The role of Staph Aureus and other germs in atopic eczema has been known for a very long time. In healthy skin, normal immune responses just below the skin surface kill any Staph that breaches the skin surface by releasing anti-microbial peptides, AMPs.
Staph Aureus colonisation occurs in patients with atopic dermatitis, which means that patients have difficulty eradicating it, as the skin stops defending itself against invasion by the germ. Why is this?
As Staph infects the skin, it secretes both alpha and delta toxins. These are the keys to understanding colonisation.
Alpha toxins produced by Staph aureus attach to the cell membrane and can cause the death of cells such as white blood cells, designed to combat infection, and can stimulate cytokine production, leading to inflammation. This allows the germ to colonise – or co-exist with our skin biology over time.
Delta toxins produced by Staph aureus target skin mast cells, releasing granules which cause further inflammation, and cause these cells to begin an allergic type response, and aggravate the need to scratch.
There are other factors by which Staph can become more toxic to skin, including super-antigens, V8 and ETA factors, and PSM (phenol soluble modulins). These factors may cause toxic shock syndrome, scalded skin syndrome, or forms of desquamation – where the skin is left completely raw.
Although there is potential for many different organisms to infect damaged atopic skin, it is Staph aureus that increases the most during flares of eczema, and is most associated with severity in eczema.
It is the toxins secreted by Staph aureus that give rise to super-resistant bacteria such as PVL-producing Staph, or MRSA. These bacteria are very difficult to eradicate because of the way they interrupt normal defence mechanisms.
It is therefore important to include an effective anti-staph antibiotic in creams used to combat atopic eczema, and to keep using such an antibacterial for long enough to ensure colonisation is properly addressed.