In vitro quantitation of Theileria parva sporozoites for use - TropMed ...

Chapter 1: Quantitation of Theileria parva sporozoites: Review of literature 23
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to feed for this process to occur. Sporozoites are about 0.75 – 1.5 µm in diameter and have a
surface coat that is 20 – 25 nm thick (Shaw et al., 1991; Shaw and Young, 1994)
Transmission to the bovine host occurs when the tick injects sporozoites suspended in the saliva as
it feeds. Purnell and Joyner (1967) demonstrated that infected ticks feeding on blood products
presented in glass capillary tubes salivated infective stages of T. parva into the blood meal in the
tube. The tick's lifespan may be reduced by virtue of being infected (Watt and Walker, 2000).
Similarly, reduced viability in Boophilus species heavily infected with Babesia has been observed
(Ouhelli et al., 1987; De Vos et al., 1989).
1.1.2.4. Cycle of Theileria parva in the bovine host
Theileria parva successively invades lymphocytes and erythrocytes. It differs in a number of
respects from other apicomplexans in that it does not have a well defined apical complex (Fawcett
et al., 1982b) and the secretory products of rhoptries and microspheres are ejected after
internalisation (Shaw et al., 1991). The sporozoite attaches to the lymphocyte and is internalized
by active endocytosis within three minutes of attachment (at 37°C) (Shaw et al., 1991). In vitro
studies have shown that attachment is a random event and not energy dependent, whereas
internalization is energy dependent and optimised at 37°C (Shaw et al., 1991). It begins with close
approximation of the parasitic and host cell membranes most possibly by legand-receptor
mechanisms. T. parva differs from its apicomplexan counterparts in that it can attach to the target
cell in any orientation (Fawcett et al., 1982b). The sporozoite is then progressively internalised by
becoming tightly apposed to the host membrane, in a "zippering" phenomenon described by
Fawcett et al. (1982b) (Figure 2). It sheds its own surface coat (Webster et al., 1985) and then
dissolves the host cell membrane to escape into the host's cytosol (Fawcett et al., 1982b) possibly
as a defensive mechanism against the host cell's lysozymes. The internalised sporozoite quickly
becomes associated with microtubules of the host cell, stabilises them (Shaw, 2003) and in the
first few days following infection, develops into a pyriform shape that resembles Babesia
piroplasms (Stagg et al., 1981).
From about day five post infection, development into a multinucleated syncytium, i.e. a
macroschizont, takes place. This stage transforms the host cell and the lymphoblast starts to divide
exponentially in synchrony with the schizont's own divisions so that both daughters cells usually
inherit parasite material (Hulliger et al., 1964; Stagg et al., 1980; Stagg et al., 1981). Rocchi et al.
(2006) showed that not all originally infected cells are transformed and that even among
transformed cells, there is sometimes failure for some daughter cells in receiving progeny