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Apart from ingestion of oocysts in the environment, the only other method of transmission of toxoplasmosis to sheep is vertical spread from mother to foetus during pregnancy. This is because sheep are herbivorous, and do not consume animal tissues containing cysts. The outcome of transplacental infection depends on the stage of pregnancy. Infection in early gestation usually causes foetal death, as the foetal immune system is immature at this stage. In mid-gestation, infection may cause the birth of weak or stillborn lambs, sometimes accompanied by a mummified sibling. Ewes infected in the third trimester normally give birth to infected but clinically normal lambs.
 
Apart from ingestion of oocysts in the environment, the only other method of transmission of toxoplasmosis to sheep is vertical spread from mother to foetus during pregnancy. This is because sheep are herbivorous, and do not consume animal tissues containing cysts. The outcome of transplacental infection depends on the stage of pregnancy. Infection in early gestation usually causes foetal death, as the foetal immune system is immature at this stage. In mid-gestation, infection may cause the birth of weak or stillborn lambs, sometimes accompanied by a mummified sibling. Ewes infected in the third trimester normally give birth to infected but clinically normal lambs.
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As well as in acute infection of the damn, transplacental transmission may occur as a result of recrudescence of an endogenous infection.
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While recrudescence
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of a persistent endogenous infection is
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a very common route of congenital infection with
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the closely related parasiteNeospora caninum in cattle
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(Innes et al. 2005; Williams et al. 2009 – this special
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issue), it is not thought to be a significant route of
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transmission for T. gondii infection in sheep (Dubey
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and Beattie, 1988; Buxton and Rodger, 2008).
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However, recent studies, (Duncanson et al. 2001;
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Williams et al. 2005, Morley et al. 2005, 2008), have
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suggested that endogenous transplacental transmission
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of T. gondii may be more important than
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was previously thought and that this route of transmission
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may be an important cause of lamb mortality.
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Data reported by Williams et al. (2005) stated
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that 53.7% of lambs in their test flocks had evidence
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of congenital T. gondii infection at birth with 46%
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of live lambs and 90% of dead lambs being positive
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for T. gondii by PCR analysis. Further work that
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followed ewes over successive pregnancies reported
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a frequency of 21% for successive T. gondii positive
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abortions, suggesting that complete protective immunity
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has not been acquired following a previous
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infection (Morley et al. 2008).
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These studies are very interesting although difficult
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to interpret with confidence as they rely heavily
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on PCR-based techniques and the methodology is
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not validated using supporting pathology, serological
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evidence or isolation of live parasites to show that
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the live lambs in the study were indeed congenitally
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infected with T. gondii as a result of endogenous
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transmission. In addition, the authors did not rule
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out other causes of abortion due to different pathogens
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on their study farm. These studies also raise
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the importance of the language we use to describe
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vertical transmission. To aid our understanding of
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this area it is important to define the difference
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between endogenous transplacental transmission and
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exogenous transplacental transmission as described
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by Trees and Williams (2005).
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A recent relevant study in this area using a full
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range of different diagnostic techniques found that,
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in contrast to the studies described above, there was
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no significant transmission from persistently infected
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sheep to their offspring (Rodger et al. 2006). In this
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study, a group of sheep previously infected with
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Elisabeth A. Innes and others 1888
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T. gondii and a group of naı¨ve control sheep were
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mated and followed through pregnancy to lambing.
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A full post-mortem was conducted on any dead lambs
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and placentas were examined using histopathological
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techniques and by T. gondii-specific PCR for evidence
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of infection. In addition, pre-colostral blood
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samples were collected from all the lambs to look
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for antibodies to T. gondii. The presence of T. gondii
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antibodies in pre-colostral blood samples is a good
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indicator that congenital transmission has occurred.
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The results showed that the group of 31 T. gondiiinfected
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sheep gave birth to 43 live healthy lambs
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and 6 stillborn lambs. There was no evidence of
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T. gondii infection in any of the tissues examined
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using T. gondii-specific PCR and histopathological
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techniques, in addition all the foetal fluid samples
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from the dead lambs and the pre-colostral serum
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samples from the live lambs were sero-negative with
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the exception of one set of twin lambs born to one
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of the infected ewes. All the T. gondii-negative ewes
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produced live T. gondii-negative lambs. Therefore
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this more complete study using a variety of scientific
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techniques to confirm transmission and infection
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showed that the rate of congenital transmission from
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persistently infected ewes was very infrequent,
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around 3.2% (Rodger et al. 2006).
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Data from previous published papers in this area
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also agree with the results of Rodger et al. that
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although endogenous transplacental transmission of
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T. gondii may occur it is very infrequent and does not
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pose a significant clinical risk. A study by Watson
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and Beverley in the UK showed that in a group of 26
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ewes that were infected in a previous pregnancy with
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T. gondii and then retained and followed through a
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subsequent pregnancy gave birth to 24 live uninfected
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lambs with only one ewe aborting a pair
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of twins (Watson and Beverley, 1971). A larger study
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in Australia examined what proportion of lambs may
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be infected as a result of a re-activation of a previous
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infection and found that a group of 135 persistently
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infected ewes produced 178 live lambs all being precolostral
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antibody negative with evidence of only one
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of the ewes having an infected placenta. In addition,
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there was no evidence of T. gondii being isolated from
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their tissues using mouse inoculation. Therefore they
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concluded that congenital transmission of T. gondii
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from ewes persistently infected with the parasite is
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very infrequent (Munday, 1972)..
      
==Signalment==
 
==Signalment==
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