Etiological and immunological aspects of equine hoof canker

Chronic equine proliferative pododermatitis (canker) is a hypertrophic hoof disease characterized by excessive proliferation of horn-producing tissues resulting from dyskeratosis of keratinocytes. Since its etiology remains unknown, this study investigated potential etiological agents and evaluated biochemical and immunological profiles. Ten horses with hoof canker and ten healthy controls of the Norik of Muran breed were included. Dermatophytes and bovine papillomavirus 1 and 2 (BPV 1/2) were not detected. Candida glabrata was the most frequently identified species in both affected and healthy groups. In horses with canker, Aspergillus fumigatus, Mucor spp., and Trichosporon spp. were also detected. Biochemical analysis showed significantly higher creatine kinase myoglobin binding activity in affected horses compared to controls (12.58 ± 5.86 vs. 4.11 ± 1.57; p < 0.01), with a slight increase in aspartate aminotransferase activity. Principal component analysis revealed substantial overlap between healthy and affected groups. Immunologically, monocyte phagocytic activity was significantly reduced in affected horses (83.78% ± 3.40 vs. 90.26% ± 2.88; p < 0.001). Affected horses had increased CD4⁺ (Th) lymphocyte counts and a higher CD4⁺:CD8⁺ ratio (p < 0.01), along with higher IgM⁺ B lymphocyte levels (27.20% ± 8.23 vs. 18.51% ± 4.53; p < 0.05). Serum IgG levels were also significantly elevated (11.15 ± 3.42 vs. 5.88 ± 1.91 mg/mL; p < 0.001). These results indicate stimulation of adaptive cellular and humoral immune responses in canker-affected horses. However, the lack of consistent pathogen detection suggests that the precise etiology of hoof canker remains unresolved and requires further investigation.