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Equine piroplasmosis (EP) is the most prevalent tickborne disease in equids in certain areas of the world and not only causes important economic losses but also leads to movement restrictions.1 EP is endemic in mainland Europe and tropical/subtropical regions of Asia, South and Central America and Africa, and the increasing movement of horses between countries contributes to the spread of the disease from endemic to non-endemic areas.2-4 To prevent the introduction of carrier animals to non-endemic countries such as the USA, Canada, Australia and Japan, only seronegative horses are allowed to be imported. Moreover, the full extent of the economic losses that can be attributed to the consequences of chronic EP infection in endemic countries is unknown. For these reasons, control of EP in endemic countries is critical for the equine industry.
The disease is caused by two haemoprotozoan parasites of the phylum Apicomplexa: Babesia caballi (intraerythrocytic) and Theileria equi (intraerythrocytic and intralymphocytic). Both parasites are transmitted by ixodid ticks of the genera Rhipicephalus, Dermacentor, Haemaphysalis, Hyalomma and Boophilus, although they have different life cycles.5 Parasites of the Babesia species have a transovarial transmission in the vector and then enter directly into the host’s red blood cells as sporozoites, where they develop into piroplasms. T equi, formerly called Babesia equi, was reclassified as Theileria species6 because of its transstadial transmission in the vector and because its sporozoites do not infect red blood cells but instead penetrate lymphocytes (or macrophages), where they then develop into schizonts. Merozoites are released when infected cells rupture and they then enter the red blood cells where they develop into piroplasms.
The management of EP cases is different depending on whether the practitioners are located in an endemic or disease-free region. For disease-free regions, the early …
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