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本文引用的文献

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Occurrence of enteric redmouth disease in rainbow trout (Oncorhynchus mykiss) on farms in Croatia.
Acta Vet Hung. 2002;50(3):283-91. doi: 10.1556/AVet.50.2002.3.4.
2
PCR detection and PFGE DNA macrorestriction analyses of clinical isolates of Pseudomonas anguilliseptica from winter disease outbreaks in sea bream Sparus aurata.对来自患冬季疾病的金头鲷(Sparus aurata)中鳗弧菌临床分离株的PCR检测和PFGE DNA宏观限制性分析
Dis Aquat Organ. 2002 Jun 21;50(1):19-27. doi: 10.3354/dao050019.
3
Role of active efflux in association with target gene mutations in fluoroquinolone resistance in clinical isolates of Vibrio cholerae.主动外排在霍乱弧菌临床分离株对氟喹诺酮耐药中与靶基因突变相关的作用。
Antimicrob Agents Chemother. 2002 Aug;46(8):2676-8. doi: 10.1128/AAC.46.8.2676-2678.2002.
4
Occurrence and phenotypic characterization of Yersinia ruckeri strains with biofilm-forming capacity in a rainbow trout farm.虹鳟养殖场中具有生物膜形成能力的鲁氏耶尔森菌菌株的发生情况及表型特征
Appl Environ Microbiol. 2002 Feb;68(2):470-5. doi: 10.1128/AEM.68.2.470-475.2002.
5
Type II topoisomerase quinolone resistance-determining regions of Aeromonas caviae, A. hydrophila, and A. sobria complexes and mutations associated with quinolone resistance.豚鼠气单胞菌、嗜水气单胞菌和温和气单胞菌复合体的II型拓扑异构酶喹诺酮耐药决定区以及与喹诺酮耐药相关的突变
Antimicrob Agents Chemother. 2002 Feb;46(2):350-9. doi: 10.1128/AAC.46.2.350-359.2002.
6
Type II topoisomerase mutations in fluoroquinolone-resistant clinical strains of Pseudomonas aeruginosa isolated in 1998 and 1999: role of target enzyme in mechanism of fluoroquinolone resistance.1998年和1999年分离出的耐氟喹诺酮铜绿假单胞菌临床菌株中的II型拓扑异构酶突变:靶酶在氟喹诺酮耐药机制中的作用
Antimicrob Agents Chemother. 2001 Aug;45(8):2263-8. doi: 10.1128/AAC.45.8.2263-2268.2001.
7
Quinolone resistance in Escherichia coli.大肠杆菌中的喹诺酮耐药性。
Vet Res. 2001 May-Aug;32(3-4):275-84. doi: 10.1051/vetres:2001124.
8
Interaction between DNA gyrase and quinolones: effects of alanine mutations at GyrA subunit residues Ser(83) and Asp(87).DNA 回旋酶与喹诺酮类药物之间的相互作用:GyrA 亚基残基 Ser(83) 和 Asp(87) 处丙氨酸突变的影响。
Antimicrob Agents Chemother. 2001 Jul;45(7):1994-2000. doi: 10.1128/AAC.45.7.1994-2000.2001.
9
Antimicrobial susceptibility of Listeria monocytogenes isolated from meningoencephalitis in sheep.从绵羊脑膜脑炎中分离出的单核细胞增生李斯特菌的抗菌药敏性
Int J Antimicrob Agents. 2001 Mar;17(3):215-20. doi: 10.1016/s0924-8579(00)00318-6.
10
Mechanisms of action of antimicrobials: focus on fluoroquinolones.抗菌药物的作用机制:聚焦于氟喹诺酮类
Clin Infect Dis. 2001 Mar 15;32 Suppl 1:S9-S15. doi: 10.1086/319370.

对喹诺酮类药物敏感性降低的鲁氏耶尔森菌临床分离株的gyrA基因分析。

Analysis of the gyrA gene of clinical Yersinia ruckeri isolates with reduced susceptibility to quinolones.

作者信息

Gibello Alicia, Porrero M Concepción, Blanco M Mar, Vela Ana I, Liébana Pilar, Moreno Miguel A, Fernández-Garayzábal José F, Domínguez Lucas

机构信息

Departamento Sanidad Animal, Facultad de Veterinaria, Universidad Complutense, 28040 Madrid, Spain.

出版信息

Appl Environ Microbiol. 2004 Jan;70(1):599-602. doi: 10.1128/AEM.70.1.599-602.2004.

DOI:10.1128/AEM.70.1.599-602.2004
PMID:14711693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC321256/
Abstract

Antimicrobial susceptibility of seven clinical strains of Yersinia ruckeri representative of those isolated between 1994 and 2002 from a fish farm with endemic enteric redmouth disease was studied. All isolates displayed indistinguishable pulsed-field gel electrophoresis restriction patterns, indicating that they represented a single strain. However, considering both inhibition zone diameters (IZD) and MICs, the isolates recovered in 2001-2002 formed a separate cluster with lower levels of susceptibility to all the quinolones tested, especially nalidixic acid (NA) and oxolinic acid (OA), compared with the isolates recovered between 1994 and 1998. Analysis of the PCR product of the quinolone resistance-determining region of the gyrA gene from clinical isolates of Y. ruckeri with reduced susceptibility to OA and NA revealed a single amino acid substitution, Ser-83 to Arg-83 (Escherichia coli numbering). Identical substitution was observed in induced OA-resistant mutant strains, which displayed IZD and MICs of quinolones similar to those of the clinical isolates of Y. ruckeri with reduced susceptibility to these antimicrobial agents. These data indicate in that for Y. ruckeri, the substitution of Ser by Arg at position 83 of the gyrA gene is associated with reduced susceptibility to quinolones.

摘要

对1994年至2002年间从一个患有地方性肠道红嘴病的养鱼场分离出的7株鲁氏耶尔森菌临床菌株的抗菌药敏性进行了研究。所有分离株显示出难以区分的脉冲场凝胶电泳限制性图谱,表明它们代表单一菌株。然而,考虑到抑菌圈直径(IZD)和最低抑菌浓度(MIC),与1994年至1998年分离出的菌株相比,2001年至2002年分离出的菌株形成了一个单独的聚类,对所有测试喹诺酮类药物的敏感性较低,尤其是萘啶酸(NA)和恶喹酸(OA)。对鲁氏耶尔森菌临床分离株中对OA和NA敏感性降低的gyrA基因喹诺酮耐药决定区的PCR产物分析显示,有一个氨基酸取代,即Ser-83突变为Arg-83(以大肠杆菌编号)。在诱导的OA耐药突变株中观察到相同的取代,这些突变株显示出的喹诺酮类药物的IZD和MIC与对这些抗菌药物敏感性降低的鲁氏耶尔森菌临床分离株相似。这些数据表明,对于鲁氏耶尔森菌,gyrA基因第83位的Ser被Arg取代与对喹诺酮类药物的敏感性降低有关。