Multidrug resistance mechanism of pathogenic bacteria by mobile genetic elements

本研究的目的是了解移动的遗传元件在病原菌耐药基因传播中的作用。(1)志贺菌属多重耐药的遗传学特征。我们描述了志贺菌耐药性的遗传基础。在2000-2004年期间在日本广岛县从人类分离的。(2)奇异变形杆菌临床分离株携带沙门氏菌基因组岛1的一个新变体，该变体包含多重抗生素耐药区域我们在奇异变形杆菌多重耐药菌株中鉴定了一个新变体SGI 1，该变体包含多重耐药基因组区域。这是第一次在沙门氏菌以外的属中报告SGI 1。(3)动物园动物作为携带整合子和抗菌素耐药基因的革兰氏阴性菌的储存库从日本广岛县动物园饲养的哺乳动物、爬行动物和鸟类中回收了总共232株革兰氏阴性菌。小行星49 ...更多信息 TEs（21.1%）表现为多药耐药表型，并携带至少一种耐药基因。PCR和DNA测序鉴定出Ⅰ类和Ⅱ类整合子及多种β-内酰胺酶编码基因，并发现一种新的ampC β-内酰胺酶基因bla_<CMY-26>。此外，还鉴定了质粒介导的喹诺酮类耐药基因qnr和aac（6 '）-Ib-cr。(4)出现头孢吡肟和头孢匹罗耐药的弗氏柠檬酸杆菌临床分离株，携带一种新型染色体编码的AmpC β-内酰胺酶，CMY-37弗氏柠檬酸杆菌菌株4306于2006年3月在巴勒斯坦从一名患者的尿液标本中分离出来。该菌株显示出独特的多药耐药表型，因为它对7-α-甲氧基-和氧亚氨基-头孢菌素类（包括头孢吡肟、头孢匹罗和单环内酰胺类）以及喹诺酮类、链霉素和甲氧苄啶-磺胺甲恶唑均耐药。分子特征表明，对7-α-甲氧基-和氧亚氨基-头孢菌素的耐药性是由于一种新的AmpC β-内酰胺酶，命名为CMY-37。系统进化分析表明CMY-37是许多质粒介导的AmpC酶的起源。少

The purpose of this study is to understand the roles of mobile genetic elements in spread of antibiotic resistance genes among pathogenic bacteria.(1) Genetic characterization of multidrug resistance in Shigella spp. from JapanWe characterized the genetic basis of antimicrobial resistance of many Shigella spp. isolated from humans during 2000-2004 in Hiroshima prefecture, Japan.(2) Proteus mirabilis clinical isolate harboring a new variant of Salmonella genomic island 1 containing the multiple antibiotic resistance regionWe identified a new variant SGI1 containing the multiple resistance genomic region in a multidrug-resistant strain of P. mirabilis. This is the first report for SGI1 in a genus other than Salmonella.(3) Zoo animals as a reservoir of Gram-negative bacteria harboring integrons and antimicrobial resistance genes A total of 232 isolates of gram-negative bacteria were recovered from mammals, reptiles and birds housed at Zoological Park, Hiroshima prefecture, Japan. 49 isola … More tes (21.1%) showed multidrug resistance phenotypes and harbored at least one antimicrobial resistance gene. PCR and DNA sequencing identified class I and class 2 integrons and many β-lactamase-encoding genes, in addition to a novel ampC β-lactamase gene, bla_<CMY-26>. Furthermore, the plasmid-mediated quinolone resistance genes, qnr and aac(6')-Ib-cr, were also identified.(4) Emergence of cefepime- and cefpirome-resistant Citrobacter freundii clinical isolate harbouring a novel chromosomally-encoded AmpC β-lactamase, CMY-37Citrobacter freundii strain 4306 was isolated from a urine specimen of a patient in March 2006 in Palestine. This strain showed a unique multidrug resistance phenotype, as it was resistant to both 7-α-methoxy- and oxyimino-cephalosporins, including cefepime, cefpirome and monobactams, in addition to quinolones, streptomycin and trimethoprim-sulfamethoxazole. Molecular characterization showed that the resistance to 7-α-methoxy- and oxyimino-cephalosporins was due to a novel AmpC β-lactamase, designated CMY-37. Phylogenetic analysis suggested that CMY-37 is the origin of many plasmid-mediated AmpC β-lactamases. Less