Eczema and Staph

Staphylococcus aureus, often referred to as “staph,” is a very common bacteria. Approximately 25-30% of healthy people carry this organism on their skin or in their nose.

There is an important distinction to be made between staph colonization and infection.

Colonization = the presence of the bacteria, but no signs of illness or infection. Staph thrives in warm, moist places; common sites of colonization include the nostrils, belly button, underarms, groin, etc.

Infection = clinical signs of illness or inflammation (e.g., localized pain/tenderness, redness, warmth, swelling; pus; fever). These are due to tissue damage caused by invasion by the bacteria. Infection requires treatment – various treatment options exist. Treatment does not always require the use of an antibiotic.


Colonization of staph does not require treatment. Most individuals are unaware if they are colonized as the bacteria presents no symptoms.

The Relationship to Eczema

The role that staph plays in eczema is just now becoming widely known and it’s changing the way eczema is being treated. A 2013 published medical study brings to light the role that staph plays in eczema – revealing that “more than 90% of AD patients are colonized with Staphylococcus aureus in the lesional skin whereas most healthy individuals do not harbor the pathogen”.

If colonization doesn’t require a treatment, and “healthy” individuals routinely carry staph on their skin, should we be concerned that the incidence of bacterial colonization is this high for individuals suffering with atopic eczema?

In a newly published 2015 medical journal title “How bacterial pathogens colonize their hosts and invade deeper tissues“, we are presented with a detailed look of when some bacteria – the aforementioned Staphylococcus aureus in particular, are able to penetrate the skin, creating infection for the host.

The human body harbors a large number of bacteria but their localization in healthy individuals is normally restricted to certain body areas such as the skin, the mucosae of buccal and nasal cavities, vagina and, most importantly, the gastrointestinal tract. The internal tissues are normally sterile. In some circumstances, however, some opportunistic pathogens are able to enter the host by taking advantage of injuries or breaches in one of the different host barriers. In addition, bona fide pathogens have evolved mechanisms to cross host barriers and reach deeper organs where they proliferate and lead to severe disease for their host.

In short, it’s not “normal” to have staph outside of the places it’s typically found – and we know that eczema lesions can be found in every area of the body. When this happens, we run the risk of colonization turning into infection – and that infection can even spread internally.

As the paper continues, we are again reassured that “some bacteria are able to enter and to proliferate inside host cells.”

In the conclusion of the journal (section 5), we are informed that “whereas most pathogens are unable to cross the skin barrier, they can however access the underlying tissues via ruptures in the skin, such as cuts, microlesions or bites (in particular for pathogens transmitted via arthropod vectors).”

While the discussion of arthropod vectors (fleas, mosquitoes, ticks, fleas, etc) are a topic for a different conversation, we find that open skin ruptures and microlesions (common with eczema) will both allow the colonization of bacteria to enter the cells and create infection.

However, increasing evidence now shows that bacteria initially thought to remain strictly extracellular can indeed be found inside host cells as exemplified by the case of Staphylococcus aureus.

In summarizing our pathogen puzzle, we now know that over 90% of eczema lesions are colonized with Staphylococcus aureus bacteria. This colonization can turn to infection at any time – whereas most people carrying staph in the usual places staph is found may never have an issue. These individuals are low risk while eczema sufferers have an extremely high risk of bacterial infection. These medical facts might well explain why a short “burst” of antibiotics does little for ongoing eczema treatments. This conventional approach may work temporarily but so long as there are open wounds and the eczema is untreated, the colonization of staph bacteria remains or returns – and thus, the risk of infection increases.

This understanding gives further insight to the success of Dr. Aron’s treatment for atopic eczema, the “Aron Regime”. Dr. Aron insists that conventional antibiotic prescriptions are not appropriate for atopic eczema, and neither are topical steroids alone. By prescribing a longer term dose of antibiotics in a heavily diluted moisturizer along with a topical steroid, the bacterial element of atopic eczema is properly addressed while inflammation is reduced and the skin continues to be moisturized. Healing can finally happen.

Dr. Aron’s is the good news we’ve been waiting to hear, for the world of eczema and red skin sufferers.

Are you curious if you have staph bacteria that puts you at risk of infection? Talk to your doctor and request a skin swab of the eczema lesion.