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PubMed1997

Macrorestriction analysis (PFGE) of serologically cross-reactive serovars of Acinetobacter baumannii and genospecies 3.

Forty-two serovar reference strains of Acinetobacter baumannii and genospecies 3, which yielded major or minor, one-way or two-way (reciprocal) serological cross-reactions, were subjected to macrorestriction (SmaI, ApaI) analysis with the aid of pulsed-field gel electrophoresis (PFGE). The PFGE patterns of serovars 3 and 21 of genospecies 3 differed by 3 (SmaI) and 2-4 (ApaI) DNA fragments and thus were closely/possibly related in their genotype. Serovars 13 and 26 of genospecies 3 differed by only 2 DNA fragments (SmaI), suggesting close genetic relatedness; however, these two particular serovars of genospecies 3 appeared to be genotypically indistinguishable following restriction with ApaI. Serovars 2, 4, and 12 of genospecies 3 appeared to be unrelated to serovar 13 of genospecies 3 (SmaI); however, restriction with ApaI indicated a possible relatedness. Genospecies 3 serovars 2 and 26 differed by 5 DNA fragments (SmaI and ApaI), implying a possible relatedness. All other cross-reactive serovars examined proved to be genotypically unrelated, i.e., differed by > or = 7 DNA fragments (SmaI restriction).

Acinetobacter↗

PubMed1997

Genotypic investigation of multidrug-resistant Acinetobacter baumannii infections in a medical intensive care unit.

Multi-resistant Acinetobacter baumannii isolates obtained from 13 hospitalized patients over a six-month period were evaluated. One patient had an isolate susceptible only to imipenem; the next three had isolates susceptible to imipenem and ampicillin/sulbactam; the next six patients had isolates which were susceptible to imipenem, amikacin, and ampicillin/sulbactam; while the final three patients had isolates which were susceptible to imipenem and ampicillin/sulbactam. Ten patients died, five within 10 days of a positive culture. Five of six patients with bacteraemia succumbed to the infection. DNA extracted from all isolates was amplified by polymerase chain reaction using four random primers (RAPD). The resulting band patterns were compared and strains identified. In addition, all isolates were biotyped. RAPD analysis and biotyping showed that there were two distinct strains involved. The first four patients were infected with one strain (genotype ¿A', biotype 9), the subsequent nine patients were infected with a second strain (genotype ¿B', biotype 1). These results suggested that there was patient-to-patient spread of strains. Institution of, and strict adherence to, isolation procedure and other infection control practices controlled the spread of infection. These data emphasize the need for active surveillance for multidrug-resistant organisms in critically ill patients, and the value of molecular typing of strains in a hospital setting to investigate spread of infection.

Acinetobacter↗

PubMedDate not supplied

The role of Acinetobacter baumannii as a nosocomial pathogen for dogs and cats in an intensive care unit.

Acinetobacter baumannii is a nosocomial pathogen associated with high morbidity and mortality in humans. Whereas infections with strains of Acinetobacter species have been reported in various situations, the importance of A baumannii as a nosocomial pathogen in veterinary hospitals has not been studied so far. In this retrospective case series, we describe 17 dogs and 2 cats from which A baumannii had been isolated during a 2 1/2-year period. In 7 dogs, A baumannii induced systemic signs of illness, whereas 12 animals showed signs of local infection. In all animals with systemic infection, and in 2 with localized infection, A baumannii contributed to the death of the animal or contributed to euthanasia; the remaining 8 dogs and both cats recovered. Molecular typing of the isolates with restriction polymorphisms of ribosomal DNA provided evidence of nosocomial spread of this pathogen and for the presence of several strains of A baumannii in the hospital environment.

Acinetobacter↗

PubMed2007

Genetics and expression of the carbapenem-hydrolyzing oxacillinase gene blaOXA-23 in Acinetobacter baumannii.

The genetic structures surrounding the plasmid-carried blaOXA-23 oxacillinase gene, encoding resistance to carbapenems, were studied in Acinetobacter baumannii. ISAba1 and the novel element ISAba4 were detected upstream of the blaOXA-23 gene, providing promoter sequences for its expression. These insertion elements were likely involved in transposition processes at the origin of acquisition of this beta-lactamase gene.

Acinetobacter baumannii↗

PubMed2005

In vitro synergy test of meropenem and sulbactam against clinical isolates of Acinetobacter baumannii.

Meropenem and imipenem are often the drugs of choice for the treatment of infections due to multidrug-resistant Acinetobacter baumannii. The present study aimed at evaluating the interaction between meropenem and sulbactam through microdilution and checkerboard methods against 48 clinical isolates of A. baumannii collected from Brazilian hospitals. All the isolates presented elevated minimum inhibitory concentration (>or=2 microg/mL) to either meropenem or sulbactam. The checkerboard method with the combination of meropenem and sulbactam demonstrated 29.2% (14/48) synergism, 47.9% (23/48) partial synergism, 10.5% (5/48) additive, 6.2% (3/48) indifference, and 6.2% (3/48) antagonism (SigmaFIC(min)=0.09 and SigmaFIC(max)=8). Thus, combinations of meropenem and sulbactam may show synergism or partial synergism for most A. baumannii isolates. Further studies may help identify treatment options for patients with infections caused by these organisms, particularly with this combination, where both drugs have time-dependent activities and might be suitable for therapy optimization studies.

Acinetobacter baumannii↗

PubMed2002

In vitro investigation of the susceptibility of Acinetobacter baumannii strains isolated from clinical specimens to ampicillin/sulbactam alone and in combination with amikacin.

The sensitivity of 52 strains of Acinetobacter baumannii was determined to 13 antimicrobial drugs. All strains tested were multiresistant. Compared with MICs of amikacin and ampicillin/sulbactam alone, there was a significant decrease in MICs for both drugs when the combination was used. The results of the in vitro study of this combination showed a synergistic or partial synergistic effect in 98% of the strains.

Acinetobacter Infections↗

PubMed2005

Treatment of pan-drug resistant Acinetobacter baumannii.

The objective of this study was to investigate the role of sulbactam in the treatment of pan-drug resistant Acinetobacter baumannii (PDRAB). We studied 89 patients with PDRAB infection treated with different antibiotic regimens. Group A (n = 39) were treated with carbapenem with sulbactam and group B (n = 30) with second and third generation cephalosporins, antipseudomonas penicillins, or fluoroquinolones with aminoglycosides. We also studied the MICs for 48 PDRAB strains by using antimicrobial agents with and without sulbactam. The clinical outcomes of the 2 groups did not differ significantly, either in terms of resolution of infection (25/59, 42% in group A vs 12/30, 40% in group B) or survival (35/59, 59% vs 17/30, 57%). However, the MICs indicated that 16 of the 48 strains were sensitive to imipenem/sulbactam, compared with only 2 of the 48 to imipenem alone. The addition of sulbactam thus reversed the response in 30% (14/46) of strains initially resistant or only intermediate sensitive to imipenem. The MICs for meropenem/sulbactam were in the sensitive range for 8 of 48 strains compared to only 3 of the meropenem alone, indicating an 11% (5/45) reversal rate when sulbactam was added to meropenem. For the 38 isolates initially resistant to both carbapenems alone, imipenem/sulbactam reversed the resistance in 16% (6/38), while meropenem/sulbactam did so in only 3% (1/38). Thus, the carbapenem-sulbactam combinations did not clearly improve clinical outcome, but they did demonstrate lower MICs for the PDRAB strains tested. It may be that aggressive, early treatment of A. baumannii infections with these agents might prevent the emergence of PDRAB strains.

Acinetobacter Infections↗

PubMed2003

Multiresistant Acinetobacter baumannii isolates in intensive care units in Greece.

One hundred and twenty-one clinical isolates of Acinetobacter baumannii recovered from the intensive care units (ICUs) of nine tertiary-care hospitals in Athens, Greece were studied in order to determine whether the increasing appearance of resistant acinetobacters is due to the spread of epidemic strains. The majority of the isolates exhibited resistance to ampicillin-sulbactam, and the most common antibiotic resistance profiles comprised resistance to nine and eight of the 11 potentially active antibiotics tested, respectively. Pulsed-field gel electrophoresis showed that 68% of the isolates, recovered from all ICUs, belonged to two clonal groups, indicating inter-hospital dissemination of multiresistant A. baumannii in our region.

Acinetobacter Infections↗

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↗

PubMed1994

Emergence of multidrug-resistant isolates of Acinetobacter baumannii.

Patterns of antimicrobial resistance during an outbreak of nosocomial infections caused by Acinetobacter baumannii were studied. The medical records of all patients admitted to the hospital between February 1993 and February 1994 from whom A. baumannii was cultured were reviewed for demographic data, confirmation of the isolation report, admission date, date of first isolation of the organism, and antimicrobial use before and after the culture and susceptibility test results were obtained. The culture and susceptibility test data were reviewed for all specimens submitted to the laboratory during the review period. A total of 87 patients (mean +/- S.D. age, 37.9 +/- 8.7 years) with nosocomial infection or colonization with A. baumannii were identified. All the patients were surgical intensive care unit residents and had predisposing factors for acinetobacter infection. A total of 107 isolates of the organism were cultured from various sites; sputum was the most common source. The number of isolates per month increased steadily beginning in September 1993 and then declined over the winter. The median time between admission and first isolation of resistant A. baumannii was 11 days. Infections were manifested clinically as pneumonia (36 patients), bacteremia (8), wound infection (6), and urinary-tract infection (2). Of the 107 isolates, all were resistant to formulary cephalosporins, extended-spectrum penicillins, quinolones, and aztreonam. Only nine isolates were susceptible to one or more aminoglycosides. All the isolates were susceptible to imipenem-cilastatin. During an outbreak of nosocomial infections with A. baumannii, all or nearly all of the 107 isolates were resistant to a broad range of antimicrobials with the exception of imipenem-cilastatin, to which all the isolates were susceptible.

Acinetobacter↗

PubMed2004

The synthetic N-terminal peptide of human lactoferrin, hLF(1-11), is highly effective against experimental infection caused by multidrug-resistant Acinetobacter baumannii.

The lactoferrin-derived peptide hLF(1-11), but not its control peptide, was highly effective against five multidrug-resistant Acinetobacter baumannii strains in vitro (3 to 4 log reduction) and against four of these strains in an experimental infection in mice (2 to 3 log reduction). Therefore, this peptide is a promising candidate as a novel agent against infections with multidrug-resistant A. baumannii.

Acinetobacter Infections↗

PubMed2005

Investigation of a nosocomial outbreak of Acinetobacter baumannii producing PER-1 extended-spectrum beta-lactamase in an intensive care unit.

We investigated an outbreak of Acinetobacter baumannii in an adult intensive care unit of Kosin University Gospel Hospital in Busan, Republic of Korea. The outbreak involved 10 cases of infection by A. baumannii producing PER-1 extended-spectrum beta-lactamase over a seven-month period, and was caused by a single pulsed-field gel electrophoresis clone. The epidemic isolates were characterized by slight synergy between clavulanic acid and cefepime. Isoelectric focusing of crude bacterial extracts detected two nitrocefin-positive bands with pI values of 8.0 and 5.3. Polymerase chain reaction amplification and characterization of the amplicons by restriction analysis and direct sequencing indicated that the epidemic isolates carried a bla(PER-1) determinant. The epidemic isolates were characterized by a multidrug-resistant phenotype that remained unchanged over the outbreak, including penicillins, beta-lactam/beta-lactamase inhibitor, extended-spectrum cephalosporins and monobactams. Isolation of infected patients and appropriate carbapenem therapy were successful in ending the outbreak. Our report indicates that the bla(PER-1) resistance determinant may become an emerging therapeutic problem.

Acinetobacter Infections↗

PubMed2006

Risk factors for the isolation of multi-drug-resistant Acinetobacter baumannii and Pseudomonas aeruginosa: a systematic review of the literature.

An understanding of the epidemiology of multi-drug-resistant (MDR) Acinetobacter baumannii and Pseudomonas aeruginosa infections is necessary in order to develop strategies to curtail their spread. For this purpose, the evidence linking the isolation of MDR A. baumannii and P. aeruginosa with specific risk factors was evaluated. PubMed was searched for the 20-year period from September 1985 to September 2005, and eligible studies were considered to be those that: (1) linked the isolation of A. baumannii and P. aeruginosa with specific risk factors; (2) described the characteristics of the affected patients in detail; and (3) provided data on the antibiotic resistance profile of the isolated micro-organisms. Fifty-five studies were found referring to A. baumannii (28 with case-control methodology and 27 outbreak investigations without case-control methodology), and 42 studies were found referring to P. aeruginosa (25 with case-control methodology and 17 outbreak investigations without case-control methodology). Although heterogeneous study designs and investigated risk factors limited this analysis, it was concluded that acquisition and spread of these micro-organisms appear to be related to a large number of variables. Among the most important were deficiencies in the implementation of infection control guidelines and the use of broad-spectrum antibiotics. Use of carbapenems and third-generation cephalosporins appear to be related to the development of an MDR phenotype by A. baumannii, while carbapenems and fluoroquinolones are implicated in MDR P. aeruginosa. The diversity of risk factors associated with the development of MDR A. baumannii and P. aeruginosa suggests that a separate outbreak investigation should be performed in each hospital setting. The development of innovative control strategies is needed in order to limit the spread of these pathogens.

Acinetobacter Infections↗

PubMed2005

Channel formation by CarO, the carbapenem resistance-associated outer membrane protein of Acinetobacter baumannii.

It has been recently shown that resistance to both imipenem and meropenem in multidrug-resistant clinical strains of Acinetobacter baumannii is associated with the loss of a heat-modifiable 25/29-kDa outer membrane protein, called CarO. This study aimed to investigate the channel-forming properties of CarO. Mass spectrometry analyses of this protein band detected another 25-kDa protein (called Omp25), together with CarO. Both proteins presented similar physicochemical parameters (M(w) and pI). We overproduced and purified the two polypeptides as His-tagged recombinant proteins. Circular dichroism analyses demonstrated that the secondary structure of these proteins was mainly a beta-strand conformation with spectra typical of porins. We studied the channel-forming properties of proteins by reconstitution into artificial lipid bilayers. In these conditions, CarO induced ion channels with a conductance value of 110 pS in 1 M KCl, whereas the Omp25 protein did not form any channels, despite its suggested porin function. The pores formed by CarO showed a slight cationic selectivity and no voltage closure. No specific imipenem binding site was found in CarO, and this protein would rather form unspecific monomeric channels.

Acinetobacter baumannii↗

PubMed2005

Investigation of a nosocomial outbreak of extended-spectrum beta-lactamase VEB-1-producing isolates of Acinetobacter baumannii in a hospital setting.

A nosocomial outbreak of epidemiologically related VEB-1 extended-spectrum beta-lactamase-producing isolates of Acinetobacter baumannii occurred in 33 patients in an intensive care unit. A case-control study identified previous treatment with third-generation cephalosporins as the only risk factor for A. baumannii acquisition. Rationale for antibiotic use should be strengthened.

Acinetobacter Infections↗

PubMed2006

Low genetic diversity of the intrinsic OXA-51-like class D carbapenemases among Acinetobacter baumannii clinical isolates in Greece.

This study examined the geographical distribution and diversity of the intrinsic OXA-51-like class D carbapenemases among Acinetobacter baumannii clones recovered in three major Greek regions from 2000 to 2005. The blaOXA-66 allele was exclusively detected among clonally distinct A. baumannii isolates recovered in the regions of Thessaloniki and Larissa. This sequence was also the most widespread among A. baumannii isolates in Athens, while less frequent were blaOXA-69 and blaOXA-65 alleles. These findings highlight the high prevalence of a specific blaOXA-51-like allele in Greece, possibly indicating that our A. baumannii clones might have originated from a common ancestor. However, the possibility that blaOXA-51-like variants, with blaOXA-66 predominating, are widely disseminated among several unrelated A. baumannii strains cannot be excluded.

Acinetobacter baumannii↗

PubMed2002

Loss of a 29-kilodalton outer membrane protein in Acinetobacter baumannii is associated with imipenem resistance.

We analyzed the possible causes of imipenem (IPM) resistance in multidrug-resistant isolates of Acinetobacter baumannii. Comparison of the outer membrane protein (OMP) profiles of two genomically related strains (Ab288 [IPM sensitive] and Ab242 [IPM resistant]) indicated the conspicuous loss of a 29-kDa polypeptide in the Ab242 strain. No carbapenemase activity was detected in any of these strains. The treatment of Ab288 with sodium salicylate resulted in IPM resistance and the loss of the 29-kDa OMP. In addition, IPM-resistant clones of Ab288 which were selected by repetitive culturing in increasing concentrations of this antibiotic also showed the absence of this 29-kDa OMP.

Acinetobacter Infections↗

PubMed2005

Reliability of the E-test method for detection of colistin resistance in clinical isolates of Acinetobacter baumannii.

We compared the E-test to the broth microdilution method for testing the susceptibility of 115 clinical isolates of Acinetobacter baumannii to colistin. Twenty-two (19.1%) strains were resistant to colistin and 93 (80.8%) strains were susceptible according to the reference broth microdilution method. A categorical agreement of 98.2% was found, with only two (1.7%) very major errors. Agreement within 1 twofold dilution between the E-test and the broth microdilution was 16.5%. Complete agreement was found for the strains for which MICs fell within the range of 0.25 to 1 microg of colistin/ml. However, there was poor concordance, particularly in extreme dilutions with higher MICs by the E-test method.

Acinetobacter Infections↗