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This is the commonest and most pathogenic of the seven species of Eimeria that infect domestic poultry. Each Eimeria species develops in a different region of the bird’s digestive tract, and co‐infections with two or more species are common. Eimeria tenella occurs throughout the world and is responsible for a great deal of economic loss. Although it can cause high flock mortality, the availability of vaccines and anticoccidial drugs coupled with effective hygiene means that most losses result from chronic and subclinical infections causing reduced growth and egg production.

The life cycle is monoxenous (i.e., involves a single host) and begins when a bird ingests an infective oocyst with its food or in its water. The oocyst releases infective sporozoites when it reaches the small intestine. Gut peristalsis moves sporozoites down the intestinal tract with the digesta and once they reach the caecum, they invade the intestinal epithelial cells. In common with the other species of Eimeria, a membrane bound parasitophorous vacuole of host cell origin surrounds all the intracellular stages. The incorporation of parasite proteins into the vacuole membrane prevents the fusion of lysosomes or other vesicles. The sporozoites travel through the epithelial cells and emerge into the lamina propria where macrophages promptly ingest them. The macrophages act as a sort of transport host and move the parasites to the glands of Lieberkuhn where they escape and invade the glandular epithelial cells. Within the epithelial cells, the parasites transform into meronts and undergo a form of asexual reproduction called merogony to produce numerous merozoites. This kills the host cell and releases the merozoites to invade other caecal epithelial cells within which they produce another generation of merozoites. The parasites kill these host cells and following their release, these second‐generation merozoites invade new epithelial cells. However, at this point, for some reason, the subsequent development can follow one of two paths. Some of the merozoites will give rise to a third generation of merozoites, whilst others undergo gametogony to produce become either macrogametocytes (female) or microgametocytes (male). The microgametocytes leave their host cell and invade those containing a macrogametocyte and fuse with it to effect fertilization. After fertilization, the macrogamete transforms into a zygote and then into an oocyst. The oocyst contains only a single cell – referred to as the sporont. The oocyst leaves the host bird in its faeces but is not infectious at this stage. It now undergoes sporogony in which four sporocysts each of which contains two sporozoites develop. This takes two or more days depending upon the environmental temperature. Therefore, prompt removal of faeces and good farm hygiene can effectively prevent the transmission of disease both within and between rearing sheds.

Serious disease primarily affects young poultry particularly those between 3 and 8 weeks of age but older birds infected for the first time later in life also suffer badly. Infected birds become listless, cease to feed, and huddle together to keep warm. Damage to the caecum results in bleeding into the gut and stains the birds’ faeces with blood. The damage allows secondary invasion by bacteria present naturally in the gut, and this extends the lesions and causes further pathology. Acutely infected birds often die from blood loss 5–6 days after infection. In addition to haemorrhages, the gut swells and thickens, so it appears ‘sausage‐like’. Birds that are still alive 9 days after infection will usually recover: a caseous (cheese‐like) plug may form in the lumen of their caecum, which is voided with the faeces.

Recovering birds develop protective, species‐specific, cell‐mediated immunity to re‐infection based on CD4+ and CD8+ T cells found in the lymphoid tissues associated with the gut (Shirley et al. 2007). Co‐infections with two or more species of Eimeria do not necessarily compromise the development of immunity (Jenkins et al. 2009).