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Predicted ages of dairy calves when colostrumderived bovine viral diarrhea virus antibodies would no longer offer protection against disease or interfere with vaccination

Claudia A. Muñoz-ZanziDepartment of Medicine and Epidemiology, University of California, Davis, CA 95616.
Present address is Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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 DVM, PhD
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Mark C. ThurmondDepartment of Medicine and Epidemiology, University of California, Davis, CA 95616.

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Wesley O. JohnsonSchool of Veterinary Medicine, and the Department of Statistics, University of California, Davis, CA 95616.

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Sharon K. HietalaCalifornia Animal Health and Food Safety Laboratory, University of California, Davis, CA 95616.

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Abstract

Objective—To develop models that could be used to predict, for dairy calves, the age at which colostrumderived bovine viral diarrhea virus (BVDV) antibodies would no longer offer protection against infection or interfere with vaccination.

Design—Prospective observational field study.

Animals—466 calves in 2 California dairy herds.

Procedure—Serum BVDV neutralizing antibody titers were measured from birth through 300 days of age. The age by which colostrum-derived BVDV antibodies had decayed sufficiently that calves were considered susceptible to BVDV infection (ie, titer ≤ 1:16) or calves became seronegative was modeled with survival analysis methods. Mixed-effects regression analysis was used to model colostrum-derived BVDV antibody titer for any given age.

Results—Half the calves in both herds became seronegative for BVDV type I by 141 days of age and for BVDV type II by 114 days of age. Rate of antibody decay was significantly associated with antibody titer at 1 to 3 days of age and with whether calves were congenitally infected with BVDV. Three-month-old calves were predicted to have a mean BVDV type-I antibody titer of 1:32 and a mean BVDV type-II antibody titer of 1:16.

Conclusions and Clinical Relevance—Results provide an improved understanding of the decay of BVDV-specific colostrum-derived antibodies in dairy calves raised under typical field conditions. Knowledge of the age when the calf herd becomes susceptible can be useful when designing vaccination programs aimed at minimizing negative effects of colostrum-derived antibodies on vaccine efficacy while maximizing overall calf herd immunity. (J Am Vet Med Assoc 2002;221:678–685)

Abstract

Objective—To develop models that could be used to predict, for dairy calves, the age at which colostrumderived bovine viral diarrhea virus (BVDV) antibodies would no longer offer protection against infection or interfere with vaccination.

Design—Prospective observational field study.

Animals—466 calves in 2 California dairy herds.

Procedure—Serum BVDV neutralizing antibody titers were measured from birth through 300 days of age. The age by which colostrum-derived BVDV antibodies had decayed sufficiently that calves were considered susceptible to BVDV infection (ie, titer ≤ 1:16) or calves became seronegative was modeled with survival analysis methods. Mixed-effects regression analysis was used to model colostrum-derived BVDV antibody titer for any given age.

Results—Half the calves in both herds became seronegative for BVDV type I by 141 days of age and for BVDV type II by 114 days of age. Rate of antibody decay was significantly associated with antibody titer at 1 to 3 days of age and with whether calves were congenitally infected with BVDV. Three-month-old calves were predicted to have a mean BVDV type-I antibody titer of 1:32 and a mean BVDV type-II antibody titer of 1:16.

Conclusions and Clinical Relevance—Results provide an improved understanding of the decay of BVDV-specific colostrum-derived antibodies in dairy calves raised under typical field conditions. Knowledge of the age when the calf herd becomes susceptible can be useful when designing vaccination programs aimed at minimizing negative effects of colostrum-derived antibodies on vaccine efficacy while maximizing overall calf herd immunity. (J Am Vet Med Assoc 2002;221:678–685)