解脲脲原体的耐药性分析及其耐氟喹诺酮的分子机制研究

目的检测128株临床分离解脲脲原体(UU)对9种药物的敏感性,并检测喹诺酮类耐药UU对5种喹诺酮药物的MIC以及gyrA和parC基因突变情况。方法应用支原体分离鉴定、计数药敏试剂盒检测UU对9种药物的敏感性,用微量肉汤稀释法检测耐药UU菌株对5种喹诺酮类药物的MIC,用PCR和DNA测序及序列比较检测基因突变。结果UU对多西环素最敏感,其次为米诺环素、交沙霉素、司帕沙星及克林霉素,对大环内酯类药物阿奇霉素和罗红霉素高度耐药。而司帕沙星、加替沙星和左氧氟沙星的MIC范围在0.25～8μg/mL,抑制UU活性强于氧氟沙星和环丙沙星。10株喹诺酮类耐药UU中有3株只有parC基因第80位TCA→TTA的突变,氨基酸由丝氨酸→亮氨酸,1株GyrA基因第95位密码子GAC→GAA的突变,氨基酸由天冬氨酸→谷氨酸。6株两者同时存在。结论在UU治疗中可首选多西环素,其次为米诺环素和交沙霉素。gyrA基因95位密码子和parC基因80位的突变密码子与UU耐喹诺酮类药物密切相关。     

淋球菌gyrA和parC基因突变与氟喹诺酮类药物关系的研究

目的：探讨淋球菌gyrA和parC基因突变与淋球菌耐氟喹诺酮类药物之间的关系。方法：①纸片扩散法检测58株淋球菌对5种氟喹诺酮类药物的敏感性。②E测定法定量检测环丙沙星的最小抑菌浓度（MIC）。③PCR技术扩增gyrA和parC基因的喹诺酮耐药决定区（QRDR）相关序列并作测序分析。结果：①对环丙沙星、氧氟沙星、氟罗沙星、洛美沙星、依诺沙星同为敏感、中介、耐药者分别为2株、4株和39株。②环丙沙星MIC为敏感、中介、耐药分别为2株、17株和39株。③环丙沙星MIC为0．004－0．016μg/mL的2株淋球菌gyrA和parC基因均未发生突变；MIC为0．064－0．094μg/mL的菌株仅发生gyrA单位点突变；而MIC≥0.25μg/mL的菌株均发生gyrA双位点突变。MIC≤0．25μg/mL的菌株无parC基因突变，而MIC≥1.0μg/mL的菌株除出现gyrA双位点突变外均同时发生parC单位点突变。④在发生突变的16株菌中，Ser91(TCC)→Phe(TTC）突变为15株。结论：①gyrA基因突变介导淋球菌对氟喹诺酮类药物低和中水平耐药，而对氟喹诺酮类药物高水平耐药需要parC基因突变的共同参与。②gyrA基因Ser91→Phe的突变是导致淋球菌对氟喹诺酮类药物耐药的关键突变。     

解脲脲原体临床分离株中喹诺酮类耐药株的筛选及其耐药基因的研究

目的：从临床分离的解脲脲原体中筛选出喹诺酮类药物耐药株,了解耐药株发生的比率。并研究耐药株中喹诺酮抗性决定区域(QRDR)出现基因变异的情况。方法：采用药敏试剂盒及96孔微量培养基稀释法收集解脲脲原体的喹诺酮耐药株。PCR扩增阳性标本测序后比较基因变异情况。结果：从104株解脲脲原体临床分离株中筛选出10株耐药株。测序结果显示有7株QRDR的gyrA基因片段中309位均出现了A→G点变异,导致相应编码的氨基酸由组氨酸变为精氨酸。结论：解脲脲原体对喹诺酮类药物的耐药与QRDR中gyrA基因的点变异可能相关。     

淋病奈瑟菌对氟喹诺酮的耐药性及GyrA耐药基因突变类型的研究

目的探讨江苏省淋病奈瑟菌(NG)对氟喹诺酮的耐药状况、耐药基因突变型的分布情况及二者之间的关系。方法采用琼脂稀释法检测江苏省三个地区临床分离的95株NG氟喹诺酮类药物的最小抑菌浓度(MIC),根据结果抽取部分菌株采用PCR法扩增gyrA基因的氟喹诺酮耐药决定区(QRDR),并进行测序分析。结果根据所测MIC,95株NG对环丙沙星100%的耐药;60株通过测序分析,检测到gyrA的五种突变形式,以gyrA出现272位碱基C→T和283位G→A的突变型的MIC最高。结论在江苏省,NG对氟喹诺酮耐药严重,氟喹诺酮药物已不再适合用于临床治疗淋病。     

山东地区解脲脲原体抗菌药物敏感性检测

目的 探讨近年来山东地区解脲脲原体抗菌药物敏感性变化趋势。 方法 对本科近6年来3984例门诊患者进行解脲脲原体培养,阳性的患者进行药物敏感性试验。 结果 Uu对喹诺酮类药物耐药严重,最高的环丙沙星耐药率接近90%。耐药率较低的药物包括四环素、美满霉素、强力霉素、克拉霉素和交沙霉素。罗红霉素和阿奇霉素的耐药率近年来有较明显的上升。 结论 山东地区Uu对喹诺酮类药物耐药严重,不宜作为经验性用药。为减少耐药性产生,宜根据药敏试验的结果足量、足疗程使用抗菌药物。在无药敏结果参考时,可以采用满霉素、强力霉素、克拉霉素及交沙霉素进行治疗。     

沙眼衣原体耐药机制研究进展

随着抗菌药物的广泛应用，沙眼衣原体耐药的报道越来越多。近年从基因水平研究发现，四环素类耐药主要是由质粒介导，喹诺酮类耐药与gyrA和parC喹诺酮耐药决定区的点突变有关，大环内酯类耐药和23SrRNA上的基因突变有关，利福平耐药则与rpoB基因的核苷酸改变有关。所有机制主要涉及基因转移和基因突变两方面。     

白头翁制剂胶体溶液对耐药解脲脲原体的体外抑制作用

目的探讨白头翁制剂胶体溶液对耐药解脲脲原体的抑菌作用。方法制备白头翁制剂胶体溶液,选用20株耐四环素解脲脲原体临床分离株,以微量肉汤稀释法测定对解脲脲原体耐药株的最低抑菌浓度。结果白头翁制剂胶体溶液(1.0mg/mL)最低抑菌浓度为(0.08±0.07)mg/mL,与阴性对照组比较差异有显著性(P<0.05)。结论白头翁制剂胶体溶液对耐药解脲脲原体有明显的抑制作用。     

解脲脲原体对四环素类药物耐药性变化及机制研究

目的分析解脲脲原体(UU)对四环素类药物的耐药性变化,并探讨其耐药机制。方法取疑似泌尿生殖道感染患者的分泌物进行解脲脲原体培养,同时检测其对多西环素、米诺环素的敏感性;分离对上述两种药物耐药的UU菌株,采用PCR试剂盒检测四环素类耐药基因TetM。结果2003～2005年间共培养检测泌尿生殖道分泌物2845例,UU阳性1213例,3年间UU对多西环素、米诺环素的耐药性没有明显变化,2003年耐药率为5.6%和7.7%,2004年为5.4%和5.5%,2005年为8.2%和7.6%。同时对多西环素、米诺环素耐药的20株UU中均检出四环素类耐药基因TetM。结论四环素类药物仍然是治疗UU感染的敏感药物;TetM耐药基因是导致UU对四环素类药物耐药的主要机制。     

脲原体耐药机制的研究进展

脲原体是最小和最简单的自我复制细胞之一。它们缺乏细胞壁,对青霉素、头孢菌素和其他β-内酰胺类抗生素或万古霉素不敏感,并且不能合成叶酸,所以对磺胺类药物或甲氧苄啶也不敏感。该综述阐述了脲原体一些可能的耐药机制,脲原体对大环内酯类抗生素产生耐药性可能是主动外排(msrD、msrB基因)或23S rRNA突变或甲基化(erm基因);对喹诺酮类抗生素产生耐药性可能是喹诺酮耐药决定区(QRDRs)的突变;对四环素类抗生素产生耐药性可能是存在tetM基因。由于不同国家不同地区的脲原体耐药情况各不相同,所以临床上需要结合实际情况进行治疗。     

广州淋球菌基因特征及其多抗原序列分型与环丙沙星耐药相关性研究

目的 探讨2014年广州市97株淋球菌环丙沙星耐药株的基因特征及其多抗原序列分型（NG-MAST）与淋球菌耐环丙沙星的相关性。 方法 用琼脂稀释法测定淋球菌对环丙沙星的最低抑菌浓度（MIC）,PCR分别扩增淋球菌的gyrA、parC基因和NG-MAST分型基因porB、tbpB基因并测序,获取耐药菌株的ST型别。 结果 97株淋球菌中95株（97.9%）对环丙沙星耐药。95株环丙沙星耐药菌株均在gyrA基因对应丝氨酸的第91和95位点上发生了突变,其中93株菌出现了parC基因突变。41株高水平耐药株（MIC ≥ 16 mg/L）中35株（85.4%）出现了parC基因87位点突变,54株低水平耐药株中32株（59.3%）出现此突变,差异有统计学意义（χ2 = 7.64,P < 0.05）。96株淋球菌分离株配对后,50株为网站已编号型别,共35个不同的ST型,其中10个ST型含有2 ~ 4个不同的分离株,ST型别中最常见ST5309。对淋球菌菌株系统进化树分析,淋球菌流行株可分为两群,第1群84株中MIC ≥ 16 mg/L的菌株39株占46.4%,第2群12株中只有1株MIC值为16 mg/L,差异有统计学意义（χ2 = 6.27,P = 0.012）。 结论 淋球菌对环丙沙星的高水平耐药主要与parC基因87位点突变相关。NG-MAST分型与环丙沙星耐药程度高低可能存在相关性。     

New fillers for the new man

ABSTRACT:  Two new collagen-based lidocaine-containing dermal fillers, ArteSense™/ArteFill™ (Artes Medical, San Diego, CA) and Evolence® (Colbar LifeScience Ltd., Herzliya, Israel), have proved to be of particular interest to men, many of whom seek a long-lasting or permanent correction. ArteFill™ has been available in the United States since 2006, and it is expected that Evolence® will reach the American market in 2008. The properties of the two products will be described, and experience based on the administration of many hundreds of syringes of both products by a Canadian dermatologist will be detailed here, with tips and precautions to optimize patient outcomes.     

Outcomes and adverse effects of ablative vs nonablative lasers for skin resurfacing: A systematic review of 1093 patients

It is generally believed that ablative laser therapies result in prolonged healing and greater adverse events when compared with nonablative lasers for skin resurfacing. To evaluate the efficacy of ablative laser use for skin resurfacing and adverse events as a consequence of treatment in comparison to other modalities, a PRISMA‐compliant systematic review (Systematic Review Registration Number: 204016) of twelve electronic databases was conducted for the terms “ablative laser” and “skin resurfacing” from March 2002 until July 2020. Studies included meta‐analyses, randomized control trials, cohort studies, and case reports to facilitate evaluation of the data. All articles were evaluated for bias. The search strategy produced 34 studies. Of 1093 patients included in the studies of interest, adverse events were reported in a total of 106 patients (9.7%). Higher rates of adverse events were described in nonablative therapies (12.2% ± 2.19%, 31 events) when compared with ablative therapy (8.28% ± 2.46%, 81 events). 147 patients (13.4%) reported no side effects, 68 (6.22%) reported expected, transient self‐resolving events, and five (0.046%) presented with hypertrophic scarring. Excluding transient events, ablative lasers had fewer complications overall when compared with nonablative lasers (2.56% ± 2.19% vs 7.48% ± 3.29%). This systematic review suggests ablative laser use for skin resurfacing is a safe and effective modality to treat a range of pathologies from photodamage and acne scars to hidradenitis suppurativa and posttraumatic scarring from basal cell carcinoma excision. Further studies are needed, but these results suggest that ablative lasers are a superior, safe, and effective modality to treat damaged skin.     

Genetic alterations in RAS‐regulated pathway in acral lentiginous melanoma

Studies integrating clinicopathological and genetic features have revealed distinct patterns of genomic aberrations in Melanoma. Distributions of BRAF or NRAS mutations and gains of several oncogenes differ among melanoma subgroups, while 9p21 deletions are found in all melanoma subtypes. In the study, status of genes involved in cell cycle progression and apoptosis was evaluated in a panel of 17 frozen primary acral melanomas. NRAS mutations were found in 17% of the tumors. In contrast, BRAF mutations were not found. Gains of AURKA gene (20q13.3) were detected in 37.5% of samples, gains of CCND1 gene (11q13) or TERT gene (5p15.33) in 31.2% and gains of NRAS gene (1p13.2) in 25%. Alterations in 9p21 were identified in 69% of tumors. Gains of 11q13 and 20q13 were mutually exclusive, and 1p13.2 gain was associated with 5p15.33. Our findings showed that alterations in RAS‐related pathways are present in 87.5% of acral lentiginous melanomas.     

Self‐resolving superficial primary cutaneous mucormycosis in a 7‐week‐old infant

A 7‐week‐old girl, born at 30 weeks' gestational age, presented to clinic for evaluation of a crop of vesicular lesions that were noted after removal of a bandage that had been in place for 4 days. A punch biopsy of the lesion revealed fungal elements that were later identified as Rhizopus spp. The lesion began to self‐resolve, and no further treatment was needed, with full resolution of the lesion by 1 month after presentation. Clinicians should be aware of the variable presentations of mucormycosis and consider fungal infection in the differential diagnosis when evaluating vulnerable patients with skin eruptions.     

Multiple New-Onset Subcutaneous Nodules of the Upper Extremity Digits: Giant Cell Tumor of Tendon Sheath and Lipoma

A black woman with the concurrent onset of two subcutaneous nodules located on the digits of her upper extremities is described. Initially, a single systemic disorder was considered; yet, the lesions differed in morphology and consistency. Microscopic examination of the nodules showed a giant cell tumor of tendon sheath and a lipoma. Although Occam's “razor” suggests that multiple lesions in the same person are more likely to represent variable manifestations of a single disorder than several different diseases in that individual, the simultaneously appearing lesions in this patient represented two different conditions.