产超广谱β-内酰胺酶大肠埃希菌和肺炎克雷伯菌的分布及耐药性分析

目的了解医院产超广谱β-内酰胺酶（ESBLs）大肠埃希菌和肺炎克雷伯菌的分布及耐药性特点。方法对我院2004年7月～2006年7月间各类临床标本分离出的大肠埃希菌307株和肺炎克雷伯菌202株，用CLSI／NCCLS推荐的表型确证法检测其ESBLs，采用K-B纸片琼脂扩散法进行药敏试验，分析产ESBLs菌株的分布及耐药性。结果大肠埃希菌和肺炎克雷伯菌产ESBLS菌株的检出率分别为38．4％（118／307）和31．7％（64／202），主要分布于尿和痰、咽拭子中，病区主要集中于肺科、神经外科、感染科、泌尿外科、ICU室。产ESBLs菌株对亚胺培南和美罗培南呈高度敏感，对哌托西林／三唑巴坦、头孢哌酮／舒巴坦、头孢西丁耐药率较低，对其他抗菌药物均出现较高耐药。结论产ESBLS的大肠埃希菌和肺炎克雷伯菌分布在不同病区的不同标本中，碳青霉烯类抗生素亚胺培南和美罗培南是治疗产ESBLS菌株感染的较佳药物。     

Fluoroquinolone resistance in pediatric bloodstream infections because of Escherichia coli and Klebsiella species

In pediatric bloodstream infections with fluoroquinolone (FQ)-resistant Escherichia coli and Klebsielia species, we noted an association between FQ resistance and extended-spectrum beta-lactamase (ESBL) production (OR, 12; 95% CI: 2.28-83.8). A case control study revealed no significant risk factors (including prior antibiotic use) for FQ resistance among ESBL E coli and Klebsiella species (ESBL-EK).     

Risk factors for fluoroquinolone resistance in nosocomial Escherichia coli and Klebsiella pneumoniae infections

BACKGROUND: The incidence of fluoroquinolone (FQ) resistance has increased markedly in recent years. Even in the common nosocomial pathogens Escherichia coli and Klebsiella pneumoniae, in which the emergence of FQ resistance was believed to be unlikely, increasing resistance to these agents has been noted. Risk factors for FQ resistance in these pathogens remain unknown. Although FQs are important components of the present antimicrobial arsenal, their continued usefulness is threatened by rising FQ resistance. OBJECTIVE: To identify risk factors for nosocomial FQ resistance. METHODS: A case-control study of hospitalized patients with infections due to FQ-resistant and FQ-susceptible E coli and K pneumoniae occurring between January 1, 1998, and June 30, 1999. RESULTS: We included 123 patients with nosocomial FQ-resistant infections and 70 randomly selected patients with nosocomial FQ-susceptible infections. Independent risk factors (adjusted odds ratio [95% confidence interval]) for FQ resistance were (1) recent FQ use (5.25 [1.81-15.26]); (2) residence in a long-term care facility (3.65 [1.64-8.15]); (3) recent aminoglycoside use (8.86 [1.71-45.99]); and (4) older age (1.03 [1.01-1.06]). CONCLUSIONS: Recent FQ use, residence in a long-term care facility, recent aminoglycoside use, and older age were all noted to be independent risk factors for FQ resistance among patients with nosocomial E coli and K pneumoniae infections. Efforts should be directed at recognition and modification of these risk factors to curb the rise in FQ resistance and preserve the utility of these agents in the treatment of common nosocomial gram-negative infections.     

Epidemiological investigation of fluoroquinolone resistance in infections due to extended-spectrum beta-lactamase-producing Escherichia coli and Klebsiella pneumoniae.

The incidence of infections due to extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli and Klebsiella pneumoniae (ESBL-EK) has increased markedly in recent years. Treatment is difficult because of frequent multidrug resistance. Although fluoroquinolones offer effective therapy for ESBL-EK infections, their usefulness is threatened by increasing fluoroquinolone resistance. To identify risk factors for fluoroquinolone resistance in ESBL-EK infections, a case-control study of all patients with ESBL-EK infections from 1 June 1997 through 30 September 1998 was conducted. Of 77 ESBL-EK infections, 43 (55.8%) were resistant to fluoroquinolones. Independent risk factors for fluoroquinolone resistance were fluoroquinolone use (odds ratio [OR], 11.20; 95% confidence interval [CI], 1.99-63.19), aminoglycoside use (OR, 5.83; 95% CI, 1.12-30.43), and long-term care facility residence (OR, 3.39; 95% CI, 1.06-10.83). The genotypes of fluoroquinolone-resistant ESBL-EK isolates were closely related. Efforts should be directed at modification of these risk factors to preserve the utility of fluoroquinolones in the treatment of ESBL-EK infections.     

老年下呼吸道感染患者肺炎克雷伯菌和大肠埃希菌耐药性分析

目的：监测老年下呼吸道感染患者肺炎克雷伯菌和大肠埃希菌的耐药性。为临床合理应用抗生素提供依据。方法：对我院下呼吸道感染患者中分离出的肺炎克雷伯菌和大肠埃希菌240株，以Kirby-Bauer(K-B)琼脂扩散法作药敏试验；以美国临床实验室标准委员会（NCCLS）1999年推荐的表型确认试验检测超广谱β－内酰胺酶（ESBLs）。结果：老年组和非老年组肺炎克雷伯菌和大肠埃希菌对14例抗生素的耐药率分别为阿莫西林93．2％和87．3％，哌拉西林57．1％和42．9％、头孢呋新51．4％和33．3％、头孢噻肟40．1％和17．5％、头孢他啶13．6％和3．2％、头孢曲松39．0％和17．5％、头孢哌酮37．3％和15．9％，头孢吡肟10．2％和3．2％、阿米卡星47．5％和34．9％，环丙沙星54．2％和38．1％、亚胺培南15．9％、头孢吡肟10．2％和3．2％、阿米卡星47．5％和34．9％、环丙沙星54．2％和38．1％，亚胺培南0和0、头孢哌酮／舒巴坦0和0、哌拉西林／三唑巴坦1．1％和0、头孢美唑9．6％和4．8％。78株肺炎克雷伯菌和大肠埃希菌被证实为产ESBLs菌，ESBLs检测出率为32．5％（78／240），其中老年组ESBLs检出率为38．4％（68／177），非老年组ESBLs检出率为15．9％（10／63）。亚胺培南，头孢哌酮／舒巴坦，哌拉西林／三唑巴坦和头孢美唑对产ESBLs菌的耐药率最低，分别为0、0、2．6％和12．8％。结论：老年下呼吸道感染患者肺炎克雷伯菌和大肠埃希菌的耐药率和ESBLs检出率均显著高于非老年患者；亚胺培南，头孢哌酮／舒巴坦、哌拉西林／三唑巴坦和头孢美唑是治疗由产ESBLs菌引起感染的有效抗生素。     

下呼吸道产超广谱β-内酰胺酶肺炎克雷伯氏菌及大肠埃希氏菌的耐药性分析

目的分析临床分离的下呼吸道产超广谱β-内酰胺酶肺炎克雷伯菌及大肠埃希菌的耐药特点,从而掌握耐药菌株的流行状况。方法按常规方法进行细菌分离、培养和菌种鉴定。采用微量液体稀释与K—B法分别对常用抗生素和头孢哌酮／舒巴坦的耐药性进行检测。结果产ESBLs肺炎克雷伯菌和大肠埃希菌对AMP、AMP／SB、PIP、CF、CFZ、CRM、CPD、CAX、CAZ、CTX、CPE和AZT的耐药率高达90％以上;对含β-内酰胺酶抑制剂的复合制剂（PIP／TB和SCF）的耐药率分别是52．6％、34．6％和39．7％、19．8％;对环丙沙星、庆大霉素、妥布霉素的耐药率较高,分别是64％、88．8％,96．2％、75％和96％、87．9％,具有多重耐药特点,但对亚胺培南敏感。结论产ESBLs肺炎克雷伯菌和大肠埃希菌对多种不同种类抗生素耐药,且具有多重耐药的特点。尤其是对青霉素、头孢菌素类耐药率高,但对碳青霉烯类抗生素敏感。     

老年肝胆疾病患者大肠埃希菌血流感染的临床特点分析

目的：分析老年肝胆疾病患者大肠埃希菌血流感染的临床特点及耐药性,为临床治疗提供依据。方法回顾性分析2009年－2012年于解放军三二医院住院的57例老年肝胆疾病患者血流感染大肠埃希菌的临床特点及药敏试验结果。计量资料组间比较采用 t 检验,计数资料组间比较采用χ2检验。结果57例老年肝胆疾病患者血流感染大肠埃希菌,其中基础疾病以肝硬化为主,感染来源以自发性细菌性腹膜炎为主,超广谱β－内酰胺酶（ESBL）阳性24株,阳性率为42．1％。二者在年龄、性别、基础疾病、原发病灶、体温峰值、白细胞计数及中性粒细胞百分比等方面比较,差异均无统计学意义（P 值均＞0．05）。除亚胺培南／西司他丁、美罗培南、头孢哌酮／舒巴坦、替卡西林／克拉维酸及米诺环素外,ESBL 阳性大肠埃希菌的耐药性均高于 ESBL 阴性大肠埃希菌,差异具有统计学意义（P 值均＜0．05）。发生感染性休克、肝性脑病及急性肾损伤患者的病死率要高于无发生者,差异有统计学意义（χ2值分别为9．541、7．622、9．733,P 值均＜0．05）。结论老年肝胆疾病患者血流感染大肠埃希菌 ESBL 阳性耐药性高,出现严重并发症者预后不良,应尽早联合抗感染治疗及预防,控制严重并发症以降低病死率。     

严重肝病伴糖尿病患者大肠埃希菌血流感染临床分析

目的：分析严重肝病伴糖尿病患者大肠埃希菌血流感染的临床特点及耐药性,为临床合理应用抗菌药物提供依据。方法回顾性分析2009年至2012年住院的严重肝病合并糖尿病血流感染大肠埃希菌患者的临床特点及药敏结果。结果严重肝病合并糖尿病血流感染大肠埃希菌患者共47例,基础疾病以肝硬化为主,感染来源以自发性细菌性腹膜炎为主,ESBL阳性22株,阳性率46．81％。ESBL阳性大肠埃希菌耐药性高于 ESBL 阴性大肠埃希菌,但两者在年龄、性别、基础疾病、原发病灶、体温峰值、白细胞计数及中性粒细胞百分比等方面比较均差异无统计学意义,发生感染性休克者的病死率要高于无感染性休克者。结论严重肝病合并糖尿病患者血流感染病情危重,预后不良,应尽早进行正确的综合治疗和抢救以降低病死率。     

Conjugal transfer of multiple antibiotic resistance from hospital isolates of Klebsiella to Escherichia coli

Six independent isolates of Klebsiella from hospital environmental sources in Malaysia were found to be resistant to at least ampicillin, carbenicillin, cefoperazone, chloramphenicol, gentamicin and tetracycline. On the basis of their antibiograms, they were divided into four antibiogroups. They transferred all or part of their multiple antibiotic resistance traits to E. coli by conjugation. The results suggest that these Klebsiella strains harbour self-transmissible R plasmids. The significance of these findings are discussed.     

Plasmid-mediated resistance to third-generation cephalosporins caused by point mutations in TEM-type penicillinase genes

Infections due to strains of Klebsiella pneumoniae, Escherichia coli, and Citrobacter freundii resistant to third-generation cephalosporins have been observed recently in France and the Federal Republic of Germany. This resistance phenotype is due to the production of new plasmid-mediated, broad-substrate-range beta-lactamases designated TEM-3 to TEM-7. DNA-DNA hybridization analysis with a probe specific for TEM-1 indicated that the corresponding genes blaT-3 to blaT-7 were variants of the structural genes for TEM-type beta-lactamases. In the present studies, a 2.5-kilobase BamHI plasmid DNA fragment encoding TEM-3 was cloned in E. coli, and the entire nucleotide sequence of blaT-3 was determined. The deduced amino acid sequence of TEM-3 differed in two positions from that of the TEM-2 enzyme: lysine (TEM-3) was substituted for glutamic acid (TEM-2) at residue 104 and serine (TEM-3) for glycine (TEM-2) at residue 238 in the numbering system of Ambler. Spontaneous mutants of TEM penicillinases with increased activity against third-generation cephalosporins were obtained in vitro by selection on cefotaxime or ceftazidime. It therefore appears that mutations in TEM-type beta-lactamases contribute to resistance to new-generation cephalosporins.     

The importance of the K1 capsule in invasive infections caused by Escherichia coli

We examined 534 clinical isolates of Escherichia coli for sensitivity to rough lipopolysaccharide-specific and K1-specific phages. Twenty-eight percent of bacteremic isolates were sensitive to rough-specific phages. Forty-two percent of these strains, against only 20% of bacteremic isolates insensitive to rough-specific phages, had K1 capsule (P less than 0.001). K1-positive strains were usually resistant to phagocytic killing, whereas strains lacking the K1 capsule were more likely to be killed regardless of capsular type. Eighty-two percent of strains were typable with O-specific, 57% with K-specific, and 74% with H-specific antisera. Sixty percent of E coli were agglutinated by only 10 O-specific antisera. K1 was the most common capsular type, followed by K5, K2, and K12, whereas four H antigens accounted for nearly half of the H-typable strains. We conclude that (1) the combination of rough-specific and K1-specific phage sensitivity defines functionally similar groups of bacteria and (2) a polyvalent vaccine against invasive E coli is possible given the relatively limited number of invasive O:K:H serotypes.     

Virulence of Escherichia coli strains with R-plasmid mediated penicillin resistance in mice infections.

Penicillinase I-, II- and III-producing R-plasmid of Escherichia coli were transferred to Escherichia coli 177, KC-14, and 444. These strains are highly virulent in mice. This study was conducted to investigate the influence of conjugative R-plasmid on the virulence of its host strains. Escherichia coli 177 after penicillinase I- or III-producing R-plasmids transfer retained parental levels of virulence. On the other hand, penicillinase II-producing transconjugants showed reduced virulence in mice. The virulence of its revertants, in which R-plasmid was eliminated by heat, were equivalent to that of the host strain. It is suggested that the decrease in the virulence of transconjugants was not due to transferred R-plasmid. The reduced virulence of the these transconjugants may be due to alterations in their components such as the lipopolysaccharides in the cell envelope.     

Phylogenetic origin and virulence genotype in relation to resistance to fluoroquinolones and/or extended-spectrum cephalosporins and cephamycins among Escherichia coli isolates from animals and humans

In Escherichia coli infection, the implications of fluoroquinolone (FQ) and extended-spectrum cephalosporin plus cephamycin (AmpC) resistance for phylogenetic origin and virulence potential are undefined, as is the influence of ecological context on these associations. Accordingly, 106 E. coli isolates exhibiting FQ and/or AmpC resistance and 98 susceptible isolates were compared with regard to phylogenetic background and virulence profiles, stratified by host group (104 predominantly extraintestinal human isolates and 100 predominantly intestinal cattle and swine isolates). Although resistant isolates exhibited significant shifts in phylogenetic distribution and virulence profiles, human and animal isolates exhibited different phylogenetic shifts, and only among human isolates did resistance predict reduced virulence. Evidence for similar strains being resistant versus susceptible was scant. The O15:K52:H1 clonal group and the closely related "clonal group A" featured prominently among resistant and susceptible human isolates, respectively. Thus, in E. coli, antibiotic resistance predicts phylogenetic background and virulence potential in a complex, context-dependent fashion.     

Clinico-epidemiological features of infections caused by CTX-M type extended spectrum beta lactamase-producing Escherichia coli in hospitalised patients

A review of medical records of 45 of 53 hospitalised patients with positive cultures for CTX-M type ESBL-producing Escherichia coli between 01 January and 31 May 2004 was conducted. The mean age of the population studied was 73.1 (+/-14.6) years and the majority (55.6%) had been under the care of the internal medicine or elderly care service. In the majority (77.8%) of instances the isolate was attributed to a clinical infection rather than colonisation and the commonest clinical specimen to yield the organism was urine, which was positive in 57.8% of patients. Acquisition of the organism was categorised as nosocomial in 68.9% of patients; in this subgroup, the median duration of inpatient stay prior to recovery of the organism was 24 (range 3-240) days. Haemodialysis-dependence was the most common of the comorbidities evaluated. The mean number of antibiotics prescribed per patient in the 30 days prior to first isolation of the organism was 1.7 (range 0-4). Furthermore, the mean number of antibiotic-days exposure per patient during this period was 13.9 (range 0-48). The most frequently received class of antibiotic was beta-lactam/beta-lactamase inhibitor combinations. Of 35 infections, 26 (74.2%) were successfully treated. Overall 12 patients with infection died (34.3%); attributable mortality was presumed in seven (20%).     

In vitro activity of cefpirome compared with other third generation cephalosporins against nosocomial isolates in Argentina

Summary Thein vitro activity of cefpirome was evaluated against strains that showed conflicting results for third generation cephalosporins. Against isolates with derepressed inducible chromosomal cephalosporinase (n=40) cefpirome was the sole cephalosporin with an MIC₉₀ in the susceptible range;Klebsiella spp. with plasmid-mediated -lactamases (broad spectrum SHV-2 or SHV-2 type) (n=40) remained most susceptible to ceftizoxime and cefpirome; against aminoglycoside-resistantPseudomonas aeruginosa (n=50), cefpirome was as active as ceftazidime and cefoperazone; against oxacillin-susceptible and oxacillin-resistantStaphylococcus spp., (n=40 each) and againstEnterococcus spp., (n=20), cefpirome was more active than other third generation cephalosporins but killing was inadequate against both oxacillin-resistant staphylococci and enterococci.

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In-Vitro-Aktivität vom Cefpirom im Vergleich zu anderen Drittgenerations-Cephalosporinen gegen nosokomiale Isolate aus Argentinien

Zusammenfassung Cefpirom wurde auf seineIn-Vitro-Aktivität gegen Stämme untersucht, die sich in ihrer Empfindlichkeit gegen Drittgenerationscephalosporine widersprüchlich verhielten. Cefpirom wies als einziges Drittgenerationscephalosporin gegen 40 Isolate mit dereprimierter induzierbarer chromosomaler Cephalosporinase MHK₉₀-Werte im empfindlichen Bereich auf. Plasmid-vermittelte -Laktamase (Breitspektrum SHV-2 oder Typ SHV-2) bildendeKlebsiella spp. (n=40) verhielten sich gegen Ceftizoxim und Cefpirom am empfindlichsten. Cefpirom war gegen aminoglykosidresistente Stämme vonPseudomonas aeruginosa (n=50) ebenso wirksam wie Ceftazidim und Cefoperazon. Cefpirom war den anderen Drittgenerationscephalosporinen überlegen in seiner Aktivität gegen oxacillinempfindliche und oxacillinresistenteStaphylococcus spp. (je 40 Isolate) und gegenEnterococcus spp. (n=20); jedoch war die Abtötung oxacillinresistenter Staphylokokken wie auch der Enterokokken nicht adäquat.

     

Infections caused by Escherichia coli resistant to norfloxacin in hospitalized cirrhotic patients

Selective intestinal decontamination with norfloxacin is useful to prevent bacterial infections in several groups of cirrhotic patients at high risk of infection. However, the emergence of infections caused by Escherichia coli resistant to quinolones has recently been observed in cirrhotic patients undergoing prophylactic norfloxacin. Our aim is to determine the characteristics of the infections caused by E. coli resistant to norfloxacin in hospitalized cirrhotic patients. One hundred and six infections caused by E. coli in 99 hospitalized cirrhotic patients were analyzed and distributed into two groups: group I (n = 67), infections caused by E. coli sensitive to norfloxacin, and group II (n = 39), infections caused by E. coli resistant to norfloxacin. The clinical and analytical characteristics at diagnosis of the infection were similar in both groups. Previous prophylaxis with norfloxacin was more frequent in group II (15/67, 22.4% vs. 32/39, 82%, P <.0001), as a result of a higher number of patients submitted to continuous long-term prophylaxis in this group, whereas previous short-term prophylaxis was similar in both groups. Infections were more frequently nosocomial-acquired in group II than in group I (17/67, 25.3% vs. 20/39, 51.2%, P =.01). The type of infections was similar in both groups: urinary tract infections 38 in group I and 24 in group II, spontaneous bacterial peritonitis 8 and 2, spontaneous bacteremia 4 and 4, and bacterascites 1 and 0, respectively (pNS). Mortality during hospitalization was similar in the two groups (4/67, 5.9% vs. 5/39, 12.8%, pNS). None of the E. coli resistant to norfloxacin were also resistant to cefotaxime and only one of them was resistant to amoxicillin-clavulanic acid. Prophylaxis with norfloxacin, usually continuous long-term prophylaxis, favors the development of infections caused by norfloxacin-resistant E. coli. Long-term antibiotic prophylaxis should therefore be restricted to highly selected groups of cirrhotic patients at high-risk of infection. Infections caused by E. coli resistant to norfloxacin show a severity similar to those caused by sensitive E. coli. No significant associated resistance between norfloxacin and the antibiotics most frequently used in the treatment of bacterial infections in cirrhotic patients has been observed.