Toxoplasmosis - Sheep

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

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 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 oocysts¹, 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 farm².

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.

Diagnosis

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. Sheep may become infected from the consumption of sporulated oocysts. Once ingested, the oocysts excyst in the small intestine, releasing sporozoites which quickly invade and multiply within the cells of the gut differentiating into tachyzoites. The tachyzoites can be found multiplying within mesenteric lymph node cells by day 4 following infection (Dubey, 1984). Toxoplasma is an obligate intracellular parasite and uses a process of endodyogeny to multiply within host cells (Ferguson, 2009). The parasitized cells then rupture releasing tachyzoites that invade other host cells. A common clinical sign is an elevated temperature in the animal which is observed co-incident with the appearance of tachyzoites in the mesenteric lymph nodes and the fever may last for a further week, during which time tachyzoites may be detected in the circulation (Dubey and Sharma, 1980; Wastling, Nicoll and Buxton, 1993). In the pregnant ewe, the tachyzoites find their way to the placenta where they invade and multiply within the maternal caruncular septa in the placentome and from there they invade the adjoining foetal trophoblast cells (Buxton and Finlayson, 1986). The immune system of the sheep is modulated during pregnancy in order to prevent rejection of the semi-allogeneic foetus. This manifests as a damping down of the pro-inflammatory immune responses such as interleukin 2 (IL-2) and interferon gamma (IFNc) at the maternal-foetal interface (Innes and Vermeulen, 2006; Entrican and Wheelhouse, 2006). This change in the immune environment of the placenta provides a favourable location for the parasite to establish and multiply.

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.

References

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