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The Theileria life cycle begins when a tick injects infectious sporozoites into the blood stream of a suitable mammal host (Figure 3.11). Theileria parva sporozoites are non‐motile and unlike those of many other apicomplexans, they do not actively invade the host cell. Instead, they make random contact with T and B‐lymphocytes and attach to host cell receptors. The host cell then internalizes the parasite and surrounds it with a vacuole membrane. The parasites do not orientate themselves in relation to the host cell, and they discharge the contents of their rhoptries and micronemes only after entering it. These chemicals cause the vacuole membrane to disperse so that the parasites lie free within the cytoplasm of the lymphocytes. The sporozoites then transform into multinucleate schizonts and induce the host cell to proliferate: the parasites are closely associated with the lymphocyte mitotic apparatus and divide with their host cell so that daughter lymphocytes are also infected. The first generation of schizonts are called ‘macroschizonts’ and these give rise to ‘macromerozoites’ that invade other lymphocytes and give rise to either more macroschizonts and macromerozoites or to microschizonts that give rise to micromerozoites. The micromerozoites may invade either lymphocytes or red blood cells. Those invading lymphocytes continue to multiply by schizogony, but those invading red blood cells differentiate into ‘piroplasms’ that do not divide any further but are infectious to the tick vector. The piroplasms are extremely small, typically 1.5–2 μm long and 0.5–1μm wide and rod‐shaped although oval, comma, and ring‐shaped forms also occur. They are a characteristic diagnostic feature of East Coast fever. The digestion of infected red blood cell within the tick gut lumen releases the piroplasms, and they differentiate into either microgametocytes or macrogametocytes. The microgametocytes and macrogametocytes fuse to form a diploid zygote, and this invades the tick gut epithelial cells where it transforms into a motile ‘kinete’ form. The kinetes make their way through the body to the tick salivary glands where they invade the type III acini cells and undergo sporogony to produce numerous infectious sporozoites.

Figure 3.11 Life cycle of Theileria parva. 1: An infected tick injects sporozoites into a cow’s bloodstream, and these are internalized by T‐ and B‐lymphocytes within which they transform into multinucleate schizonts. 2: Schizogony results in the formation of merozoites that are released when the host cell dies. 3: Infected lymphocytes are induced to divide and the parasites infect each new cell as it forms. The first generation of schizonts (macroschizonts) form ‘macromerozoites’ that invade other lymphocytes and give rise to either more macroschizonts and macromerozoites or to microschizonts that give rise to micromerozoites. The micromerozoites invade either lymphocytes or red blood cells. 4: Micromerozoites invading red blood cells differentiate into piroplasms that do not divide any further but are infectious to the tick vector. 5: The piroplasms are released within the tick gut lumen and differentiate into either microgametes or macrogametes. The microgametes and macrogametes fuse to form a diploid zygote, and this invades the tick gut epithelial cells where it transforms into a motile kinete. 6: The kinetes make their way through the tick’s body to its salivary glands where they undergo sporogony to produce sporozoites. The sporozoites are released into the saliva and are transmitted when the tick feeds. Drawings not to scale.