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→Transmission to Sheep
Sheep are often kept in an environment that is significantly contaminated with oocysts, and infection follows ingestion of infected food, primarily contaminated pasture. Fields treated with manure or bedding from buildings to which cats have access result in high levels of ovine toxoplasmosis, and insecure storage of supplementary feeds also poses a risk.
Sheep are often kept in an environment that is significantly contaminated with oocysts, and infection follows ingestion of infected food, primarily contaminated pasture. Fields treated with manure or bedding from buildings to which cats have access result in high levels of ovine toxoplasmosis, and insecure storage of supplementary feeds also poses a risk.
Oocysts in the environment
Members of the cat family are the definitive hosts of
the parasite and tend to become infected for the first
time when they start hunting and eating wild rodents
and birds already infected with T. gondii. Following
consumption of T. gondii cysts, the parasites excyst
in the gut of the cat and invade and infect host cells.
Sexual development of the parasite takes place in the
gut of the cat resulting in the production of oocysts
which are shed in the faeces. Shedding usually occurs
around 3–10 days after initial infection and may
continue for 2–3 weeks (Dubey and Beattie, 1988).
During this period a cat may shed over 100 million
oocysts and experimental studies in sheep have shown
that a dose of only 200 oocysts may cause abortion in
previously naı¨ve pregnant sheep (McColgan, Buxton
and Blewett, 1988). The importance of oocysts as a
source of infection for sheep, has been supported by
studies showing an association with infection and
contamination of feed or grazing land with sporulated
oocysts (Plant, Richardson and Moyle, 1974;
Faull, Clarkson and Winter, 1986) and also work
showing an association with cats on farms and
prevalence of T. gondii in sheep (Skjerve et al. 1998).
Further studies looking at development of specific
antibodies in sheep, as an indicator of exposure to
T. gondii, have shown that there is an increase in seroprevalence
associated with age. This indicates that
there is extensive environmental contamination with
T. gondii oocysts and that most infections in sheep
occur following exposure to the parasite after birth
(Waldeland, 1977; Blewett, 1983; Lunden,Nasholm
and Uggla, 1994). Recent studies have indicated that
there is widespread environmental contamination
with T. gondii oocysts (Dabritz et al. 2007).
Congenital transmission
Primary infection during pregnancy. As sheep are
not carnivores, consumption of tissues infected with
T. gondii bradyzoites contained within tissue cysts
is not considered to be a route of transmission in
these animals. The only other route of transmission
is vertical from mother to foetus during pregnancy
(Buxton and Rodger, 2008). The stage of pregnancy
when transplacental transmission of T. gondii takes
place is important in determining the clinical outcome.
If infection occurs early in gestation, when the
foetal immune system is relatively immature, foetal
death is likely to occur. Infection at mid-gestation
can result in birth of a stillborn or weak lamb which
may have an accompanying small mummified foetus,
whereas infection in later gestation may result in
birth of a live, clinically normal, but infected lamb
(Buxton, 1990). The birth of clinically normal but
infected lambs usually occurs as a result of a primary
infection in the third trimester of pregnancy,
although it is also possible that transplacental transmission
may occur as a result of recrudescence of an
endogenous infection (Trees and Williams, 2005).
Recrudescence of an endogenous infection. While recrudescence
of a persistent endogenous infection is
a very common route of congenital infection with
the closely related parasiteNeospora caninum in cattle
(Innes et al. 2005; Williams et al. 2009 – this special
issue), it is not thought to be a significant route of
transmission for T. gondii infection in sheep (Dubey
and Beattie, 1988; Buxton and Rodger, 2008).
However, recent studies, (Duncanson et al. 2001;
Williams et al. 2005, Morley et al. 2005, 2008), have
suggested that endogenous transplacental transmission
of T. gondii may be more important than
was previously thought and that this route of transmission
may be an important cause of lamb mortality.
Data reported by Williams et al. (2005) stated
that 53.7% of lambs in their test flocks had evidence
of congenital T. gondii infection at birth with 46%
of live lambs and 90% of dead lambs being positive
for T. gondii by PCR analysis. Further work that
followed ewes over successive pregnancies reported
a frequency of 21% for successive T. gondii positive
abortions, suggesting that complete protective immunity
has not been acquired following a previous
infection (Morley et al. 2008).
These studies are very interesting although difficult
to interpret with confidence as they rely heavily
on PCR-based techniques and the methodology is
not validated using supporting pathology, serological
evidence or isolation of live parasites to show that
the live lambs in the study were indeed congenitally
infected with T. gondii as a result of endogenous
transmission. In addition, the authors did not rule
out other causes of abortion due to different pathogens
on their study farm. These studies also raise
the importance of the language we use to describe
vertical transmission. To aid our understanding of
this area it is important to define the difference
between endogenous transplacental transmission and
exogenous transplacental transmission as described
by Trees and Williams (2005).
A recent relevant study in this area using a full
range of different diagnostic techniques found that,
in contrast to the studies described above, there was
no significant transmission from persistently infected
sheep to their offspring (Rodger et al. 2006). In this
study, a group of sheep previously infected with
Elisabeth A. Innes and others 1888
T. gondii and a group of naı¨ve control sheep were
mated and followed through pregnancy to lambing.
A full post-mortem was conducted on any dead lambs
and placentas were examined using histopathological
techniques and by T. gondii-specific PCR for evidence
of infection. In addition, pre-colostral blood
samples were collected from all the lambs to look
for antibodies to T. gondii. The presence of T. gondii
antibodies in pre-colostral blood samples is a good
indicator that congenital transmission has occurred.
The results showed that the group of 31 T. gondiiinfected
sheep gave birth to 43 live healthy lambs
and 6 stillborn lambs. There was no evidence of
T. gondii infection in any of the tissues examined
using T. gondii-specific PCR and histopathological
techniques, in addition all the foetal fluid samples
from the dead lambs and the pre-colostral serum
samples from the live lambs were sero-negative with
the exception of one set of twin lambs born to one
of the infected ewes. All the T. gondii-negative ewes
produced live T. gondii-negative lambs. Therefore
this more complete study using a variety of scientific
techniques to confirm transmission and infection
showed that the rate of congenital transmission from
persistently infected ewes was very infrequent,
around 3.2% (Rodger et al. 2006).
Data from previous published papers in this area
also agree with the results of Rodger et al. that
although endogenous transplacental transmission of
T. gondii may occur it is very infrequent and does not
pose a significant clinical risk. A study by Watson
and Beverley in the UK showed that in a group of 26
ewes that were infected in a previous pregnancy with
T. gondii and then retained and followed through a
subsequent pregnancy gave birth to 24 live uninfected
lambs with only one ewe aborting a pair
of twins (Watson and Beverley, 1971). A larger study
in Australia examined what proportion of lambs may
be infected as a result of a re-activation of a previous
infection and found that a group of 135 persistently
infected ewes produced 178 live lambs all being precolostral
antibody negative with evidence of only one
of the ewes having an infected placenta. In addition,
there was no evidence of T. gondii being isolated from
their tissues using mouse inoculation. Therefore they
concluded that congenital transmission of T. gondii
from ewes persistently infected with the parasite is
very infrequent (Munday, 1972)..
==Signalment==
==Signalment==