Lecture 10: Bovine Viruses 1 Flashcards
What are examples of diseases in the Genus Pestivirus
- Genus: Pestivirus (NADL/Singer strains are most common in vx)
o Border disease virus
o Classical swine fever
o BVD1
o BVD2
What is the taxonomy of BVDV
Pestivirus
o 1a and 2a in vx – 2b not in vaccine but is more prevalent
o Enveloped
What are is the target(s) species for BVDV
- Target: bovine, wildlife (pig/deer/goat/rabbit)
o Wildlife reservoir: must be susceptible, shed, and maintain BVDV + contact with cattle to allow spill back
How is BVDV transmitted in 3 main affected species
- Transmit (pigs): raw milk
- Transmit (sheep): trans-placental
- Transmit (cow): oronasal
How is BVDV clinically affecting pigs
- Clinically (pigs): poor conception/abortion/stillborn – subclinical
How is BVDV clinically affecting to sheep
- Clinically (sheep): hairy shakers (kids)
How is BVDV clinically affecting to cows
- 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
Why is there different outcomes for BVDV infection at 2-4 mo vs 5-9 mo
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
What is mucosal dz? Who does it infect
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
What is the pathogenesis of BVDV?
- 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
How is BVDV controlled in NA and Europe
o CA: BVDV screening/ProAction/vx
o Europe: kill the persistently infected (legislative change)
What methods are used to screen for BVDV
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
What is a ‘wreck’ in relation to BVDV
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)
What are the main impacts of BLV
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
How is BLV transmitted
blood
colostrum/milk
natural breeding
in utero
What is the prevalence of BLV in NA
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)
What is the pathology of BLV
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
How is BLV transmitted
Transmit: blood/colostrum/milk/in utero/natural breeding (mucosal)
What are the consequencees of BLV infection
- Asymptomatic
- Persistent lymphocytosis: 30% infected
a. Persistently higher than normal WBC - Leukemia/lymphoma: 0.1-10% infected
a. Enzootic bovine leukosis
What are the clinical features of leukemia induced by BLV
- 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
How to diagnose BLV
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
How to control BLV
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…)
Are proviruses silent
no
they can produce products 5 >3’ and 3’ > 5’ in DNA
research is ongoing
