Transport of oxytetracycline, chlortetracycline, and ivermectin in surface runoff from irrigated pasture.

The transport of oxytetracycline, chlortetracycline, and ivermectin from manure was assessed via surface runoff on irrigated pasture. Surface runoff plots in the Sierra Foothills of Northern California were used to evaluate the effects of irrigation water application rates, pharmaceutical application conditions, vegetative cover, and vegetative filter strip length on the pharmaceutical discharge in surface runoff. Experiments were designed to permit the maximum potential transport of pharmaceuticals to surface runoff water, which included pre-irrigation to saturate soil, trimming grass where manure was applied, and laying a continuous manure strip perpendicular to the flow of water. However, due to high sorption of the pharmaceuticals to manure and soil, less than 0.1% of applied pharmaceuticals were detected in runoff water. Results demonstrated an increase of pharmaceutical transport in surface runoff with increased pharmaceutical concentration in manure, the concentration of pharmaceuticals in runoff water remained constant with increased irrigation flow rate, and no appreciable decrease in pharmaceutical runoff was produced with the vegetative filter strip length increased from 30.5 to 91.5 cm. Most of the applied pharmaceuticals were retained in the manure or within the upper 5 cm of soil directly beneath the manure application sites. As this study evaluated conditions for high transport potential, the data suggest that the risk for significant chlortetracycline, oxytetracycline, and ivermectin transport to surface water from cattle manure on irrigated pasture is low.

Host-derived nitrate boosts growth of E. coli in the inflamed gut.

Changes in the microbial community structure are observed in individuals with intestinal inflammatory disorders. These changes are often characterized by a depletion of obligate anaerobic bacteria, whereas the relative abundance of facultative anaerobic Enterobacteriaceae increases. The mechanisms by which the host response shapes the microbial community structure, however, remain unknown. We show that nitrate generated as a by-product of the inflammatory response conferred a growth advantage to the commensal bacterium Escherichia coli in the large intestine of mice. Mice deficient in inducible nitric oxide synthase did not support the growth of E. coli by nitrate respiration, suggesting that the nitrate generated during inflammation was host-derived. Thus, the inflammatory host response selectively enhances the growth of commensal Enterobacteriaceae by generating electron acceptors for anaerobic respiration.