Flaviviridae Flashcards
Which genus of Flaviridae contains many important veterinary pathogens including BVD and swine fever?
Pestivirus
What is important about the maturation of Flaviviridae virions?
Immature have prM and E that form a tight, heterodimeric complex. Upon maturation, lose prM and rearrangement of E protein into homodimers
Where does flaviviridae replication occur?
Cytoplasm
Describe the genome of flaviviridae?
Linear, positive sense, single stranded RNA that is cleaved by viral and host proteases
What two important veterinary diseases come from genus pestivirus?
BVD and swine fever/hog cholera
Which is the most common type of BVDV?
Non-cytopathogenic–does not induce apoptosis!
Crosses placenta, invades fetus, results in persistent infection in calves
Congenital, reproductive, enteric disorders
What mutation results in the cytopathogenic form of BVDV?
NCP biotype; production of nonstructural protein NS3 that induces apoptosis
Mucosal disease in cattle persistently infected with this biotype
T or F: Both BVDV types exhibit cp and noncp viruses
True! They both have cytopathogenic and noncytopathogenic viruses
Which type of BVDV is more common?
BVDV type 1 is more frequently detected than BVDV type 2
If a cow is infected 2-4 months into gestation, what is the outcome of her pregnancy?
Persistent infection! AKA PI calves
*Then the cow becomes naturally immune
If the cow is infected 1 month into gestation, what is the outcome of her pregnancy?
Embryo death
If the cow is infected 5-9 months into gestation, what is the outcome of her pregnancy?
Abortion, deformities, normal calves
T or F: PI calves shed the BVDV continually into the environment
True!
What are the two outcomes of PI calves?
- May survive, continue to shed virus, develop antibodies
- Superinfection with cytopathogenic virus and/or mutation of non-cytopathogenic virus to cytopathogenic virus aka there is no protection against this strain and mucosal disease develops
How is BVDV transmitted?
Through nasal discharge, urine, milk, semen, saliva and commonly through PI calves! Also transplacental, contact with aborted fetus, etc.
What are some outcomes of BVDV infection in immunocompetent non-preggers cattle?
Subclinical/mild disease, diarrhea in calves, thrombocytopenia, hemorrhageic syndrome, immunosuppression
What are some outcomes of BVDV in immunocompetent pregger cattle?
Conception failure, death of embryo, abortion, fetal mummification, stillbirths, congenital defects, PI calves
T or F: immunotolerant cattle (calves) may develop mucosal disease
True
What are some congenital defects arising from BVDV infection?
Abortion, nervous system defects, cerebellar hypoplasia, stargazing, hydraencephaly, rigid joints, porencephaly
What are some clinical findings in the mucosal (acute) form of BVDV?
Severe diarrhea, ulcerated nose/mouth/gums/tongue, esophageal erosions, Peyer’s patches erosions, rumen erosions, hemorrhages in abomasum, coronary band ulceration (some animals)
What are some clinical findings in the mucosal (Chronic) form of BVDV?
Diarrhea, inappetence, emaciation, rough hair, chronic bloat, hoof deformities, chronic erosions on skin and oral cavity
T or F: Classical swine fever and BVDV are antigenically related
True!
How many antigenic types of CSF exist?
Only one! But more virulent strains exist
What ‘list’ is this viral disease on, according to the OIE?
List A! It causes HUGE losses to the pig industry!
T or F: CSF has been eradicated from the USA, where it is believed to have originated?
True! in 1978
It is endemic in South Africa, Far East Asia
How can CSF be transmitted?
Direct contact, fecal oral, aerosol, fomites, vets, farm workers, feeding garbage containing pork scraps!
Infected pigs shed it in feces, urine, saliva, nasal discharge
Pregnant sows can also transplacentally transmit it to a PI calf/piglet
Where is the primary site of invasion of CSF?
The tonsil–there it goes to the lymphatic vessels and blood capillaries–then to the spleen, peripheral lymph nodes
What is the end result of pathogenesis of CSF? i.e. on the molecular/immunology level?
B lymphocyte deficiency, immunosuppression, depletion of CD4, CD8, macrophage activation, pro-inflammatory cytokine release, vascular epithelium degeneration, thrombosis, hemorrhages, release of TNF alpha in virus infected lymph nodes, lymphocyte apoptosis
What are clinical signs of the peracute and acute forms of CSF?
Drowsiness, depression, piled or huddled together piglets, hyperemia, cyanosis of ears, conjunctivitis, diarrhea, purplish discoloration of skin, nervous signs as well
What might you find upon necropsy of a peracute/acutely infected pig?
Necrotic foci in tonsil, inflamed lymph nodes, enlarged spleen, hemorrhage in bladder, ‘turkey egg kidney,’ pelvic hemorrhage of kidney, petechiae in lung and kidney, venous congestion of brain, button ulcers on colon**
How might you diagnose CSF?
Elisa, virus isolation, PCR, FAT
How might you control CSF?
Immediately notify authorities! Quarantine, slaughter, incineration of carcus, disinfectant, avoid feeding uncooked pork products to pigs (cannibalism duh), vaccination in endemic areas
T or F: it is impossible to differentiate animals vaccinated with LAV vaccines from animals infected with the field strain using serology
True! They lead to the same antibody response
Can differentiate them using DIVA: subunit marker vaccines!
To what genus does West Nile Virus (WNV) belong?
Genus flavivirus!
In what areas is WNV considered endemic?
Africa, Asia, Australia, Middle East, Europe, and the U.S.
It is zoonotic!
Which animal is the reservoir for WNV?
The bird–then infects mosquitos
Incidental infection to horses
Which lineage/sublineage is the most common in humans?
Sublineage 1a
*Only lineages 1 and 2 have been implicated in humans but at least 7 lineages exist
Describe the pathogenesis of WNV
Bite in skin, taken up by DC and Langerhans cells, taken to lymph nodes, leads to viremia and infection of peripheral organs
What are the three West Nile neuro-invasive diseases we should be worried about?
WN virus encephalitis
WN menengitis
WN meningoencephalitis
What other conditions can result from WNV?
West Nile fever, myocarditis, hepatitis, nephritis, rashes, asymptomatic
What are the predominant clinical signs in WNV infected horses and is it common?
8% develop neurological symptoms
Most are asymptomatic
Encephalomyelitis with ataxia are predominant clinical signs
What species does Louping ill most effect?
Sheep and red grouse (bird)
Tick-borne, zoonotic, viral disease
Caused by a member of the genus flavivirus
How many subtypes of Louping ill have been identified?
FOUR. Who cares?
Which tick is the vector for Louping ill
Ixodes ricinus! Common in British Isles, Scotland, Ireland, N. England, Wales
What two types of transmission are common with looping ill?
Transtadial and tarnsovarial
What does clinical disease of looping ill look like?
Replication of virus in brain, severe CNS inflammation, brainstem necrosis so ataxia, muscle termors, jerky, stiff movements, bounding gate
Morbidity/mortality ranges from 5-60%
Just remember that louping ill is a viral zoonosis**
Ok?
Is there a vaccination available for louping ill?
Yes, formalin killed tissue cultured vaccine
Tick control is also important
