In case #1, veterinarians observed uncommon BVDV presentations such as these tongue lesions.
In case #1, veterinarians observed uncommon BVDV presentations such as these tongue lesions.

If you ask a practitioner to describe a “typical” outbreak of bovine viral diarrhea (BVD) you might get a variety of answers. In fact, the more experience one has with BVD the less willing one might be to give a definitive answer. The clinical manifestations that are lumped under the term BVD are many and varied and include respiratory, reproductive and enteric disease. Multiple “forms” of BVD are recognized. Among these are acute uncomplicated BVD, severe acute BVD (including hemorrhagic syndrome), acute BVD-respiratory disease, acute BVD-reproductive disease, persistent infection and mucosal disease. Many practitioners have a mental check list of clinical signs that would lead them to test for BVD and, conversely, a check list of signs that they would not associate with BVD. This article will discuss cases which, at first blush, “just didn’t look like BVD.”

The collection of disease syndromes referred to as BVD is caused by infection with any one of three different species of virus: bovine viral diarrhea virus type 1 (BVDV1), bovine viral diarrhea virus type 2 (BVDV2) and a newly emerging group of viruses called HoBi-like viruses. So far the only BVD pathogens found in the United States are BVDV1 and BVDV2. All BVD pathogens may exist as one of two biotypes — cytopathic and noncytopathic. This designation has nothing to do with virulence but reflects whether or not viral infection of cultured epithelial cells results in cell death. In nature, viruses from the noncytopathic biotype predominate by a large margin and all high-virulence viruses are noncytopathic. In general, cytopathic viruses are only isolated from mucosal disease cases  and are thought to arise from noncytopathic viruses via genetic recombination. There is a wide range of virulence among the noncytopathic viruses circulating in the field. However, most highly virulent viruses are rare. While it appears both biotypes may cross the placenta and infect the fetus, only viruses from the noncytopathic biotype establish persistent infection in the fetus. Because the immune system of the persistently infected fetus does not recognize viral proteins as foreign, the virus is never cleared, thus setting up a lifelong infection. While persistently infected animals (PIs) are the major vector for introducing BVD into herds and PIs tend to have more health problems than normal animals, most of the economic damage resulting from BVD is associated with acute infections.

When BVD doesn’t look like BVDCase #1 — Severe oral and mucosal lesions associated with acute BVD infection
Bill Hessman, Haskell County Animal Hospital LLC, was called in to consult on a disease outbreak in the fall of 2008 in a northwest Texas feedlot. The high morbidity and mortality plus severity of lesions initially raised concerns about the presence of a new pathogen or the introduction of a foreign pathogen into the herd. Signs included fever and extensive ulcerative lesions of the larynx, trachea and esophagus. Two lots of heifers were involved in the outbreak. Of the 159 calves in lot A, 119 became ill and 45 died. Of the 45 mortalities, 22 had marked mucosal lesions. Losses were smaller in lot B, with 79 out of 160 animals sick and six dying. Three of the six dead animals had extensive mucosal lesions. The lesions observed were described in the Journal of Veterinary Diagnostic Investigation thusly:

“Grossly, the mucosal lesions observed on necropsy varied dramatically. Lesions were observed in the oral cavity on buccal surfaces and tongue, and in the larynx, trachea and esophagus. Small infrequent, 1-3 mm, irregular but sharp-edged ulcerations without gross necrotic material were observed in the esophagus of some animals but others had extensive, multifocal, 1mm to 1 cm, circular to ovoid mucosal ulcerations involving the majority of the esophagus with and without necrotic debris. Yet other animals with esophageal involvement showed more proliferative, raised, necrotic lesions. The lesions varied in size from 1-5 mm, circular, raised lesions to up to 1 cm wide and 4 cm long coalescing, raised, proliferative lesions. Some animals showed extensive, coalescing ulcerations involving greater than 50 percent of the upper esophageal mucosa, which contained firm, yellowish, plaque-like necrotic debris that was not proliferative.

“Mucosal lesions of the larynx showed large, 1 cm, circular to ovoid mucosal ulcerations with necrotic material but in other animals the lesions were small circular (3-5 mm), raised, proliferative lesions. Gross lesions of the tongue were observed in two animals. One animal showed circular, 3-5 mm ulcerations but the other animal had circular, raised, proliferative, 3-8 mm lesions.”

Based on the severe oral lesions, differential diagnosis included vesicular stomatitis, papular stomatitis and footand- mouth disease. Samples from 11 of the dead calves were tested by virus isolation and immunohistochemistry (IHC) in Robert Fulton’s lab in the Department of Veterinary Pathobiology at Oklahoma State University. At least one tissue from each of the 11 fatalities was positive for BVDV by IHC. Comparison of sequences from the isolated viruses, conducted at the National Animal Disease Center, demonstrated that the same BVDV2 strain was isolated from animals in both lots. Due to the timing of the mortalities, it is hypothesized that the BVDV2 infection originated in lot A and then spread to lot B. No further outbreaks of this disease were subsequently seen in this feedlot.

When BVD doesn’t look like BVDCase #2 — Late-term abortions and severe skeletal deformities
BVD reproductive losses are usually associated with early-term abortions. However, in case #2, the clinical presentation was lateterm abortions, preterm calves and congenital defects. Further, the skeletal deformities observed following BVD fetal infections are rarely as severe as those seen in this case, worked up by Patricia Blanchard, of the California Animal Health and Food Safety Laboratory, University of California- Davis. The outbreak occurred in a group of 37 first-calf heifers. At 1 week of age these heifers had been vaccinated with a killed vaccine. From 5 months to 12 months of age these heifers were housed at heifer ranch A. No vaccinations were given at ranch A.

At 12 months of age they were moved to heifer ranch B. Heifer ranch B also housed heifers from three other dairies. A second dose of killed vaccine was delivered at arrival at ranch B. The heifers were six- to seven-months pregnant when they were returned to the home dairy. Approximately eight weeks before the onset of abortions in the heifers, an outbreak of pyrexia and diarrhea was observed in postpartum cows in the herd. Over a four-week period in May 2004, 19 out of 37 heifers aborted or gave birth two to four weeks early. In the first week of the outbreak, seven heifers delivered seven either stillborn or premature live calves that had severe deformations including notably shortened mandibles.

One calf had particularly severe congenital defects including absence of forelimbs, cleft palate and no bone covering the dorsal central 9 cm of the brain. Tissues from four of the calves were submitted for testing. BVDV infection was confirmed in all four calves. Phylogenetic analysis, conducted at the National Animal Disease Center, identified the virus as a BVDV1 strain. Experimental infection of calves with this virus resulted in a more pronounced clinical presentation than that typically observed with BVDV1 strains. The clinical presentation included pyrexia, leukopenia and thrombocytopenia. Experimental infection of fetuses in the first trimester of pregnancy led to persistent infection but not fetal deformities. It may be that the congenital deformities observed were due to infections that occurred later in gestation.

When BVD doesn’t look like BVDCase #3 — Congenital tremor
BVD in utero can result in morphologic defects in the CNS. Grossly observable congenital neural abnormalities such as cerebellar hypoplasia, hydranencephaly, internal hydrocephalus, microencephaly and proencephaly are commonly associated with BVD. Due to recent reports, we are now beginning to realize that such gross abnormalities may be only the tip of the iceberg and that defects that can only be observed microscopically may play a bigger role than previously thought. A 2009 paper in the Veterinary Record reported an association between BVD and congenital tremor. This study was based on characterization of 23 different outbreaks of neurological disease in England and Wales occurring between 1991 and 2007. The most common clinical presentation was tremor apparent in calves from birth.

Most of the calves were recumbent or only able to stand with support, but none had clear macroscopic skeletal or visceral abnormalities. Upon necropsy it was found that all the calves had diffuse neuraxial hypomyelination and that BVDV antigen was present. A similar finding was observed by Brian Porter, Department of Veterinary Pathobiology, Texas A&M, in a longhorn calf submitted to the Texas A&M Veterinary Teaching Hospital. The newborn calf was unable to rise, exhibited generalized tremors, ataxia and horizontal and vertical nystagmus. The calf was euthanized at 8 days of age and necropsied. The brain and spinal cord appeared normal by gross examination. Macroscopically the most notable observation was that myelin sheaths were absent or markedly thinner in comparison with normal calves. IHC for BVDV antigen was positive for a number of cell types in the CNS. The infecting virus was identified as a BVDV2 strain by researchers at the National Animal Disease Center. These findings suggest that BVD should be considered as one of the main differential diagnoses of congenital tremor in calves.

Due to the sheer number of different clinical presentations existing under the BVD umbrella, diagnosing BVD based on clinical signs is not advisable. Thus diagnosis relies upon testing of samples in diagnostic laboratories. In the United States, most of the diagnostic effort has been focused on identifying and culling animals persistently infected with BVD pathogens.

The Academy of Veterinary Consultants recommends that testing for animals persistently infected with a BVD pathogen be incorporated into both beef and dairy biosecurity plans. However, as case #1 illustrates, outbreaks of acute BVD can result in substantial losses. Based on surveillance data, it is estimated that 85 percent of cattle in the United States have been exposed to a BVD pathogen, and 10 percent of herds currently harbor a persistently infected animal. The question is not whether practitioners will witness an outbreak of BVD but when they will witness it. Their ability to recognize BVD when they see it depends on regularly including BVD as a differential in their case workups.

Suggested reading
Blanchard PC, Ridpath JF, Walker JB, Hietala SK: 2010, An outbreak of late-term abortions, premature births, and congenital deformities associated with a bovine viral diarrhea virus 1 subtype b that induces thrombocytopenia. J Vet Diagn Invest 22:128-131.

Evermann JF, Barrington GM: 2005, Clinical features. In: Bovine viral diarrhea virus: Diagnosis, Management and Control, eds. Goyal SM, Ridpath JF, pp. 105-120. Blackwell Publishing, Ames, IA.

Hessman BE, Sjeklocha DB, Fulton RW, Ridpath JF, Johnson BJ, McElroy DR: 2012, Acute bovine viral diarrhea associated with extensive mucosal lesions, high morbidity, and mortality in a commercial feedlot. J Vet Diagn Invest 24:397-404.

Porter BF, Ridpath JF, Calise DV, Payne HR, Janke JJ, Baxter DG, Edwards JF: 2010, Hypomyelination associated with bovine viral diarrhea virus type 2 infection in a longhorn calf. Vet Pathol 47:658-663.


BVD forms associated with acute infections


Age, reproductive status, contributing factors

Clinical presentation

Acute BVD

  • immunocompetent animal in good health
  • typical virulence virus
  • either cytopathic or noncytopathic biotype
  • infecting virus may belong to BVDV1, BVDV2 or HoBi like species
  • 70 – 90 % of cases subclinical
  • mild short duration low grade pyrexia
  • leukopenia
  • loss of function in remaining immune cells
  • immune suppression may outlast viremia
  • limited viral shed

Severe acute BVD

  • high virulence BVDV (typically BVDV2 but outbreaks have been associated with BVDV1)
  • age of animal not a factor in clinical presentation
  • pyrexia greater than 105 C lasting more than 4 days
  • profuse diarrhea
  • pronounced immune tissue depletion
  • may observe death loss
  • may see lesions over Peyers patches

Hemorrhagic syndrome

  • only reported with BVDV2 infections
  • age of animal not a factor in clinical presentation
  • clinical presentation the same as for severe acute BVDV with the following additions;
    • bloody diarrhea
    • thrombocytopenia
    • petechial hemorrhages on tongue, palate, gum line
    • bleeding from injection sites or insect bites

Reproductive failure

  • infecting virus may belong to BVDV1, BVDV2 or HoBi like species
  • Abortions most common during the first trimester although late term abortions may occur
    • 6-10% of infectious abortions in cattle
    • fetal reabsorption
    • mummification
    • reduction in conception rates

Fetal infections

  • in field most commonly observed with noncytopathic virus although cytopathic virus can infect under experimental conditions
  • infecting virus may belong to BVDV1, BVDV2 or HoBi like species
  • Outcome dependent on stage of gestation


  • Congenital defects particularly of the central nervous system
  • Persistent infection if exposed between 30-125 days gestation to a noncytopathic virus
  • Ataxia, remors, wide-based stance, stumbling, “dummy calves”, failure or inability to nurse

Respiratory disease

  • While HoBi-like, BVDV1 and BVDV2 infections may result in primary acute respiratory disease under some conditions, these pathogens are thought to function more to predispose animals to respiratory disease
  • Bovine respiratory disease complex (BRDC)

BVD forms associated with persistent infections

Chronic BVD

  • Persistent infection with a noncytopathic BVDV1 or BVDV2*
  • Persistent loose feces or intermittent diarrhea
  • Ill thrift
  • Anorexia
  • Chronic recurrent bloat
  • Interdigital erosions
  • Chronic laminitis
  • alopecia

Mucosal disease

  • Persistent infection with a noncytopathic BVDV1 or BVDV2 followed by superinfection with a cytopathic BVDV1 or BVDV2*
  •   Case fatality rate approaches 100%
  • pyrexia, anorexia, tachycardia, polypnea, profuse watery diarrhea
  • erosions and ulcers may be present on tongue, palate, gingival, interdigital regions, coronary bands, teats, vulva and prepuce
  • necrotizing ulcers and erosions throughout the GI tract

*While these forms of BDV have not been observed with HoBi-like viruses, this might be due to recent emergence and limited observation rather than an inability of this species of virus to cause this form of the disease.