ABSTRACT
AIMS: This study assessed the effects of the therapeutic use of Tylan® in a large-scale turkey production facility on the selection of macrolide-resistant Campylobacter. METHODS AND RESULTS: A flock of production turkeys (c. 30,000 birds) was followed from brooding to slaughter, and the effects of macrolide application was assessed in one half of the flock from finishing stage to final product and compared against the control barn where no macrolide was used. Overall, Campylobacter prevalence in turkeys was almost 100% by 4 weeks of age. When Campylobacter prevalence was assessed in relation to treatment, high levels of macrolide resistance were evident in this group following treatment, with Campylobacter coli becoming the dominant strain type. Over time, and in the absence of a selection agent, the population of resistant strains decreased suggesting that there was a fitness cost associated with macrolide resistance carriage and persistence. Macrolide resistance was detected in the control barn at a very low level (four isolates recovered during the study), suggesting that the creation or selection of macrolide-resistant Campylobacter was correlated with the treatment regime used. Molecular analysis of a selection of macrolide-resistant Campylobacter recovered was assessed using PCR, RFLP and sequence analysis of the 23S rRNA. The majority of isolates displaying high-level macrolide resistance (>256 µg ml(-1)) possessed an A2075G transition mutation in the 23S rRNA and the CmeABC efflux pump. CONCLUSIONS: These studies suggest that macrolide resistance can be promoted through the application of treatment during the grow-out phase and once established in a production facility has the potential to persist and be transferred to final product. SIGNIFICANCE AND IMPACT OF THE STUDY: The study highlights the prudent use of antimicrobials in treatment of disease in poultry. Of significance is the presence of macrolide-resistant Campylobacter in poultry production and finished product as a consequence of macrolide usage.
Subject(s)
Anti-Bacterial Agents/pharmacology , Campylobacter/drug effects , Turkeys/microbiology , Tylosin/pharmacology , Animals , Anti-Bacterial Agents/administration & dosage , Anti-Bacterial Agents/therapeutic use , Campylobacter/isolation & purification , Campylobacter coli/drug effects , Campylobacter coli/isolation & purification , Campylobacter jejuni/drug effects , Campylobacter jejuni/genetics , Campylobacter jejuni/isolation & purification , Drug Resistance, Bacterial , Tylosin/administration & dosage , Tylosin/therapeutic useABSTRACT
We investigated in rats the effect of 4 wk of hypodynamia on the respiration of mitochondria isolated from four distinct muscles [soleus, extensor digitorum longus, tibial anterior, and gastrocnemius (Gas)] and from subsarcolemmal (SS) and intermyofibrillar (IMF) regions of mixed hindlimb muscles that mainly contained the four cited muscles. With pyruvate plus malate as respiratory substrate, 4 wk of hindlimb suspension produced an 18% decrease in state 3 respiration for IMF mitochondria compared with those in the control group (P < 0.05). The SS mitochondria state 3 were not significantly changed. Concerning the four single muscles, the mitochondrial respiration was significantly decreased in the Gas muscle, which showed a 59% decrease in state 3 with pyruvate + malate (P < 0.05). The other muscles presented no significant decrease in respiratory rate in comparison with the control group. With succinate + rotenone, there was no significant difference in the respiratory rate compared with the respective control group, whatever the mitochondrial origin (SS, or IMF, or from single muscle). We conclude that 4 wk of hindlimb suspension alters the respiration of IMF mitochondria in hindlimb skeletal muscles and seems to act negatively on complex I of the electron-transport chain or prior sites. The muscle mitochondria most affected are those isolated from the Gas muscle.
Subject(s)
Hindlimb Suspension/adverse effects , Mitochondria, Muscle/metabolism , Muscle, Skeletal/metabolism , Animals , Body Weight/physiology , Cell Respiration , Citrate (si)-Synthase/metabolism , Male , Mitochondria, Muscle/enzymology , Muscle Fibers, Fast-Twitch/metabolism , Muscle Fibers, Fast-Twitch/ultrastructure , Muscle Fibers, Slow-Twitch/metabolism , Muscle Fibers, Slow-Twitch/ultrastructure , Muscle, Skeletal/enzymology , Muscle, Skeletal/ultrastructure , Myofibrils/metabolism , Proteins/metabolism , Rats , Rats, Wistar , Sarcolemma/metabolismABSTRACT
We investigated NaHCO3 infusion effects on plasma lactate removal by forearm muscles and performance during intensive leg exercise. Seven subjects performed the force-velocity (FV) test with placebo and NaHCO3 (2 mEq.min-1) with a double-blind crossover protocol. Blood samples for arterial ([LA]A) and venous ([LA]V) lactate determinations were taken 1) at rest before infusion, and 2, 6, 10, 14, 18, and 22 min following its start; and 2) at the end of each exercise bout. The arteriovenous difference ([LA]A-V) was determined for each sampling. NaHCO3 significantly increased arterial bicarbonate concentration and pH during rest (P < 0.001; P < 0.001) and the FV test (P < 0.001; P < 0.05). During the test, [LA]A and [LA]V were significantly higher with NaHCO3 (P < 0.05, P < 0.001). At test onset, [LA]A-V became positive and increased until the braking force of 6 kg, with NaHCO3 and placebo, with values significantly lower for NaHCO3 (P < 0.001). Peak anaerobic power (Wanae, peak) and the corresponding braking force (Fmax) were also determined. Fmax was significantly increased with NaHCO3 (P < 0.001). In conclusion, the increasing rise in [LA]A and [LA]V induced by NaHCO3 may be partly explained by a decreased rate of lactate uptake by forearm skeletal muscles. NaHCO3 did not improve Wanae, peak, but improved Fmax, thus increasing FV duration.