172 Award Talk: The complexities of liver abscess etiology through the lens of an experimental model.

Abstract Liver abscesses (LA) in cattle are a multifactorial, polymicrobial disease first identified over a century ago. In the past decade, LA research efforts to understand the disease have increased as abscess prevalence and economic losses have risen. Extreme variations in LA prevalence across and within breed-type, region, management system, and diet composition, coupled with our inability to diagnose LA before harvest, emphasize the complex nature of this disease. The dogma of LA formation has centered around feeding high-concentrate, grain-based diets and the acidosis-rumenitis complex that allows Fusobacterium translocation from the rumen to portal circulation. To test this dogma, an experimental challenge model was developed in which repeated bouts of subacute ruminal acidosis (SARA) in combination with intraruminal inoculation with bacteria commonly found in LA resulted in 50% LA prevalence in steers. This model, and subsequent variations, have not only confirmed the aforementioned theory of LA, but have brought to light new questions and theories suggesting that the hindgut and other pathogens, besides Fusobacterium, may also play a role in LA disease etiology. In one study, steers were subjected to 4 bouts of SARA followed by bacterial inoculation which resulted in 80% LA prevalence; however, no rumenitis was present at harvest. In a follow-up study, LA occurred in steers not subjected to a high-starch diet or SARA bouts but received bacterial inoculation. These studies suggest that acidosis or rumenitis may not be necessary for LA formation. When Salmonella was introduced into this model, the prevalence and severity of LA increased, suggesting that other bacterial pathogens may also play a role in abscess formation and severity. Importantly, no LA have been observed in cattle that have not been inoculated, regardless of dietary treatment, confirming that pathogen presence and concentration is a likely driver for LA prevalence. As new questions regarding LA etiology emerge following this series of experimental studies, this model provides a foundation to elucidate LA formation and resolution. Further, this LA model offers a mechanism to test potential prevention and mitigation methods while simultaneously providing a framework to identify predictive and diagnostic biomarkers of LA in cattle prior to harvest.