Staph aureus throws a party in untreated eczema patches

We are not alone. Wherever we go, we carry our personal microbiological party along with us--in our gut, in our intestine, and naturally on our skin. We're crawling, even the healthiest of us, with ten bacteria, viruses, protozoa, etc. for every cell in our body.

New research has revealed an interesting difference between the skin microbiomes of patients who do and don't use pharmaceuticals to control their eczema. A recent study in the journal Genome Research finds that Staphylococcus aureus has pooped the party--it dominates the population of bacteria in untreated skin. On the skin of patients who use steroids, calcineurin inhibitors such as Protopic, or antibiotics, S. aureus shares its living quarters much more equitably with its bacterial cousins.

The authors of the paper, led by Heidi Kong and Julia Segre at NIH, used a technique called "16S ribosomal RNA bacterial gene sequencing" to catalog the bacterial population in two body locations at which eczema commonly occurs--the insides of the elbows and the backs of the knees--in 12 kids with eczema and 11 healthy controls.

(They used this type of sequencing because the method usually used to assay bacteria, which is to swab and try to grow a culture, may favor the growth of certain species over others. 16S sequencing provides a snapshot of all bacteria species present at any one time.)

S. aureus dominates flareup regions in patients who don't treat eczema. (Fig 3A.  from Kong et al.)

In the controls and the eczema patients before flareups, the bacterial populations were quite similar, with the eczema patients hosting populations in which S. aureus owned twice as much market share as it did in the controls.But during flares, the main finding was that in the patients who didn't treat their eczema (to be specific: they hadn't taken an oral antibiotic for the previous 4 weeks, or applied a topical treatment in the previous week), 90% of the bacterial population was Staphylococcus, compared to 20% for the patients who had treated their skin.

The scientists observed other shifts in the bacterial population on untreated skin, too. Several other species increased their relative numbers--especially Staphylococcus epidermidis, often thought to be a "commensal"--which I take to mean relatively harmless--species on healthy skin. It appears that S. aureus and S.epidermidis have some kind of symbiotic relationship--the two are helping each other out, or one is parasitic on the other in some way.

Very interesting research, although there's not much for an eczema patient to take away. Naively, one might think that this shows it is better to treat one's eczema than not. But there was nothing about the eczema in untreated skin being worse; the number of patients in the study is small; and there's a lot of variation (of course) among the data for the patients who treated their skin. What did they treat it with? We don't know. Could it be that applying a steroid helps keep down the S. aureus population? That would be weird indeed, because S. aureus folliculitis is a known side effect of strong steroid use. I'll go out on a limb and say that antibiotics are probably better than steroids for keeping S. aureus down in the short term.

One small frustrating point is that the 16S sequencing technique doesn't seem to provide absolute numbers. I'll exaggerate to make the point: Maybe there are 100 bacteria total in your elbow to start, 20 of which are S. aureus, and during a flare there are now 100,000 bacteria, but 90,000 of them are S. aureus. Or maybe there are 90 billion S. aureus out of 100 billion during a flare. This paper doesn't give you any idea of the scale.