1998～2002年广州地区淋球菌对抗生素耐药性的变迁

目的 :了解 1998～ 2 0 0 2年广州地区淋球菌对 5种抗生素的耐药性的变迁及产青霉素酶淋球菌(PPNG)和高水平耐四环素淋球菌 (TRNG)的流行状况。方法 :用琼脂稀释法测定最低抑菌浓度 (MIC)以及用纸片碘量法检测β-内酰胺酶。结果 :60 3株淋球菌检出 PPNG 64株 (10 .6% )、TRNG 83株 (13 .7% ) ,1998～ 2 0 0 2年 ,PPNG、TRNG流行率及环丙沙星耐药率 ,经μ检验 ,P<0 .0 1,差异有显著性。头孢曲松、壮观霉素未发现耐药菌株 ,壮观霉素抗菌活性最强。结论 :持续监测淋球菌的耐药性十分重要     

2003年广州地区淋球菌对抗生素耐药性结果分析

目的了解广州地区淋球菌对抗生素的耐药性及PPNG和TRNG的流行状况.方法用琼脂稀释法测定最低抑菌浓度(MIC)以及用纸片碘量法检测β-内酰胺酶.结果 116株淋球菌检出PPNG30株(25.9%)、TRNG36株(31%)、环丙沙星耐药率达93.1%,头孢三嗪、壮观霉素未发现耐药菌株,且抗菌活性最强.结论持续监测淋球菌的耐药性十分重要.     

广州地区淋球菌抗生素耐药性及质粒图谱研究

目的：了解广州地区淋球菌对抗生素的耐药性及质粒图谱。方法：用琼脂稀释法测定5种抗生素对167株菌的最低抑菌浓度（MIC）及用破裂解法分析160株菌的质粒图谱。结果：167株淋球菌检出PPN9株（5．4％）,TRNG16株（9．6％）,环丙沙星耐药率达78．4％,头孢三嗪,壮观霉素未发现耐药菌株。160株菌其质粒谱型2．6Md 4.5Md(24.4%),2.6Md 4.5Md 24.5Md(20.6%),2.6Md 24.5Md(20.6%),4.5Md检出率（45％）24.5Md检出率（41．3％）。结论：表明了广州地区淋球菌抗生素的耐药性和质粒图谱,有助于淋病的治疗和防治。     

2010年广州地区淋球菌耐药监测结果分析

目的了解广州地区淋球菌对抗生素耐药性的变化及PPNG和TRNG的流行趋势。方法用琼脂稀释法测定头孢曲松、大观霉素、环丙沙星、阿奇霉素和四环素的最低抑菌浓度（MIC）;用纸片碘量法检测β-内酰胺酶。结果83株淋球菌检出PPNG24株（28．9％）、TRNG50株（60．2％）、环丙沙星耐药率高达98．8％,高度耐药株（MIC≥16mg／L）43株（51．8％）,而76株淋球菌中阿奇霉素耐药株11株（14．5％）,均未出现对头孢曲松、大观霉素耐药的菌株,抗菌活性强。结论合理规范使用抗生素及动态监测淋球菌耐药性变迁是临床减少淋球菌耐药菌株出现的有效办法。     

结核分枝杆菌利福平耐药性的研究进展

本旨在阐明结核分枝杆菌耐利福平分离株rpoB基因突变的规律,以及rpoB基因突变与利福平最低抑菌浓度(MIC)的关系。结核分枝杆菌的rpoB基因突变是引起利福平耐药性的主要原因,耐利福平分离株的rpoB基因突变主要集中在507～533位密码子的81bp的区域内,约80％的菌株发生531位或526位密码子突变。不同类型rpoB基因突变的结核分枝杆菌对利福平的耐受性也不同,通常发生531位密码子突变的菌株的MIC≥64μg／ml。     

淋球菌耐药性与耐药质粒的研究

为了解湛江地区淋球菌耐药现状及耐药质粒的分布,并初步探讨其相互关系,对１９９８￣１９９９年广东省湛江地区健康鉴定出的９８株淋球菌流行株,应用纸片扩散法测定细胞对１０种抗生素的敏感性,并采用碱裂解法进行质粒抽提,分析耐药质粒的分布情况,选取ＮＧ４、ＮＧ３１、ＮＧ４３、ＮＧ７０进行细菌的接合试验,以观察耐药质粒能否通过接合进行传递以及传递后受体菌耐药性的变化。结果显示６．１２％菌株对全部抗生素敏感,４８．９６％的菌株对３种及３种以上的抗生素耐药;共检出四种不同分子量的质闰,７．４ｋｂ和４．２ｋｂ质粒检出率较高,分别为５９．１６％和６７．３２％,质粒谱型１２种,以７．４ｋｇ＋４．２ｋｇ和３９．５ｋｇ＋７．４ｋｇ＋４．２ｋｇ为主,占３８．７６％。在细菌的接合传递试验中,ＮＧ４３可通过接合传递将其耐药性传递给淋球菌及大肠     

羧甲基壳聚糖对5株口腔颌面部感染细菌的抑菌性能的评价

目的 研究羧甲基壳聚糖对5株口腔颌面部感染细菌的抑菌性能,为在临床应用提供相关资料。方法 采用液体梯度稀释法分别测定羧甲基壳聚糖对牙龈卟啉菌、中间普氏菌、金黄色葡萄球菌、大肠埃希菌和铜绿假单胞菌的最低抑菌浓度（MIC）。结果 羧甲基壳聚糖对5株菌的MIC分别为：20、5、2.5、5、10 g/L。结论 羧甲基壳聚糖对口腔颌面部感染重要相关细菌具有抑菌作用。     

郴州地区淋病奈瑟菌耐药性特点分析

目的 了解郴州市区域内病奈瑟菌耐药性特点,为临床用药提供依据。方法 收集郴州市区域内12家医院门诊病人泌尿生殖道分泌物中分离的255株淋球菌,并作为药敏试验,分析其特点。结果 255株淋球菌对青霉素100％耐药,对复方新诺明、氨苄、青霉素、四环素等耐药严重,同时耐毒霉素、头孢三嗪、环丙沙星等交叉耐药现象严重。结论 临床上治疗淋病须以体外药敏试验为依据用药,以提高疗效和减少耐药菌株的产生。     

56例儿童淋球菌检测结果分析

淋病是侵犯泌尿生殖系统为主的性病 ,除急性外 ,还呈慢性经过 ,甚至有无症状感染者 ,这种无症状感染者因不被注意 ,具有流行病学上的重要意义。因此 ,快速、准确的淋菌检测结果 ,为临床提供重要的诊治依据 ,为此我们对 5 6例患儿的不同标本进行相同的系统检测 ,现报道如下。1　材料与方法1 1　病例选择　随机选择拟似淋病患儿 5 6例 ,其中男 2 1例 ,女 35例 ,年龄最小出生后 3d ,最大 14岁 ,父母均患淋病者 35例 ,单方患淋病者 15例。人均取材 3次者 2 1例 ,取材2次者 2 5例 ,取材 1次者 11例 ,合计取材 12 1份次。1 2　方法　 (1)眼分泌物…     

三种方法检测淋球菌的结果分析

淋病奈瑟氏菌(N.gonoyyhoeac简称淋球菌),淋病快速纸片法和涂片革兰染色镜检操作简便、快速、价廉。从定性反应和形态上观察疑诊淋病,要确诊尚需细菌培养。本文就疑诊淋病患者标本在纸片法,涂片镜检的同时进行细菌培养,现报道如下。1　材料与方法1.1　病例选择　随机选择?..     

Chromosomal location of antibiotic resistance genes in Neisseria gonorrhoeae.

Transformation with purified plasmid and chromosomal deoxyribonucleic acid from a clinical isolate of Neisseria gonorrhoeae showed that each of seven loci affecting drug resistance (penA, penB, ery, str, tet, chl, and env) was chromosomal.     

Loss of low-level antibiotic resistance in Neisseria gonorrhoeae due to env mutations.

Mutations (env) which resulted in increased sensitivity of gonococci to diverse compounds were studied by transformation. Strains carrying an env mutation were more sensitive than wild-type strains to several antibiotics, dyes, and detergents. The env mutations resulted in complete phenotypic suppression of low-level resistance to these same drugs determined by mutation at ery. Recombination was observed in transformation crosses between various env mutants. The env locus was not linked to the cluster of antibiotic resistance genes near str and spc.     

淋病奈瑟球菌的耐药性检测

目的了解淋病奈瑟球菌对临床常见药物的耐药性。方法采用琼脂稀释法测定13种抗菌药物对35株淋病奈瑟球菌的MICs;Nitrocefin(头孢硝噻酚)纸片检测β-内酰胺酶,并采用PCR测定其基因型。结果淋病奈瑟球菌对青霉素、四环素、环丙沙星与头孢呋辛的耐药率分别为65．7％、60．0％、88．6％与14．3％,对第3、4代头孢菌素、大观霉素非常敏感,耐药率均为0％;42．9％的菌株产生TEM型β-内酰胺酶。结论淋病奈瑟球菌对青霉素、四环素类和氟喹诺酮类的耐药性高,治疗宜选用第3、4代头孢菌素和大观霉素等,同时加强耐药性监测。     

Intrinsic penicillin resistance in penicillinase-producing Neisseria gonorrhoeae strains

The minimal inhibitory concentrations (MICs) of ampicillin for fifty strains of beta-lactamase-producing Neisseria gonorrhoeae (PPNG) isolated in Japan ranged from 1.56 to 200 micrograms/ml, and all the strains harbored a 4.5 megadalton plasmid. These strains were classified into two groups: dicloxacillin-susceptible (28%) and -resistant group (72%). A linear correlation was found in the dicloxacillin-susceptible strains between their beta-lactamase activity and the susceptibility to ampicillin, but not in the dicloxacillin-resistant strains. This suggests that the high ampicillin resistance in PPNG is due not only to acquiring the beta-lactamase producing plasmid, but also to some intrinsic resistance of the strains. To investigate a cause of the high ampicillin resistance, the beta-lactamase-producing plasmid, pTMS1, was transferred by conjugation to a penicillin-susceptible gonococcal strain as well as to its isogenic multiply antibiotic-resistant transformants, and the susceptibility of the transconjugants to ampicillin was determined. Acquisition of pTMS1 by a penicillin-susceptible strain resulted in a 32-fold increase in resistance to ampicillin, whereas the increase was 128-fold for its isogenic strains which contain some chromosomal mutations. These results suggest that reduced permeability of the outer membrane to ampicillin underlies the high ampicillin resistance of PPNG.     

Porin-mediated antibiotic resistance in Neisseria gonorrhoeae: ion, solute, and antibiotic permeation through PIB proteins with penB mutations

Neisseria gonorrhoeae has two porins, PIA and PIB, whose genes (porA and porB, respectively) are alleles of a single por locus. We recently demonstrated that penB mutations at positions 120 and 121 in PIB, which are presumed to reside in loop 3 that forms the pore constriction zone, confer intermediate-level resistance to penicillin and tetracycline (M. Olesky, M. Hobbs, and R. A. Nicholas, Antimicrob. Agents Chemother. 46:2811-2820, 2002). In the present study, we investigated the electrophysiological properties as well as solute and antibiotic permeation rates of recombinant PIB proteins containing penB mutations (G120K, G120D/A121D, G120P/A121P, and G120R/A121H). In planar lipid bilayers, the predominant conducting state of each porin variant was 30 to 40% of the wild type, even though the anion selectivity and maximum channel conductance of each PIB variant was similar to that of the wild type. Liposome-swelling experiments revealed no significant differences in the permeation of sugars or beta-lactam antibiotics through the wild type or PIB variants. Although these results are seemingly contradictory with the ability of these variants to increase antibiotic resistance, they are consistent with MIC data showing that these porin mutations confer resistance only in strains containing an mtrR mutation, which increases expression of the MtrC-MtrD-MtrE efflux pump. Moreover, both the mtrR and penB mutations were required to decrease in vivo permeation rates below those observed in the parental strain containing either mtrR or porin mutations alone. Thus, these data demonstrate a novel mechanism of porin-mediated resistance in which mutations in PIB have no affect on antibiotic permeation alone but instead act synergistically with the MtrC-MtrD-MtrE efflux pump in the development of antibiotic resistance in gonococci.