Theileria sergenti proliferates in SCID mice with bovine erythrocyte transfusion

1992 
The unavailability of in vitro or in vivo experimental systems has been the major factor ham- pering the progress of research studies on Theileria sergenti, causative agent of theileriosis, a major disease of cattle in Japan. We report the first successful prop- agation of T. sergenti in SCID mice into which unin- fected bovine erythrocytes (Bo-RBC) were supplied pe- riodically. The infectivity of T. sergenti proliferated in an SCID mouse was ascertained by successful transfer of infection into another SCID mouse into which un- infected Bo-RBC were supplied periodically. Theileriosis, caused by the intraerythrocytic protozoan Theileria sergenti, has been one of the most serious problems among infectious diseases of cattle in Japan. It is highly prevalent among grazing cattle as the vector tick, Haemaphysalis longicornis, is widely distributed in Japanese pastures. The parasite infection by itself causes only mild anemia, but when it is combined with other factors, such as other infections, stress, and shipping and delivery, the disease becomes se- vere and occasionally results in fatal infection (Takahashi, 1976). The majority of infected cat- tle are long-term carriers of T. sergenti, which makes the disease control and eradication very difficult. Although many scientists have been working on this parasite, practical measures for control have yet to be developed. The main lim- iting factor is the unavailability of experimental systems. Attempts to develop an in vitro culture system have not been successful and small lab- oratory animals susceptible to this parasite have not been found. Thus, virtually all experiments have to be conducted with, or rely for the source of material on, cattle. Here, we report the first successful propagation of T. sergenti apart from the natural hosts by use of a mutant mouse hav- ing severe combined immune deficiency (C.B- 17 scid/scid, hereafter designated as SCID) (Bosma et al., 1983). SCID mice lack functional T and B lymphocytes and are, therefore, immunologi- cally incompetent for rejecting not only allografts but also cells of other species (McCune et al.,
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