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The occurrence of nitrofuran metabolites in the tissues of chickens exposed to very low dietary concentrations of the nitrofurans.

The global problem of food products contaminated by residues of the banned carcinogenic nitrofuran drugs has prompted research into how such residues accumulate in tissues. In the study described here, two aspects have been investigated where the nitrofurans accumulate in tissues from chickens exposed to either a dietary or an environmental source of contamination. Twenty groups of broilers were fed a diet containing one of the nitrofurans: furazolidone, nitrofurazone, nitrofurantoin or furaltadone at concentrations of 30, 100, 300, 1000 and 3000 microg kg(-1). At the lowest concentration of furazolidone contamination (0.01% of the therapeutic dose) tissue bound AOZ metabolite residues were detected in liver (1.1 +/- 0.2 microg kg(-1)) and in muscle (0.33 +/- 0.03 microg kg(-1)). Similar results were obtained for AMOZ (0.6 +/- 0.2 microg kg(-1) in liver), the tissue bound metabolite of furaltadone. There was no appreciable accumulation of nitrofurantoin in chicken muscle. The AHD metabolite was not detected in muscle from birds fed nitrofurantoin at either 30 or 100 microg kg(-1). For nitrofurazone the concentrations of the SEM metabolite were higher in muscle than in liver for all dietary concentrations. The potential for a contaminated environment to cause nitrofuran residues in chickens was investigated. Six chickens were placed in a pen that was previously occupied by birds fed a diet containing 3000 microg kg(-1) of furazolidone. After 24 hours' exposure of the chickens to the litter in the pen, AOZ residues of 0.13 +/- 0.04 and 0.10 +/- 0.03 microg kg(-1) were detected in liver and muscle, respectively. The results of both experiments have implications for the poultry industry in trying to eliminate nitrofurans from their production systems, and for regulatory analysts faced with the detection of low concentrations of the drugs, both in tissues and in feedingstuffs.

Animal Feed↗

Mechanism of nitrofuran resistance in Salmonella enteritidis phage type 4 and interpretation of nitrofuran susceptibility tests.

The mechanism of nitrofuran resistance in Salmonella enteritidis phage type 4 was studied. Nitrofuran reductase activity was inversely related to the furazolidone MIC for the organism. Strains with low-level nitrofuran resistance, typically found in almost all isolates of S. enteritidis PT4, had intermediate nitrofuran reductase activity. Disc diffusion tests with furazolidone, 15 or 50 micrograms discs, and nitrofurantoin, 50 or 300 micrograms discs, failed to distinguish reliably between susceptible populations and those with low-level resistance. In order to detect low-level resistance to nitrofurans a dilution method should be used with a furazolidone breakpoint of 1 mg/l or a nitrofurantoin breakpoint of 16 mg/l.

Drug Resistance, Microbial↗