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| | ===Clinical Signs=== | | ===Clinical Signs=== |
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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. The sporozoites ingested excyst in the digestive tract and penetrate the intestinal epithelium, before reaching the mesenteric lymph nodes around day 4 post-infection. Here, they cause lymphomegaly and focal necrosis before contributing to a parisitaemia from day 5. Pyrexia is associated with the development of parasitaemia. |
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| − | Abortions and neonatal mortality occur when
| + | Following dissemination of ''T. gondii'' in the blood, many tissues become infected. Parasitaemia ends when the maternal immune response becomes effective, and protozoa start to encyst as bradizoites. In pregnant animals, the uterus is an immunoprivileged site, and the outcome of foetal infection is influenced by the stage of gestation. In early pregnancy, the foetus is unable to mount any immune response, and so cannot inhibit parasite multiplication. The foetus rapidly dies and is resorbed. In mid-gestation, infection can again be fatal. This causes a mummified foetus which is often twinned with a lamb that dies later in gestation, or is born weakly. Because the foetal immune system is well developed in late pregnancy, infection at this stage will be resisted, and the lamb will be born infected but alive. Infection of the placentome has a different pathogenesis. Multiplication of ''Toxoplasma gondii'' in the placenta causes multiple foci of necrosis, which continue to expand throughout gestation. If this renders placental function non-viable, abortion may occur in late gestation. |
| − | sheep, (and goats) suffer a primary infection during
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| − | pregnancy5. In the UK, toxoplasmosis is a primary
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| − | cause of loss in 10-20% of flocks with an abortion
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| − | problem, giving an annual incidence in the breeding
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| − | ewe population of 1-2%2223. Sporulated T. gondii
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| − | oocysts, ingested by susceptible pregnant sheep,
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| − | excyst in the digestive tract and release sporozoites
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| − | to penetrate the intestinal epithelium. By 4 days,
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| − | organisms can be found in the mesenteric lymph
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| − | nodes, where they multiply causing marked lymph
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| − | node enlargement, sometimes with focal necrosis24.
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| − | Around the 5th day toxoplasms are released to cause
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| − | a parasitaemia, which may last until the 12th
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| − | day25,26. Coinciding with the parasitaemia the ewe
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| − | displays a febrile response which can exceed 41°C
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| − | around day 6 or 727.
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| − | Many tissues become infected in this way. The
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| − | cessation of the parasitaemia coincides with the onset
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| − | ofan effective maternal immnune response and infection
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| − | then persists as bradyzoites within tissue cysts.
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| − | In pregnant animals the gravid uterus is an | |
| − | 'immunologically privileged' site28. On the uterine
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| − | side maternal immunological responses are suppreied
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| − | while the ability of the fetus, with its placenta, to
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| − | recognize and respond to a pathogen commences
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| − | during the first half of gestation and develops for the
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| − | remainder of pregnancy, so that lambs at birth are
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| − | immunocompetent. During a T. gondii parasitaemia
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| − | in the dam, tachyzoites are able to parasitise
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| − | the caruncular septa, the maternal tissues of the
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| − | placentome. They then invade adjacent trophoblast
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| − | cells of the fetal villi, and firom there, the rest of the
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| − | fetus, between 5 and 10 days after the onset of
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| − | parasitaemia9. However, the outcome of infection is
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| − | influenced by the stage of gestation at which it | |
| − | commences.
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| − | Infection in early gestation is rapidly fatal18'30 due
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| − | to the absence of a fetal immune response to inhibit | |
| − | parasite multiplication29. Subsequent resorption of | |
| − | the fetus can be mistaken for infertility30. Infection
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| − | in mid gestation may also be fatal and give rise to
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| − | a mummified fetus often alongside a sibling which is | |
| − | born alive but weakly or which dies late in gestation. | |
| − | Infection in late pregnancy will normally cause fetal
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| − | infection but because, at this stage, the competence | |
| − | of the fetal immune system is well advanced, the
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| − | parasite will be resisted and the lamb born live,
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| − | infected and immune 8. When infection in the | |
| − | placentome is initiated, parasite multiplication causes | |
| − | multiple foci of necrosis29. These foci of tissue
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| − | damage expand throughout the remainder of gestation
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| − | until abortion or birth when they may be macroscopically
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| − | visible as white spots in the cotyledons of
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| − | the shed placenta, a feature used to aid diagnozsis"31.
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| − | Diagnosis is also helped by histological examination
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| − | of the brain where there may be both primary | |
| − | and secondary lesions32'33. Glial foci, surrounding a
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| − | necrotic and sometimes mineralized centre, often
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| − | associated with a mild lymphoid meningitis, represent
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| − | a fetal immune response following direct damage by
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| − | parasite multiplication. Focal leukomalacia is also
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| − | common and is thought to be due to fetal anoxia in
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| − | late gestation caused by advanced focal necrosis in
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| − | the placentome preventing sufficient oxygen transfer
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| − | from mother to fetus33. Focal inflammatory lesions
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| − | and associated diffuse lymphoid infiltrates may also
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| − | be found in the liver, lung and heart and less
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| − | frequently in kidneys and skeletal muscle33.
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| − | The ovine fetal immune system starts to respond to
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| − | T. gondii at or soon after 60 days gestation when both
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| − | humoral and cellular reactions can be detected29.
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| − | Specific circulating anti-T. gondii IgM and IgG,
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| − | detectable after 30 days of maternal infection, can
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| − | be used in the diagnosis of T. gondii abortion29.
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| − | Infection ofpregnant and non-pregnant ewes provokes
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| − | substantial iunity, so that a uterine T. gondii
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| − | infection will not develop in a future gestation2l.
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| | ===Laboratory Tests=== | | ===Laboratory Tests=== |