中华检验医学杂志
中華檢驗醫學雜誌
중화검험의학잡지
CHINESE JOURNAL OF LABORATORY MEDICINE
2012年
7期
625-629
,共5页
沙雷菌,黏质%抗药性,细菌%卡巴配能类%聚合酶链反应
沙雷菌,黏質%抗藥性,細菌%卡巴配能類%聚閤酶鏈反應
사뢰균,점질%항약성,세균%잡파배능류%취합매련반응
Serratia marcescens%Drug resistance,bacterial%Carbapenems%Polymerase chain reaction
目的 探讨黏质沙雷菌分离株的整体耐药特点,研究其对碳青霉烯类药物耐药的主要机制.方法 收集2007至2010年从宁波市第一医院不同病区分离(剔除重复菌株)黏质沙雷菌247株,用Vitek2 -Compact及配套革兰阴性杆菌药敏卡(GNS)检测其药敏情况,对筛选出的20株耐碳青霉烯类菌株进行PCR检测其耐药基因.结果 黏质沙雷菌对头孢曲松、氨曲南、环丙沙星的耐药率较高,分别为70.4％( 174/247)、64.8％ (160/247)、57.4％ (142/247)；对阿米卡星、庆大霉素、亚胺培南、美罗培南的耐药率较低,分别为:3.5％( 8/229)、5.4％( 13/241)、5.9％(14/237)、8.1％ (20/247).PCR检测20株对碳青霉烯类抗生素耐药的黏质沙雷菌中,1、7、12和16号的AmpC染色体基因表达是阴性参考菌株的98.3、102.3、121.5、87.3倍；共有12株黏质沙雷菌分离株同时携带CTX-M型超广谱β内酰胺酶(ESBLs)和KPC-2型碳青霉烯类酶.黏质沙雷菌所携带的CTX-M以CTX-M1、CTX-M2、CTX-M9为主；2株菌携带有SHV基因；2株菌携带有SME基因；2株菌携带有TEM基因；5株菌膜孔蛋白基因ompC和ompF均缺失；仅1株ompC基因缺失；2株菌ompF基因缺失.结论 黏质沙雷菌对β内酰胺类药物耐药的原因比较复杂,以产β内酰胺酶为主.开展对耐药菌株的进化和多耐药基因的研究,有利于合理应用抗菌药物,降低抗生索对耐药菌的选择压力及控制耐药菌株的蔓延.
目的 探討黏質沙雷菌分離株的整體耐藥特點,研究其對碳青黴烯類藥物耐藥的主要機製.方法 收集2007至2010年從寧波市第一醫院不同病區分離(剔除重複菌株)黏質沙雷菌247株,用Vitek2 -Compact及配套革蘭陰性桿菌藥敏卡(GNS)檢測其藥敏情況,對篩選齣的20株耐碳青黴烯類菌株進行PCR檢測其耐藥基因.結果 黏質沙雷菌對頭孢麯鬆、氨麯南、環丙沙星的耐藥率較高,分彆為70.4％( 174/247)、64.8％ (160/247)、57.4％ (142/247)；對阿米卡星、慶大黴素、亞胺培南、美囉培南的耐藥率較低,分彆為:3.5％( 8/229)、5.4％( 13/241)、5.9％(14/237)、8.1％ (20/247).PCR檢測20株對碳青黴烯類抗生素耐藥的黏質沙雷菌中,1、7、12和16號的AmpC染色體基因錶達是陰性參攷菌株的98.3、102.3、121.5、87.3倍；共有12株黏質沙雷菌分離株同時攜帶CTX-M型超廣譜β內酰胺酶(ESBLs)和KPC-2型碳青黴烯類酶.黏質沙雷菌所攜帶的CTX-M以CTX-M1、CTX-M2、CTX-M9為主；2株菌攜帶有SHV基因；2株菌攜帶有SME基因；2株菌攜帶有TEM基因；5株菌膜孔蛋白基因ompC和ompF均缺失；僅1株ompC基因缺失；2株菌ompF基因缺失.結論 黏質沙雷菌對β內酰胺類藥物耐藥的原因比較複雜,以產β內酰胺酶為主.開展對耐藥菌株的進化和多耐藥基因的研究,有利于閤理應用抗菌藥物,降低抗生索對耐藥菌的選擇壓力及控製耐藥菌株的蔓延.
목적 탐토점질사뢰균분리주적정체내약특점,연구기대탄청매희류약물내약적주요궤제.방법 수집2007지2010년종저파시제일의원불동병구분리(척제중복균주)점질사뢰균247주,용Vitek2 -Compact급배투혁란음성간균약민잡(GNS)검측기약민정황,대사선출적20주내탄청매희류균주진행PCR검측기내약기인.결과 점질사뢰균대두포곡송、안곡남、배병사성적내약솔교고,분별위70.4％( 174/247)、64.8％ (160/247)、57.4％ (142/247)；대아미잡성、경대매소、아알배남、미라배남적내약솔교저,분별위:3.5％( 8/229)、5.4％( 13/241)、5.9％(14/237)、8.1％ (20/247).PCR검측20주대탄청매희류항생소내약적점질사뢰균중,1、7、12화16호적AmpC염색체기인표체시음성삼고균주적98.3、102.3、121.5、87.3배；공유12주점질사뢰균분리주동시휴대CTX-M형초엄보β내선알매(ESBLs)화KPC-2형탄청매희류매.점질사뢰균소휴대적CTX-M이CTX-M1、CTX-M2、CTX-M9위주；2주균휴대유SHV기인；2주균휴대유SME기인；2주균휴대유TEM기인；5주균막공단백기인ompC화ompF균결실；부1주ompC기인결실；2주균ompF기인결실.결론 점질사뢰균대β내선알류약물내약적원인비교복잡,이산β내선알매위주.개전대내약균주적진화화다내약기인적연구,유리우합리응용항균약물,강저항생색대내약균적선택압력급공제내약균주적만연.
Objective To find out the antimicrobial resistance of clinical sequential isolates of Serratia marcescens,investigate the primary antimicrobial resistant mechanism of Serratia marcescens to β-lactams antibiotics.Methods Review the antimicrobial resistance data of 247 Serratia marcescens isolates collected sequentially from different clinical wards during 2007 to 2010 in the First Hospital of Ningbo,which their antimicrobial susceptihility testing was got by using Vitek2-Compact system and matching products of gram-negative susceptibility card (GNS).The antimicrobial resistant genes of 20 carbapenems resistant isolates were detected by PCR.Results The Serratia marcescens resistant rates to ceftriaxone,aztreonarn and ciprofloxacin in our hospital were 70.4％ ( 174/247 ),64.8％ ( 160/247 ),57.4％ ( 142/247),respectively,the resistant rates were lower to amikacin,gentamicin,imipenem and meropenem,which were 3.5％ ( 8/229 ),5.4％ ( 13/241 ),5.9％ ( 14/237 ),8.1％ ( 20/247 ),respectively.PCR experiment showed that the expression levels of the AmpC gene in 4 strains were higher than that of the negative reference strains.The expression levels were 98.3,102.3,121.5,87.3 times compared to the negative reference strains,respectively.Twelve strains (strain no.2,3,5,6,9,10,14,15,16,17,18 and 19) produce both blaCTX-M and blaKPC-2 enzymes.Highly deteced hlaCTX-M of Serratia marcescens in our hospital included CTX-M1,CTX-M2,CTX-M9.Isolates no.7 and 18 were carrying blaSHV gene,Isolates no.8 and 13 were carrying blaSME,Isolates no.11 and 20 were carrying blaTEM.There were 5 strains (no.3,4,5,7 and 16) lose the outer membrane protein (OMP) genes ompC and ompF.Two strains( no.1 and 12 ) lose OMP gene ompF only,and one strain ( no.20 ) was lose OMP gene ompC only.Conclusions The cause of β-lactam antibiotics resistance of Serratia marcescens was complicated,and the most important mechanism is producing β-1actams and loss of OMP.Understanding the evolution and drug resistant mechanisms will help for best use of antibiotics and reducing the selection of antibiotics to resistant isolates.
