Bovine Viral Diarrhoea Virus

Antigenicity

• RNA virus closely related to Classical Swine Fever and Border Disease Virus
• 2 Serological Types
  • BVDV-1 is traditional, existing as two biotypes
    • BVDV-1nc: noncytopathogenic
    • BVDV-1c: cytopathogenic
  • BVDV-2 is an emerging hemorrhagic virus

Hosts

• Cattle

Pathogenesis

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

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

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

Pathology

• 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

Histology

• 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

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.

Diagnosis

• 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

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

A pestivirus which may result in abortion of fresh, autolysed or mummified foetuses. Calves may also be born alive and may be weak, uncoordinated due to cerebellar hypoplasia (cerebellar hypoplasia also seen with feline panleukopenia infection).