肺炎克雷伯细菌及其荚膜

肺炎克雷伯细菌及其荚膜
肺炎克雷伯细菌及其荚膜

Klebsiella pneumoniae Bacteremia and Capsular Serotypes, Taiwan Chun-Hsing Liao, Yu-Tsung Huang, Chih-Cheng Lai, Cheng-Yu Chang, Fang-Yeh Chu, Meng-Shiuan Hsu, Hsin-Sui Hsu, and Po-Ren Hsueh

Capsular serotypes of 225 Klebsiella pneumoniae isolates in Taiwan were identi ? ed by using PCR. Patients infected with K1 serotypes (41 isolates) had increased community-onset bacteremia, more nonfatal diseases and liver abscesses, lower Pittsburgh bacteremia scores and mortality rates, and fewer urinary tract infections than patients infected with non–K1/K2 serotypes (147 isolates).

K

lebsiella pneumoniae bacteria cause a variety of infections (1,2). Geographic differences in this organism have been recognized, and a high prevalence of liver abscesses has been observed for >20 years in persons in Taiwan infected with K . pneumoniae (3,4). K1 and K2 are the major capsular serotypes that cause liver abscesses and have increased virulence (4–7). In contrast, only limited information is available about serotypes causing K. pneumoniae bacteremia (3,5).

Yu et al. grouped K1 and K2 serotypes and compared clinical characteristics for patients with K. pneumoniae bacteremia with those for patients infected with non–K1/K2 serotypes (3). Recent evidence suggests that K1 is a major cause of primary liver abscesses and has greater potential for causing metastasis, and that K2 is a major cause of secondary liver abscesses (6,8). We examined the distribution and clinical characteristics of serotypes that cause K. pneumoniae bacteremia from 225 patients (9) and performed PCR-based genotyping to identify capsular serotypes (10).

The Study

The study was conducted at Far-Eastern Memorial Hospital in Taipei, Taiwan. Patients with K . pneumoniae bacteremia were identi ? ed during January 1–December

31, 2007. Identi ? cation of K . pneumoniae was based on

colony morphologic features and biochemical reactions

(11). Data on time until positive blood culture results were

obtained from the automated blood culture system at the hospital. Data for each patient were included only once (at

the time of the ? rst detection of bacteremia). Patients <18

years of age and those not admitted to our hospital were

excluded. Inactive malignancy was not included as an

underlying illness. In-hospital and 14-day mortality rates

were assessed. For 225 available bacterial isolates, cps genotyping was performed (10).

A total of 231 patients with K . pneumoniae bacteremia were observed at the hospital during the study; 225 isolates from 225 patients were used. A total of 133 (59%) of these patients had community-onset bacteremia (bacteremia identi ? ed in an emergency department). The in-hospital mortality rate was 32.4%. Among 225 isolates, 41 (18.2%) were identi ? ed as K1 serotype, 37 (16.4%) as K2, 15 (6.7%) as K57, and 8 (3.6%) as K54. The K1 serotype was found predominantly in community-onset infections (36 [87.8%] of 41 patients compared with 75 [51.0%] of 147 patients infected with non–K1/K2 serotypes; odds ratio [OR] 6.91, 95% con ? dence interval [CI] 2.57–18.60) (online Appendix Table 1, https://www.360docs.net/doc/60413034.html,/EID/content/17/6/1113-appT1.htm).

Underlying illness was classi ? ed as nonfatal in 75.6% of patients with K1 bacteremia (53.7% of patients with non–K1/K2 bacteremia; OR 2.67, 95% CI 1.22–5.84). A lower percentage of patients with K1 bacteremia had surgery in the previous 3 months (9.8% vs. 30.6%; OR 0.25, 95% CI 0.09–0.73). Patients with K1 bacteremia had lower mean ± SD Pittsburgh bacteremia scores than those with non–K1/K2 bacteremia (2.7 ± 3.1 vs. 4.4 ± 4.7; OR 0.90, 95% CI 0.81–0.99), but the time until a positive blood culture was obtained was not different. K1 serotype was more common in patients with liver abscesses (46.3% vs. 4.1%; OR 20.3, 95% CI 7.31–56.40) and less common in patients with urinary tract infections (UTIs) (4.9% vs. 20.4%; OR 0.20, 95% CI 0.05–0.88). The in-hospital mortality rate for patients with K1 bacteremia was lower that that for patients with non–K1/K2 bacteremia (14.6% vs. 34.7%; OR 0.32, 95% CI 0.13–0.82).

No differences were found in clinical characteristics for patients with K2 bacteremia and those with non–K1/K2 bacteremia except for a higher frequency of liver abscesses in patients with K2 bacteremia (13.5% vs. 4.1%; OR 3.67, 95% CI 1.06–12.8). For patients infected with K54 and K57 serotypes, 1 K57 serotype caused liver abscesses; no abscesses were found in patients infected with a K54 serotype. The in-hospital mortality rate was 50% (4/8) for patients with K54 bacteremia and 53.3% (8/15) for patients with K57 bacteremia.

Patients infected with a K1 serotype had lower mean ± SD Pittsburgh bacteremia scores (2.7 ± 3.1 vs. 5.0 ± 5.3;

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Author af ? liations: Far Eastern Memorial Hospital, Taipei, Taiwan (C.-H. Liao, C.-C. Lai, C.-Y . Chang, F.-Y . Chu, M.-S. Hsu, H.-S. Hsu); and National Taiwan University College of Medicine, Taipei (Y .-T. Huang, P .-R. Hsueh)DOI: 10.3201/eid1706.100811

OR 0.88, 95% CI 0.78–0.98, p = 0.002) and lower 14-day and in-hospital mortality rates (9.8% vs. 27.0%; OR 0.29, 95% CI 0.08–1.03, p = 0.06; and 14.6% vs. 43.2%; OR 0.23, 95% CI 0.08–0.67, p = 0.007) than patients infected with K2 serotypes. A higher percentage of patients with K1 bacteremia had liver abscesses at the site of infection (46.3% vs. 13.5%; OR 5.53, 95% CI 1.80–17.02, p = 0.003).

Characteristics of patients with community-onset K. pneumoniae bacteremia were also analyzed (online Appendix Table 2, https://www.360docs.net/doc/60413034.html,/EID/content/17/6/1113-appT2.htm). Patients infected with a K1 serotype were more likely to have liver abscesses and less likely to have UTIs or biliary tract infections (OR 11.5, 95% CI 3.99–33.20; OR 0.20, 95% CI 0.04–0.92; and OR 0.25, 95% CI 0.07–0.91, respectively).

In our patients, K1 and K2 serotypes were found at similar frequencies (18.2% and 16.4%, respectively), which differs from results of Fung et al., in which the K1 serotype was more common (K1 30.8% and K2 5.1%) (12). Despite reported virulence of the K1 serotype, it was primarily responsible for community-onset bacteremia in patients with less severe underlying illness and associated with lower mortality rates. Moreover, the K1 serotype is associated with liver abscesses and lower mortality rates (2–7). Liver abscesses were found in 46% of patients with K1 bacteremia, and a K1 serotype was found in 63.3% of patients with liver abscesses.

Conclusions

Management of liver abscesses has improved in Taiwan because of increased physician awareness (13). Mortality rates for patients with K. pneumoniae bacteremia were lower in patients with UTIs or biliary tract infections (5,14), which were less common in patients infected with a K1 serotype. Thus, patient outcomes depend more on underlying conditions and severity of sepsis than on bacterial serotypes (5,9,14).

In our previous study of the interval until a positive blood culture for K. pneumoniae bacteremia was obtained

(9), we found that higher Pittsburgh bacteremia scores,

a time until a positive blood culture <7 hours, and active malignancy were associated with death. In this study, we found no difference in time until a positive blood culture was obtained for patients infected with different serotypes. This interval for patients infected with K1 serotypes was slightly longer than that for patients infected with K2 and non–K1/K2 serotypes. This ?nding may have resulted from a higher percentage of community-onset infections and liver abscesses and less severe underlying illness in patients infected with a K1 serotype.

Studies investigating K. pneumoniae bacteremia have grouped K1 and K2 serotypes (3,7). However, such grouping may be problematic because evidence suggests that the K1 serotype is the major cause of primary liver abscesses (6). Another report showed that the genetic background of serotype K2 is diversi? ed, and only 1 of the 2 major K2 clones was highly virulent in mice (15). These ?ndings are consistent with our clinical observations. Differences in symptoms of patients infected with K2 and non–K1/K2 serotypes were minimal, despite slightly more liver abscesses among patients infected with K2 serotypes, which was lower than for patients infected with K1 serotypes. Because of different serotyping methods used (3,5,15), caution is required when interpreting data from various studies.

Despite greater virulence of the K1 serotype, it is predominant in patients with community-onset infections and in those with less severe underlying illness. Although the K1 serotype is the major cause of liver abscesses, it results in a lower mortality rate, which can be attributed to host factors.

Dr Liao is an infectious diseases specialist in the Department of Internal Medicine, Far-Eastern Memorial Hospital, Taipei, Taiwan. His research interests are clinical characteristics, epidemiology, and pathogenesis of bacterial infections, particularly methicillin-resistant Staphylococcus aureus and Klebsiella pneumoniae.

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肺炎克雷伯菌研究进展

J OURNAL OF C LINICAL M ICROBIOLOGY,Aug.2007,p.2723–2725Vol.45,No.8 0095-1137/07/$08.00?0doi:10.1128/JCM.00015-07 Evaluation of Methods To Identify the Klebsiella pneumoniae Carbapenemase in Enterobacteriaceae? K.F.Anderson,*D.R.Lonsway,J.K.Rasheed,J.Biddle,B.Jensen,L.K.McDougal, R.B.Carey,A.Thompson,S.Stocker,B.Limbago,and J.B.Patel Centers for Disease Control and Prevention,Division of Healthcare Quality Promotion,Atlanta,Georgia Received3January2007/Returned for modi?cation13February2007/Accepted6June2007 The Klebsiella pneumoniae carbapenem(KPC)?-lactamase occurs in Enterobacteriaceae and can confer resistance to all?-lactam agents including carbapenems.The enzyme may confer low-level carbapenem resistance,and the failure of susceptibility methods to identify this resistance has been reported.Automated and nonautomated methods for carbapenem susceptibility were evaluated for identi?cation of KPC-mediated resistance.Ertapenem was a more sensitive indicator of KPC resistance than meropenem and imipenem independently of the method used.Carbapenemase production could be con?rmed with the modi?ed Hodge test. Carbapenems are commonly used to treat infections caused by multidrug-resistant Enterobacteriaceae.In the United States and other locations,an increasingly common mechanism of carbapenem resistance is the Klebsiella pneumoniae carbapen-emase(KPC)(2,10,15,18,19,24,26,27).The KPC?-lacta-mase occurs most commonly in K.pneumonia e,but it has also been reported sporadically in other species of Enterobacteria-ceae(Klebsiella oxytoca,Enterobacter spp.,Escherichia coli,Sal-monella spp.,Citrobacter freundii,and Serratia spp.)and Pseudomonas aeruginosa(4,10–12,17,23,28).The KPC en-zyme confers resistance to all?-lactam agents including peni-cillins,cephalosporins,monobactams,and carbapenems(1,21, 27,28).Some isolates containing KPC demonstrate low-level carbapenem resistance,but when combined with other cellular changes,such as porin loss,the carbapenem MIC increases (21,26).The gene encoding the KPC enzyme is usually?anked by transposon-related sequences and has been identi?ed on conjugative plasmids;therefore,the potential for dissemina-tion is signi?cant(17,26–28).Several outbreaks of KPC-pro-ducing bacteria have occurred in the northeast United States (2,26).Isolates that acquired this enzyme are usually resistant to several other classes of antimicrobial agents used as treat-ment https://www.360docs.net/doc/60413034.html,boratory identi?cation of KPC-producing clinical isolates will be critical for limiting the spread of this resistance mechanism.The failure of automated susceptibility testing systems to detect KPC-mediated resistance was previ-ously noted(5,22). We evaluated commonly used susceptibility testing methods to identify the most sensitive conditions for KPC detection with31 KPC-producing Enterobacteriaceae isolates(25of K.pneumoniae, 2of K.oxytoca,1of E.coli,1of Enterobacter spp.,1of Citrobacter freundii,and1of Salmonella spp.).These were isolated from different patients who were hospitalized in13different healthcare institutions from seven different states:Maryland(one),New Jersey(two),New York(four),Pennsylvania(two),Michigan (two),Missouri(one),and North Carolina(one).The presence of bla KPC was determined using previously described oligonucleo-tide primers and cycling conditions(27).Enzyme activity was demonstrated in all isolates by isoelectric focusing(6,16). To measure the speci?city of methods to detect KPC-medi-ated resistance,45isolates(26of K.pneumoniae,9of K.oxy-toca,and10of E.coli)were chosen for testing.All45isolates were negative for bla KPC by PCR.These isolates were submit-ted to the CDC for reference susceptibility https://www.360docs.net/doc/60413034.html,ing the reference broth microdilution(BMD)method,all isolates met the CLSI extended-spectrum?-lactamase(ESBL)screening test criteria;that is,they demonstrated reduced susceptibility to at least one extended-spectrum cephalosporin(7,8).Twenty-six isolates were positive by the CLSI ESBL broth con?rmatory test, and the other isolates were presumed to have another broad-spectrum?-lactamase or other mechanism of cephalosporin resistance.Five isolates were nonsusceptible to a carbapenem (imipenem,meropenem,or ertapenem)by BMD.Since two of the isolates were ESBL producers by BMD and the other three isolates produced an AmpC-type enzyme as demonstrated by isoelectric focusing and PCR(20),it is likely that the mechanism of reduced carbapenem susceptibility is a combination of a cepha-loporinase and porin loss(3,9,13). Meropenem,imipenem,and ertapenem susceptibilities were determined by BMD using cation-adjusted Mueller-Hinton broth in panels that were prepared in-house(7),disk diffusion(Becton Dickinson,Sparks,MD)(8),Etest(AB Biodisk,Piscataway,NJ), Microscan Autoscan using the NM32panel(Dade Behring,West Sacramento,CA),and the Vitek2test using the AST GN14card (bioMe′rieux,Durham,NC).Susceptibility testing of meropenem and imipenem was performed with the Phoenix test using the NEG MIC30panel or NEG MIC112panel(Becton Dickinson, Sparks,MD),the Vitek Legacy test using the GNS-122and GNS-127panels(bioMe′rieux,Durham,NC),and the Sensititre Auto Reader using the GN2F panel(Trek Diagnostics,West Lake, OH).All methods were performed according to the manufactur-ers’recommendations.Quality control testing of susceptibility *Corresponding author.Mailing address:Centers for Disease Con- trol and Prevention,Mail Stop G-08,1600Clifton Road NE,Atlanta, GA30333.Phone:(404)639-2824.Fax:(404)639-1381.E-mail:ebi2 @https://www.360docs.net/doc/60413034.html,. ?Published ahead of print on20June2007. 2723 on August 19, 2015 by guest https://www.360docs.net/doc/60413034.html,/ Downloaded from

肺炎克雷伯杆菌肺炎

克雷白杆菌肺炎(Klebsiella pneumonia):近20余年来,该菌已成为院内获得性肺炎的主要致病菌,耐药株不断增加,且产生超广谱酶,成为防治中的难点。本病多见于中年以上男性,起病急、高热、咳嗽、痰多及胸痛,可有发绀、气急、心悸,约半数患者有畏寒,可早期出现休克。临床表现类似因为的肺炎球菌肺炎,但其痰常呈粘稠脓性,量多、带血,灰绿色或砖红色、胶冻状,但此类典型的痰液并不多见。胸部X线表现常呈多样性,包括大叶实变,好发于右肺上叶、双肺下叶,有多发性蜂窝状肺脓肿、叶间隙下坠。严重病例有呼吸衰竭、周围循环衰竭。慢性病程者表现为咳嗽、咳痰、衰弱、贫血等。克雷白杆菌肺炎的预后较差,病死率高。 临床表现:①发病骤起,出现呼吸困难; ②年长儿有大量黏稠血性痰,但婴儿少见; ③由于气道被黏液梗阻,肺部体征较少或完全缺乏; ④病情极为严重,发展迅速,患儿常呈休克状态; ⑤X线胸片示肺段或大叶性致密实变阴影,其边缘往往膨胀凸出。可迅速发展到 邻近肺段,以上叶后段及下叶前段较多见; ⑥常见并发症为肺脓肿,可呈多房性蜂窝状,日后形成纤维性变;其次为脓 胸及胸膜肥厚。治疗尚缺乏有效抗菌药物。 临床病理: 肺炎克雷白杆菌为革兰阴性杆菌,常存在于人体上呼吸道和肠道,当机体抵抗力 降低时,便经呼吸道进入肺内而引起大叶或小叶融合性实变,以上叶较为多见。病变中渗出液粘稠而重,致使叶间隙下坠。细菌具有荚膜,在肺泡内生长繁殖时,引起组织坏死、液化、形成单个或多发性脓肿。病变累及胸膜、心包时,可引起渗出性或脓性积液。病灶纤维组织增生活跃,易于机化;纤维素性胸腔积液可早期出现粘连。在院内感染的败血症中,克雷白杆菌以及绿脓杆菌和沙雷菌等均为重要病原菌,病死率较高。 老年体弱患者有急性肺炎、中毒症状严重、且有血性粘稠痰者,应考虑本病。确诊有赖于痰细菌学检查,并与葡萄球菌、结核菌或其他革兰阴性杆菌所致肺炎相鉴别。年老、白细胞减少、菌血症及原有严重疾病者预后较差。 与支气管扩张症区别 支气管扩张症是常见的慢性支气管化脓性疾病,大多数继发于呼吸道感染和支气 管阻塞,尤其是儿童和青年时期麻疹、百日咳后的支气管肺炎,由于破环支气管管壁, 形成管腔扩张和变形。 临床表现:慢性咳嗽伴大量脓痰和反复咯血。若有厌氧菌混合感染,则有臭味。 咯血可反复发生,程度不等,从小量痰血至大量咯血,咯血量与病情严重程度有时不 一致,支气管扩张咯血后一般无明显中毒症状。 与肺炎球菌肺炎区别 肺炎球菌肺炎是由肺炎球菌或肺炎链球菌所引起,占院外感染肺炎中的半数以上。肺段或肺叶呈急性炎性实变,临床上症状轻或不典型病较为多见。起病多急骤,有高热,体温在数小时内可以升到39-40℃,可呈稽留热,与脉率相平行。患侧胸部疼痛,可放射到肩部、腹部,咳嗽或深呼吸时加剧。痰少,可带血丝或呈铁锈色。胃纳锐减,偶有恶心、呕吐、腹痛或腹泻,有时误诊为急腹症。

关于肺炎克雷伯菌的临床分布与药敏结果

肺炎克雷伯菌的临床分布及耐药性 【摘要】目的了解我院临床分离肺炎克雷伯菌临床分布及耐药性。方法回顾性分析黄山市人民医院2010年10月-2011年10月间临床分离肺炎克雷伯菌对常用抗菌药物的耐药性,统计其临床分布。结果342株肺炎克雷伯菌主要来源于痰标本240株(占70.1%),尿液31株(占9.1%),血16株(占4.6%),分泌物14株(占4%),科室分布主要见于ICU110株(占32.2%),脑外52株(占15.2%),呼吸内科32株(占9.4%)药敏结果显示肺炎克雷伯菌对氨苄西林耐药率最高,达94.7%,对亚胺培南耐药率最低,仅为8.2%,厄他培南次之,耐药率为10.7%,对阿米卡星、妥布霉素、哌拉西林、头孢替坦、的耐药率分别为11.5%、13.5%、15.2%、16.1%,其余药物中,除环丙沙星(23.4%)外,对头孢唑林、胺苄西林、氨曲南、头孢匹美,庆大霉素、左旋氧氟沙星、复方新诺明、呋喃妥因、头孢他啶的耐药率均在30%以上。342株肺炎克雷伯菌中发现25株泛耐药菌株(占7.3%)。结论本院临床分离的肺炎克雷伯菌主要分离自痰液标本,以ICU、呼吸内科及脑外科为主,耐药性较为严重并存在泛耐药株。 【关键词】肺炎克雷伯菌抗生素耐药性 肺炎克雷伯菌属革兰阴性杆菌,常寄殖于呼吸道和肠道,是下呼吸道感染的重要病原菌,常引起典型的原发性肺炎及肺外感染,如肠炎、婴儿脑膜炎、败血症、泌尿系感染等。随着临床广谱抗生素的应用,肺炎克雷伯菌已经成为医院感染的重要病原菌,近年来肺炎克雷伯菌的感染率与耐药率明显升高,呈上升趋势。为进一步了解我院肺炎克雷伯菌耐药状况及临床分布,本研究针对2010.10-2011.10间临床分离的342株肺炎克雷伯菌进行耐药性分析,结果报道如下: 材料与方法 一、材料 (一)细菌收集我院2010.10~2011.10间临床分离的肺炎克雷伯菌株,共342株(剔除同一患者7天内同一部位的重复菌株),质控菌株为大肠埃希菌ATCC25922,铜绿假单胞菌ATCC27853,购自卫生部临检中心。 (二)仪器与试剂VITEK-2全自动微生物鉴定与药敏分析仪,NG鉴定卡,AST-NG药敏卡,VITEK比浊计购自法国Bio-Merieux公司;自制0.45%的生理盐水。 (三)药物种类AST-NG药敏卡带有氨苄西林、头孢唑林、胺苄西林、氨曲南、头孢匹美,庆大霉素、左旋氧氟沙星、复方新诺明、呋喃妥因、头孢他啶、哌拉西林,环丙沙星,阿米卡星、头孢替坦、亚胺培南、厄他培南、妥布霉素 (四)培养基细菌培养用中国蓝玫瑰酸琼脂粉,分纯培养用MH琼脂粉,均购自杭州

肺炎克雷伯杆菌肺炎

克雷白杆菌肺炎(Klebsiella pneumonia):近20余年来,该菌已成为院内获得性肺炎得主要致病菌,耐药株不断增加,且产生超广谱酶,成为防治中得难点、本病多见于中年以上男性,起病急、高热、咳嗽、痰多及胸痛,可有发绀、气急、心悸,约半数患者有畏寒,可早期出现休克。临床表现类似因为得肺炎球菌肺炎,但其痰常呈粘稠脓性,量多、带血,灰绿色或砖红色、胶冻状,但此类典型得痰液并不多见。胸部X线表现常呈多样性,包括大叶实变,好发于右肺上叶、双肺下叶,有多发性蜂窝状肺脓肿、叶间隙下坠、严重病例有呼吸衰竭、周围循环衰竭。慢性病程者表现为咳嗽、咳痰、衰弱、贫血等、克雷白杆菌肺炎得预后较差,病死率高。 临床表现:①发病骤起,出现呼吸困难; ②年长儿有大量黏稠血性痰,但婴儿少见; ③由于气道被黏液梗阻,肺部体征较少或完全缺乏; ④病情极为严重,发展迅速,患儿常呈休克状态; ⑤X线胸片示肺段或大叶性致密实变阴影,其边缘往往膨胀凸出、可迅速发展到邻近肺段,以上叶后段及下叶前段较多见; ⑥常见并发症为肺脓肿,可呈多房性蜂窝状,日后形成纤维性变;其次为脓胸及胸膜肥厚。治疗尚缺乏有效抗菌药物。 临床病理: 肺炎克雷白杆菌为革兰阴性杆菌,常存在于人体上呼吸道与肠道,当机体抵抗力降低时,便经呼吸道进入肺内而引起大叶或小叶融合性实变,以上叶较为多见。病变中渗出液粘稠而重,致使叶间隙下坠、细菌具有荚膜,在肺泡内生长繁殖时,引起组织坏死、液化、形成单个或多发性脓肿。病变累及胸膜、心包时,可引起渗出性或脓性积液。病灶纤维组织增生活跃,易于机化;纤维素性胸腔积液可早期出现粘连。在院内感染得败血症中,克雷白杆菌以及绿脓杆菌与沙雷菌等均为重要病原菌,病死率较高。 老年体弱患者有急性肺炎、中毒症状严重、且有血性粘稠痰者,应考虑本病。确诊有赖于痰细菌学检查,并与葡萄球菌、结核菌或其她革兰阴性杆菌所致肺炎相鉴别。年老、白细胞减少、菌血症及原有严重疾病者预后较差、 与支气管扩张症区别 支气管扩张症就是常见得慢性支气管化脓性疾病,大多数继发于呼吸道感染与支气管阻塞,尤其就是儿童与青年时期麻疹、百日咳后得支气管肺炎,由于破环支气管管壁,形成管腔扩张与变形。 临床表现:慢性咳嗽伴大量脓痰与反复咯血。若有厌氧菌混合感染,则有臭味。咯血可反复发生,程度不等,从小量痰血至大量咯血,咯血量与病情严重程度有时不一致, 支气管扩张咯血后一般无明显中毒症状。 与肺炎球菌肺炎区别 肺炎球菌肺炎就是由肺炎球菌或肺炎链球菌所引起,占院外感染肺炎中得半数以上、肺段或肺叶呈急性炎性实变,临床上症状轻或不典型病较为多见、起病多急骤,有高热,体温在数小时内可以升到39-40℃,可呈稽留热,与脉率相平行。患侧胸部疼痛,可放射到肩部、腹部,咳嗽或深呼吸时加剧。痰少,可带血丝或呈铁锈色。胃纳锐减,偶有恶心、呕吐、腹痛或腹泻,有时误诊为急腹症、 辅助检查:

肺炎克雷伯菌肺炎的临床诊治

【摘要】目的分析下呼吸道肺炎克雷伯杆菌感染的发病特点、药敏情况及治疗转归。了解产超广谱β-内酰胺酶(esbls)菌株耐药情况。方法回顾性分析37例肺炎克雷伯杆菌感染患者的临床特点、病原菌的耐药性、抗菌治疗及转归。结果该组病例以中老年患者为主,排菌及肺空洞形成占大多数,临床症状不典型,合并症及混合菌感染多,主要依靠病原学并结合临床、x线检查作为诊断依据.容易产esbls菌株,且有增长趋势,亚胺培南是首选抗感染用药。结论肺结核患者院内下呼吸道感染是一个值得关注的问题,警惕es-bls菌株的产生,治疗上应根据药敏联合应用抗生素. 【关键词】肺炎克雷白杆菌肺炎克雷伯杆菌(k1ebsiellapneumoniae),又称肺炎杆菌,是引起肺炎最多的革兰阴性杆菌,其所致的肺炎占细菌性肺炎的1%~5%,平均为2%,在社区获得性和医院获得性革兰阴性杆菌肺炎中分别18%~64%和30%,院内肺炎杆菌肺炎的发病约为6.6/10000~8.0/10000,肺炎杆菌占医院内肺炎全部病原体的7%~11%。虽有不少前瞻和回顾性调查,但肺炎杆菌在社会人群中的确切发病率甚难估计。近年来,随着对肺炎杆菌高效抗菌药物如第三代头孢菌素、氟喹诺酮类药物的不断问世与推广,和耐药严重的铜绿假单胞菌及其他假单胞菌、不动杆菌和阴沟杆菌等引起的肺炎比例增加,肺炎杆菌临床分离率有下降趋势。肺炎杆菌肺炎的病死率较高,为20%~50%,也有70%的报道,尤其在酗酒者。 1临床资料本组37例,其中男34例,女3例,年龄18~27岁。病程1~11d。临床表现:发热25例,咳嗽26例,咳浓痰20例,痰中带血7例,砖红色痰6例。肺部体征:湿啰音17例,干啰音4例。胸部x线检查:肺实变阴影6例,斑片状致密影有小空腔或空洞10例,肺纹理增多、紊乱,表现为支气管周围炎11例。实验室检查:白细胞总数高于正常15例,中性粒细胞&0.75的23例。 2诊断与鉴别诊断 2.1诊断男性,长期嗜酒,有慢性支气管炎或其他肺部疾病、糖尿病、恶性肿瘤、器官移植或粒细胞减少症等免疫抑制,或建立人工气道机械通气的患者,出现发热、咳嗽、呼吸困难及肺部湿啰音,外周血中性粒细胞增加,结合x线有肺部炎性浸润表现提示细菌性肺炎时,均应考虑肺炎杆菌的可能,特别是当青霉素或依托红霉素及其他大环内酰类抗生素治疗无效时。肺炎杆菌的临床表现、实验室和x线检查多不具有特征性。咯砖红色痰虽为其典型表现,但临床上并不多见。合格的痰标本涂片找见较多革兰阴性杆菌,尤其大量聚集在脓细胞和支气管的假复层纤毛柱状上皮细胞周围并带有荚膜者,更应考虑肺炎杆菌的可能,但此不是确诊依据。痰培养分离肺炎杆菌有利于诊断,但应与定植于口咽部的污染菌相鉴别。有认为连续两次以上经涂片筛选的痰标本分离到肺炎杆菌或定量培养分离的肺炎杆菌浓度≥109cfu/ml,可诊断为肺炎杆菌肺炎。对重症、难治或免疫抑制病例,使用防污染下呼吸道标本采样技术如经环甲膜穿刺气管吸引(ti’a)、防污染双套管毛刷采样(psb)、支气管肺泡灌洗(bal)和经皮穿刺吸引(la)等,从这些标本分离出肺炎杆菌则可确诊本病。 2.2鉴别诊断微生物学检查是确诊肺炎杆菌肺炎的惟一依据,也是与其他细菌性肺炎相鉴别的重要方法。 3治疗肺炎杆菌肺炎的治疗包括抗感染治疗和支持治疗。 3.1对症及支持治疗包括保持气道通畅、祛痰、止咳、给氧、纠正水、电解质和酸碱失衡、补充营养等。 3.2抗感染治疗及早使用有效抗生素是治愈的关键。在应用抗生素治疗前,肺炎杆菌感染的死亡率51%~97%;在抗生素治疗下,病死率已有明显下降。但由于肺炎杆菌耐药率较高,病死率为20%~30%,远超过肺炎链球菌肺炎。具有抗肺炎杆菌作用的抗菌药物较多,包括第一、第二和第三代头孢菌素、广谱青霉素、氨基糖苷类抗生素、氟喹诺酮类及其他,如亚胺培南和氨曲南等。高效、低毒、价廉是考虑选择抗菌药物的最重要因素。

肺炎克雷伯菌耐药机制的研究进展

肺炎克雷伯菌耐药机制的研究进展 肺炎克雷伯菌是临床分离和医院获得性感染最常见的致病菌之一,其主要耐药机制包括产生抗菌药物灭活酶、抗菌药物渗透障碍(生物被膜和外膜孔蛋白缺失)、药物作用靶位的改变、主动外排泵系统的亢进作用、整合子等。肺炎克雷伯菌耐药机制的研究对于控制耐药菌的播散和合理使用抗生素都具有重要的意义。本文就上述耐药机制的研究进展进行综述。 肺炎克雷伯菌(KPN)是重要的条件致病菌和医源性感染菌之一。近年来,由于临床上抗菌药物的大量应用和滥用,致使KPN耐药率居高不下,直接影响到临床治疗效果。Amazian等[1]研究显示,肺炎克雷伯菌占地中海地区医院内感染的9.2%;2011年全国医院感染监控网医院感染病原菌分布调查显示KPN占9.03%,成为国内医院感染的第二大病原菌[2]。国外曾经报道一组由多重耐药KPN引起医院内感染的暴发流行,死亡率高达40%[3]。KPN主要耐药机制包括产生抗菌药物灭活酶、药物作用靶位的改变、抗菌药物渗透障碍(生物被膜、外膜孔蛋白缺失)、主动外排泵系统的亢进作用等,同时抗菌药物耐药基因借助质粒、转座子、整合子的播散也是耐药菌株临床加剧的重要原因。本文对上述耐药机制的研究进展作一简要综述。 1 产生抗菌药物灭活酶 细菌可产生许多能引起抗菌药物灭活的酶,主要包括β-内酰胺酶、氨基糖苷类钝化酶(AME)。KPN对β-内酰胺类药物耐药的主要机制之一是产生β-内酰胺酶。它可通过水解β-内酰胺环,使β-内酰胺类药物水解从而失去抗菌活性,其水解率是细菌耐药性的主要决定因素。KPN产生的β-内酰胺酶主要包括产超广谱β-内酰胺酶(ESBLs)、质粒介导的AmpC酶、耐酶抑制剂的β-内酰胺酶(IRBLs)及碳青霉烯酶(KPC酶)等。 1.1 产超广谱β-内酰胺酶(ESBLs)ESBLs是KPN耐药产生的最主要的一类酶。1983年由德国报告了世界上第一例ESBLs,1994年在中国医学科学院北京协和医院发现国内首例ESBLs感染,迄今已报告的ESBLs的代表菌株有肺炎克雷伯杆菌、大肠杆菌等。ESBLs是由质粒介导的丝氨酸蛋白衍生物,通过水解青霉素、广谱及超广谱头孢菌素及单环β-内酰胺类药物的β-内酰胺酶,导致此类抗菌药物耐药,可被β-内酰胺酶抑制剂如克拉维酸钾所抑制,但罗燕萍等[4]报道,产ESBLs的PKN对酶抑制剂复合抗生素也有较高的耐药率。 ESBLs以TEM型和SHV型最常见,CTX-M型是我国的主要基因型。TEM 型ESBLs主要对青霉素、氨苄西林及头孢他啶等一代头孢菌素耐药,但对头孢噻肟敏感,对舒巴坦和克拉维酸耐药是所有CTX-M型酶的特点。SHV型ESBLs 由质粒介导或染色体编码产生,主要引起细菌对第一代头孢菌素和青霉素耐药,SHV-1型对阿莫西林、氨苄西林等青霉素类抗菌药物有较强的水解作用。目前用于治疗产ESBLs菌所致感染的药物有碳青霉烯类、头霉素类抗生素,亚胺培南具有超广谱、高效的抗菌活性,是治疗ESBLs菌感染的首选药物。

肺炎克雷伯细菌及其荚膜

Klebsiella pneumoniae Bacteremia and Capsular Serotypes, Taiwan Chun-Hsing Liao, Yu-Tsung Huang, Chih-Cheng Lai, Cheng-Yu Chang, Fang-Yeh Chu, Meng-Shiuan Hsu, Hsin-Sui Hsu, and Po-Ren Hsueh Capsular serotypes of 225 Klebsiella pneumoniae isolates in Taiwan were identi ? ed by using PCR. Patients infected with K1 serotypes (41 isolates) had increased community-onset bacteremia, more nonfatal diseases and liver abscesses, lower Pittsburgh bacteremia scores and mortality rates, and fewer urinary tract infections than patients infected with non–K1/K2 serotypes (147 isolates). K lebsiella pneumoniae bacteria cause a variety of infections (1,2). Geographic differences in this organism have been recognized, and a high prevalence of liver abscesses has been observed for >20 years in persons in Taiwan infected with K . pneumoniae (3,4). K1 and K2 are the major capsular serotypes that cause liver abscesses and have increased virulence (4–7). In contrast, only limited information is available about serotypes causing K. pneumoniae bacteremia (3,5). Yu et al. grouped K1 and K2 serotypes and compared clinical characteristics for patients with K. pneumoniae bacteremia with those for patients infected with non–K1/K2 serotypes (3). Recent evidence suggests that K1 is a major cause of primary liver abscesses and has greater potential for causing metastasis, and that K2 is a major cause of secondary liver abscesses (6,8). We examined the distribution and clinical characteristics of serotypes that cause K. pneumoniae bacteremia from 225 patients (9) and performed PCR-based genotyping to identify capsular serotypes (10). The Study The study was conducted at Far-Eastern Memorial Hospital in Taipei, Taiwan. Patients with K . pneumoniae bacteremia were identi ? ed during January 1–December 31, 2007. Identi ? cation of K . pneumoniae was based on colony morphologic features and biochemical reactions (11). Data on time until positive blood culture results were obtained from the automated blood culture system at the hospital. Data for each patient were included only once (at the time of the ? rst detection of bacteremia). Patients <18 years of age and those not admitted to our hospital were excluded. Inactive malignancy was not included as an underlying illness. In-hospital and 14-day mortality rates were assessed. For 225 available bacterial isolates, cps genotyping was performed (10). A total of 231 patients with K . pneumoniae bacteremia were observed at the hospital during the study; 225 isolates from 225 patients were used. A total of 133 (59%) of these patients had community-onset bacteremia (bacteremia identi ? ed in an emergency department). The in-hospital mortality rate was 32.4%. Among 225 isolates, 41 (18.2%) were identi ? ed as K1 serotype, 37 (16.4%) as K2, 15 (6.7%) as K57, and 8 (3.6%) as K54. The K1 serotype was found predominantly in community-onset infections (36 [87.8%] of 41 patients compared with 75 [51.0%] of 147 patients infected with non–K1/K2 serotypes; odds ratio [OR] 6.91, 95% con ? dence interval [CI] 2.57–18.60) (online Appendix Table 1, https://www.360docs.net/doc/60413034.html,/EID/content/17/6/1113-appT1.htm). Underlying illness was classi ? ed as nonfatal in 75.6% of patients with K1 bacteremia (53.7% of patients with non–K1/K2 bacteremia; OR 2.67, 95% CI 1.22–5.84). A lower percentage of patients with K1 bacteremia had surgery in the previous 3 months (9.8% vs. 30.6%; OR 0.25, 95% CI 0.09–0.73). Patients with K1 bacteremia had lower mean ± SD Pittsburgh bacteremia scores than those with non–K1/K2 bacteremia (2.7 ± 3.1 vs. 4.4 ± 4.7; OR 0.90, 95% CI 0.81–0.99), but the time until a positive blood culture was obtained was not different. K1 serotype was more common in patients with liver abscesses (46.3% vs. 4.1%; OR 20.3, 95% CI 7.31–56.40) and less common in patients with urinary tract infections (UTIs) (4.9% vs. 20.4%; OR 0.20, 95% CI 0.05–0.88). The in-hospital mortality rate for patients with K1 bacteremia was lower that that for patients with non–K1/K2 bacteremia (14.6% vs. 34.7%; OR 0.32, 95% CI 0.13–0.82). No differences were found in clinical characteristics for patients with K2 bacteremia and those with non–K1/K2 bacteremia except for a higher frequency of liver abscesses in patients with K2 bacteremia (13.5% vs. 4.1%; OR 3.67, 95% CI 1.06–12.8). For patients infected with K54 and K57 serotypes, 1 K57 serotype caused liver abscesses; no abscesses were found in patients infected with a K54 serotype. The in-hospital mortality rate was 50% (4/8) for patients with K54 bacteremia and 53.3% (8/15) for patients with K57 bacteremia. Patients infected with a K1 serotype had lower mean ± SD Pittsburgh bacteremia scores (2.7 ± 3.1 vs. 5.0 ± 5.3; Emerging Infectious Diseases ? https://www.360docs.net/doc/60413034.html,/eid ? Vol. 17, No. 6, June 2011 1113 Author af ? liations: Far Eastern Memorial Hospital, Taipei, Taiwan (C.-H. Liao, C.-C. Lai, C.-Y . Chang, F.-Y . Chu, M.-S. Hsu, H.-S. Hsu); and National Taiwan University College of Medicine, Taipei (Y .-T. Huang, P .-R. Hsueh)DOI: 10.3201/eid1706.100811

对肺炎克雷伯菌碳青霉烯酶的研究进展

文章编号:167328640(2010)0120063204 中图分类号:R378.1 文献标识码:A 对肺炎克雷伯菌碳青霉烯酶的研究进展 汤 瑾1 , 李 卿2 , 蒋燕群 1 (1.上海交通大学附属上海市第六人民医院检验科,上海200233;2.上海市临床检验中心,上海200126) 关键词:碳青霉烯酶;肺炎克雷伯菌;检测作者简介:汤 瑾,女,1975年生,学士,主管技师,主要从事细菌耐药监测及相关研究。通讯作者:蒋燕群,联系电话:02126436918128735。 碳青霉烯类抗菌药物在临床上可用于多重耐 药的细菌感染,随着临床上碳青霉烯类抗菌药物的广泛使用,产生了对亚胺培南或美罗培南耐药的肠杆菌。至今为止对碳青霉烯类耐药的肠杆菌还比较少见,1998至2001年美国的net w ork 监测中没有发现此类细菌。调查了1996至2000年间24家美国医院分离的1123株肺炎克雷伯菌,只 找到了4株耐药菌株(在同一个中心)[1] 。肺炎克雷伯菌碳青霉烯酶(Klebsiella pneum oniae carbapene mase ,KPC 酶)最早在一株亚胺培南耐药的肺炎克雷伯菌中被发现。从2000年以后,KPC 酶家族陆续在美国的新英格兰和亚特兰大地区被发现,主要在克雷伯菌属中,也在其他菌株中被发现。由于肠杆菌是临床上重要的医院感染菌,其对碳青霉烯类抗菌药物的耐药给临床抗感染治疗带来了极大困难。 一、碳青霉烯酶的分类 碳青霉烯酶是指能够明显水解亚胺培南或美罗培南的一类β2内酰胺酶,包括Ambler 分子分 类为A 、B 、D 3类酶[2,3] 。A 类为丝氨酸酶,其活性部位具有丝氨酸结构,属于Bush 分群中的第2f 亚组。A 类碳青霉烯酶少见,包括阴沟肠杆菌(I M I 21和NMC 2A )、黏质沙雷菌中由染色体介导的NMC 2A 、S me 21、S me 22、S me 23、I M I 21酶,以及肺炎克雷伯菌、铜绿假单胞菌中质粒介导的KPC 21、 GES 22酶[4] 。这类酶都是青霉素酶,他们对亚胺培南的水解活性强于美罗培南,可以引起青霉素类、氨曲南、碳青霉烯类耐药,而对第3代头孢菌素通常敏感。三唑巴坦、克拉维酸可以抑制此类酶,但不被乙二胺四乙酸(E DT A )所抑制。 Amble 分类D 类为丝氨酸酶,属于Bush 分群中的第2d 亚组,其活性部位具有丝氨酸结构,由bla OXA 等位基因编码,仅见于不动杆菌。 Amble 分类B 类是金属酶,属于Bush 分类3组,是一种需金属离子发挥活性的β2内酰胺酶,由bla I M P 、bla V I M 、blaSP M 和blaGI M 编码,可被 EDT A 所抑制[2] ,染色体介导或质粒介导,存在于多种不同革兰阳性和革兰阴性细菌中。金属酶均可明显水解亚胺培南,能水解除单环类抗菌药物以外的绝大多数β2内酰胺类抗菌药物,但对于其他 β2内酰胺类抗菌药物的水解能力有较大差异[5] 。临床使用亚胺培南等碳青霉烯类抗菌药物大大增加,导致金属β2内酰胺酶产生率有不断上升的趋势。目前尚未开发出有效的金属酶抑制剂。 细菌对碳青酶烯类抗菌药物耐药除了产水解碳青霉烯类β2内酰胺酶外,耐药机制还可能涉及如下几个方面:(1)高产AmpC 酶伴膜孔蛋白Omp 缺失,如阴沟肠杆菌、产气肠杆菌、弗劳地柠檬酸杆菌、大肠埃希菌及肺炎克雷伯菌。革兰阴性菌的细胞壁外膜的蛋白通道是药物进入细菌的重要途径,膜孔蛋白对β2内酰胺类抗菌药物的导入作用有其特异性,当某种膜孔蛋白表达减少或缺失时,相应的抗菌药物就不能进入细菌发挥作用;(2)青霉素结合蛋白改变。β2内酰胺类抗菌药物通过膜孔蛋白进入周质间隙,然后与青霉素结合蛋白结合而发挥抗菌作用,此蛋白发生结构变化,β2内酰胺类抗菌药物与之亲和力下降或不与其结合,则不能有效干扰细菌细胞壁的合成而产生耐药;(3)主动外排系统的活跃。细菌细胞内膜存在能量依赖性蛋白外排泵,通过主动外排作用将药物从菌体排出,使达到作用靶位的药量 明显减少,不足以发挥杀菌或抑菌作用[6,7] 。 二、KPC 酶的研究进展1.KPC 21酶 2001年有学者在美国北卡罗来纳州肺炎克雷伯菌中发现由质粒介导的KPC 21酶[8] 。耐药表型表现出高度亚胺培南和美罗培南耐药性[最低抑菌浓度(M I C )均为16μg/mL ],当存在克拉维酸时,针对亚胺培南和美罗培南的β2内酰胺酶活性被抑制;对头孢菌素类抗菌药物和氨曲南也耐药。KPC 21基因由大约50kb 的非

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