Variation in the OC Locus of Acinetobacter baumannii Genomes Predicts Extensive Structural Diversity in the Lipooligosaccharide

Kenyon, Johanna J.; Nigro, Steven J.; Hall, Ruth M.

doi:10.1371/journal.pone.0107833

Cited by 60 publications

(93 citation statements)

References 36 publications

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“…In any case, targeted mutagenesis and random mutagenesis of genes involved in synthesis of the LOS core oligosaccharide have shown that this component is a major contributor to Acinetobacter survival and virulence (33)(34)(35). The cluster of genes that synthesize the sugar component of LOS are extremely diverse among Acinetobacter spp., and a number of different structures have been determined or predicted (36). Modification of the LOS has also been shown to impart resistance to antimicrobials, similar to the findings for other bacterial species.…”

Section: Cell Surfacesupporting

confidence: 52%

Pathogenic Acinetobacter: from the Cell Surface to Infinity and Beyond

2016

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The genus Acinetobacter encompasses multiple nosocomial opportunistic pathogens that are of increasing worldwide relevance because of their ability to survive exposure to various antimicrobial and sterilization agents. Among these, Acinetobacter baumannii, Acinetobacter nosocomialis, and Acinetobacter pittii are the most frequently isolated in hospitals around the world. Despite the growing incidence of multidrug-resistant Acinetobacter spp., little is known about the factors that contribute to pathogenesis. New strategies for treating and managing infections caused by multidrug-resistant Acinetobacter strains are urgently needed, and this requires a detailed understanding of the pathobiology of these organisms. In recent years, some virulence factors important for Acinetobacter colonization have started to emerge. In this review, we focus on several recently described virulence factors that act at the bacterial surface level, such as the capsule, O-linked protein glycosylation, and adhesins. Furthermore, we describe the current knowledge regarding the type II and type VI secretion systems present in these strains.

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Section: Cell Surfacesupporting

confidence: 52%

Pathogenic Acinetobacter: from the Cell Surface to Infinity and Beyond

2016

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“…Analysis of the OC locus of strain K50 revealed that it is 98% identical to the OC locus of A. baumannii strain RBH4, classified as OCL1 (Table S4). This OC arrangement is widely distributed in CC1 and CC2 isolates and has been identified in several A. baumannii strains belonging to various sequence types, including ST158 (24). Although many of the antibiotic resistance determinants in A. baumannii are commonly organized within resistance islands (AbaR [A. baumannii resistance island]), none of the previously described AbaR regions was identified in the chromosome of strain K50.…”

Section: Sequencing and Phylogenetic And Comparative Analyses Of The mentioning

confidence: 98%

Complete Genome Sequencing of Acinetobacter baumannii Strain K50 Discloses the Large Conjugative Plasmid pK50a Encoding Carbapenemase OXA-23 and Extended-Spectrum β-Lactamase GES-11

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Eikmeyer³

et al. 2018

Antimicrob Agents Chemother

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Multidrug-resistant (MDR) strains appeared as serious emerging nosocomial pathogens in clinical environments and especially in intensive care units (ICUs). strain K50, recovered from a hospitalized patient in Kuwait, exhibited resistance to carbapenems and additionally to ciprofloxacin, chloramphenicol, sulfonamides, amikacin, and gentamicin. Genome sequencing revealed that the strain possesses two plasmids, pK50a (79.6 kb) and pK50b (9.5 kb), and a 3.75-Mb chromosome. K50 exhibits an average nucleotide identity (ANI) of 99.98% to the previously reported Iraqi clinical isolate AA-014, even though the latter strain lacked plasmid pK50a. Strain K50 belongs to sequence type 158 (ST158) (Pasteur scheme) and ST499 (Oxford scheme). Plasmid pK50a is a member of the Aci6 (replication group 6 [RG6]) group of plasmids and carries a conjugative transfer module and two antibiotic resistance gene regions. The transposon Tn carries the carbapenemase gene , whereas a class 1 integron harbors the resistance genes, ,, Δ, and , conferring resistance to all β-lactams and reduced susceptibility to carbapenems and resistance to aminoglycosides, trimethoprim, quaternary ammonium compounds, and sulfamethoxazole, respectively. The class 1 integron is flanked by MITEs (miniature inverted-repeat transposable elements) delimiting the element at its insertion site.

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“…A. baumannii does not contain genes involved in lipopolysaccharide (LPS) O-antigen ligase activity (Kenyon and Hall, 2013;Weber et al, 2015), synthesizing instead a lipooligosaccharide (LOS) consisting of an outer core oligosaccharide (OCL) linked to Lipid A (Kenyon and Hall, 2013;Kenyon et al, 2014a); at least twelve distinct OCL structures have been inferred from genomic data (Kenyon et al, 2014b). We mapped all Thai isolates against an A. baumannii specific databases for capsular and LOS loci (KL and OCL, resp.…”

Section: Genes Associated With Capsules and Outer Corementioning

confidence: 99%

Genomic and Phenotypic Analyses of Acinetobacter baumannii Isolates From Three Tertiary Care Hospitals in Thailand

et al. 2020

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Antibiotic resistant strains of Acinetobacter baumannii are responsible for a large and increasing burden of nosocomial infections in Thailand and other countries of Southeast Asia. New approaches to their control and treatment are urgently needed and an attractive strategy is to remove the bacterial polysaccharide capsule, and thus the protection from the host's immune system. To examine phylogenetic relationships, distribution of capsule chemotypes, acquired antibiotic resistance determinants, susceptibility to complement and other traits associated with systemic infection, we sequenced 191 isolates from three tertiary referral hospitals in Thailand and used phenotypic assays to characterize key aspects of infectivity. Several distinct lineages were circulating in three hospitals and the majority belonged to global clonal group 2 (GC2). Very high levels of resistance to carbapenems and other front-line antibiotics were found, as were a number of widespread plasmid replicons. A high diversity of capsule genotypes was encountered, with only three of these (KL6, KL10, and KL47) showing more than 10% frequency. Almost 90% of GC2 isolates belonged to the most common capsule genotypes and were fully resistant to the bactericidal action of human serum complement, most likely protected by their polysaccharide capsule, which represents a key determinant of virulence for systemic infection. Our study further highlights the importance to develop therapeutic strategies to remove the polysaccharide capsule from extensively drug-resistant A. baumanii during the course of systemic infection.

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Variation in the OC Locus of Acinetobacter baumannii Genomes Predicts Extensive Structural Diversity in the Lipooligosaccharide

Cited by 60 publications

References 36 publications

Pathogenic Acinetobacter: from the Cell Surface to Infinity and Beyond

Pathogenic Acinetobacter: from the Cell Surface to Infinity and Beyond

Complete Genome Sequencing of Acinetobacter baumannii Strain K50 Discloses the Large Conjugative Plasmid pK50a Encoding Carbapenemase OXA-23 and Extended-Spectrum β-Lactamase GES-11

Genomic and Phenotypic Analyses of Acinetobacter baumannii Isolates From Three Tertiary Care Hospitals in Thailand

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