Bovine Viral Diarrhoea (BVD) Flashcards

1
Q

BVD Background

A
  • The disease was reported in 1946 in the USA
  • Initially, clinical cases at that time were associated with high fever, diarrhoea, mucosa lesions and leukopenia
  • Until the late 1980s, effective BVD control was hindered by its widespread distribution and lack of cost-effective diagnostic tools.
  • The stealthy nature of the disease prevented farmers and veterinarians from recognizing its full economic impact
  • It took at least 40 years to fully recognize the extent of the effects caused by BVDV infections
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2
Q

Why is BVD important?

A
  • poor fertility
  • high level of dz in calves
  • poor weight gain
  • scours
  • low milk yields

economic impact:
- Poor reproductive performances
- Growth retardation
- Reduced milk yield
- Increased susceptibility to other diseases
- Early culling increased mortality among youngstock

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3
Q

BVD - Aetiology

A
  • Pestivirus Single-stranded RNA virus
  • Antigenic variations of the viral surface proteins result in two types of BVDV: type 1 and type 2
  • BVDV can be cytopathogenic (CP) or Non -CP

UK:
- BVDv Type 1: prevalent
- BVDv Type 2: rare

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4
Q

BVDv subtypes

A
  • BVDV-1 (Pestivirus A) and BVDV-2 (Pestivirus B), which are further divided into subtypes
  • There are currently 17 recognized subgenotypes of BVDV type 1 (designated 1a–1q) and 3 subgenotypes of type 2 (designated 2a–2c)

UK:
- BVDv Type 1: prevalent
- BVDv Type 2: rare

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5
Q

BVD - host range

A
  • BVDV includes most even-toed ungulates
  • Many species can be affected, domestic cattle seem to be the primary host
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6
Q

BVD transmission

A
  • Nose-to-nose contact is the main route for the transmission of infection
  • Most commonly by introducing infected animal(s) to herd
  • And/or contact at boundaries, shows etc
  • Virus survives very poorly in the environment, on fomites etc.
    – Survives ~4w in the environment
  • PIs are generally much more important sources of infection
  • Most transmission is via nasopharyngeal secretions (faeces are a poor source)
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7
Q

BVD - Pathogenesis

A
  • Lymphoid tissue is the primary target of BVDV
  • BVD is associated with a reduction in the number of T lymphocytes in blood and diminished function of T lymphocyte (thymocytes, lymphocytes, monocytes, macrophages, and dendritic cells)
  • However, viral replication occurs in a variety of cell types located in the integument, alimentary canal, nervous system, respiratory tract, and immune system
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8
Q

BVD infection: non-pregnant animals - CS

A

Not pregnant = transient infection

  • Subclinical or clinical (dull, decreased appetite, D+)
  • No clear/specific CS
  • Shed low levels for up to 3 weeks
  • Antibodies present from 2-4 weeks pi and persist for several years

Respiratory infections:
- Worse with BVD
- e.g. BVDV + other viruses (IBR + RSV) + bacteria (M.haemolytica)

Enteric infections:
- Worse with BVD
- e.g. BVDV + other viruses (corona + rota) + bacteria (Salmonella spp)

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9
Q

BVD infection during pregnancy - CS

A
  • Lowered herd fertility
  • Increased number of barren cows
  • Decreased number of newborn calves
  • Can cause an inflammation of the ovaries -> impaired ovarian function

Wide variety of possible CS:
- PI calf
- Normal calf
- Abortion
- Congenital defects
– e.g. e.g. cerebellar hypoplasia arthrogryposis, microphthalmia, cataracts, hydrocephalus, musculoskeletal malformations, and alopecia
- Embryo loss

Stage of gestation (~) & outcome:
- 0-30d = embryo loss
- 30-120d = PI calf (Ab -ve, Ag +ve)
- 90-210 = normal calf or congenital defects or abortion (Ab +ve, Ag -ve)
- 190-270 = normal calf (Ab +ve, Ag -ve)

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10
Q

PI animal

A

= persistently infected
= persistent transmission
- BVDv seen as part of normal self
- no antibodies ever produced
- may go undetected or may show CS
- shed large quantities of virus
- 0.5-2% of national population are PI animals

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11
Q

BVD infection during pregnancy - PI

A
  • PI dam -> PI calf (100% chance)
    – ~7% of all PI calves come from a PI cow
  • Pregnant, BVD naive cow + BVD -> PI calf
    – 93% of all PI calves come from acute infection of the dam
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12
Q

Acute BVD infection during pregnancy - PI CS

A
  • PI’s often small and stunted but can be clinically completely normal until they develop MD
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13
Q

BVD mucosal dz - CS

A
  • Mucosal dz = transmitting whilst alive
  • Fatal condition
  • Clinical signs: weight loss, bloody D+, dehydration and ulcerated lesions in mouth, nose and interdigital space
  • Virus mutates from non-cytopathic to cytopathic form (ie cell killing form)
  • Transmission of cp strain = potential for MD in other PIs
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14
Q

BVD infection in bulls - CS

A
  • Can be PI
  • Can be acutely infected
  • Rare: the virus can ‘hide’ in testicles “immunologically privileged site”
    – Hence, it can be blood Ab positive, antigen negative, yet still spreading viru
    – Only identified by semen sample
  • Potential to introduce virus to herd
  • Test before bringing new bull in
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15
Q

BVD 1 CS

A
  • Acute infection
    – Mild systemic illness
    – Reduced reproductive performance
    – Immunosuppression
  • Mucosal disease (PI animals)
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16
Q

BVD 2 CS

A
  • Acute severe haemorrhagic syndrome
  • Has been seen in UK but not very recently/widely

Acute infection:
- generally severe disease often fatal, usually adults
- virus clearance 28 – 38 days
- thrombocytopenia, diarrhoea, haemorrhagic disease
- weak cross-protection to Type 1 BVDV antibodies

17
Q

BVD – Diagnosis

A
  • Viral antigen and antibody tests
  • Both can be identified in blood and milk
    – Ag also skin, hair, semen, tracheal fluid, follicular fluid
  • Both can be used on bulk milk (dairy herds)
    – Viral Ag can be detected in bulk milk from 1 PI in 300 cows
18
Q

Early identification of PI calves

A
  • Virus can be readily identified in blood samples pre-colostrum or from older calves (> 8 months)
    – Detection in blood can be hampered in younger animals by maternal antibodies
  • Possible to look for viral Ag in calves of any age by using ear tissue samples, where high levels of antibody are less likely
19
Q

BVD diagnosis on individual level

A
  • Presence of virus (i.e. Ag) can mean
    – Animal is a PI
    – Animal is acutely infected
    -> Viraemia following acute infection lasts up to 2 weeks
  • So, to demonstrate PI animal:
    – 2 positive antigen tests >3 weeks apart
    – Usually, PIs have low/no antibody levels in both samples
  • PI animals represent the major reservoir of infection
    – Cull if discovered
  • Sensitivity and specificity of both Ab and Ag test rel. good
    – But no test is perfect… always bear this in mind, especially important when screening high numbers
  • Paired serology in acute infections can be difficult due to a slow response
    – After abortions with BVD – it won’t necessarily give a rising titre
  • Care with buying pregnant cattle (the calf may be a PI)
    – The “Trojan horse” effect
  • Some PI animals can make antibodies (rare)
20
Q

BVD diagnosis at herd level

A

Main questions:
- Is BVD present in the herd?
- Are PI calves being produced?

Antibody level:
- <0.1 = naive animal
- 0.1-0.35 = low level of exposure
- 0.35-0.70 = moderate level of exposure
- >0.7 = recent or active exposure

21
Q

BVD diagnosis at herd level - tag & test

A

– Newer way to tell whether PIs are being produced
– More expensive (as test every animal)
– But also shows which individuals are PIs
–> Allows culling
–> Normal also to test dam where PI revealed
– Becoming a more common approach

22
Q

BVD diagnosis at herd level - blood sampling a heifer cohort

A
  • Blood sample for Ab from ~ 8 months of age (maternal Ab)
    – Usually, sample 8-10 from the group
    – It should be Ab negative (and Ag if it was tested)
  • If Ab positive
    – must have seroconverted due to infection from a PI
    OR
  • Contact with an adult (acute infection or PI)
  • A useful measure of whether the infection is active in a herd
23
Q

Basic approach to BVD control

A
  • Evaluate current herd status
  • Assess the routes by which virus could enter the herd and spread within the herd
  • Eradication by removal of PIs and preventing new cases
24
Q

BVD – Diagnosis

A
  • Initial screening commonly…
    – Bulk milk Ab +/- Ag test (dairy)
    – Youngstock cohort tests (dairy and beef herds)
  • Calf tag/test results useful
    – But normally only have these once the farmer embarks on a control programme
  • PM of the spleen
  • Abortion results -> can use aborted foetuses
25
Q

BVD – Management - Eradication programme

A

Requires a committed farmer and excellent biosecurity

Need to identify and remove any PI animals
- Often via tag and test (i.e. from “now” onwards)
– Generally also test bulk milk for antigens to identify adult PIs
- Time-consuming and costly (lab fees)
- Even when PIs have gone, the virus can still be present and slow spread via acute infection is theoretically possible

Herd will become completely naïve; re-infection could result in large losses

Commonly stop Ag testing calves at some point (often 1 year after the last positive) and rely on bulk milk antibodies to detect the incursion

Protect the breeding herd and stop the birth of PI animals
- With time, any existing PIs will be culled out naturally
- Must ensure protection before first breeding
- Bovilis BVD (Intervet), Bovidec (Novartis) and Bovela (Boehringer) currently available in the UK

Care: PI animals are sometimes still produced even after a long period of vaccination
- As PI cows will still have PI calves
- Can be important for calf health

26
Q

BVD – Management - Vaccination & eradication

A

Adopt vaccination and monitor for Pis
- Usually vaccinate now plus tag & test calves born from now on
– Again, usually stop this 1 year after the last positive
- +/- adult herd testing to detect/remove PIs at the start

Leads to the most rapid and complete resolution of BVD problems within the herd and protects against re-infection: especially useful if…
- Hard/impossible to adopt biosecurity measures to keep disease out (e.g. “flying herd”)
- Large number of adult PIs and/or farmers unwilling to test/cull adults

Two main types of vaccines:
1. Inactivated (CP bovine viral diarrhoea (BVD) virus type 1)
- No replication in vivo, no viraemia following vaccination

  1. Modified live (BVDV Type 1 & 2 non-cytopathic)
    - MLV result in transient viraemia following vaccination o MLV vaccinated animals will test antigen positive for 2wks following vaccination
27
Q

BVD – Management - Do nothing

A
  • A proportion of the herd will acquire natural immunity
  • But this is random, and immunity will wane over time
  • Losses that occur as a result of infection can be significant – but are very variable and can be hidden
  • If the herd is only monitored through bulk milk Ab and is consistently low/medium positive, this is still a fairly common option, but is this appropriate?
28
Q

BVD – National control programmes

A
  • Voluntary national control schemes in England and Wales
  • Compulsory scheme in Scotland
    – Mandatory screening, restrictions on untested or “non-negative” herds
29
Q

BVD summary

A
  • aetiology: infectious dz caused by a pestivirus
  • transmission: horizontally and vertically
  • diagnosis of the individual: skin biopsies and blood samples
  • diagnosis of the herd: bulk milk
  • control strategies:
    – rigorous biosecurity measures (i.e. quarantine)
    – systematic testing
    – culling of PI animals
    – maintaining high herd immunity through vaccination