Written By: Bradford P Smith, DVM, DACVIM, Professor Emeritus
Perhaps that is what makes BVDV such an intriguing pathogen…it has worldwide distribution, has very complex biology and it seems to have many ways to do harm. The history is long and convoluted. At first it was thought that there were two separate viruses, one that caused BVD and one that caused mucosal disease, a fulminant fatal condition. Later research demonstrated that in utero fetal infection with a biotype called noncytopathic or NCP (because it does not cause visible cytopathic effects in cell culture) could result in an immunotolerant carrier calf, which later would develop a super infection with the cytopathic (CP) biotype and show mucosal disease. Still later it was determined that the CP biotype can occur by molecular rearrangement of the original NCP biotype, as well as by exposure to an external CP biotype. The antigenic relationship of the CP and NCP biotypes determines whether mucosal disease, chronic BVD, and even chronic BVD followed by recovery occurs. The literature is full of papers about BVDV.
In addition to all this complexity, BVDV can cause early embryonic death, congenital defects and abortion. In feedlot animals, it is immunosuppressive and a contributor to bovine respiratory disease complex (shipping fever). Small wonder then that there are many vaccines available, and that new information is constantly emerging. As you learn about BVDV, be prepared to find out that something different has just been discovered. We certainly don’t have all the answers yet! Be sure to visit the BVDV PowerPage at VetPrep.com to review notes which review some of the most important details about this complicated disease.