D. Glenn Kennedy

Intact nitrofurazone is present in whole eyes of chickens fed varying levels of this banned antibiotic and may therefore be used as an alternative to the controversial marker residue, semicarbazide, to monitor for abuse of this drug in primary production.

Nitrofuran metabolite residues AOZ, AMOZ, AHD and SEM were detected at parts per million concentrations in retina of pigs fed therapeutic doses of nitrofuran antibiotics. Discovery of this residue depot may allow widespread technology transfer to laboratories lacking LC-MS/MS thus improving global monitoring of these drugs.

Carbadox cannot be used in food-producing animals within the European Union following the adoption of Commission Regulation EC 2788/98/EC. Monitoring of the longest remaining residue—quinoxaline-2-carboxylic acid (QCA)—is the most effective way of enforcing the prohibition on its use. The study was under taken to determine if QCA could be passed from pig to pig following the exposure of unmedicated animals to housing that had previously contained medicated animals. Drug-withdrawal studies were also carried out on medicated animals. Distinction between treated animals and those exposed to QCA might be required by competent national authorities to determine whether a positive result for QCA in tissue is truly ‘violative’. Comparison of the ratio concentrations of QCA in tissues and body fluids was made to determine if they could be used as criteria for discrimination between illegally treated animals and environmental contamination.

A method is described for the quantitative determination of quinoxaline-2-carboxylic acid (QCA), the marker residue for the veterinary drug carbadox, in swine liver. Tissue is subjected to alkaline hydrolysis followed by liquid–liquid extraction. QCA residues are cleaned up using automated solid phase extraction (SPE), before a final liquid–liquid extraction step. Analysis is based on LC coupled to positive ion electrospray MS-MS, monitoring product ions at m/z 129, 102 and 75 for QCA and at m/z 106 for the internal standard (d₄-QCA). The method has been validated according to draft revised EU criteria for analysis of veterinary drug residues, and is suitable for monitoring tissues taken under national surveillance schemes. The method has been validated at 3, 10, 30, 100 and 300 μg kg⁻¹. The method performance characteristics, CCα (decision limit) and CCβ (detection limit) were determined to be 0.16 and 0.27 μg kg⁻¹, respectively. The described method, which is relatively rapid and applicable to large sample numbers, correlates well (r² = 0.9799) with a widely used GC-MS assay for QCA.

Sheep fed diets containing less than 70 micrograms Co per kg develop vitamin B12 deficiency. When sheep were fed diets containing 20 micrograms Co per kg or less, mean rumen succinate concentrations increased by more than one hundred-fold within 2 days. This increase was matched by an equimolar decrease in mean rumen propionate concentrations. When diets containing more than 20 micrograms Co per kg were fed to sheep, no such changes occurred. The synthesis of succinyl CoA from propionyl CoA in liver is impaired in ovine cobalt deficiency. We suggested that, paradoxically, accumulation of rumen succinate could reduce the effects of vitamin B12 deficiency on methylmalonyl CoA mutase and consequently result in lower plasma methylmalonic acid (MMA) concentrations than would arise by feeding diets that did not affect rumen succinate concentrations. This hypothesis was tested by feeding diets containing 4, 40 and 1000 micrograms Co per kg to sheep for 23 weeks. However, sheep fed 40 micrograms Co per kg did not have mean plasma MMA concentrations that were higher than those in the sheep fed 4 micrograms Co per kg, indicating that rumen succinate accumulation did not ameliorate the effects of Co deficiency.