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1. (Article ID: 5397)
 
Arbatsky NP, Kasimova AA, Shashkov AS, Shneider MM, Popova AV, Shagin DA, Shelenkov AA, Mikhailova YV, Yanushevich YG, Azizov IS, Edelstein MV, Hall RM, Kenyon JJ, Knirel YA
Structure of the K128 capsular polysaccharide produced by Acinetobacter baumannii KZ-1093 from Kazakhstan
Carbohydrate Research 485 (2019) 107814
 

The structure of the K128 capsular polysaccharide (CPS) produced by Acinetobacter baumannii isolate KZ-1093 from Kazakhstan was established by sugar analysis and Smith degradation along with 1D and 2D 1H and 13C NMR spectroscopy. The CPS was found to consist of branched pentasaccharide repeating units containing only neutral sugars, and its composition and topology are closely related to those of the A. baumannii K116 CPS. The K128 and K116 oligosaccharide units differ in the linkage between the disaccharide side chain and the main chain, with a β-(1→6) linkage in K128 replacing a β-(1→4) linkage in K116. The linkages between the repeating units in the K128 and K116 CPSs are also different, with K128 units linked by β-d-GalpNAc-(1→4)-d-Galp, and β-d-GalpNAc-(1→3)-d-Galp linkages between K116 units. The KZ-1093 genome was sequenced and the CPS biosynthesis gene cluster at the chromosomal K locus was designated KL128. Consistent with the CPS structures, KL128 differs from KL116 in one glycosyltransferase gene and the gene for the Wzy polymerase. In KL128, the gtr200 glycosyltransferase gene replaces gtr76 in KL116, and Gtr200 was therefore assigned to the different β-d-GalpNAc-(1→6)-d-Galp linkage in K128. Similarly, the WzyK128 polymerase could be assigned to the β-d-GalpNAc-(1→4)-d-Galp linkage between the K128 units.

Acinetobacter baumannii, capsular polysaccharide, glycosyltransferase, Wzy polymerase, K locus

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2. (Article ID: 6078)
 
Kasimova AA, Cahill SM, Shpirt AM, Dudnik AG, Shneider MM, Popova AV, Shelenkov AA, Mikhailova YV, Chizhov AO, Kenyon JJ, Knirel YA
The K139 capsular polysaccharide produced by Acinetobacter baumannii MAR17-1041 belongs to a group of related structures including K14, K37 and K116
International Journal of Biological Macromolecules 193(PtB) (2021) 2297-2302
 

Capsular polysaccharide (CPS) is a key target for bacteriophage and vaccine therapies currently being developed for treatment of infections caused by the extensively antibiotic resistant bacterial species, Acinetobacter baumannii. Identification of new CPS structures and the genetics that drive their synthesis underpins tailored treatment strategies. A novel CPS biosynthesis gene cluster, designated KL139, was identified in the whole genome sequence of a multiply antibiotic resistant clinical isolate, A. baumannii MAR-17-1041, recovered in Russia in 2017. CPS material extracted from A. baumannii MAR-17-1041 was studied by sugar analysis and Smith degradation along with one- and two-dimensional 1H and 13C NMR spectroscopy, and the structure was found to include a branched pentasaccharide repeating unit containing neutral carbohydrates. This structure closely resembles the topology of the A. baumannii K14 CPS but differs in the presence of d-Glcp in place of a d-Galp sugar in the repeat-unit main chain. The difference was attributed to a change in the sequence for two glycosyltransferases. These two proteins are also encoded by the A. baumannii KL37 gene cluster, and a multiple sequence alignment of KL139 with KL14 and KL37 revealed a hybrid relationship. The global distribution of KL139 was also assessed by probing 9065 A. baumannii genomes available in the NCBI non-redundant and WGS databases for the KL139 gene cluster. KL139 was found in 16 genomes from four different countries. Eleven of these isolates belong to the multidrug resistant global lineage, ST25.

Acinetobacter baumannii, capsular polysaccharide, K locus, K139

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3. (Article ID: 6199)
 
Arbatsky NP, Kasimova AA, Shashkov AS, Shneider MM, Popova AV, Shagin DA, Shelenkov AS, Mikhailova YV, Yanushevich YG, Hall RM, Kenyon JJ
Involvement of a Phage-Encoded Wzy Protein in the Polymerization of K127 Units To Form the Capsular Polysaccharide of Acinetobacter baumannii Isolate 36-1454
Microbiology Spectrum 10(3) (2022) e0150321
 

A comprehensive understanding of capsular polysaccharide (CPS) diversity is critical to implementation of phage therapy to treat panresistant Acinetobacter baumannii infections. Predictions from genome sequences can assist identification of the CPS type but can be complicated if genes outside the K locus (CPS biosynthesis gene cluster) are involved. Here, the CPS produced by A. baumannii clinical isolate 36-1454 carrying a novel K locus, KL127, was determined and compared to other CPSs. KL127 differs from KL128 in only two of the glycosyltransferase (gtr) genes. The K127 unit in 36-1454 CPS was the pentasaccharide β-D-Glcp-(1→6)-D-β-GalpNAc-(1→6)-α-D-Galp-(1→6)-β-D-Glсp-(1→3)-β-D-GalpNAc in which D-Glcp at position 4 replaces d-Galp in K128, and the glycosyltransferases encoded by the different gtr genes form the surrounding linkages. However, although the KL127 and KL128 gene clusters encode nearly identical Wzy polymerases, the linkages between K units that form the CPS chains are different, i.e., β-D-GalpNAc-(1→3)-D-Galp in 36-1454 (K127) and β-D-GalpNAc-(1→4)-D-Galp in KZ-1093 (K128). The linkage between K127 units in 36-1454 is the same as the K-unit linkage in five known CPS structures, and a gene encoding a Wzy protein related to the Wzy of the corresponding K loci was found encoded in a prophage genome in the 36-1454 chromosome. Closely related Wzy proteins were encoded in unrelated phage in available KL127-carrying genomes. However, a clinical isolate, KZ-1257, carrying KL127 but not the prophage was found, and K127 units in the KZ-1257 CPS were β-D-GalpNAc-(1→4)-D-Galp linked, confirming that WzyKL127 forms this linkage and thus that the phage-encoded WzyPh1 forms the β-D-GalpNAc-(1→3)-D-Galp linkage in 36-1454. IMPORTANCE Bacteriophage therapy is an attractive innovative treatment for infections caused by extensively drug resistant Acinetobacter baumannii, for which there are few effective antibiotic treatments remaining. Capsular polysaccharide (CPS) is a primary receptor for many lytic bacteriophages, and thus knowledge of the chemical structures of CPS produced by the species will underpin the identification of suitable phages for therapeutic cocktails. However, recent research has shown that some isolates carry additional genes outside of the CPS biosynthesis K locus, which can modify the CPS structure. These changes can subsequently alter phage receptor sites and may be a method utilized for natural phage resistance. Hence, it is critical to understand the genetics that drive CPS synthesis and the extent to which genes outside of the K locus can affect the CPS structure.

Acinetobacter baumannii, capsular polysaccharide, phage, Wzy polymerase, K locus, K127

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4. (Article ID: 6474)
 
Timoshina OY, Kasimova AA, Shneider MM, Arbatsky NP, Shashkov AS, Shelenkov AA, Mikhailova YV, Popova AV, Hall RM, Knirel YA, Kenyon JJ
Loss of a Branch Sugar in the Acinetobacter baumannii K3-Type Capsular Polysaccharide Due To Frameshifts in the gtr6 Glycosyltransferase Gene Leads To Susceptibility To Phage APK37.1
Microbiology Spectrum 11(1) (2023) e0363122
 

The type of capsular polysaccharide (CPS) on the cell surface of Acinetobacter baumannii can determine the specificity of lytic bacteriophage under consideration for therapeutic use. Here, we report the isolation of a phage on an extensively antibiotic resistant ST2 A. baumannii isolate AB5001 that carries the KL3 CPS biosynthesis gene cluster predicting a K3-type CPS. As the phage did not infect isolates carrying KL3 or KL22 and known to produce K3 CPS, the structure of the CPS isolated from A. baumannii AB5001 was determined. AB5001 produced a variant CPS form, K3-v1, that lacks the β-d-GlсpNAc side chain attached to the d-Galp residue in the K3 structure. Inspection of the KL3 sequence in the genomes of AB5001 and other phage-susceptible isolates with a KL3 locus revealed single-base deletions in gtr6, causing loss of the Gtr6 glycosyltransferase that adds the missing d-GlсpNAc side chain to the K3 CPS. Hence, the presence of this sugar profoundly restricts the ability of the phage to digest the CPS. The 41-kb linear double-stranded DNA (dsDNA) phage genome was identical to the genome of a phage isolated on a K37-producing isolate and thus was named APK37.1. APK37.1 also infected isolates carrying KL116. Consistent with this, K3-v1 resembles the K37 and K116 structures. APK37.1 is a Friunavirus belonging to the Autographiviridae family. The phage-encoded tail spike depolymerase DpoAPK37.1 was not closely related to Dpo encoded by other sequenced Friunaviruses, including APK37 and APK116. IMPORTANCE Lytic bacteriophage have potential for the treatment of otherwise untreatable extensively antibiotic-resistant bacteria. For Acinetobacter baumannii, most phage exhibit specificity for the type of capsular polysaccharide (CPS) produced on the cell surface. However, resistance can arise via mutations in CPS genes that abolish this phage receptor. Here, we show that single-base deletions in a CPS gene result in alteration of the final structure rather than deletion of the capsule layer and hence affect the ability of a newly reported podophage to infect strains producing the K3 CPS.

Acinetobacter baumannii, capsular polysaccharide, K locus, APK37.1, K3-v1, KL3

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