Clonal expansion and microevolution of quinolone-resistant Salmonella enterica serotype Typhi in Vietnam from 1996 to 2004
Clonal expansion and microevolution of quinolone-resistant Salmonella enterica serotype Typhi in Vietnam from 1996 to 2004
复制标题
1996 年至 2004 年越南耐喹诺酮肠炎沙门氏菌血清型 Typhi 的克隆扩增和微进化
DOI：
10.1128/jcm.00948-07
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发表时间：
2007-11-01
影响因子：
9.4
通讯作者：
Weill, Francois-Xavier
中科院分区：
文献类型：
--
作者：
Le, Thi Anh Hong;Fabre, Laetitia;Weill, Francois-Xavier
从1996年至2004年越南各地的散发病例和小规模暴发中收集了对萘啶酸（Nal(r)）耐药的伤寒沙门氏菌临床分离株（n = 91）。采用Vi噬菌体分型、PstI核糖分型、XbaI和SpeI脉冲场凝胶电泳（PFGE）和单核苷酸多态性（SNP） 4种方法对分离菌株进行分型和比较。结果表明，65%的分离株不能用Vi噬菌体分型。相比之下，核型分型和SNP分析方法（准确性更高）表明，所有Nal(r)分离株属于先前发现的单克隆（核型3a，单倍型H58），主要由质粒编码的多药耐药血清型伤寒分离株组成。PFGE证实了该克隆中微进化的发生。我们确定了两个主要的PFGE组合谱：X1-S1和X3-S6。X3-S6在1996年至2002年期间占主导地位，但在2002年之后被XI-SI取代。然而，PFGE的辛普森指数为0.78，不被认为是调查越南伤寒疫情的最佳歧视性方法。研究期间喹诺酮类药物耐药率上升，多药耐药率下降。2002 - 2004年，越南南部80.6%的分离株仅对Nal耐药。大多数菌株（94%）耐药的机制是gyrA的喹诺酮类药物耐药染色体区域发生突变，导致Ser83Phe氨基酸取代。未检测到质粒定位的qnrA、qnrB或qnrS。
Salmonella enterica serotype Typhi clinical isolates (n = 91) resistant to nalidixic acid (Nal(r)) were collected from sporadic cases and minor outbreaks throughout Vietnam between 1996 and 2004. These isolates were typed and compared by four methods: Vi phage typing, PstI ribotyping, XbaI and SpeI pulsed-field gel electrophoresis (PFGE), and single-nucleotide polymorphism (SNP) analysis. The results indicated that 65% of the isolates were not typeable by Vi phage typing. In contrast, the ribotyping and, with more accuracy, the SNP analysis methods indicated that all Nal(r) isolates belonged to a single clone (ribotype 3a, haplotype H58) that was found previously and that largely consisted of plasmid-encoded multidrug-resistant serotype Typhi isolates. PFGE demonstrated the occurrence of microevolution within this clone. We identified two major combined PFGE profiles: X1-S1 and X3-S6. X3-S6 predominated between 1996 and 2002 but was replaced by XI-SI after 2002. Nevertheless, PFGE, with a Simpson's index of 0.78, was not considered an optimal discriminatory method for investigating typhoid fever outbreaks in Vietnam. The rate of quinolone resistance increased and the rate of multidrug resistance decreased during the study period. From 2002 to 2004, 80.6% of the isolates from South Vietnam were resistant only to Nal. The mechanism of Nal resistance in most of the isolates (94%) was a mutation in the quinolone resistance-determining chromosomal region of gyrA that led to the amino acid substitution Ser83Phe. No plasmid-located qnrA, qnrB, or qnrS was detected.