The Magnitude and patterns of ruminal hydrogen sulfide production, blood thiamine concentration, and mean pulmonary arterial pressure in feedlot steers consuming water of different sulfate concentrations
DOI:
https://doi.org/10.21423/bovine-vol39no1p16-22Keywords:
arteries, blood pressure, cerebrocortical necrosis, drinking water, hydrogen sulfide, polioencephalomalacia, rumen, rumen gases, steers, thiamin, toxicity, water qualityAbstract
Twenty-seven single-source, yearling crossbred steers (713 lb; 324 kg) were used to evaluate the effect of water sulfate concentration on the patterns and magnitude of ruminal gas cap hydrogen sulfide, blood thiamine concentration and mean pulmonary arterial blood pressure (mPAP). Target water sulfate concentrations were 125, 500 and 2000 mg sulfate/L of drinking water, while the observed water sulfate concentrations were 136, 583 and 2,360 mg/L. Ruminal gas cap hydrogen sulfide concentrations were measured three times per week for 10 weeks, then once a week for seven additional weeks. On days 29 and 113, whole-blood samples were collected and analyzed for thiamine concentration. Pulmonary arterial blood pressures were measured on day 100. Ruminal gas cap hydrogen sulfide concentrations decreased to day 15, then increased and peaked by day 31, and finally decreased and remained relatively stable. The peak in hydrogen sulfide concentration was associated with an event of polioencephalomalacia in the treatment group consuming water with 2,360 mg/L sulfate, and the greatest frequency of polioencephalomalacia events in cattle in an adjacent commercial feedlot consuming water with a similar sulfate concentration. Ruminal hydrogen sulfide concentration increased with increasing water sulfate concentration (P<0.05). A treatment effect on blood thiamine concentration was not detected (P=0.29). Mean pulmonary arterial pressure increased linearly with increasing water sulfate concentration (P<0.05). Ruminal gas cap hydrogen sulfide concentrations greater than 1000 ppm provide evidence of excessive sulfur consumption. Pathological concentrations of ruminal sulfides appear central to the pathogenesis of sulfur-associated polioencephalomalacia.