Eczema is a chronic inflammatory skin condition characterized by intensely itchy, dry, and inflamed patches of skin. The disease is not caused by a single microbe but rather by internal biological factors. Microbes from the skin’s surface play a significant secondary role in exacerbating symptoms and driving severe, persistent flares, determining the overall severity of the condition.
The Underlying Cause of Eczema
The root of eczema lies in a combination of genetic predisposition and an overactive immune response within the body. A major factor is the presence of mutations in the filaggrin gene (FLG), which is responsible for producing a protein incorporated into the outermost layer of the skin. This protein is necessary for the proper formation of the skin barrier and for maintaining hydration, and its deficiency leads to a structurally compromised surface. The resulting defective skin barrier allows moisture to escape easily and permits foreign substances, such as allergens and irritants, to penetrate the deeper layers of the skin.
Once irritants breach this weakened barrier, the immune system mounts an exaggerated response. Eczema is associated with a dysregulation of the immune system involving T-helper type 2 (Th2) cells. This immune profile promotes inflammation, which further damages the skin barrier in a self-perpetuating cycle of inflammation and damage. The primary disease process is internal immune and structural dysfunction, setting the stage for microbial communities to thrive.
The Significant Role of Bacterial Colonization
The most notable microbial complication in eczema involves the bacterium Staphylococcus aureus, which colonizes the skin of most patients with moderate-to-severe disease. While it is found on healthy skin, the colonization rate on eczematous skin can exceed 80%, compared to less than 5% on healthy skin. The damaged skin barrier and a deficiency in natural antimicrobial peptides in the skin create an ideal niche for this bacteria to multiply.
Staphylococcus aureus exacerbates inflammation by producing superantigens, such as Staphylococcal Enterotoxin B (SEB) and Toxic Shock Syndrome Toxin-1 (TSST-1). These toxins bypass normal immune pathways, causing massive, non-specific activation of T-cells that intensifies the inflammatory reaction. This intense immune stimulation contributes to the persistent redness, oozing, and crusting seen during severe flares. Superantigens also induce resistance to topical corticosteroids in T-cells, making treatment more difficult.
The high bacterial load and the presence of these toxins contribute to the severity of the disease rather than causing the initial condition. Reducing the burden of S. aureus colonization is a major goal in managing flares, as it directly reduces inflammation driven by these superantigens. The colonization also contributes to the risk of secondary skin infection, presenting as impetigo or cellulitis.
Fungal Involvement and Eczema Types
Fungi, particularly the yeast genus Malassezia, have a well-documented role in certain subtypes of eczema, such as seborrheic dermatitis. Malassezia species are lipophilic, meaning they thrive in oil-rich areas of the skin like the scalp, face, and upper chest. Seborrheic dermatitis is considered a form of eczema where the inflammatory response is triggered by the proliferation of this yeast and the irritating byproducts it creates from metabolizing skin oils.
The presence of Malassezia can also contribute to head and neck atopic dermatitis, where inflammation is localized to sebaceous areas. In these cases, the patient’s immune system exhibits an exaggerated reaction to the yeast, leading to characteristic scaling and redness. This reaction is distinct from a generalized atopic dermatitis flare, where Malassezia is less central to the pathology.
Yeast-driven inflammation must be distinguished from true dermatophyte infections, such as ringworm, which are caused by different types of fungi and are contagious. While ringworm is a true infection requiring antifungal treatment, Malassezia involvement in eczema is a reaction to a commensal organism that has overgrown or triggered an immune response. Clinical improvement seen with antifungal treatments in seborrheic dermatitis underscores the yeast’s role in driving the inflammatory cycle.
Managing Microbial Complications
Medical professionals manage microbial complications in eczema by first determining the presence and type of microbe through clinical assessment or a skin swab for culture and sensitivity testing. Identifying the specific organism, whether it is S. aureus or Malassezia, directs the subsequent treatment strategy. Targeted therapies are then used to reduce the microbial load on the compromised skin surface.
For excessive bacterial colonization, a strategy involves the use of diluted sodium hypochlorite baths. These baths are prepared at a low concentration, which is safe for the skin and reduces the S. aureus population. In cases where a frank bacterial skin infection is present, a short course of topical or oral antibiotics may be prescribed to clear the infection.
If a flare is suspected to be driven by Malassezia, especially in seborrheic areas, antifungal creams or shampoos are used to limit the growth of the yeast. Reducing the microbe population helps to break the cycle of inflammation and immune overreaction. The ongoing management of eczema requires consistent use of moisturizers and anti-inflammatory medication to repair the underlying barrier defect and keep the microbial environment balanced.