Picornaviridae Flashcards
What’s the structure of picornaviridae? how do they look in electron micrographs?
Spherical, non-enveloped, icosahedral, ~30nm diameter.
They look smooth and round in elctron micrographs.
What kind of genome do picornaviridae have?
single molecules of linear, positive sense, ssRNA, 7-8.8kb in size
T/F picornaviridae RNA is non-infectious
false
genomic RNA is infectious
what is VPg?
it is a protein linked covalently to the 5’ end of picornaviridae RNA
T/F picornaviridae replicate in the nucleus
false. picornaviridae replicate in the cytoplasm
picornaviridae RNA acts as mRNA, which is translated into ____________
a polyprotein. this polyprotein is cleaved to yield 11 or 12 individual proteins.
what is characteristic of picornaviridae pathogenesis?
most of them cause rapid cell death with characteristic CPE (cytopathic effects)
how many genera of picornaviridae are there, and what’s an important difference between them?
there are 29, and a big difference is their stabilities at low pH
What is the etiology of Foot-and-Mouth Disease? (FMD)
Aphthovirus
t/f Foot-and-Mouth disease has a high economic impact
True. Massively expensive losses
i.e. loss of milk, draught power, weight, dead animals
fertility issues, delay in sale of livestock/products
cost of vaccination, diagnostics, culling
what are some other names for Foot-and-Mouth Disease?
Aphthovirus fever, epidemic aphthae
“aphtha” greek for small ulcer
how many types of aphthovirus are there?
at least seven serotypes
at least 80 subtypes, with new emerging
Which aphthovirus serotypes are present in south america?
O, A, and C
Which aphthovirus serotypes are present in Africa?
O, A, C, SAT 1, 2, and 3
Which aphthovirus serotypes are present in asia, part of the middle east, and eastern europe?
O,A,C, Asia 1
Name the 5 places which are aphthovirus free, and which one of those experiences periodic epizootics.
Oceania, the Caribbean, North America, Central America, and Western Europe.
Western europe experiences periodic epizootics.
What hosts does Foot-and-Mouth disease affect?
all cloven footed animals
cattle, sheep, goats, buffalo, swine, camels, etc
Horses are GENETICALLY RESISTANT
Where is FMD still enzootic?
Much of africa, asia, and the middle east
how long can FMD virus survive in the environment?
14 days in a stall, and as long as 20 weeks on sacks and hay
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.
False: viruses in muscles are inactivated within 48 hours of slaughter, but survive for longer periods in bone marrow, viscera, and blood clots.
t/f - FMD virus infectivity is destroyed by high temperature (>56C) and UV light
true
what chemicals and acid conditions are FMD viruses sensitive to?
sensitive to acid, and alkaline (stable at pH 6-9)
sodium hydroxide, sodium carbonate, and citric or acetic acid are all effective disinfectants
How is FMD transmitted?
- 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
what is the pathogenesis of FMD?
inhalation/ingestion –> oropharyngeal infection –> viremia –> spread to different organs and tissues –> replication in epidermal cells –> characteristic vesicular lesions
describe the vesicle formation in FMD
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.
t/f FMD lesions are prone to secondary infections
true. vesicles are highly prone to bacterial inf
What is Tiger Heart?
focal necrosis of cardiac muscle, occurs due to FMD. commonly seen in fatal FMD cases in young calves, lambs, goats, pigs and buffalo
small gray foci, streaks of irreuglar size and shape
striped appearance
often leads to sudden death by heart failure.
where may FMD persist after recovery?
the pharynx of some animals
how long is the FMD virus detectable?
cattle up to 2 years
sheep up to 6 months
virus persistence does not occur in swine
t/f FMD has low morbidity, and high mortality
false - FMD has high morbidity and low mortality.
what are the clinical signs of FMD in cattle?
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
what would you see with a FMD infection combined with secondary bact infection in cattle?
mastitis, mucopurulent nasal discharge
t/f you may see lameness in cattle infected w FMD
true. foot lesions may cause lameness
Tiger heart affects calves of what age?
up to six months
t/f FMD may lead to abortion of cattle
true. even the virus does not cross the placenta, cattle may abort due to fever
What are Hairy Panters?
animals with:
chronic syndrome of anemia, diabetes mellitus, overgrown hair, poor heat tolerance.
probably due to endocrine damage. associated w FMD
Clinical signs of FMD in pigs?
lameness is often first
vesicles in the mouth are usually less prominent than in cattle
large vesicles which quickly rupture often develop on the snout
FMD in sheep and goats?
mostly subclinical infections
if dz occurs, very mild
How should we sample tissue for suspected FMD?
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)
what tests can be done for FMD?
ELISA is preferred
virus isolation
RT-PCR
Tests for antibodies to the nonstructural proteins (NSP) of FMD virus:
Distinguish infected animals from vaccinated animals (DIVA)
Is FMD a reportable disease?
Yes
How do you control FMD in disease free countries?
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
How do you control FMD in endemic countries?
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
Is FMD a zoonotic disease?
Yes. Most human infections are subclinical.
Fever, anorexia, vesiculation on the skin/mucous membranes.
What genus is avian encephalomyelitis virus?
Tremovirus
What is the typical host for avian encephalomyelitis?
Mostly observed in chickens 1 to 3 wks of age
mild dz has also been observed in turkey, quail, and pheasant
Where is avian encephalomyelitis found?
worldwide
how is avian encephalomyelitis transmitted?
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.
What is another name for avian encephalomyelitis?
Epidemic tremor
what is the incubation period for avian encephalomyelitis?
Incubation period depends on the route of infection:
Vertical transmission: 1-7 days
Horizontal transmission: 11 days or more
What is the usual pathogenesis of avian encephalomyelitis?
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
t/f - In AEV, gross lesions are seen in the brain of infected birds
False - gross lesions are not seen in the brain. Histological lesions typical of viral encephalitis are present throughout the CNS, without peripheral involvement.
What histological lesions are typical of avian encephalomyelitis?
central chromatolysis of neurons in the medulla oblongata is very suggestive.
often accompanied by neuronal necrosis and satellitosis, neuronophagia, and gliosis.
what are typical clinical signs of AEV infection, when seen in a young chicken?
Ataxia, leg weakness progressing from paresis to paralysis and recumbency.
fine tremors of the head and neck in some birds
prostration, blindness, coma, death
mortality exceeding 50% in an initial outbreak
what is typical of recovery from AEV?
surviving birds of acute infection may develop a cataract (blue corneal opacity)
recovered birds may have CNS deficiencies
affected chicks are normally destroyed, as they rarely recover
what clinical signs are typical of AEV infection in laying hens?
no neuro signs
sudden 5-10% drop in egg production, usually lasting for <2wk, followed by return to normal
no deterioration in egg shell quality
hatchability may drop as much as 5% during decline, due to late embryonic mortality
How do you diagnose AEV?
- 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
How do you control AEV?
- 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
Does AEV cause dz in people or other mammals?
No, it does not.
Which genus of Picornaviridae cause encephalomyocarditis?
Cardiovirus
What two kinds of strains of cardiovirus have been identified?
Encephalotropic as well as cardiotropic strains
What are the natural hosts of encephalomyocarditis virus, and to which animals is it transmitted?
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.
T/F - encephalomyocarditis virus is transmitted to pigs from mother to piglet.
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
Clinical features of encephalomyocarditis virus include?
- 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
T/F - in encephalomyocarditis infections, enlargement of the right ventricle with multifocal necrosis may be grossly apparent
True - white patches appear on myocardium
T/F - in young pigs, suppurative meningoencephalitis is present with encephalomyocarditis infection.
False - in young pigs, nonsuppurative meningoencephalitis is present.
What are three major reproductive consequences of encephalomyocarditis virus infections in pigs?
- near-term abortions (107-111 days into gestation)
- stillbirth
- mummification
