Duman Muhammed, Altun Soner, Cengiz Murat, Saticioglu Izzet Burcin, Buyukekiz Ayse Gul, Sahinturk Pinar
Uludag University, Faculty of Veterinary Medicine, Aquatic Animal Disease Department, 16059 Bursa, Turkey.
Dis Aquat Organ. 2017 Jun 19;125(1):31-44. doi: 10.3354/dao03132.
In this study, we compared 142 Yersinia ruckeri isolates collected between 2013 and 2016 from 6 different regions in Turkey. A total of 18 different genogroups were found, though most of the isolates clustered into the same genogroup as serotype O1. As immunization of fish with inactivated Y. ruckeri by injection, immersion, or feeding provide minimal protection against Y. ruckeri infection in Turkey, many fish producers use antimicrobials unrestrictedly, resulting in antimicrobial resistance in aquatic pathogens. Accordingly, we investigated resistance to the antimicrobials most commonly used to treat yersiniosis. More than 80% of the Y. ruckeri isolates were susceptible to sulfamethoxazole-trimethoprim (SXT), florfenicol (FFC), and tetracycline, whereas none were susceptible to sulfamethoxazole. The most commonly used antimicrobials (SXT and FFC) can be effectively administered because the resistance levels to these drugs are the lowest among those reported for agents used to control enteric red mouth disease (12.6 and 14.7%, respectively). In conclusion, to the best of our knowledge, this study is the first characterization of the antimicrobial resistance genes floR, sulI, tetC, tetD, and tetE in Y. ruckeri isolates from aquaculture. Additionally, we detected the sulII gene but not the tetA, tetB, tetM, tetS, or sulIII genes.
在本研究中，我们比较了2013年至2016年间从土耳其6个不同地区收集的142株鲁氏耶尔森菌分离株。共发现了18个不同的基因群，不过大多数分离株与O1血清型聚为同一基因群。在土耳其，通过注射、浸浴或投喂用灭活鲁氏耶尔森菌对鱼进行免疫，对鲁氏耶尔森菌感染提供的保护极小，许多养鱼户无限制地使用抗菌药物，导致水生病原菌产生抗菌药物耐药性。因此，我们调查了对最常用于治疗耶尔森菌病的抗菌药物的耐药情况。超过80%的鲁氏耶尔森菌分离株对磺胺甲恶唑-甲氧苄啶（SXT）、氟苯尼考（FFC）和四环素敏感，而对磺胺甲恶唑均不敏感。最常用的抗菌药物（SXT和FFC）可以有效使用，因为对这些药物的耐药水平在用于控制肠型红嘴病的药物中是最低的（分别为12.6%和14.7%）。总之，据我们所知，本研究首次对水产养殖中鲁氏耶尔森菌分离株的抗菌药物耐药基因floR、sulI、tetC、tetD和tetE进行了表征。此外，我们检测到了sulII基因，但未检测到tetA、tetB、tetM、tetS或sulIII基因。
