Membrane and cell wall responses in Staphylococcus aureus to changes in environmental parameters representative of the human wound site

Staphylococcus aureus is renowned pathogen and significant burden on the healthcare system, as it is a major cause of both community and nosocomial infections. Strains of S. aureus (MRSA and VRSA) exhibit forms of resistance to all known antibiotic classes. S. aureus has the capability of surviving in harsh and dynamic environments as a consequence of coevolution with its host. The invasion of a wound site by a commensal bacterium is a common opportunistic transition and can lead to a state of chronic infection. As the bacterium enters the wound it will be confronted with an array of environmental stresses including changes in temperature, pH and osmotic pressure differentials. Common adaptation strategies include formation of biofilms, small colony variants (SCV) as well as changes in the composition of the cell membrane and cell wall. The cell membrane provides a selective barrier between the cytoplasm and the external environment and houses essential integral and transmembrane proteins. It facilitates diffusion and alterations in membrane composition resulting in changes in fluidity which are crucial for survival. Alteration of the properties of the membrane can be achieved via adjusting in the distribution of fatty acids within the phospholipids. The mechanisms and rates of adaptation have not been characterized for Staphylococci. Results to date have determined that changes in pH and osmotic pressure similar to those that may be experienced in the wound site, impart significant changes in the fatty acid composition of the bacterial membrane in 1~2 hours. Understanding the process of membrane alteration is ultimately important in S. aureus as the fatty acid biosynthetic pathway is unique to bacteria and is fundamental to the bacterium’s persistence in an infection scenario. Targeting this adaptation process may offer new insights for developing antimicrobial control of staphylococcal infections.