Staphylococcus aureus Colonization

In a recent review article, Piewngam and Otto examined the epidemiology, mechanisms, and clinical implications of Staphylococcus aureus (S. aureus) colonization, while evaluating both current and emerging strategies for decolonization.¹ The authors emphasize that while topical antibiotics such as mupirocin and antiseptics like chlorhexidine remain the mainstays of current practice, their long-term effectiveness is limited by recolonization, microbial resistance, and disruption of the healthy microbiome. Novel approaches, including targeted bacteriocins, phage therapy, and probiotic-based strategies, show promise but require further investigation to determine safety, efficacy, and durability.

Background and Results

S. aureus is a major cause of infectious disease–related mortality worldwide, capable of producing a wide spectrum of illnesses from mild skin infections to life-threatening bacteremia. Most infections arise from asymptomatic colonization, which occurs primarily in the nose, intestine, moist skin areas (groin, axilla), pharynx, and vagina.¹ Nasal and intestinal colonization rates are approximately 20% to 30% in adults, with the intestine potentially serving as an important source for recolonization at other sites.¹

In atopic dermatitis (AD), S. aureus colonization is especially prevalent, with more than 70% of patients showing skin or nasal colonization compared to 10% to 20% in healthy individuals.² AD skin provides an attractive environment due to impaired barrier function, reduced production of antimicrobial peptides, and altered microbiota. S. aureus exacerbates disease through multiple mechanisms, including:

Production of toxins and superantigens that activate T cells and amplify skin inflammation.³

Induction of Th2-skewed immune responses, promoting chronic inflammation and pruritus.³

Triggering of IL-23/IL-17–driven pathways that contribute to systemic immune activation.⁴

Evidence suggests that higher colonization density in AD correlates with increased disease severity.² Reducing bacterial load via antimicrobial or microbiome-based interventions has been associated with symptom improvement.

Beyond AD, S. aureus colonization is relevant in surgical site infections, prosthetic device-associated infections, bacteremia, and autoimmune conditions. The organism’s adaptation to the skin involves genetic and phenotypic changes, including resistance to antimicrobial peptides, biofilm formation, and evasion of innate immunity.5

Current decolonization strategies include intranasal mupirocin and topical antiseptics such as chlorhexidine. These are most effective for short-term, targeted use but often fail to achieve long-term eradication due to recolonization from untreated body sites or environmental reservoirs.¹

Emerging strategies include:

Targeted bacteriocins such as lugdunin from Staphylococcus lugdunensis or lantibiotics from Staphylococcus hominis that inhibit S. aureus growth without harming commensals.¹

Phage-derived lysins and bacteriophage therapy that selectively kill S. aureus.¹

Probiotic strategies, such as oral Bacillus subtilis spores producing fengycins that inhibit S. aureus quorum sensing, leading to a reduction in colonization of more than 95% reduction without altering gut microbiota.¹

Quorum-sensing inhibitors from skin commensals that prevent S. aureus biofilm formation and persistence.¹

Although these strategies show promise in preclinical and early clinical studies, they require further evaluation and long-term safety data to establish real-world efficacy.

Clinical Implications

This comprehensive review, supported by additional literature, underscores the complex interplay between S. aureus colonization, host factors, and environmental influences. In AD, colonization is more than an incidental finding; it is an active driver of inflammation and disease exacerbation.⁶ Addressing colonization may therefore improve both infectious and inflammatory outcomes.

However, decolonization is rarely permanent, especially when systemic or environmental sources remain untreated. Traditional topical regimens remain useful for high-risk patients but must be applied with care to avoid resistance and microbiome disruption.¹

Future strategies are likely to integrate microbiome-preserving and host-targeted approaches, potentially combining bacteriocins, probiotics, and immune-modulating agents. These methods hold promise for sustained control of colonization, reduced infection rates, and improved quality of life for patients with chronic inflammatory skin diseases such as AD. 

1. Piewngam P, Otto M. Staphylococcus aureus colonisation and strategies for decolonisation. Lancet Microbe. 2024;5(9):e606-e618. https://doi.org/10.1016/S2666-5247(24)00040-5

2. Ogonowska P, et al. Colonization with Staphylococcus aureus in atopic dermatitis patients: attempts to reveal the unknown. Front Microbiol. 2021;11:567090. https://doi.org/10.3389/fmicb.2020.567090

3. Chen H, et al. Exploring the role of Staphylococcus aureus in inflammatory diseases. Toxins (Basel). 2022;14(7):464. https://doi.org/10.3390/toxins14070464

4. Terui H, et al. Staphylococcus aureus skin colonization promotes SLE-like autoimmune inflammation via neutrophil activation and the IL-23/IL-17 axis. Sci Immunol. 2022;7(78):eabm9811. https://doi.org/10.1126/sciimmunol.abm9811

5. Gehrke AKE, et al. Staphylococcus aureus adaptation to the skin in health and persistent/recurrent infections. Antibiotics (Basel). 2023;12(10):1520. https://doi.org/10.3390/antibiotics12101520

6. Gallo RL, Horswill AR. Staphylococcus aureus: the bug behind the itch in atopic dermatitis. J Invest Dermatol. 2024;144(5):950-953. https://doi.org/10.1016/j.jid.2024.01.001

Peter Lio, MD

• Dermatologist
• Clinical Assistant Professor of Dermatology and Pediatrics
• Northwestern University School of Medicine
  Chicago

 Somto Ndubisi

• Medical student
• Ross University School of Medicine