Whole-Genome Pyrosequencing of an Epidemic Multidrug-Resistant
            <i>Acinetobacter baumannii</i>
            Strain Belonging to the European Clone II Group

Iacono, Michele; Villa, Laura; Fortini, Daniela; Bordoni, Roberta; Imperi, Francesco; Bonnal, Raoul Jean Pierre; Sicheritz-Pontén, Thomas; Bellis, Gianluca De; Visca, Paolo; Cassone, Antonio; Carattoli, Alessandra

doi:10.1128/aac.01643-07

Cited by 251 publications

(249 citation statements)

References 39 publications

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“…CP000521; Smith et al, 2007). (Barbe et al, 2004), 'Acinetobacter oleivorans' DR1 (Jung et al, 2010), A. baumannii AB0057, AB900 and AB307-0294 (Adams et al, 2008), ACICU (Iacono et al, 2008), 17978 (Smith et al, 2007), and SDF and AYE (Vallenet et al, 2008). Table 1 provides specific strain descriptions.…”

Section: Methodsmentioning

confidence: 99%

Diverse responses to UV light exposure in Acinetobacter include the capacity for DNA damage-induced mutagenesis in the opportunistic pathogens Acinetobacter baumannii and Acinetobacter ursingii

et al. 2012

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Error-prone and error-free DNA damage repair responses that are induced in most bacteria after exposure to various chemicals, antibiotics or radiation sources were surveyed across the genus Acinetobacter. The error-prone SOS mutagenesis response occurs when DNA damage induces a cell's umuDC-or dinP-encoded error-prone polymerases. The model strain Acinetobacter baylyi ADP1 possesses an unusual, regulatory umuD allele (umuDAb) with an extended 59 region and only incomplete fragments of umuC. Diverse Acinetobacter species were investigated for the presence of umuDC and their ability to conduct UV-induced mutagenesis. Unlike ADP1, most Acinetobacter strains possessed multiple umuDC loci containing either umuDAb or a umuD allele resembling that of Escherichia coli. The nearly omnipresent umuDAb allele was the ancestral umuD in Acinetobacter, with horizontal gene transfer accounting for over half of the umuDC operons. Despite multiple umuD(Ab)C operons in many strains, only three species conducted UV-induced mutagenesis: Acinetobacter baumannii, Acinetobacter ursingii and Acinetobacter beijerinckii. The type of umuDC locus or mutagenesis phenotype a strain possessed was not correlated with its error-free response of survival after UV exposure, but similar diversity was apparent. The survival of 30 Acinetobacter strains after UV treatment ranged over five orders of magnitude, with the Acinetobacter calcoaceticus-A. baumannii (Acb) complex and haemolytic strains having lower survival than non-Acb or non-haemolytic strains. These observations demonstrate that a genus can possess a range of DNA damage response mechanisms, and suggest that DNA damage-induced mutation could be an important part of the evolution of the emerging pathogens A. baumannii and A. ursingii. INTRODUCTIONWhen bacteria are exposed to DNA-damaging agents, such as UV light or chemical mutagens, a wide variety of SOS response genes (genes that play critical roles in repairing damaged DNA) are specifically induced (Friedberg et al., 1995;Walker, 1996). In the model developed by experimentation in Escherichia coli, SOS genes are negatively regulated by the LexA repressor binding to the SOS box in the promoter (Mount et al., 1972). DNA damage causes the activation of RecA, which facilitates LexA self-cleavage and releases the repression of SOS genes such as umuDC (Little et al., 1980;1981). UmuD initially causes a pause in cell division while DNA repair and replication occurs (Opperman et al., 1999). However, within minutes, UmuD homodimerizes and carries out intermolecular self-cleavage, facilitated by activated RecA* interaction (Nohmi et al., 1988). Two cleaved UmuD9 molecules then associate with UmuC to form DNA polymerase V, which carries out error-prone, trans-lesion DNA replication (SOS mutagenesis) (Reuven et al., 1999;Tang et al., 1999). Another errorprone polymerase commonly involved in SOS mutagenesis as part of the DNA damage response is DinP (also called DinB), DNA polymerase IV, which can function either by itself (Kim et al., 1997) or with U...

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Section: Methodsmentioning

confidence: 99%

Diverse responses to UV light exposure in Acinetobacter include the capacity for DNA damage-induced mutagenesis in the opportunistic pathogens Acinetobacter baumannii and Acinetobacter ursingii

et al. 2012

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“…genomes sequenced to date originate from strains that occupy three distinct environmental niches: a free-living soil organism, a human body louse symbiont, and a series of multidrug-resistant and drug-susceptible clinical isolates (4,15,115,233,248). Thus, as well as being able to assess the overall conservation of transcription components in Acinetobacter spp.…”

Section: Rna Transcriptionmentioning

confidence: 99%

“…Currently, complete genome sequences are available for seven Acinetobacter strains: the highly transformable laboratory strain A. baylyi ADP1 (15); a human body louse symbiont, A. baumannii SDF (248); and the human pathogens A. baumannii strains ATCC 17978 (233), AYE (248), ACICU (115), AB0057 (4), and AB307-0294 (4). At least eight additional genome sequence projects are currently in progress or at draft assembly stage at the time of writing of this review.…”

Section: Introductionmentioning

confidence: 99%

Essential Biological Processes of an Emerging Pathogen: DNA Replication, Transcription, and Cell Division in Acinetobacter spp

Robinson

Brzoska

Turner

et al. 2010

Microbiol Mol Biol Rev

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SUMMARY Within the last 15 years, members of the bacterial genus Acinetobacter have risen from relative obscurity to be among the most important sources of hospital-acquired infections. The driving force for this has been the remarkable ability of these organisms to acquire antibiotic resistance determinants, with some strains now showing resistance to every antibiotic in clinical use. There is an urgent need for new antibacterial compounds to combat the threat imposed by Acinetobacter spp. and other intractable bacterial pathogens. The essential processes of chromosomal DNA replication, transcription, and cell division are attractive targets for the rational design of antimicrobial drugs. The goal of this review is to examine the wealth of genome sequence and gene knockout data now available for Acinetobacter spp., highlighting those aspects of essential systems that are most suitable as drug targets. Acinetobacter spp. show several key differences from other pathogenic gammaproteobacteria, particularly in global stress response pathways. The involvement of these pathways in short- and long-term antibiotic survival suggests that Acinetobacter spp. cope with antibiotic-induced stress differently from other microorganisms.

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“…Among the most widespread are three particular lineages, commonly referred to as European clonal (EC) lineages I, II, and III (16,17). To gain insight into the success of these lineages, groups have sequenced the genomes of select representatives (18)(19)(20)(21). Among the most notable features of these A. baumannii genomes was an observed propensity for horizontal gene transfer, with the most striking examples being large genomic islands enriched in transposable elements and antibiotic resistance determinants (21).…”

mentioning

confidence: 99%

Genome-wide recombination drives diversification of epidemic strains of Acinetobacter baumannii

Snitkin

Zelazny

Montero

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

155

160

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Acinetobacter baumannii is an emerging human pathogen and a significant cause of nosocomial infections among hospital patients worldwide. The enormous increase in multidrug resistance among hospital isolates and the recent emergence of pandrug-resistant strains underscores the urgency to understand how A. baumannii evolves in hospital environments. To this end, we undertook a genomic study of a polyclonal outbreak of multidrugresistant A. baumannii at the research-based National Institutes of Health Clinical Center. Comparing the complete genome sequences of the three dominant outbreak strain types enabled us to conclude that, despite all belonging to the same epidemic lineage, the three strains diverged before their arrival at the National Institutes of Health. The simultaneous presence of three divergent strains from this lineage supports its increasing prevalence in international hospitals and suggests an ongoing adaptation to the hospital environment. Further genomic comparisons uncovered that much of the diversification that occurred since the divergence of the three outbreak strains was mediated by homologous recombination across 20% of their genomes. Inspection of recombinant regions revealed that several regions were associated with either the loss or swapping out of genes encoding proteins that are exposed to the cell surface or that synthesize cell-surface molecules. Extending our analysis to a larger set of international clinical isolates revealed a previously unappreciated ability of A. baumannii to vary surface molecules through horizontal gene transfer, with subsequent intraspecies dissemination by homologous recombination. These findings have immediate implications in surveillance, prevention, and treatment of A. baumannii infections. bacterial evolution | microbial genomics | clinical microbiology | hospital epidemiology | hospital infection

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Whole-Genome Pyrosequencing of an Epidemic Multidrug-Resistant Acinetobacter baumannii Strain Belonging to the European Clone II Group

Cited by 251 publications

References 39 publications

Diverse responses to UV light exposure in Acinetobacter include the capacity for DNA damage-induced mutagenesis in the opportunistic pathogens Acinetobacter baumannii and Acinetobacter ursingii

Diverse responses to UV light exposure in Acinetobacter include the capacity for DNA damage-induced mutagenesis in the opportunistic pathogens Acinetobacter baumannii and Acinetobacter ursingii

Essential Biological Processes of an Emerging Pathogen: DNA Replication, Transcription, and Cell Division in Acinetobacter spp

Genome-wide recombination drives diversification of epidemic strains of Acinetobacter baumannii

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