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Flashcards in Flaviviridae Deck (35):

most important genus for vet medicine



general characteristics flaviviridae

spherical virion, replication in cytoplasm


two biotypes of Bovine Viral Diarrhea Virus (BVDV)

Non cytopathic and cytopathic


BVDV Noncytopathic-

uncleaved NS2-3, doe snot induce apoptosis, most common, cross placenta, invade fetus, persistent in calves
-can cause congenital, repro or enteric disorders


BVDV Cytopathic

arise from mutation of ncp biotype in persistently infected calves, non structural protein NS3 by cleavage of NS2-3, induce apoptosis, mucosal disease in cattle with persistently infected with ncp biotype


mechanism of conversion of ncp or noncytopathic

inserts cellular sequences into NS2-3 gene of BvDV genomes leads to additional cleavage so NS2-3 and release NS3


genotypes of BVDV

type 1 or 2, 1 is more detected than two, both 1 and 2 can have both biotypes


BVDV in non pregnant cow

mild infection, scours, milk drop, reduced WBCs


BVDV in pregnant first month

embryonic death


BVDV in 2-4 months of pregnancy

persistent infection in calves


BVDV months 5-9 of pregnancy

abortion early, then deformities, followed by no affect in late term


persistent infection progressed to mucosal disease

persistently infect calves (PI) can show decreased weight gain and stunted growth and will continuously shed virus into environment
with 2 outcomes
1. will survive, shed virus, and develop antibodies to both biotypes
2. will be infected with super antigen or mutation occurs where calf doesn't recognize cytopathic strain as foreign (no production)-> mucosal disease


PI calves

main source of BVDV direct contact transmission because of constant shedding


BVDV infection in Immunocompetent non-pregnant cattle

subclinical, diarrhea


BVDV immunocompetent pregnant cattle

conception failure, embryonic mortality, abortion, fetal mummification, stillbirths, congenital defects, birth of stunted or PI calves


BVDV immunotolerent cattle

mucosal disease (acute, chronic), appear ill and weak, secondary infection susceptibility


congenital defects from BVDV

abortion, cerebral hypoplasia, stargazing, porencephaly, hydroencephaly (dome head), rigid joints


mucosal disease BVDV acute form

ulceration of tongue, ulcerated nose and mouth, runny nose, ulcerations in gum, diarrhea, esophageal erosion, rumen ulceration, hemorrhagic focal lesions in abomasum, erosions and necrosis of peyers patches


mucosal disease chronic BVDV

diarrhea, inappetence, emaciation, rough hair, chronic bloat


BVDV diagnosis of PI calves

PCR on pooled skin samples, skin IHC, skin ELISA, SNAP BVD


Hog Cholera (CSF) or Classic Swine Fever

caused by Pestivirus, indistinguishable from African Swine Fever, related to BVD, one antigenic version infecting pigs domestic or wild, OIE List A disease


CSF distribution

not in USA since 1978, South America and Far East Asia, Except Japan and Korea


CSF transmission

direct contact, fecal oral, aerosol, fomites, vets and farm workers, feeding garbage. healthy pig can inhale, ingest or get by insemination. Shed in urine and nasal discharge


Path CSF

comes in through tonsil->peyers patches->early immunosuppression, depletion of CD1, CD4, CD8; macrophage activation and release of proinflamm cytokines; degeneration of vascular epithelium, thrombosis, hemorrhages; release of TNF-alpha in virus affected lymph nodes and apoptosis of lymphocytes; B-cells deficiency due to destruction of germinal centers of lymphoid tissues


Peracute and acute forms of CSF show

hyperemia, huddling infections, cyanosis of ears, blotchy purple skin, diarrhea, hemorrhage in urinary bladder, turkey egg kidneys, button ulcer colon, abortion or stillbirth, nervous signs-running or goose stepping


Dx for CSF

ELISA used most often


CSF control

OIE list A notifiable disease, quarantine farms, slaughter and proper disposal of carcass, such as incineration, **avoid feeding uncooked garbage and meat products to pigs


West Nile Virus

mosquito borne in genus flavivirus,endemic to africa australia, asia, the middle east, and europe


WNV transmission

birds are reservoirs, blood transfusions, breast feeding, lab accidents, organ transplants, and intrauterine all ways to transmit


WNV lineages

7 exist, only lineage 1 and 2 are affecting humans (1a)


clinical forms of WNV in humans

fever, cutaneous, no neuro (myocarditis, hepatitis, nephritis) and neuro-WNE West Nile enceph., WNM West Nile Meningitis, and meningoencephalitis


WNV signs in horses

mostly asymptomatic, 8% develop neuro, encephalomyelitis with ataxia are predominant clinical signs


Louping ILL

tick bourne, zoonotic , viral in sheep, and red grouse, caused by flavivirus, 4 subtypes, found in british isles , ioxides ricinus


louping ILL transmission

tick at any stage is infective


loupe ILL path and clinical signs

replication of virus in brain, severe inflammation of CNS, necrosis of brainstem and ventral horn neurons, affected stand apart, may have ataxia, muscle tremors, lack of coordination, jerky