Genetic variability in the sdrD gene in Staphylococcus aureus from healthy nasal carriers

Abstract

BackgroundStaphylococcus aureus cell wall anchored Serine Aspartate repeat containing protein D (SdrD) is a member of the microbial surface component recognising adhesive matrix molecules (MSCRAMMs). It is involved in the bacterial adhesion and virulence. However the extent of genetic variation in S. aureus sdrD gene within isolates from healthy carriers are not known. The aim of this study was to evaluate allelic variation of the sdrD gene among S. aureus from healthy nasal carriers.ResultsThe sdrD A region from 48 S. aureus isolates from healthy carriers were analysed and classified into seven variants. Variations in the sdrD A region were concentrated in the N2 and N3 subdomains. Sequence analysis of the entire sdrD gene of representative isolates revealed variations in the SD repeat and the EF motifs of the B repeat. In silico structural modelling indicates that there are no differences in the SdrD structure of the 7 variants. Variable amino acid residues mapped onto the 3D structure revealed that the variations are surface located, exist within the groove between the N2-N3 subdomains and distributed mainly on the N3 subdomain. Comparison of adhesion to keratinocytes in an in vitro cell adhesion assay, using NCTC 8325–4∆sdrD strains expressing the various sdrD gene variants, indicated a significant difference between only two complements while others showed no major difference in their adhesion.ConclusionsThis study provides evidence of sequence variations across the different domains of SdrD from S. aureus isolated from healthy nasal carriers. Proper understanding of these variations is necessary in the study of S. aureus pathogenesis.Electronic supplementary materialThe online version of this article (10.1186/s12866-018-1179-7) contains supplementary material, which is available to authorized users.

The genetic feature and virulence determinant of highly virulent community-associated MRSA ST338-SCCmec Vb in China

“…All ST338 isolates as well as ST59-SCCmec Vb strains harboured similar virulence factors and genomic islands; however, the former lacked the clfA, clfB, ebp, cna, sdrC, and sdrD genes found in MW2 and USA300. ClfA promotes bacterial colonization and adhesion [45]; clfB, sdrC, and sdrD mediate adhesion to human nasal mucosa [46][47][48]; and Cna is involved in tissue colonization [49]. Experiments in mice and human alveolar epithelial cells showed that ST338 had a lower nasal colonization capacity than MW2, which is consistent with its lack of adhesion factor genes (clfA, clfB, ebp, sdrC, and sdrD).…”

The intra-host evolutionary landscape and pathoadaptation of persistent Staphylococcus aureus in chronic rhinosinusitis

“…To our knowledge, such recombination has not been previously reported in S. aureus. While it is known that serine-aspartate repeat MSCRAMM proteins are variable and contribute to biofilm formation [93,94], more work needs to be done to characterise the relationship between divergent serine-aspartate repeat MSCRAMM proteins and their relationship to within-host adaptation.…”

The Intra-Host Evolutionary Landscape And Pathoadaptation Of PersistentStaphylococcus aureusIn Chronic Rhinosinusitis

“…To our knowledge, such recombination has not been previously reported in S. aureus . While it is known that serine-aspartate repeat MSCRAMM proteins are variable and contribute to biofilm formation (Ajayi et al, 2018; Barbu, Mackenzie, Foster, & Hook, 2014), more work needs to be done to characterise the relationship between divergent serine-aspartate repeat MSCRAMM proteins and their relationship to within-host adaptation.…”