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Abstract
Staphylococcus aureus is an opportunistic pathogen of humans and warm-blooded animals and presents a growing threat in terms of multi-drug resistance. Despite numerous studies, the basis of staphylococcal virulence and switching between commensal and pathogenic phenotypes is not fully understood. Using genomics, we show here that S. aureus strains exhibiting virulent (VIR) and non-virulent (NVIR) phenotypes in a chicken embryo infection model genetically fall into two separate groups, with the VIR group being much more cohesive than the NVIR group. Significantly, the genes encoding known staphylococcal virulence factors, such as clumping factors, are either found in different allelic variants in the genomes of NVIR strains (compared to VIR strains) or are inactive pseudogenes. Moreover, the pyruvate carboxylase and gamma-aminobutyrate permease genes, which were previously linked with virulence, are pseudogenized in NVIR strain ch22. Further, we use comprehensive proteomics tools to characterize strains that show opposing phenotypes in a chicken embryo virulence model. VIR strain CH21 had an elevated level of diapolycopene oxygenase involved in staphyloxanthin production (protection against free radicals) and expressed a higher level of immunoglobulin-binding protein Sbi on its surface compared to NVIR strain ch22. Furthermore, joint genomic and proteomic approaches linked the elevated production of superoxide dismutase and DNA-binding protein by NVIR strain ch22 with gene duplications.
Highlights
The genetic determinants and protein effectors that are responsible for the virulence of Staphylococcus aureus escape our full understanding despite a number of comprehensive studies
We evaluated the virulence in a chicken embryo infection model of a number of poultry originating strains of Staphylococcus aureus on a background of their genetic relationships
To determine the genomic basis of phenotypic differences between the selected strains, in this study, we obtained the genomic sequences of five highly virulent strains (CH3, CH5, CH9, CH21, and CH23) and four strains characterized by low virulence
Summary
The genetic determinants and protein effectors that are responsible for the virulence of Staphylococcus aureus escape our full understanding despite a number of comprehensive studies. Factors correlated with high pathogenicity in the group of genetically related S. aureus had little effect on the mortality rates associated with infections caused by bacteria from other clonal complexes (Recker et al, 2017). This finding indicates both the genetic and phenotypic basis of staphylococcal virulence. Despite the high heterogeneity of the analyzed proteomes, we were able to identify alpha-hemolysin and bifunctional autolysin as indicators of virulence, whereas glutamylendopeptidase production was characteristic of nonvirulent strains (Bonar et al, 2016) This prior study, did not take into account surface-attached proteins, which may contain additional virulence factors. It is rather the combined differential expression of multiple factors that determines the virulence of CH21; the rationale behind this conclusion is discussed in our communication
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