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Home Topics Infectious Diseases Infections A-Z Toxoplasmosis General Information ›  Information for Health Professionals: Toxoplasmosis

Information for Health Professionals: Toxoplasmosis

Toxoplasmosis is a zoonotic disease caused by a ubiquitous protozoan parasite called Toxoplasma gondii, which can infect all mammal and bird species throughout the world. It has been estimated that up to one billion people have been exposed to the parasite worldwide (1), however seroprevalence varies widely between countries.

In the UK, cases are diagnosed by the Toxoplasma Reference Unit, and quarterly data published in the Health Protection Report. About 400 cases are diagnosed annually.

Most healthy people who acquire toxoplasma infection do not experience any significant symptoms, however about 10% of people develop a mild to moderate self limiting flu-like or glandular fever-like illness. Lymphadenopathy is the most common manifestation, lasting up to 4-6 weeks but fatigue, sore throat, myalgia, (or, very rarely, rashes, arthralgia or hepatosplenomegaly) may occur. In rare cases symptoms may persist for many months or years and may be due to chronic active infection.

The disease may be more severe in immunocompromised persons. Infection acquired during pregnancy can be transmitted to the foetus and can lead to foetal abortion or congenital malformation.

Following the acute active stage of the infection the parasite persists in the body for many years or decades in the form of cysts, particularly in heart and skeletal muscle and nervous system tissues. In immunocompetent persons these cysts are considered not pose a health risk.  While some researchers have suggested possible links between toxoplasma infection and behavioural changes, psychiatric illnesses, and other chronic conditions, there is probably insufficient evidence at this time to draw any firm conclusions.

Life cycle

Toxoplasma gondii has a complicated life cycle, and requires an animal host to develop. Virtually all warm blooded animals can act as intermediate hosts of T. gondii, but the parasite's life cycle is completed only in cats and several species of wild felidae, which are therefore termed the 'definitive host'.
There are three infectious stages in the life cycle of T. gondii:

  • Sporozoites are found in oocysts, which are produced when the parasite replicates in the intestine of a cat, and are shed in the cat's faeces for 7-21 days during acute infection. The oocysts then develop (sporulate) over a period of 1-21 days in the faeces, and become infective when ingested by mammals, including humans.
  • Tachyzoites are found in the tissues of warm blooded animals. Infection with this stage of the parasite causes a strong inflammatory response and leads to clinical manifestations of the disease.
  • Bradyzoites form cysts in animal tissues, particularly the brain, skeletal and heart muscles where they may remain for many years without detection. Tissue cysts can contain many thousands of bradyzoites.

The life cycle of T. gondii may continue indefinitely through the transmission of tissue cysts between intermediate hosts. Click here for the life cycle of T. gondii.


Humans are infected with T. gondii by four major routes:

  • Ingesting water, food or soil contaminated with the faeces of infected cats
  • Transmission from a newly infected mother to the foetus
  • Ingesting or handling undercooked or raw meat (mainly pork or lamb) that contains tissue cysts
  • Receiving organ transplants or, very rarely, blood products from donors with acute or latent toxoplasmosis

Other than from mother to fetus, direct human to human transmission has not been reported.

Toxoplasmosis in the immunocompromised

Toxoplasmosis in immunocompromised individuals usually occurs as a result of reactivation of chronic infection, and may be very severe. The nature and severity of symptoms varies according to the cause and degree of the immunosuppression. The central nervous system is usually affected, but reactivation can also occur in the periphery resulting in a range of systemic symptoms. Both toxoplasmic encephalitis and systemic toxoplasmosis have been reported in individuals with immuno-deficiencies due to a range of causes (2). The clinical presentation may include changes in mental status, seizures, motor problems, speech abnormalities, movement disorders and neuropsychiatric findings. There may also be signs of infection such as fever and malaise.

T. gondii can also be transmitted by organ transplantation from an infected donor to an uninfected recipient, and this is an important cause of disease in recipients of heart, heart-lung, kidney, liver and liver-pancreas transplants, and to a lesser extent, kidney. T. gondii transmission has also been reported, although rarely, via blood or leucocytes from infected individuals (3).

T. gondii is an important opportunistic pathogen in patients with AIDS, and can cause severe encephalitis. In the vast majority of patients disease occurs due to reactivation of latent toxoplasma infection, and the most frequent manifestation is toxoplasmic encephalitis. It has been reported that 30-50% of AIDS patients with latent T. gondii infection may develop toxoplasmic encephalitis, usually once they are severely immunosuppressed (4). However, recent improvements in treatment for HIV such as HAART have reduced the overall burden of disease associated with toxoplasma in this clinical group.

Congenital toxoplasmosis

Acute toxoplasma infection acquired during pregnancy is often asymptomatic and when clinical symptoms occur they are the same as in other immunocompetent individuals (5). However, when a previously uninfected woman becomes infected with T. gondii for the first time during pregnancy, the infection can be passed to the unborn foetus and cause congenital toxoplasmosis. Congenital toxoplasmosis may cause abortion, neonatal death or foetal abnormalities, and can significantly reduce the quality of life in children who survive a prenatal infection (1).

If T. gondii infection is acquired before conception, the development of protective immunity will usually prevent transmission to the foetus. However, women who are immunocompromised due to HIV infection or systemic lupus erythematosus may, depending on their level of immunocompromise, transmit the parasite months or years after having acquired infection.

The effect of congenital toxoplasmosis on the fetus varies according to the stage of development at the time of transmission. Maternal infection early in pregnancy is rarely transmitted, however if transmission occurs the effects are severe. Significant manifestations include central nervous system damage, meningoencephalitis, hydrocephalus, chorioretinitis and intracranial calcifications, blindness and epilepsy. Foetal death or spontaneous abortion occurs in about 10% of cases (2). Signs of generalised infection may also be present including jaundice, rash, hepatosplenomegaly, fever, anaemia and thrombocytopaenia (5). The clinical signs of toxoplasmosis are often similar to those caused by other congenital infections, including cytomegalovirus, herpes simplex virus, rubella and syphilis.

Transmission later in pregnancy is more common, and is asymptomatic in up to 85% of cases. The infant may, however, develop clinical symptoms months or years after birth, usually eye lesions.

Ocular toxoplasmosis

T. gondii can infect the eye and cause an acute inflammatory lesion of the retina, which slowly resolves to leave scarring, causing toxoplasmic chorioretinitis. Eye disease can occur in congenital or postnatally acquired toxoplasmosis due to acute infection or reactivation. It has been estimated that about one third of prenatally infected children may develop eye disease later in life (2). Although ocular toxoplasmosis in adults has generally been seen as a late manifestation and reactivation of congenital disease, it has been increasingly reported in association with acute infection (3). Current estimates for the UK are that individuals infected in later life may account for as many, if not slightly more, cases than congenital infection.


Diagnosis of toxoplasmosis is complicated by the fact that the parasite can be present in an acute, chronic, latent or reactivated form. In patients who are immunocompetent, initial tests are carried out to detect IgG and IgM antibodies. In those who are immunocompromised diagnosis usually involves direct detection of the parasite either by microscopy, parasite culture, and/or nucleic acid detection. Eye testing and radiological studies are used to aid diagnosis of congenital infection.

In pregnant women laboratory investigation is used to determine whether the pregnancy is at risk. If tests confirm that infection took place before conception, then further investigation is unnecessary.  If the woman is found to be uninfected, then advice can be given on measures to reduce the risk of infection while pregnant.  However, if a pregnancy is considered to be at risk of transmission from mother to foetus, further clinical and laboratory investigation of the foetus may be considered.  Concurrent anti-toxoplasma treatment (spiramycin) aimed at reducing the risk of transmission from mother to foetus can also be considered.  It should be noted that, while some studies have suggested a significant reduction in transmission rates associated with the use of spiramycin, other studies have detected no significant benefits. Thus, the precise choice of management option will depend upon a range of factors including stage of pregnancy and parental choice, which, in some cases, might be elective termination. Flowchart: Investigation of toxoplasmosis in pregnancy (PDF, 43 KB)

If foetal infection is either strongly suspected or confirmed, management options include intervention with more effective but potentially more toxic anti-toxoplasma therapy, or a reconsideration of elective termination. Flowchart: Investigation of toxoplasmosis in the foetus (PDF, 44 KB)

Where unequivocal exclusion or confirmation of congenital toxoplasma infection was not possible during prenatal investigation, tests are carried out on the neonate to determine whether treatment and further clinical investigation are necessary. If infection is confirmed in the neonate appropriate management may, again, depend on a range of factors such as clinical presentation at birth, and may include treatment and clinical follow-up.

The table below summarises the range of laboratory investigations that are helpful in assessing risk to a pregnancy from toxoplasma, and confirming or excluding congenital toxoplasma infection in the foetus and neonate;

Table: diagnostic tests for toxoplasmosis

Toxoplasma test

Pregnant women:

Foetus: amniotic fluid
Foetus: blood Neonate: cord or neonatal blood

Amniotic fluid

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IgG avidity
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IgG immunoblot
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(a) as matched sample with neonatal blood
(a) and (b) must be tested as paired samples for comparison
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Immunocompetent adults do not usually require treatment, unless symptoms are severe or persistent. Treatment in pregnant women and immunocompromised individuals is more complicated and advice varies according to the stage of infection. However, a range of treatments are available if treatment is considered to be indicated.


Limiting exposure to cats, their litter, and soil contaminated with cat faeces is important, particularly when pregnant. Cat litter should be disposed of daily and hands should be thoroughly washed after handling cats, their litter, faeces or soil. Thorough hygiene practices are important when preparing raw meat, ensuring that surfaces and utensils which have touched raw meat are thoroughly washed, hands are thoroughly washed after handling raw meat. Meat should be well cooked, to an internal temperature of over 60°C and until it is no longer pink in the middle. Gloves should be worn when gardening or handling soil.

Neonatal screening has been implemented in several countries. No vaccine is currently available for use in humans.


1. Sukthana Y. Toxoplasmosis: beyond animals to humans. Trends Parasitol 2006; 22(3):137-42.
2.Tenter AM, Heckeroth AR, Weiss LM. Toxoplasma gondii: from animals to humans. Int J Parasitol 2000; 30(12-13):1217-58.
3 . Montoya JG, Liesenfeld O. Toxoplasmosis. Lancet 2004;363(9425):1965-76.
4 . Mariuz P, Steigbigel RT. Toxoplasma infection in HIV-infected patients. In: Joynson D.H.M, Wreghitt TG, editors. Toxoplasmosis: A comprehensive clinical guide. Cambridge: Cambridge University Press; 2001. p. 147-77.
5 . Thulliez P. Maternal and foetal infection. In: Joynson D.H.M, Wreghitt TG, editors. Toxoplasmosis: A comprehensive clinical guide. Cambridge: Cambridge University Press; 2001. p. 193-213

Last reviewed: 25 August 2011