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PubMed1998

[Virulence and its relationship to antibiotic resistance].

PATHOGENIC ISLANDS: Certain DNA blocks inserted into the chromosome of most Gram negative bacteria originated in pathogens found in plants. VIRULENCE-ANTIBIOTIC INTERACTIONS: During the invasive phase, the bacterial cell covers itself with adhesins which facilitate its adherence to tissues. The bacterial cell produces a fibronectin which protects its defense systems. Antibiotics favor bacterial resistance by increasing the expression of surface adhesins and fibronectin production. PENICILLIN RESISTANT PNEUMOCOCCI: Experimental models have demonstrated that mortality in mice and host resistance to pneumococcal infection are related to the type of capsule and not to antibiotic resistance. QUORUM SENSING: The bacterial inoculum regulates the production of virulence factors in vivo via quorum sensing. This regulation can play an important role in Pseudomonas aeruginosa infections. ACINETOBACTER BAUMANNI VIRULENCE: Long poorly understood, factors favoring A. baumanni virulence appear to result from bacterial production of IROMPs in the extracellular growth medium in response to iron depletion during the exponential growth phase.

Acinetobacter↗
PubMed2002

Opportunistic colonization of Ralstonia solanacearum-infected plants by Acinetobacter sp. and its natural competence development.

The behavior of the soil bacterium Acinetobacter sp. BD413 was monitored in Ralstonia solanacearum-infected and non-infected tomato plants after direct injection into the stem or natural infection by roots. In healthy plants, Acinetobacter sp. BD413 failed to colonize plant tissue. In plants infected simultaneously by the pathogen R. solanacearum,the Acinetobacter population increased linearly to about 3.1 x 10(7) cells per gram plant material and was maintained at a high level until the death of the plant. Moreover, Acinetobacter sp. BD413 was found to develop a competent state when multiplying in planta, indicating it could possibly be transformed by bacterial or plant DNA.

Acinetobacter↗
PubMed2003

The epidemiology of multidrug-resistant Acinetobacter baumannii: does the community represent a reservoir?

OBJECTIVE: To explore the role of the community as a potential reservoir for Acinetobacter baumannii. DESIGN: Antimicrobial resistance patterns and genotypes of A. baumannii isolates from patients in two Manhattan hospitals were compared with those of A. baumannii isolates from the hands of community members. RESULTS: A total of 103 isolates from two hospitals (hospital A, 81; hospital B, 22) and 23 isolates from community residents were studied. Of the hospital isolates, 36.6% were multidrug resistant (hospital A, 68.2%; hospital B, 27.8%). In contrast, there were no multidrug-resistant isolates from the community (P < .005 between hospital and community). The prevalence of A. baumannii on the hands of community residents was 10.4% (23 of 222). By molecular typing, 42 strains of A. baumannii were identified. Of the isolates from hospital A and hospital B, 55.6% (45 of 81) and 68.2% (15 of 22), respectively, were indistinguishable or closely related. In contrast, most community (83.3%) isolates were unrelated (P = .001 between hospital and community). CONCLUSION: Acinetobacter isolates from the community, characterized by a large variety of unrelated strains (83.3%), were distinct from the hospital isolates, of which 58.3% were closely related. The absence of multidrug-resistant strains in the community compared with 36.8% prevalence among hospital isolates suggests that the reservoir for epidemic strains resides in the hospital environment itself. To our knowledge, this is the first study to examine the community as a potential reservoir for hospital strains of A. baumannii.

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↗
PubMed1996

A comparative study of different PCR-based DNA fingerprinting techniques for typing of the Acinetobacter calcoaceticus-A. baumannii complex.

Different PCR-based DNA fingerprinting techniques were evaluated for typing 26 clinical isolates belonging to the Acinetobacter calcoaceticus-A. baumannii complex. Seven isolates belonged to a previously defined outbreak while 19 isolates were unrelated epidemiologically. The PCR-based DNA fingerprinting techniques used were: (i) repetitive extragenic palindromic (REP) PCR; (ii) enterobacterial repetitive intergenic consensus (ERIC) PCR; (iii) randomly amplified polymorphic DNA with M13 forward primer; (iv) restriction analysis of the amplified 16S rRNA gene (ARDRA-16S); and (v) restriction analysis of an amplified region containing the 16S-23S rRNA spacer region and part of the 23S rRNA gene (ARDRA 23S + spacer). The discrimination index for the PCR-based DNA fingerprinting techniques was: 0.99 for REP; 0.94 for ERIC; 0.87 for M13; 0.60 for ARDRA-16S digested with Hpa II and <0.50 for ARDRA 23S + spacer. It was concluded that REP-PCR possessed high discriminatory power and reproducibility in comparison with the other PCR-based DNA fingerprinting techniques, and is a simple and rapid typing method for use in epidemiological studies of isolates belonging to the A. calcoaceticus-A. baumannii complex.

Acinetobacter↗
PubMed2006

Nosocomial spread of OXA-58-positive carbapenem-resistant Acinetobacter baumannii isolates in a paediatric hospital in Greece.

Twelve non-repetitive Acinetobacter baumannii isolates producing the carbapenem-hydrolysing oxacillinase OXA-58 were recovered from patients in the same paediatric hospital in Athens, Greece, between November 2003 and May 2005. All isolates were clonally related, but the bla(OXA-58) gene was not always plasmid-located and there were variations in the DNA sequences surrounding the OXA-58 gene in different isolates. This study emphasises the importance of the bla(OXA-58) carbapenemase gene in conferring carbapenem resistance among A. baumannii isolates in Greece.

Acinetobacter Infections↗
PubMed2006

Comparison of Acinetobacter baumannii isolates from the United Kingdom and the United States that were associated with repatriated casualties of the Iraq conflict.

Acinetobacter isolates associated with casualties from the Iraq conflict from the United States were compared with those from the United Kingdom by pulsed-field gel electrophoresis and integron analysis. Representatives of the main outbreak strain associated with casualties from both countries were indistinguishable in DNA profile. Two further outbreak strains were common to both sets of isolates.

Acinetobacter Infections↗
PubMed2004

Comparison of Acinetobacter baumannii isolates from United Kingdom hospitals with predominant Northern European genotypes by amplified-fragment length polymorphism analysis.

Acinetobacter baumannii isolates collected between 1999 and 2001 from 46 United Kingdom hospitals were compared with previously identified northern European genotypes by amplified-fragment length polymorphism (AFLP) analysis. Two predominant northern European genotypes associated with outbreaks in the mid-1980s had been superseded by new outbreak-associated genotypes.

Acinetobacter Infections↗
PubMed1996

Clusters of nosocomial cross-infection due to Acinetobacter baumannii and genospecies 3: comparison of serotyping with macrorestriction analysis of genomic DNA with pulsed-field gel electrophoresis.

Triplets of isolates representing 20 putative clusters of nosocomial cross-infection due to Acinetobacter baumannii and genospecies 3 were examined comparatively using serotyping and analysis of restriction fragments (SmaI and ApaI) of genomic DNA with the aid of pulsed-field gel electrophoresis. Carbon source assimilation tests disclosed phenotypic variation among 6 to 20 triplets of isolates. Two misleading results of serotyping were encountered. With respect to the presumptive cluster No. 9, one of the genospecies 3 (originally serovar 4) isolates proved to be polyagglutinable upon repeat examination; this particular putative cluster was shown to be a pseudocluster by comparison of the macrorestriction profiles of the respective triple isolates. A strain of A. baumannii serovar 15 had infected 8 patients in a surgical intensive care unit, while a second, genotypically totally different strain of identical serovar had caused infection in one additional patient. With this exception, the correlation between serotyping and analysis of macrorestriction profiles was excellent.

Acinetobacter↗
PubMedDate not supplied

Infections caused by Acinetobacter species and their susceptibility to 14 antibiotics in Lagos University Teaching Hospital, Lagos.

Acinetobacter spp are well recognised as causes of nosocomial infections particularly in patients with immature or defective body defence system. Information concerning these organisms are lacking in this environment. For this reason the pattern of infection and the antimicrobial susceptibility profiles of these organisms isolated over a one-year period were studied. A total of 58 (3%) of the 2001 isolates from all clinical specimens received in the laboratory during the year were Acinetobacter spp. The 58 Acinetobacter spp constituted 5.5% of all the 1051 NLF-GNB isolated, and caused 4.6% of all the 1261 nosocomial infections. Thirty-seven (63%) and 17 (30%) of the Acinetobacter isolates were from wound infections and UTI respectively. All the infections were nosocomially acquired and were associated with compromised host immunity, defective body defence, surgery or urinary catheterization; with Acinetobacter baumannii being the predominant species. There was an apparent male predominance over females by a ratio of 1. 9:1 in the infections, particularly from 45 years and above. One hundred percent and 96.6% of the isolates were susceptible to cefoperazone-sulbactam and travofloxacin respectively. Forty-five (77.6%) were susceptible to cefotaxime, 49 (84.5%) to ampicillin-sulbactam, 34 (58.6%) to ceftazidime, 38 (65.6%) to ticarcillin-clavulanic acid and 41 (70.7%) to ciprofloxacin. Generally the Acinetobacter spp showed multiple resistance to the range of antibiotics tested. All the isolates produced beta-lactamase.

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↗