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Taylor Viro Final > picorna > Flashcards

picorna Flashcards

1
Q

What’s the structure of picornaviridae? how do they look in electron micrographs?

A

Spherical, non-enveloped, icosahedral, ~30nm diameter.They look smooth and round in elctron micrographs.

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2
Q

What kind of genome do picornaviridae have?

A

single molecules of linear, positive sense, ssRNA, 7-8.8kb in size

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3
Q

T/F picornaviridae RNA is non-infectious

A

falsegenomic RNA is infectious

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4
Q

what is VPg?

A

it is a protein linked covalently to the 5’ end of picornaviridae RNA

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5
Q

T/F picornaviridae replicate in the nucleus

A

false. picornaviridae replicate in the cytoplasm

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6
Q

picornaviridae RNA acts as mRNA, which is translated into ____________

A

a polyprotein. this polyprotein is cleaved to yield 11 or 12 individual proteins.

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7
Q

what is characteristic of picornaviridae pathogenesis?

A

most of them cause rapid cell death with characteristic CPE (cytopathic effects)

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8
Q

how many genera of picornaviridae are there, and what’s an important difference between them?

A

there are 29, and a big difference is their stabilities at low pH

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9
Q

What is the etiology of Foot-and-Mouth Disease? (FMD)

A

Aphthovirus

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10
Q

t/f Foot-and-Mouth disease has a high economic impact

A

True. Massively expensive lossesi.e. loss of milk, draught power, weight, dead animalsfertility issues, delay in sale of livestock/productscost of vaccination, diagnostics, culling

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11
Q

what are some other names for Foot-and-Mouth Disease?

A

Aphthovirus fever, epidemic aphthae”aphtha” greek for small ulcer

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12
Q

how many types of aphthovirus are there?

A

at least seven serotypesat least 80 subtypes, with new emerging

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13
Q

Which aphthovirus serotypes are present in south america?

A

O, A, and C

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14
Q

Which aphthovirus serotypes are present in Africa?

A

O, A, C, SAT 1, 2, and 3

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15
Q

Which aphthovirus serotypes are present in asia, part of the middle east, and eastern europe?

A

O,A,C, Asia 1

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16
Q

Name the 5 places which are aphthovirus free, and which one of those experiences periodic epizootics.

A

Oceania, the Caribbean, North America, Central America, and Western Europe.Western europe experiences periodic epizootics.

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17
Q

What hosts does Foot-and-Mouth disease affect?

A

all cloven footed animalscattle, sheep, goats, buffalo, swine, camels, etcHorses are GENETICALLY RESISTANT

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18
Q

Where is FMD still enzootic?

A

Much of africa, asia, and the middle east

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19
Q

how long can FMD virus survive in the environment?

A

14 days in a stall, and as long as 20 weeks on sacks and hay

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20
Q

T/F - FMD viruses in muscle are inactivated within 72 hours of slaughter, but are inactivated more quickly in bone marrow, viscera, and blood clots.

A

False: viruses in muscles are inactivated within 48 hours of slaughter, but survive for longer periods in bone marrow, viscera, and blood clots.

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21
Q

t/f - FMD virus infectivity is destroyed by high temperature (>56C) and UV light

A

true

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22
Q

what chemicals and acid conditions are FMD viruses sensitive to?

A

sensitive to acid, and alkaline (stable at pH 6-9)sodium hydroxide, sodium carbonate, and citric or acetic acid are all effective disinfectants

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23
Q

How is FMD transmitted?

A

-mostly inhalation; infected animals generate lots of aerosols-ingestions of infected food-contact b/w infected and healthy animals-contaminated animal products (milk, meat, semen)-contaminated fomites-spreads over long distances, asymptomatic carriers-mechanical transmission by birds, rodents, arthropods

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24
Q

what is the pathogenesis of FMD?

A

inhalation/ingestion –> oropharyngeal infection –> viremia –> spread to different organs and tissues –> replication in epidermal cells –> characteristic vesicular lesions

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25
Q

describe the vesicle formation in FMD

A

initial hyperemic areas develop into vesicles, some of which coalesce to form large blisters. vesicles are filled with clear yellow fluid. may rupture leaving raw wounds.

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26
Q

t/f FMD lesions are prone to secondary infections

A

true. vesicles are highly prone to bacterial inf

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27
Q

What is Tiger Heart?

A

focal necrosis of cardiac muscle, occurs due to FMD. commonly seen in fatal FMD cases in young calves, lambs, goats, pigs and buffalosmall gray foci, streaks of irreuglar size and shapestriped appearanceoften leads to sudden death by heart failure.

28
Q

where may FMD persist after recovery?

A

the pharynx of some animals

29
Q

how long is the FMD virus detectable?

A

cattle up to 2 yearssheep up to 6 monthsvirus persistence does not occur in swine

30
Q

t/f FMD has low morbidity, and high mortality

A

false - FMD has high morbidity and low mortality.

31
Q

what are the clinical signs of FMD in cattle?

A

fever, anorexia, depression, decrease in milk production.w/in 24 hours, drooling, and development of vesicles on the tongue and gums.vesicles may be found in the interdigital skin and coronary band of the feet, and on the teats.vesicles rupture, producing large, crater-like ulcers

32
Q

what would you see with a FMD infection combined with secondary bact infection in cattle?

A

mastitis, mucopurulent nasal discharge

33
Q

t/f you may see lameness in cattle infected w FMD

A

true. foot lesions may cause lameness

34
Q

Tiger heart affects calves of what age?

A

up to six months

35
Q

t/f FMD may lead to abortion of cattle

A

true. even the virus does not cross the placenta, cattle may abort due to fever

36
Q

What are Hairy Panters?

A

animals with:chronic syndrome of anemia, diabetes mellitus, overgrown hair, poor heat tolerance.probably due to endocrine damage. associated w FMD

37
Q

Clinical signs of FMD in pigs?

A

lameness is often firstvesicles in the mouth are usually less prominent than in cattlelarge vesicles which quickly rupture often develop on the snout

38
Q

FMD in sheep and goats?

A

mostly subclinical infectionsif dz occurs, very mild

39
Q

How should we sample tissue for suspected FMD?

A

samples of vesicular epithelium of vesicular fluid should be sent in phosphate buffered saline (pH 7.4 to prevent destruction of FMD virus and antigen)

40
Q

what tests can be done for FMD?

A

ELISA is preferredvirus isolationRT-PCRTests for antibodies to the nonstructural proteins (NSP) of FMD virus: Distinguish infected animals from vaccinated animals (DIVA)

41
Q

Is FMD a reportable disease?

A

Yes

42
Q

How do you control FMD in disease free countries?

A

Quarantines and movement restrictions, slaughter of affected and exposed animals, & cleaning and disinfection of affected premises, equipment and vehicles.  Infected carcasses must be disposed of safely by incineration, or deep burial. Vaccination around the affected premises.  Rodents and other vectors may be killed to prevent mechanical transmission. Ban on swill feeding. Proper inactivation of virus in milk, meat, hides, wool. Federal law prohibits importation of animals, or animal products from infected countries

43
Q

How do you control FMD in endemic countries?

A

 Vaccination using inactivated and modified live vaccines. FMDV vaccines only protect animals from the serotype(s) contained in the vaccine. Imposition of quarantine and slaughter in an outbreak

44
Q

Is FMD a zoonotic disease?

A

Yes. Most human infections are subclinical.Fever, anorexia, vesiculation on the skin/mucous membranes.

45
Q

What genus is avian encephalomyelitis virus?

A

Tremovirus

46
Q

What is the typical host for avian encephalomyelitis?

A

Mostly observed in chickens 1 to 3 wks of agemild dz has also been observed in turkey, quail, and pheasant

47
Q

Where is avian encephalomyelitis found?

A

worldwide

48
Q

how is avian encephalomyelitis transmitted?

A

 The major mode of transmission is by a fecal–oral route Transmission via the egg may occur during the brief viremic phase of the disease in laying hens.

49
Q

What is another name for avian encephalomyelitis?

A

Epidemic tremor

50
Q

what is the incubation period for avian encephalomyelitis?

A

 Incubation period depends on the route of infection: Vertical transmission: 1-7 days Horizontal transmission: 11 days or more

51
Q

What is the usual pathogenesis of avian encephalomyelitis?

A

young chick exposed orally to field strains of AEV, primary infection of alimentary tract –> viremia –> infection of pancreas and other viscera –> infection of CNS –> encephalomyelitis

52
Q

t/f - In AEV, gross lesions are seen in the brain of infected birds

A

False - gross lesions are not seen in the brain. Histological lesions typical of viral encephalitis are present throughout the CNS, without peripheral involvement.

53
Q

What histological lesions are typical of avian encephalomyelitis?

A

central chromatolysis of neurons in the medulla oblongata is very suggestive.often accompanied by neuronal necrosis and satellitosis, neuronophagia, and gliosis.

54
Q

what are typical clinical signs of AEV infection, when seen in a young chicken?

A

Ataxia, leg weakness progressing from paresis to paralysis and recumbency.fine tremors of the head and neck in some birdsprostration, blindness, coma, deathmortality exceeding 50% in an initial outbreak

55
Q

what is typical of recovery from AEV?

A

surviving birds of acute infection may develop a cataract (blue corneal opacity)recovered birds may have CNS deficienciesaffected chicks are normally destroyed, as they rarely recover

56
Q

what clinical signs are typical of AEV infection in laying hens?

A

no neuro signssudden 5-10% drop in egg production, usually lasting for <2wk, followed by return to normalno deterioration in egg shell qualityhatchability may drop as much as 5% during decline, due to late embryonic mortality

57
Q

How do you diagnose AEV?

A

-clinical signs-no macro lesions of CNS; based on histo-tissues collected for virus isolation must include brain, duodenum, pancreas. isolation in yolk sac of embryonated eggs or cell culture-demonstration of AEV antigen in brain, spinal cord, and other tissues by immunohistochemical staining is a reliable method of diagnosis

58
Q

How do you control AEV?

A

-depopulation-immunization of breeder pullets at 10-15 wk of age with live vaccine prevents vertical trans, provides chicks with maternal immunity-AEV vaccine is usually combines with fowlpox vaccine, given by wing-web inoculation

59
Q

Does AEV cause dz in people or other mammals?

A

No, it does not.

60
Q

Which genus of Picornaviridae cause encephalomyocarditis?

A

Cardiovirus

61
Q

What two kinds of strains of cardiovirus have been identified?

A

Encephalotropic as well as cardiotropic strains

62
Q

What are the natural hosts of encephalomyocarditis virus, and to which animals is it transmitted?

A

The natural hosts are rodents, and the virus is transmitted to many animals, with severe epizootics of myocarditis with fatalities reported in swine and wildlife, especially elephants.

63
Q

T/F - encephalomyocarditis virus is transmitted to pigs from mother to piglet.

A

a little of both. Pigs are infected by eating feed or drinking water contaminated w/ rodent urine/feces. Transplacental infection MAY occur in fetuses NEAR FULL TERM, with many of them developing myocardial lesions

64
Q

Clinical features of encephalomyocarditis virus include?

A

-acute and subacute deaths almost always attributed to the viral effects on myocardium.-pigs show cardiac insufficiency, pulmonary edema, frothy transudation into respiratory tract.-histo; animals show multifocal or diffuse interstitial myocarditis and necrosis of cardiac muscle cells and Purkinje fibers

65
Q

T/F - in encephalomyocarditis infections, enlargement of the right ventricle with multifocal necrosis may be grossly apparent

A

True - white patches appear on myocardium

66
Q

T/F - in young pigs, suppurative meningoencephalitis is present with encephalomyocarditis infection.

A

False - in young pigs, nonsuppurative meningoencephalitis is present.

67
Q

What are three major reproductive consequences of encephalomyocarditis virus infections in pigs?

A

-near-term abortions (107-111 days into gestation)-stillbirth-mummification

Taylor Viro Final (12 decks)

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