Zoonotic bacterial populations, gut fermentation characteristics and methane production in feedlot steers during oral nitroethane treatment and after the feeding of an experimental chlorate product.

Nitroethane inhibits the growth of certain zoonotic pathogens such as Campylobacter and Salmonella spp., foodborne pathogens estimated to cause millions of human infections each year, and enhances the Salmonella- and Escherichia coli-killing effect of an experimental chlorate product being developed as a feed additive to kill these bacteria immediately pre-harvest. Limited studies have shown that nitroethane inhibits ruminal methane production, which represents a loss of 2-12% of the host's gross energy intake and contributes to global warming and destruction of the ozone layer. The present study was conducted to assess the effects of 14-day oral nitroethane administration, 0 (0X), 80 (1X) or 160 (2X)mg nitroethane/kg body weight per day on ruminal and fecal E. coli and Campylobacter, ruminal and fecal methane-producing and nitroethane-reducing activity, whole animal methane emissions, and ruminal and fecal fermentation balance in Holstein steers (n=6 per treatment) averaging 403+/-26 (SD) kg BW. An experimental chlorate product was fed the day following the last nitroethane administration to determine effects on E. coli and Campylobacter. The experimental chlorate product decreased (P<0.001) fecal, but not ruminal (P>0.05) E. coli concentrations by 1000- and 10-fold by 24 and 48 h, respectively, after chlorate feeding when compared to pre-treatment concentrations (>5.7 log(10) colony forming units/g). No effects (P>0.05) of nitroethane or the experimental chlorate product were observed on fecal Campylobacter concentrations; Campylobacter were not recovered from ruminal contents. Nitroethane treatment decreased (P<0.01) ruminal (8.46, 7.91 and 4.74+/-0.78 micromol/g/h) and fecal (3.90, 1.36 and 1.38+/-0.50 micromol/g/h) methane-producing activity for treatments 0X, 1X and 2X, respectively. Administration of nitroethane increased (P<0.001) nitroethane-reducing activity in ruminal, but not fecal samples. Day of study affected ruminal (P<0.0001) but not fecal (P>0.05) methane-producing and nitroethane-reducing activities (P<0.01); treatment by day interactions were not observed (P>0.05). Ruminal accumulations of acetate decreased (P<0.05) in 2X-treated steers when compared with 0X- and 1X-treated steers, but no effect (P>0.05) of nitroethane was observed on propionate, butyrate or the acetate to propionate ratio. Whole animal methane emissions, expressed as L/day or as a proportion of gross energy intake (%GEI), were unaffected by nitroethane treatment (P>0.05), and were not correlated (P>0.05) with ruminal methane-producing activity. These results demonstrate that oral nitroethane administration reduces ruminal methane-producing activity but suggest that a microbial adaptation, likely due to an in situ enrichment of ruminal nitroethane-reducing bacteria, may cause depletion of nitroethane, at least at the 1X administration dose, to concentrations too low to be effective. Further research is warranted to determine if the optimization of dosage of nitroethane or related nitrocompouds can maintain the enteropathogen control and anti-methanogen effect in fed steers.