肺炎克雷伯杆菌临床分离株对5种常用消毒剂的抗性研究

摘要 目的 观察临床分离肺炎克雷伯杆菌对常用消毒剂的抗性及消毒剂抗性基因携带情况,分析消毒剂与抗菌药物间的交叉耐药性、消毒剂抗性基因和抗菌药物耐药的相关性。方法 采用微量肉汤稀释法和PCR技术,测定5种消毒剂对44株肺炎克雷伯杆菌的MIC值,并对qacE△1基因携带情况进行筛查。结果 44株肺炎克雷伯杆菌对醋酸氯己定和三氯生的MIC值均高于质控菌大肠杆菌(ATCC 25922),对抗菌药物交叉耐药率分别为55.6%和77.8%,对季铵盐类消毒剂抗性升高不明显。共筛查出22株携带qacE△1基因,不同医院检出率存在差异。qacE△1在抗菌药物耐药菌株中的检出率要高于敏感菌株,且抗菌药物耐药株与敏感株的qacE△1基因检出率存在地区差异。结论 肺炎克雷伯杆菌临床株对醋酸氯己定和三氯生具有更高的抗性,qacE△1基因的检出率存在地区差异性。长期不合理暴露于此两种消毒剂的菌株在持续的选择压力下可能增强消毒剂抗性和抗菌药物交叉耐药性。     

临床分离肺炎克雷伯杆菌对消毒剂耐药性观察

摘要 目的 观察临床分离的肺炎克雷伯杆菌对常用消毒剂的耐药情况及抗消毒剂基因携带状况。方法采用琼脂扩散法和聚合酶链反应法,对96株临床肺炎克雷伯杆菌抗消毒剂和抗性基因携带情况进行检测。结果3种季铵盐和三氯生对96株肺炎克雷伯杆菌的MIC值均高于标准菌株,氯己定对96株肺炎克雷伯菌中的93株MIC值高于标准株。临床分离的肺炎克雷伯菌qacEΔ1和qacE携带率均为76.0%;qacE-qacEΔ1携带率为70.8%。qacE、qacEΔ1和sugE(c)阳性菌株对三氯生、溴化铵、苯扎氯铵和醋酸氯己定等消毒剂抗性较阴性菌株强。结论该医院临床分离的肺炎克雷伯杆菌对3类低效消毒剂显示出抗力增强的趋势,消毒剂抗性基因携带率也比较高,提示慎用低效消毒剂消毒关键性物品。     

医院感染耐碳青霉烯类肠杆菌科分布及耐药性分析

摘要 目的 了解临床分离耐碳青霉烯类肠杆菌科分布及其耐药情况,为指导临床合理使用抗菌药物提供参考。方法 通过细菌分离鉴定技术,对某医院住院患者送检病原学标本进行检测与分析。结果 从该医院住院患者送检标本中共分离耐碳青霉烯类肠杆菌科（CRE）细菌322株,包括肺炎克雷伯菌198株（含臭鼻克雷伯菌1株）、粘质沙雷菌78株和大肠埃希菌46株。CRE菌株主要分离自重症监护室、神经外科和呼吸内科病房送检的标〖JP2〗本;居首位的标本是痰液,占68.42%。临床分离的CRE菌株对常用抗菌药物高度耐药。结论 医院感染CRE细菌主要是肺炎克雷伯菌、粘质沙雷菌和大肠埃希菌,耐药严重,多见于呼吸道感染,应当依据药敏结果选用抗菌药物。     

某综合医院下呼吸道感染肺炎克雷伯菌耐药性分析

〖HT5”H〗摘要 目的 对某综合医院下呼吸道肺炎克雷伯菌感染及耐药情况进行调查。方法 对2015-2017年临床送检的下呼吸道标本进行病原菌的分离鉴定及药敏试验。结果 分离出486株肺炎克雷伯菌,主要来自呼吸内科、儿科和ICU,产超广谱β-内酰胺酶(ESBLs)肺炎克雷伯菌占37.65%。肺炎克雷伯菌对临床常用多种抗菌药物耐药率呈上升趋势,产ESBLs菌株的耐药率高于非产ESBLs菌株。结论 该医院下呼吸道感染肺炎克雷伯菌产ESBLs检出率及耐药率呈逐年上升趋势,临床应根据药敏结果合理应用抗菌药物。     

住院肝病患者肺部感染肺炎克雷伯菌及其耐药性分析

摘要 目的 了解住院肝病患者肺部感染肺炎克雷伯菌及其耐药情况,为临床合理应用抗菌药物提供依据。方法通过细菌分离鉴定和药敏试验方法,对山东某传染病专科医院住院肝病患者送检痰标本进行病原菌检测和分析。结果从65例住院肝病并发肺部感染患者痰标本中分离出65株肺炎克雷伯菌,其中检出产超广谱β-内酰胺酶菌株（ESBLs）21株,占32.31%。从痰液分离的肺炎克雷伯菌对18种临床常用抗菌药物均不同程度耐药,产ESBLs菌株耐药率明显高于非ESBLs菌株。临床分离的肺炎克雷伯菌仅对亚胺培南/西司他丁和美罗培南等碳青霉烯类比较敏感。结论住院肝病患者肺部感染的肺炎克雷伯菌中产ESBLs菌株比例较高,耐药严重,仅对碳青霉烯类抗菌药物敏感,提示应根据药敏试验结果选用抗菌药物。     

医院环境中分离致病菌对三种消毒剂的抗性研究

摘要 目的 研究医院环境表面分离的致病菌对常用消毒剂抗性变化情况,为科学使用化学消毒剂提供参考。方法采用稀释法和基因扩增技术,对医院环境中分离的致病菌抗消毒剂情况和抗性基因携带率进行检测与分析。结果苯扎溴铵对铜绿假单胞菌中的3株MIC和MBC值低于标准菌株;对3株肺炎克雷伯菌和鲍曼不动杆菌的MIC和MBC值高于标准菌株。葡萄糖酸氯己定对铜绿假单胞菌的MIC值和MIC值有2株高于标准株,有9株低于标准株;对肺炎克雷伯和鲍曼不动杆菌的MIC值和MBC值均与标准菌株相同。二氧化氯对铜绿假单胞菌中的MIC和MBC值有6株高于标准株,有2株低于标准株;对肺炎克雷伯菌的MIC和MBC值均低于标准菌株,对鲍曼不动杆菌的MIC、MBC值均高于标准菌株。医院分离的铜绿假单胞菌检出qacE△1-sul 1基因携带率为79.17%,其他两种致病菌均未检出携带抗性基因。结论医院物体表面分离的致病菌中仅少部分菌株对3种消毒剂产生了抗性,多数则比较敏感,对医院环境病原菌抗消毒剂情况予以关注非常必要。     

社区获得感染耐甲氧西林金黄色葡萄球菌耐药性与消毒剂抗性关系研究

摘要 目的 研究医院门诊患者社区获得感染耐甲氧西林金黄色葡萄球菌（CA-MRSA）耐药性和消毒剂抗性分布情况，为医院进行有效消毒提供参考。方法 采用药敏试验和最小抑菌浓度（MIC）检测方法，对医院门诊患者送检病原学标本分离的CA-MRSA进行检测。结果 医院门诊患者送检标本分离的21株CA-MRSA对常用抗菌药物普遍耐药，并呈现多重耐药现象。CA-MRSA菌株对含氯消毒剂、葡萄糖氯己定醇和聚维酮碘的抗性率分别为47.62%、47.62%和33.33%。CA-MRSA菌株耐药性与消毒剂抗性的相关系数rp=0.28，无统计学意义。结论 门诊分离的CA-MRSA菌株呈现多重耐药，对消毒剂抗性有所增加，耐药性与消毒剂抗性无明显相关性。     

我国五省市碳青霉烯药物不敏感肠杆菌耐药机制分析

摘要 目的 〖HT5"SS〗了解我国五省市六家三甲医院碳青霉烯类抗生素不敏感肠杆菌KPC耐药基因携带和膜蛋白缺失情况。方法 收集2012年10月-2014年12月碳青霉烯类抗生素不敏感大肠埃希菌和肺炎克雷伯菌共135株。运用改良Hodge试验进行KPC表型初步筛选,PCR法进行KPC耐药基因和膜蛋白基因检测。多位点序列分析（MLST）和脉冲场凝胶电泳（PFGE）对KPC酶阳性菌株进行同源性分析。结果 共有115株菌Hodge试验阳性。65株菌检测到KPC耐药基因,有13株菌所测膜蛋白全部缺失。8株KPC阳性大肠埃希菌ST131型占主导地位;57株KPC阳性肺炎克雷伯菌主导型别是ST11。PFGE结果显示部分菌株同源性较高。结论 KPC酶在碳青霉烯类抗菌药物不敏感的菌株中起主导作用,而膜蛋白的缺失也是导致耐药的一个协同因素。不同地区菌株的主要耐药机制和主导分子型别一致,同时某些医院存在部分分子型别小规模流行,临床工作中应特别注意监控,以防大规模扩散和地区间传播。     

产ESBL肺炎克雷伯菌血流感染及危险因素分析

〖HT5"H〗摘要 目的 〖HT5"SS〗研究产ESBLs肺炎克雷伯菌血流感染现状及其危险因素。 方法 通过病原菌分离鉴定和药敏试验方法，对某医院住院患者肺炎克雷伯菌血流感染病例现状进行调查与分析。 结果 共调查肺炎克雷伯菌血流感染病例75例，分离到肺炎克雷伯菌75株，其中产ESBLs菌株占30.7%。产ESBLs肺炎克雷伯菌对庆大霉素、氨苄西林、复方新诺明、头孢他啶、头孢噻肟和头孢吡肟耐药率均达50%以上；临床分离的肺炎克雷伯菌中已经产生耐碳青霉烯类菌株；近3个月内有手术史和住院史易引发肺炎克雷伯菌感染。 结论 血流感染的肺炎克雷伯菌中产ESBLs比率较高，临床用药前应评估危险因素，合理选用抗菌药物。     

重病监护病房鲍曼不动杆菌消毒剂耐药基因检测

摘要 目的 了解江苏省内医院ICU鲍曼不动杆菌（Ab）药敏及消毒剂耐药基因携带情况。 方法 用PCR法检测2016年7家医院ICU采集的224株Ab的qacE△1-sulI基因携带情况,采用VITEK2系统对菌株进行药物敏感分析。结果 徐州市F医院ICU采集的携带qacE△1-sulI基因的Ab最多（30株）。药敏分析结果显示除哌拉西林他唑巴坦等6种抗菌药物外,采集的Ab对其他抗菌药物的耐药率均高于50%。卡方检验结果显示qacE△1-sulI基因阳性菌株和阴性菌株,除氨苄西林等5种抗菌药物外,对其他的抗菌药物的耐药率差别均存在显著的统计学差异。结论 〖JP3〗徐州F医院ICU采集的鲍曼不动杆菌qacE△1-sulI基因携带率较高,qacE△1-sulI基因不仅与磺胺类抗菌药物耐药有关,与其他抗菌药物存在统计学关联。医院应加强针对性消毒措施。     

Gefitinib reverses breast cancer resistance protein-mediated drug resistance

Breast cancer resistance protein (BCRP) is an ATP binding cassette transporter that confers resistance to a series of anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone. In this study, we evaluated the possible interaction of gefitinib, a selective epidermal growth factor receptor tyrosine kinase inhibitor, with BCRP. BCRP-transduced human epidermoid carcinoma A431 (A431/BCRP) cells acquired cellular resistance to gefitinib, suggesting that BCRP could be one of the determinants of gefitinib sensitivity in a certain sort of cells. Next, the effect of gefitinib on BCRP-mediated drug resistance was examined. Gefitinib reversed SN-38 resistance in BCRP-transduced human myelogenous leukemia K562 (K562/BCRP) or BCRP-transduced murine lymphocytic leukemia P388 (P388/BCRP) cells but not in these parental cells. In addition, gefitinib sensitized human colon cancer HT-29 cells, which endogenously express BCRP, to SN-38. Gefitinib increased intracellular accumulation of topotecan in K562/BCRP cells and suppressed ATP-dependent transport of estrone 3-sulfate, a substrate of BCRP, in membrane vesicles from K562/BCRP cells. These results suggest that gefitinib may overcome BCRP-mediated drug resistance by inhibiting the pump function of BCRP. Furthermore, P388/BCRP-transplanted mice treated with combination of irinotecan and gefitinib survived significantly longer than those treated with irinotecan alone or gefitinib alone. In conclusion, gefitinib is shown to interact with BCRP. BCRP expression in a certain sort of cells is supposed to be one of the determinants of gefitinib sensitivity. Gefitinib inhibits the transporter function of BCRP and reverses BCRP-mediated drug resistance both in vitro and in vivo.     

Gentamicin resistance in Pseudomonas aeruginosa: R-factor-mediated resistance

By disk diffusion antimicrobial susceptibility testing, 11% of 313 consecutive strains of Pseudomonas aeruginosa, examined during July to October 1973, were resistant to gentamicin (minimal inhibitory concentration 12.5 to >100 mug/ml), and a further 31% were moderately resistant (6.25 to 12.5 mug/ml) to gentamicin at the University of Alberta Hospital in Edmonton, Canada. Of 45 gentamicin-resistant strains from that hospital, none possessed R-factors or gentamicin-inactivating enzymes. Eight of 13 strains obtained from three American sources, which contained gentamicin-acetylating (12 strains) or -adenylating (1 strain) activity, conjugally transferred both gentamicin resistance and antibiotic-inactivating activity. P. aeruginosa recipients were much more effective for detection of transferable gentamicin resistance than Escherichia coli recipients, although not all P. aeruginosa were equally as effective as recipients. One strain, POW 151, transferred resistance to both carbenicillin and gentamicin as well as to several other antibiotics. R-factors detected belonged to P-2 and P-3 (Com 6, C) incompatibility groups. Expression of gentamicin resistance due to acetylation of gentamicin was subject to marked phenotypic lag, especially in recipient strain P. aeruginosa 280. This was shown to result in the failure to detect gentamicin resistance transfer if the concentration of gentamicin in selection media was too high (>2.5 mug/ml for strain 280). Some but not all recipients were changed in pyocine type upon acquisition of R-factors.     

Insulin resistance

Insulin resistance is closely associated with fat accumulation in liver. Thus, it has been suggested that insulin resistance is one of the important factor in development of non-alcoholic steatohepatitis(NASH). For example, insulin resistance in adipocyte results in increased lipolysis and delivery of free fatty acids(FFAs) to the liver, which induce fatty liver. If there is insulin resistance in skeletal muscle, hyperinsulinemia and/or hyperglycemia might increase fat accumulation in liver, through, at least in part, increased sterol-regulatory element binding protein-1c(SREBP-1c) activation. However, hepatic insulin resistance might prevent fat accumulation in liver, because insulin strongly induces lipogenesis. Thus, the tissue specific insulin resistance should be considered in the pathogenesis of NASH.     

Aspirin resistance

OBJECTIVE: To review the literature addressing the problem of aspirin resistance in patients with vascular disease. DATA SOURCES: A MEDLINE search (1966-February 2002) was performed. Key search terms included aspirin, resistance, resistant, failure, tolerance, and nonresponder. English-language studies were identified as well as pertinent references from these articles. DATA SYNTHESIS: Aspirin resistance has been reported in patients with cardiovascular, cerebrovascular, and peripheral vascular disease. Because of differences in the definition of resistance, variations in detection methods, and a lack of controlled trials, the true significance of the problem remains unknown. Multiple mechanisms for resistance have been proposed, including increased reactivity to platelet aggregating factors, genetic polymorphism, and alternate pathways for thromboxane synthesis. The studies to date have failed to demonstrate consistent relationships between aspirin's platelet-inhibiting effects, the impact of dosage escalation, and clinical outcomes. CONCLUSIONS: For many patients, aspirin is an effective antithrombotic agent. However, patients taking aspirin may demonstrate highly variable responses to in vitro tests for platelet aggregation and may experience breakthrough thromboembolic events. Although this phenomenon has been termed aspirin resistance, the lack of a uniform definition or agreement on diagnostic criteria precludes definitive recommendations at this time. In addition, strategies are needed to identify patients at risk for aspirin resistance who might benefit from alternative or combined antiplatelet therapy.     

Antibiotic resistance

Resistance to antibiotics is economically and physiologically costly. Control of antibiotic resistance will require aggressive implementation of numerous strategies. Ongoing surveillance is needed to monitor known antibiotic types and to be able to identify the development of other potential types. Early intervention is needed to combat the rising rate of resistance. Persistent use of hygiene measures and controlled use of antibiotics will limit the spread of antibiotic resistance. Health care providers need to monitor adherence to control measures. Hand and environmental control measures remain a critical component of staff education activities. Active management of infections with non-pharmacologic treatments should be promoted. Motivational campaigns will reinforce positive infection control behaviors. Consistent surveillance of antibiotic use will help fulfill the CDC directive to combat antibiotic resistance and keep the population healthy.     

Insulin resistance

There are several mechanisms about high blood pressure induced by insulin resistance in type 2 diabetes. Hyperinsulinemia is rare in Japanese type 2 diabetic patients. Therefore, hyperinsulinemia is not a major cause of high blood pressure in Japanese type 2 diabetic patients. Diabetic nephropathy was associated with high blood pressure. There was a relation between diabetic nephropathy and insulin resistance. Coexistence of essential hypertension with type 2 diabetes. Both essential hypertension and type 2 diabetes were related with insulin resistance. Vascular endothelial dysfunction was associated with insulin resistance. High blood pressure was partially caused by the endothelial dysfunction. The degree of insulin induced vasodilation was reduced in the type 2 diabetic patients with insulin resistance.