r*sr expansion of parasitized cells

Schizont in?






Figure 1 Distribution of the two most economically important Theileria species, T. parva and T. annulata. The distribution of the tick vectors is wider than these parasites and hence the potential for spread is high.

Piroplasms in erythrocytes

Figure 2 Life cycle of Theileria parva. Sexual cycle is obligatory and occurs in the tick. Transformation and clonal expansion of infected cells has only been described In T. parva, T. annulata, T. taurotragi and T. hirci. All stages except zygotes and kinetes are haploid. The transmission is trans-stadial, thus larvae and nymphs of three host ticks become infected when feeding on an Infected host and the resultant nymphs and adults transmit the parasite.

Figure 1 Distribution of the two most economically important Theileria species, T. parva and T. annulata. The distribution of the tick vectors is wider than these parasites and hence the potential for spread is high.

13 Theileria annulata ^Theileria parva

13 Theileria annulata ^Theileria parva schizonts of T. parva, T. annulata, T. taurotragi and T. hirci induce the host cells to transform and proliferate. Casein kinase II in the host cell and the parasite may be involved in the signaling of this proliferation. During host cell division schizonts associate closely with the mitotic spindle and divide synchronously with the cell, resulting in clonal expansion of infected cells. Between 3 and 4 days after infection, some schizonts undergo merogony to produce large numbers of merozoites. These escape following the rupture of the host cells and invade erythrocytes, where they develop into piroplasms.

Ticks become infected when taking a blood meal from infected animals. Within the ticks the parasites undergo a complicated development, including a sexual cycle, to produce motile kinetes, which migrate to the salivary glands where they undergo a process of maturation to produce infective sporozoites.

The clinical signs of theileriosis are predominantly associated with the schizont stage. Infected animals develop pyrexia and enlarged lymph nodes, coinciding with the appearance of intracellular schizonts. Infected cells rapidly spread to other lymphoid tissues causing generalized lymphadenopathy. With the emergence of host killer cells and rupture of infected cells a lymphodestructive phase follows which results in severe leukopenia. The animals quickly lose condition, develop respiratory distress and frequently die within 10-15 days with massive pulmonary edema and severe gastroenteritis. Anemia, associated with erythrocytic merogony is an additional feature in animals infected with T. annulata and T. hirci.

A number of Theileria-specific antigens have been identified and characterized (Table 2). An antigen referred to as the polymorphic immunodominant molecule (PIM) of T. parva is present in all the stages of the parasite and varies considerably in size among the different stocks. The PIM gene shows highly conserved terminal sequences flanking a central variable region. Some antibodies specific for the PIM antigen neutralize sporozoite infectivity for lymphocytes in vitro. However, cattle immunized with recombinant PIM are not protected against T. parva challenge. The role of PIM in the induction of cell-mediated immune responses is currently being evaluated-

The 67 kDa antigen of T. parva is localized on the surface of sporozoites. The gene coding for this antigen has been sequenced and characterized. It is present as a single copy, has a small 29 bp intron and is highly conserved among different stocks of cattle-derived T. parva. Murine monoclonal antibodies

Table 2 Antigens of different Theileria species

Species Molecular Method of Localization Identified Application weight (kDa) identification function

T. parva

T. annulata

T. mutans

T. sergenti/orientalis/buffeli

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