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Toxoplasmosis 

Toxoplasmosis

Chapter:
Toxoplasmosis
Author(s):

Oliver Liesenfeld

and Eskild Petersen

DOI:
10.1093/med/9780199204854.003.070804_update_005

Update:

This chapter was reviewed in December 2014 and minor changes made.

Updated on 30 Jul 2015. The previous version of this content can be found here.
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date: 28 March 2017

Toxoplasma gondii is a protozoan parasite with worldwide distribution that infects up to one-third of the world’s population. Human infection is acquired through ingestion in water or food of oocysts shed by cats, or by ingestion of bradyzoites released from cysts contained in uncooked or undercooked meat (e.g. sheep, swine, cattle). Following invasion in the intestine, tachyzoites rapidly disseminate throughout the host. Immune mechanisms mediate the formation of cysts, primarily in the brain, eye, and skeletal and heart muscles, where they persist for the life of the host. Presence of infection may be established by direct detection of the parasite in clinical samples (often by polymerase chain reaction, PCR) or by serological techniques.

Clinical features and treatment

Immunocompetent adults and children—primary infection is usually subclinical, but some patients develop cervical lymphadenopathy; specific treatment is not usually required.

Ocular disease—choroidoretinitis; treatment with pyrimethamine and sulphadiazine is usually recommended if there are severe inflammatory responses and/or proximity of retinal lesions to the fovea or optic disk.

Immunocompromised patients—the central nervous system is the most commonly affected site. Reactivation of latent infection can cause life-threatening encephalitis. Empirical anti-T. gondii therapy is given to patients with single or multiple ring-enhancing brain lesions on imaging, positive serology, and advanced immunodeficiency, most commonly with the combination of pyrimethamine/sulphadiazine and folinic acid. Patients with suspected cerebral T.gondii infection should be tested for HIV.

Congenital toxoplasmosis—infection acquired in early pregnancy may cause severe damage to the fetus or intrauterine death; infection in the second and third trimesters goes unnoticed in the newborn in most cases, but signs of disease, e.g. chorioretinitis, may occur later in life. Suspected or established maternal infection acquired during pregnancy must be confirmed by prenatal diagnosis of fetal infection using PCR on amniotic fluid: if this is positive it is highly probable that the fetus is infected and pyrimethamine/sulphadiazine and folinic acid should be given and continued throughout the pregnancy.

Prevention

Prevention of infection by avoiding ingestion is the strategy of choice in seronegative people. Trimethoprim-sulfamethoxazole can be used for primary and secondary prophylaxis of seropositive immunocompromised patients or seronegative recipients of organ transplants from seropositive donors. Spiramycin can be used for secondary prevention of transmission from the acutely infected mother to her fetus.

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