Clinicians have known for decades that people with atopic dermatitis (eczema) are prone to Staph. infections (Staphylococcus aureus) on their skin. And we have also known that treatment of the infection can be critical to improving their eczema. Even when the rash is not obviously infected, nearly always Staph can be recovered from the patches of eczema.
In other words, even when the skin lesions of atopic dermatitis are not obviously infected, they are colonized, often heavily, by Staph. aureus.
The role of Staph in atopic dermatitis has become a hot topic with the recent focus on the normal skin microbiome and its disruption in disease. Like the gut, skin is normally colonized by a large number of microorganisms. Prominent among its ‘normal flora’ are several good varieties of Staphylococcus. These ‘good’ Staph growing on normal skin are usually able to keep the ‘bad’ Staph. (Staph.aureus, that is) at bay.
The ‘bad’ Staph. are known to produce a variety of toxins and proteases (enzymes that digest proteins) that can weaken the barrier and stir up the immune system – both of which are key components in the ‘pathogenesis’ (causation) of atopic dermatitis (or ‘eczema’). This leads to the obvious question: does colonization of the skin with Staph. aureus lead to the development of eczema?
Could Staph. aureus be the ‘egg’ that hatches the atopic dermatitis ‘chicken’?
A recent study out of Lausanne, Switzerland provides evidence that this could indeed by the case. Because most cases of atopic dermatitis develop in the first 2 years of life, these authors took a cohort of 149 newborns and followed them for 2 years or until a clinical diagnosis of atopic dermatitis was established. Some of the infants were considered high risk, because of a family history of ‘atopy’ (or allergy). At birth and then at regular intervals, the skin was cultured at two sites and the infants examined for signs of eczema.
They found a positive association between colonization of the skin by Staph. aureus and the development of atopic dermatitis. And most intriguingly, that this colonization preceded the development of eczema by two months on average. They also found, conversely, that colonization with a ‘good’ strain of Staph. (Staph. hominis) declined on the atopic dermatitis skin.
These studies suggest that its not that atopic dermatitis skin provides a fertile field for the growth of Staph. aureus, but that these ‘bad’ Staph. could indeed be provoking the eczema to develop in the first place.
It has also been known for decades that not only are the lesions of atopic dermatitis colonized – even the clinically uninvolved areas of skin, as well as often the nasal mucosa, of eczema patients will harbor Staph. Aureus – without showing any signs of infection. And we’ve also known that the uninvolved skin of eczema patients is not entirely normal, either. Its often drier (low moisture content), has an impaired skin barrier, and shows subtle signs of eczema under the microscope.
These authors did not measure other skin functions, particularly the skin’s barrier function, to see whether a defective skin barrier (our prediction) is the real ‘egg’ here. In other studies we have shown that the skin’s permeability barrier is intimately linked to its antimicrobial barrier. Whatever disrupts the permeability barrier will also affect its antimicrobial barrier. These barriers are joined hand in glove.
Thus, it is entirely possible that an impaired skin barrier leads to colonization with ‘bad’ Staph. which in turn promotes the development of atopic dermatitis. Hopefully, the next large prospective study will measure both barrier function and Staph. colonization to sort out which of these two scenarios is the most likely.
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