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Nature of the disease
Toxoplasmosis is an infectious disease caused by the coccidia Toxoplasma gondii. The definitive host is a Felid but it can affect a wide range of species as intermediate hosts including humans. It frequently manifests as abortion and stillbirths in sheep and by encephalitis, pneumonia and neonatal mortality in all species.

Apart from the losses in sheep the impact is relatively small and the importance of the disease lies in its potential threat to humans.

FAO List C disease
Susceptible species
Toxoplasmosis naturally occurs in a wide range of domestic and wild animals and birds. Domestic cats predominate as reservoir for zoonotic transmission as they are the definitive hosts (were the parasite reproduce).

Pigs, sheep, goats and humans are the more susceptible to the disease, cattle and horses being less susceptible. Within each species, young animals and those with a weaker immune system (e.g. sick, pregnant, old) are more susceptible to the disease.

Clinically, sheep flocks are commonly affected with abortions and neonatal deaths being seen. Within the Pacific region, serological surveys indicate that goats are the species most frequently exposed to infection.

Toxoplasmosis occurs in most parts of the world. However, it seems to be absent from, at least, French Polynesia, Kiribati and Vanuatu.
Clinical signs
Recent observations showed that toxoplasmosis is uncommon in cattle. Calves are more susceptible than adults and the clinical signs of orally affected calves include diarrhea, anorexia, poor weight gain, depression, weakness, dyspnea and fever. In some casejust a lymphadenopathy. Congenitally affected calves show fever, dyspnoea, coughing, sneezing and neurological signs.

If the disease occurs in adults, symptoms include fever, dyspnoea, and nervous signs, followed by lethargy. Stillborn calves and neonatal deaths may be seen.

Pigs less than 3 weeks old are the more susceptible. Clinical signs include debility, weakness, incoordination, fever, wasting, dyspnoea and cough. In adults cough and tremors predominate. In pregnant sows abortion, stillborn and premature are common.

Lambs affected after birth show fever and dyspnoea. In pregnant ewes, abortions and stillbirths are common, abortions tend to occur in the last 3-4 weeks of pregnancy. Symptoms in adults are uncommon and include fever, dyspnoea, and tremor.

The clinical disease appears to be rare in horses, however symptoms include progressive neurological signs, including ataxia, circling, paresis and apparent blindness.

Cats are the definitive host, with infection common but clinical illness rare. Symptoms may include:

  • Loss of weight,
  • Pneumonia,
  • Encephalitis,
  • Fever

In young cats dyspnoea associated with bronchopneumonia may be seen. Infection may be fatal in young kittens.

In Poultry symptoms can be sudden death or anorexia, emaciation, pallor, diarrhoa and blindness.

The infection is very common in humans, but clinical disease is of low incidence and occurs only sporadically. Postnatal infection is less severe disease and commonly presents as a generalised lymphadenopathy that may resolve without treatment in a few weeks.
Congenital infection results in systemic disease often with severe neuropathological changes. Rarely, serious ocular or systemic toxoplasmosis can be acquired by older individuals or reactivated in immuno-compromised individuals. Clinical signs include:

  • Fever,
  • Skin eruption,
  • Malaise,
  • Myalgia and arthralgia,
  • Cervical lymphadenopathy,
  • Pneumonia,
  • Myocarditis,
  • Meningoencephalitis,
  • Chorioretinitis
Post-mortem findings
In cattle, multiple, proliferative necrotic granulomas in the lungs and nervous system are characteristic. If there is visceral involvement pneumonitis, hydrothorax, ascites, lymphadenitis, intestinal ulceration and necrotic foci in internal organs may be seen.

In sheep there may be involvement of the uterine wall, placenta and foetus. In the foetus focal necrotic lesions may be seen in the brain, liver, lungs and in the foetal membranes.

In horses haemorrhagic lesions may be seen in the brain and spinal cord. These may also be seen in sheep.

Differential diagnosis
There is a wide range of symptoms and lesions that may be produced with toxoplasmosis in domestic animals and the disease may be difficult to recognise.

Clinical syndromes of encephalopathy in new-born animals occur with vitamin A deficiency and as congenital defects after vaccination of pregnant dams with attenuated bluetongue and hog cholera vaccines.
Other cause of abortion in sheep include:

  • Brucellosis,
  • Vibriosis,
  • Enzootic abortion,
  • Listeriosis,
  • Salmonellosis

Neurological signs can also be produced by:

  • Virus or bacterial infections,
  • Cerebral oedema,
  • Space-occupying lesions,
  • Hypoglycaemia,
  • Poisons (e.g. salt, lead, arsenic, mercury)

There are also a wide range of cause of respiratory distress that may need to be considered.

Specimens required for diagnosis
Blood samples and faeces should be collected to establish the diagnosis in cats.

Tissue samples collected from animals and aborted foetuses should include brain and lungs.

In humans, the disease is diagnosed by serology.

Laboratory tests available include serology ( ELISA, Fulton test, Indirect Fluorescent Antibody test (Ig G), isolation, DNA-probe with PCR and microscopic demonstration of organisms in smear or sections.

The demonstration of cysts does not establish a causal relationship to clinical illness, since cysts may be found in both acute and chronic infections. However, finding tachyzoites in blood or body fluids confirms active infection.

Cats are responsible for maintaining and spreading infection. The sexual reproduction of the parasite only occurs in this specie. Cats faces contain occysts that can infect all species through food contamination. Cats can become infected by eating chronically infected birds, rodents, raw meat, etc.
There are three modes of spread by which animals can become infected:
  • Oocysts from the cat’s faeces
  • Trophozoites or bradyzooites in the flesh of prey or food
  • Transplacental — if trophozoites are present in the blood stream, the foetus may become infected

Transmission to humans occurs via eating raw or undercooked meat containing cysts; by ingesting sporulated oocysts from cat faeces; or transplacentally.

Freezing of meat to -20o C for 2 days or heating to 60o C kills cysts. Under appropriate environmental conditions, oocysts passed in cat faeces can remain infective for a year or more.


Risk of introduction
Toxoplasmosis is most likely to be introduced to new areas with deliberate or accidental importation of cats. Unapparent infection is common in cats.

The risk of introduction by contaminated meat exists but the probability of transmission of the disease is low if the meat is properly cooked.

Control / vaccines
Cats can be treated with a 5-7 day course of sulphamezathine. Antimicrobials such as spiramycin, clindamycin sulphonamides, diphenylsulphones and pyrimenthamine have been shown to be effective against trophozoites and can be used against acute and chronic toxoplasmosis.

In humans, the treatment of choice is pyrimethamine plus either trisulphapyrimidines or sulfadiazine. Folic acid is given to avoid the haematological effects of pyrimethamine-induced folate deficiency.

Children's play areas should be protected from cat and dog faeces.

Pregnant women should take measures to prevent infection by avoiding contact with cat faeces and avoid working in soil or gardens that could be contaminated by cats, etc. and by thoroughly cooking meat. Hands should be washed after handling raw meat and before eating or touching the face.

Vaccines are under development for both humans and animals.

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  • DUBEY JP (1998), Toxoplasmosis, Sarcocystosis, Isosporosis, and Cyclosporosis In Zoonoses, ed by SR PALMER, Lord SOULSEY and D.I.H. SIMPSON, Oxford University Press, Bath Press, Avon, 1998, p.579-597
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  • SOULSBY EJL, Helminths, Toxoplasma In Helminths, Arthropods and Protozoa of Domesticated Animals, Lea and Febiger Inc, 7th ed, 1982, Philadelphia, p 670-682
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