SEARCH · PubMed Health

Results for “Acinetobacter baumannii”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

PubMed2006

[Prevalence of the tetA and tetB genes as mechanisms of resistance to tetracycline and minocycline in Acinetobacter baumannii clinical isolates].

INTRODUCTION: Two hundred twenty-one Acinetobacter baumannii clinical strains were collected from 25 hospitals in Spain. The aim of this study was to analyze the prevalence of the tetA and tetB genes in a collection of A. baumannii strains that were not epidemiologically related. METHODS: The strains were distributed in 79 clones by genomic DNA analysis with low frequency restriction enzymes and pulsed-field gel electrophoresis. The MICs for tetracycline and minocycline were determined by the E-test. One strain representing each of the tetracycline-resistant clones was analyzed by polymerase chain reaction (PCR) with specific primers for the tetA and tetB genes. RESULTS: Fifty-nine (74.7%) out of the 79 clones were tetracycline-resistant (MIC > or = 16 mg/l) and 40 (50.6% of the total) were also minocycline-resistant (MIC > 1 mg/l). One strain representative of each tetracycline-resistant clone was taken to study the prevalence of the tetA and tetB genes. The PCR analysis showed that 39 strains representing the same number of clones (66%) had the tetB gene, while only 8 (13.6%) were positive for the tetA gene. Twelve strains did not have any of these genes. None of the analyzed strains had both genes. CONCLUSION: Although resistance to tetracycline in Acinetobacter baumannii clinical isolates is greater than that to minocycline, the tetB gene, which affects both antimicrobial agents, has a higher prevalence than the tetA gene, which affects only tetracycline.

Acinetobacter baumannii↗

PubMed2003

[Mechanism of carbapenems resistance in Acinetobacter baumannii].

OBJECTIVE: To investigate the mechanism of carbapenems resistance in Acinetobacter baumannii. METHODS: WHONET-5 software was used to analyze the trend of carbapenem resistance in Acinetobacter baumannii collected from 1999 to 2001 at Peking Union Medical College Hospital. Analytical isoelectric focusing was used to measure the pI of the beta-lactamase. Conjugation experiment was used to study the transfer of carbapenem resistance and plasmid DNA was extracted and purified with Qiagen Plasmid Mini Kit. The homology of the isolates was determined by pulsed field gel electrophoresis (PFGE). Integrase genes and blaIMP-, blaVIM-, blaOXA- genes for resistant isolates were amplified and sequenced. RESULTS: Imipenem resistance in A. baumannii was ranged from 1.8%-8.5%, but only 9 resistant isolates were viable. They were co-resistant to other carbapenems, ceftazidime, aztreonam, and gentamicin, and four isolates were resistant to ciprofloxacin. Impipenem resistance could not be transferred to susceptible strains. No plasmid was extracted. Each isolate produced TEM-1, AmpC, and two enzymes (pI 6.7, 6.0), which can not be inhibited by cloxacillin and clavulanic acid. Each isolate had class I intergase gene. Nine isolates were all negative for PCR of blaIMP- and blaVIM- genes, but positive for blaOXA-23 specific PCR. Sequencing found 100% homology with blaOXA-23. PFGE found 3 clones (A type: 5 isolates; B type: 3 isolates; C type: 1 isolate). Control isolates (imipenem-susceptible, but ceftazidime, ciprofloxacin, and gentamicin resistant) were also A clone. CONCLUSIONS: Production of OXA-23 carbapenemase in A. baumannii was one of the main mechanisms of carbapenems resistance at our hospital. It brings concern that imipenem-resistant clone has evoluted from nosocomial multiple-resistant strains.

Acinetobacter baumannii↗

PubMed2006

In-vitro activity of polymyxin B in combination with imipenem, rifampicin and azithromycin versus multidrug resistant strains of Acinetobacter baumannii producing OXA-23 carbapenemases.

BACKGROUND: Acinetobacter baumannii has emerged as a major nosocomial pathogen worldwide. Many of the circulating strains exhibit multi-drug resistance remaining consistently susceptible only to polymyxins. In-vitro studies have reported that polymyxins combined with carbapenems, rifampicin or azithromycin are synergistic against these strains despite in-vitro resistance to these agents alone. The use of antimicrobial combinations have therefore been advocated for the treatment of severe A. baumannii infection in man. In order to determine whether such combinations are synergistic against the prevalent clones of multi-drug resistant A. baumannii causing infection in the UK, we performed synergy testing against representative isolates using two rapid Etest methods. METHODS: The activity of polymyxin in combination with imipenem, azithromycin or rifampicin was assessed against five strains of multi-drug resistant A. baumannii encoding OXA-23 carbapenemases. Synergy studies were performed by Etest-agar dilution and a combined Etest strip method. Synergy was defined as a FICI of < or = 0.5. RESULTS: All strains were resistant to beta-lactams, carbapenems, quinolones and aminoglycosides but susceptible to polymyxins. Marked synergy was not seen with polymyxin in combination with imipenem, rifampicin or azithromycin against any of the strains. Borderline synergy (FICI = 0.5) was seen against one strain belonging to OXA-23 clonal group 2, using the Etest-agar dilution method only. CONCLUSION: In-vitro synergy with polymxyin in combination with imipenem, rifampicin or azithromycin is highly strain and method dependent. As reliable synergy could not be demonstrated against the prevalent UK multi-drug resistant strains, use of such combinations should not be used for empirical treatment of these infections in the UK. The optimal treatment for serious multi-drug A. baumannii infection and the role of combination therapy should be addressed in a prospective clinical trial.

Acinetobacter baumannii↗

PubMed2000

Cloning, nucleotide sequencing, and analysis of the gene encoding an AmpC beta-lactamase in Acinetobacter baumannii.

A clinical strain of Acinetobacter baumannii (strain Ab RYC 52763/97) that was isolated during an outbreak in our hospital and that was resistant to all beta-lactam antibiotics tested produced three beta-lactamases: a TEM-1-type (pI, 5.4) plasmid-mediated beta-lactamase, a chromosomally mediated OXA-derived (pI, 9.0) beta-lactamase, and a presumptive chromosomal cephalosporinase (pI, 9.4). The nucleotide sequence of the chromosomal cephalosporinase gene shows for the first time the gene encoding an AmpC beta-lactamase in A. baumannii. In addition, we report here the biochemical properties of this A. baumannii AmpC beta-lactamase.

Acinetobacter↗

PubMed2001

[Postsurgical meningitis caused by Acinetobacter baumannii: study of 22 cases and review of the literature].

BACKGROUND: Postsurgical Acinetobacter baumannii meningitis is associated with relevant morbidity and mortality. It has been related to neurosurgery, intraventricular catheters (IC) or CSF fistula. Thus, features, epidemiology and clinical course of this infection were studied. METHODS: Retrospective analysis of 22 episodes of nosocomial postsurgical Acinetobacter baumannii meningitis. Twenty episodes occurred in males. The mean age of patients was 46 years (range: 16-83 years). RESULTS: All patients were admitted to the ICU. In 50% of patients a history of intraventricular hemorrhage was recorded, 36% had had a skull fracture and the remaining patients had a brain tumor. In 18 cases the portal of entry was considered to be IC, in two an epidural catheter, and in two a CSF fistula. Patients showed a clinical picture indistinguishable from other types of meningitis, fever being the most common symptom (100%). CSF findings were consistent with bacterial meningitis. In one case the microorganism was recovered from blood. Fifteen patients recovered, three died as a direct result of the infection, and the remaining patients relapsed. Non recovery of patients was significantly associated with non removal of catheter (p < 0.05). CONCLUSIONS: Postsurgical Acinetobacter baumannii meningitis occurs frequently in patients previously colonized with this microorganism in other sites and is enhanced by the presence of an IC. Catheter removal is essential for recovery of patients.

Acinetobacter Infections↗

PubMed2002

Nosocomial bacteremia due to Acinetobacter baumannii: epidemiology, clinical features and treatment.

Acinetobacter baumannii is an important cause of nosocomial infections in many hospitals. It is difficult to control and infection caused is difficult to treat due to its high resistance in the environment and its ability to develop resistance to antimicrobials. Bacteremia, followed by respiratory tract and surgical wound infections, is the most significant infection caused by A. baumannii. The known risk factors for A. baumannii bacteremia are invasive procedures and the use of broad-spectrum antimicrobials. Consequently, episodes of bacteremia due to A. baumannii occur most frequently in critically-ill patients admitted to an intensive care unit. The clinical manifestations of bacteremia by A. baumannii are not specific. The most common sources of bacteremia are intravascular catheters and the respiratory tract. A. baumannii bacteremia is associated with a high crude mortality rate, but it is difficult to distinguish morbidity and mortality attributable to A. baumannii from that attributable to the common and severe co-morbidity in these patients. A. baumannii is a bacterium that appears to have a propensity for developing multiple antimicrobial resistance extremely rapidly. These data are disturbing because the therapeutic possibilities decrease while inappropriate antimicrobial treatment contributes to patient mortality. Generally, imipenem is the most active agent against A. baumannii. However, the description of imipenem-resistant A. baumannii strains is becoming increasingly common. The usual treatment for A. baumannii bacteremia is an active beta-lactam alone, preferably one with a limited spectrum. Before beginning treatment of a bacteremia by A. baumannii, it is very important to carry out a clinical evaluation of the patient to eliminate the possibility of a pseudobacteremia, and thereby avoid unnecessary treatment.

Acinetobacter Infections↗

PubMed2006

In vitro postantibiotic effect of colistin on multidrug-resistant Acinetobacter baumannii.

Infections by multidrug-resistant Acinetobacter baumannii constitute an increasing threat for critically ill patients. Colistin is often the only antimicrobial retaining activity against these strains. The postantibiotic effect (PAE) of colistin was studied on 19 isolates of A. baumannii resistant to ampicillin/sulbactam, ciprofloxacin, and carbapenems with the viable count method. The mean PAEs of 1x MIC and 4x MIC concentrations of colistin on the tested isolates were 3.90 and 4.48 h, respectively, indicating that a modified dosage scheme with increased dosing intervals might retain activity whereas minimizing the incidence of adverse effects.

Acinetobacter baumannii↗

PubMed2006

Global comparison of the membrane subproteomes between a multidrug-resistant Acinetobacter baumannii strain and a reference strain.

Acinetobacter baumannii causes severe infections in compromised patients. We combined SDS-PAGE, two-dimensional gel electrophoresis and mass spectrometry (LC-MS/MS and MALDI-TOF) to separate and characterize the proteins of the cell envelope of this bacterium. In total, 135 proteins (inner and outer membrane proteins) were identified. In this analysis, we described the expression by this bacterium of RND-type efflux systems and some potential virulence factors. We then compared the membrane subproteome of a clinical multidrug-resistant (MDR) isolate with that of a reference strain. We found that the MDR strain expressed lower levels of the penicillin-binding-protein 1b, produced a CarO protein having different primary and quaternary structures to that of the reference strain, and expressed OmpW isoforms. We also showed that the clinical strain has a high ability to form biofilms consistent with the accumulation of some outer membrane proteins (OMPs) such as NlpE or CsuD that have already been described as involved in bacterial adhesion. These features may partly explain the MDR emergence of the clinical isolate.

Acinetobacter baumannii↗

PubMed1999

Six-year prospective study of risk and prognostic factors in patients with nosocomial sepsis caused by Acinetobacter baumannii.

In this prospective study, the risk factors associated with nosocomial sepsis Caused by Acinetobacter baumannii or Pseudomonas aeruginosa were compared. Prior use of broad-spectrum antibiotics, urinary tract catheter, prior surgery, and mechanical ventilation were significantly associated with nosocomial sepsis caused by Acinetobacter baumannii. The mean prognostic factors significantly associated with mortality were known focus of infection, multiresistant Acinetobacter baumannii, and inappropriate antibiotic treatment. Adequate knowledge of these findings is important to ensure appropriate management of patients and rational use of antibiotics.

Acinetobacter↗

PubMed1998

Adherence of Acinetobacter baumannii to rat bladder tissue.

Acinetobacter baumannii, an important nosocomial pathogen, causes severe infections in patients of intensive care units, but its pathogenic attributes are unknown. Previously, the adherence of A. baumannii to cell lines has been negative in the authors' laboratory. In this work, the adherence of strains of A. baumannii of various biotypes to small pieces of rat bladder tissue was investigated. Tissue pieces were submerged into cultures of A. baumannii and sessile cells were counted after removing planktonic bacteria. Fimbriae and sessile cells were examined by transmission and scanning electron microscopy, respectively. In contrast to a uropathogenic strain of Escherichia coli, all cultures exhibited a mannose- and galactose-resistant agglutination of human group O red blood cells as well as mannose- and galactose-resistant adherence to the bladder tissue. Inhibition of exopolysaccharide synthesis did not modify adherence. Indeed, adherence, apparently unrelated to these fimbriae or to the exopolysaccharide, may be a factor contributing to the pathogenicity of A. baumannii in the urinary tract or in other tissues.

Acinetobacter↗

PubMed1996

Relevance of digestive tract colonization in the epidemiology of nosocomial infections due to multiresistant Acinetobacter baumannii.

Fecal colonization with multiresistant Acinetobacter baumannii was evaluated in 189 consecutive patients in intensive care units (ICUs) during two different 2-month periods (October-November 1993 and May-June 1994). Rectal swabs were obtained weekly from admission to discharge from the ICU. Overall, 77 patients (41%) had multiresistant A. baumannii fecal colonization; colonization was detected in 55 (71%) of the patients within the first week of their ICU stay. Clinical infections due to multiresistant A. baumannii occurred more frequently in patients with fecal colonization than in those without fecal colonization (26% vs. 5%, respectively; P < .001). The reinforcement of isolation measures between study periods reduced both the number of fecal carriers of multiresistant A. baumannii (from 52% to 31%; P < .01) and the number of patients with multiresistant A. baumannii infections (from 17% to 11%; no statistical significance). The digestive tract of ICU patients could be an important epidemiologic reservoir for multiresistant A. baumannii infections in hospital outbreaks. Further prospective studies should be undertaken to define the relative significance of digestive tract colonization compared with other body site colonizations.

Acinetobacter↗

PubMed1999

Regulation of polyphosphate kinase gene expression in Acinetobacter baumannii 252.

A strain of Acinetobacter baumannii cultured in butyric acid media was found to take up phosphate following a period of phosphate release. PCR was used to clone the polyphosphate kinase (ppk) gene from the strain. The promoter for the ppk gene was functional in the heterologous Escherichia coli host. Using RT-PCR, transcription of the ppk gene was found to be regulated by phosphate concentration.

5' Untranslated Regions↗

PubMed1993

Effect of iron-limiting conditions on growth of clinical isolates of Acinetobacter baumannii.

Different clinical isolates of Acinetobacter baumannii, typed by plasmid profile, were able to grow in iron-chelated medium by secreting iron-regulated siderophores. This iron-scavenging phenotype was associated with the production of iron-repressible catechol. Siderophore utilization bioassays showed the presence of 2,3-dihydroxybenzoic acid in the growth medium, and neither enterobactin nor aerobactin was detected in culture supernatants obtained under iron-deficient conditions.

Acinetobacter↗

PubMed1992

Esterase electrophoresis compared with biotyping for epidemiological typing of Acinetobacter baumannii strains.

Forty-nine Acinetobacter baumannii strains belonging to three biotypes and isolated from four hospitals were differentiated by electrophoretic typing of their esterases. Six main kinds of esterases were distinguished by their spectra of hydrolytic activity toward seven synthetic substrates. The electrophoretic variations of these enzymes were used to define ten zymotypes among the three biotypes. Esterase electrophoresis appeared to be more sensitive than biotyping, and could represent an additional marker for epidemiological analysis.

Acinetobacter↗

PubMed1997

Cloning and nucleotide sequence analysis of a gene encoding an OXA-derived beta-lactamase in Acinetobacter baumannii.

A clinical strain of Acinetobacter baumannii (strain Ab41) that was resistant to all beta-lactam antibiotics tested except ceftazidime, ceftriaxone, ceftizoxime, and imipenem produced three beta-lactamases: a presumptive chromosomal cephalosporinase, a TEM-1-like beta-lactamase (pI 5.4), and a novel OXA-derived beta-lactamase named OXA-21 (pI 7.0). The gene encoding OXA-21 was located in an integron. The nucleotide sequence showed three mutations compared with the sequence of OXA-3, with two being silent; the nonsilent mutation generated a substitution of Ile-217 to Met.

Acinetobacter↗

PubMed2006

Epidemiology of Acinetobacter baumannii in a university hospital in Turkey.

OBJECTIVE: Molecular epidemiologic surveillance of Acinetobacter baumannii by polymerase chain reaction-randomly amplified polymorphic DNA analysis in a university hospital for 3 consecutive study periods. RESULTS: Twelve different Acinetobacter baumannii genotypes (A-L) were detected. Although only 2 genotypes were detected during the first period and genotype A appeared to be the most common genotype, genotype D was included in these genotypes during the second study period. Genotype A completely disappeared during the third period. Although the presence of genotype C and the genotype D continued during the third period, 9 new genotypes were detected during this period. Genotype A appeared to be the most common genotype in the hospital (detected in 19 different clinics). The distribution of genotypes in clinical samples correlated with patient traffic between them. Some genotypes were found in both clinical and environmental samples. Seventeen different antibiotypes were detected, according to antibiotic susceptibility profiles. CONCLUSIONS: Environmental contamination, airborne transmission, patient transfer, and cross-contamination play important roles in epidemics caused by A. baumannii in our hospital. The distribution of genotypes can change over time, so antibiotyping is not appropriate for the epidemiological analysis of A. baumanii infection.

Acinetobacter Infections↗

PubMed1992

Identification of an epidemic strain of Acinetobacter baumannii using electrophoretic typing methods.

Nosocomial infections due to Acinetobacter baumannii dramatically increased in a Lebanese medical center following an outbreak of hostilities in Lebanon in 1984. The incidence of infection caused by this organism has remained high in this institution, thus requiring the implementation of a strain typing system to aid in infection control. Three methods were investigated for their utility in differentiating among a representative group of 36 nosocomial Acinetobacter baumannii isolates obtained over a 10 month period from specimens of hospitalized patients. Isolates were typed by antibiogram analyses, plasmid fingerprinting, and total cell protein profiles. Only three distinct total cell protein profiles were detected, with one pattern accounting for 26 (72.2%) of the isolates. However, eight different plasmid profiles were observed, with 20 (55.5%) isolates having the same profile. Eleven distinct antibiograms were seen with the most prevalent pattern occurring in 21 isolates. Twenty of the 21 (95%) isolates with the common antibiogram also had the same plasmid profile and total protein profile (44.4% of total isolates). The combination of these three typing methods was useful in tracing the spread of these organisms in the medical center. The data obtained suggest the distribution of a common strain among at least six wards of this hospital.

Acinetobacter↗

PubMed2006

Multidrug-resistant genes are associated with an 86-kb island in Acinetobacter baumannii.

A strain of multidrug-resistant Acinetobacter baumannii that caused a 26% mortality rate in a French epidemic was characterized and compared with an antibiotic-susceptible strain of A. baumannii. The multiresistant strain carries many of its antibiotic-resistance genes on an 86-kb region, whereas the susceptible strain lacks these genes in a homologous region. Characterization of this multidrug-resistant A. baumannii strain highlights the limited options for current therapy and raises concerns for future treatment options in an era in which few novel antibiotics are being developed.

Acinetobacter baumannii↗