103 Development of a Novel, Experimental, Minimally Invasive Model to Investigate the Genesis and Etiology of Liver Abscesses in Cattle

Abstract

Abstract Most research surrounding liver abscesses involves post-hoc evaluation of naturally occurring abscesses in production settings. Few studies have been designed to experimentally induce abscesses with the purpose of identifying a time course, causality, and associated physiological implications. Therefore, we set out to develop a minimally invasive, reliable, and repeatable model to induce liver abscesses in calves in a controlled research environment to elucidate the genesis and etiology of the disease, with the ultimate goal of developing abscess reduction strategies. Experiment 1 was an attempt to induce abscesses by intraruminal inoculation with Fusobacterium necrophorum, Salmonella lubbock, and Truperella pyogenes (FST) following an intravenous lipopolysaccharide challenge. Holstein steers were harvested 3- and 10-d after inoculation, but no abscesses were detected. Experiments 2 and 3 involved diet manipulation by cycling calves on and off a high-starch, acidotic diet followed by intraruminal inoculation of microbes. In Experiment 2, Holstein calves were fed a negative control diet, an acidotic diet, and an acidotic diet plus bacterial inoculation with FST. No abscesses formed in the control or acidotic diet calves, but 43% of calves fed the acidotic diet with FST inoculation formed liver abscesses, suggesting that acidosis alone is insufficient to produce abscesses. In Experiment 3, treatments consisted of Holstein steers fed a negative control, an acidotic diet, an acidotic diet plus ruminal Fusobacterium necrophorum (F), and an acidotic diet plus Fusobacterium and Salmonella (FS). Again, there were no abscesses in the control or calves fed an acidotic diet alone; however, 40% of calves receiving F presented with an abscess, and 50% of the calves that received FS presented with abscesses. These data suggest that ruminal acidosis in conjunction with a ruminal load of pathogens commonly associated with liver abscesses provides a model that will induce liver abscesses. While the role of barrier dysfunction in the rumen and the lower gastrointestinal tract in formation of abscesses is not fully understood, this work provides a foundation to further explore the etiology of this disease and potential mitigation strategies.