Bovine Viral Diarrhoea Virus

Description

Across the globe, cattle of all ages are affected by bovine viral diarrhoea virus (BVDV). The virus gives rise to productive and reproductive losses, causing significant economic impact

Virus

Classification

Over 60 years ago, the viral aetiology of the disease bovine viral diarrhoea was established. In the 1960s-70s, bovine viral diarrhoea virus (BVDV), together with related agents causing disease in sheep and swine, was assigned to the newly-penned “Pestivirus” genus. At this stage, Pestiviruses were considered to be non-arthropod-borne togaviruses, although it was later realised by sequencing of genomic RNA they are more taxonomically suited to the family Flaviviridae (Collett et al, 1988; Meyers et al, 1989), where they reside today.

The Flaviviridae are primarily spread via arthropod vectors, particularly mosquitoes and ticks. Genera within the family include the Flaviviruses, which cause disease in both man (such as yellow fever virus and West Nile virus) and animals (for example, louping ill), and Hepacivirus, which contains Hepatitis C virus only.

Pestiviruses, however, are not arthropod-borne, and include pathogens of cattle (BVDV), sheep and pigs. The porcine Pestivirus, classical swine fever virus (CSFV), was first documented in 1833 in Ohio (quoted by Hanson, 1957). Acute disease (classical swine fever) typically includes a raised body temperature, inco-ordination of movement and hyperaemia of the skin followed by petechial or extensive haemorrhage (Dahle and Leiss, 1992).

Border disease, caused by Border disease virus (BDV) is the ovine pestivirus and was described by Hughes et al. in 1959. Congenital infection results in the birth of “hairy shaker” lambs, which suffer tonic-clonic tremors and have hairy rather than woolly coats (Sawyer, 1992). Severity of clinical signs can vary within a flock and among litter-mates.

Transmission and Epidemiology

Epidemiology

• A major concern is that it can be confused with FMD (especially as it often occurs with clinical signs of salivation and depression)
• Virus is widespread: 60-70% exposure by 4 years of age
  • Often may sweep through a whole colony of young stock causing profuse diarrhoea (perhaps febrile) for a few days and then recover
  • Due to primary exposure to cytopathic strain of virus
• PI cows:
  • 100% vertical transmission to offspring
  • Are infected with BVDV-1nc and NEVER BVDV-1c
  • Are often antibody-negative (though they can show low levels of Ab to heterologous virus)
  • Show a wide range of clinical signs:
    • Severe congenital damage (ataxia)
    • Poor body condition
    • Increased susceptibility to enteric and respiratory disease
  • Act as the herd reservoir of BVDV
  • Can ONLY be identified by blood testing
• Transfer via semen, direct contact with acutely infected animals, or vertical from dam to offspring
• Transfer can be iatrogenic: repeated use of needles and gloves, etc.

Pathogenesis

BVDV-1c

• Infects cattle regardless of age
• Usually mild: diarrhoea with recovery in 10 dyas
• Immunosuppression can lead to secondary infection

BVDV-2nc

• Transient thrombocytopenia and leukopenia over 2 weeks
• Hemorrhages
• Secondary infection
• Death

BVDV-1nc

• Transplacental infection of naive heifers
• Outcome depends on age of fetus at contraction
  • 0-110 days: abortion or persistently infected (PI) calves born
  • 110-220 days: congenital damage with noticeable CNS and musculoskeletal lesions
  • 220 days to term: active immunity developed

Mucosal Disease

• Mucosal disease is caused by a superinfection of PI animals with a second homologous cytopathic biotype (eg BVDV-1nc followed by BVDV-1c)
• Infection typically occurs between 6-18 months of age but is variable
• Superinfection will quickly spread horizontally among PI animals
• Invariable fatal
• Characterized by oral and enteric erosions, particularly overlying Peyer's patches, and ulceration of the feet
• Animals can show anorexia, depression and/or diarrhoea for 2-5 days before death
• Vaccination can lead to iatrogenic infection in undiagnosed PI calves

Diagnosis

Laboratory Tests

• Traditional test: virus isolation followed by serology on infected cells
• ELISA for virus antigen in animals with persistent viremia (will show up 3-8 days post-infection)
• PI calves often appear virus negative as a result of receiving neutralizing Ab in colostrum: can be countered by RT-PCR
• Paired serum samples from cows with acute BVDV
• Herd sampling by ELISA for antibody on bulk milk

Pathology

Small erosions of MDV/BVDV - vesicles are microscopic (Courtesy of Alun Williams (RVC))

Coalescing lesions of BVDV (Courtesy of Alun Williams (RVC))

• Mucosal Disease: erosive condition produces small multiple, cleanly punched out lesion in mouth
• Neutrophils invade the ulcer and if bacterial colonisation occurs, further excavation follows. Either:

1. This lesion develops a granular base and becomes diphtheritic.
2. If bacterial colonisation does not take place, healing occurs within fourteen days.

• Seen in most parts of mouth (or maybe on muzzle) e.g. dental pad, cheeks, sides of tongue
• Lesions extend throughout gut with particularly big ulcers in small intestine over Peyers patches. Necrosis occurs in lymph nodes and spleen

• No vesicular stage, prickle cells die off from surface resulting in layer of necrotic debris over epithelial layer
• Infection penetrates inward through stratum germinativum.
• Epithelium does not recover as animal does not recover

Treatment and Control

• No known treatment to reverse persistent infection or to cure mucosal disease
• BUT, without exposure to BVDV, the whole herd is at risk as there is no developed immunity
• Vaccination of dams before pregnancy will prevent PI calves being born
  • Beta-propiolactone inactivated vaccine
  • Combine with screening for antigen and removal of PI animals