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PubMed2006

Outbreak of infection by carbapenem-resistant Acinetobacter baumannii producing the carbapenemase OXA-58 in Belgium.

Carbapenem-resistant Acinetobacter baumannii isolates were obtained from 17 patients between September 2004 and August 2005 at the Academisch Ziekenhuis Vrije Universiteit Brussel, Brussels, Belgium. These multidrug-resistant isolates, which belonged to a single clone, remained susceptible to colistin and tigecycline only and produced the carbapenem-hydrolyzing oxacillinase OXA-58. This study highlights the importance of the intercountry spread of this beta-lactamase-mediated resistance mechanism and its epidemic evolution.

Acinetobacter Infections↗
PubMed1989

Laboratory investigation of hospital outbreak caused by two different multiresistant Acinetobacter calcoaceticus subsp. anitratus strains.

During a 7-month period, from December 1986 to June 1987, multiresistant strains of Acinetobacter calcoaceticus subsp. anitratus were isolated from 25 patients in a respiratory intensive care unit. The biochemical characteristics defined two groups of strains, group 1 (14 strains) and group 2 (11 strains). Both groups had the same biochemical characteristics, but group 2 strains could assimilate adipate and phenyl acetate. Moreover, of 16 antibiotics tested only netilmicin and imipenem had some inhibitory activity for group 1 strains; group 2 strains were susceptible to mezlocillin, piperacillin, and ticarcillin. Plasmid profiles of the groups were also different. The results of a laboratory investigation (biochemical characteristics, antibiotic susceptibility, and plasmid isolation) identified two different A. calcoaceticus subsp. anitratus strains as the causes of the outbreak.

Acinetobacter↗
PubMed1992

Use of pulsed-field gel electrophoresis for investigation of hospital outbreaks of Acinetobacter baumannii.

Genomic DNAs from taxonomically and epidemiologically well-defined strains of Acinetobacter baumannii were digested with restriction endonucleases that cleave with low frequency, and the fragments were separated by pulse-field gel electrophoresis. Restriction fragment length polymorphisms were observed. Restriction fragment length polymorphism analysis can be used as an epidemiological tool to delineate outbreaks of nosocomial infections caused by A. baumannii.

Acinetobacter↗
PubMed1993

Correlation of typing methods for Acinetobacter isolates from hospital outbreaks.

Four methods, namely, biotyping, cell envelope protein electrophoresis, ribotyping, and comparison of antibiograms, were used for strain identification of Acinetobacter isolates from five outbreaks in hospitals. There was good agreement among the methods for the identification of an index strain, but biotyping and the comparison of antibiograms were the least discriminatory.

Acinetobacter↗
PubMed1993

Epidemiological study of an Acinetobacter baumannii outbreak by using polymerase chain reaction fingerprinting.

A polymerase chain reaction (PCR) technique was applied to the fingerprinting of different strains of Acinetobacter baumannii from a cluster of patients infected or colonized with the incriminated pathogen. The DNA was extracted by boiling and was subjected to PCR amplification by using the core sequence of the M13 phase as a single primer. The amplified products were separated by agarose gel electrophoresis and were detected by staining with ethidium bromide. In 1990, 49 multiresistant A. baumannii strains were isolated from 13 patients from the same intensive care unit of the Charité Hospital; 45 of these outbreak isolates obtained from 12 patients showed the same PCR patterns, indicating an epidemiological relatedness of these strains. Four strains isolated from the same patient belonged to another genetic group, as revealed by a distinct amplification pattern. Another single subtype of A. baumannii was identified as the causative agent in patients during a second outbreak at a different intensive care unit in the same hospital. Seventeen isolates recovered from 10 immunocompromised patients had the same amplification patterns, which were distinct from all other PCR profiles. Five strains were obtained from two other hospitals; three isolates from the hospital of Magdeburg, Germany, had identical PCR patterns which, however, could be clearly distinguished from the patterns of all other strains. The remaining two isolates displayed individual patterns of amplified fragments. PCR fingerprinting may provide a useful and particularly rapid identification technique for epidemiological investigations of nosocomial infections.

Acinetobacter↗
PubMed1994

Comparison of four different methods for epidemiologic typing of Acinetobacter baumannii.

A set of 103 epidemiologically well-defined Acinetobacter baumannii isolates obtained from nine hospital outbreaks and 21 unrelated strains were characterized by pulsed-field gel electrophoresis (PFGE) of total genomic DNA digested with ApaI. Among outbreak strains, eight different patterns and five possible variants were identified by PFGE. Results were compared with those from traditional typing methods such as plasmid profile analysis, antimicrobial susceptibility, and biotyping. Plasmid analysis revealed six different and two related patterns; one outbreak strain lacked plasmids. A total of 16 of the 21 unrelated strains harbored plasmids and exhibited unique patterns. Epidemiologically unrelated strains were placed into only two biotypes and had similar antimicrobial susceptibility patterns but were clearly distinguished by PFGE. PFGE of A. baumannii chromosomal DNA yielded reproducible and easily readable results and showed excellent discriminatory power. However, plasmid profile analysis may provide a cost-effective first step in epidemiological typing of A. baumannii isolates obtained from well-defined hospital outbreaks.

Acinetobacter↗
PubMed1995

Identification of Acinetobacter isolates in the A. calcoaceticus-A. baumannii complex by restriction analysis of the 16S-23S rRNA intergenic-spacer sequences.

Members of the genus Acinetobacter are reported to be involved in hospital-acquired infections with an increasing frequency. However, clinical laboratories still lack simple methods that allow complete identification of some pathogenic species, i.e., those corresponding to A. baumannii (DNA group or genospecies 2), unnamed genospecies 3 and 13, and two new genospecies that have recently been described. In fact, a complete discrimination between these species is possible only by DNA-DNA hybridization or ribotyping. Both of these techniques are complex and time-consuming and cannot be performed in most clinical laboratories. As a consequence, isolates belonging to these genospecies are often not differentiated and included, together with the environmental genospecies 1, in the A. calcoaceticus-A. baumannii complex. In this report, a simple and rapid method for the identification of the genospecies belonging to the A. calcoaceticus-A. baumannii complex is proposed. It is based on the combined digestion by the restriction endonuclease AluI and NdeII of the DNA fragments resulting from the amplification of the 16S-23S rRNA intergenic spacer sequences. The analysis of 36 strains characterized by DNA-DNA hybridization in previous studies showed that the restriction profiles obtained are highly reproducible and characteristic for each genospecies. Moreover, extending this study to 68 clinical strains, which were assigned to the A. calcoaceticus-A. baumannii complex by phenotypic tests, confirmed the existence of a panel of limited and well-conserved restriction patterns and allowed the identification of the strains tested. This study thus proposes the detection of restriction length polymorphism in the spacer sequences between the 16S and 23S rRNA genes as a method for the identification of isolates in the A. calcoaceticus-A. baumannii complex.

Acinetobacter↗
PubMed1996

Comparison of outbreak and nonoutbreak Acinetobacter baumannii strains by genotypic and phenotypic methods.

Thirty-one Acinetobacter baumannii strains, comprising 14 strains from 14 outbreaks in different northwestern European cities and 17 sporadic strains, were compared by investigating various properties of the strains including biotype, antibiogram, cell envelope protein electrophoretic profile, ribotype pattern, and the band pattern generated by a novel genomic fingerprinting method, named AFLP, which is based on the selective amplification of restriction fragments. Results showed that 12 strains from unrelated outbreaks were linked together in two clusters according to their similarities by these typing methods, whereas sporadic strains were more heterogeneous. Outbreak strains appeared to be markedly more resistant to antibiotics than nonoutbreak strains. The uniformity of typing characters in two sets of outbreak strains suggests that strains in each cluster have a common clonal origin.

Acinetobacter↗
PubMed1998

In vitro activities of ampicillin-sulbactam and amoxicillin-clavulanic acid against Acinetobacter baumannii.

In vitro susceptibility patterns of newer beta-lactamase-inhibiting antibiotics ampicillin-sulbactam (A/S) and amoxicillin-clavulanic acid (A/C) for 100 consecutive isolates of Acinetobacter baumannii obtained from various clinical samples were studied. The A/C MIC for 86% of the strains was more than 16/8 microgram/ml, whereas there was an A/S MIC of more than 16/8 microgram/ml for only 38% of the strains. This showed that A/S has significantly superior in vitro activity compared to A/C against A. baumannii, although, theoretically, both should have similar activities. The therapeutic superiority of A/S over A/C needs to be studied, or else the breakpoints for these agents in in vitro tests need to be redefined.

Acinetobacter↗
PubMed1999

Application of infrequent-restriction-site PCR to clinical isolates of Acinetobacter baumannii and Serratia marcescens.

We applied infrequent-restriction-site PCR (IRS-PCR) to the investigation of an outbreak caused by 23 isolates of Acinetobacter baumannii in an intensive care unit from November 1996 to May 1997 and a pseudoepidemic caused by 16 isolates of Serratia marcescens in a delivery room from May to September 1996. In the epidemiologic investigation of the outbreak caused by A. baumannii, environmental sampling and screening of all health care workers revealed the same species from the Y piece of a mechanical ventilator and the hands of two health care personnel. IRS-PCR showed that all outbreak-related strains were genotypically identical and that three strains from surveillance cultures were also identical to the outbreak-related strains. In a pseudoepidemic caused by S. marcescens, IRS-PCR identified two different genotypes, and among them one genotype was predominant (15 of 16 [93.8%] isolates). Extensive surveillance failed to find any source of S. marcescens. Validation of the result of IRS-PCR by comparison with that of field inversion gel electrophoresis (FIGE) showed that they were completely concordant. These results suggest that IRS-PCR is comparable to FIGE for molecular epidemiologic studies. In addition, IRS-PCR was less laborious and less time-consuming than FIGE. To our knowledge, this is the first report of the application of IRS-PCR to A. baumannii and S. marcescens.

Acinetobacter↗
PubMed1999

Spread of amikacin resistance in Acinetobacter baumannii strains isolated in Spain due to an epidemic strain.

Sixteen amikacin-resistant clinical Acinetobacter baumannii isolates from nine different hospitals in Spain were investigated to determine whether the high incidence of amikacin-resistant A. baumannii was due to the dissemination of an amikacin-resistant strain or to the spread of an amikacin resistance gene. The epidemiological relationship studied by repetitive extragenic palindromic PCR and low-frequency restriction analysis of chromosomal DNA showed that the same clone was isolated in eight of nine hospitals, although other clones were also found. The strains were studied for the presence of the aph(3')-VIa and aac(6')-I genes, which encode enzymes which inactivate amikacin, by PCR. All 16 clinical isolates had positive PCRs with primers specific for the amplification of the aph(3')-VIa gene, whereas none had a positive reaction for the amplification of the aac(6')-I gene. Therefore, the high incidence of amikacin resistance among clinical A. baumannii isolates in Spain was mainly due to an epidemic strain, although the spread of the aph(3')-VI gene cannot be ruled out.

Acinetobacter↗
PubMed1999

Epidemiological study of an Acinetobacter baumannii outbreak by using a combination of antibiotyping and ribotyping.

From June to November 1994 (period 1) and from February to June 1995 (period 2), multiresistant Acinetobacter baumannii strains were isolated in intensive care units and surgical wards of the Amiens Teaching Hospital Center (Amiens, France). Eighteen isolates were obtained from 17 (1%) of 1,706 patients admitted during both of these periods, giving an incidence rate of nosocomial infection per 1,000 patient days of 0.6%. Of 17 infected patients, 9 had pneumonia, 3 had urinary tract infection, 2 had peritonitis, 1 had septicemia, 1 had a catheter infection, and 1 had pneumonia and urinary tract infection. According to typing results, four antibiotic resistance profiles were detected: a, b, c, and d; seven ribotypes were distinguished by both restriction enzymes EcoRI and SalI (A, B, C, D, E, F, and G). By combining antibiotyping and ribotyping, we obtained eight groups of strains (groups I to VIII). Group I contained five strains (strains 4, 5, 7, 8, and 9) which had antibiogram pattern a and ribopattern A and constituted the outbreak strains. The strains of group II (strains 3, 10, 11, 13, and 14) were closely related to outbreak strain A and appeared to be variants of ribotype A (A2 [strain 3]; A4 [strain 10]; A5 [strains 11, 13, and 14]). Groups III, IV, V, VI, VII, and VIII included strains which were epidemiologically unrelated to the strains of group I and were considered nonoutbreak strains.

Acinetobacter↗
PubMed2000

Emergence and rapid spread of carbapenem resistance during a large and sustained hospital outbreak of multiresistant Acinetobacter baumannii.

Beginning in 1992, a sustained outbreak of multiresistant Acinetobacter baumannii infections was noted in our 1,000-bed hospital in Barcelona, Spain, resulting in considerable overuse of imipenem, to which the organisms were uniformly susceptible. In January 1997, carbapenem-resistant (CR) A. baumannii strains emerged and rapidly disseminated in the intensive care units (ICUs), prompting us to conduct a prospective investigation. It was an 18-month longitudinal intervention study aimed at the identification of the clinical and microbiological epidemiology of the outbreak and its response to a multicomponent infection control strategy. From January 1997 to June 1998, clinical samples from 153 (8%) of 1,836 consecutive ICU patients were found to contain CR A. baumannii. Isolates were verified to be A. baumannii by restriction analysis of the 16S-23S ribosomal genes and the intergenic spacer region. Molecular typing by repetitive extragenic palindromic sequence-based PCR and pulsed-field gel electrophoresis showed that the emergence of carbapenem resistance was not by the selection of resistant mutants but was by the introduction of two new epidemic clones that were different from those responsible for the endemic. Multivariate regression analysis selected those patients with previous carriage of CR A. baumannii (relative risk [RR], 35.3; 95% confidence interval [CI], 7.2 to 173.1), those patients who had previously received therapy with carbapenems (RR, 4.6; 95% CI, 1.3 to 15.6), or those who were admitted into a ward with a high density of patients infected with CR A. baumannii (RR, 1.7; 95% CI, 1.2 to 2.5) to be at a significantly greater risk for the development of clinical colonization or infection with CR A. baumannii strains. In accordance, a combined infection control strategy was designed and implemented, including the sequential closure of all ICUs for decontamination, strict compliance with cross-transmission prevention protocols, and a program that restricted the use of carbapenem. Subsequently, a sharp reduction in the incidence rates of infection or colonization with A. baumannii, whether resistant or susceptible to carbapenems, was shown, although an alarming dominance of the carbapenem-resistant clones was shown at the end of the study.

Acinetobacter↗
PubMed2000

Detection of carbapenemase-producing Acinetobacter baumannii in a hospital.

Acinetobacter baumannii strains resistant to both imipenem (IPM) and ceftazidime (CAZ) were isolated from 1994 through 1996 at Gunma University Hospital. Nine isolates from different inpatients were examined for carbapenem-hydrolyzing activity and for the carbapemase gene bla(IMP) by the PCR method. All nine isolates were carbapenemase-producing strains that hydrolyzed IPM and that harbored bla(IMP). The bla(IMP) gene was transmissible by conjugation to an IPM-susceptible recipient strain of A. baumannii and conferred resistance to IPM, CAZ, cefotaxime (CTX), ampicillin (AMP), and piperacillin (PIP). Either intermediate or high-level resistance to amikacin (AMK) was transferred from two and five strains, respectively, concomitantly with bla(IMP), and gentamicin (GEN) resistance was also transferred in one instance of high-level AMK resistance. Comparative examination of clinical isolates for resistance patterns to nine drugs, IPM, CAZ, CTX, aztreonam, AMP, PIP, AMK, GEN, and norfloxacin, in addition to pulsed-field gel electrophoresis patterns with NotI-digested genomic DNA, confirmed nosocomial transmission of infections involving carbapenemase-producing A. baumannii strains.

Acinetobacter↗
PubMed2000

Characterization of a nosocomial outbreak caused by a multiresistant Acinetobacter baumannii strain with a carbapenem-hydrolyzing enzyme: high-level carbapenem resistance in A. baumannii is not due solely to the presence of beta-lactamases.

From February to November 1997, 29 inpatients at Ramón y Cajal Hospital, Madrid, Spain, were determined to be either colonized or infected with imipenem- and meropenem-resistant Acinetobacter baumannii (IMRAB) strains (MICs, 128 to 256 microg/ml). A wide antibiotic multiresistance profile was observed with IMRAB strains. For typing IMRAB isolates, pulsed-field gel electrophoresis was used. For comparative purposes, 30 imipenem- and meropenem-susceptible A. baumannii (IMSAB) strains isolated before, during, and after the outbreak were included in this study. The molecular-typing results showed that the outbreak was caused by a single IMRAB strain (genotype A). By cloning experiments we identified a class D beta-lactamase (OXA-24) encoded in the chromosomal DNA of this IMRAB strain which showed carbapenem hydrolysis. Moreover, the outer membrane profile of the IMRAB strain showed a reduction in the expression of two porins at 22 and 33 kDa when compared with genetically related IMSAB isolates. In addition no efflux mechanisms were identified in the IMRAB strains. In summary, we report here the molecular characterization of a nosocomial outbreak caused by one multiresistant A. baumannii epidemic strain that harbors a carbapenem-hydrolyzing enzyme. Although alterations in the penicillin-binding proteins cannot be ruled out, the reduction in the expression of two porins and the presence of this OXA-derived beta-lactamase are involved in the carbapenem resistance of the epidemic nosocomial IMRAB strain.

Acinetobacter↗
PubMed2001

Acinetobacter baumannii at a tertiary-care teaching hospital in Jerusalem, Israel.

In a retrospective 10-year analysis of 3,536 patient-unique isolates, Acinetobacter baumannii imipenem susceptibility declined from 98.1 (1990) to 64.1% (2000), and ciprofloxacin susceptibility decreased from 50.5 to 13.1%. Imipenem median zone diameters decreased from 27. 7 (1997) to 18.8 mm (2000). No outbreaks were detected. Two clusters were identified for 41 strains genotyped by pulsed-field gel electrophoresis, but imipenem resistance was not clonal.

Acinetobacter↗