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PubMed2002

Distribution of beta-lactamases in Acinetobacter baumannii clinical isolates and the effect of Syn 2190 (AmpC inhibitor) on the MICs of different beta-lactam antibiotics.

The distribution of beta-lactamases in a group of 20 epidemiologically well defined Acinetobacter baumannii clinical isolates and the in vitro activity of Syn 2190, a novel beta-lactamase AmpC inhibitor, were determined. Twenty-five per cent of the strains carried and expressed a TEM-type beta-lactamase, whereas 35% had an OXA-type beta-lactamase. In nine out of 11 (82%) ceftazidime-resistant and four out of 13 (30.7%) cefepime-resistant strains, the MIC of these beta-lactam antibiotics decreased when determined in the presence of Syn 2190. Thus, our results suggest that in a high percentage of A. baumannii clinical isolates the increased production of AmpC, in combination or not with other resistance mechanisms, contributes to the resistance pattern in A. baumannii to beta-lactams.

Acinetobacter Infections↗
PubMed2003

Partial characterization of a transposon containing the tet(A) determinant in a clinical isolate of Acinetobacter baumannii.

A genomic library from one clinical isolate of Acinetobacter baumannii was obtained to find genes responsible for tetracycline resistance. Escherichia coli DH5alpha-MDR transformants, selected on Mueller-Hinton agar supplemented with tetracycline 18 mg/L, were thoroughly characterized. In one clone, with an insert of 7,070 bp, it was found that the resistance to tetracycline was mediated by the tet(A) gene (1,200 bp) which encodes a tetracycline efflux pump. This gene was recovered together with tetR(A) (651 bp), the tet(A) repressor. Moreover, the partial sequence (2,008 bp) of a transposase gene, tnpA, and 1,316 bp corresponding to an IS, similar to that described in one strain of Salmonella typhi (IS4321), were found. In this A. baumannii clinical isolate, the tet(A) gene is located in a transposon. The structure of this transposon is similar to that of Tn1721, with the tet(A), tetR(A) and the regions between these genes, being closely related to those of Tn1721. The data indicate horizontal transfer of tetracycline resistance genes between A. baumannii and other genera sharing the same ecological niches.

Acinetobacter Infections↗
PubMed2003

Frequencies and mechanisms of resistance to moxifloxacin in nosocomial isolates of Acinetobacter baumannii.

OBJECTIVES: To compare the in vitro activity of moxifloxacin and ciprofloxacin against 226 nosocomial isolates of Acinetobacter baumannii from 44 hospitals in the UK. METHODS: MICs of ciprofloxacin and moxifloxacin were determined by Etest. PCR analysis was used to detect chromosomal mutations in the gyrA and parC genes. Isolates resistant to ciprofloxacin and susceptible to moxifloxacin were examined for the ability to generate spontaneous moxifloxacin-resistant isolates. RESULTS: Of 226 isolates, 49.1% were resistant to ciprofloxacin and 39.4% were moxifloxacin-resistant according to BSAC criteria. Approximately 20% of isolates resistant to ciprofloxacin remained susceptible to moxifloxacin. A GyrA mutation at Ser-83 was found in all ciprofloxacin-resistant isolates. Single mutations in both the gyrA and parC genes at codons Ser-83 and Ser-80, respectively, were found in ciprofloxacin- and moxifloxacin-resistant isolates. Isolates that were ciprofloxacin-resistant but moxifloxacin-susceptible generated spontaneous moxifloxacin-resistant mutants when grown on medium containing up to 8x their initial MIC. However, these mutants were not stable and none displayed high-level moxifloxacin resistance. CONCLUSIONS: Moxifloxacin retained in vitro activity against some ciprofloxacin-resistant clinical A. baumannii isolates. Mutations in both gyrA and parC were necessary for resistance to moxifloxacin in most isolates of A. baumannii.

Acinetobacter Infections↗
PubMed2004

In vitro and in vivo activity of meropenem and sulbactam against a multidrug-resistant Acinetobacter baumannii strain.

OBJECTIVES: The potential therapeutic role of meropenem combined with sulbactam against a clinical endemic isolate of multidrug-resistant Acinetobacter baumannii, Ab-153, was investigated. METHODS: The antimicrobial susceptibility of Ab-153 to various drugs was studied by the agar dilution method and Etest strips. The antibacterial activity of meropenem and sulbactam were investigated by a time-kill study in vitro and further examined for therapeutic efficacy in vivo in a murine model. RESULTS: In the time-kill study, at a concentration of 0.5 x MIC (4 mg/L) of meropenem, 1 x MIC (8 mg/L) of sulbactam and both in combination, only the combination demonstrated bactericidal effects and there was at least a 5 log(10) reduction in bacterial colony counts after 48 h, compared with either drug alone. BALB/c mice infected with 2.1-2.6 x 10(7) cfu of Ab-153 were treated with 20 mg/kg meropenem every 8 h, 40 mg/kg sulbactam every 8 h or both in combination. The survival rate of mice in the combination group was significantly higher than that in the meropenem-treated or sulbactam-treated group (87% versus 35%, P = 0.0004; 87% versus 30%, P = 0.0002). CONCLUSIONS: Meropenem in conjunction with sulbactam can exhibit more potent antimicrobial activity against Ab-153 than meropenem or sulbactam alone.

Acinetobacter Infections↗
PubMed2004

Long-term dissemination of an OXA-40 carbapenemase-producing Acinetobacter baumannii clone in the Iberian Peninsula.

OBJECTIVE: The main objectives of this study were to assess the clonal relatedness of Acinetobacter baumannii carbapenem-resistant isolates recovered from the Iberian Peninsula and to investigate the production of carbapenemases. METHODS: One hundred and sixty-two imipenem-resistant A. baumannii isolates were collected from 1998 to 2003 in three Portuguese university hospitals. An imipenem-resistant isolate (988FFP strain) recovered in 1995 from a smaller hospital unit, was also included, as well as an OXA-40-producing A. baumannii Spanish strain (SM28). Susceptibility tests were carried out by disc diffusion and Etest methods. DNA fingerprints were obtained by PFGE of ApaI-digested chromosomal DNA. Carbapenemase activity was determined by a bioassay and spectrophotometry. The detection of the blaOXA-40 gene was conducted through PCR analysis, cloning and nucleotide sequencing. RESULTS: All the isolates presented a similar multi-resistance pattern, including imipenem (MIC >32 mg/L). The Iberian isolates showed an identical PFGE pattern with minor band variations, including isolate 988FFP collected in 1995. PCR results revealed a blaOXA-type gene in 65 isolates and nucleotide sequence analysis revealed the presence of the blaOXA-40 gene in seven representative Portuguese isolates from the various geographically dispersed hospitals. CONCLUSIONS: Our results indicate that a multi-resistant epidemic clone of A. baumannii, carrying blaOXA-40, is disseminated in the Iberian Peninsula, persisting in Portugal since 1995.

Acinetobacter Infections↗
PubMed2004

Selection of topoisomerase mutations and overexpression of adeB mRNA transcripts during an outbreak of Acinetobacter baumannii.

OBJECTIVES: To investigate the mechanism of ciprofloxacin resistance in isolates of Acinetobacter baumannii during two hospital outbreaks and to determine the expression level of the gene encoding the AdeB efflux pump. METHODS: Isolates were previously typed by PFGE and their MICs determined by broth microdilution. The gyrA and parC genes were sequenced and the adeB gene examined by real-time reverse transcription PCR (RT-PCR). RESULTS: Two clonal lineages were responsible for the two hospital outbreaks. In both outbreaks, ciprofloxacin susceptibility was reduced during the course of the outbreak when compared with the index isolates. Mutations in gyrA and parC were found to have occurred during the outbreak. The MICs of non-fluoroquinolone antibiotics were raised in one clonal lineage and this was associated with a >10-fold increase in mRNA transcripts for adeB. CONCLUSIONS: We have witnessed the appearance of gyrA and parC mutations during outbreaks of A. baumannii. In parallel with these mutations, we observed up-regulation of the adeB gene associated with a decrease in susceptibility to non-fluoroquinolone antibiotics. These data illustrate the propensity for A. baumannii to develop multi-drug resistance rapidly.

Acinetobacter Infections↗
PubMed2004

Antibiotic combinations for serious infections caused by carbapenem-resistant Acinetobacter baumannii in a mouse pneumonia model.

OBJECTIVES: Successful therapy of carbapenem-resistant Acinetobacter baumannii strains has been reported with colistin, but recently we argued against its use as monotherapy because of the poor results obtained in a mouse pneumonia model. Our aim was to identify antibiotic combinations that were valid therapeutic alternatives in the same model. METHODS: We used two carbapenem-resistant A. baumannii strains (D and E; MICs of imipenem, 8 and 512 mg/L, respectively). MICs of tobramycin, rifampicin and colistin for both strains were 8, 8 and 0.5 mg/L, respectively. RESULTS: In infections caused by strain D, lung bacterial counts (log(10) cfu/g, mean +/- s.d.) were: controls (10.86+/-0.25), imipenem (5.99+/-0.59, P < 0.05 versus controls), and colistin (10.43 +/- 1.09); imipenem + tobramycin was the most active combination (5.46+/-0.62, P < 0.05 versus controls). In infections caused by strain E, results were: controls (10.82+/-0.33), rifampicin (5.62+/-0.26, P < 0.05 versus controls), colistin (8.38+/-1.22, P < 0.05 versus controls), and imipenem (11.01+/-0.2); rifampicin + imipenem (3.79+/-0.99) and rifampicin + tobramycin (3.96+/-0.30) were the most active combinations (P < 0.05); results with rifampicin + colistin (5.59+/-1.17) were similar to those with rifampicin alone. CONCLUSIONS: Our data indicate that imipenem can still be the best alternative for carbapenem-resistant A. baumannii infections with moderate levels of imipenem resistance, preferably combined with aminoglycosides. For strains highly resistant to imipenem, a combination of rifampicin with imipenem, tobramycin or colistin may be useful, if resistance to rifampicin is only moderate.

Acinetobacter Infections↗
PubMed2004

A nosocomial outbreak of Acinetobacter baumannii isolates expressing the carbapenem-hydrolysing oxacillinase OXA-58.

OBJECTIVE: The aim of this study was to analyse the spread of the bla(OXA-58) gene as a source of carbapenem resistance in Acinetobacter baumannii in the burns unit of a university hospital in Toulouse in 2003-2004. METHODS: Six carbapenem-resistant A. baumannii isolates from six patients, and a carbapenem-resistant environmental A. baumannii isolate were collected in the burns unit of the Rangueil hospital (Toulouse). Susceptibility tests were carried out by disc diffusion and agar dilution methods. The detection of the bla(OXA-58) gene was conducted by PCR followed by sequence analysis. Plasmids were extracted and hybridized with a probe specific for bla(OXA-58). DNA fingerprints were obtained by pulsed-field gel electrophoresis of ApaI- or SmaI-digested chromosomal DNA of the tested strains. RESULTS: The multidrug-resistant clinical isolates had a similar 30 kb plasmid that encoded the carbapenem-hydrolysing beta-lactamase OXA-58. These isolates were clonally related. The unrelated environmental carbapenem-resistant A. baumannii isolate had a similar bla(OXA-58)-carrying plasmid, suggesting spread of this gene. CONCLUSIONS: A novel oxacillinase was the source of carbapenem resistance in the A. baumannii isolates. Its gene was plasmid-, but not integron-borne.

Acinetobacter Infections↗
PubMed2006

Outbreak of multiple clones of imipenem-resistant Acinetobacter baumannii isolates expressing OXA-58 carbapenemase in an intensive care unit.

OBJECTIVES: To investigate the resistance mechanisms and the genetic relationship of imipenem-resistant Acinetobacter baumannii isolates recovered in the intensive care unit (ICU) of a tertiary care hospital. METHODS: Imipenem-resistant A. baumannii clinical and environmental isolates were collected in the ICU of the Red Cross General Hospital, Athens, Greece between March and October 2002. The isolates were tested by Etest MBL, PCR, RT-PCR and sequencing for carbapenemase-encoding genes, PFGE and synergy experiments using meropenem and the efflux pump inhibitor carbonyl cyanide chlorophenylhydrazone. RESULTS: During the study period, 15 clinical and two environmental imipenem-resistant (MIC 8 to >128 mg/L) A. baumannii isolates were recovered. PFGE showed six different clones that included both clinical and environmental isolates. All 17 isolates were negative by Etest MBL and PCR for genes bla(IMP), bla(VIM), bla(SPM), bla(OXA-23-like) and bla(OXA-24-like). Genes bla(OXA-51-like) and bla(OXA-58-like) were amplified from 15 and 14 isolates, respectively. Sequencing of bla(OXA-51-like) amplicons identified bla(OXA-66) (nine cases) and bla(OXA-69) (six cases), whereas bla(OXA-58-like) sequences were classical bla(OXA-58). Reverse transcriptase-PCR showed that bla(OXA-51-like) genes were expressed in 12 and bla(OXA-58) in 10 isolates; in these isolates, inhibition of OXA enzymes by 200 mM of NaCl reduced carbapenem MICs by up to 4-fold. Overexpression of proton-gradient dependent efflux pumps did not contribute to carbapenem resistance in any isolate. Similarly, although AmpC expression was demonstrated in eight isolates, inhibition of AmpC with cloxacillin did not reduce the MICs of carbapenems significantly. CONCLUSIONS: These findings indicate wide dissemination of OXA-58 carbapenemase, which contributes, at least partially, to the imipenem resistance of unrelated A. baumannii isolates in our ICU.

Acinetobacter Infections↗
PubMed2006

Evolution of multidrug-resistant Acinetobacter baumannii isolates obtained from elderly patients with respiratory tract infections.

OBJECTIVES: To study the evolution between 1999 and 2002 and mechanisms of antibiotic resistance in a multidrug-resistant Acinetobacter baumannii clone predominant in isolates from elderly patients with respiratory tract infections. METHODS: Susceptibility to antimicrobials was determined using an agar dilution method. Bacterial clones were identified by PCR-fingerprinting and PFGE with ApaI. Carbapenemases were detected by phenotypic tests; by PCR with primers specific for bla (OXA-40), bla(IMP), bla(VIM-1) and bla(VIM-2); and by hybridization with DNA probes. Class 1 integrons were detected using PCR. RESULTS: In 1999 isolates were grouped into two main genotypes: clone I (33%) and clone II (55%). These were also detected in 2002 with a different distribution: clone I (69%), clone II (22%). Resistance to amikacin, meropenem and imipenem increased significantly in clone I over this time, whereas clone II was not affected. In 2002, the incidence of bla(OXA-40) rose to 91% in clone I isolates with some also harbouring bla(VIM-2) and bla(IMP) genes. Different class 1 integrons were detected ranging in size from 550 to 1200 bp. No relationship was found between carbapenemases and class 1 integrons. CONCLUSIONS: In elderly patients, a single clone became predominant among A. baumannii isolates, coinciding with an increase in antibiotic resistance rates. The majority of isolates harboured the bla(OXA-40) carbapenemase gene and some of them also harboured bla(VIM-2) and bla(IMP) genes. The presence of class 1 integrons also increased over time.

Acinetobacter Infections↗
PubMed2006

Comparison of mortality of patients with Acinetobacter baumannii bacteraemia receiving appropriate and inappropriate empirical therapy.

OBJECTIVES: To evaluate the effect of inappropriate empirical antimicrobial treatment on the mortality of patients with Acinetobacter baumannii bacteraemia. METHODS: Retrospective cohort study of patients with A. baumannii bacteraemia hospitalized at the Henry Dunant hospital from January 2002 to December 2004. RESULTS: Among 40 patients with A. baumannii bacteraemia, 22 (55%) and 18 (45%) received inappropriate and appropriate antibiotic therapy, respectively, during the 3 day period after obtaining the blood culture(s) from which the pathogen was isolated. Failure to cure the infection was more common in the first group [16/22 patients (72.7%) versus 5/18 (27.8%), P = 0.005]. Although without statistical significance, probably due to the small number of studied patients, considerably increased mortality was noted in the first group compared with the second group [13/22 patients (59.1%) versus 6/18 (33.3%), P = 0.10]. CONCLUSIONS: A. baumannii bacteraemia was associated with worse outcome regarding the cure of infection in patients who received inappropriate empirical antimicrobial treatment compared with those who received appropriate treatment.

Acinetobacter Infections↗
PubMed2006

Emergence of PER and VEB extended-spectrum beta-lactamases in Acinetobacter baumannii in Belgium.

OBJECTIVES: Strains of Acinetobacter baumannii producing the extended-spectrum beta-lactamase (ESBL) PER-1 are widespread in Turkey and have also been reported from Korea and France. In contrast, A. baumannii producing the ESBL VEB-1 have only been reported from France, where one strain was responsible for a nationwide outbreak in 2003-2004. Here we describe the emergence of strains of A. baumannii producing VEB-1 and PER- 1 in Belgium. METHODS: Belgian hospitals were alerted in December 2003 to the emergence in France of VEB-1-producing A. baumannii susceptible only to meropenem and colistin. Isolates with a compatible susceptibility profile were sent to a single central laboratory for VEB-1 confirmation, molecular characterization and typing. RESULTS: From December 2003 to March 2005, three hospitals located close to the French border and one in the Brussels area reported isolation of eight A. baumannii isolates compatible with the French epidemic clone. Using PCR, six were identified as VEB-1-positive and two as PER-1-positive. All the VEB-1-positive isolates were clonally related by PFGE and by integron analysis to the French epidemic strain. The PER-1-positive strains were indistinguishable by PFGE but not related to the known French isolate or to several Turkish isolates. Both genes were chromosomally encoded. CONCLUSIONS: This work illustrates the inter-country spread of VEB-1-producing A. baumannii isolates as well as the emergence of PER-1-producing A. baumannii strains in Belgium.

Acinetobacter Infections↗
PubMed2006

Rifampicin/imipenem combination in the treatment of carbapenem-resistant Acinetobacter baumannii infections.

BACKGROUND: In the setting of a large endemic of Acinetobacter baumannii infections, treatment of those due to carbapenem-resistant strains, susceptible only to colistin, has become a major problem in our hospital during the past years. Successful results have been reported using colistin, but clinical experience with this antibiotic is limited. In our experimental studies using these strains in a mouse pneumonia model, the best results were observed with a combination of rifampicin and imipenem. METHODS: From July 2000 to September 2001, we performed a pilot study with patients suffering from serious infections due to carbapenem-resistant A. baumannii. Patients were treated with a rifampicin/imipenem combination and followed up prospectively. Cultures were repeated during and after treatment, and in vitro activity of rifampicin was monitored. Genotyping of these strains was performed by means of PFGE. RESULTS: Ten patients were selected: four with ventilator-associated pneumonia, and six with other infections (one catheter-related bacteraemia, five surgical infections). Three patients died, two of whom were considered therapeutic failures. In five of the seven patients who were cured, other procedures were also performed such as surgical drainage or catheter removal. In vitro development of high resistance to rifampicin was shown in seven (70%). PFGE demonstrated that initial isolates and high-resistant strains belonged to the same clones. CONCLUSIONS: The results of our study argue against the use of a rifampicin/imipenem combination for the treatment of carbapenem-resistant A. baumannii infections. However, combinations of rifampicin with other antibiotics merit further studies.

Acinetobacter Infections↗
PubMed2006

Prevention of rifampicin resistance in Acinetobacter baumannii in an experimental pneumonia murine model, using rifampicin associated with imipenem or sulbactam.

OBJECTIVES: To examine the development of rifampicin resistance in multidrug-resistant Acinetobacter baumannii exposed to rifampicin and the prevention of the appearance of rifampicin-resistant mutants when rifampicin is used in association with imipenem or sulbactam. METHODS: A clinical strain of multidrug-resistant A. baumannii was used to examine the frequency of resistance to rifampicin in vivo, in a pneumonia model in immunocompetent C57BL/6 mice. The in vitro and in vivo prevention of the development of resistance to rifampicin was analysed using rifampicin alone or in association with imipenem or sulbactam, in time-kill studies and in the experimental murine pneumonia, respectively. RESULTS: Rifampicin-resistant mutants were found at 48 and 72 h, both in vitro and in vivo, when rifampicin was used alone, with the MIC increasing from 4 to > or =128 mg/L. The in vivo frequency of rifampicin-resistant mutants was 3 x 10(-6). On the contrary, no resistant mutants appeared after 72 h, in vitro or in vivo, when rifampicin was employed in association with imipenem or sulbactam. After six daily passages in rifampicin-free agar plates the resistant mutants maintained the high resistance to rifampicin (> or =128 mg/L). CONCLUSIONS: These results suggest that rifampicin must not be used alone in the treatment of infections caused by multidrug-resistant A. baumannii. In these cases, rifampicin may be used in combination with imipenem or sulbactam, which prevent the development of resistance to rifampicin.

Acinetobacter Infections↗
PubMed2006

Cure of multiresistant Acinetobacter baumannii central nervous system infections with intraventricular or intrathecal colistin: case series and literature review.

OBJECTIVES: CNS infections due to multiresistant Acinetobacter baumannii (MRAB) are an emerging problem in neurosurgical patients. Colistin remains one of the few remaining treatment options for MRAB but has poor CNS penetration. We describe our experience with intraventricular or intrathecal colistin for this infection. METHODS: Cases known to have received intraventricular or intrathecal colistin for CNS infections due to MRAB were retrospectively reviewed regarding colistin treatment, colistin efficacy and adverse events. RESULTS: Five patients were identified. All were admissions to the neurosurgical ICU and all were cured of their CNS infections. Three cases were complicated by drug-induced aseptic meningitis or ventriculitis. CONCLUSIONS: This largest case series to date shows that direct instillation of colistin into the CNS may cause chemical meningitis or ventriculitis but it is an effective treatment option for MRAB CNS infection. Further study of dosing regimens is needed.

Acinetobacter Infections↗
PubMed1978

Acinetobacter calcoaceticus outbreak associated with peritoneal dialysis.

Investigation of an outbreak of contamination of dialysis drainage fluid with Acinetobacter calcoaceticus var. anitratus identified a previously unrecognized source for dialysis associated infections. Over a 4-month period, 25 peritoneal dialysis treatments were administered to 13 hospital patients. Of the 25 treatments for which culture results were available, 14 were associated with dialysis drainage fluid cultures positive for A. calcoaceticus. A water bath used to warm bottles of peritoneal dialysate before use was the reservoir for the bacteria, and investigation showed in vitro that bath water could contaminate the dialysate. It appears likely that the dialysate became contaminated when the prong of the fluid administration set was inserted through the rubber bung on the dialysate bottles. This outbreak illustrates the potential importance of environmental reservoirs in infections complicating peritoneal dialysis.

Acinetobacter↗
PubMed1990

Epidemic bacteremia due to Acinetobacter baumannii in five intensive care units.

From March 5, 1986 to September 4, 1987, Acinetobacter baumannii (AB) was isolated from blood or vascular catheter-tip cultures of 75 patients in five intensive care units at a hospital in New Jersey. To identify risk factors for AB bacteremia in the intensive care units, a case-control study was conducted. Characteristics of 72 case-patients were compared with those of 37 controls. Case-patients were more likely than controls to have had peripheral arterial catheters (odds ratio (OR) = 7.0, p less than 0.001), mechanical ventilation (OR = 5.8, p less than 0.001), hyperalimentation (OR = 5.7, p less than 0.001), or pulmonary arterial catheters (OR = 3.9, p less than 0.001). Arterial catheters were used with reusable pressure transducers for intravascular pressure monitoring. A logistic regression analysis identified four independent risk factors: transducers, ventilation, hyperalimentation, and days of transducer use at an insertion site. The strongest influence on the risk of AB bacteremia was exerted by number of days of transducer usage. Cultures of 70 transducer diaphragms or domes, 42 in-use and 28 in-storage, were positive for AB in 21% and 46%, respectively. Plasmid analysis showed that patient blood cultures and transducer isolates were identical. Transducers were wiped with alcohol in the units between patient uses. Since reusable transducers appeared to be the source of this outbreak, it is recommended that reusable transducers receive either high level disinfection or sterilization between patient uses.

Acinetobacter↗
PubMed1995

Nosocomial bacteremia due to Acinetobacter baumannii. Clinical features, epidemiology, and predictors of mortality.

To study the possible predisposing factors, clinical features, molecular epidemiology, and factors affecting mortality associated with bacteremia due to Acinetobacter baumannii, we reviewed 87 episodes of A. baumannii bacteremia occurring in 79 patients hospitalized at 2 university tertiary care centers and 4 community-based hospitals during a recent 18-month period. Plasmid DNA analysis and analysis of genomic DNA with pulsed-field gel electrophoresis was performed to investigate possible epidemiologic relationship. All patients acquired their infections in the hospital, and no seasonal variation was observed. Among patients with A. baumannii bacteremia, 91% were hospitalized in an intensive care unit, 99% had indwelling vascular catheters, 81% received prior broad spectrum antimicrobial therapy, 70% were mechanically ventilated, and 47% had major surgical procedures. In 39 cases (45%) the infection was related to indwelling vascular access devices. Other infections included pneumonia (9%), tracheobronchitis (22%), meningitis (2%), and burn wound infections (4%). Septic shock occurred in 30% of patients. All isolates were multidrug resistant. Polymicrobial bacteremia was observed in 35% of cases. The crude mortality rate was 44%. Death was considered attributable to A. baumannii bacteremia in 15 (19%) patients. All patients with pneumonia as the primary site of infection died. Using multivariate analysis, we identified 3 independent predictors of mortality: the presence of a rapidly or ultimately fatal underlying disease (p = 0.0009), septic shock at the onset of bacteremia (p = 0.0013), and mechanical ventilation (p = 0.016). Epidemiologic typing revealed that 82 episodes were associated with different hospital outbreaks of infection, and only 7 episodes were due to epidemiologically unrelated strains.

Acinetobacter Infections↗