The comparative pharmacokinetic profile of cefquinome was studied in sheep and goats following repeated intramuscular (IM) administrations of 2 mg/kg body weight. Cefquinome concentrations in serum were determined by microbiological assay technique using Micrococcus luteus (ATCC 9341) as test organism. Following intramuscular injection of cefquinome in sheep and goats, the disposition curves were best described by two-compartment open model in both sheep and goats. The pharmacokinetics of cefquinome did not differ significantly between sheep and goats; similar intramuscular dose rate of cefquinome should therefore be applicable to both species. On comparing the data of serum levels of repeated intramuscular injections with first intramuscular injection, it was revealed that repeated intramuscular injections of cefquinome have cumulative effect in both species sheep and goats. The in vitro serum protein-binding tendency was 15.65% in sheep and 14.42% in goats. The serum concentrations of cefquinome along 24 h after injection in this study were exceeding the MICs of different susceptible microorganisms responsible for serious disease problems. These findings indicate successful use of cefquinome in sheep and goats.

This study was designed to investigate the possible developmental teratogenicity of norfloxacin in rats. Forty pregnant female rats were divided into four equal groups. Group A received norfloxacin in a dose of 500 mg/kg·b·wt/day orally from 6th to 15th day of gestation. Groups B and C received 1000 and 2000 mg/kg·b·wt/day orally for the same period, respectively; Group D behaved as control and received 0.5 mL distilled water orally for the same period. The dams were killed on 20th day of gestation and their fetuses were subjected to morphological, visceral, and skeletal examinations. Norfloxacin significantly decreased the number of viable fetuses, increased the number of resorbed fetuses, and induced retardation in growth of viable fetuses; some visceral and skeletal defects in these fetuses were seen and these effects were dose dependant. Conclusively, norfloxacin caused some fetal defects and abnormalities, so it is advisable to avoid using this drug during pregnancy.

In this study, powders were evaluated for their anticoccidial effects. In in vitro, sporulated oocysts of mixed Eimeria species isolated from naturally infected chickens were randomly assigned to 10, 5, 2.5, 1.25, 0.6, 0.3, 0.2 and 0.08 g turmeric and garlic powders /liter distilled water (g/L). The efficacy of garlic was higher (up to 80%) than turmeric (up to 66.6%) at different concentrations. In the in vivo study, one-day old chicks were divided into 7 equal groups. All groups were infected with 10.000 viable sporulated oocysts of mixed Eimeria spp. orally except G7 (-ve control). G1 and G2 were infected and supplemented with turmeric powder at 10 and 5 g/L, respectively, G3 and G4 were infected and supplemented with garlic powder at 10 and 5 g/L, respectively. G5 was infected and treated with Amprolium at 1.25 g/L, G6 (+ve control) infected, non-treated and G7 was non-infected & non-treated. Clinical signs and lesion score were less sever in garlic supplemented groups compared with turmeric supplemented groups. Reduction of total oocyst count in garlic supplemented group more than turmeric supplemented group. It is concluded that Garlic powder was more effective than turmeric powder in treatment and control of coccidiosis.

Aims: The present study was designed to assess the comparative bio-equivalence of Doxysol ® and Doxymed ® in healthy broiler chickens after oral administration of both products in a dose of 20 mg doxycycline/kg.b.wt. Materials and Methods: Twenty broiler chickens were divided into two groups. The first group was designed to study the pharmacokinetics of Doxysol, while the 2nd group was designed to study the pharmacokinetics of Doxymed. Each broiler chickens in both groups were injected intravenously with 20 mg doxycycline/kg.b.wt. Blood samples were obtained from the wing vein and collected immediately before and at 5, 15, 30 minute, 1, 2, 4, 6, 8, 12 and 24 hours after a single intravenous or oral administration. Results: Doxycycline in both products obeyed a two compartments open model following I.V. injection in a dose of 20 mg/kg.b.wt. The disposition kinetics of Doxysol ® and Doxymed ® following oral administration of 20 mg doxycycline base/kg.b.wt. revealed that the maximum blood concentration [Cmax.] were 4.70 and 4.65 μg/ml and attained at [tmax.] of 1.30 and 1.40 hours, respectively. Doxycycline in Doxysol ® and Doxymed ® was eliminated with half-lives [t0.5(β)] equal to 1.98 and 2.31 hours, respectively. The mean systemic bioavailability of doxycycline in Doxysol ® and Doxymed ® after oral administration in healthy chickens was 92.57 and 88.21%, respectively. Conclusion: Doxymed ® is bioequivalent to Doxysol ® since Cmax test/Cmax reference and AUCtest/AUCreference ratios were 99% and 90%, respectively.

Although the combination of antibiotics is generally well-tolerated, they may have nephrotoxic effects. This study investigated whether tigecycline (TG) and gentamicin (GM) co-administration could accelerate renal damage. Male Wistar rats were randomly divided into six experimental groups: the control, TG7 (tigecycline, 7 mg/kg), TG14 (tigecycline, 14 mg/kg), GM (gentamicin, 80 mg/kg), TG7+GM, and TG14+GM groups. The combination of TG and GM evoked renal damage seen by the disruption of kidney function tests. The perturbation of renal tissue was mainly confounded to the TG and GM-induced oxidative damage, which was exhibited by marked increases in renal MDA (malondialdehyde) along with a drastic reduction in GSH (reduced-glutathione) content and CAT (catalase) activity compared to their individual treatments. More obvious apoptotic events and inflammation were also revealed by elevating the annexin-V and interleukin-6 (IL-6) levels, aside from the upregulation of renal PCNA (proliferating cell nuclear antigen) expression in the TG and GM concurrent treatment. The principal component analysis indicated that creatinine, urea, annexin-V, IL-6, and MDA all played a role in discriminating the TG and GM combined toxicity. Oxidative stress, inflammatory response, and apoptosis were the key mechanisms involved in this potentiated toxicity.