Staphylococcus epidermidis
Staphylococcus epidermidis is a type of bacterium that lives on the top layers of our skin (the epidermis) and is usually harmless. This bacterium is found all over our body, but it loves to live in moist places where we sweat from, like our armpits.
Staphylococcus epidermidis has an important job on the skin. It teaches our cells the difference between bacteria that are good for us, and ones that are bad for us and could cause infections.
However, Staphylococcus epidermidis is what is known as an ‘opportunistic bacterium’. This means that when we are healthy, it helps us to keep our skin barrier strong and stop infection, but if we have a cut, or an operation, or if we are very ill, then it takes advantage of this and can move from the surface of our skin and into the wound causing an infection.
Normally, our body has a strong immune system that can get rid of infections, but Staphylococcus epidermidis can grow with other bacteria in a biofilm. When it is in a biofilm it is hidden and harder for our body to find. Bacteria in a biofilm also stick together in clumps which take our immune system much longer to kill than if they were floating around on their own. The longer the bacteria stay alive, the more they can grow and spread.
Within a biofilm, bacteria are stuck together by a molecular ‘glue’ and protected from various components of the immune system – and from antibiotics. This can reduce antibiotic efficacy by 10 – 1000-fold. The molecular components of that ‘glue’ are known as adhesins, which are either sugar- or protein-based compounds. A lot of the time, Staphylococcus epidermidis biofilms have both sugar- and protein-based adhesins. Treatments are available that dissolve these adhesins. However, any treatments that only dissolve one type of adhesin will leave the other type unharmed, and the biofilm will survive.
One adhesin that is very well researched is called polysaccharide intercellular adhesin (PIA). It is a long chain of sugars that extend out from bacteria, allowing nearby bacterial cells to stick to each other. Interestingly, this long chain structure is also thought to mask key surface characteristics of S. epidermidis, meaning our body doesn’t recognise them and they escape the immune system.
The main treatment option for biofilms focuses on disrupting their structure and creating a window where the bacteria are more vulnerable to antibiotic treatments. This is known as ‘biofilm-based wound care’ and can cure up to 75% of patients with infected chronic wounds.
Alongside shielding bacteria from antibiotics, the mechanical barrier provided by a biofilm also protects them from being killed by our body’s protective neutrophils. Bacterial cells that are stuck together by the adhesive properties of a biofilm are an obstacle to the neutrophils’ ability to internalise, or ‘eat’ bacteria by a proves called phagocytosis; this is because the biofilm components must be broken down first, before the actual bacteria themselves can be broken down. This has been called ‘frustrated phagocytosis’ (de Vor et al., 2020).
Staphylococcus species are major components of wound microenvironments; they are found everywhere on undamaged skin and act as a reservoir of infection should the skin become damaged (Cogen et al. 2008). In diabetic foot ulcers, Staphylococcus species were identified in up to 98% of wounds (Loesche et al., 2017).
The life cycle of a staphylococcal biofilm can be divided into initial adherence to living or non-living surfaces, biofilm accumulation (characterised by the expression of adhesins (Schommer et al., 2011)), and dispersal to initiate other sites of infection (Rohde et al., 2005). Staphylococcus epidermidis biofilms express factors that can bind to a number of components laid down in a wound during the healing process, such as collagen (Foster, 2020). This makes these biofilms well suited to colonising wound environments leading to chronic infections and poor healing.
Once a certain density of bacterial cells is reached within a biofilm, the biofilm degrades in response to changing environmental cues (mediated through the quorum sensing system (Schilcher and Horswill, 2020)). Not only does degradation of the biofilm assist in perpetuating the infection, but it also allows some cells to be recognised by the immune system, thereby re-stimulating the host inflammatory response. Maintenance of inflammation leads to host tissue damage and the release of more nutrients that bacteria can use in the form of fluid leaching from the wound (Wolcott et al., 2008).
Further reading on Staphylococcus epidermidis
Cogen, A. L., Nizet, V. and Gallo, R. L. (2008) ‘Skin microbiota: A source of disease or defence?’ British Journal of Dermatology, vol. 158(3), pp. 442-55. https://doi.org/10.1111/j.1365-2133.2008.08437.x.
de Vor, L., Rooijakkers, S. H. M. and van Strijp, J. A. G. (2020) ‘Staphylococci evade the innate immune response by disarming neutrophils and forming biofilms’, FEBS Letters, vol. 594(16), pp. 2556-69 https://doi.org/10.1002/1873-3468.13767.
Foster, T. J. (2020) ‘Surface proteins of Staphylococcus epidermidis’, Frontiers in Microbiology, vol. 11, https://doi.org/10.3389/fmicb.2020.01829.
Loesche, M., Gardner, S. E., Kalan, L., Horwinski, J., Zheng, Q., Hodkinson, B. P., Tyldsley, A. S., Franciscus, C. L., Hillis, S. L., Mehta, S., Margolis, D. J. and Grice, E. A. (2017) ‘Temporal stability in chronic wound microbiota is associated with poor healing’, Journal of Investigative Dermatology, vol. 137(1), pp. 237–44, https://doi.org/10.1016/j.jid.2016.08.009.
Rohde, H., Burdelski, C., Bartscht, K., Hussain, M., Buck, F., Horstkotte, M. A., Knobloch, J. K. M., Heilmann, C., Herrmann, M. and Mack, D. (2005) ‘Induction of Staphylococcus epidermidis biofilm formation via proteolytic processing of the accumulation-associated protein by staphylococcal and host proteases’, Molecular Microbiology, vol. 55 (6), pp. 1883–95, https://doi.org/10.1111/j.1365-2958.2005.04515.x.
Schilcher, K. and Horswill, A. R. (2020) ‘Staphylococcal biofilm development: Structure, regulation, and treatment strategies’, Microbiology and Molecular Biology Reviews, vol. 84 (3), https://doi.org/10.1128/MMBR.00026-19.
Schommer, N. N., Christner, M., Hentschke, M., Ruckdeschel, K., Aepfelbacher, M. and Rohde, H. (2011) ‘Staphylococcus epidermidis uses distinct mechanisms of biofilm formation to interfere with phagocytosis and activation of mouse macrophage-like cells 774A.1′, Infection and Immunity, vol 79(6), pp. 2267–76, https://doi.org/10.1128/IAI.01142-10.
Wolcott, R. D., Rhoads, D. D. and Dowd, S. E. (2008) ‘Biofilms and chronic wound inflammation’, Journal of Wound Care, vol. 17(8), pp. 333-41, https://doi.org/10.12968/jowc.2008.17.8.30796.