Species identification and molecular characterization of Acinetobacter spp. blood culture isolates from Norway

Karah, Nabil; Haldorsen, Bjørg; Hegstad, Kristin; Simonsen, Gunnar Skov; Sundsfjord, Arnfinn; Samuelsen, Ørjan

doi:10.1093/jac/dkq521

Cited by 106 publications

(81 citation statements)

References 32 publications

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“…In addition, the proportions of Acinetobacter baumannii and Acinetobacter genospecies 3 were approximately equal in the Netherland,[17] and Acinetobacter genospecies 13TU was the most prevalent genospecies in Norwegian blood cultures. [18] It is a pity that by far there is no such report about the genospecies identification of the Acinetobacter baumannii group in the mainland of China, further studies are needed.…”

Section: Resultsmentioning

confidence: 99%

TheAcinetobacter baumanniigroup:a systemic review

Zhang

Qiao

2013

World Journal of Emergency Medicine

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BACKGROUND:The Acinetobacter baumannii group, including Acinetobacter baumannii, Acinetobacter genomospecies 3 and 13TU, is phenotypically indistinguishable and uniformly identified as Acinetobacter baumannii by laboratories of clinical microbiology. This review aimed to demonstrate the differences among them.METHODS:Literatures associated with the Acinetobacter baumannii group were identified and selected from PubMed databases and relevant journals.RESULTS:Acinetobacter genospecies 3 and 13TU possess a certain proportion in clinical isolates. There were considerable differences in epidemiologic features, clinical manifestations, antimicrobial resistances and therapeutic options among the Acinetobacter baumannii group. Compared with Acinetobacter genomospecies 3 and 13TU, Acinetobacter baumannii with a higher resistance to antimicrobial agents are easier to be treated inappropriately, and present a worse outcome in patients.CONCLUSION:The Acinetobacter baumannii group comprises three distinct clinical entities, and their clinical value are not equal.

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Section: Resultsmentioning

confidence: 99%

TheAcinetobacter baumanniigroup:a systemic review

Zhang

Qiao

2013

World Journal of Emergency Medicine

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“…However, opportunistic infections are also caused by Acinetobacter lwoffii, Acinetobacter ursingii (Turton et al, 2010) or strains in the Acinetobacter calcoaceticus-A. baumannii (Acb) complex (Gerner-Smidt et al, 1991), most commonly by genomic groups 13TU and 3 (Chuang et al, 2011;Karah et al, 2011) which correspond to the species Acinetobacter nosocomialis and Acinetobacter pittii, respectively (Nemec et al, 2011). The genome of the non-pathogenic, naturally competent A. baylyi ADP1 has been sequenced (Barbe et al, 2004), and strain ADP1 serves as an excellent model organism for genetic and metabolic engineering (de Berardinis et al, 2009;Metzgar et al, 2004).…”

Section: Introductionmentioning

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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“…Infections with A. baumannii have been associated with high attributable mortality and increased length of hospital stay, with multidrug resistance often being a predictor of poor clinical outcomes (5, 6). However, the frequencies of A. nosocomialis and A. pittii as human pathogens are increasingly recognized (7,8). Several studies have shown that these different species within the ACB complex exhibit unique epidemiologic niches, drug resistance patterns, and virulence characteristics within the nosocomial environment (9, 10).…”

mentioning

confidence: 99%

Utility of Whole-Genome Sequencing in Characterizing Acinetobacter Epidemiology and Analyzing Hospital Outbreaks

2016

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bAcinetobacter baumannii frequently causes nosocomial infections and outbreaks. Whole-genome sequencing (WGS) is a promising technique for strain typing and outbreak investigations. We compared the performance of conventional methods with WGS for strain typing clinical Acinetobacter isolates and analyzing a carbapenem-resistant A. baumannii (CRAB) outbreak. We performed two band-based typing techniques (pulsed-field gel electrophoresis and repetitive extragenic palindromic-PCR), multilocus sequence type (MLST) analysis, and WGS on 148 Acinetobacter calcoaceticus-A. baumannii complex bloodstream isolates collected from a single hospital from 2005 to 2012. Phylogenetic trees inferred from core-genome single nucleotide polymorphisms (SNPs) confirmed three Acinetobacter species within this collection. Four major A. baumannii clonal lineages (as defined by MLST) circulated during the study, three of which are globally distributed and one of which is novel. WGS indicated that a threshold of 2,500 core SNPs accurately distinguished A. baumannii isolates from different clonal lineages. The bandbased techniques performed poorly in assigning isolates to clonal lineages and exhibited little agreement with sequence-based techniques. After applying WGS to a CRAB outbreak that occurred during the study, we identified a threshold of 2.5 core SNPs that distinguished nonoutbreak from outbreak strains. WGS was more discriminatory than the band-based techniques and was used to construct a more accurate transmission map that resolved many of the plausible transmission routes suggested by epidemiologic links. Our study demonstrates that WGS is superior to conventional techniques for A. baumannii strain typing and outbreak analysis. These findings support the incorporation of WGS into health care infection prevention efforts.A n important role of clinical microbiology is to identify relationships between bacterial isolates. At a broad level, phenotypic and genotypic tests are used to categorize bacterial isolates into the same or different species. Within a bacterial species, techniques are used to group isolates into clonal lineages, which are groups of closely related bacteria that share a recent common ancestor but have spread regionally or globally. At a more local level, infection control practitioners must determine whether a group of isolates constitutes a hospital outbreak by ascertaining whether the isolates have a degree of similarity consistent with a common source within the hospital. Once isolates belonging to a hospital outbreak have been identified, similarities and differences between these isolates can be exploited to generate a transmission map to aid in finding the source of the outbreak and in disrupting ongoing pathways of transmission. For some groups of bacteria, such as Acinetobacter, discernment at each level has medically important consequences and therefore must be accomplished by hospital-associated clinical microbiology laboratories.Within the Acinetobacter genus, the Acinetobacter calcoaceticusAcinetobac...

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Species identification and molecular characterization of Acinetobacter spp. blood culture isolates from Norway

Cited by 106 publications

References 32 publications

TheAcinetobacter baumanniigroup:a systemic review

TheAcinetobacter baumanniigroup:a systemic review

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

Utility of Whole-Genome Sequencing in Characterizing Acinetobacter Epidemiology and Analyzing Hospital Outbreaks

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