Abstract

Acinetobacter baumannii A118, a strain isolated from the blood of an infected patient, is naturally competent and unlike most clinical strains, is susceptible to a variety of different antibiotics including those usually used for selection in genetic manipulations. These characteristics make strain A118 a convenient model for genetic studies of A. baumannii. To identify potential virulence factors, its complete genome was analyzed and compared to other A. baumannii genomes. A. baumannii A118 includes gene clusters coding for the acinetobactin and baumannoferrin iron acquisition systems. Iron-regulated expression of the BauA outer membrane receptor for ferric-acinetobactin complexes was confirmed as well as the utilization of acinetobactin. A. baumannii A118 also possesses the feoABC genes, which code for the main bacterial ferrous uptake system. The functionality of baumannoferrin was suggested by the ability of A. baumannii A118 culture supernatants to cross feed an indicator BauA-deficient strain plated on iron-limiting media. A. baumannii A118 behaved as non-motile but included the csuA/BABCDE chaperone-usher pilus assembly operon and produced biofilms on polystyrene and glass surfaces. While a known capsular polysaccharide (K) locus was identified, the outer core polysaccharide (OC) locus, which belongs to group B, showed differences with available sequences. Our results show that despite being susceptible to most antibiotics, strain A118 conserves known virulence-related traits enhancing its value as model to study A. baumannii pathogenicity.

Highlights

  • Acinetobacter baumannii infections used to be rare a few decades ago (Hartstein et al, 1988)

  • To facilitate its use as model of infection we identify the presence of genes and functions previously associated with A. baumannii pathogenicity

  • There is an urgent need to find answers to the problem of infections with bacteria belonging to the ESKAPE group (Boucher et al, 2013), which includes A. baumannii

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Summary

Introduction

Acinetobacter baumannii infections used to be rare a few decades ago (Hartstein et al, 1988). Its importance as an opportunistic human pathogen kept increasing and it is responsible for a growing number of community and nosocomial infections including bacteremia, urinary tract infections, wound infections, meningitis, and pneumonia (Maragakis and Perl, 2008; Zurawski et al, 2012; McConnell et al, 2013; Harding et al, 2018). Recent studies identified pathogenic and resistance islands (Fournier et al, 2006; Smith et al, 2007; Post et al, 2010; Krizova et al, 2011) as well as several potential virulence factors (Harding et al, 2018) such as iron and other micronutrients uptake (Zimbler et al, 2009; Gaddy et al, 2012; Moore et al, 2014; Penwell et al, 2015), motility (Mussi et al, 2010; Eijkelkamp et al, 2013; Wood et al, 2018), production of cytotoxic and protection factors (Russo et al, 2010; Jin et al, 2011), and adhesion and biofilm formation on abiotic and biotic surfaces (Gaddy et al, 2009; Longo et al, 2014)

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