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This species occurs throughout the world but is particularly common in tropical and subtropical countries. The first cases were recognised in people returning from the battlefields during the First World War, hence the species name (Latin bellum = war). It only infects humans and there do not appear to be any paratenic hosts (Dubey and Almeria 2019). It causes diarrhoea and is frequently associated with persons suffering from AIDS or immunosuppressive illnesses.

The life cycle begins when we ingest oocysts (17–37 × 8–21 μm) containing infective sporozoites (Figure 3.13). In common with other members of the genus, each oocyst contains two sporocysts and each sporocyst contains four sporozoites. The sporozoites emerge in the small intestine and invade the epithelial cells where they transform into merozoites that divide to produce more merozoites that in turn divide in a cycle that repeats many times. This destroys the host cell and releases the parasites so that they can invade new host cells. In serious infections, this results in the loss of large areas of the gut lining and allows secondary invasion by gut microbes. Presumably, the parasites gain access to the circulation because tissue cysts develop in variety of organs distant from the gastrointestinal tract. For example, within the spleen, liver, and lymph nodes. Each cyst contains a single parasite (zoite) (i.e., they are monozoic) that resembles a typical coccidian sporozoite. The formation of tissue cysts usually occurs in immunocompromised patients but their role in pathology and relapses is uncertain. There is a suggestion that in pigs, the formation of tissue cysts by C. suis contributes to the maintenance of immunity to the parasite (Shrestha et al. 2015). Nowadays, few animals get the opportunity to eat humans, so the tissue cysts probably play no role in transmission of C. belli. The importance of tissue cysts in the transmission of other mammalian Cystoisospora species is uncertain.

Figure 3.13 Life cycle of Isospora belli. 1: Infection commences following ingestion of a sporulated oocyst. The oocyst releases eight sporozoites when it reaches the small intestine and these invade the gut epithelial cells where they transform into merozoites. The merozoites divide asexually to produce more merozoites. 2: Merozoite forming a multinucleate meront that gives rise to microgametocytes (male). 3: Merozoite giving rise to a macrogametocyte (female). Fusion of a male and a female gamete results in the formation of a zygote, and this develops into an oocyst. 4: Sporulation of the oocyst occurs before it is released in the host’s faeces. Drawings not to scale.

At some point, the merozoites transform into multinucleate meronts and these give rise to microgametes (male) or macrogametes (female). Unless the microgametes and macrogametes occur within the same cell (which is possible), the microgametes leave their host cell to locate a macrogamete and their fusion results in the formation of a zygote that then develops into an oocyst. The death of the host cell releases the oocyst into the gut lumen and leaves the body with the faeces. The oocyst then undergoes sporulation to produce two sporocysts, each of which contains four sporozoites. Transmission is therefore passive by faecal–oral contamination. Environmental conditions probably heavily influence the time taken for sporulation. For example, in some Isospora species, temperatures below 20 °C inhibit sporulation, but it takes less than 16 hours at 30 °C. Nevertheless, transmission is probably through infected food or water rather than direct contact. For example, through not washing one’s hands after defaecation or by contacting an article touched by such a person. This is therefore distinct from Cryptosporidium parvum in which the oocysts are immediately infective after shedding.