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PubMed2005

Multi-drug-resistant Acinetobacter baumannii intra-abdominal abscess.

BACKGROUND: Multi-drug-resistant bacteria are rarely isolated from patients with acute appendicitis. METHODS: Case report and literature review. RESULTS: We report an unusual case of post-appendectomy intra-abdominal abscess with intra- operative cultures that grew multi-drug-resistant Acinetobacter baumannii. An 11-year-old boy underwent open appendectomy for perforated appendicitis. He developed a superficial surgical site infection at the Penrose drain site on the seventh postoperative day; cultures grew multi-drug-resistant Acinetobacter baumannii. A computed tomography scan revealed an intra- abdominal abscess. Open drainage was performed, and intra-operative cultures grew the same multi-drug-resistant A. baumannii along with Escherichia coli. CONCLUSIONS: Post-operative therapy with ceftriaxone may have predisposed the patient to nosocomial infection caused by multi-drug-resistant A. baumannii.

Abdominal Abscess↗
PubMed1993

Effect of sulbactam on infections caused by imipenem-resistant Acinetobacter calcoaceticus biotype anitratus.

A recent outbreak of multiresistant strains of Acinetobacter calcoaceticus biotype anitratus was observed mostly, but not exclusively, in the surgical intensive care unit in our hospital. Disk diffusion and microdilution susceptibility studies demonstrated resistance to imipenem, all aminoglycosides, and all individual beta-lactam antibiotics. Only ampicillin plus sulbactam, cefoperazone plus sulbactam, and polymyxin produced zone sizes and MICs in the susceptible ranges. Determination of MICs and MBCs demonstrated that sulbactam was the antimicrobial agent responsible for the killing of these organisms. Nine of 10 patients who were infected with imipenem-resistant Acinetobacter strains and received ampicillin plus sulbactam for > 3 days improved clinically, and in many cases organisms were eradicated from the site of isolation.

Acinetobacter Infections↗
PubMed1995

Bactericidal in-vitro activity of beta-lactams and beta-lactamase inhibitors, alone or associated, against clinical strains of Acinetobacter baumannii: effect of combination with aminoglycosides.

Five Acinetobacter baumannii strains of various phenotypes were selected on the basis of the results of a national survey in France in 1991. beta-Lactamases in Acinetobacter isolates were characterized by isoelectrofocusing. We carried out a 24 h time-kill study to assess the bactericidal effect of antibiotic alone or in combination against A. baumannii strains. The initial inoculum was 10(6) cfu/mL. Antibiotics were tested at MIC x 2 when an antibiotic was tested alone and at the MIC for each combination including ticarcillin, piperacillin, ceftazidime or imipenem with or without amikacin or netilmicin and/or beta-lactamase inhibitors. Concentration of inhibitors were: 2 mg/L for clavulanic acid, 4 mg/L for tazobactam and 8 mg/L for sulbactam. Sulbactam and tazobactam showed an intrinsic in-vitro activity against strains susceptible to ticarcillin. A complete killing at 24 h was observed when beta-lactams were combined with amikacin in comparison with antibiotics alone. Synergy was lost when the strain presented a low resistance level to beta-lactams or aminoglycosides except for ticarcillin. Combinations of sulbactam with ticarcillin showed the best bactericidal activity against strains multiresistant to beta-lactams.

Acinetobacter↗
PubMed2025

Characterization of blaOXA-542-mediated carbapenem resistance in Acinetobacter baumannii.

BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) causes multiple anatomical site infections, representing a significant public health threat. AIM: This study reports the isolation and characterization of a carbapenem-resistant A. baumannii harbouring blaOXA-542, followed by a comprehensive investigation of its antimicrobial resistance mechanisms and genomic characteristics. METHODS: Firstly, antimicrobial susceptibility testing was performed using the broth microdilution method. Subsequently, whole-genome sequencing was employed to identify and characterize the resistance and virulence determinants. The functional validation of resistance mechanisms was performed by gene knockdown and construction of expression vectors. The fitness cost of β-lactamase expression was identified by a bacterial growth kinetic test. Molecular docking was utilized to predict potential binding sites of β-lactamase and carbapenems. Finally, the genetic characteristics of the isolates were analysed through comparative genomics analyses and phylogenetic tree construction. RESULTS AND CONCLUSIONS: The results demonstrated that blaOXA-542 confers resistance to carbapenem and penicillin in A. baumannii and Escherichia coli while exhibiting no significant impact on cephalosporins. The ability of blaOXA-542 to hydrolyze meropenem was further confirmed by modified carbapenem inactivation assay (mCIM). Expression of blaOXA-542 in E. coli BL21 showed no significant growth rate alteration. Comparative analysis of the blaOXA-542 genetic environment revealed a close association with Acinetobacter pitti. This study reports the emergence of blaOXA-542-mediated carbapenem and penicillin resistance in a novel A. baumannii lineage (ST2795Pas/ST3464Oxf), highlighting the urgent need for rational antibiotic use against specific pathogens.

Acinetobacter baumannii↗
PubMed2005

OXA (beta)-lactamases in Acinetobacter: the story so far.

The emergence of carbapenem resistance in Acinetobacter baumannii has become a global concern since these beta-lactams are often the only effective treatment left against many multiresistant strains. A recent development has been the discovery of a novel group of narrow-spectrum OXA beta-lactamases in carbapenem-resistant strains, some of which have acquired the ability to hydrolyse the carbapenems. The first of these was found in a strain isolated in Edinburgh before imipenem was in use in the hospital. Whether these carbapenemases have been acquired or are part of the genetic make-up of this species has yet to be determined. More importantly, however, they represent an important stage in the evolution of antibiotic resistance in Acinetobacter. This paper discusses the emergence of these unusual enzymes over the past decade.

Acinetobacter↗
PubMed2006

High prevalence of OXA-51-type class D beta-lactamases among ceftazidime-resistant clinical isolates of Acinetobacter spp.: co-existence with OXA-58 in multiple centres.

OBJECTIVES: This study was designed to demonstrate the prevalence of the newly discovered carbapenem-hydrolysing class D enzymes, OXA-51-type and OXA-58, among clinical isolates of Acinetobacter spp. METHODS: A total of 72 isolates from six centres were studied. Isolates were screened by PCR with specific primers for bla(OXA-51-type) and bla(OXA-58). PCR products were sequence-analysed. Plasmids were digested with EcoRV and genomic DNAs were digested with PvuII. Hybridization experiments were done with digoxigenin-labelled specific probes. Macro-restriction analysis was done on SmaI-digested genomic DNAs. RESULTS: A total of 56 (77.8%) isolates were positive for bla(OXA-51-type) genes. Sequence analysis of the products from 23 selected isolates revealed the occurrence of multiple alleles in all contributing centres. The bla(OXA-58) gene was detected among 10 isolates from five centres. All were also positive for bla(OXA-51-type) genes. Among the bla(OXA-58)-positive isolates, two from the same centre were positive for a novel OXA-51 allele (OXA-86). Southern hybridization of plasmids and of genomic DNAs suggested that bla(OXA-51-type) genes are located on chromosomes whereas bla(OXA-58) genes are plasmid borne in these 10 isolates. Plasmid profiles and pulsed-field gel electrophoresis patterns indicated the spread of the bla(OXA-58) gene among multiple clones. The bla(OXA-51-type) and bla(OXA-58) co-carrier strains were mostly associated with a pandrug-resistant phenotype. CONCLUSIONS: This study indicated that bla(OXA-58)-bearing plasmids are readily spreading among multiple clones of the bla(OXA-51-type)-bearing clinical isolates of Acinetobacter spp. Since these isolates are highly resistant to antibiotics this finding indicates the existence of a significant problem in Turkish hospitals.

Acinetobacter↗
PubMed2006

Successful organ transplantation from donors with Acinetobacter baumannii septic shock.

Donor bacteremia with severe sepsis, especially due to gram-negative organisms, has been considered a contraindication to transplantation. Over a 6-month period we prospectively collected standardized data on all brain-dead, heart-beating organ donors with gram negative bacteremia and septic shock and the recipients of their organs in hospitals throughout Israel. Donors were treated with appropriate antibiotics for at least 48 hr prior to organ retrieval while recipients received 7 days of culture-specific antibiotics following transplantation. In total, 12 organs were transplanted (5 kidneys, 2 livers, 3 lungs and 2 hearts) from 3 donors with Acinetobacter baumannii bacteremia and septic shock. All patients were alive with good graft function 60 days following transplantation, apart from one of the heart recipients who died of primary nonfunction on the second postoperative day. Two recipients developed postoperative infections, none with Acinetobacter sp. (one Pseudomonas sp. urinary tract infection, one Klebsiella sp. central venous catheter sepsis).

Acinetobacter Infections↗
PubMed2001

Carriage of class 1 integrons and antibiotic resistance in clinical isolates of Acinetobacter baumannii from northern Spain.

A collection of 70 clinical isolates of Acinetobacter baumannii from Bilbao in northern Spain was examined by PCR for the presence of class 1 integron structures. The organisms comprised 21 distinct RAPD genotypes, with 10 distinct antibiogram patterns. Four different integron structures were detected in a total of 59 (84%) of the 70 isolates, with two predominant integron structures found in 20 and 30 isolates each. No clear antibiogram differences could be correlated with the presence or absence of integron structures, but sequence analysis of two of the internal integron regions indicated homology with genes encoding ANT(2'') adenyltransferase activity and AAC(6')-Ib acetyltransferase activity. Phenotypic analysis of aminoglycoside resistance profiles indicated that many isolates produced a combination of aminoglycoside-modifying enzymes, with most of the observed resistance to amikacin being associated with a gene encoding APH(3')-VI phosphotransferase, as detected by PCR. RAPD analysis indicated that all the Bilbao isolates producing APH(3')-VI were distinct from an epidemic integron-carrying and APH(3')-VI-producing Acinetobacter strain found in other regions of Spain. It is concluded that, although class 1 integrons are widely disseminated amongst clinical isolates of A. baumannii from the Bilbao region of Spain, at present they are not playing a major role in the dissemination of antibiotic resistance genes in this region.

Acinetobacter↗
PubMed2002

Population structure and antibiotic resistance of Acinetobacter DNA group 2 and 13TU isolates from hospitals in the UK.

A total of 287 Acinetobacter isolates belonging to DNA groups 2 (A. baumannii) and 13TU was collected consecutively from 46 hospitals and typed by randomly amplified polymorphic DNA fingerprinting with primers DAF-4 and ERIC-2. With a similarity coefficient of >/=72% as a cut-off value, 37 clusters of genotypically similar isolates (genotypes) were recognised. Four major clusters, found in 15, 12, 12 and 8 hospitals respectively, accounted for 42% of isolates, but only three of these predominant clusters were associated with outbreaks of infection in individual hospitals. Many of the isolates were resistant to multiple antibiotics, including expanded-spectrum beta-lactam agents, aminoglycosides, tetracyclines and fluoroquinolones, but >98% remained susceptible to carbapenems and colistin. Overall, the study demonstrated that a heterogeneous population of Acinetobacter DNA group 2 and 13TU isolates, frequently showing multiple resistance to antibiotics, was causing infections in UK hospitals, and that four predominant genotypes appeared to have disseminated among geographically distinct locations.

Acinetobacter↗
PubMed1997

Clinical importance and antibiotic resistance of Acinetobacter spp. Proceedings of a symposium held on 4-5 November 1996 at Eilat, Israel.

Members of the genus Acinetobacter, particularly multiresistant strains of A. baumannii, are implicated in a wide spectrum of nosocomial infections, including bacteraemia, secondary meningitis and urinary tract infection, but have now assumed a particularly important role as agents of nosocomial pneumonia in intensive care units (ICUs). Rapid genotyping methods for the identification and typing of these organisms have allowed a better appreciation of the epidemiology and survival of these organisms in the hospital environment. Their emergence as significant pathogens seems to be related partly to their survival ability and partly to their ability to develop resistance rapidly to the major groups of antibiotics, resulting in a considerable selective advantage in environments (such as ICUs) with widespread and heavy uses of antibiotics. Molecular and biochemical mechanisms of resistance to the major beta-lactam, aminoglycoside and quinolone groups of antibiotics have now been elucidated in some detail for these organisms, and experimental models, including a mouse model of A. baumannii pneumonia, have been developed to examine the efficacy of different therapeutic regimens for difficult-to-treat-infections caused by these bacteria. 'Non-classic' antibiotic combinations--such as ticarcillin with clavulanic acid and sulbactam--seem to show promise for treating systemic infections caused by otherwise multiresistant strains, but revised screening procedures in the pharmaceutical industry may be required in the near future to select novel compounds with activity against multiresistant Acinetobacter spp. and other emerging gram-negative, non-fermentative bacilli in general.

Acinetobacter↗
PubMed1999

Genotypic and phenotypic similarity of multiresistant Acinetobacter baumannii isolates in the Czech Republic.

The diversity of 103 clinical isolates of the Acinetobacter calcoaceticus-Acinetobacter baumannii complex obtained between 1991 and 1997 from 17 Czech hospitals was studied by ribotyping, biotyping, plasmid profiling and antibiotic susceptibility testing. According to the EcoRI ribotypes, all but one of these isolates were identified to the DNA group level: 77 isolates were allocated to DNA group 2 (A. baumannii), 14 to DNA group 3, 10 to DNA group 13 sensu Tjernberg and Ursing and one to DNA group 1 (A. calcoaceticus). In total, 50 different EcoRI ribotypes and 10 biotypes were observed. Plasmids were found in 92% of the isolates and a high variability in plasmid profiles was found in isolates of the same DNA group. The combination of typing profiles allowed two predominant groups (termed A and B) to be distinguished among the A. baumannii isolates (37 and eight isolates, respectively) that shared a specific ribotype and were highly similar in other properties. These two groups comprised both sporadic and outbreak isolates and were found in most localities. Group A and B isolates were markedly more resistant to antibiotics than most of the remaining isolates, thus representing 85% of all multiresistant isolates. The features of groups A and B corresponded to those of two epidemic clones identified recently among hospital strains in north-western Europe.

Acinetobacter Infections↗
PubMed1975

Acinetobacter anitratus infections in man.

During a period of 17 months, 142 strains of Acinetobacter anitratus were isolated from 140 patients. They were examined for biochemical characteristics, antibiotic susceptibilities to 15 chemotherapeutic drugs and clinical and epidemiologic features. Biochemical studies were necessary for positive identification of this gram negative rod. Many isolates were susceptible to kanamycin, gentamicin, polymixin B, cotrimoxazole and nalidixic acid. Most isolates were hospital acquired and had been cultured from a number of anatomic sites in the presence of a variety of clinical situations. Acinetobacter anitratus was the primary infecting organism in two cases of septicaemia (one fatal), two pneumonias, two wound infections and six urinary tract infections. Because of its potential pathogenicity this organism should not be dismissed as a harmless commensal by laboratory staff and clinicians.

Acinetobacter↗
PubMed2005

The emergence of multidrug resistant Acinetobacter species: a major concern in the hospital setting.

Acinetobacter spp. have emerged in recent years as a major cause of nosocomial infections that are associated with significant morbidity and mortality. Developing resistance patterns have prompted the suggestion that we are closer to the end of the antibiotic era with Acinetobacter than with methicillin-resistant Staphylococcus aureus (J Hosp Infect58, 2004, 167).

Acinetobacter Infections↗
PubMed1996

High resolution DNA fingerprinting of Acinetobacter outbreak strains.

AFLP is a novel high resolution fingerprinting method that can be used to delineate intraspecific relationships among a large variety of organisms, including bacteria. In the present study, this method was tested for its usefulness in the epidemiological typing of Acinetobacter strains. A total of 25 Acinetobacter strains originating from five hospital outbreaks in three countries were used. Isolates from the same outbreak displayed identical banding patterns and each set of outbreak strains could be found in one particular AFLP cluster. These data are in good agreement with the results obtained by other typing methods previously used on the same set of strains, indicating that AFLP analysis may be a valuable alternative in epidemiological typing.

Acinetobacter↗
PubMed2000

Molecular characterization of integrons in Acinetobacter baumannii: description of a hybrid class 2 integron.

Twenty Acinetobacter baumannii strains resistant to various antibiotics were analyzed for integron content and sequences of the amplification products. Sixteen clinical isolates had a class 1 integron, 2 contained an additional class 1 or class 2 integron, but no class 3 integron was detected. Thirteen strains had integrons with a single cassette: aac(3)-Ia (9 strains), ant(2")-Ia (2 strains), or aac(6')-Ib (2 strains); 1 had aac(6')-Ib and oxa20 cassettes and an unknown gene; and 1 had an integron containing ant(2")-Ia and an oxa3 cassette truncated by IS6100. The remaining strains harbored class 1 integrons with gene cassettes previously found in Enterobacteriaceae. One integron had a hybrid structure composed of intI2 and the 3' conserved segment of class 1 integrons. These data indicate that integrons play a major role in multidrug resistance in Acinetobacter.

Acinetobacter↗
PubMed2001

IMP-4, a novel metallo-beta-lactamase from nosocomial Acinetobacter spp. collected in Hong Kong between 1994 and 1998.

Between 1994 and 1998, 97 imipenem-resistant Acinetobacter isolates were identified at the Prince of Wales Hospital, Hong Kong, China. A bla(IMP) PCR product was obtained from 23 of 35 viable cultures; 12 isolates belonged to genomic DNA group 3, 8 belonged to group 2 (Acinetobacter baumannii), 2 belonged to group 13TU, and 1 belonged to group 1. The bla(IMP) homologues were sequenced from two isolates from genomic DNA group 2 and one isolate each from groups 3 and 13TU. The four sequences included an identical 738-bp open reading frame, predicted to encode a polypeptide of 246 amino acids, with 95.6% homology to IMP-1 and 89.3% homology to IMP-2. The new enzyme, designated IMP-4, was partially purified. It had a pI of 8.0 and was strongly active against imipenem and meropenem, with V(max) values 53 and 8% of that for penicillin G, respectively. Strong activity was also seen against oxyimino-aminothiazolyl cephalosporins but not against aztreonam. Hydrolytic activity was inhibited by EDTA but not by clavulanate or tazobactam. Carbapenem MICs for most bla(IMP)-positive isolates were 4 to 32 microg/ml, but one isolate with the intact gene was susceptible, with imipenem and meropenem MICs of 0.25 and 0.5 microg/ml, respectively. The latter isolate did not produce the band with a pI of 8.0, and gene expression was inferred to have been lost. None of the isolates studied in detail contained extrachromosomal DNA, and carbapenem resistance was not transmissible to Escherichia coli. Nevertheless, the presence of bla(IMP-4) in different genomic DNA groups implies horizontal transfer, and sequences resembling a GTTRRRY integrase-dependent recombination motif were identified in the flanking regions of bla(IMP-4).

Acinetobacter↗
PubMed2004

In vitro double and triple synergistic activities of Polymyxin B, imipenem, and rifampin against multidrug-resistant Acinetobacter baumannii.

Eight unrelated clinical Acinetobacter baumannii isolates resistant to all commonly used antibiotics were subjected to three-dimensional checkerboard microtiter plate dilution and time-kill studies at one-fourth of their MICs of polymyxin B, imipenem, and rifampin. Synergy was demonstrated with combinations of polymyxin B and imipenem, polymyxin B and rifampin, and polymyxin B, imipenem, and rifampin. Double combinations of polymyxin B and imipenem and of polymyxin B and rifampin were bactericidal for seven of eight isolates, and triple combinations were bactericidal for all isolates within 24 h. Future clinical studies using double and triple therapy with these antibacterials may provide an effective option against potentially lethal infection due to multiresistant Acinetobacter baumannii.

Acinetobacter Infections↗