Eczema (atopic dermatitis) is a chronic skin condition characterized by persistent inflammation, intense itching, and dry, scaly patches. While it affects millions globally, it is fundamentally a disorder of the immune system and the skin barrier, not a primary infection. Microbes become relevant only as secondary factors that trigger flare-ups and worsen the underlying disease.
Eczema as an Inflammatory Skin Barrier Disorder
Eczema is primarily a genetically influenced condition where the outermost layer of the skin, the epidermal barrier, fails to function correctly. This defect is often linked to mutations in the filaggrin gene, which compromises the structural integrity of skin cells. A deficiency in this protein reduces the production of natural moisturizing factors.
This structural weakness leads to a significant increase in Transepidermal Water Loss (TEWL), causing the characteristic extreme dryness of eczematous skin. The barrier is also weakened by an altered lipid composition, specifically a reduction in essential fats called ceramides that function as the “mortar” holding the skin cells together.
This compromised barrier allows allergens, irritants, and environmental pollutants to penetrate the skin more easily. Once these substances cross the barrier, they trigger an overactive immune response in the deeper layers. This internal immune reaction is the source of the chronic inflammation, redness, and severe itching that defines eczema. The resulting inflammation further damages the skin barrier, creating a self-perpetuating cycle of dysfunction and symptoms.
The Role of Bacteria in Eczema Flares
While eczema is not caused by bacteria, up to 90% of patients experience significant colonization of their lesions by the bacterium Staphylococcus aureus (S. aureus). This overgrowth, known as dysbiosis, is encouraged by the altered environment of eczematous skin, including a higher surface pH and reduced levels of natural antimicrobial peptides.
The presence of S. aureus is a major driver of flare-ups because the bacterium secretes numerous toxins. These virulence factors, such as hemolysins and superantigens, directly damage the skin cells and further compromise the already fragile epidermal barrier. Specifically, superantigens released by the bacteria can cause a disproportionate activation of the immune system, leading to a massive inflammatory reaction.
This exaggerated immune response exacerbates the redness, swelling, and itching associated with a flare. The bacteria’s toxins also contribute to the breakdown of the skin’s microbiome diversity, reinforcing the cycle of colonization and inflammation. Therefore, the bacteria are not the initiating cause but an opportunistic microbe that aggressively worsens the condition.
Fungal Involvement in Specific Eczema Types
The question of fungal involvement is generally less central to the overall eczema narrative but becomes important in specific types of the condition. The most common fungus implicated is the yeast Malassezia, a normal inhabitant of the skin that thrives in areas rich in sebum, or skin oil. This yeast is strongly linked to seborrheic dermatitis, an eczematous condition that typically affects the scalp, face, and chest.
In susceptible people, an overgrowth of Malassezia triggers an inflammatory response, which is a reaction to the yeast itself or its metabolic byproducts. As the yeast breaks down the sebum, it produces irritating fatty acids that can disrupt the skin barrier and induce an immune reaction. This process results in the scaly, inflamed patches characteristic of seborrheic dermatitis.
It is important to distinguish this inflammatory reaction from true fungal infections like ringworm, which is caused by dermatophytes and can sometimes look like eczema. While ringworm is a primary infection, Malassezia involvement is primarily an immune sensitivity to an overgrowth of a normal skin organism. Effective management of these specific eczema types often requires addressing the yeast population alongside the inflammation.
Treating Eczema: Targeting Inflammation and Microbes
Effective management of eczema requires a comprehensive approach that recognizes its dual nature as an inflammatory barrier defect complicated by microbial factors. The first line of defense focuses on restoring the skin barrier and reducing inflammation. Daily application of moisturizers, particularly those formulated with ceramides, helps repair the deficient lipid layer and minimize Transepidermal Water Loss.
Inflammation is addressed using anti-inflammatory medications, such as topical corticosteroids or calcineurin inhibitors, which work to calm the overactive immune system. Simultaneously, microbial management is necessary to control the secondary factors that drive flares. This may involve using antiseptic washes or targeted antibiotics to reduce the load of S. aureus during acute infections.
Where Malassezia is implicated, antifungal treatments may be used to control the yeast population, often alongside anti-inflammatory agents. Research is also moving toward novel therapies, such as the topical application of beneficial bacteria, to rebalance the skin’s natural microbiome and suppress the growth of harmful organisms. The overall goal is to control the environment of the skin, not to simply treat a primary infection.