picornaviridae Flashcards
picornaviridae general
spherical, non enveloped, visions appear smooth and round
single molecule linear + sense RNA, VPg protein links to 5’ end and genomic RNA is infectious
picornaviridae genome
cytoplasmic replication, virion RNA acts as mRNA and is translated to polyprotein to yield 11-12 proteins, most cause cytopathic effects and rapid cel death, very stable at low pH, 29 genera
foot and mouth disease FMD
seven serotypes, 80 subtypes, OAC in SA, OAC sAT 123 in Africa western europe and north and central america virus free
FMD hosts
all cloven footed domestic and wild animals, horses are genetical resistant
FMD distribution
africa, asia, middle east, none in North and Central America
FMD stability
stable pH6-9, broken down by citric or acetic acid
FMD transmission
mostly through inhalation, can move in wind or inside animal carriers
FMD path
inhalation/ingestion->oropharyngeal infection->viremia->spread to different organs and tissues->replication in epidermal cells->characteristic vesicular lesions
**vesicles filled with clear fluid
FMD path myocardial lesion
tiger heart, focal necrosis of cardiac muscle
-seen in fatal FMD cases in young animals, streaks of irregular size and shape are visible in myocardium, sudden death from heart failure
FMD Path
usually founding the pharynx, needs prolonged period of recovery, virus detectable in cattle up to two years and sheep after six months, virus persistence doesn’t occur in swine
FMD clinical signs
most severe in cattle and intensively reared pigs, sheep and goat develop subclinical infections, morbidity high and mortality low
FMD cattle clinical signs
fever anorexia depression
decreased milk production, drooling, vesicles around coronary band, crater ulcers from ruptured vesicles
secondary bacterial infections, myocarditis in calves up to 6 months of age, abortion, chronic Diabetes mellitus from endocrine damage
FMD clinical sign in swine
lameness is often the first sign of foot and mouth disease, vesicles in mouth less prominent, more on snout
FMD in sheep and goats
mostly subclinical infections, if disease occurs its mostly mild
FMD Dx
sampling fluid, ELISA, test for antibodies
FMD control
notifiable disease, quarantines in disease free countries, infected carcasses must be disposed of properly, vaccination around affected areas, rodent control, ban on swill feeding
FMD zoonosis
most human infections are subclinical, clinical signs show fever anorexia, vesiculation
tremovirus
avian encephalomyelitis
most seen in chickens 1-3 weeks old, fecal oral transmission or by egg
avian encephalomyelitis path
incubation period depends on the route of infection, vertical transmission 1-7 days, horizontal 11 days or more. no gross lesions
histology of central chromatolysis of neurons in the medulla oblongata
avian encephalomyelitis clinical signs
young chickens exhibit nervous disease -ataxia leg weakness , paralysis and recumbency, prostration blindness coma and death, may develop cataracts
laying chickens-no neuro signs, no deterioration in egg shell, hatch ability may drop, late embryonic mortality
avian encephalomyelitis Dx and control
Dx-virus isolation from brain and duodenum with pancreas, yolk sac of embryonated eggs, demonstration of AE virus antigen brain, spinal cord and other tissues, immunoflourescent staining. for control immunize with breeder pellets, commercial live vaccine AE vaccine combined with fowlpox, AE doesn’t infect humans or other mammals
encephalomyocarditis
genus: cardiovirus
tropic to heart and brain, hosts are rodents, epizootics to swine and other wildlife, pigs infected from water contamination and transplacental infection
encephalomyocarditis clinical features
myocardial effects contribute to acute and subacute deaths, nonsuppurative meningoencephalitis in young pigs, reproductive issues/late term abortions
