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PubMed2004

In vitro activities of the beta-lactamase inhibitors clavulanic acid, sulbactam, and tazobactam alone or in combination with beta-lactams against epidemiologically characterized multidrug-resistant Acinetobacter baumannii strains.

Acinetobacter baumannii is an important nosocomial pathogen usually in the context of serious underlying disease. Multidrug resistance in these organisms is frequent. The beta-lactamase inhibitors clavulanic acid, sulbactam, and tazobactam have intrinsic activity against Acinetobacter strains. To evaluate their potential therapeutic usefulness, we determined the in vitro activity of ampicillin, sulbactam, ampicillin-sulbactam, cefoperazone, cefoperazone-sulbactam, piperacillin, piperacillin-sulbactam, tazobactam, piperacillin-tazobactam, amoxicillin, clavulanic acid, amoxicillin-clavulanic acid, ticarcillin, and ticarcillin-clavulanic acid against multidrug-resistant A. baumannii. All isolates were epidemiologically characterized by RAPD [random(ly) amplified polymorphic DNA] analysis and/or pulsed-field gel electrophoresis and represented different strain types, including sporadic strains, as well as outbreak-related strains. The MICs were determined by agar dilution on Mueller-Hinton agar (using fixed concentrations, as well as fixed ratios for beta-lactamase inhibitors) and the E-test. The majority of E-test results were within two dilutions of those recorded by agar dilution, with the exception of piperacillin-tazobactam. Sulbactam was superior to clavulanic acid and tazobactam and may represent an alternative treatment option for infections due to multiresistant A. baumannii strains. beta-Lactamase inhibitors have intrinsic activity but do not enhance activity of beta-lactams against A. baumannii. Testing with the inhibitor added at a fixed concentration as recommended for piperacillin-tazobactam and ticarcillin-clavulanic acid by the National Committee for Clinical Laboratory Standards may falsely suggest high activity or gives uninterpretable results due to trailing. If combinations are used for testing, fixed ratios may give more useful results.

Acinetobacter Infections↗
PubMed2000

Antibody response to lipopolysaccharide in patients colonized or infected with an endemic strain of Acinetobacter genomic species 13 sensu Tjernberg and Ursing.

The levels of antilipopolysaccharide (anti-LPS) antibodies in patients colonized with an endemic Acinetobacter strain were compared to those in patients with bloodstream infections. Seropositivity and seronegativity correlated with positive and negative blood cultures, respectively, indicating that determination of the level of anti-LPS antibodies is useful for diagnosing Acinetobacter infections.

Acinetobacter↗
PubMed2006

Occurrence of carbapenem-resistant Acinetobacter baumannii clones at multiple hospitals in London and Southeast England.

From late 2003 to the end of 2005, the Health Protection Agency's national reference laboratories received approximately 1,600 referrals of Acinetobacter spp., including 419 and 58 examples, respectively, of two carbapenem-resistant Acinetobacter baumannii lineages, designated OXA-23 clones 1 and 2. Representatives of these clones were obtained from 40 and 8 hospitals, respectively, in London or elsewhere in Southeast England. Both clones had blaOXA-23-like genes, as well as the intrinsic (but downregulated) blaOXA-51-like carbapenemase genes typical of A. baumannii. Both were highly multiresistant: only colistin and tigecycline remained active versus OXA-23 clone 1 isolates; OXA-23 clone 2 isolates were also susceptible to amikacin and minocycline. These lineages increase the burden created by the southeast (SE) clone, a previously reported A. baumannii lineage with variable carbapenem resistance contingent on upregulation of the blaOXA-51-like gene. Known since 2000, the SE clone had been referred from over 40 hospitals by the end of 2005, with 627 representatives received by the reference laboratories. The OXA-23 clone 2 is now in decline, but OXA-23 clone 1 continues to be referred from new sites, as does the SE clone. Their spread is forcing the use of unorthodox therapies, principally colistin and tigecycline, although the optimal regimens remain uncertain.

Acinetobacter Infections↗
PubMed2006

Horizontal gene transfer in a polyclonal outbreak of carbapenem-resistant Acinetobacter baumannii.

In the last few years, phenotypically carbapenem resistant Acinetobacter strains have been identified throughout the world, including in many of the hospitals and intensive care units (ICUs) of Australia. Genotyping of Australian ICU outbreak-associated isolates by pulsed-field gel electrophoresis of whole genomic DNA indicated that different strains were cocirculating within one hospital. The carbapenem-resistant phenotype of these and other Australian isolates was found to be due to carbapenem-hydrolyzing activity associated with the presence of the blaOXA-23 gene. In all resistant strains examined, the blaOXA-23 gene was adjacent to the insertion sequence ISAba1 in a structure that has been found in Acinetobacter baumannii strains of a similar phenotype from around the world; blaOXA-51-like genes were also found in all A. baumannii strains but were not consistently associated with ISAba1, which is believed to provide the promoter required for expression of linked antibiotic resistance genes. Most isolates were also found to contain additional antibiotic resistance genes within the cassette arrays of class 1 integrons. The same cassette arrays, in addition to the ISAba1-blaOXA-23 structure, were found within unrelated strains, but no common plasmid carrying these accessory genetic elements could be identified. It therefore appears that antibiotic resistance genes are readily exchanged between cocirculating strains in epidemics of phenotypically indistinguishable organisms. Epidemiological investigation of major outbreaks should include whole-genome typing as well as analysis of potentially transmissible resistance genes and their vehicles.

Acinetobacter Infections↗
PubMed1989

Acinetobacter baumannii serotyping for delineation of outbreaks of nosocomial cross-infection.

A total of 152 clinical isolates of Acinetobacter baumannii from 152 patients were identified by carbon source utilization tests and examined serologically. Polyclonal rabbit immune sera against A. baumannii strains were used in checkerboard tube agglutination tests, and 20 serovars were identified. One (serovar 19) cross-reacted with genospecies 3 (serovar 3), a closely related member of the genus Acinetobacter. Several outbreaks of nosocomial cross-infection caused by serovars 4 and 10 were delineated.

Acinetobacter↗
PubMed1998

Survival of Acinetobacter baumannii on dry surfaces: comparison of outbreak and sporadic isolates.

Acinetobacter spp. are important nosocomial pathogens reported with increasing frequency in outbreaks of cross-infection during the past 2 decades. The majority of such outbreaks are caused by Acinetobacter baumannii. To investigate whether desiccation tolerance may be involved in the ability of certain strains of A. baumannii to cause hospital outbreaks, a blind study was carried out with 39 epidemiologically well-characterized clinical isolates of A. baumannii for which survival times were determined under simulated hospital conditions. The survival times on glass coverslips of 22 strains isolated from eight well-defined hospital outbreaks in a German metropolitan area were compared with the survival times of 17 sporadic strains not involved in outbreaks but rather isolated from inpatients in the same geographic area. All sporadic isolates have been shown by pulsed-field gel electrophoresis to represent different strain types. There was no statistically significant difference between the survival times of sporadic strains of A. baumannii and outbreak strains (27.2 versus 26.5 days, respectively; P < or = 0.44) by the Wilcoxon-Mann-Whitney test. All investigated A. baumannii strains, irrespective of their areas of endemicity or epidemic occurrence, have the ability to survive for a long time on dry surfaces. Antimicrobial susceptibility testing showed that A. baumannii outbreak strains were significantly more resistant to various broad-spectrum antimicrobial agents than sporadic strains. Both desiccation tolerance and multidrug resistance may contribute to their maintenance in the hospital setting and may explain in part their propensity to cause prolonged outbreaks of nosocomial infection.

Acinetobacter↗
PubMed2000

Pseudo-outbreak of imipenem-resistant Acinetobacter baumannii resulting from false susceptibility testing by a rapid automated system.

Introduction of the Vitek GNS-506 susceptibility testing cards in the Hippokration General Hospital, Thessaloniki, Greece, resulted in an apparently high prevalence of imipenem-resistant Acinetobacter baumannii. When 35 of these isolates were further tested by disk diffusion, broth microdilution, and agar dilution assays, 32 were imipenem sensitive by all tests and three were sensitive or intermediate, depending on the method. The pseudoresistant acinetobacters did not form a genetically homogeneous group. It is suggested that the detection of imipenem-resistant A. baumannii isolates by this system should be confirmed by an additional susceptibility test.

Acinetobacter↗
PubMed2003

Outbreak of extended-spectrum beta-lactamase VEB-1-producing isolates of Acinetobacter baumannii in a French hospital.

Twelve clonally related and multidrug-resistant Acinetobacter baumannii isolates were recovered during a 4-month period from 12 patients hospitalized at the Valenciennes Hospital in France. Antibiograms determined by the double-disk diffusion technique on cloxacillin-containing plates detected a clavulanic acid-inhibited extended-spectrum beta-lactamase (ESBL). PCR and sequencing identified the gene encoding the Ambler class A ESBL VEB-1. This gene was located on the chromosome and was part of a class 1 integron identical to that previously identified in Pseudomonas aeruginosa isolates from Thailand. Additionally, seven clonally related bla(VEB-1)-positive A. baumannii strains were identified in the immediate environment of the hospitalized patients. This is the first report of the ESBL VEB-1 in Acinetobacter spp. and the first description of VEB-1-producing strains as a source of an outbreak occurring outside Southeast Asia. This report underlines the difficulty of the identification of ESBLs in A. baumannii.

Acinetobacter Infections↗
PubMed2004

Antimicrobial susceptibility testing of Acinetobacter spp. by NCCLS broth microdilution and disk diffusion methods.

Although both broth microdilution (BMD) and disk diffusion (DD) are listed by NCCLS as acceptable methods for testing Acinetobacter spp. for antimicrobial susceptibility, few studies have compared the results generated by the two methods. We tested 196 isolates of Acinetobacter spp. from nine U.S. hospitals and from the Centers for Disease Control culture collection by using BMD and DD and clinically appropriate antimicrobial agents. Categorical results for amikacin, ciprofloxacin, gatifloxacin, gentamicin, imipenem, levofloxacin, meropenem, tobramycin, and trimethoprim-sulfamethoxazole were comparable for the two methods: there was only one very major (VM) error, with tobramycin, and only one major (M) error, with meropenem, when DD results were compared with BMD results. However, VM errors were frequent with the beta-lactams and beta-lactam-beta-lactam inhibitor combinations, while M errors were often observed with tetracyclines. For BMD, tests frequently exhibited subtle growth patterns that were difficult to interpret, especially for beta-lactams. If subtle growth (i.e., granular, small button, or "starry" growth) was considered positive, error rates between BMD and DD were unacceptably high for ampicillin-sulbactam (VM error, 9.8%; minor [m] error, 16.1%), piperacillin (VM error, 5.7%; m error, 13.5%), piperacillin-tazobactam (VM error, 9.3%; m error, 12.9%), ceftazidime (VM error, 6.2%; m error, 11.4%), cefepime (VM error, 6.2%; m error, 13.0%), cefotaxime (m error, 21.2%), ceftriaxone (m error, 23.3%), tetracycline (M error, 11.4%; m error, 32.1%), and doxycycline (M error, 2.6%). When subtle growth patterns were ignored, the agreement still did not achieve acceptable levels. To determine if the problems with BMD testing occurred in other laboratories, we sent frozen BMD panels containing beta-lactam drugs and nine isolates to six labs with experience in performing BMD and DD. Among these laboratories, cefepime MICs ranged from < or =8 to > or =32 microg/ml for four of the nine strains, confirming the problem in interpreting BMD results. Discrepancies between the categorical interpretations of BMD and DD tests were noted primarily with cefepime and piperacillin, for which the BMD results were typically more resistant. Clinical laboratories should be aware of these discrepancies. At present, there are no data to indicate which method provides more clinically relevant information.

Acinetobacter↗
PubMed2004

Dissemination of a clone of unusual phenotype of pandrug-resistant Acinetobacter baumannii at a university hospital in Taiwan.

From December 2002 to February 2003, 15 isolates of pandrug-resistant unidentified Acinetobacter species were recovered from seven patients treated on different wards or intensive care units. Both 16S-23S rRNA intergenic spacer PCR-restriction fragment length polymorphism profiles and sequence analysis of these isolates identified them as Acinetobacter baumannii. This pandrug-resistant A. baumannii strain with an unusual phenotype could persist in humans for long periods and was widely disseminated throughout the hospital.

Acinetobacter Infections↗
PubMed2005

Development of a multilocus sequence typing scheme for characterization of clinical isolates of Acinetobacter baumannii.

In this study a multilocus sequence typing (MLST) scheme for Acinetobacter baumannii was developed and evaluated by using 40 clinical A. baumannii isolates recovered from outbreaks in Spanish and German hospitals during the years 1990 to 2001, as well as isolates from other European hospitals and two DSMZ reference strains of A. baumannii. For comparison, two isolates of Acinetobacter species 13 (sensu Tjernberg and Ursing), two clinical isolates, and three DSMZ strains of A. calcoaceticus (both belonging to the A. calcoaceticus-A. baumannii complex) were also investigated. Primers were designed for conserved regions of housekeeping genes, and 305- to 513-bp internal fragments of seven such genes-gltA, gyrB, gdhB, recA, cpn60, gpi, and rpoD-were sequenced for all strains. The number of alleles at individual loci ranged from 6 to 12, and a total of 20 allelic profiles or sequence types were distinguished among the investigated A. baumannii strains. The MLST data were in high concordance with the epidemiologic typing results generated by pulsed-field gel electrophoresis and amplified fragment length polymorphism fingerprinting. The MLST scheme provides a high level of resolution and an excellent tool for studying the population structure and long-term epidemiology of A. baumannii.

Acinetobacter Infections↗
PubMed2006

Nosocomial bacteremia due to an as yet unclassified acinetobacter genomic species 17-like strain.

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.

Acinetobacter↗
PubMed1989

Use of protein profiles to identify Acinetobacter calcoaceticus in a respiratory care unit.

The presence of acinetobacters in a respiratory care unit was prospectively studied because of an increase in the number of isolations of Acinetobacter calcoaceticus. Cell envelope protein electrophoresis was used to distinguish strains. Eleven protein patterns were observed in isolates from patients and their environment. One pattern (pattern 1) was seen in several patients and environmental samples. Another pattern (pattern 2) was identified repeatedly in samples from skin and mucous membranes of patients in the same ward. After thorough cleaning was undertaken throughout the unit, the pattern 1 strain was no longer cultivated from clinical samples. It is concluded that cell envelope protein electrophoresis is a useful method for tracing epidemic strains of A calcoaceticus.

Acinetobacter↗
PubMed1995

A case of Acinetobacter calcoaceticus pneumonia.

A case of community acquired pneumonia with Acinetobacter calcoaceticus is presented. Acinetobacter must be considered in the differential diagnosis of Gram negative coccobacillary pneumonia.

Acinetobacter Infections↗
PubMedDate not supplied

Exposure of clinical isolates of Acinetobacter baumannii and genospecies 3 to defibrinated human blood with and without added human 'natural' or (patient) immune antibodies.

Fresh defibrinated blood (65% v/v) from 2 human donors failed to completely kill strains of Acinetobacter baumannii and genospecies 3, representing four serovars each. Although colony counts were reduced > or = 90%, there invariably occurred rebound growth following extended incubation. Neither selected serovar-specific or isolate-homologous (following experimental bacteremia) rabbit immune sera nor three intravenously applicable IgG preparations augmented the bactericidal activity of human blood against six selected strains of A. baumannii and genospecies 3, despite documented antibody contents of all sera and IgG preparations employed. The majority of the sera from 22 patients who were early reconvalescent from systemic infection due to A. baumannii or genospecies 3, showed raised IgM antibody titers, and all sera demonstrated markedly elevated IgG antibody titers as determined with an enzyme-linked immunoassay. Defibrinated blood from donors B and T failed to completely kill the bacteria inocula of these 22 Acinetobacter isolates. Only one patient serum enhanced the bactericidal activity of human blood in the absence of antimicrobial drug(s), and only 1 patient serum with large amounts of detectable antimicrobial drug(s) effected complete killing of the homologous bacterial inoculum.

Acinetobacter↗
PubMed1984

Phage-types and susceptibility to 26 antibiotics of nosocomial strains of Acinetobacter isolated in Portugal.

Sixty-two strains of Acinetobacter calcoaceticus isolated from pathological samples or from the environment in several hospitals in Lisbon, were studied by means of two complementary phage-typing systems. Eighteen phage-types or sub-types, one group of uncommon types (9.6%) and one group of untypable strains (20.9%) were found. A new phage-type (No. 104) and a new sub-type (No. 18) were defined among the Portuguese strains. The in vitro activity of 26 antibiotics against 48 nosocomial strains was studied by the Kirby-Bauer method. The most active antibiotics were, in decreasing order, amikacin, carbenicillin, tobramycin, minocycline, dibekacin, doxycycline, sisomycin, trimethoprim-sulphamethoxacole, ticarcillin and piperacillin. The strains were also tested against 4 new beta-lactam antibiotics, and the MICs were determined by an agar dilution method. N-formimidoyl-thienamycin was found to be the most active against Acinetobacter and ceftazidime was considerably more active than apalcillin and cefotaxime.

Acinetobacter↗
PubMed1997

Risk factors for infection by Acinetobacter baumannii in intubated patients with nosocomial pneumonia.

STUDY OBJECTIVE: To investigate the epidemiology of infection by Acinetobacter baumannii in patients with ventilator-associated pneumonia (VAP). DESIGN: Prospective clinical study. SETTING: Three medical-surgical ICUs in teaching hospitals. PATIENTS: We followed up 707 mechanically ventilated patients and 148 episodes of VAP with etiologic diagnosis. RESULTS: A baumannii was isolated in 12 (8.1%) episodes in 148 patients. Five of these episodes were directly responsible for death. Using logistic regression analysis, the risk of VAP due to A baumannii was found to be high in patients with neurosurgery (odds ratio [OR]=10.03; 95% confidence interval [CI]=1.55 to 64.90), ARDS (OR=9.73; 95% CI=1.60 to 59.24), head trauma (OR=5.17; 95% CI=0.88 to 30.34), and large-volume pulmonary aspiration (OR=2.90; 95% CI=0.80 to 10.53). CONCLUSIONS: Intubated patients who develop pneumonia and have any of the above factors are at an increased risk of Acinetobacter infection.

Acinetobacter↗