AmpC cephalosporinase hyperproduction in Acinetobacter baumannii clinical strains
AmpC cephalosporinase hyperproduction in Acinetobacter baumannii clinical strains
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DOI：
10.1093/jac/dkg407
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发表时间：
2003-10-01
影响因子：
5.2
通讯作者：
Reynaud, A
中科院分区：
文献类型：
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作者：
Corvec, S;Caroff, N;Reynaud, A
目的：比较不同程度对-内酰胺耐药的鲍曼不动杆菌ampC基因的遗传环境。方法：对42株鲍曼不动杆菌临床菌株的β -内酰胺耐药及β -内酰胺酶产生规律进行了研究。在C类头孢菌素酶抑制剂氯西林（500 mg/L）存在或不存在的情况下，测定了各种β -内酰胺类药物的mic。采用PCR和DNA测序方法对ampC基因及其5′邻近序列进行了分析。建立了RT-PCR方法来评估ampC的转录水平。结果：菌株分为3个耐药组：一是头孢他啶MIC≤8 mg/L的菌株（20株，占47.6%）；其次，头孢他啶MIC为32 mg/L的菌株（8株，19%），在氯西林的存在下降低了4倍；头孢他啶MIC≥256mg /L的菌株（14株，33.4%）在氯西林的存在下没有降低。在所有耐药菌株（II和III组）中，但在头孢他啶敏感菌株（I组）中未检测到，在ampC基因上游检测到一个1180 bp的插入序列，显示了插入序列的所有特征。根据RT-PCR实验，具有该插入物的分离株过表达ampC。结论：鲍曼不动杆菌临床分离株ampC上游存在插入序列，可能包括一个强启动子，可能导致ampC过度表达，导致高水平头孢他啶耐药性。
Objective: To compare the genetic environments of ampC genes in different Acinetobacter baumannii isolates showing different levels of beta-lactam resistance.Methods: The patterns of beta-lactam resistance and beta-lactamase production were investigated for 42 A. baumannii clinical strains. The MICs of various beta-lactams were determined in the presence or absence of the class C cephalosporinase inhibitor, cloxacillin (500 mg/L). The ampC gene and its 5' adjacent sequence were analysed by PCR and DNA sequencing. An RT-PCR method was developed to evaluate ampC transcript levels.Results: Strains fell into three resistance groups: first, strains with a ceftazidime MIC less than or equal to 8 mg/L (20 strains, 47.6%); secondly, strains with a ceftazidime MIC 32 mg/L, which was reduced four-fold in the presence of cloxacillin (eight strains, 19%); and thirdly, strains with a ceftazidime MIC greater than or equal to 256 mg/L, which did not decrease in the presence of cloxacillin (14 strains, 33.4%). In all of the resistant isolates (groups II and III), but not in any of the ceftazidime-susceptible isolates (group I), a 1180 bp insert showing all the characteristics of an insertion sequence was detected upstream from the ampC gene. Isolates having this insert overexpress ampC, according to RT-PCR experiments.Conclusion: Presence of an insertion sequence upstream of ampC in A. baumannii clinical isolates, possibly including a strong promoter, has the potential to cause over-expression of AmpC, resulting in high-level ceftazidime resistance.