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The life cycle begins when ticks inject infective sporozoites are into the mammal bloodstream and these then invade the red blood cells (Figure 3.12). Initially, the host cell encloses the sporozoites within a membrane‐bound vacuole. However, the parasites escape from this and therefore come into intimate contact with the erythrocyte cytoplasm. The sporozoites now transform into the merozoite stage that divides by binary fission and accumulates within the cell and eventually kill it. The merozoites are usually pear shaped (in Babesia bigemina they are 4–5 μm long × 2–3 μm wide) and in blood smears, they are seen singly or in pairs. When their host cell dies, the parasites are released, and they re‐infect other red blood cells. Mechanical transmission between hosts can occur – for example, via re‐used needles and veterinary instruments and blood transfusions. In susceptible hosts, the parasitaemia builds up rapidly and 70–80% of the red blood cells can become infected. Some merozoites transform into oval‐shaped gamonts and these develop no further unless a suitable tick vector ingests them.

Table 3.2 The distribution, vectors, and host ranges of representative Babesia species of medical and veterinary importance.

Species of Babesia	Distribution	Mammal host	Tick vector
Babesia Bigemina	Central & South America, North & South Africa, Australia, Asia (not in UK)	Cattle, water buffalo, zebu, deer	Various species of Rhipicephalus and also Ixodes ricinus
Babesia bovis	Central & South America, North & South Africa, Australia, Asia, Southern Europe (not in UK)	Cattle, deer	Various species of Rhipicephalus and also Ixodes ricinus
Babesia divergens	Northern Europe, including UK	Cattle	Ixodes ricinus
Babesia Microti	North‐eastern USA, Europe	Rodents, human infections increasingly reported	Ixodes dammini, Ixodes scapularis
Babesia Ovis	Southern Europe, Middle East, Africa	Sheep, goats	Various species of Rhipicephalus
Babesia Canis	Southern Europe, Middle East, Africa, Asia, Central, South and North America	Dogs and other caniids	Various species of Ixodes, Dermacentor variabilis, Haemaphysalis leachi

Figure 3.12 Life cycle of Babesia spp: 1: An infected tick injects saliva containing sporozoites into the bloodstream and these invade red blood cells. The sporozoites transform into merozoites that divide asexually until they kill their host cell, and they then infect other red blood cells. Some merozoites transform into oval‐shaped gamonts, and these develop no further unless a suitable tick vector ingests them. 2: Within a tick’s gut, the gamonts invade the intestinal cells and differentiate into gametocytes (ray bodies). Once they are mature, the gametocytes leave the tick gut cells and fuse to produce a zygote. 3A: Zygotes transform into motile primary kinetes that invade other cell types within which they transform and multiply to form secondary motile kinetes. 3B: Primary kinetes that invaded the tick oocytes result in the young tick emerging from its egg already infected, and in these, the parasites ultimately invade their salivary glands. 4: Secondary kinetes that parasitize the salivary glands transform into sporonts, and these give rise to infectious sporozoites. Drawings not to scale.

When a tick ingests blood from an infected host, it digests the Babesia merozoites along with the red blood cells they parasitize. The gamonts, however, survive and invade the cells lining the tick’s gut. Within these intestinal cells the gamonts differentiate into gametocytes that are referred to as ‘ray bodies’ (derived from the original German ‘strahlenkörper’ that is still used by some authors), which are globular with one or two thorn‐like projections. Once they are mature, the ray bodies leave the gut cells and two of them fuse to produce a zygote. The zygote then transforms into a motile kinete that invades several other cell types including muscles, Malpighian tubules, and in female ticks the ovaries and oocytes. Within these cells, they transform and multiply to form numerous secondary motile kinetes. Upon release, the secondary kinetes parasitize other cells including the salivary glands. Within the salivary glands, the kinetes transform into sporonts, and these give rise to numerous infectious sporozoites. Those primary kinetes that invaded the tick oocytes result in the young tick emerging from its egg already infected, and in these the parasites ultimately invade their salivary glands. For one‐host ticks, trans‐ovarial transmission of the infection is essential if they are to function as effective vectors. This is because they usually spend their whole life on a single animal and therefore cannot transmit infections directly from one host to another. For two‐ and three‐host ticks, transovarial transmission may be of less importance for the parasite. This is because the ticks drop off and re‐attach to new hosts between moults. Therefore, the ticks have greater opportunity to spread the infection. Many parasites that grow and develop within blood‐feeding vectors damage their vector in the process (e.g., sand‐flies and Leishmania spp.) but Babesia microti facilitates the feeding and improves the survival of its tick host, Ixodes trianguliceps (Randolph 1991). Whether similar Babesia‐tick relationships occur in other Babesia species is uncertain.