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Virology > VSV & BLuetongue > Flashcards

VSV & BLuetongue Flashcards

1
Q

What doe “Rhabdo-“ mean?

A

rod (bullet-shaped)

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2
Q

What genus does Vesicular stomatitis virus belong to?

A

Vesiculovirus

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3
Q

What are the physical characteristics of VSV?

A
  • Enveloped
  • (-)ssRNA
  • 11Kb genome
  • 5 distinct proteins
  • G: neutralizing epitopes
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4
Q

What species are affected by VSV?

A
  • Horses, Cattle, Swine
    • wildlife, very rare in sheep, goats, llamas, alpacas
  • Zoonotic potential
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5
Q

How many serogroups of VSV are there?

A
  • 2 serogroups - distinct NAb
    • New Jersey
    • Indiana
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6
Q

What is the geographical spread of VSV?

A
  • Limited to the Americas
    • sporadic outbreaks in US
      • limited to western states since 1980s
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7
Q

How does VSV affect humans?

A
  • Most cases asymptomatic
  • Can cause flu-like illness
    • Headache, fever, muscle aches, weakness for 3-5 days
    • Rare - vesicles and encephalitis
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8
Q

When does VSV occur?

A
  • Seasonal variation - vector availability
  • May to October
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9
Q

Why is VSV important?

A
  • Reportable disease
  • May result in trade restrictions
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10
Q

How is VSV transmitted?

A
  • Direct: contact with infected animals - mucosa and skin
    • Indirect: contaminated shared feed and water stations
  • Blood-feeding insects:
    • sandflies, black flies, biting midgets
      • Biological vectors
      • Associated with water sources, typically warmer months
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11
Q

How do insects spread VSV?

A
  • Insect pick up VSV from feeding on infected animals
    • replicate the virus
    • secrete it from their salivary glands when they feed again
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12
Q

What are the clinical signs of VSV infection?

A
  • Incubation period 2-8d
    • Fever - before or same time lesions appear
    • Broad tissue tropism
  • Typically self-limiting, resolves in 10-14 days
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13
Q

How prevalent is VSV? How fatl?

A
  • Morbidity rate generally low in herd: 10-20%
    • Previous exposure, underlying immunity, route of exposure
  • Seroprevalence may be high - approaching 100%
  • Mortality rare
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14
Q

How are VSV and FMDV similar?

A
  • Identical clinical presentation to FMDV
    • Excessive salivation: ptyalism )often 1st sign)
    • Vesicles, ulceration, erosion of various sizes of the oral and nasal mucosa, mucocutaneous junction of lips, sloughing of the epithelial surface of tongue
      • Coronary bands, foot lesions, and lameness
      • Prepuce, vulva, and teat lesions , possible 2° mastitis
      • loss of appetite, reluctance to eat/drink
    • Crusting lesions of the muzzle, ventral abdomen, ears, sheath, and udder
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15
Q

When were significant outbreaks of VSV?

A
  • 2005/2006
    • 9 states, 445 premises
    • 584+ equines cases
    • 202+ bovine cases
  • 2009
    • 2 states, 5 premises
    • 7+ equine cases
  • 2012
    • 2 states, 36 premises
    • 51+ equine cases
  • 2015/2016
    • 823 VSV-affected premises confirmed or suspected in 8 states
  • 2019
    • 1144VSV affected premises confirmed or suspected in 8 states
  • 2020
    • 326 VSV affected premises confirmed or suspected in 8 states
    • KS: 196 affected premises
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16
Q

How is VSV diagnosed?

A
  • REPORT to Authorities/Regulatory Veterinarians
    • Samples collected FAD diagnostician
    • Zoonotic - PPE should be worn when handling affected animals
  • Antibody detection
  • VI/PCR or active vesicular lesions
    • Vesicular fluid, epithelial tags from lesions, lesion or mucosal swab
    • Typically no viremia
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17
Q

What are the DDx for VSV?

A
  • FMDV
  • SVDV
  • VESV
  • SVA
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18
Q

How is VSV managed?

A
  • No specific treatment available
  • Soft feed for pain associated with oral lesions
  • Cleaning wounds with mild antiseptics (prevent 2° infections)
  • Reduce exposure to vector
    • Shelter/housing, insecticides, eliminate insect breeding areas
    • Pasture away from moving water (streams, rivers)
  • Isolate affected animals, quarantine
    • Premises containing affected animals are quarantined for at leas 14 days from the onset of lesions in the last affected animal
  • Biosecurity, disinfecting equipment/fomites
  • Commercial vaccines not available in US
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19
Q

Is there a vaccine for VSV?

A
  • Commercial vaccines are NOT available in the US
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20
Q

What is the triad of Vesicular Diseases?

A
  • Vesicles
  • Fever
  • Lameness
  • All vesicular diseases are clinically indistinguishable
  • All require testing to confirm diagnosis
21
Q

What Family and Genus are Bluetongue Virus part of?

A
  • Reoviridae
    • REO - Respiratory, enteric orphan viruses
  • Orbivirus - BTV, EHDV
22
Q

What are the characteristics of BTV?

A
  • dsRNA 19kb
  • Nonenveloped
  • Segmented genome - 10
  • >26 different serotypes worldwide
    • >13 in US
23
Q

What is BTV?

A
  • Non-contagious infectious arthropod-borne viral disease of domestic and wild ruminants (known for >100y)
  • Geographical restriction due to climate and environmental conditions needed to support Culicoides biting midge vectors
  • In US: C. sonorensis and insignis
    • detected in southern and western states
24
Q

What type of vector are biting midges for BTV?

A
  • Biological vector:
    • virus replicates in midge
    • vector becomes infected by blood from an infected ruminant
    • Etiological cycle between vector and susceptible ruminant
25
Q

Why are Culicoides biting midges important?

A
  • >1400 species worldwide
  • Different species transmit BTV, EHDV (many other viruses) in distinct global ecosystems
26
Q

How is BTV transmitted?

A
  • Virus has high affinity for blood cells
    • initially all blood cells than only erythrocytes
      • NO replication in RBC
    • Prolonged viremia in presence of NAb
      • Not persistent, generally < 60 days
      • May be up to 11 weeks in cattle
      • Can contribute to year-round transmission
  • Primary Route: Vector
    • Virus in secretions/excretions minimal
      • direct/indirect/aerosol transmission unlikely
    • Semen from viremic bulls potential source through natural breeding or AI
    • Transplacental transmission in cattle reported
27
Q

What animals are primarily effected by BTV? Mortality?

A
  • Most common in sheep - principally European sheep reeds
  • Peracute to chronic course
  • Mortality rate highly variable 2-90%
    • Peracute: may die within 7-9 d
      • severe pulmonary edema, dyspnea, frothing from nostrils
    • Chronic: may die after 3-5 seeks
      • secondary bacterial infections
  • Mild cases usually recover rapidly
28
Q

What production losses does BTV cause?

A
  • Deaths
  • unthriftiness
  • wool breaks
  • Reproductive losses
29
Q

What are the clinical signs of BTV in sheep?

A
  • Incubation: 4-6 days
    • Fever (105-107.5F)
    • Listless/depression, reluctance to move
    • edema of lips, nose, face, submandibular region, eyelids, ears
    • Congestion/hyperemia of mouth, nose, nasal cavities, conjunctiva, and coronary bands
    • lameness, hoof defects
    • Serous nasal discharge (mucopurulent) dyspnea
    • Sore muzzle
    • Blue tongue
      • some have severe edema and cyanosis of tongue
    • Reduced appetite, erosions/ulcers can occur in oral cavity
    • Dermatitis may result in abnormal wool growth
    • Muscle loss, torticollis
30
Q

What is the pathogenesis of BTV that allows for the clinical signs in sheep?

A
  • Vascular endothelial damage
    • Increased capillary permeability, intravascular coagulation
      • edema, congestion, hemorrhage, inflammation, necrosis
31
Q

What is the pathogenesis and clinical signs of BTV in cattle?

A
  • C/S rare but similar to sheep:
    • Fever
    • Increased respiratory rate
    • lacrimation
    • salivation
    • stiffness
    • Oral vesicles and ulcers
    • hyperesthesia
    • dermatitis
32
Q

What are the clinical signs of BTV in pregnant cattle/sheep?

A
  • May abort or deliver malformed calves/lambs
    • infection in early gestation
    • Cerebral malformation
      • Hydranencephaly, ,porencephaly
      • Ataxia and blindness at birth
33
Q

What are the clinical signs of BTV in WTD and pronghorn?

A
  • Severe hemorrhagic disease leading to sudden death
34
Q

What are the characteristic lesions of BTV found at necropsy?

A
  • Petechiae, ecchymoses, or hemorrhage in wall and base of pulmonary artery
  • Focal necrosis of papillary muscle of left ventricle
  • Ulcers/hemorrhage/necrosis in oral cavity, tongue, esophageal groove, and omasal folds
  • SQ, IM and LN edema and hemorrhage, skeletal myonecrosis and hemorrhage, myocardial and intestinal hemorrhage, pleural and pericardial effusion, pulmonary edema, pericarditis, and pneumonia
  • Characterized by vascular permeability, thrombosis and tissue infarction
35
Q

How is BTV diagnosed?

A
  • Consistent clinical signs and pathology
  • VI/PCR
    • whole blood in anticoagulant
    • Spleen, ln, bone marrow
  • Antibody response detected 7-14dpi, generally lifelong
    • AGID, ELISA
  • Identity of isolate (serotype)
    • can be performed on both virus and Ab
36
Q

How is BTV managed?

A
  • No specific treatment
    • Rest, soft food, husbandry
    • Controlling secondary infections
  • Vaccination
  • Control of vectors
37
Q

What is the BTV vaccine?

A
  • Modified live virus (MLV) and Inactivated vaccines commercially available
  • In US:
    • monovalent (BTV 10) MLV vaccine available for use in sheep
  • MLV vaccine can cause abortion or malformation of fetuses when given in the first half (ewe) or first trimester (cow) of pregnancy
  • Vaccination with different serotypes does NOT provide consistent cross-protection
  • MLV vaccines should NOT be used during Culicoides season:
    • insects may transmits the vaccine virus
      • potential for reassortment, new viral strains
38
Q

does BTV undergo genetic shift?

A
  • Genetic shift by reassortment of gene segments during infection of insects or animals with more than 1 strain/serotype of BTV
39
Q

What are some concerns about the future of BTV?

A
  • Climate changes: increased range of environment supportive of the vector?
  • Additional emerging serotypes?
    • different species virulence
    • origin of virus
40
Q

What are the characteristics of Epizootic hemorrhagic disease virus (EHDV)

A
  • dsRNA virus
  • Nonenveloped
  • Segmented genome
  • >10 different serotypes worldwide
41
Q

What is EHDV?

A
  • Non-contagious infectious arthropod-borne viral disease of domestic and wild ruminants
    • Historically, a disease of WTD in NA - rarely a clinical disease of cattle
      • Ibaraki virus - outbreak in Japan 1959
  • Emerging disease in cattle: OIE notifiable since 2008
  • Biological vector: Culicoides biting midge
  • Immunological cross-reactivity with BTV
  • Seasonal due to vector
  • REPORTABLE
42
Q

What animals are hosts to EHDV

A
  • WTD most important
    • Morbidity and Mortality may be as high as 90%
      • varies between years and geographical locations
  • Other wild ruminants may seroconvert:
    • mule deer, pronghorn, black-tailed deer, red deer, elk, moose, bighorn sheep
  • Cattle: subclinical infection common, outbreaks rare
  • Culicoides sp. transmit virus to ruminants after external extrinsic period of 10-14 days
43
Q

What is the Pathogenesis of EHDV

A
  • Viremia can be prolonged > 50d in the presence of NAb
    • Virus associated with RBC
  • Virus infects endothelium all tissues affected
44
Q

What are the clinical signs of EHDV in WTD?

A
  • Incubation: 5-10d
    • Fever, weakness, reduced appetite, excessive salivation, head and neck edema, hyperemia of conjunctiva and mucus membranes of oral cavity, coronitis, stomatitis
    • Prolonged disease: ulcers on dental pad, hard palate, and tongu
    • Terminal: excessive bleeding, bloody diarrhea, hematuria, death
45
Q

What are the clinical signs of EHDV in cattle

A
  • Incubation: 5-10d
    • Acute disease similar to BTV;
    • fever, reduced appetite, conjunctival edema, redness and crusting of nose and lips, oculonasal discharge, stomatitis, salivation, lameness, tongue edema, oronasal erosion, dyspnea, coronitis, difficulty swallowing
    • Abortions/stillbirths reported
    • Mortality low (<10%)
46
Q

What lesions are common in WTD with EHDV

A
  • Widespread hemorrhage and edema
    • especially in heart and GIT
47
Q

jHow is EHDV diagnosed?

A
  • REPORTABLE
  • Differentials:
    • WTD: BTV, FMDV
    • Cattle, BTV, BVDV, FMDV, IBR, VSV, MCFV
  • FAD investigation
  • VI/PCR
    • whole blood in anticoagulant
    • spleen, lungs, ln, liver
  • Serology: paired serum samples
    • AGID, ELISA, SN
48
Q

How is EHDV managed?

A
  • Control Vector
    • insecticides, repellents on susceptible ruminants, management of culicoides breeding areas
  • NO VACCINE commercially available for preventing EHDV in US

Virology (37 decks)

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