Atopic dermatitis (AD), commonly known as eczema, is a chronic, inflammatory skin condition involving intense itching and a compromised skin barrier. Although not caused by bacteria alone, the severity of eczema is strongly linked to the presence of Staphylococcus aureus (Staph). This bacterium colonizes the skin of most individuals with eczema, thriving on the damaged tissue and actively worsening inflammation. Understanding this interaction is necessary for effective disease management.
The Compromised Skin Barrier
The skin barrier in individuals with eczema is structurally compromised, creating an ideal environment for S. aureus colonization. A significant factor is often a genetic variation in the filaggrin protein, which helps form the skin’s protective layer. Defects in this protein lead to a thinner, less robust outer layer, resulting in increased transepidermal water loss and characteristic dryness.
This disrupted barrier allows microbes and irritants to enter the skin and moisture to escape. Filaggrin is broken down into natural moisturizing factors that maintain skin hydration and a slightly acidic pH. When filaggrin is defective, the skin’s surface pH becomes higher, or more alkaline.
This higher pH shifts the skin’s microbiome balance, favoring opportunistic pathogens like S. aureus over beneficial bacteria. Healthy skin produces antimicrobial peptides (AMPs) as a defense. In eczema, the production of these natural antibiotics is often reduced, diminishing the skin’s ability to suppress S. aureus.
The combination of a fragile physical barrier, dryness, and reduced defenses allows S. aureus to colonize eczematous skin at rates as high as 90%, compared to 5–10% in healthy individuals. This colonization is found in both affected and unaffected skin areas. The presence of the bacteria is directly correlated with greater disease severity.
Mechanisms of Staph-Driven Eczema Worsening
Once S. aureus colonizes the compromised skin, it actively worsens eczema symptoms by releasing toxic substances. These bacterial products exacerbate inflammation, trigger the immune system, and further degrade the skin’s fragile structure. This creates a vicious cycle of inflammation, itching, and colonization that drives chronic disease flares.
Toxin Production
S. aureus releases several toxins and enzymes that directly attack skin cells and the barrier. Alpha-toxin and delta-toxin are cytolytic, meaning they damage and kill keratinocytes, the primary cells of the epidermis. Delta-toxin also stimulates mast cells, which release histamine and inflammatory mediators, increasing redness and the sensation of itch.
The bacteria also secrete proteases, enzymes that break down proteins. These proteases cleave structural proteins like desmoglein-1, further disrupting the epidermal barrier. This enzymatic destruction increases water loss and allows allergens and irritants to penetrate more easily, fueling the inflammatory response.
Superantigens
S. aureus worsens eczema through the production of superantigens, such as staphylococcal enterotoxins. These substances bypass the typical, highly specific immune recognition process. Superantigens bind broadly to T-cells and antigen-presenting cells, forcing the immune system into a state of hyperactivation.
This massive, non-specific activation leads to the widespread release of pro-inflammatory cytokines, driving systemic inflammation and intensifying the eczema rash. Superantigens can also act as allergens, promoting the production of IgE antibodies specific to the bacterial toxins. This IgE response contributes to the allergic nature of atopic dermatitis and is linked to increased disease severity and persistent itching.
Biofilm Formation
S. aureus forms biofilms, which are protective communities of bacteria encased in a self-produced matrix. This shield makes the bacteria highly resistant to the host’s immune defenses and topical antimicrobial treatments. Biofilms create a persistent reservoir of bacteria on the skin surface.
The presence of a biofilm ensures a continuous local release of toxins and proteases, perpetuating chronic inflammation and barrier dysfunction. Biofilms can colonize structures like eccrine ducts, making them difficult to eradicate and contributing to recurrent eczema flares. This resilience is why bacterial colonization is challenging to manage in severe cases.
Strategies for Reducing Bacterial Colonization
Reducing the load of S. aureus is an important part of managing eczema severity, breaking the cycle of inflammation driven by bacterial toxins. Strategies focus on topical treatments to suppress the bacteria and intensive moisturizing to rebuild the skin’s natural defenses. These approaches aim to limit microbes without causing undue resistance or irritation.
Topical Antimicrobials
When there are signs of localized infection, such as crusting or weeping, topical antibiotics like mupirocin may be prescribed for a short duration. These treatments directly target the bacteria, but their use is restricted to prevent antibiotic resistance. Mupirocin is often applied intermittently to the inside of the nose, as the nasal cavity is a common reservoir for S. aureus that can reinfect the skin.
Dilute Bleach Baths
A common strategy for reducing overall bacterial load is the use of dilute bleach baths, which employ sodium hypochlorite. When added to bathwater, the hypochlorite acts as a broad-spectrum antiseptic, helping to kill S. aureus on the skin surface. The recommended concentration is very low (approximately 0.005%), achieved by adding a half-cup of standard bleach to a full 40-gallon bathtub of water.
Patients typically soak in this solution for 5 to 10 minutes, two to three times a week. This practice can significantly reduce eczema severity, particularly in submerged areas. The benefit comes from the reduction of bacterial toxins and the suppression of the microbial population on the skin.
Antiseptic Washes
Other antiseptic alternatives are available for individuals who cannot tolerate bleach baths. Washes containing ingredients like chlorhexidine or triclosan cleanse the skin and lower the bacterial count without traditional antibiotics. These washes help manage the skin microbiome and prevent the overgrowth of pathogenic species like S. aureus.
The Importance of Emollients
While antibacterial measures address the microbial component, the long-term goal remains restoring the skin barrier. Consistent application of emollients (moisturizers) is fundamental to this process. Emollients help reduce transdermal water loss and repair the compromised physical structure of the skin.
A healthy, intact skin barrier is naturally more resistant to bacterial colonization and less prone to damage that allows S. aureus to thrive. Applying emollients immediately after bathing reinforces the skin’s structure, creating an unfavorable environment for the bacteria and helping maintain clinical improvements.