Is Psoriasis a Fungal Condition?
No, psoriasis is definitively not a fungal infection—it is a chronic immune-mediated inflammatory disease with genetic predisposition, characterized by dysregulated T-cell activation and keratinocyte hyperproliferation. 1
Pathophysiology of Psoriasis
Psoriasis is fundamentally an immune-mediated organ-specific inflammatory disease in which intralesional inflammation primes basal stem keratinocytes to hyperproliferate and perpetuate the disease process. 1 The disease mechanism involves:
Genetic basis: The HLA-Cw6 allele (PSORS1) represents the major susceptibility gene, with at least 8 chromosomal loci identified for psoriasis linkage. 2
Immune dysregulation: The disease is driven by T-cell mediated autoimmune responses, particularly involving TH1 and TH17 T-helper cell subsets that play central roles in pathogenesis. 1, 2
Inflammatory cascade: TH17 cells secrete cytokines including IL-22, which promotes keratinocyte proliferation and augments production of antimicrobial peptides. 1
Cellular infiltration: Resolution of psoriasis is associated with decreased lesional infiltration of T cells, dermal dendritic cells, Langerhans cells, and neutrophils. 1
Evidence Supporting Immune-Mediated Mechanism
The immune-mediated nature of psoriasis is conclusively demonstrated by:
Treatment response: The efficacy of immunosuppressive drugs such as methotrexate, cyclosporine, immune-targeting biologic agents, and TNF-blocking biologics proves the immunologic basis. 1
Cytokine involvement: Exacerbation of psoriasis occurs with certain cytokine therapies such as interferons alfa, beta, and gamma; IL-2; and granulocyte colony-stimulating factor. 1
Biologic success: FDA-approved biologics targeting specific immune pathways (TNF-α inhibitors, IL-17 inhibitors, IL-23 inhibitors) achieve significant disease control, which would be impossible if psoriasis were fungal. 1, 3
Clinical Distinction from Fungal Infections
Psoriasis presents with pathognomonic features distinct from fungal infections:
Classic presentation: Well-demarcated, erythematous (salmon-colored) plaques with silvery scale on extensor surfaces (elbows, knees), scalp, and presacral region. 1, 4, 5
Distribution pattern: Symmetric involvement of extensor surfaces, unlike the asymmetric or annular patterns typical of fungal infections. 4
Chronicity and relapse: Psoriasis follows a relapsing course driven by immune activation, not infectious spread. 1
Common Pitfall to Avoid
Do not confuse psoriasis with fungal infections based solely on scaling or erythema. The key distinguishing features are:
- Psoriasis has well-demarcated plaques with silvery scale on extensor surfaces 4, 5
- Fungal infections typically show peripheral scale with central clearing, positive KOH preparation, and respond to antifungal therapy
- Psoriasis requires immunosuppressive or immune-modulating therapy, not antifungal treatment 1