Atopic Dermatitis & Staph aureus
The Connection Between Atopic Dermatitis and Staphylococcus aureus
Atopic dermatitis (AD), often referred to as eczema, is a chronic skin condition characterised by itchy, inflamed skin. While its exact cause is multifaceted, one factor has consistently emerged as a critical player in the condition: the presence of the bacteria Staphylococcus aureus on the skin
S. aureus is a bacterium commonly found on the skin and mucous membranes of healthy individuals and usually causes no harm. However, in the context of atopic dermatitis, where the skin is dry, scratched or grazed, S. aureus concentrations on the skin are often elevated, leading to complications.
S. aureus impacts AD in several ways:
Colonisation and Skin Barrier Dysfunction:
AD patients often have a compromised skin barrier, making it easier for S. aureus to colonise.
The bacteria thrive on the damaged, dry skin typical of AD, exacerbating the condition.
Triggering Inflammation:
S. aureus produces toxins called superantigens (SAGs) that can trigger an immune response, leading to increased inflammation and worsening of AD symptoms.
This inflammation perpetuates the "itch-scratch" cycle, a hallmark of AD.
Imbalance in Skin Microbiome:
Healthy skin maintains a balance of various microorganisms, keeping each other in check. In AD, this balance is disrupted, with S. aureus often dominating.
This imbalance can reduce the diversity of beneficial microbes, further weakening the skin’s defence mechanisms.
Causes of barrier disruption, which allow for S. aureus and other bacterial overgrowth include:
The itch and scratch cycle which breaks the surface of the skin or other mechanical disruptors such as topical allergens (latex, nickel), cosmetics / soaps, dust mites
Genetics leading to a poor barrier formation e.g, FLG, an aggregating protein which provides structural integrity. Loss of function is associated with moderate to severe AD.
pH alterations usually from soaps, cosmetics, hard water, diet, sweat
Environmental e.g., low humidity environments, which lead to trans epidermal water loss (TEWL) from the skin, and dry skin is sensitive skin.
Sustained stress – leads to a reduction in lipid content in the skin along with structural proteins and an increase int TEWL.
Overgrowth of S. aureus is not just a consequence of atopic dermatitis but also a driver of its severity. Managing its concentration can reduce skin inflammation, improve symptoms like itching and redness and help restore the skin’s natural barrier function.
Barrier Dysfunction
Reducing barrier protection can lead to skin infections and progression.
I use a naturopathic perspective and work holistically, from the inside out to manage skin conditions but a complicating factor with AD in particular, is the potential for SAGs production from S. aureus. Alongside managing internal causes, reducing the bacterial load and restoring the skin barrier is critical to managing the condition as it prevents bacterial penetration of the skin and translocation, which can lead to skin infections and progression.
An important first step is to restore the skin’s pH, which means acidifying. A healthy skin pH is approximately 4.1-5.5. A pH within this range helps to suppress bacterial overgrowth but the pH of the skin is out of range, it allows for recurrent colonisation post treatment. An alkaline pH doesn’t just allow for colonisation, it can also disrupt normal skin function and repair.
This is why eczema / AD frequently reoccurs post steroids or antibacterial / antibiotic creams. An analogy I frequently use in clinic is that such treatments work in the short term, but they are akin to burning or pulling out the weeds in a garden and leaving the garden bare without planting, mulching and rebuilding the soil. The soil is denuded and so the only things that grow again are the weeds. In this case the pH and acid mantle are disrupted allowing for bacterial overgrowth.
Some strategies I use to acidify the skin include:
Application of dilute white vinegar (1 part vinegar to 40 parts water)
Choosing moisturising creams that have a pH less than 5.5. Some examples include Eucerin Eczema Relief Cream or Cetaphil cream. There are natural creams that have a pH less than 5.5 however, often the pH is not clearly indicated so check with the manufacturers before use.
Once the microbial load has been decreased, alternative creams can be used to moisturise skin.
It is also important to reduce microbial load by topically targeting SAGs contributing to progression and flares.
Topically applied Colloidal Silver can be used to breakdown bacterial biofilms. Biofims are protective layers used by bacteria to protect their environment. A useful analogy might be to see a biofilm as bacteria building a brick house rather than one made of straw.
Use of herbs such as neem, myrrh, calendula and berberine containing herbs such as barberry or Oregon grape in creams.
Black Seed Oil – for staph aureus, particularly good for hand eczema.
Dilute essential oils – three I like to use in topical creams or gels include lemongrass, tea tree or sandalwood. Please note the application of essential oils to damaged skin needs to be done with care and specificity, and used incorrectly, they can easily irritate skin.
Black Seed Oil
Antimicrobial & anti-inflammatory
Once the bacterial load has reduced and pH restored, then it is critical to restore barrier function. This topic will be covered in a separate article.
Understanding the connection between atopic dermatitis and S. aureus highlights the importance of a comprehensive approach to managing this chronic condition. While conventional treatments like steroids and antibiotics may provide temporary relief, they do not address the root causes of bacterial overgrowth and skin barrier dysfunction. By focusing on restoring the skin's pH, reducing microbial load, and strengthening the skin barrier, the cycle of recurrent flares and inflammation can be addressed. A holistic approach that combines targeted topical treatments with internal support can significantly improve symptoms and long-term skin health.