血培养常见革兰阴性杆菌耐药性分析

目的 了解医院血培养中常见革兰阴性杆菌的耐药性,为临床合理应用抗菌药物提供依据.方法 BacT/Alert 3D全自动血培养仪进行血液培养,Microscan Autoscan-4微生物分析仪进行细菌鉴定及药敏试验.结果血培养阳性率6.9%,革兰阴性杆菌、革兰阳性球菌、真菌分别占52.1%、46.1%、1.8%,主要革兰阴性杆菌为大肠埃希菌、肺炎克雷伯菌、铜绿假单胞菌.大肠埃希菌、肺炎克雷伯菌超广谱β-内酰胺酶(ESBLs)检出率分别为33.1%、20.7%,两菌对哑胺培南、哌拉西林/他唑巴坦、阿米卡星的耐药率较低(0～10.3%),铜绿假单胞菌对受测试的10种药物的耐药率较低(0～10.5%).结论血培养分离的革兰阴性杆菌具有不同的耐药特点,及时规范的血培养检查有助于诊断与治疗.     

革兰阴性杆菌高产AmpC酶的检测及耐药性分析

目的：了解革兰阴性杆菌高产AmpC酶检出的情况及其对10种常用抗菌药物的耐药性分析。方法：对我院2001～2004年临床标本分离出的273株革兰阴性杆菌，用粗提酶头孢西丁三维试验检测高产AmpC酶并分析其对10种常用抗菌药物的耐药性。结果：273株革兰阴性杆菌中，高产AmpC酶菌株共74株．检出率为27．1％；除对亚胺培南、头孢吡肟耐药性较低外，它们对其他抗菌药物高度耐药，耐药率大多数高于80％；产AmpC酶菌株耐药性明显高于非产酶菌株。结论：高产AmpC酶的革兰阴性杆菌日益增多．耐药性强，临床治疗应首选碳青霉烯类抗生素和第四代头孢菌素。     

临床主要革兰阴性杆菌分布及耐药性变迁

目的：了解近3a临床主要G^-杆菌分布及耐药性变迁,为合理使用抗生素提供帮助。方法：VATEK32鉴定仪对临床分离菌进行鉴定及药敏实验。结果：检出的G杆菌以大肠埃希菌、肺炎克雷伯菌、鲍氏不动杆菌、铜绿假单胞菌为主,鲍氏不动杆菌呈上升趋势,抗生素的耐药率逐年升高。结论：G^-杆菌耐药性非常严重,鲍氏不动杆菌出现广泛耐药,应加强病原菌耐药性监测,防止医院感染暴发。     

医院感染革兰阴性杆菌产AmpC酶状况及耐药性检测分析

目的 探讨产头孢菌素酶(AmpC酶)革兰阴性杆菌医院内感染现状及对药物敏感性的影响.方法 对临床标本进行分离鉴定,采用K-B法对常规药物进行耐药性检测,采用美国国家临床实验室标准化委员会(NCCLS)推荐的三维法检测AmpC酶.结果 在331株革兰阴性杆菌中检出产AmpC酶109株,产酶率为18.4%,产酶菌株对第3代头孢菌素、头霉素类、环丙沙星及含酶抑制剂复合物药物敏感率下降明显,对亚胺培南、头孢吡肟、丁胺卡那耐药率较低,分别为3.28%(2/61)、44.26%(27/61)、31.1%(19/61),产酶菌株对抗菌药物的耐药率明显高于非产酶菌株.结论 革兰阴性杆菌耐药与产AmpC酶有关,治疗该菌感染应选用亚胺培南、第4代头孢菌素等.     

呼吸道感染常见的革兰阴性杆菌菌群分布及耐药分析

为了解我院患标本中分离到的细菌菌群分布及耐药情况,对我院2003-01～2005-06呼吸道感染患送检的痰标本中培养获得的236株常见的革兰阴性杆菌进行药敏试验,现报告如下.     

中国大陆革兰阴性杆菌耐药性研究进展

近年来,国内外越来越多的细菌耐药研究资料给人们展示了目前细菌耐药的新特点,现试从国内革兰阴性杆菌的埘药现状、耐药机制、分子流行病学特征等方面来揭示国内革兰阴性杆菌耐药之规律。     

头孢哌酮他唑巴坦钠对非发酵革兰阴性杆菌的敏感性监测

目的 通过临床分离253株非发酵革兰阴性杆菌对常见临床抗生素的敏感性比较,评价头孢哌酮他唑巴坦对非发酵革兰阴性杆菌的抗菌活性.方法 用全自动细菌分析系统对河南信阳市第一人民医院2006-01-2008-06临床分离的非发酵革兰阴性杆菌进行鉴定药敏试验.结果 非发酵革兰阴性杆菌中分离率占前三位的为铜绿假单胞菌、鲍曼不动杆菌和嗜麦芽窄食单胞菌.非发酵革兰阴性杆菌对头孢哌酮他唑巴坦的敏感度,明显高于其他临床常见抗生素.结论 头孢哌酮一他巴唑坦钠对非发酵革兰阴性杆菌具有良好的抗菌作用,可广泛应用于对其敏感的临床常见致病菌感染疾病的治疗.     

鼓楼医院4年血培养检出革兰阴性杆菌情况及耐药性分析

目的探讨血培养阳性病原菌中革兰阴性杆菌的分布及耐药性分析。方法血液标本在BacT/A-lert 120全自动培养仪中培养,采用BioMerieux API系统鉴定。结果 1 263株血培养阳性分离菌中,革兰阴性杆菌553株,占43.8%。其中大肠埃希菌、肺炎克雷伯菌和铜绿假单胞菌最为常见。除嗜麦芽窄食单胞菌外,其余革兰阴性杆菌对亚胺培南、头孢哌酮/舒巴坦的耐药率较低。结论血培养阳性病原菌中革兰阴性杆菌的总体耐药性较强,临床应根据药敏结果选择抗生素,防止抗感染治疗的失败。     

2643株临床分离革兰阴性杆菌耐药性分析

目的对临床分离的革兰阴性杆菌的分布及耐药性进行分析,为临床合理应用抗生素提供依据。方法用Walkaway40型全自动细菌鉴定仪,对临床分离革兰阴性杆菌进行来源监测及耐药试验以及统计学分析。结果2643株革兰阴性杆菌中分离率居前五位的依次为大肠埃希菌（28．5％）、铜绿假单胞菌（17．3％）、肺炎克雷伯菌（14．7％）、阴沟肠杆菌（9．4％）、鲍曼不动杆菌（7．5％）。不同来源的标本病原菌分布不同：呼吸道标本以铜绿假单胞菌为主,其余标本以大肠埃希菌为主。药敏结果显示,肠杆菌科对头孢哌酮／舒巴坦和亚胺培南耐药率低于10．5％,对氨苄西林、美洛西林、复方新诺明、庆大霉素、头孢曲松、头孢噻肟耐药率达49．4％～97．4％。铜绿假单胞菌和鲍曼不动杆菌对头孢哌酮／舒巴坦和亚胺培南耐药率低于12．7％,对氨苄西林、美洛西林、复方新诺明、庆大霉素、头孢噻肟、头孢曲松、丁胺卡那、头孢他啶耐药率达50．2％～90．2％。结论大肠埃希菌、铜绿假单胞菌、肺炎克雷伯菌、阴沟肠杆菌、鲍曼不动杆菌是临床分离的主要革兰阴性杆菌,而且耐药情况严重,应加强耐药性监测,合理使用抗生素,以减少耐药菌株的传播流行。     

临床常见革兰阴性杆菌分布特点及耐药性调查

目的了解医院革兰阴性(G-)杆菌的分布及耐药情况,为临床合理使用抗生素提供依据。方法对2010年解放军第88医院分离出的所有G-杆菌的耐药情况进行回顾性分析。结果分离出G-杆菌660株,分离前四位的为铜绿假单胞菌、肺炎克雷伯菌、大肠埃希菌、鲍氏不动杆菌。对肠杆菌科敏感率最高的是亚胺培南和美罗培南,铜绿假单胞菌对于头孢吡肟、美罗培南和舒普深的耐药率相对较低,鲍氏不动杆菌对米诺环素的耐药率相对较低。结论碳青霉烯类对肠杆菌科仍保持高活性,对非发酵菌的体外抗菌活性较差。     

Antibiotic Susceptibility Testing of Gram-Negative Nonfermentative Bacilli

A study was undertaken to determine if current methods of antibiotic susceptibility testing could be successfully applied to the gram-negative nonfermentative bacilli. Using clinical isolates and reference strains, experiments were conducted on the inherent reliability of the Bauer-Kirby method, as well as the effect of certain modifications on the method such as elimination of the 2- to 5-h incubation in broth and use of different agar media. Results obtained using these modifications were compared to the results obtained by the standard method. It was shown that the two modifications investigated had a significant effect on the interpretation of zone diameters. It was further shown that the standard Bauer-Kirby method with some exceptions correlates with minimal inhibitory concentrations as determined by broth dilution methods. Results suggest that the Bauer-Kirby method may be a reliable technique for testing the antibiotic susceptibility of the nonfermentative bacilli.     

1137株非发酵革兰阴性菌耐药情况分析

目的 对非发酵菌的临床特征及耐药情况进行分析,为临床医生合理应用抗生素提供依据.方法 应用VITEK2Compact全自动微生物分析仪鉴定临床菌株,WHONET5.6分析软件对2011年1月～2012年3月分离的1 137株非发酵革兰阴性菌进行回顾性分析,并对2011年第一季度和2012年第一季度非发酵革兰阴性杆菌耐药情况进行比较.结果 2011年1月～2012年3月共检出非发酵菌1 137株,占临床分离率的28％(1 137/4 040).其中,铜绿假单胞菌占54.5％(620株),鲍曼不动杆菌占37.6％(428株),嗜麦芽窄食单胞菌占4.0％(45株).非发酵菌临床标本主要来源于痰液,其次为尿液和血液标本.鲍曼不动杆菌对β-内酰胺类、氨基糖苷类、氟喹诺酮类和磺胺类的耐药率均＞50％,鲍曼不动杆菌对抗生素的耐药率分别为亚胺培南59.8％,庆大霉素68.8％,妥布霉素69.8％,左旋氧氟沙星69.5％,头孢吡肟75.3％和头孢他啶69.5％.铜绿假单胞菌对抗生素的耐药率分别为亚胺培南39.1％,庆大霉素18.9％,妥布霉素7.3％,左旋氧氟沙星21.4％,头孢吡肟39.8％和头孢他啶36.6％.2012年第一季度比2011年同季度的耐药情况严重,其中,非发酵革兰阴性杆菌对亚胺培南的耐药情况加重最为明显.结论 非发酵菌感染及耐药情况比较严重,所以控制院内感染并指导临床经验用药,监测非发酵菌临床分布特征和耐药情况刻不容缓.     

Synergistic Activity of Trimethoprim and Amikacin Against Gram-Negative Bacilli

The in vitro effect of trimethoprim on the inhibitory and bactericidal activity of amikacin against 20 strains each of Klebsiella pneumoniae and Serratia marcescens, 15 strains of Escherichia coli, and 10 strains of Pseudomonas aeruginosa was examined by the checkerboard technique in microtiter plates. Trimethoprim had a synergistic effect on the inhibitory and bactericidal activity of amikacin against the majority of non-pseudomonas strains tested. The mean +/- standard deviation fractional inhibitory concentration indexes were 0.59 +/- 0.19 for the Klebsiella strains, 0.48 +/- 0.18 for the Serratia strains, and 0.60 +/- 0.22 for the E. coli strains tested. Respective mean +/- standard deviation fractional bactericidal concentration indexes for these organisms were 0.55 +/- 0.17, 0.54 +/- 0.29, and 0.61 +/- 0.22. A total of 40% of the Klebsiella strains, 80% of the Serratia strains, and 46% of the E. coli strains had a fractional inhibitory concentration equal to or less than 0.25 for both of these antimicrobial agents and were considered to be synergistically inhibited by the combination. By applying this criterion to bactericidal activity, synergy was demonstrated against 50, 65, and 46% of these strains, respectively. All of the Enterobacteriaceae tested were inhibited by clinically achievable concentrations of trimethoprim and amikacin. Antagonism was not demonstrated with any of the organisms tested. Trimethoprim had no antibacterial effect on the Pseudomonas strains and did not alter amikacin's activity against these bacteria.     

Surveillance of Gentamicin-Resistant Gram-Negative Bacilli in a General Hospital

Aerobic gram-negative bacilli isolated from clinical specimens from 1 January to 31 December 1976 were tested for gentamicin and tobramycin resistance by standardized disk testing. For Pseudomonas isolates, gentamicin resistance was 17.1% and tobramycin resistance was 2.8%. For other gram-negative bacilli, gentamicin resistance was 5.5% and tobramycin resistance was 5.4%. Seventy-four patients from whom gentamicin-resistant organisms were isolated from 1 January to 30 June 1976 were studied prospectively. These patients were elderly, had serious underlying diseases, and had received prior antibiotic therapy. Eleven patients carried gentamicin-resistant organisms at the time of transfer to our hospital from community hospitals or nursing homes. Of the 82 isolates from these 74 patients, 52 were from the urine. Pseudomonas was found most frequently (32 isolates), followed by Klebsiella (15 isolates), Enterobacter (10 isolates), Serratia (10 isolates), and Proteus (9 isolates). Only 3 of 32 Pseudomonas isolates caused symptomatic infection, while 16 of 50 other gram-negative bacilli were responsible for symptomatic infection. Although amikacin was the most active drug against gentamicin-resistant gram-negative bacilli and had not been used in our hospital at the time of this study, 25% of Pseudomonas and 18% of all gram-negative bacilli showed resistance to this aminoglycoside.     

Emergence of Imipenem-Resistant Gram-Negative Bacilli in Intestinal Flora of Intensive Care Patients

Intestinal flora contains a reservoir of Gram-negative bacilli (GNB) resistant to cephalosporins, which are potentially pathogenic for intensive care unit (ICU) patients; this has led to increasing use of carbapenems. The emergence of carbapenem resistance is a major concern for ICUs. Therefore, in this study, we aimed to assess the intestinal carriage of imipenem-resistant GNB (IR-GNB) in intensive care patients. For 6 months, 523 consecutive ICU patients were screened for rectal IR-GNB colonization upon admission and weekly thereafter. The phenotypes and genotypes of all isolates were determined, and a case control study was performed to identify risk factors for colonization. The IR-GNB colonization rate increased regularly from 5.6% after 1 week to 58.6% after 6 weeks in the ICU. In all, 56 IR-GNB strains were collected from 50 patients: 36 Pseudomonas aeruginosa strains, 12 Stenotrophomonas maltophilia strains, 6 Enterobacteriaceae strains, and 2 Acinetobacter baumannii strains. In P. aeruginosa, imipenem resistance was due to chromosomally encoded resistance (32 strains) or carbapenemase production (4 strains). In the Enterobacteriaceae strains, resistance was due to AmpC cephalosporinase and/or extended-spectrum β-lactamase production with porin loss. Genomic comparison showed that the strains were highly diverse, with 8 exceptions (4 VIM-2 carbapenemase-producing P. aeruginosa strains, 2 Klebsiella pneumoniae strains, and 2 S. maltophilia strains). The main risk factor for IR-GNB colonization was prior imipenem exposure. The odds ratio for colonization was already as high as 5.9 (95% confidence interval [95% CI], 1.5 to 25.7) after 1 to 3 days of exposure and increased to 7.8 (95% CI, 2.4 to 29.8) thereafter. In conclusion, even brief exposure to imipenem is a major risk factor for IR-GNB carriage.     

Is There Complete Cross-Resistance of Gram-Negative Bacilli to Gentamicin and Tobramycin?

No cross-resistance between gentamicin and tobramycin was found among 19 recent clinical isolates representing four genera of gram-negative bacilli.     

Combined Activity of Clavulanic Acid and Ticarcillin Against Ticarcillin-Resistant, Gram-Negative Bacilli

Fifty-one clinical isolates of ticarcillin-resistant, gram-negative bacilli were tested for susceptibility to combinations of ticarcillin and clavulanic acid (BRL 14151), a potent beta-lactamase inhibitor. Minimal inhibitory concentrations (MICs) were measured by a microdilution method, and minimal bactericidal concentrations for selected strains were measured by the broth dilution method. Ticarcillin MICs were >/=128 mug/ml for all and >/=512 mug/ml for 38 (75%) of the strains. Thirty-nine strains of Enterobacteriaceae tested included Escherichia coli (14), Klebsiella pneumoniae (16), Citrobacter sp. (3), Enterobacter sp. (3), Salmonella enteritidis (1), Serratia marcescens (1), and Proteus mirabilis (1). Ticarcillin MICs for 34 strains (88%) were lowered at least threefold by the addition of 1.0 mug of clavulanic acid per ml. Against 33 strains (85%), the MICs were 64 mug or less per ml in the presence of 5 mug of clavulanic acid per ml. In contrast, the MICs for seven of eight strains of Pseudomonas aeruginosa were unaffected by the addition of up to 10 mug of clavulanic acid per ml. Ticarcillin with 5 mug of clavulanic acid per ml was bactericidal against ticarcillin-resistant (MIC >/= 2,048 mug/ml) E. coli, K. pneumoniae, Enterobacter, and P. mirabilis.     

Activity of Three Aminoglycosides and Two Penicillins Against Four Species of Gram-Negative Bacilli

Three aminoglycoside antibiotics and two penicillins were compared for their in vitro activity against 60 isolates of Serratia, Pseudomonas, Proteus mirabilis, and indole-positive Proteus sp. Testing was done by the agar dilution method using Mueller-Hinton broth solidified with 1.5% agar. The activity of amikacin, aminodeoxybutirosin, and gentamicin against Proteus and Pseudomonas, as related to their peak blood levels, showed no significant differences. Amikacin was the most active against Serratia marcescens. Results using Mueller-Hinton media in broth dilution tests correlated with the agar dilution method except for Pseudomonas aeruginosa. The minimal inhibitory concentration for aminoglycosides in agar was considerably greater than the minimal inhibitory concentration in Mueller-Hinton broth, and the disparity was related to the higher divalent cation concentration of agar. BL-P1654 and carbenicillin were similar except that carbenicillin was much more active against indole-positive Proteus sp. Additionally, the ratio of bactericidal to bacteriostatic concentrations of BL-P1654 was considerably greater than for carbenicillin.     

Effect of Clindamycin on the In Vitro Activity of Amikacin and Gentamicin Against Gram-Negative Bacilli

The in vitro effect of clindamycin on the inhibitory and bactericidal activity of amikacin (BB-K8) and gentamicin against Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa was examined by the checkerboard technique in microtiter plates. Clindamycin (15 μg/ml) produced statistically significant increases in the minimal bactericidal concentrations of amikacin and gentamicin against E. coli and Klebsiellae at 2 and 4 h of incubation. The minimal bactericidal concentration against P. aeruginosa was not affected. Higher concentrations of clindamycin (20 to 25 μg/ml) reduced the minimal inhibitory and bactericidal concentrations of amikacin and gentamicin for E. coli at 18 h of incubation. The synergistic bactericidal activity of amikacin and carbenicillin against E. coli, but not P. aeruginosa, was also inhibited slightly by clindamycin (15 μg/ml). The clinical implications of this inhibition of the early bactericidal in vitro activity of aminoglycosides by clindamycin remain to be determined. Although these in vitro results have not been studied in clinical infections, it is conceivable that slight interference in early bacterial killing could alter the outcome of infection in the immunosuppressed patient.     

Mechanism of Synergistic Effects of β-Lactam Antibiotic Combinations on Gram-Negative Bacilli

These studies were undertaken to elucidate further the mechanism of synergism of pairs of beta-lactam antibiotics on beta-lactamase-producing gram-negative bacilli. Three strains of gram-negative bacilli which elaborate beta-lactamase enzymes with widely differing properties were employed. The antibacterial effects of beta-lactam antibiotics, singly and in combination, on the three organisms investigated were exactly those which would have been predicted on the basis of the enzymological properties of the beta-lactamases elaborated by these organisms. The findings thus support the hypothesis that the synergistic antibacterial effects of combinations of beta-lactam antibiotics on these organisms were due to inhibition of the enzyme by one of the agents and killing of the organism by the other, which was protected from enzymatic hydrolysis, rather than the alternative possibility that the synergistic effects were due simply to the combined antibacterial actions of the two drugs.