Abstract
Holstein steers (n = 40; initial body weight [BW] = 96.0 ± 10.5 kg) were individually housed in a climate-controlled barn to evaluate potential models for the genesis of liver abscesses (LA). In this 2 × 2 factorial, steers were balanced by BW and randomly assigned to one of two treatments: 1) intravenous saline injection followed by intraruminal bacterial inoculation with Fusobacterium necrophorum subsp. necrophorum (1 × 109 colony forming unit [CFU]/mL) and Salmonella enterica serovar Lubbock (1 × 106 CFU/mL; CON; n = 20 steers); or 2) intravenous injection with 0.25 µg/kg BW of lipopolysaccharide (LPS; Escherichia coli O111:B4) followed by intraruminal bacterial inoculation of F. necrophorum subsp. necrophorum (1 × 109 CFU/mL) and S. enterica serovar Lubbock (1 × 106 CFU/mL; LBI; n = 20 steers) and 1 of 2 harvest dates (3 or 10 d post LPS infusion). Body weights were recorded on days -4, -1, 3, and 10, and blood was collected for hematology on days -4, 3, and 10, relative to LPS infusion on day 0. Intraruminal bacterial inoculation occurred on day 1. Steers from each treatment group were harvested at two different time points on day 3 or 10 to perform gross pathological examination of the lung, rumen, liver, LA (if present), and colon. Feed disappearance was less for LBI than CON (P < 0.01); however, BW did not differ (P = 0.33) between treatments. Neither treatment nor time differed for hematology (P ≥ 0.13), and no gross pathological differences were noted in the lung, liver, LA, or colon (P ≥ 0.25). A treatment × harvest date interaction was noted for ruminal pathology in which LBI had an increased percentage of abnormal rumen scores on day 3 (P < 0.01). These results suggest that an LPS challenge in combination with intraruminal bacterial inoculation of pathogens commonly isolated from LA was not sufficient to induce LA in steers within 3 or 10 d (P = 0.95) when compared to CON. Further evaluation is needed to produce a viable model to investigate the genesis and prevention of LA in cattle.