Lecture 10: Bovine Viruses 1 Flashcards

1
Q

What are examples of diseases in the Genus Pestivirus

A
  • Genus: Pestivirus (NADL/Singer strains are most common in vx)
    o Border disease virus
    o Classical swine fever
    o BVD1
    o BVD2
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2
Q

What is the taxonomy of BVDV

A

Pestivirus
o 1a and 2a in vx – 2b not in vaccine but is more prevalent
o Enveloped

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3
Q

What are is the target(s) species for BVDV

A
  • Target: bovine, wildlife (pig/deer/goat/rabbit)
    o Wildlife reservoir: must be susceptible, shed, and maintain BVDV + contact with cattle to allow spill back
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4
Q

How is BVDV transmitted in 3 main affected species

A
  • Transmit (pigs): raw milk
  • Transmit (sheep): trans-placental
  • Transmit (cow): oronasal
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5
Q

How is BVDV clinically affecting pigs

A
  • Clinically (pigs): poor conception/abortion/stillborn – subclinical
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6
Q

How is BVDV clinically affecting to sheep

A
  • Clinically (sheep): hairy shakers (kids)
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7
Q

How is BVDV clinically affecting to cows

A
  • Clinically (cow):
    o Infected 1 mo in utero: embryonic death

o Infected 2-4 mo in utero: persistent infected calf (Ig negative) or abortion or malformation

o Infected 5-9 mo in utero: normal (Ig positive) or abortion or malformation

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8
Q

Why is there different outcomes for BVDV infection at 2-4 mo vs 5-9 mo

A

o Infected 2-4 mo in utero: persistent infected calf (Ig negative) or abortion or malformation
 Will shed disease in high quantities
 Immune system is not developed – virus is recognized as self
 look like malignant catarrhal fever – deterioration of mucosal surface
* mucosal disease: mutated persistently infecting virus (converts from non-cytopathic to cytopathic)

o Infected 5-9 mo in utero: normal (Ig positive) or abortion or malformation
 Immune system is more developed – recognize as non-self

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9
Q

What is mucosal dz? Who does it infect

A

Persistently infected calves with BVDV

  • mucosal disease: mutated persistently infecting virus (converts from non-cytopathic to cytopathic)
    o ulcers on mucosal surfaces
    o NS2 and NS3 genes – non structural viral proteins that split in genome
    o Cannot transmit cytopathic form between calves
    o Not recoverable – euthanasia indicated
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10
Q

What is the pathogenesis of BVDV?

A
  • Path: lymphatic spread from tonsil to regional LN to blood
    o Found in lymphoid tissue in GI/lung (thymus/bone marrow/spleen)
    o All organs are BVDV positive
    o Result in immunosuppression
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11
Q

How is BVDV controlled in NA and Europe

A

o CA: BVDV screening/ProAction/vx
o Europe: kill the persistently infected (legislative change)

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12
Q

What methods are used to screen for BVDV

A

o Serology (ELISA antigen and/or antibody)/bulk tank PCR (only target milk producing animals) test calves
 Target: unvaccinated and low maternal Ig levels – find PI’s
 Test whole herd serology: if whole herd is negative = no BVDV
* If some +/- = there are persistently infected + generally infected animals

o Individual sample (blood/ear notch/milk)
 Ear notch: best for finding PI
 Blood: use capture ELISA, but won’t identify virus that is covered in Ig

o Vaccination: modified live and killed
 Effective but must be strain specific (can be vaccinated for one type and infected by another)
 1a and 2a in vx – 2b not in vaccine but is more prevalent

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13
Q

What is a ‘wreck’ in relation to BVDV

A

o Wrecks: unvaccinated herds introduced to virus with synchronous breeding
 Result in almost all calves being PI
 Mainly affecting beef – cow calf
 Vaccinate with cytopathic strains of BVDV – if vx PI with cytopathic strain they will develop mucosal dz (will occur in 25% of PI’s) – not recommended (low efficacy/inhumane euthanasia)

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14
Q

What are the main impacts of BLV

A

Impacts: dairy industry
* 3% less milk/cow
* 23% more likely to be culled/die
* If clinical = death, and carcass condemnation
* Animal welfare/export restrictions/consumer concerns

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15
Q

How is BLV transmitted

A

blood
colostrum/milk
natural breeding
in utero

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16
Q

What is the prevalence of BLV in NA

A

Prevalence: rising prevenance in NA (~80% herds in AB positive)
* If you have a positive herd = approx. 40% of animals are infected (wide range = difficult to manage)

17
Q

What is the pathology of BLV

A

Path: lifelong infection
* Infect B cells (CD5+ B cells) – unsure mechanism, includes polyclonal expansion of B cells
* Result in and increase of B cells and decrease of T cells

18
Q

How is BLV transmitted

A

Transmit: blood/colostrum/milk/in utero/natural breeding (mucosal)

19
Q

What are the consequencees of BLV infection

A
  1. Asymptomatic
  2. Persistent lymphocytosis: 30% infected
    a. Persistently higher than normal WBC
  3. Leukemia/lymphoma: 0.1-10% infected
    a. Enzootic bovine leukosis
20
Q

What are the clinical features of leukemia induced by BLV

A
  1. Leukemia/lymphoma: 0.1-10% infected
    a. Enzootic bovine leukosis
    b. Prevalence of this form indicated high number of positive animals in herd
    c. Also persistent infection
    d. Clinically
    i. Tumor formation: provirus induces genes (oncogene/TSG) upstream and/or downstream from insertion
    ii. Exophtalmus: due to retrobulbar process (tumor growing behind eyes)
    iii. Generalized edema
    iv. Lymphomegaly
    v. Cardiac/splenic/intestinal lymphosarcoma
21
Q

How to diagnose BLV

A

Dx: Ig ELISA (at 36d post infection), PCR on cDNA (26d post infection)
* Identify proviral load – variation in peak proviral load
o High proviral load: more likely to transmit and have induced leukemia
 Reduce HPL animals = reduce transmission
o Low proviral load

  • Lymphocyte count related to proviral load
22
Q

How to control BLV

A

Control
* Screen: antibody test: quick/reliable/cheap – blood and/or milk
o Identify positive and negative animals
* Reduce risk of transmission (don’t use pooled colostrum/re-used needles…)
* Biosecurity (transport/new animals introduced…)

23
Q

Are proviruses silent

A

no

they can produce products 5 >3’ and 3’ > 5’ in DNA

research is ongoing