primary vector?

A

the british isles, mainly the upland areas of Scotland, Ireland, northern England and Wales.

Ixodes ricinus tick

53
Q

describe Louping ill transmission cycle

A

tick larvae/nymphs take blood meal from viremic host –> nymph or adult female bites uninfected sheep

no evidence for transovarial spread into tick eggs

54
Q

louping ill clinical disease is associated with replication of virus in _____, severe inflammation of _____, and necrosis of ____________.

A

brain; CNS; brainstem and ventral horn neurons

55
Q

clinical signs of louping ill?

A

Affected animals stand apart, exhibit ataxia, muscle tremors, incoordination of hind limbs, jerky, stiff movements and a bounding gait (Hence the name Louping Ill, where loup (as in Scottish) or leaping is observed in extreme cases)

56
Q

is louping ill zoonotic?

A

YESSSSSSS

VIROLOGY FINAL (18 decks)

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