Difference between revisions of "Toxoplasmosis - Sheep"

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==Introduction==
+
 
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Toxoplasmosis is the disease caused by ''[[Toxoplasma gondii]]'',  an intracelluler protozoan parasite. Although the definitive host is the cat, ''T. gondii'' can infect all mammals including man and is a significant cause of abortion in sheep and goats. Toxoplasmosis does not seem to cause disease in cattle.
+
==Description==
 +
 
 +
Toxoplasmosis is the disease caused by ''Toxoplasma gondii'',  an intracelluler protozoan parasite. Although the definitive host is the cat, ''T. gondii'' can infect all mammals including man and is a significant cause of abortion in sheep and goats. Toxoplasmosis does not seem to cause disease in cattle.
 
[[Image:Toxoplasmosis Life Cycle.jpg|thumb|right|300px| Life cycle of ''Toxoplasma gondii''. Source: Wikimedia Commons; Author: LadyofHats (2010)]]
 
[[Image:Toxoplasmosis Life Cycle.jpg|thumb|right|300px| Life cycle of ''Toxoplasma gondii''. Source: Wikimedia Commons; Author: LadyofHats (2010)]]
 +
===Life Cycle===
 +
 +
There are three infectious stages of ''Toxoplasma gondii'': 1) sporozoites; 2) actively reproducing tachyzoites; and 3) slowly multiplying bradyzoites. Tachyzoites and bradyzoites are found in tissue cysts, whereas sporozoites are containted within oocysts, which are excreted in the faeces. This means that the protozoa can be transmitted by ingestion of oocyst-contaminated food or water, or by consumption of infected tissue.
 +
 +
In naive cats, ''Toxoplasma gondii'' undergoes an enteroepithelial life cycle. Cats ingests intermediate hosts containing tissue cysts, which release bradyzoites in the gastrointestinal tract. The bradyzoites penetrate the small intestinal epithelium and sexual reproductio ensues, eventually resulting the production of oocysts. Oocysts are passed in the cat's faeces and sporulate to become infectious once in the environment. These can then be ingested by other mammals, including sheep.
 +
 +
When sheep ingest oocysts, ''T.gondii'' intiates extraintestinal replication. This process is the same for all hosts, and also occurs when carnivores ingest tissue cysts in other animals. Sporozoites (or bradyzoites, if cysts are consumed) are released in the intestine to infect the intestinal epithelium where they replicate. This produces tachyzoites, which reproduce asexually within the infected cell. When the infected cell ruptures, tachyzoites are released and disseminate via blood and lymph to infect other tissues. Tachyzoites then replicate intracellularly again and the process continues until the host becomes immune or dies. If the infected cell does not burst, tachyzoites eventually encyst as bradyzoites and persist for the life of the host. Cyst are most commonly found in the brain or skeletal muscle, and are a source of infection for carnivorous hosts.
 +
 
==Transmission to Sheep==
 
==Transmission to Sheep==
 +
 
===Oocysts in the Environment===
 
===Oocysts in the Environment===
−
As the definitive hosts of ''Toxoplasma gondii'', cats become infected when they hunt and eat infected wild rodents and birds. Rodents are a particularly important source of [[Toxoplasmosis - Cat and Dog|feline infection]], as they can pass ''T. gondii'' infection to their offspring without causing clinical disease. This means that a farm may develop a reservoir of ''T. gondii'' tissue cysts with the potential to cause feline infection and massive oocyst excretion when a cat is introduced to the environment. Between days 3 and 14 post-infection, cats shed over 100 million of oocysts in their faeces. Studies have shown an association between ovine toxoplasma infection, and the contamination of feed or grazing with sporulated oocysts<sup>1</sup>, highligting the importance of oocysts as a source of infection for sheep. It has also been demonstrated that the prevalence of ovine toxoplasmosis varies with the presence of cats on a farm<sup>2</sup>.
+
 
 +
Infected cats shed oocysts continuously between days 3 and 14 post-infection. During this time, hundreds of millions of oocysts may be shed. The main sources of feline toxoplasma infection are chronically infected birds and rodents. Rodents are particularly important since they can pass ''T. gondii'' infection to their offspring without causing clinical disease. This means that a farm may develop a reservoir of ''T. gondii'' tissue cysts with the potential to cause feline infection and massive oocyst excretion. In turn, environments may easily become contaminated with a high oocyst burden when a cat is introduced.
 +
 
 +
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.
 +
 
 +
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===
 
===Congenital Transmission===
 +
 
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.
 +
 +
As well as in acute infection of the damn, transplacental transmission may occur as a result of 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==
−
Ovine toxoplasmosis is only clinically apparent when primary infection of a pregnant animal occurs.
 
  
 
==Diagnosis==
 
==Diagnosis==
−
A combination of clinical signs and (histo)pathology are most commonly used to make a diagnosis of ovine toxoplasmosis, but serology may be of use in some cases.
 
  
 
===Clinical Signs===
 
===Clinical Signs===
−
The signs of toxoplasmosis in sheep manifest following the exposure of a naive pregnant ewe to 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.
 
  
−
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 bradyzoites. 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 a flock, this is visible clinically as large numbers of barren ewes. In mid-gestation (70-120 days), infection can again be fatal. This causes a mummified foetus which is often twinned with a lamb that is stillborn or weak. Abortion due to infection at 70-120 days gestation tends to occur in very late pregnancy. Because the foetal immune system is well developed in late pregnancy, infection at this stage will be resisted, and the lamb will be born transiently infected but alive.
+
*Clinical outbreaks of toxoplasmosis are '''sporadic'''
 +
**Immunity is acquired before tupping
 +
**Significant ill-effects are unlikely if immune ewes are infected during pregnancy
 +
**Not shed from sheep to sheep so predicting outbreaks is difficult
  
 
===Laboratory Tests===
 
===Laboratory Tests===
−
Serology may be used for the laboratory diagnosis of toxoplasmosis. Ideally, the indirect fluorescent antibody test is used to detect antibody in the foetal fluids, as this is the most reliable method. If abortion products are not available, a latex agglutination test can be performed on maternal blood. Anti-''Toxoplasma gondii'' IgG antibodies can be detected in the maternal circulation from thirty days post-infection and remain increased for years afterwards. This means that for clinical diagnosis, IgG titres must be measured in paired serum samples taken 3-4 weeks apart, and must show at least a four-fold increase in titre<sup>3</sup>. In an outbreak of disease, this time scale may be too great to be useful. IgM antibodies become apparent sooner after infection and persist for a much shorter time, and so increased IgM titres are consistent with recent infection.
 
  
 
===Pathology===
 
===Pathology===
−
Multiplication of ''Toxoplasma gondii'' in the placenta causes multiple foci of necrosis, which limit effective function during pregnancy. After birth, these areas of necrosis are visible as white spots on the cotyledons. The intercotyledonary areas appear normal.
 
  
−
Histologically, foetal tissues may display changes. In the brain, glial foci surround a necrotic centre and represent a foetal immune response to damage initiated by parasite multiplication. An associated mild lymphoid meningitis is often seen. Focal leukomalacia is also common and is thought to be due to foetal anoxia in late gestation, caused by extensive necrosis of the placentome. Focal inflammatory lesions with diffuse lymphoid infiltrates can be found in many other tissues, including the liver, lung and heart. The kidneys and skeletal muscle are less frequently affected.
+
Aborted ewes show focal necrotic placentitis with white lesions in the cotyledons and foetal tissue
  
 
==Treatment==
 
==Treatment==
−
In the event of an outbreak, little can be done to prevent further spread since transmission is via contaminated food or water rather than sheep-to-sheep contact. Since environmental contamination is related to the behaviour of cats, numbers should be limited. Keeping an older, neutered male cat may help ward of other felines: since most cats seroconvert at a young age, adults are unlikely to shed oocysts to contribute to contamination. Rodents and other vermin transmit toxoplasmosis to cats, and so populations should also be controlled. Animals should be prevented from gaining access to sheep feed or bedding.
 
  
−
Previously, monensin has been given in sheep feed in the lead up to lambing. Although this was shown to reduce perinatal lamb mortality related to ''Toxoplasma'' infection, monensin is no longer licensed for sheep and should not be used.
+
*Toxovax vaccine
 +
***Live, avirulent strain of ''Toxoplasma''
 +
***Does not form bradyzoites or tissue cysts
 +
***Killed by host immune system
 +
***Single dose given 6 weeks before tupping
 +
***Protects for 2 years
 +
***Immunity boosted by natural challenge
 +
**Medicated feed can be given daily during the main risk period
 +
***14 weeks before lambing
 +
**The best method of protection is to prevent cats from contaminating the pasture, lambing sheds and feed stores
  
−
The best method of controlling ovine toxoplasmosis is therefore by vaccination. A live vaccine containing tachyzoites of the avirulent S48 strain is available. These tachyzoites do not cause pathology or form bradyzoites or tissues cysts. A single dose of vaccine is administered intramuscularly at least 3 weeks (and up to four months) prior to mating, from an age of five months. The vaccine is known to protect against toxoplasmosis for at least two lambing seasons.
+
The extent of environmental
 +
contamination with T. gondii oocysts is thus
 +
related to the distribution and behaviour of cats.
 +
Measures to reduce environmental contamination
 +
by oocysts should be aimed at reducing the number
 +
of cats capable of shedding oocysts. This would include
 +
attempts to limit their breeding. If male cats are
 +
caught, neutered and returned to their colonies the
 +
stability ofthe colony is maintained; fertile male cats
 +
do not challenge the neutered males12 and breeding
 +
is controlled. Thus the maintenance ofa small healthy
 +
population of mature cats will reduce oocyst excretion
 +
as well as help to control rodents. Sheep feed should be
 +
kept covered at all times to prevent its contamination
 +
by cat faeces.
  
 
==Prognosis==
 
==Prognosis==
−
An outbreak of toxoplasmosis can cause significant lamb losses. However, ewes rarely show ill effects, and will not abort again in subsequent lambings. Vaccination gives excellent control of toxoplasmosis.
 
−
 
−
{{Learning
 
−
|literature search = [http://www.cabdirect.org/search.html?q=%28toxoplasmosis%29+AND+od%3A%28sheep%29 Toxoplasmosis in sheep publications]
 
−
}}
 
  
 
==Links==
 
==Links==
−
 
−
<big>'''[[Toxoplasmosis - Cat and Dog|Feline and Canine Toxoplasmosis]]
 
−
 
−
'''[[Toxoplasmosis - Human|Human Toxoplasmosis]]</big>
 
−
 
−
*[http://www.moredun.org.uk/feature-article.asp?ref=111 Toxoplasma infection: vaccination as a control strategy (Moredun Insititute)]
 
−
*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/52200.htm The Merck Veterinary Manual - Toxoplasmosis]
 
−
*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/110305.htm The Merck Veterinary Manual - Abortion in Sheep]
 
−
*[http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/zoonoses/lambing.htm#toxoplasmosis Defra: Zoonoses during the lambing season]
 
  
 
==References==
 
==References==
  
−
#Plant, J Wet al (1974) Toxoplasma infection and abortion in sheep associated with feeding of grain contaminated with cat faeces. ''Australian Veterinary Journal'', '''50''', 19–21.
 
−
#Skjerve, E et al (1998). Risk factors for the presence of antibodies to Toxoplasma gondii in Norwegian slaughter lambs. ''Preventative Veterinary Medicine'', '''35''', 219–227.
 
−
#Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial''
 
 
#Buxton, D (1990) Ovine toxoplasmosis: a review. ''Journal of the Royal Society of Medicine'', '''83''', 509-511.
 
#Buxton, D (1990) Ovine toxoplasmosis: a review. ''Journal of the Royal Society of Medicine'', '''83''', 509-511.
 
#Innes, E A et al (2009) Ovine toxoplasmosis. ''Parastiology'', '''136''', 1887–1894.
 
#Innes, E A et al (2009) Ovine toxoplasmosis. ''Parastiology'', '''136''', 1887–1894.
 
#Buxton, D et all (2007) Toxoplasma gondii and ovine toxoplasmosis: New aspects of an old story. ''Veterinary Parasitology'', '''147''', 25-28.
 
#Buxton, D et all (2007) Toxoplasma gondii and ovine toxoplasmosis: New aspects of an old story. ''Veterinary Parasitology'', '''147''', 25-28.
 
#Dubey, J P (2009) Toxoplasmosis in sheep — The last 20 years. ''Veterinary Parasitology'', '''163''', 1-14.
 
#Dubey, J P (2009) Toxoplasmosis in sheep — The last 20 years. ''Veterinary Parasitology'', '''163''', 1-14.
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+
[[Category:Tissue_Cyst_Forming_Coccidia]][[Category:Sheep]]
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[[Category:To_Do_-_Lizzie]]
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{{review}}
 
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{{OpenPages}}
 
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[[Category:Sheep Parasites]][[Category:Reproductive Diseases - Sheep]]
 
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[[Category:Brian Aldridge reviewing]]
 

Revision as of 15:25, 13 August 2010


 This article is still under construction.


Description

Toxoplasmosis is the disease caused by Toxoplasma gondii, an intracelluler protozoan parasite. Although the definitive host is the cat, T. gondii can infect all mammals including man and is a significant cause of abortion in sheep and goats. Toxoplasmosis does not seem to cause disease in cattle.

Life cycle of Toxoplasma gondii. Source: Wikimedia Commons; Author: LadyofHats (2010)

Life Cycle

There are three infectious stages of Toxoplasma gondii: 1) sporozoites; 2) actively reproducing tachyzoites; and 3) slowly multiplying bradyzoites. Tachyzoites and bradyzoites are found in tissue cysts, whereas sporozoites are containted within oocysts, which are excreted in the faeces. This means that the protozoa can be transmitted by ingestion of oocyst-contaminated food or water, or by consumption of infected tissue.

In naive cats, Toxoplasma gondii undergoes an enteroepithelial life cycle. Cats ingests intermediate hosts containing tissue cysts, which release bradyzoites in the gastrointestinal tract. The bradyzoites penetrate the small intestinal epithelium and sexual reproductio ensues, eventually resulting the production of oocysts. Oocysts are passed in the cat's faeces and sporulate to become infectious once in the environment. These can then be ingested by other mammals, including sheep.

When sheep ingest oocysts, T.gondii intiates extraintestinal replication. This process is the same for all hosts, and also occurs when carnivores ingest tissue cysts in other animals. Sporozoites (or bradyzoites, if cysts are consumed) are released in the intestine to infect the intestinal epithelium where they replicate. This produces tachyzoites, which reproduce asexually within the infected cell. When the infected cell ruptures, tachyzoites are released and disseminate via blood and lymph to infect other tissues. Tachyzoites then replicate intracellularly again and the process continues until the host becomes immune or dies. If the infected cell does not burst, tachyzoites eventually encyst as bradyzoites and persist for the life of the host. Cyst are most commonly found in the brain or skeletal muscle, and are a source of infection for carnivorous hosts.

Transmission to Sheep

Oocysts in the Environment

Infected cats shed oocysts continuously between days 3 and 14 post-infection. During this time, hundreds of millions of oocysts may be shed. The main sources of feline toxoplasma infection are chronically infected birds and rodents. Rodents are particularly important since they can pass T. gondii infection to their offspring without causing clinical disease. This means that a farm may develop a reservoir of T. gondii tissue cysts with the potential to cause feline infection and massive oocyst excretion. In turn, environments may easily become contaminated with a high oocyst burden when a cat is introduced.

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.

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

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.

As well as in acute infection of the damn, transplacental transmission may occur as a result of 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

Diagnosis

Clinical Signs

  • Clinical outbreaks of toxoplasmosis are sporadic
    • Immunity is acquired before tupping
    • Significant ill-effects are unlikely if immune ewes are infected during pregnancy
    • Not shed from sheep to sheep so predicting outbreaks is difficult

Laboratory Tests

Pathology

Aborted ewes show focal necrotic placentitis with white lesions in the cotyledons and foetal tissue

Treatment

  • Toxovax vaccine
      • Live, avirulent strain of Toxoplasma
      • Does not form bradyzoites or tissue cysts
      • Killed by host immune system
      • Single dose given 6 weeks before tupping
      • Protects for 2 years
      • Immunity boosted by natural challenge
    • Medicated feed can be given daily during the main risk period
      • 14 weeks before lambing
    • The best method of protection is to prevent cats from contaminating the pasture, lambing sheds and feed stores

The extent of environmental contamination with T. gondii oocysts is thus related to the distribution and behaviour of cats. Measures to reduce environmental contamination by oocysts should be aimed at reducing the number of cats capable of shedding oocysts. This would include attempts to limit their breeding. If male cats are caught, neutered and returned to their colonies the stability ofthe colony is maintained; fertile male cats do not challenge the neutered males12 and breeding is controlled. Thus the maintenance ofa small healthy population of mature cats will reduce oocyst excretion as well as help to control rodents. Sheep feed should be kept covered at all times to prevent its contamination by cat faeces.

Prognosis

Links

References

  1. Buxton, D (1990) Ovine toxoplasmosis: a review. Journal of the Royal Society of Medicine, 83, 509-511.
  2. Innes, E A et al (2009) Ovine toxoplasmosis. Parastiology, 136, 1887–1894.
  3. Buxton, D et all (2007) Toxoplasma gondii and ovine toxoplasmosis: New aspects of an old story. Veterinary Parasitology, 147, 25-28.
  4. Dubey, J P (2009) Toxoplasmosis in sheep — The last 20 years. Veterinary Parasitology, 163, 1-14.
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