Figure 1. Illustration representing Staphylococcus aureus on inflamed skin (Getty Images).
Staphylococcus aureus (S. aureus) is now confirmed as a direct trigger of the eczema itch, but if we stop there we may be missing more clinically useful questions: what is allowing it to thrive and how do we address this before Staph takes hold?
Key clinical terms: atopic dermatitis, eczema, pruritus, Staphylococcus aureus, skin microbiome, acid mantle, V8 protease, PAR1, skin barrier function
Itch is the defining and most debilitating symptom of eczema (atopic dermatitis), profoundly affecting quality of life, sleep and psychological wellbeing in both children and adults. While the causes of the associated itch are multifactorial, evidence implicates S. aureus as a key microbial driver of itch and an active participant in the itch–scratch–inflammation cycle.
S. Aureus is Common on Eczema, and not by Chance
A proliferation of S. aureus is found on the skin lesions of 70% of individuals with eczema, compared with less than 5% of healthy-skinned individuals (Totté et al., 2016).
This disproportionate colonisation is not incidental.
In eczema, the acid mantle, skin microbiome and barrier are disrupted, creating the ideal conditions in which S. aureus thrive, with reduced competition from protective, skin ‘friendly’ bacteria (Nakatsuji et al., 2023, as cited in Gallo & Horswill, 2024).
The result is a compromised skin surface where staph thrives, multiplies and directly triggers the itch.
How S. Aureus Bypasses Inflammation to Trigger Itch
Until recently, the mechanism by which S. aureus directly induces itch remained poorly understood. In a landmark study by Deng et al. (2023), it was established that epicutaneous exposure to S. aureus causes robust itch and scratch-induced skin damage in murine models, while subcutaneous infection did not produce the same response—a finding that highlights the significance of surface colonisation over deep tissue infection, and is directly relevant to the pattern seen in eczema.
A toxin produced by S. aureus, called serine protease V8, has been identified as the key itch-triggering factor, activating PAR1 on itch-sensing nerves in the skin to send a signal directly to the brain (Deng et al., 2023; Gallo et al., 2024). This triggers the urge to scratch.
Importantly, Deng et al. (2023) demonstrated that itch and skin inflammation are not the same process and do not require each other. Bacterial strains that caused less inflammation still triggered itch and blocking the PAR1 receptor reduced itch without reducing inflammation scores. This tells us that the V8–PAR1 pathway drives itch directly through the nervous system, independently of the inflammatory mediators that most eczema treatments are designed to target.
This research helps to explain why a patient's skin can become less inflamed through medical treatments and still be intensely itchy.
Figure 2. The itch of eczema is not caused by inflammation alone, it is triggered directly by S. aureus, which releases a toxin that activates itch-sensing nerves independently of the inflammatory response (Deng et al., 2023).
The scratching that follows then damages the skin barrier further, allowing S. aureus to penetrate more deeply, and it is at this point that secondary skin infections may develop (Deng et al., 2023). Impetigo, cellulitis and recurrent infected eczema are well-recognised clinical consequences of this cycle.
In severe flares, S. aureus induces epidermal thickening and elevation of Th2 and Th17 cells, driving inflammation (Byrd et al., 2017). This reinforces a straightforward but clinically important principle: making the skin environment inhospitable to S. aureus before colonisation takes hold is more beneficial to a person's quality of life, rather than treating infected eczema after the damage has been done.
If we can address the conditions that allow S. aureus to thrive in the first place, we may be able to stop the cycle before it starts and improve an eczema patient's quality of life.
Which raises the question: what allows S. aureus to thrive there in the first place?
Why S. Aureus Thrives on Eczema: The pH Problem
An elevated skin pH above 5.5 is linked to multiple inflammatory and infectious skin conditions, including acne vulgaris, dry skin, seborrheic dermatitis, ichthyosis vulgaris, candidiasis and diaper dermatitis (Brooks et al, 2025; Hülpüsch, 2020).
Multiple studies have also consistently demonstrated that eczema-prone skin has an elevated stratum corneum pH, typically in the range of 5.5–6.5 (Rippke et al., 2004; Brooks et al, 2025; Hülpüsch, 2020). Interestingly, skin pH becomes even more alkaline during flares and the higher the pH, the more severe the eczema presents (Kong et al., 2012).
The clinical consequences may be significant.
Research has demonstrated that S. aureus thrives at elevated skin pH 5.7–6.2 in eczematous skin (Hülpüsch, 2020) (Figure 3). At an elevated pH of 6.0–7.0, S. aureus adhesion to keratinocytes may increase, the efficacy of antimicrobial peptides may be reduced and the structural integrity of stratum corneum lipids, including ceramides and free fatty acids, may be compromised (Rippke et al., 2004).
Figure 3. Illustration of human skin. When skin surface pH is above 6.0 the protective microbiome may dislodge, stratum corneum dries and cracks and provides an optimal environment for Staphylococcus aureus to thrive.
The pH of Healthy Skin Leaves Clues
In contrast, healthy skin typically has an acidic pH under 5.0, with an average pH of 4.7 when pH is not skewed by tap water or skincare (Lambers et al, 2006). This acid mantle is crucial for skin barrier function, it provides antibacterial protection and promotes adherence of the microbiome to the skin’s surface (Li, et al. 2023; Lambers et al, 2006).
Even a small rise in skin pH can disrupt the skin's natural defence against bacteria, speed up skin cell shedding and trigger pro-inflammatory cytokines (inflammation). These are changes commonly seen in eczema-prone skin (Ng et al, 2024).
Furthermore, studies show that Staph colonisation is markedly reduced in an acidic environment around pH 5.0 and under. (Rippke et al., 2004).
Figure 4. Illustration of human skin. When skin surface pH is below 5.0 the natural microbiome adheres to skin and forms a protective barrier.
The Role of Lactic Acid in Restoring the Acid Mantle
Lactic acid (lactate) is a component of the stratum corneum, produced via sweat secretion and keratinocyte metabolism. In eczematous skin, stratum corneum lactate levels are significantly reduced compared to levels in healthy skin, correlating with pH elevation and compromised barrier function (Sugawara et al., 2012).
Within a low pH skincare product, topical lactic acid may help restore stratum corneum acidity through two complementary mechanisms. First, it directly lowers surface pH, creating an environment less hospitable to S. aureus colonisation and growth (Costa & Horswill, 2022; Hayashi et al., 2021). Second, in an acidic environment around pH 4.5, lactic acid may exert a bacteriostatic effect on S. aureus that is independent of pH reduction alone (Rippke et al., 2004), working synergistically to suppress bacterial growth.
Topical low pH emollients formulated at pH 4.5–5.0 have been shown to support barrier recovery and may reduce S. aureus colonisation in eczema. In contrast, soaps and cleansers with a pH at or above 5.5 may contribute to disruption of the acid mantle and create conditions that favour bacterial overgrowth and the itch that follows.
It is worth noting that so-called "pH balanced" skincare products may not offer the protection the term implies. This claim has its roots in a widely held belief within the skincare and cosmetic chemistry industry that pH 5.5–6.0 represents healthy skin pH — a reference range that has since been disproven. Lambers et al. (2006) demonstrated that healthy skin surface pH is on average below 5.0, and that the 5.5–6.0 range more accurately reflects the pH of eczema-affected or elderly skin (Rippke et al., 2004; Lambers et al., 2006). Despite this, the outdated figure continues to inform product formulation and marketing across the skincare industry, meaning many products labelled "pH balanced" may inadvertently maintain the very skin conditions associated with eczema, rather than supporting recovery from it.
Clinical Implications: Why Treating Staph Alone may not be Enough & What to Include in Treatment Plans
The evidence reviewed here suggests several practical considerations in the management of eczema-associated itch:
- S. aureus surface colonisation may be a direct and independent trigger of itch, operating independently of classic inflammatory cytokine cascades (Deng et al., 2023).
- Skin surface pH elevation in eczema may create a favourable environment for S. aureus colonisation and reduce the efficacy of the skin's own antimicrobial defence mechanisms (Rippke et al., 2004).
- Topical skincare formulated at pH 4.5–5.0 and containing lactic acid may support restoration of the acid mantle, inhibit S. aureus colonisation and contribute to a reduction in bacterially mediated itch (Hayashi et al., 2021; Costa & Horswill, 2022).
- Clinicians may consider advising patients to avoid alkaline soaps and cleansers, even pH balanced skincare, which may disrupt the acid mantle and facilitate S. aureus overgrowth.
Figure 5. Salt baths, clay baths, bleach baths and soap all share a common problem—they are all alkaline, meaning any of them used alone without pH restoration afterwards may contribute to the alkaline skin environment that favours S. aureus colonisation on eczema.
A Note on Bleach Baths
Dilute bleach baths, where bleach is added to lukewarm water, are commonly recommended to reduce S. aureus colonisation in eczema and some studies report improvements in barrier function and itch. However, household bleach has a pH of approximately 11–13, which is strongly alkaline and may temporarily elevate an already-alkaline skin surface. This could inadvertently recreate the conditions that allow S. aureus to re-establish on eczema. Clinicians may wish to reconsider bleach baths as a standalone intervention, or consider following each bath with rinsing and a low pH emollient formulated at pH 4.5 to help restore the acid mantle.
Staph is not the Whole Story but it's the Clue we Needed
Staphylococcus aureus is not merely a commensal opportunist in eczema—it may be an active and direct driver of itch, independent of classical inflammatory mediators.
The role of elevated skin pH in facilitating S. aureus colonisation provides a compelling mechanistic rationale for low pH, lactic acid-containing skincare as part of a comprehensive eczema management strategy. Maintaining the acid mantle at physiological pH 4.5–5.0 may represent one of the most accessible and evidence-informed approaches to interrupting the itch–scratch–colonisation cycle at its source.
Putting the Evidence into Practice
For clinicians seeking to recommend a low pH emollient and cleanser for eczema patients, Skin Friend's low pH skincare range is formulated at pH 4.5–5.0 and contains lactic acid, developed specifically to support the acid mantle and microbiome in eczema-prone skin. Product information is available at skinfriend.com.au.
References:
Deng L, Costa F, Blake KJ, Choi S, Chandrabalan A, Yousuf MS, et al. S. aureus drives itch and scratch-induced skin damage through a V8 protease–PAR1 axis. Cell. 2023;186(24):5375–5393.e25.
Gallo RL, Horswill AR. Staphylococcus aureus: the bug behind the itch in atopic dermatitis. J Invest Dermatol. 2024;144(5):950–953.
Totté JEE, et al. Prevalence and odds of Staphylococcus aureus carriage in atopic dermatitis: a systematic review and meta-analysis. Br J Dermatol. 2016;175(4):687–695.
Rippke F, Schreiner V, Doering T, Maibach HI. Stratum corneum pH in atopic dermatitis: impact on skin barrier function and colonization with Staphylococcus aureus. Am J Clin Dermatol. 2004;5(4):217–223.
Lambers H, Piessens S, Bloem A, Pronk H, Finkel P. Natural skin surface pH is on average below 5, which is beneficial for its resident flora. Int J Cosmet Sci. 2006;28(5):359–370.
Costa FG, Horswill AR. Overcoming pH defenses on the skin to establish infections. PLoS Pathog. 2022;18(5):e1010512.
Hayashi K, Nagano Y, Sakata K, et al. Analysis of hand environment factors contributing to the hand surface infection barrier imparted by lactic acid. Skin Res Technol. 2021;27(6):1135–1144.
Byrd AL, et al. Staphylococcus aureus and Staphylococcus epidermidis strain diversity underlying pediatric atopic dermatitis. Sci Transl Med. 2017;9(397):eaal4651.
Sugawara T, et al. Decreased lactate and potassium levels in natural moisturizing factor from the stratum corneum of mild atopic dermatitis patients are involved with the reduced hydration state. J Dermatol Sci. 2012;67(3):196–201.
