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- Author or Editor: David J. Steffen x
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Abstract
Objective—To evaluate protection resulting from use of a modified-live noncytopathic bovine viral diarrhea virus (BVDV) type 1 vaccine against systemic infection and clinical disease in calves challenged with type 2 BVDV.
Animals—10 calves, 5 to 7 months of age.
Procedures—Calves were allocated (n = 5/group) to be nonvaccinated or vaccinated SC on day 0 with BVDV 1 (WRL strain). Calves in both groups were challenged intranasally with BVDV type 2 isolate 890 on day 21. Rectal temperatures and clinical signs of disease were recorded daily, and total and differential WBC and platelet counts were performed. Histologic examinations and immunohistochemical analyses to detect lesions and distribution of viral antigens, respectively, were performed.
Results—After challenge exposure to BVDV type 2, nonvaccinated calves developed high rectal temperatures, increased respiratory rates, viremia, leukopenia, lymphopenia, and infection of the thymus. Vaccinated calves did not develop high rectal temperatures or clinical signs of respiratory tract disease. Vaccinated calves appeared to be protected against systemic replication of virus in that they did not develop leukopenia, lymphopenia, viremia, or infection of target organs, and infectious virus was not detected in peripheral blood mononuclear cells or the thymus.
Conclusions and Clinical Relevance—The modified-live BVDV type 1 vaccine protected against systemic infection and disease after experimental challenge exposure with BVDV type 2. The vaccine protected calves against infection and viremia and prevented infection of target lymphoid cells.
Abstract
Objective—To evaluate protection against systemic infection and clinical disease provided by use of a modified-live noncytopathic bovine viral diarrhea virus (BVDV) type 1 vaccine in calves challenged with NY-1 BVDV.
Animals—10 calves, 5 to 7 months of age.
Procedures—Calves were allocated (n = 5/group) to be nonvaccinated or vaccinated SC on day 0 with BVDV type 1 (WRL strain). Calves in both groups were challenged intranasally with NY-1 BVDV on day 21. Calves' rectal temperatures and clinical signs of disease were recorded daily, total and differential WBC and platelet counts were performed, and serum neutralizing antibody titers against NY-1 BVDV were determined. Histologic examinations and immunohistochemical analyses to detect gross lesions and distribution of viral antigens, respectively, were performed.
Results—After challenge exposure to NY-1 BVDV, nonvaccinated calves developed high rectal temperatures, increased respiratory rates, viremia, leukopenia, lymphopenia, and infection of the thymus. Vaccinated calves did not develop high rectal temperatures or clinical signs of respiratory tract disease. Vaccinated calves appeared to be protected against systemic replication of virus in that they did not develop leukopenia, lymphopenia, viremia, or infection of target organs, and infectious virus was not detected in peripheral blood mononuclear cells or the thymus.
Conclusions and Clinical Relevance—The modifiedlive BVDV vaccine protected calves against systemic infection and disease after experimental challenge exposure with NY-1 BVDV. The vaccine protected calves against infection and viremia and prevented infection of target lymphoid cells. (Am J Vet Res 2005;66:1785–1791)
Abstract
Objective—To determine the comparative virulence of 5 isolates of bovine viral diarrhea virus (BVDV) type II by inoculating 6- to 9-month-old beef calves with isolates originating from the tissues of cattle affected with naturally occurring, transient, acute, nonfatal infections or naturally occurring, peracute, fatal infections.
Animals—22 calves that were 6 to 9 months old.
Procedure—The study used BVDV isolates 17011, 713, and 5521 that originated from fetuses aborted from cows with transient, nonfatal, acute BVDV infections and isolates 23025 and 17583 that originated from the tissues of cattle with peracute, fatal BVDV infections. Calves were allotted to 6 groups (1, mockinfected control calves [n = 2]; 2, inoculated with BVDV 17011 [4]; 3, inoculated with BVDV 713 [4]; 4, inoculated with BVDV 5521 [4]; 5, inoculated with BVDV 23025 [4]; and 6, inoculated with BVDV 17583 [4]). Rectal temperatures and clinical signs of disease were recorded daily. Total and differential WBC and platelet counts were performed. Histologic examination and immunohistochemical analysis were conducted to detect lesions and distribution of viral antigens, respectively.
Results—Calves inoculated with BVDV 23025 or 17583 developed more severe clinical signs of disease (fever and diarrhea), more severe lymphopenia, and more severe lesions (alimentary epithelial necrosis, lymphoid depletion, and BVDV antigen deposition in lymphatic tissues), compared with calves inoculated with BVDV 713, 5521, or 17011.
Conclusions and Clinical Relevance—Relative severity of experimentally induced infections corresponded to severity of clinical signs of naturally occurring infections with respective BVDV isolates. (Am J Vet Res 2002;63:1379–1384)
Abstract
Objective—To compare experimentally induced concurrent infection with bovine viral diarrhea virus (BVDV) and bovine rotavirus (BRV) with infection of either virus alone in calves.
Animals—Seventeen 1-day-old gnotobiotic calves.
Procedure—Calves were allotted to 8 treatments as follows: group 1, mock-infected control calves (n = 2); group 2, inoculated with BVDV on day 1 (2); groups 3, 5, and 7, inoculated with BRV on days 1 (2), 4 (1), or 7 (2), respectively; and groups 4, 6, and 8, inoculated with BVDV on day 1 and with BRV on days 1 (2), 4 (2), or 7 (4), respectively. Concentrations of BVDV in serum and ileal tissues were measured, and BRV shedding in feces was determined. Histologic examination and immunohistochemical analysis were conducted to detect lesions and viral antigens.
Results—Neonatal calves inoculated with BVDV alone or with BVDV on day 1 and BRV on day 7 developed villus atrophy and submucosal inflammation of the intestines. Concurrent BVDV and BRV infections acted synergistically in the intestinal tract, causing more severe enteric disease than infection with either virus alone. Severe lymphoid depletion was associated with BVDV infection in calves regardlesss of concurrent BRV infection.
Conclusions and Clinical Relevance—Infection with BVDV played direct and indirect roles in enteritis in neonatal calves, causing villus atrophy in the duodenum and submucosal inflammation of the intestines. Also, BVDV potentiated effects of BRV. Concurrent infection with BVDV and BRV resulted in more severe enteric disease in neonatal calves than infection with BRV or BVDV alone. (Am J Vet Res 2002;63:1179–1186)
Abstract
Objective—To characterize the influence of the viral protein Npro on virulence of bovine viral diarrhea virus (BVDV) and on type I interferon responses in calves.
Animals—10 calves, 4 to 6 months of age.
Procedures—BVDV virulence and type I interferon responses of calves (n = 5) infected with a noncytopathic BVDV with a deleted Npro were compared with those of calves (5) infected with a noncytopathic BVDV with a functional Npro. Rectal temperatures, clinical signs, platelet counts, and total and differential WBC counts were evaluted daily. Histologic examinations and immunohistochemical analyses of tissues were conducted to assess lesions and distribution of viral antigens, respectively. Serum type I interferon concentrations were determined.
Results—Calves infected with Npro-deleted BVDV developed leukopenia and lymphopenia, without developing increased rectal temperatures or lymphoid depletion of target lymphoid organs. There was minimal antigen deposition in lymphoid organs. Calves infected with Npro BVDV developed increased rectal temperatures, leukopenia, lymphopenia, and lymphoid depletion with marked BVDV antigen deposition in lymphatic tissues. Interferon type I responses were detected in both groups of calves.
Conclusions and Clinical Relevance—Deletion of Npro resulted in attenuation of BVDV as evidenced by reduced virulence in calves, compared with BVDV with a functional Npro. Deletion of Npro did not affect induction of type I interferon. The Npro-deleted BVDV mutant may represent a safe noncytopathic virus candidate for vaccine development.
Abstract
Objective—To determine outcome of equids in the western United States with clinical signs of West Nile virus (WNV) infection and identify factors associated with risk of death in infected equids.
Design—Cross-sectional study.
Animals—484 equids in Nebraska and Colorado.
Procedure—Owners of 484 equids with laboratoryconfirmed West Nile virus infection in Nebraska and Colorado were contacted by telephone, and a questionnaire was used to obtain information on signalment, management, clinical signs, date of disease onset, duration of disease, WNV vaccination status, and health status at the time of the interview.
Results—137 of 482 (28.4%) animals died or were euthanatized. Ataxia, lethargy, muscle fasciculations, and weakness were the most common clinical signs of disease. Animals ≥ 3 years old were more likely to die than were animals ≤ 2 years old. Unvaccinated equids were twice as likely to die as were animals that had been vaccinated at least once prior to the onset of disease. Animals that were recumbent and unable to rise were 78 times as likely to die as were animals that never lost the ability to rise. Females were 2.9 times as likely to die as males. Two hundred seventy-one of 339 (79.9%) animals that survived recovered fully; mean duration of disease for these animals was 22.3 days.
Conclusions and Clinical Relevance—Among equids with WNV infection, age, vaccination status, an inability to rise, and sex were associated with the risk of death. (J Am Vet Med Assoc 2004;225:267–274)
Abstract
Objective—To determine the prevalence of bovine viral diarrhea virus (BVDV)–infected alpaca herds in the United States and investigate factors associated with seropositive herd status and, subsequently, determine the proportion of animals within seropositive alpaca herds that are persistently infected (PI) carriers for BVDV, obtain information regarding previous herd exposure to BVDV, determine titers of anti-BVDV antibodies of dams, and ascertain whether individual seropositive crias had received supplemental colostrum at birth.
Design—Prevalence study.
Animals—63 alpaca herds with ≥ 12 registered female alpacas.
Procedures—250 alpaca breeders were randomly selected from 562 eligible herds listed in the Alpaca Owner and Breeders Association membership directory and mailed a voluntary participation request. Sixty-three alpaca breeders participated in the study. From each herd, blood samples from ≥ 4 crias were tested for BVDV, BVDV RNA, and serum neutralizing antibodies against BVDV. A region of the genome of BVDV recovered from PI crias was sequenced to determine genetic homology.
Results—Among the 63 herds, 16 (25.4%) had seropositive crias and 4 (6.3%) had PI crias. Infections in 3 of the 4 herds with PI crias were linked as evidence by the genetic homologies of viruses. In addition to PI crias, feeding supplemental colostrum was associated with herd seropositivity.
Conclusions and Clinical Relevance—Results confirmed the importance of BVDV infections in alpacas in the United States and highlighted the importance of determining the BVDV infection status of animals before they are commingled to limit exposure of herds to BVDV infection.