Isolates of bovine viral diarrhea virus (BVDV) were segregated into two groups based on comparison of sequences from the 5' untranslated region (UTR) of the viral genome. Phylogenic analysis suggested that these groups, termed BVDV I and BVDV II, are as different from each other as reference BVDV (BVDV-NADL, BVDV-SD-1, BVDV-Osloss) are from hog cholera virus. Polymerase chain reaction (PCR) tests, based on the 5' untranslated region and the genomic region coding for the p125 polypeptide, were designed to differentiate between BVDV I and BVDV II. Using these tests, 76 of 140 isolates of BVDV were identified as BVDV II. Antigenic and pathologic differences were noted between BVDV I and BVDV II viruses. Among BVDV I were viruses commonly used in vaccine production, diagnostic tests, and research. BVDV II was isolated predominantly from fetal bovine sera, persistently infected calves born to dams vaccinated against BVDV, and cattle that had died from an acute form of BVDV termed hemorrhagic syndrome.

In 1993, noncytopathic bovine viral diarrhea virus (BVDV) strains with enhanced virulence caused unprecedented outbreaks of severe acute bovine viral diarrhea (BVD) in dairy, beef, and veal herds in Ontario (Canada). Fever, pneumonia, diarrhea, and sudden death occurred in all age groups of cattle. Abortions often occurred in pregnant animals. Gross lesions in the alimentary tract were similar to those associated with mucosal disease, especially in animals >6 months of age. Cattle of all age groups had microscopic lesions in the alimentary tract similar to those seen with mucosal disease. The epidemic peaked in the summer of 1993, with 15% of all bovine accessions from diseased cattle presented to the diagnostic laboratory being associated with BVDV. The virus strains involved in the outbreak were analyzed using monoclonal and polyclonal antibodies and the polymerase chain reaction. The virus isolates from these outbreaks of severe disease were determined to be type 2 BVDV. Type 2 BVDV has been present in Ontario at least since 1981 without causing widespread outbreaks of severe acute BVD, which suggests that type 2 designation in itself does not imply enhanced virulence. Cattle properly vaccinated with type 1 BVDV vaccines appear to be protected from clinical disease.

This study charted 237 fatal cases of bovine respiratory disease (BRD) observed from May 2002 to May 2003 in a single Oklahoma feed yard. Postmortem lung samples were used for agent identification and histopathology. Late in the study, 94 skin samples (ear notches) were tested for Bovine viral diarrhea virus (BVDV) by immunohistochemistry (IHC). Bovine respiratory disease morbidity was 14.7%, and the mortality rate of all causes was 1.3%, with more than half (53.8%) attributed to BRD (0.7% total of all causes). The agents isolated were the following: Mannheimia haemolytica (25.0%), Pasteurella multocida (24.5%), Histophilus somni (10.0%), Arcanobacterium pyogenes (35.0%), Salmonella spp. (0.5%), and Mycoplasma spp. (71.4%). Viruses recovered by cell culture were BVDV-1a noncytopathic (NCP; 2.7%), BVDV-1a cytopathic (CP) vaccine strain (1.8%), BVDV-1b NCP (2.7%), BVDV-2a NCP (3.2%), BVDV-2b CP (0.5%), and Bovine herpesvirus 1 (2.3%). Gel-based polymerase chain reaction (PCR) assays were 4.6% positive for Bovine respiratory syncytial virus and 10.8% positive for Bovine coronavirus. Bovine viral diarrhea virus IHC testing was positive in 5.3% of the animals. The mean values were determined for the treatment data: fatal disease onset (32.65 days), treatment interval (29.15 days), number of antibiotic treatments (2.65), number of different antibiotics (1.89), and day of death (61.81 days). Lesions included the following: 1) duration: acute (21%), subacute (15%), chronic (40.2%), healing (2.8%), normal (18.1%), and autolyzed (2.8%); 2) type of pneumonia: lobar bronchopneumonia (LBP; 27.1 %), LBP with pleuritis (49.1 %), interstitial pneumonia (5.1 %), bronchointerstitial pneumonia (1.4%), septic (0.9%), embolic foci (0.5%), other (2.8%), normal (10.3%), and autolyzed (2.8%); and 3) bronchiolar lesions: bronchiolitis obliterans (39.7%), bronchiolar necrosis (26.6%), bronchiolitis obliterans/bronchiolar necrosis (1.4%), other bronchiolar lesions (6.5%), and bronchiolar lesion negative (25.7%). Statistically significant relationships were present among the agents, lesions, and the animal treatment, disease onset, and mortality data. Clinical illnesses observed in this study were lengthier than those reported 16–20 years ago, based on fatal disease onset, treatment interval, and day of death.

Summary: A noncytopathic bovine viral diarrhea virus (bvdv), bvdv-890, isolated from a yearling heifer that died with extensive internal hemorrhages, was compared for virulence in calves with noncytopathic bvdv-TGAN, isolated from an apparently healthy persistently infected calf. After challenge exposure with bvdv-890, nonimmune calves (n = 7) developed fever > 40 C, diarrhea, leukopenia, lymphopenia, neutropenia, and thrombocytopenia. Most calves (n = 6) died or were euthanatized by 19 days after challenge exposure. Challenge exposure with bvdv-890 did not induce disease in 2 calves that had congenital persistent infection with bvdv or in 3 calves that had neutralizing antibody titer > 4 against bvdv-890. After challenge exposure with bvdv-TGAN, nonimmune calves (n = 7) developed fever > 40 C and, rarely, diarrhea or lymphopenia. All of those calves survived challenge exposure. The average maximal titer of bvdv-890 isolated from serum was 1,000 times that of bvdv-TGAN. In calves infected with bvdv-890, the average maximal percentages of lymphocytes and platelets associated with virus were greater than those found in calves infected with bvdv-TGAN. Additional findings of epidemiologic significance were prolonged shedding of virus and delayed production of viral-neutralizing antibody in 1 calf challenge-exposed with bvdv-890. Also, after production of neutralizing antibody, mutant virus that was refractory to neutralization was isolated from calves challenge-exposed with bvdv-TGAN.