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ABSTRACT: The members of the genus Acinetobacter are Gram-negative cocobacilli that are frequently found in the environment but also in the hospital setting where they have been associated with outbreaks of nosocomial infections. Among them, Acinetobacter baumannii has emerged as the most common pathogenic species involved in hospital-acquired infections. One reason for this emergence may be its persistence in the hospital wards, in particular in the intensive care unit; this persistence could be partially explained by the capacity of these microorganisms to form biofilm. Therefore, our main objective was to study the prevalence of the two main types of biofilm formed by the most relevant Acinetobacter species, comparing biofilm formation between the different species.
Biofilm formation at the air-liquid and solid-liquid interfaces was investigated in different Acinetobacter spp. and it appeared to be generally more important at 25°C than at 37°C. The biofilm formation at the solid-liquid interface by the members of the ACB-complex was at least 3 times higher than the other species (80-91% versus 5-24%). In addition, only the isolates belonging to this complex were able to form biofilm at the air-liquid interface; between 9% and 36% of the tested isolates formed this type of pellicle. Finally, within the ACB-complex, the biofilm formed at the air-liquid interface was almost 4 times higher for A. baumannii and Acinetobacter G13TU than for Acinetobacter G3 (36%, 27% & 9% respectively).
Overall, this study has shown the capacity of the Acinetobacter spp to form two different types of biofilm: solid-liquid and air-liquid interfaces. This ability was generally higher at 25°C which might contribute to their persistence in the inanimate hospital environment. Our work has also demonstrated for the first time the ability of the members of the ACB-complex to form biofilm at the air-liquid interface, a feature that was not observed in other Acinetobacter species.
BMC Research Notes 01/2011; 4:5.
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ABSTRACT: Non-Acinetobacter baumannii spp. are emerging among clinical Acinetobacter isolates causing nosocomial infections, and some (such as genomospecies 13TU) appear to be multidrug resistant. The prevalence of non-Acinetobacter baumannii spp. in the hospital setting is likely understated due to poor identification techniques. We report the first identification of an AdeABC-type efflux pump in an Acinetobacter genomospecies 13TU clinical isolate, its contribution to multidrug resistance, and the coexistence of three Ade-type efflux pumps in this strain.
Antimicrobial Agents and Chemotherapy 01/2011; 55(3):1285-6. · 4.84 Impact Factor
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José A Martínez,
Esther Delgado, Sara Martí,
Francesc Marco,
Jordi Vila,
Josep Mensa,
Antoni Torres,
Carles Codina,
Antoni Trilla,
Alex Soriano,
Aitor Alquezar,
Pedro Castro,
José M Nicolás
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ABSTRACT: To assess the role of antipseudomonal agents on Pseudomonas aeruginosa colonization and acquisition of resistance.
Prospective cohort study.
Two medical intensive care units.
346 patients admitted for >or= 48 h.
Analysis of data from an 8-month study comparing a mixing versus a cycling strategy of antibiotic use.
Surveillance cultures from nares, pharynx, rectum, and respiratory secretions were obtained thrice weekly. Acquisition of resistance was defined as the isolation, after 48 h of ICU stay, of an isolate resistant to a given antibiotic if culture of admission samples were either negative or positive for a susceptible isolate. Emergence of resistance refers to the conversion of a defined pulsotype from susceptible to non-susceptible. Forty-four (13%) patients acquired 52 strains of P. aeruginosa. Administration of piperacillin-tazobactam for >or= 3 days (OR 2.6, 95% CI 1.09-6.27) and use of amikacin for >or= 3 days (OR 2.6, 95% CI 1.04-6.7) were positively associated with acquisition of P. aeruginosa, whereas use of quinolones (OR 0.27, 95% CI 0.1-0.7) and antipseudomonal cephalosporins (OR 0.27, 95% CI 0.08-0.9) was protective. Exposure to quinolones and cephalosporins was not associated with the acquisition of resistance, whereas it was linked with usage of all other agents. Neither quinolones nor cephalosporins were a major determinant on the emergence of resistance to themselves, as resistance to these antibiotics developed at a similar frequency in non-exposed patients.
In critically ill patients, quinolones and antipseudomonal cephalosporins may prevent the acquisition of P. aeruginosa and may have a negligible influence on the acquisition and emergence of resistance.
European Journal of Intensive Care Medicine 10/2008; 35(3):439-47. · 5.17 Impact Factor
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Jesús Oteo,
Carmen García-Estébanez,
Silvia Migueláñez,
José Campos, Sara Martí,
Jordi Vila,
Maria Angeles Domínguez,
Fernando Docobo,
Nieves Larrosa,
Alvaro Pascual,
Vicente Pintado,
Pere Coll
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ABSTRACT: To investigate relevant clinical and microbiological features of Acinetobacter baumannii in Spanish hospitals and to establish the genotypic diversity of imipenem resistant isolates.
Seven Spanish hospitals collected 354 consecutive isolates that were subjected to antimicrobial susceptibility testing by standard methods. Further genetic analysis was determined by PFGE in a subset of 135 isolates from three hospitals selected because each of them presented high-, medium-, and low imipenem resistance rates.
Most isolates were from males (61.9%), age >65 years (52.3%), admitted to ICU (35.6%), and isolated from the respiratory tract (31.1%). Rates of carbapenem- and sulbactam resistance were 44.9% and 39.9%, respectively. Colistin was active against multiresistant isolates. Rates of imipenem resistance varied according to individual hospital (average: 43.8%; range: 13.5%-85.0%), medical department (more prevalent in ICU), and clinical sample (higher in isolates from the respiratory tract). Of the 135 isolates studied by PFGE (64 of them imipenem-resistant), 115 (85.1%) were distributed among 14 clusters and 20 were unrelated. Of the imipenem-resistant isolates, 45 (70.3%) belonged to six clusters that also had imipenem- susceptible isolates; 14 constituted four exclusive clusters, and five were unrelated.
Acquisition of imipenem resistance in A. baumannii is likely due to both clonal and non-clonal dissemination; resistance rates strongly vary between different hospitals and even between different hospital departments.
The Journal of infection 10/2007; 55(3):260-6. · 4.13 Impact Factor
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ABSTRACT: Acinetobacter baumannii is an opportunistic pathogen, causing infections mainly in patients in intensive care units where the extensive use of antimicrobial agents can select for the emergence of multiresistant strains. In fact, since strains resistant to all antimicrobial agents have been reported, A. baumannii is considered the paradigm of multiresistant bacteria. Both acquired and intrinsic resistance can contribute to multiresistance. The ability to acquire multidrug resistance can be due to either the acquisition of genetic elements carrying multiple resistant determinants or mutations affecting the expression of porins and/or efflux pump(s), which can affect unrelated antimicrobial agents. Meanwhile, intrinsic resistance can be generated by the interplay of decreased permeability and constitutive expression of active efflux systems and it too can affect unrelated antimicrobial agents. This review is focused on the current knowledge of porins and efflux pump(s) in this microorganism.
Journal of Antimicrobial Chemotherapy 07/2007; 59(6):1210-5. · 5.07 Impact Factor
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ABSTRACT: We describe a case of bacteremia due to an as yet unclassified Acinetobacter genomic species 17-like strain. The recognition of this microorganism as non-Acinetobacter baumannii may have important epidemiological implications, as it relieves the hospital of the implementation of barrier precautions for patients infected or colonized as may be necessary with a multiresistant A. baumannii epidemic.
Journal of Clinical Microbiology 05/2006; 44(4):1587-9. · 4.15 Impact Factor
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ABSTRACT: Acinetobacter baumannii is a multiresistant opportunistic nosocomial pathogen. A protein fraction was purified and analyzed by 2-DE. Twenty-nine major protein spots were selected for protein identification using trypsin digestion and MS analysis. As the A. baumannii genome has not yet been described, protein identification was performed by homology with other Acinetobacter species in the NCBi database. We identified ribosomal proteins, chaperones, elongation factors and outer membrane proteins (Omp), such as OmpA and the 33-36-kDa OMP. Proteomic analysis of A. baumannii provides a platform for further studies in antimicrobial resistance.
Proteomics 05/2006; 6 Suppl 1:S82-7. · 4.43 Impact Factor
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ABSTRACT: 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.
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.
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.
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.
Enfermedades Infecciosas y Microbiología Clínica 02/2006; 24(2):77-80. · 1.49 Impact Factor
