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.
3.4.3.2 Babesia bigemina
The different species of Babesia vary in their pathogenicity and distribution but they share many similarities, so we shall discuss only one of them, Babesia bigemina, in detail. This species was once a major cause of disease in North America, where it caused ‘Texas fever’ in infected cattle. Following successful eradication campaigns, B. bigemina is of much less economic importance in the USA today, but it remains a serious problem in Central and South America, North and South Africa, Australia, and Asia. It is principally a disease of cattle, although it also infects water buffalo, zebu, and deer. Ticks belonging to the genus Rhipicephalus are responsible for most of the transmissions, and these have a widespread distribution in tropical and subtropical countries.
Cattle normally acquire their infection from others that have recovered from the disease but continue to harbour a subclinical infection. The pathology associated with B. bigemina is unusual in that adult cattle tend to be more severely affected than the young are. This is particularly the case in cattle not previously exposed to the parasite or the local strain – for example those transported to a new region or country or following exposure to infected ticks newly introduced into the area. High‐performance milking cows imported into Africa from temperate regions are at particular risk of succumbing to severe disease symptoms. In Mexico, white‐tailed deer (Odocoileus virginianus texanus) have high seroprevalence for both B. bigemina and Babesia bovis but how important these (and other wildlife) might be as reservoirs of infection is uncertain.
A host of variables, including the age and immune status of the host (e.g., previous exposure and vaccination status) and the strain of the parasite influence the pathogenicity. The damage is primarily associated with the loss of function and destruction of the red blood cells. Lysing of infected erythrocytes releases haemoglobin into the blood stream. The destruction of small numbers of red blood cells has little effect and many infections are sub‐clinical. However, the rapid destruction of numerous cells in a short period can overload the body’s ability to remove the waste material. Consequently, haemoglobin and its breakdown products accumulate resulting in jaundice and their appearance in the urine – and hence the common name for the infection of ‘red water fever’