醋酸氯己定与替硝唑联合药敏试验观察

目的研究醋酸氯己定与替硝唑协同抗菌效果。方法采用棋盘方阵稀释法,对醋酸氯己定与替硝唑联合应用体外抗菌作用进行了观察。结果测定替硝唑和醋酸氯己定对金黄色葡萄球菌、铜绿假单胞菌、产气荚膜梭菌和脆弱拟杆菌的MIC值,替硝唑分别为200、200、1、1μg/ml,醋酸氯己定分别为0.06、4、1、4μg/ml。替硝唑与醋酸氯己定联合应用对上述4种试验菌的MIC值与各自的单方相比较无变化,两药相加无相关作用,但相互也不干扰对方的抗菌作用。结论应用于创伤涂膜剂中的醋酸氯己定和替硝唑两种主要抗菌成分既无协同作用或相加作用,但也不互相干扰。     

两种临床分离细菌对醋酸氯己定抗力测定

目的研究医院临床分离致病性大肠杆菌和金黄色葡萄球菌对醋酸氯己定的抗性力水平。方法采用肉汤稀释法测定两种16株临床分离细菌对醋酸氯己定抗力水平,并同相应标准菌株作平行比较。结果大肠杆菌临床株对醋酸氯己定的MIC为1~2 mg/L,标准菌株对醋酸氯己定的MIC为2 mg/L;有3株大肠杆菌的MIC低于标准菌株。金黄色葡萄球菌临床株对醋酸氯己定的MIC为0.98~1.95 mg/L,标准株对醋酸氯己定的MIC为0.98mg/L;有2株临床株的MIC高于标准菌株。大肠杆菌临床株对醋酸氯己定的MBC为4~8 mg/L,标准菌株对醋酸氯己定的MBC为2 mg/L;大肠杆菌临床株的MBC均高于标准菌株。金黄色葡萄球菌临床株对醋酸氯己定的MBC为15.6~125 mg/L,标准菌株的MBC为62.5 mg/L;有3株金黄色葡萄球菌临床株MBC高于标准株。结论临床分离的大肠杆菌和金黄色葡萄球菌对醋酸氯己定抗力多数比标准株强,只有个别菌株低于标准株。     

战创伤涂膜剂对常见化脓菌的抗菌活性研究

目的测定战创伤涂膜剂对常见化脓菌的最低抑菌浓度（minimum inhibitory concentration,MIC）和最低杀菌浓度（minimum bactericidal concentration,MBC）。方法以培养基稀释战创伤涂膜剂、氯己定甲硝唑乳膏至不同浓度,分别加入化脓菌标准菌株大肠埃希菌、金黄色葡萄球菌、铜绿假单胞菌、奇异变形杆菌悬液,菌液浓度为10^5cfu／ml,培养后观察细菌生长情况,确定两药的MIC和MBC并进行比较。结果战创伤涂膜剂对大肠埃希菌、金黄色葡萄球菌、铜绿假单胞菌、奇异变形杆菌的MIC分别为0．0625μg／ml、2μg／ml、4μg／ml、8μg／ml,MBC分别为0．125μg／ml、4μg／ml、4μg／ml、8μg／ml。氯己定甲硝唑乳膏对大肠埃希菌、金黄色葡萄球菌、铜绿假单胞菌、奇异变形杆菌的MIC分别为1μg／ml、8μg／ml、〉32μg／ml、〉32μg／ml,MBC分别为2μg／ml、16μg／ml、〉32μg／ml、〉32μg／ml。两药对金黄色葡萄球菌的杀菌率均达到99％以上。结论战创伤涂膜剂对常见化脓菌有良好的抑菌、杀菌作用。     

战创伤涂膜剂对厌氧菌体外抗菌实验研究

目的测定战创伤涂膜剂对产气荚膜梭菌（有芽孢菌）和脆弱拟杆菌（无芽孢菌）标准菌株的最低抑菌浓度（minimum inhibitory concentration,MIC）和最低杀菌浓度（minimum bactericidal concentration,MBC）。方法应用培养基将涂膜剂、氯已定甲硝唑乳膏稀释至不同浓度,分别加入产气荚膜梭菌和脆弱拟杆菌悬液,控制菌液浓度为10^5 efu／ml,厌氧培养后观察细菌生长情况,确定两药的MIC和MBC并进行比较。结果涂膜剂体外对脆弱拟杆菌、产气荚膜梭菌MIC均为1μg／ml,MBC分别为1μg／ml、2μg/ml。氯已定甲硝唑乳膏对脆弱拟杆菌、产气荚膜梭菌MIC分别为4μg／ml、1μg／ml,MBC为8μg／ml、2μg／ml。两药杀菌率均〉99％。结论涂膜剂对有芽孢和无芽孢类厌氧菌有良好的抑落、杀菌作用。     

两种植物挥发油体外抗菌作用试验观察

目的观察金银花和山楂果核挥发油体外抗菌效果,为实际应用提供科学依据。方法采用稀释法对两种植物挥发油体外最小抑菌浓度和最小杀菌浓度进行了测定。结果金银花挥发油对革兰阴性菌株的MIC50和MIC90值均≥128μg/ml,对金黄色葡萄球菌MIC90值≥128μg/ml、MIC50值为64μg/ml。山楂果核挥发油对所有试验菌株的MIC50值在16～64μg/ml范围;MIC90值在64～128μg/ml。山楂果核挥发油作用15 min,对大肠杆菌和金黄色葡萄球菌MBC值在32～64μg/ml范围;金银花挥发油作用60 min,对上述两种细菌MBC值为64μg/ml。结论两种植物挥发油对试验菌株都具有良好的体外抗菌效果,但其MIC和MBC值均明显高于两种对照药物。     

比阿培南和亚胺培南对呼吸道和泌尿道致病菌的体外抗菌活性比较

目的研究比阿培南和亚胺培南对呼吸道和泌尿道致病菌的体外抗菌活性。方法采用琼脂二倍稀释法，测定比阿培南和亚胺培南对294株呼吸道和泌尿道致病菌的MIC。结果比阿培南对所有测试菌的MIC价MIC90和敏感率范围分别为≤0．03～4μg／ml、0．06～〉128μg／ml及90％～100％，亚胺培南为≤0．03—2μg／ml、0．06～〉128μg／ml及86．7％～100％。比阿培南对金黄色葡萄球菌、表皮葡萄球菌的MIC90（4，1μg／ml）是亚胺培南MIC90（2，0．25μg/ml）的2—4倍，对大肠埃希菌、阴沟肠杆菌、奇异变形杆菌、铜绿假单胞菌、鲍曼不动杆菌的MIC90（0．125—4μg／ml）是亚胺培南MIC90（0．5～8μg／ml）的1／4～1／2，对肠球菌属、肺炎链球菌、肺炎克雷伯菌、流感嗜血杆菌的MIC90与亚胺培南相当，分别为〉128、0．06、0．5、2μg／ml。结论比阿培南对革兰阳性菌和革兰阴性菌均具有广谱抗菌活性，其中对革兰阴性菌的作用优于亚胺培南，对革兰阳性菌的作用稍差于亚胺培南。     

日化杀菌产品中醋酸氯己定含量测定方法的研究

为准确测定日化产品中醋酸氯己定含量,采用紫外分光光度法和高效液相色谱法,在实验室进行了试验研究。结果,测得线性范围:紫外分光光度法为 2~20μg/ml,高效液相色谱分析法为 20 ~200μg/ml;线性相关系数分别为R=0. 9998和 0. 9997。回收率:紫外分光光度法对液体样品中醋酸氯己定测定回收率为 93. 4% ~101. 4%和 94. 8% ~100. 3%;高效液相色谱分析法对牙膏中醋酸氯己定测定回收率为 85. 3% ~94. 1%和 90. 6% ~98. 5%。经过对 6种含醋酸氯己定产品测定,两种分析方法测得结果与产品标量相符。结论,两种分析方法测定常见产品中醋酸氯己定含量,样品预处理方法简单,精密度和回收率高,分离准确快速,适合于常规分析。     

广泛药物耐药铜绿假单胞菌与鲍曼不动杆菌对多粘菌素B的MIC值分布调查

目的通过检测多粘菌素B体外对广泛药物耐药(extensive drug-resistant,XDR)的铜绿假单胞菌与鲍曼不动杆菌的最低抑菌浓度(MIC)的分布上,来评价其对此类细菌的抗菌活性,为临床治疗、控制感染提供依据。方法用纸片扩散法检测临床分离的288株细菌(铜绿假单胞菌130株,鲍曼不动杆菌158株)对临床常见的25种抗菌药物的敏感性以确定其中广泛药物耐药菌;用E-试验检测多粘菌素B及临床常用11种抗菌药物MIC值,分析菌株的MIC值分布情况。结果 288株细菌经K-B法确认均为XDR菌株,对临床常用的11种抗菌药物的敏感性均低于15%;对多粘菌素B的MIC值均≤2μg/ml;130株铜绿假单胞菌的MIC值分布情况为0.125μg/ml1株、0.19μg/ml2株、0.25μg/ml9株、0.38μg/ml37株、0.5μg/ml48株、0.75μg/ml19株、1.0μg/ml11株、1.5μg/ml4株,MIC50为0.5μg/ml,MIC90为1.0μg/ml;158株鲍曼不动杆菌的MIC值分布情况为0.125μg/ml1株、0.19μg/ml3株、0.25μg/ml12株、0.38μg/ml45株、0.5μg/ml56株、0.75μg/ml21株、1.0μg/ml13株、1.5μg/ml7株、2.0μg/ml1株,MIC50为0.5μg/ml,MIC90为1.0μg/ml。结论多粘菌素B体外对广泛药物耐药铜绿假单胞菌与鲍曼不动杆菌均敏感,本地区临床未发现有多粘菌素B耐药株;但存在敏感区域内的高MIC值菌株,应引起临床重视。     

塞克硝唑对厌氧菌抑菌效果研究

目的观察塞克硝唑对厌氧菌的抑菌效果.方法采用琼脂平板稀释法测定塞克硝唑对200株厌氧菌的抑菌浓度（MIC）,实验中以替硝唑和甲硝唑作为厌氧菌抑菌试验的对照.结果塞克硝唑、替硝唑和甲硝唑对120株革兰阴性厌氧菌的MIC90分别为1～4μg/ml、1～2μg/ml和4～8μg/ml,对80株革兰阳性厌氧菌的MIC90分别为4～8μg/ml、4～16μg/ml和16～32μg/ml.结论试验药物中塞克硝唑抑制革兰阳性厌氧菌较替硝唑稍强,甲硝唑对厌氧菌的抑制作用均不如塞克硝唑和替硝唑.     

抗菌肽lycosin-I对铜绿假单胞菌临床分离株的体外抗菌活性分析

目的探讨lycosin-I对铜绿假单胞菌的体外抗菌活性。方法随机收集中南大学湘雅二医院铜绿假单胞菌临床分离株,其中铜绿假单胞菌的多重耐药菌10株,非耐药菌10株。应用微量肉汤稀释法检测lycosin-I对铜绿假单胞菌的体外最低抑菌浓度(MIC);选取铜绿假单胞菌的多重耐药菌的代表株Isolate 8(MIC为8μg/m L)和非耐药菌的代表株Isolate 12(MIC为8μg/m L),检测4×MIC浓度lycosin-I的杀菌动力学;体外构建适宜环境,培养代表株24 h,定点测定其600 nm处吸光度并绘制生长曲线;在培养环境中分别添加5 mmol/L钙离子或镁离子,检测lycosin-I杀菌能力的盐耐受性。结果 Lycosin-I在体外条件下对铜绿假单胞菌的多重耐药菌和非耐药菌均表现出良好的体外抗菌活性:lycosin-I抗铜绿假单胞菌多重耐药菌的MIC为12(8,32)μg/m L,非耐药菌的MIC为12(8,32)μg/m L,两组MIC差异无统计学意义(U=42,P0.05)。4×MIC浓度的lycosin-I在60 min时即可杀灭约50%的铜绿假单胞菌多重耐药菌和非耐药菌。体外培养24 h,可见在MIC以下浓度(0,2,4μg/m L)lycosin-I干预下铜绿假单胞菌多重耐药菌和非耐药菌于6~16 h快速生长,18 h后生长速度趋于平缓;在MIC浓度(8μg/m L)lycosin-I干预下,细菌均难以生长。5 mmol/L Ca2+或Mg2+可以减弱lycosin-I的体外抗菌活性,Ca2+的加入使lycosin-I抗铜绿假单胞菌的多重耐药菌和非耐药菌的MIC值均由原来的8μg/m L升高至64μg/m L,Mg2+的加入则均使MIC值由原来的8μg/m L升高至32μg/m L。但是当lycosin-I处于较高浓度状态(64μg/m L或32μg/m L)时,其仍然可以保持较好的抗铜绿假单胞菌多重耐药菌和非耐药菌活性。结论 Lycosin-I在体外条件下可以有效抑制铜绿假单胞菌浮游菌的生长,具有一定的盐耐受性,有望发展成为一种新型抗菌药物。     

替硝唑对厌氧菌体外抗菌活性的观察研究

目的 测定替硝唑对产气荚膜梭菌（有芽孢菌）和脆弱拟杆菌（无芽孢菌）标准菌株的最低抑菌浓度（mininmm inhibitory concentration,M1C）和最低杀菌浓度（minimum bactericidal concentration,MBC）。方法应用培养基稀释替硝唑至不同浓度,然后分别加入产气荚膜梭菌及脆弱拟杆菌悬液,菌液浓度为10^5cfu／ml,厌氧培养后观察细菌生长情况,确定MIC和MBC。结果替硝唑对脆弱拟杆菌、产气荚膜梭菌的MIC均为1μg／ml,MBC均为2μg／ml。结论替硝唑对有芽孢和无芽孢类厌氧菌都有良好的抑菌、杀菌作用。     

纳米银妇科抑菌喷剂体外抗菌效果的观察

目的观察纳米银妇科抑菌喷剂的体外抗菌效果,为实际应用提供依据。方法采用抑菌环试验和悬液定量试验方法,对该纳米银妇科抑菌喷剂体外抗菌效果进行实验室观察。结果纳米银妇科抑菌喷剂对大肠杆菌、金黄色葡萄球菌、铜绿假单胞菌和白色念珠菌的最低抑菌浓度分别为3.15μg/ml、6.3μg/ml、3.15μg/ml和6.3μg/ml,最低杀菌浓度分别为12.6μg/ml、25.2μg/ml、12.6μg/ml和25.2μg/ml。银含量为25.2μg/ml的纳米银妇科抑菌喷剂对上述四个菌种作用2 min,杀菌率均达到90%以上。结论纳米银妇科抑菌喷剂对大肠杆菌、金黄葡萄球菌、铜绿假单胞菌和白色念珠菌均具有较强的抑杀作用。     

Pharmacodynamics of razupenem (PZ601) studied in an in vitro pharmacokinetic model of infection

Simulations of administration of razupenem at 1 g every 12 h by 1-h intravenous (i.v.) infusion were performed in an in vitro pharmacokinetic model of infection. The antibacterial effect of this razupenem dosing regimen against six strains of Staphylococcus aureus (one methicillin-sensitive S. aureus [MSSA] strain [MIC, 0.015 μg/ml] and five methicillin-resistant S. aureus [MRSA] strains [MIC range, 0.09 to 3 μg/ml]) and five strains of Enterobacteriaceae (three Escherichia coli strains [two containing extended-spectrum β-lactamases {ESBLs}] and two Enterobacter sp. strains [one with an AmpC enzyme and the other with a raised razupenem MIC; MIC range, 0.09 to 6 μg/ml]) was assessed. Against the MSSA and MRSA strains, razupenem produced a >3.5-log-unit reduction in viable count after 24 h. There were no changes in population profiles. In a second series of experiments, over 5 days there was rapid initial clearance of MRSA from the model followed by regrowth after 48 h. MRSA colonies appeared on 2× MIC recovery medium after 72 h with strain 33820 (MIC, 3.0 μg/ml) and at 120 h with strain 27706 (MIC, 1.5 μg/ml). Against E. coli and Enterobacter spp., razupenem produced a >3.5-log-unit reduction in bacterial counts for all strains except that with an MIC of 6 μg/ml, where razupenem had a notably poorer antibacterial effect. Population profiles were unchanged after 48 h of exposure to razupenem except for Enterobacter strain 34425 (MIC, 6.0 μg/ml), where colonies were recovered from media containing 2×, 4×, and 8× MIC. In dose-ranging studies with MRSA strains, the percentage of the dosing interval that the free drug concentration remained higher than the pathogen MIC (fT>MIC) for a 24-h bacteriostatic effect was 5.0% ± 1.4%, and that for a 1-log-unit reduction in count was 12.5% ± 5.8%. Population profiles indicated growth on 2× MIC recovery medium at fT>MIC values of 1 to 35% but not at a value of >35%. In a similar set of experiments with Enterobacteriaceae, the fT>MIC for a 24-h bacteriostatic effect was 34.2% ± 7.6% and that for a 1-log-unit reduction in count was 42.5% ± 7.8%. Population analysis profiles indicated growth on recovery media with 2×, 4×, and 8× MIC at fT>MICs in the range of 1 to 69% but rarely at values of ≥ 70%. In conclusion, razupenem at simulated human doses of 1 g i.v. every 12 h has a marked antibacterial effect on MSSA and MRSA strains with MICs of ≤ 3.0 μg/ml and Enterobacteriaceae with MICs of ≤ 0.4 μg/ml. fT>MIC targets of ≥ 35% for MRSA and ≥ 70% for Enterobacteriaceae should provide significant antibacterial effects combined with low risks of changing pathogen antibiotic population profiles.     

氯己定对4株温和气单胞菌的抑制与杀灭作用

采用对倍稀释系列浓度定性试验法 ,测定醋酸氯己定对不同来源的 4株温和气单胞菌的最小抑菌浓度和最小杀菌浓度。结果 ,北京从临床标本分离的 3株与沈阳临床分离株对氯己定的抗力无明显差别。氯己定对它们的最小抑菌浓度与最小杀菌浓度分别为 13 6mg/L与 2 7 2mg/L。     

Antibacterial activity of sphingoid bases and fatty acids against Gram-positive and Gram-negative bacteria

There is growing evidence that the role of lipids in innate immunity is more important than previously realized. How lipids interact with bacteria to achieve a level of protection, however, is still poorly understood. To begin to address the mechanisms of antibacterial activity, we determined MICs and minimum bactericidal concentrations (MBCs) of lipids common to the skin and oral cavity--the sphingoid bases D-sphingosine, phytosphingosine, and dihydrosphingosine and the fatty acids sapienic acid and lauric acid--against four Gram-negative bacteria and seven Gram-positive bacteria. Exact Kruskal-Wallis tests of these values showed differences among lipid treatments (P < 0.0001) for each bacterial species except Serratia marcescens and Pseudomonas aeruginosa. D-sphingosine (MBC range, 0.3 to 19.6 μg/ml), dihydrosphingosine (MBC range, 0.6 to 39.1 μg/ml), and phytosphingosine (MBC range, 3.3 to 62.5 μg/ml) were active against all bacteria except S. marcescens and P. aeruginosa (MBC > 500 μg/ml). Sapienic acid (MBC range, 31.3 to 375.0 μg/ml) was active against Streptococcus sanguinis, Streptococcus mitis, and Fusobacterium nucleatum but not active against Escherichia coli, Staphylococcus aureus, S. marcescens, P. aeruginosa, Corynebacterium bovis, Corynebacterium striatum, and Corynebacterium jeikeium (MBC > 500 μg/ml). Lauric acid (MBC range, 6.8 to 375.0 μg/ml) was active against all bacteria except E. coli, S. marcescens, and P. aeruginosa (MBC > 500 μg/ml). Complete killing was achieved as early as 0.5 h for some lipids but took as long as 24 h for others. Hence, sphingoid bases and fatty acids have different antibacterial activities and may have potential for prophylactic or therapeutic intervention in infection.