Staphylococci: Colonizers and Pathogens of Human Skin

Rosanna Coates; Josephine Moran; Malcolm J Horsburgh

Disclosures

Future Microbiol. 2014;9(1):75-91. 

In This Article

Desiccation, Osmotic & Matric Stress Resistance Mechanisms

Desiccation tolerance is important for staphylococcal transmission and may affect survival on the skin if the RH falls below the threshold for growth. When S. aureus or S. epidermidis are grown at RH levels approaching their growth limit they become larger, form thicker cell walls and form cuboidal packs of eight cells rather than their typical grape-like clusters.[123,124] Similar observations were made for staphylococcal autolysin mutants, revealing that this morphological switch is likely to be autolysin controlled.[124] These morphology changes could limit water loss and osmotic stress by reducing surface area:volume ratio to maintain turgor pressure. Staphylococci grown at low RH are more hydrophilic, which aids water acquisition.[124] Desiccation tolerance, or its recovery from being subjected to this stress, requires antioxidant activity (catalase, alkylhydroperoxide reductase), regulatory activity via accessory σ factor B and the ClpX protease.[125]

The ability to produce the polysaccharide intercellular adhesin (PIA) in staphylococci might contribute to desiccation tolerance. de Goffau et al. identified high tolerance to low RH in the PIA-producer RP62a.[123] PIA might act similarly to Pseudomonas aeruginosa exopolysaccharide (EPS) to limit desiccation.[126] EPS slows the rate of water loss to increase the time for bacteria to adapt; EPS also slows rehydration to aid adaptation.[126]

Ebh is a giant (~1.1 MDa) cell wall-associated protein found in S. aureus and S. epidermidis. Ebh mutants exposed to high salt conditions reveal invaginated vacuoles along their septum within the first 30 min, suggesting that this contributes to initial osmotic stress resistance via a role in cell wall and membrane architecture.[127]

Membrane zwitterionic phospholipids decrease in conditions of increasing salinity in both Gram-positive and -negative bacteria. Cardiolipin (CL) contributes to osmotic stress resistance and CL synthase of E. coli is induced in response to osmotic stress and catalyzes the conversion of peptidoglycan into CL and glycerol. S. aureus encodes two CL synthase genes, and mutation of both genes reduced long-term survival in high salinity media;[128] however, levels of CL did not significantly increase in response to 2.7 M NaCl. In its annular phase, CL is theorized to regulate the mechanosensitive channel MscL and the osmosensory transporter ProP.[129] CL also decreases membrane fluidity in the bulk lipid phase.[128]

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