Toxoplasma gondii

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Product Description

Toxoplasma gondii

Toxoplasma gondii is an obligate intracellular protozoan parasite that causes toxoplasmosis in humans and warm-blooded animals. Cats and other felidae serve as the definite host producing oocysts, an environmentally resistant form. Cats acquire toxoplasmosis by eating infected prey (rodents, birds) which are intermediate hosts, as are humans.

Sample: 0,5 ml EDTA-blood, Rectal swab

Modes of transmission

Transmission occurs predominantly via ingestion of the tissue cysts, ingestion of oocysts from contaminated food or water, or congenital transmission. Infected cats excrete oocysts in large numbers with excretion occurring for up to 2 weeks following infection. Once shed, the oocyst sporulates in 1 to 5 days, becoming infective and may remain infective for more than 1 year.

Congenital transmission occurs during acute toxoplasmosis in a seronegative mother when tachyzoites present in the blood may cross the placenta and infect the fetus. During the first trimester, transmission is relatively low (< 20%) but increases to near 80% by the end of the pregnancy.

Clinical signs

The tachyzoite is present during acute infection. Tachyzoites are capable of infecting every type of nucleated cell and disseminate throughout the body. Due to the host immune response tachyzoites are eliminated from the host within a few weeks following acute infection. The bradyzoite differentiates from the tachyzoite stage and is prevalent in chronic infections. Bradyzoite replication does not lead to rupture of the host cell but rather, vacuoles containing bradyzoites mature into cysts. Brain and muscle are the most common sites of the chronic, latent infection, although cysts have also been found in lung, liver, kidney and other visceral organs.

Acquired acute infections are asymptomatic in at least 80% of immune competent individuals. Those with clinical disease most commonly present with lymphadenopathy of the head and neck region. Lymphadenopathy may also be accompanied by fever, malaise, sore throat, rash and hepatosplenomegaly. Acute infection terminates after 2 to 3 weeks of infection. In immune competent hosts chronic infection is typically asymptomatic. In contrast, in chronically infected individuals with immune deficiency reactivation of the latent infection can occur. In reactivation in the brain bradyzoites convert to the actively replicating tachyzoites resulting in necrotizing encephalitis.

Congenital transmission occurs almost solely in seronegative women who have acute infection during pregnancy and is not seen in women who are seropositive before pregnancy. The classic triad of symptoms of congenital toxoplasmosis is chorioretinitis, hydrocephalus, and intracranial calcifications.

Ocular Toxoplasmosis can be acquired congenitally, can be a postnatal acquired infection, or can be the result of disease reactivation in immune-compromised and pregnant individuals. The disease typically causes chorioretinitis with recurrence episodes of inflammation and subsequent healing. These bouts of recurrent chorioretinitis overtime result in blurred vision, photophobia, loss of central vision and blindness.

Cerebral Toxoplasmosis usually is due to reactivation of a latent infection in the brain. It causes unifocal or multifocal lesions. Clinical symptoms include headache, fever, seizures, mental confusion, ataxia, lethargy and visual alterations.

Over the past decade there has been an increasing interest in the possibility of an association of Toxoplasma gondii infection and schizophrenia and other psychiatric disorders.


Acquired Toxoplasmosis is mostly self limited and resolves without specific treatment or with symptomatic management. Treatment with pyrimethamine and sulfadiazine for is effective and is used for severe cases and cerebral toxoplasmosis. Folinic acid is usually added to prevent bone marrow suppression. Spiramycin is often used for treatment of pregnant women. Treatment of the neonatal infant during the first year of life and longer has been demonstrated to significantly improve clinical outcome. Anti-toxoplasmic therapy is effective for treating ocular toxoplasmosis, but it does not avoid recurrences.


Washing hands and fruits and vegetables is a part of prevention, as is cooking meat. Prenatal testing is possible, in case of seronegative results, caution should be increased.


Fetal involvement is most severe when maternal toxoplasmosis is contracted early in pregnancy leading to spontaneous abortion, hydrocephalus and mental retardation. Conversely, infection in the third trimester is often asymptomatic, with development of chorioretinitis commonly occurring later in life, and possibly leading to blindness.


Toxoplasmosis is one of the most common infections in humans and warm-blooded animals, with a worldwide distribution. In humans, toxoplasmosis has been found in all parts of the world and it is estimated about one-third of the world’s population is infected with latent toxoplasmosis.

The seroprevalence for Toxoplasma gondii in cats is 30 to 40%. Congenital transmission rates are found to be 19.8%.


Halonen, S.K., and Weiss, L.M. (2013). TOXOPLASMOSIS. Handb Clin Neurol 114, 125–145.3

Wahab, T., Edvinsson, B., Palm, D., Lindh, J. (2010). Comparison of the AF146527 and B1 repeated elements, two real-time PCR targets used for detection of Toxoplasma gondii. Journal of Clinical Microbiology, 48 (2), pp. 591-592.