Antibiotic resistance among clinical isolates of Acinetobacter in the UK, and in vitro evaluation of tigecycline (GAR-936)

Antibiotic resistance among clinical isolates of Acinetobacter in the UK, and in vitro evaluation of tigecycline (GAR-936)
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DOI:
10.1093/jac/49.3.479
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发表时间:
2002-03-01
影响因子:
5.2
通讯作者:
Woodford, N
Woodford, N
中科院分区:
医学2区
文献类型:
--
作者:
Henwood, CJ;Gatward, T;Woodford, N

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对595株不动杆菌进行药敏试验。2000年,从英国54个哨兵实验室的常规临床标本中分离出。鲍曼不动杆菌复合体的分离株(基因组群2、3和13TU;n=443)通过tDNA间隔区的PCR指纹图谱与其他基因组群(n=152)区分开来。在IsoSensitest琼脂上测定阿米卡星、头孢噻肟、头孢他啶、环丙沙星、粘菌素、庆大霉素、亚胺培南、美罗培南、米诺环素、哌拉西林、哌拉西林/他唑巴坦、利福平、舒巴坦和四环素的MIC,并尽可能使用BSAC断点进行解释。对新的甘环素类药物替吉环素(GAR-936)也进行了试验。对头孢菌素、氨基糖苷类和环丙沙星的耐药性普遍存在,但碳青霉烯类、粘菌素、舒巴坦、米诺环素和替格环素对80%的分离菌都有活性。鲍曼不动杆菌对头孢他啶、头孢他啶、哌拉西林、哌拉西林/他唑巴坦、环丙沙星、庆大霉素和四环素的耐药率高于其他基因组组,但对粘菌素的耐药率较低;不同基因组组对阿米卡星、碳青霉烯类、利福平和舒巴坦的敏感性无显著差异。四环素类化合物的相对活性为米诺环素和四环素。从6个中心收到13株碳青霉烯类耐药菌株(MIC大于或等于8 mg/L;2.2%);4个中心发出单一菌株;1个发出3个,1个发出6个。在其中一个菌株中检测到一个blA(IMP)等位基因,而其余12个菌株要么具有碳青霉烯酶非依赖抗性,要么是碳青霉烯酶活性与其他抗性机制相结合而未被检测到。总之,碳青霉烯类、粘菌素和米诺环素对收集到的不动杆菌保持了最大的活性。替格环素的活性不如米诺环素,但这两种药物都克服了四环素的大部分耐药性。
A survey was conducted of the antimicrobial susceptibilities of 595 Acinetobacter spp. isolated from routine clinical specimens in 54 sentinel laboratories throughout the UK during 2000. Isolates of the Acinetobacter baumannii complex (genomic groups 2, 3 and 13TU; n=443) were distinguished from other genomic groups (n=152) by PCR fingerprinting of tDNA spacer regions. MICs of amikacin, cefotaxime, ceftazidime, ciprofloxacin, colistin, gentamicin, imipenem, meropenem, minocycline, piperacillin, piperacillin/tazobactam, rifampicin, sulbactam and tetracycline were determined on IsoSensitest agar and interpreted, wherever possible, using BSAC breakpoints. Tigecycline (GAR-936), a new glycylcycline, was also tested. Resistance to cephalosporins, aminoglycosides and ciprofloxacin was widespread, but carbapenems, colistin, sulbactam, minocycline and tigecycline were each active against >80% of the isolates. Isolates of A. baumannii were more often resistant to cefotaxime, ceftazidime, piperacillin, piperacillin/tazobactam, ciprofloxacin, gentamicin and tetracyclines than those belonging to other genomic groups, but were less often resistant to colistin; no significant differences between genomic groups were noted in the susceptibilities to amikacin, carbapenems, rifampicin or sulbactam. The relative activities of the tetracyclines were minocycline > tigecycline > tetracycline. Thirteen carbapenem-resistant isolates (MICs greater than or equal to 8 mg/L; 2.2%) were received from six centres; four centres sent single isolates; one sent three and one sent six. An allele of bla(IMP) was detected in one of these isolates, but the other 12 isolates either had carbapenemase-independent resistance, or undetectable carbapenemase activity combined with other resistance mechanisms. In conclusion, carbapenems, colistin and minocycline retained greatest activity against the Acinetobacter isolates collected. Tigecycline was less active than minocycline, but both agents overcame most tetracycline resistance.