Abstract
BackgroundDiverse mechanisms (increased cell wall thickness, low cross linking, decreased autolysis, etc.) have been reported for Staphylococcus aureus strains with intermediate vancomycin susceptibility (VISA). This study was conducted to identify common mechanisms responsible for decreased vancomycin susceptibility in a VISA strain pair.ResultsTranscriptional profiling of the clinical heterogeneous VISA isolate SA137/93A and its spontaneous homogeneous mutant strain SA137/93G pointed to an increased capsule production in the strain pair compared to a susceptible control. Furthermore, transcript quantification of the gene cap5E, which is essential for capsule biosynthesis, revealed elevated levels in the VISA strains SA137/93A, SA137/93G and Mu50 in comparison with susceptible strains Reynolds, Newman and SA1450/94. The increased expression was observed in bacteria from exponential as well as stationary growth phase. However, suppression of type 5 capsule formation by expression of antisense RNA did not increase vancomycin susceptibility in the VISA strain SA137/93G. Likewise, construction of inducible mutants of S. aureus Newman or repair of capsule biosynthesis of S. aureus HG001 and S. aureus 1450/94 did not influence resistance to vancomycin. Furthermore, purified type 5 polysaccharide did not protect indicator strains from the action of vancomycin.ConclusionsThe VISA strain tested in this study displayed an increased production of type 5 capsular polysaccharide. However, the production of capsule material did not protect strain SA137/93G and three vancomycin sensitive strains in the presence of vancomycin and thus is not part of the resistance mechanism; however it may represent a by-product of VISA life style that is often characterized by a high sigma factor B activity.
Highlights
Diverse mechanisms have been reported for Staphylococcus aureus strains with intermediate vancomycin susceptibility (VISA)
We found that the genes encoding capsule biosynthesis were the only genes with higher expression in both vancomycin intermediately resistant S. aureus (VISA) strains and tested whether the staphylococcal type 5 capsular polysaccharide (CP5) might be involved in vancomycin resistance of this strain
The microarray results showed that all ORFs present in the VISA strain SA137/93A were present in strain SA1450/94
Summary
Diverse mechanisms (increased cell wall thickness, low cross linking, decreased autolysis, etc.) have been reported for Staphylococcus aureus strains with intermediate vancomycin susceptibility (VISA). Pulsed-field gel electrophoresis (PFGE) profiles, phage typing and MLST sequencing of the strains showed that they were members of the Iberian clone (ST247) which was prevalent in Germany in the early 1990’s under the designation “Northern German epidemic strain” Both strains possess a thickened cell wall [4]. Strain SA137/93A displays an IS256 insertion in the promoter region of the essential two-component system yycFG (walRK) which leads to an increased expression of this system [27] Both insertions were shown to correlate with a decrease in susceptibility to vancomycin, the difference in the vancomycin resistance level of the strain pair could be mainly attributed to the disruption of tcaA in SA137/93G [27]. The absence of mecA contributed to the higher vancomycin resistance of strain SA137/93G [4]
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