LAUSR

The pursuit of a reduction in liver abscess disease prevalence in feedlot cattle is of great importance to animal health management and beef industry stakeholder profitability. Disease effects are multifaceted, but primarily materialize in lost feedlot performance, liver condemnation, and reduced carcass weight and quality grade. The impact is further magnified by the increased prevalence of severe, A-plus liver score type disease that is associated with carcass trim and condemnation as well as increased days on feed due to reduced average daily gain and diminished feed conversion. Liver abscess disease in cattle has long been considered to be caused by damage to the ruminal lining (rumenitis) subsequent to ruminal acidosis, followed by translocation of bacteria across the ruminal wall into the portal venous circulation, and culminating in colonization of the liver for abscess formation(s). As a result of bacterial culture frequency, Fusobacterium necrophorum ssp. necrophorum is widely considered the primary etiology even though numerous other bacteria have been isolated from liver abscesses. However, the acidosis-rumenitis-liver abscess disease complex is more complicated than the decades-long, widely accepted dogma. Portions of this are still accurate, but there is much to be learned about the pathobiology of this disease relative to where the etiological agent(s) are translocating from the gastrointestinal tract into the portal venous circulation to evade the host immune responses and multiply in the liver to form an abscess(es). To better understand the pathophysiology of this disease, recent research has been focused on model development and monitoring the time course of liver abscess formation in the live animal. Therefore, the objective of this presentation will be to highlight results of model development efforts and diagnostics to help further elucidate the challenges the beef industry faces for improving industry knowledge for the pathogenesis of liver abscess disease in feedlot cattle.