牙周源性牙周牙髓联合病变常见病原菌的分布及其意义

目的研究牙周源性牙周牙髓联合病变常见病原菌分布及其相关性,为临床治疗提供依据。方法选择2018年1月至2020年6月于新疆维吾尔自治区人民医院口腔科就诊的牙周源性牙周牙髓联合病变患者43例43颗牙作为实验组,重度牙周炎患者41例41颗牙作为对照组。分别采集根管内组织和龈下菌斑,构建含有8种待测细菌基因片段的重组质粒,建立定量标准,应用实时荧光定量PCR技术检测福赛斯坦纳菌(Tannerella forsythia,Tf)、牙龈卟啉单胞菌(Porphyromonas gingivalis,Pg)、具核梭杆菌(Fusobacterium nu?cleatum,Fn)、中间普氏菌(Prevotella intermedia,Pi)、齿垢密螺旋体(Treponema denticola,Td)、消化性链球菌(Digestive streptococcus,Ds)、粪肠球菌(Enterococcus faecalis,Ef)、牙髓卟啉单胞菌(Porphyromanus endodontics,Pe)数量。结果实验组根管内组织与其龈下菌斑中Ds、Pe数量差异无统计学意义(Ρ>0.05),其余6种病原菌数量差异均有统计学意义(P<0.05);实验组与对照组龈下菌斑中Ds数量差异无统计学意义(P=0.241),其余7种病原菌数量差异均有统计学意义(P<0.05);实验组根管内组织与其龈下菌斑中Ef、Pe、Pg、Td、Tf细菌数量密切相关,Ef(r=0.347,Ρ<0.05)、Pe(r=0.363,Ρ<0.05)、Pg(r=0.437,Ρ<0.01)、Td(r=0.471,Ρ<0.01)、Tf(r=0.679,Ρ<0.01)。结论牙周源性牙周牙髓联合病变常见病原菌在根管内组织中数量低于龈下菌斑但根管内病原菌数量与龈下菌斑密切相关,临床治疗期间在控制牙周组织感染的同时,还应重视牙髓组织感染的控制。     

血流感染病原菌的临床分布及耐药性分析

目的分析长海医院2009年1月至2013年12月血流感染病原菌的菌种构成比、临床分布及耐药性分析,指导临床合理使用抗菌药物。方法采用VITEK2-Compact系统鉴定细菌及药敏试验。采用WHONET5.6软件分析血培养标本所分离的病原菌分布情况和药敏试验结果。结果 1 641株血流感染病原菌中,革兰阳性菌373株(22.74%),肠杆菌科细菌933株(56.85%),非发酵菌291株(17.73%),真菌44株(2.68%)。分离率为前5位的病原菌分别是大肠埃希菌、肺炎克雷伯菌、鲍曼不动杆菌、铜绿假单胞菌和凝固酶阴性葡萄球菌。药敏试验结果显示,耐甲氧西林金黄色葡萄球菌为61.70%,未发现对万古霉素耐药的葡萄球菌,耐万古霉素肠球菌为4.23%,肺炎克雷伯菌对亚胺培南耐药率达到13.30%,非发酵菌表现为多重耐药。结论长海医院血流感染以肠杆菌科细菌为主,其次为阳性球菌和非发酵菌,除细菌外,念珠菌血流感染也越来越常见,临床应重视血流感染的病原菌及耐药趋势,控制院内感染。     

冬春季呼吸道感染病原菌的分布及耐药性监测

目的 了解冬春季呼吸道感染病原菌分布及耐药性情况。方法标本分离培养后，予以鉴定到种并进行相应的药敏试验。结果376株病原菌中，G^-杆菌占46．3％，其中铜绿假单胞菌和肺炎克雷伯菌为主要菌种，除嗜麦芽窄食单胞菌外，亚胺培南的耐药率最低；G^ 球菌中耐甲氧西林的葡萄球菌(MRS)的出现率相当高，MRSA和MRCNS的感染率分别高达82．3％和86．7％，无万古霉素耐药株；条件致病菌和真菌，特别是白色念珠菌的感染率上升。结论依据病原菌的分布及耐药性变化合理选择抗生素是减少或延缓细菌耐药性产生的关键。     

475株血培养阳性病原菌的分布和耐药性分析

目的：了解血培养阳性病原菌的分布和耐药性,指导临床用药。方法收集2012～2013年送检的血液标本,BD9240血培养仪进行血培养,阳性菌株采用 VITEC-2 COMPACT 全自动细菌鉴定系统进行鉴定,药敏试验联合纸片扩散法和全自动仪器法,按照2012年 CLSI 判读结果。结果送检血培养标本7874份,共检出病原菌746株,阳性率为9．5％。以患者分析,剔除多次重复送检分离的菌株,阳性标本475株,其中革兰阳性菌223株,占47．0％,分别为凝固酶阴性葡萄球菌32％,金黄色葡萄球菌4％株,链球菌属7．8％,肠球菌属2．3％;革兰阴性菌241株,占50．7％,包括大肠埃希菌23％,肺炎克雷伯菌12％,鲍曼不动杆菌4％,阴沟肠杆菌3％,铜绿假单胞菌1％;真菌11株,占2．3％,包括白色念珠菌0．6％,近平滑念珠菌0．9％。其中,共检出厌氧菌4株,包括脆弱拟杆菌2株,多形拟杆菌和产气荚膜梭菌各1株;同时,也检出5株较罕见的病原菌,包括猪链球菌2株,布鲁氏菌、诺卡菌属和马尔尼菲青霉菌各1株。其中,产 ESBL 的大肠埃希菌占47．5％,肺炎克雷伯菌占16．7％;MRSA 检出率为35．0％,MRCNS 为78％;肠杆菌科细菌对碳青酶烯类抗菌药物仍高度敏感,总耐药率均小于4％,主要的耐药菌株为肺炎克雷伯菌,对美罗培南耐药率达3．6％;鲍曼不动杆菌、铜绿假单胞菌等非发酵菌耐药率相对较高;未发现万古霉素、利奈唑烷等不敏感的葡萄球菌。结论血培养污染率较高,应加强采血规范;引起血流感染的病原菌种类繁多,且耐药率较高,加强耐药检测刻不容缓。     

上海市活动性类风湿关节炎患者医院感染的流行病学调查

目的调查活动性类风湿关节炎（rheumatoidarthritis,RA）患者医院感染的发生率,致病微生物病原学及临床特征。方法对2009年1月-2011年12月上海市12所医院风湿免疫科收住的2452例活动性RA患者进行医院感染的前瞻性调查,并对患者人口学及临床特征进行描述。结果共有503例患者（20．51％）发生721例次感染,其中呼吸道感染40．97％、尿路感染22．35％皮肤和软组织感染8．58％。主要致病微生物为常见病原菌（623株,86．40％）,包括大肠埃希菌226株（31．35％）、铜绿假单胞菌40株（5．55％）、鲍曼不动杆菌48株（5．42％）、肠球菌属144株（16．25％）和甲氧西林耐药金葡菌（MRsA）15株（2．08％）、甲氧西林耐药凝固阴性葡萄球菌（MRCNS）7株（0．97％）,其他为真菌（74株,10．26％）、疱疹病毒（16株,2．21％）和结核分枝杆菌（8株,1．10％）。结论活动性RA患者常见医院感染为呼吸道感染、泌尿生殖道感染和皮肤软组织感染。主要病原菌为大肠埃希菌、铜绿假单胞菌、鲍曼不动杆菌、葡萄球菌属和肠球菌属等耐药菌。     

正气辨析

正气属中医学的气学范围,是一身之气或人气相对邪气时的称谓,是指人体内具有抗病、祛邪、调节、修复等作用的一类细微物质;正气以其运动而发挥防御、调节、修复等作用,具有物质运动的自然科学属性。正气分布到腑腑经络,则为脏腑经络之气;分布到脉之内外,则为营气和卫气。脏腑经络之气和营卫之气的防御、修复和调节作用,可因其构成成分和所在部位的不同而有所区别,但都是正气的功能体现。     

Aggregatibacter actinomycetemcomitans–Induced Bone Loss and Antibody Response in Three Rat Strains

Background: The aim of this study is to compare the colonization, immunoglobulin (Ig) G response, and alveolar bone loss in Aggregatibacter actinomycetemcomitans (Aa)–inoculated Fawn Hooded Hypertensive (FHH), Dahl Salt‐Sensitive (DSS), and Brown Norway (BN) rats. Methods: Each rat strain was divided into wild‐type Aa‐inoculated and non‐inoculated control groups. Blood taken at 12 weeks after inoculation was assessed for Aa‐specific IgG antibodies by an enzyme‐linked immunosorbent assay. Colonization was assessed 12 weeks postinoculation. Bone loss was estimated by measuring the distance from the cemento‐enamel junction (CEJ) to the alveolar bone crest (ABC) at 20 molar sites. Colonization and antibody levels were compared by using the Student t test. Diseased rats were defined as having two sites per quadrant with CEJ–ABC distances that were significantly greater than the control CEJ–ABC distances. Results: The Aa colonization of FHH rats was significantly higher than in other strains (P <0.05). The Aa‐specific IgG levels in the DSS Aa‐inoculated group were significantly higher than in its control group (P <0.05). Only FHH rats showed Aa disease‐associated bone loss (P = 0.0021). Conclusions: Aa colonized and caused more disease in FHH rats than in the other rat strains. The rat strains each responded differently to the same Aa strain.     

Clarithromycin suppresses the periodontal bacteria-accelerated abdominal aortic aneurysms in mice

Aoyama N, Suzuki J‐I, Ogawa M, Watanabe R, Kobayashi N, Hanatani T, Yoshida A, Ashigaki N, Izumi Y, Isobe M. Clarithromycin suppresses the periodontal bacteria‐accelerated abdominal aortic aneurysms in mice. J Periodont Res 2012; 47: 463–469. © 2011 John Wiley & Sons A/S Background and Objective: Although clarithromycin (CAM) has many biological functions, including regulation of MMPs, little is known about its effect on abdominal aortic aneurysms. Periodontopathic bacteria have been reported to be associated with several kinds of circulatory diseases. The purpose of this study was therefore to clarify the effect of CAM on periodontopathic bacteria‐accelerated abdominal aortic aneurysms. Material and Methods: Abdominal aortic aneurysm was produced in mice by the peri‐aortic application of 0.25 m CaCl₂. The mice were inoculated once per week with live Porphyromonas gingivalis, which is one of the major periodontopathic bacteria. Test mice (n = 8) were given a daily oral dose of CAM, while control mice (n = 13) were not. Results: Four weeks after the operation, the P. gingivalis‐injected and CAM‐treated mice showed a significant decrease in the aortic diameter in comparison with the mice only injected with P. gingivalis. Histopathologically, the samples obtained from the P. gingivalis‐injected and CAM‐treated mice showed less elastic degradation. Moreover, the plasma MMP‐2 concentration of the CAM‐treated mice decreased significantly. Conclusion: These findings suggest that CAM administration is useful to suppress periodontal bacteria‐accelerated abdominal aortic aneurysms via MMP regulation.