Determination of six illegal antibiotics in chicken jerky dog treats.

In 2007 chicken jerky dog treats were implicated in causing illnesses and death in dogs in several countries. Affected dogs were diagnosed with acquired Fanconi syndrome, which is characterized by kidney malfunction. Known causes of this condition include a chemical assault by various contaminants including certain drugs. For this reason investigations into possible causes of the illnesses included antibiotics that may be used in animal husbandry. Targeted analyte screens of individual imported chicken jerky dog treats using LC-MS/MS detected six illegal antibiotics in imported products of several brands. Trimethoprim, tilmicosin, enrofloxacin, sulfaclozine, and sulfamethoxazole are not allowed in chicken at any level and were found as high as 2800 ng/g (ppb). Sulfaquinoxaline was found in chicken jerky treats as high as 800 ng/g, which is well above the U.S. FDA tolerance of 100 ng/g. Although there is no evidence these contaminants were responsible for the dog illnesses, their misuse could contribute to antibiotic-resistant strains of bacteria.

Evaluation of the aquatic toxicity of two veterinary sulfonamides using five test organisms.

The aquatic toxicity of sulfaquinoxaline (SQO) and sulfaguanidine (SGD) was evaluated on the following test organisms: Daphnia magna (reproduction test), Pseudokirchneriella subcapitata, Scenedesmus dimorphus, Synecococcus leopoliensis (algal growth inhibition test) and Lemna gibba (duckweed growth inhibition test). Furthermore, the additivity of the two compounds was measured on D. magna (acute immobilisation test) and P. subcapitata (algal growth inhibition test) using the isobologram method. Results show that SQO and SGD are more toxic to green algae and daphnids, respectively, than other veterinary sulfonamides (SAs) and that their mixtures have a less then additive interaction. Taking into account the highest concentrations detected so far in surface waters for SQO (0.112 µg L(-1)) and for SGD (0.145 µg L(-1)) and the lowest NOECs obtained with the five test organisms, divided by an assessment factor of 10, the following PNECs and risk quotients (RQs) were calculated. SQO: PNEC 2 µg L(-1); RQ 0.056. SGD: PNEC 39.5 µg L(-1); RQ 0.004. Consequently, at the concentrations actually detected in the aquatic environment, the two SAs alone should not harm the freshwater organisms. However, it seems advisable, for veterinary mass treatments, the use of other SAs that have a lesser impact on the aquatic environment. Furthermore, considering the high probability of having complex mixtures of different SAs residues in water, each individual contamination should be evaluated by applying to the SAs mixtures the conservative criteria of additivity.

Interaction between lead toxicity and some sulphonamides in rabbits: effect on certain blood constituents and serum enzymes.

Two main equal groups of clinically healthy, non pregnant rabbits were classified into 4 subgroups (5 rabbits each). The 1st and 2nd subgroups were treated with sulphaquinoxaline or sulphadiazine in a single oral dose of 100 mg/kg b. wt., while the 3rd and 4th subgroups received a repeated oral dose of 100 mg/kg b. wt., daily for 5 successive days, respectively. The second main group received lead acetate in a dose of 4.2 mg/kg b. wt. per day for 2 months, then was classified as in case of the 1st main group and administered the respective sulphonamides in their recommended doses. The experimental lead intoxication was found to decrease the free delta-aminolevulinic acid dehydratase (delta-ALA-D) activity in blood of lead intoxicated rabbits after 4 and 8 weeks. Also, the ratio of free and with glutathione reactivated delta-ALA-D was increased 2.9 and 2.2 after 4 and 8 weeks, respectively as compared with before lead administration (1.19), indicating toxicity. The sulphonamide/creatinine ratio was increased after administration of both sulphonamides but higher in lead intoxicated rabbits as compared with healthy ones. The AST/ALT ratio was decreased 4 and 8 weeks after lead exposure. The AST, ALT and AST/ALT ratio, alkaline phosphatase, urea and creatinine were not altered in healthy rabbits. Repeated oral administration of sulphadiazine caused a significant increase in serum AST, ALT, alkaline phosphatase and creatinine level in healthy and lead intoxicated rabbits. On the other hand, AST/ALT ratio in both healthy and lead intoxicated rabbits was found to decrease 1 h after the last dose as compared with before treatment.

Experimental and field sulfaquinoxaline toxicosis in Leghorn chickens.

Mortality of 47% occurred in a commercial flock of 20-week-old leghorn pullets treated with 0.05% sulfaquinoxaline in the feed. The drug was given for 2-3 days, removed for 2 days, and fed again for 2-3 days. Gross lesions consisted of disseminated hemorrhages, bone marrow pallor, a variety of changes suggesting septicemia, and overwhelming bacterial infection. Experimental feeding of sulfaquinoxaline at 0.05% in the feed at a schedule of 3 days on, 3 days off, and 2 days on successfully reproduced the essential features and gross lesions of the field toxicosis. Mortalities of 32.5% and 43.5% were observed in sulfaquinoxaline-treated groups. A high incidence of gangrenous dermatitis occurred in chickens with the experimental toxicosis, but it was not observed in the field case.