Canine babesiosis is a tick-borne disease caused by the protozoan parasites of the genus Babesia. One of the significant clinical manifestations of canine babesiosis is anemia, which can range from mild to severe and contribute to the morbidity and mortality of affected dogs. The underlying mechanisms leading to anemia in canine babesiosis are complex and multifactorial. This comprehensive review aims to elucidate the pathogenesis of anemia in canine babesiosis, with a particular focus on the possible contribution of pro-inflammatory cytokines and chemokines. Numerous studies have implicated the involvement of pro-inflammatory mediators in the development of anemia, including interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and various chemokines. The dysregulation of these immune mediators can result in erythrocyte destruction, altered erythropoiesis, and dysregulation of iron metabolism. Understanding the intricate interplay between pro-inflammatory cytokines, chemokines, and the pathogenesis of anemia in canine babesiosis is crucial for the development of targeted therapeutic interventions and improved management strategies for this debilitating disease.

Canine babesiosis, pro-inflammatory cytokines, chemokines

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