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Acinetobacter baumannii causes severe, fulminant, community-acquired pneumonia (CAP) in tropical and subtropical regions. We compared the population structure, virulence and antimicrobial resistance determinants of northern Australian community-onset A. baumannii strains with local and global strains. We performed whole-genome sequencing on 55 clinical and five throat colonization A. baumannii isolates collected in northern Australia between 1994 and 2016. Clinical isolates included CAP (n=41), healthcare-associated pneumonia (n=7) and nosocomial bloodstream (n=7) isolates. We also included 93 publicly available international A. baumannii genome sequences in the analyses. Patients with A. baumannii CAP were almost all critically unwell; 82% required intensive care unit admission and 18% died during their inpatient stay. Wholegenome phylogenetic analysis demonstrated that community-onset strains were not phylogenetically distinct from nosocomial strains. Some non-multidrug-resistant local strains were closely related to multidrug-resistant strains from geographically distant locations. Pasteur sequence type (ST)10 was the dominant ST and accounted for 31/60 (52 %) northern Australian strains; the remainder belonged to a diverse range of STs. The most recent common ancestor for ST10 was estimated to have occurred in 1738 (95% highest posterior density, 1626–1826), with evidence of multiple introduction events between Australia and Southeast Asia between then and the present day. Virulence genes associated with biofilm formation and the type 6 secretion system (T6SS) were absent in many strains, and were not associated with in-hospital mortality. All strains were susceptible to gentamicin and meropenem; none carried an AbaR resistance island. Our results suggest that international dissemination of A. baumannii is occurring in the community on a contemporary timescale. Genes associated with biofilm formation and the T6SS may not be required for survival in community

In the version of this article initially published, in the subsection ‘GAS vaccine target variation’ in the Results, the text “The analyses revealed that 2,083 isolates carry the J8.0 allele of the M protein” should have read “The analyses revealed that 37% of the 2,083 isolates carry the J8.0 allele of the M protein.” The error has been corrected in the HTML and PDF versions of the article., SCOPUS: er.j, DecretOANoAutActif, info:eu-repo/semantics/published

Group A Streptococcus (GAS; Streptococcus pyogenes) is a bacterial pathogen for which a commercial vaccine for humans is not available. Employing the advantages of high-throughput DNA sequencing technology to vaccine design, we have analyzed 2,083 globally sampled GAS genomes. The global GAS population structure reveals extensive genomic heterogeneity driven by homologous recombination and overlaid with high levels of accessory gene plasticity. We identified the existence of more than 290 clinically associated genomic phylogroups across 22 countries, highlighting challenges in designing vaccines of global utility. To determine vaccine candidate coverage, we investigated all of the previously described GAS candidate antigens for gene carriage and gene sequence heterogeneity. Only 15 of 28 vaccine antigen candidates were found to have both low naturally occurring sequence variation and high (>99%) coverage across this diverse GAS population. This technological platform for vaccine coverage determination is equally applicable to prospective GAS vaccine antigens identified in future studies., info:eu-repo/semantics/published

David AB Dance,1 Vanaporn Wuthiekanun,2 Derek Sarovich,3 Erin P Price,3 Direk Limmathurotsakul,4 Bart J Currie,5 Trinh Thanh Trung61Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit, Vientiane, Lao PDR; 2Mahidol-Oxford Tropical Medicine Research Unit, Bangkok, Thailand; 3University of the Sunshine Coast, Sippy Downs, QLD, Australia; 4Microbiology, Mahidol-Oxford Tropical Medicine Research Unit, Bangkok, Thailand; 5Infectious Diseases, Menzies School of Health Research, Darwin, NT, Australia; 6Vietnam National University, Hanoi, VietnamWe are writing, on behalf of the International Melioidosis Society Committee, as a group of researchers and clinicians with longstanding experience of melioidosis and Burkholderia pseudomallei as we have some concerns about the above paper that was published in your journal recently.1 Although we believe that melioidosis is undoubtedly being under-diagnosed in Indonesia,2,3 we are not convinced that the isolate in this case is B.pseudomallei based on the information provided by the authors. Although it is difficult to be certain from the photographs in Figure 2, the colonies do not appear typical of the species to the microbiologists amongst us, who have seen several thousand isolates of B.pseudomallei over the past 30 years. Furthermore, the authors do not report whether the isolate was oxidase positive or negative. We believe that more comprehensive methods of confirming the identity, particularly genomic analysis, should have been undertaken before publishing the case.4 Unfortunately, the postamplification 16s analysis described in the paper might not have been able to distinguish between B.pseudomallei and other Burkholderia species (particularly B.thailandensis and several as-yet-uncharacterized Burkholderia spp.), and we would have recommended additional testing, for example, multilocus se