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