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Principles and practice of Clinical parasitology - Gillespie S.

Gillespie S. Principles and practice of Clinical parasitology - Wiley publishing , 2001. - 675 p.
ISBN 0-471-97729-2
Download (direct link): principlesandpracticeofclin2001.pdf
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Babesia Life-cycle
Most work on the life-cycles of Babesia species that are known to infect man has been done on
B. microti, which is discussed below. Readers are referred to reviews for information on the life cycles of other Babesia species, such as B. equi and B. canis (Mehlhorn and Shein, 1984).
The tick ingests intraerythrocytic forms of B. microti when feeding on an infected host. They are first evident in the tick gut after approximately 10 hours of feeding (Telford et al., 1993) (Figure 4.2). A peritrophic membrane forms in the gut of the feeding tick, dividing the gut into ecto- and endoperitrophic spaces. The latter contains the blood meal, including intact erythrocytes containing B. microti (Rudzinska et al., 1983). After hours of residence in the endoperitrophic space, organelles appear within
102
PRINCIPLES AND PRACTICE OF CLINICAL PARASITOLOGY
Babesia life-cycle in tick
' Gut cell -f, (10-16 hours)
Salivary glands
(8-10 Months)
Tick
life-cycle
Hosts
for
tick
Babesia life-cycle in host
(2 Years)
Erythrocytic cycle
F'g- 4.2 The life-cycle of Babesia microti
B. microti. These organelles are thought to be gametes, which emerge from the erythrocyte and fuse to form a zygote 14-18 hours after repletion of the feeding tick (Rudzinska et al., 1982). The zygotes possess a unique structure shaped like an arrowhead and possibly containing proteolytic enzymes. The arrowhead structure is required for the passage of B. microti through the peritrophic membrane and into the ectoperitrophic space. The arrowhead structure of the invading organism contacts the epithelial cell of the tick gut. At the point of contact, the membrane of the host cell invaginates and eventually encircles the parasite, resulting in its endocytosis. Once within the host cell, B. microti is covered by its own plasma membrane as the host cell membrane appears to disintegrate. The arrowhead structure is no longer present (Rudzinska et al., 1983). The zygote is translocated to the basal lamina of the host cell and enters the hemolymph, at which point an ookinete stage is achieved. Ookinetes invade cells of the salivary gland of the tick prior to feeding of the nymphal form and undergo hypertrophy to form sporoblasts (Karakashian
et al., 1983). The sporoblasts are dormant and are thought to remain so throughout the winter. Temperature elevation, through contact of the tick with a mammalian host and feeding of the nymph, stimulates the development of
B. microti (Karakashian et al., 1983; Telford et al., 1993). Within the host cell, a large mesh-work is formed by the sporoblast. Approximately 44-65 hours after attachment of the tick to a mammalian host, sporozoites form from within the meshwork and mature through simultaneous nuclear and cytoplasmic division. The mature sporozoites separate from the sporoblast through a process of budding, forming organisms which are 2.2 x 0.8 pm in size (Karakashian et al., 1983). During the final hours of attachment of the tick to the host, thousands of sporozoites are deposited into the skin.
The direct invasion of sporozoites into mammalian host erythrocytes has not been demonstrated for B. microti and the process by which sporozoites transform into merozoites is not understood (Telford et al., 1993). However,
BABESIOSIS
103
for B. equi, sporozoites directly invade lymphocytes and transform into merozoites, which then leave the lymphocyte and invade the erythrocyte. The existence of lymphocyte invasion by B. microti is controversial (Mehlhorn and Shein, 1984; Telford et al., 1993).
The role of complement in the invasion of erythrocytes by B. microti is uncertain. However, there is evidence that an intact host alternative complement pathway and an erythrocyte C3b receptor is necessary for the penetration of rat erythrocytes by B. rodhaini (Jack and Ward, 1980). In the presence of the parasite, complement is activated and C3b is fixed to the surface of the merozoite. Presumably, the fixed C3b binds to the C3 receptor on the erythrocyte surface. In addition, erythrocytes bearing surface C3 are also infected. These data suggest that complement-mediated changes of the erythrocyte and/or the B. rhodaini merozoite facilitate the process of invasion.
The merozoite enters the mammalian erythrocyte through invagination of the host cell membrane. The anterior end of the merozoite, which contains complex apical organelles, attaches to the erythrocyte membrane, which invaginates and then encompasses the merozoite. A parasitophorous vacuole is formed, composed of two membranes, one derived from the host cell and one derived from the merozoite and containing the developing trophozoite. The host cell membrane disintegrates, leaving B. microti free within the host cell cytoplasm. This is an important difference from the life cycle of Plasmodium species (Telford et al., 1993).
Within the erythrocytes, maturing trophozoites develop organelles, such as polar rings and double membrane segments. Some of these segments represent bud precursors. Via asynchronous budding, two to four merozoites are formed. The rare but diagnostic tetramere seen with light microscopy of erythrocytes parasitized by B. microti is a representation of four merozoites within the parental Babesia (Figure
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