Family - Flaviviridae
Genus - Pestivirus
Biotypes - Cytopathic and non-cytopathic
Genotypes - BVDV I and BVDV II

BVDV is one of 3 pestiviruses: classical swine fever (Hog Cholera Virus), Border Disease Virus in Sheep, and BVDV, also known as mucosal disease virus.  These are single-stranded, enveloped RNA virus.  There is antigenic variation however cross-protection has been demonstrated allowing for more efficient vaccinations.1  The two biotypes can be differentiated:


  • Most common and most important economically
  • Able to cross the placenta resulting in persistently infected (PI) animals calves
  • Can be isolated from animal dying of mucosal disease

  • May mutate from non-cytopathic biotype
  • Can NOT cross the placenta
  • Associated as the cause of mucosal disease in animals already PI with the non-cytopathic biotype
  • Causes cell vaculation and cell death

Clinical Signs:

Clinical signs can vary from subclinical-death depending on a number of factors including duration, organ system involved, age at infection, immune status, pregnancy status, environmental stress, genetic diversity, antigenic variation and virulence of the BVDV strain. 

Infection of the NON-pregnant, Immunocompetent Animals
Subclinical BVDV
  • Affects all ages and sexes
  • Produces subtle-to-unrecognizable signs
    • transient inappetence, depression, fever, mild diarrhea, leucopenia which all recovers in a few days
  • Animals develop serum neutralizing antibodies to eliminate the virus
  • Subclinical BVDV cases may account for a portion of the serologically positive animals
Peracute BVDV

and Hemorrhagic Syndrome
  • Associated with non-cytopathic biotype
  • Occurs in animals affected with the peracute form of BVDV
  • CBC indicates a low platelet number
  • Clinical signs include bloody diarrhea, petechial and ecchymosed hemorrhage of the sclera of the eye, epitaxis, and abnormal bleeding
  • Animals may also show clinical signs related to osteopetrosis, anemia, thrombocytopenia, and bone marrow necrosis
  • Case fatality rate is ~25%
  • Controversial evidence indicates that postnatal infection can lead to immunosuppression

Infection of Immunocompetent Pregnant Cattle and Fetal Infection
Infection prior to insemination
  • Failure to ovulate or delayed ovulation
  • Decreased conception rates
  • Ovaritis in heifers
Insemination of cattle with contaminated Semen
  • 1st mating has poor conception rates.  The 2nd mating after that  has normal conception rates and will produce non-affected calves.
  • Semen (fresh or frozen) can be contaminated, but is not always,  by PI bulls or bulls with acute postnatal transient infection. 
  • Contamination can also be carried through infected bovine serum used for transportation or diluent of embryo transfer
Infection during embryonic period 0-45days of gestation
  • the zona pellucida helps stop the virus from access to the embryonic cells
  • the pregnant animals may show signs of viremia for 8-17days after infection
Infection during the late embryonic -early fetal period  45-125 of gestation

  • Fetal infection can lead to a wide range of abnormalities and outcomes
  • day 50-day 100 - abortion may occur a few days to several months after the infection has caused fetal death or mummification
  •  fetuses affected with the non-cytopathic biotype may become persistently infected (PI) calves.  Only the non-cytopathic biotype can affect the fetus itself as the cytopathic biotype cannot cross the placenta.
    •  PI calves:  
      • may appear health and yet still shed BVDV
      • may have retarded growth associated with decreased serum thyroid hormone levels
      • have an increased chance of  being immunotolerant to the homologous strain of virus and developing mucosal disease

Mucosal disease occurs when PI animals are infected with a cytopathic strain post-natally.  It has recently been demonstrated in studies that mucosal diseases can affect immunocompetent animals as well although it is more widely seen in PI animals.    Mucosal disease usually affects animals 6-24 months of age.

  • Sudden onset
  • Morbidity is low but case fatality is >90%
  • Clinical signs include: erosions of the oral cavity, external nares and pharynx, mucopurulent nasal discharge, laminitis, coronitis, or erosive lesions on the skin of the interdigitating cleft of all 4 feet, depression, anorexia, salivation, fever (40-41°C), tachycardia, polypnea, decreased ruminal contraction, profuse and foul smelling diarrhea which may be watery, mucosy, or bloody. 
  • Dehydration is progressive and death occurs 5-7 days after the onset of signs

  • Acute cases that do not end in death can become chronically ill with diarrhea, inappetance, progressive emaciation, rough dry hair coat, chronic bloat, and/or hoof deformities.
  • Characteristic failure of healing leads to shallow erosive lesions covered with scabs on the scrotum, preputial orifice and vulva, between the legs, and on the junction between the skin-horn junction around the dew claw, interdigitating cleft and heels.

Infection 125-175 days of gestation
  • Congential defects occur because the final stage of organogenesis of the nervous system and immune system are occurring at this time.
  • Defects seen may include cerebellar hyperplasia, and ocular abnormalities  such as retinal atrophy, optic neuritis, cataract, micro-ophtalmia with retinal dysphasia.
Infection 180days - term
  • The fetus at this time has a fully competent immune system and the virus will elicit an immune response eliminating the virus.                                              
Transmission and Pathogenesis:
The major source of virus in the herd is nasal discharge, saliva, semen, feces, urine, tears, milk, and/or aborted fetuses from PI animals.  PI animals can shed large amounts of virus throughout their entire life.  Acutely affected animals also shed the virus but to a lesser extent.  Transmission occurs with direct contact with these secretions or indirect contact via blood feeding insects, or fomites such as rectal gloves or reused needles.  BVDV does not stay in the environment past 2 week and is susceptible to common disinfectants.4

Diagnosis is based on herd history, including vaccination history, clinical signs, gross lesions, and laboratory diagnostic tests.  Diagnostic tests available include:
Diagnositc Test Available Samples Required/Used
Viral isolation
Kidney, lung, spleen
Fluorescent antibodies Kidney, lung, spleen
Immunohistochemistry Kidney, lung, spleen
Fetal Antibody titre
Pleural fluid serum
Gross Pathology 
Congenital deformities
Major organs

Treatment and Control
There is no treatment for BVDV.  If the acute form is suspected, supportive care and prevention of 2° bacterial infection with broad spectrum antibiotics, fluids, electrolytes, and vitamins may lessen the chance of a loss.4  

Control is in the hands of prevention.  Vaccinating and biosecurity are the best two preventative measures to prevent the introduction of BVDV into to a herd.  Biosecurity should involved the testing of entering animals, purchasing animals only from herds with well managed vaccination programs, isolation of new additions, and use of only AI semen that has bbeen tested, and reducing human traffic that may be potentially contaminated.3  Vaccines are available as both inactivated and modified live.  (SEE VACCINATIONS AVAILABLE)

Economic Importance:
The highest economic impact occurs in the first 2-3 years after herd has been infected.  Losses are due to:
  Neonatal mortality Prenatal growth retardation increased risk of mastitis and decreased milk production
Still births retained placentas Post-natal growth retardation  decreased reproductive capabilities   
Congenital defects Early disposal of PI calves Deaths due to mucosal disease  decreased weight gains