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1. (Article ID: 5458)
 
Kenyon JJ, Arbatsky NP, Shashkov AS, Shneider MM, Popova AV, Hall RM, Knirel YA
Production of the K16 capsular polysaccharide by Acinetobacter baumannii ST25 isolate D4 involves a novel glycosyltransferase encoded in the KL16 gene cluster
International Journal of Biological Macromolecules 128 (2019) 101-106
 

A new capsular polysaccharide (CPS) biosynthesis gene cluster, KL16, was found in the genome sequence of a clinical Acinetobacter baumannii ST25 isolate, D4. The variable part of KL16 contains a module of genes for synthesis of 5,7-diacetamido-3,5,7,9-tetradeoxy-l-glycero-l-manno-non-2-ulosonic acid (5,7-di-N-acetylpseudaminic acid, Pse5Ac7Ac), a gene encoding ItrA3 that initiates the CPS synthesis with d-GlcpNAc, and two glycosyltransferase (Gtr) genes. The K16 CPS was studied by sugar analysis and Smith degradation along with 1D and 2D 1H and 13C NMR spectroscopy, and shown to be built up of linear trisaccharide repeats containing d-galactose (d-Gal), N-acetyl-d-glucosamine (d-GlcNAc), and Pse5Ac7Ac. The d-Galp residue is linked to the d-GlcpNAc initiating sugar via a β-(1→3) linkage evidently formed by a Gtr5 variant, Gtr5K16, encoded in KL16. This reveals an altered or relaxed substrate specificity of this variant as the majority of Gtr5-type glycosyltransferases have previously been shown to form a β-d-Galp-(1→3)-d-GalpNAc linkage. The β-Psep5Ac7Ac-(2→4)-d-Galp linkage is predicted to be formed by the other glycosyltransferase, Gtr37, which does not match members of any known glycosyltransferase family.

Acinetobacter baumannii, capsular polysaccharide, 5, glycosyltransferase, 7-Di-N-acetylpseudaminic acid, KL16 K locus

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2. (Article ID: 5500)
 
Singh JK, Adams FG, Brown MH
Diversity and Function of Capsular Polysaccharide in Acinetobacter baumannii
Frontiers in Microbiology 9 (2019) 3301
 

The Gram-negative opportunistic bacterium Acinetobacter baumannii is a significant cause of hospital-borne infections worldwide. Alarmingly, the rapid development of antimicrobial resistance coupled with the remarkable ability of isolates to persist on surfaces for extended periods of time has led to infiltration of A. baumannii into our healthcare environments. A major virulence determinant of A. baumannii is the presence of a capsule that surrounds the bacterial surface. This capsule is comprised of tightly packed repeating polysaccharide units which forms a barrier around the bacterial cell wall, providing protection from environmental pressures including desiccation and disinfection regimes as well as host immune responses such as serum complement. Additionally, capsule has been shown to confer resistance to a range of clinically relevant antimicrobial compounds. Distressingly, treatment options for A. baumannii infections are becoming increasingly limited, and the urgency to develop effective infection control strategies and therapies to combat infections is apparent. An increased understanding of the contribution of capsule to the pathobiology of A. baumannii is required to determine its feasibility as a target for new strategies to combat drug resistant infections. Significant variation in capsular polysaccharide structures between A. baumannii isolates has been identified, with over 100 distinct capsule types, incorporating a vast variety of sugars. This review examines the studies undertaken to elucidate capsule diversity and advance our understanding of the role of capsule in A. baumannii pathogenesis.

polysaccharide, Acinetobacter, Acinetobacter baumannii, capsule, virulence factor, persistence

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