Skin Microbiome

The skin microbiome is the community of bacteria, fungi and viruses living on the skin. Its make-up depends on local pH, moisture, sebum and skin shape (Edslev, Acta Derm Venereol 2020). In healthy skin the main staphylococci are harmless “commensal” Coagulase-Negative Staphylococci such as S. epidermidis and S. hominis. Some strains of these make antimicrobial substances that kill or block Staphylococcus aureus. In Atopic Dermatitis the picture shifts. Bacterial diversity falls, S. aureus increases, and the shift tracks how severe the eczema is. S. aureus colonises about 70% of eczema lesions and 39% of non-lesional skin (Totté, BJD 2016). Commensal strains that can kill S. aureus are less common on eczema skin than on healthy skin (Nakatsuji, cited by Edslev 2020).

Staphylococcus aureus [part-of] Skin Microbiome Coagulase-Negative Staphylococci [part-of] Skin Microbiome Coagulase-Negative Staphylococci [opposes] Staphylococcus aureus Skin Microbiome [relates] Atopic Dermatitis

S. aureus dominance in flares (Kong 2012). The landmark NIH study by Kong et al. (Genome Research 2012) sequenced bacterial DNA from the elbow and knee creases of 12 children with moderate to severe eczema and 11 controls. Samples were taken at baseline, during a flare, and 10–14 days after flare treatment. Bacterial diversity dropped during flares. In flares where the child had had no recent treatment, S. aureus made up about 65% of the bacteria, against about 15% in flares where the child had been using treatment intermittently. The Staphylococcus proportion correlated with worse severity, and it fell again after treatment. Diversity was higher with even intermittent treatment (Topical Corticosteroids, antibiotics, Bleach Baths), and diversity recovered before the eczema improved. Streptococcus, Propionibacterium and Corynebacterium increased after therapy. Later reviews confirm the pattern in children and adults. In paediatric flares S. aureus often exceeds 40% of skin bacteria, and its abundance stays slightly above healthy-control levels after the flare (Edslev 2020). Low Filaggrin, loss of Natural Moisturising Factor and a raised Skin pH all favour S. aureus (Skin Barrier Dysfunction).

Staphylococcus aureus [worsens] Atopic Dermatitis Skin Barrier Dysfunction [causes] Staphylococcus aureus Skin pH [relates] Skin Microbiome Topical Corticosteroids [relates] Skin Microbiome

Conflict: [Kong et al., Genome Research, 2012] found the commensal S. epidermidis also rose significantly during untreated flares, alongside S. aureus. [Edslev et al., Acta Derm Venereol, 2020], citing paediatric flare data, says there was no change in S. epidermidis, S. hominis or S. capitis during or after a flare, and frames commensal staph as protective and depleted. Unresolved — add to open_questions.

Microbiome transplant and bacteriotherapy trials. If eczema skin lacks protective commensals, putting them back could treat it (Bacteriotherapy). Myles et al. at NIAID (JCI Insight 2018) ran the first-in-human open-label trial of live Roseomonas mucosa, a Gram-negative commensal collected from healthy volunteers, given in sugar water. Ten adults and five children aged 9–14 applied it twice weekly (16 weeks for children). There were no adverse events. 4 of 5 children improved by more than 50% on SCORAD (mean −78%). Steroid use fell, and the ratio of S. aureus to commensal staph dropped. There was no placebo arm, and the trial was later expanded to children aged 3–17. Nakatsuji et al. (Nature Medicine 2021) ran a double-blind randomised phase 1 trial of Staphylococcus hominis A9, a strain from healthy skin that kills S. aureus and blocks its inflammatory toxin. It was applied to the forearms of 54 adults with S. aureus-positive eczema for 1 week. It was safe and cut S. aureus, but eczema severity was not significantly better overall. Benefit appeared only in a post-hoc analysis of people whose S. aureus strain the A9 strain could kill. The placebo-controlled follow-up of R. mucosa (FB-401, 154 people aged 2 and over, 16 weeks) failed: about 58% on FB-401 and 60% on placebo reached EASI-50 (Dermatology 2024). No bacteriotherapy is licensed, and no trial has shown benefit in toddlers. Oral Probiotics are a different approach: they target gut bacteria, not skin.

Roseomonas mucosa [treats] Atopic Dermatitis Bacteriotherapy [opposes] Staphylococcus aureus Roseomonas mucosa [part-of] Bacteriotherapy Probiotics [relates] Skin Microbiome

Links to emollients, bleach and antibiotics. Ordinary eczema care already shifts the microbiome. One study found emollient use lowered the proportion of Staphylococcus on lesional skin, though long-term effects are unstudied (Edslev 2020) (Emollient Therapy). Bleach Baths aim to cut bacterial load. In Kong’s data one child had higher diversity in a flare after intermittent bleach baths. But reviews disagree on whether bleach beats plain water (Chopra 2017) or gives a modest gain with low-certainty S. aureus reduction (Bakaa 2022). Dupilumab raised diversity and lowered S. aureus over 16 weeks, an effect lost 18 weeks after stopping. Topical Fusidic Acid also suppresses protective commensals, and fusidic-acid-resistant S. aureus is now common on eczema skin. This is one reason guidance discourages routine antibiotics (Infected Eczema).

Emollient Therapy [relates] Skin Microbiome Bleach Baths [relates] Skin Microbiome Fusidic Acid [worsens] Skin Microbiome Dupilumab [relates] Skin Microbiome

Connections

  • Skin Barrier Dysfunction — dysbiosis and barrier failure reinforce each other, source: Edslev 2020
  • Staphylococcus aureus — colonises ~70% of AD lesions, 39% non-lesional skin, source: Totté BJD 2016
  • Bleach Baths — aim to cut bacterial load; may slightly reduce S. aureus (low certainty), source: Bakaa 2022
  • Coagulase-Negative Staphylococci — protective commensals, depleted/strain-shifted in AD, source: Edslev 2020; Kong 2012
  • Roseomonas mucosa — first-in-human topical microbiome transplant, source: Myles JCI Insight 2018
  • Roseomonas mucosa — FB-401 RCT (ages 2+) no better than placebo, source: Dermatology 2024
  • Bacteriotherapy — S. hominis A9 phase 1 RCT, source: Nakatsuji Nat Med 2021
  • Emollient Therapy — emollients lowered Staphylococcus proportion in one study, source: Edslev 2020
  • Fusidic Acid — also inhibits commensals; resistance common, source: Edslev 2020
  • Dupilumab — raised diversity, lowered S. aureus while on treatment, source: Edslev 2020
  • Probiotics — oral gut-targeted approach, distinct from skin bacteriotherapy, source: Probiotics note
  • Filaggrin — FLG loss favours S. aureus colonisation, source: Edslev 2020