Bovine Viral Diarrhoea (BVD) Flashcards
BVD Background
- 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
Why is BVD important?
- 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
BVD - Aetiology
- 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
BVDv subtypes
- 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
BVD - host range
- BVDV includes most even-toed ungulates
- Many species can be affected, domestic cattle seem to be the primary host
BVD transmission
- 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)
BVD - Pathogenesis
- 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
BVD infection: non-pregnant animals - CS
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)
BVD infection during pregnancy - CS
- 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)
PI animal
= 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
BVD infection during pregnancy - PI
- 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
Acute BVD infection during pregnancy - PI CS
- PI’s often small and stunted but can be clinically completely normal until they develop MD
BVD mucosal dz - CS
- 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
BVD infection in bulls - CS
- 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
BVD 1 CS
- Acute infection
– Mild systemic illness
– Reduced reproductive performance
– Immunosuppression - Mucosal disease (PI animals)