Development of a novel, experimental, and minimally invasive model to investigate the genesis and etiology of liver abscesses in cattle

Authors: Broadway, Paul; NAGARAJA, T - Kansas State University; LAWRENCE, TY - West Texas A & M University; AMACHAWADI, RAGHAVENDRA - Kansas State University; Carroll, Jeffery - Jeff Carroll; Sanchez, Nicole; GALYEAN, MICHAEL - Texas Tech University; HALES, KRISTIN - Texas Tech University

Submitted to: Journal of Animal Science Supplement
Publication Type: Abstract Only
Publication Acceptance Date: 4/17/2023
Publication Date: 11/1/2023
Citation: Broadway, P.R., Nagaraja, T.G., Lawrence, T.E., Amachawadi, R., Carroll, J.A., Sanchez, N.C., Galyean, M.L., Hales, K.E. 2023. Development of a novel, experimental, and minimally invasive model to investigate the genesis and etiology of liver abscesses in cattle. Journal of Animal Science Supplement.

Interpretive Summary:

Technical Abstract: Most research surrounding liver abscesses involves post hoc evaluation of naturally occurring abscesses in production settings. Few studies have tried to experimentally induce abscesses with the purpose of identifying a time course, causality, and associated physiological implications. Therefore, the objective of these studies was to create 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 and intervention strategies. Experiment 1 sought to induce abscesses by intraruminal inoculation with Fusobacterium, Salmonella, and Truperella following an intravenous lipopolysaccharide challenge. Steers were harvested three- and ten-days post inoculation yet yielded no liver abscesses. Experiments 2 and 3 utilized diet manipulation by cycling calves on and off an acidotic diet followed by intraruminal inoculation. Experiment 2 consisted of a negative control, those fed an acidotic diet, and those fed an acidotic diet plus bacterial inoculation. No abscesses formed in the control nor acidotic diet calves; however, 50% of calves fed the acidotic diet plus bacterial inoculation formed liver abscesses, thus suggesting that acidosis alone is insufficient to produce a liver abscess. In experiment 3, treatments consisted of a negative control, calves fed an acidotic diet, calves that received an acidotic diet plus Fusobacterium necrophorum, and calves that received an acidotic diet plus Fusobacterium and Salmonella. Again, there were no abscesses in the control nor calves given an acidotic diet alone; however, 40% of calves receiving Fusobacterium presented with an abscess. Furthermore, 50% of the calves that received Fusobacterium plus Salmonella presented with abscesses. These data suggest that ruminal acidosis plus the presence of pathogens commonly associated with liver abscesses aare necessary to induce liver abscesses. While the role of barrier dysfunction in the rumen and the lower gastrointestinal tract are not yet fully understood, this work provides a foundation to further explore the etiology of this disease and potential mitigation strategies.