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The signs of toxoplasmosis in sheep manifest following the exposure of a naive pregnant ewe to infectious oocysts. This results in primary infection of the ewe and causes transplacental infection of the foetus. Typical clinical signs are therefore abortion and the birth of stillborn or weak lambs. Stillborn or week lambs are often accompanied by a second, mummified foetus.
 
The signs of toxoplasmosis in sheep manifest following the exposure of a naive pregnant ewe to infectious oocysts. This results in primary infection of the ewe and causes transplacental infection of the foetus. Typical clinical signs are therefore abortion and the birth of stillborn or weak lambs. Stillborn or week lambs are often accompanied by a second, mummified foetus.
Sheep may become
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infected from the consumption of sporulated oocysts.
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Once ingested, the oocysts excyst in the small intestine,
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releasing sporozoites which quickly invade and
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multiply within the cells of the gut differentiating
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into tachyzoites. The tachyzoites can be found
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multiplying within mesenteric lymph node cells by
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day 4 following infection (Dubey, 1984). Toxoplasma
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is an obligate intracellular parasite and uses a process
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of endodyogeny to multiply within host cells
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(Ferguson, 2009). The parasitized cells then rupture
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releasing tachyzoites that invade other host cells. A
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common clinical sign is an elevated temperature in
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the animal which is observed co-incident with the
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appearance of tachyzoites in the mesenteric lymph
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nodes and the fever may last for a further week,
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during which time tachyzoites may be detected in
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the circulation (Dubey and Sharma, 1980; Wastling,
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Nicoll and Buxton, 1993). In the pregnant ewe, the
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tachyzoites find their way to the placenta where they
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invade and multiply within the maternal caruncular
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septa in the placentome and from there they invade
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the adjoining foetal trophoblast cells (Buxton and
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Finlayson, 1986). The immune system of the sheep
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is modulated during pregnancy in order to prevent
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rejection of the semi-allogeneic foetus. This manifests
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as a damping down of the pro-inflammatory
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immune responses such as interleukin 2 (IL-2) and
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interferon gamma (IFNc) at the maternal-foetal
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interface (Innes and Vermeulen, 2006; Entrican and
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Wheelhouse, 2006). This change in the immune
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environment of the placenta provides a favourable
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location for the parasite to establish and multiply.
      
===Laboratory Tests===
 
===Laboratory Tests===
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