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===Clinical Signs===
 
===Clinical Signs===
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*Clinical outbreaks of toxoplasmosis are '''sporadic'''
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The disease toxoplasmosis in sheep usually manifests
**Immunity is acquired before tupping
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following a primary infection of a pregnant ewe,
**Significant ill-effects are unlikely if immune ewes are infected during pregnancy
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resulting in placental invasion and transplacental
**Not shed from sheep to sheep so predicting outbreaks is difficult
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infection of the foetus. Typical clinical signs are
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abortion and production of stillborn or weak lambs
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often along with a small,mummified foetus. Placental
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tissue from infected ewes may also show characteristic
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gross white spot lesions which are visible to
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the naked eye and are areas of necrosis in the tissue
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which will limit its effective function in supporting
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the pregnancy (Buxton, 1990). 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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