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Fig. 45.3 Life cycle of Toxoplasma gondii.

As humans are omnivores, they most commonly become infected by eating raw or undercooked meat containing tissue cysts. Otherwise infection is acquired by ingesting plant or other material contaminated with oocysts. Less common but important routes of infection include ingestion of unpasteurized goat's milk, transplacental infection, and infection via transfusion or organ transplantation. It is possible that the fur of dogs which have rolled in contaminated soil may also be a source of infection.

Domestic cats that are shedding oocysts are ubiquitous. In regions of the world with warm, moist soil conditions, cat feces become infectious within a day. Such locales will have a higher prevalence of T. gondii antibody within the population. A particularly high rate is seen in many countries in South America, where the prevalence of antibody-positive individuals reaches 80% to 90% by the fifth decade of life. In other countries and cultures, T. gondii infection occurs predominantly by ingestion of tissue cysts. Some religions prohibit the ingestion of certain potential animal sources, thus reducing the prevalence of infection. Both cooking styles and eating habits will also affect antibody prevalence. For example, the proportionately greater consumption of raw or undercooked meat in France compared with other European countries has resulted in high antibody prevalence, which may exceed 50% of the population by the age of 10 years.

Congenital infection most often occurs by reactivation of latent-phase bradyzoites in the pregnant woman, although a newly acquired acute infection will have the same result. Thus in countries where antibody prevalence is high, it follows that congenital infection will also be more prevalent and the screening of individuals becomes more important. The damaging effects on the fetus are most significant if transplacental infection occurs in the first trimester of pregnancy. Fortunately, fetal infection more readily occurs in the third trimester.
As already noted, there are a few occupational risk factors for toxoplasmosis. The best documented risk is in abattoir workers, such as butchers and meat inspectors. Veterinarians whose work requires close contact with animals may also have increased antibody titers to T. gondii. Individuals who are immunosuppressed due to malignancy, infectious diseases (AIDS), or treatment such as chemotherapy are at increased risk for developing toxoplasmosis. Organisms which have been latent for years may rapidly disseminate and result in overwhelming infection in immunosuppressed individuals.

The histopathological findings vary with the immune response of the patient. The intestinal mucosal proliferation of Toxoplasma tachyzoites is followed by spread to the lymph nodes and then dissemination. The patient's clinical state is relative to the cell-mediated immunity. When there has been prolonged infection or in those who have been treated, there will be few toxoplasma in the tissues but scarring may be evident.

Within the intestine there may be ulceration, with multiple Toxoplasma tachyzoites. In about 10% of patients there may be hepatic enlargement with fibrosis and chronic inflammation. Areas of eosinophilic necrosis may be found, with surrounding clusters of Toxoplasma organisms. Liver function tests can be abnormal. In the lungs there may be interstitial pneumonia, but it is usually difficult to find the organisms: in those who are immunodeficient there may be concomitant infections such as with Pneumocystis carinii. In the central nervous system there will be glial nodules, often with surrounding inflammatory cells. The tachyzoites multiply within vessel walls, in the ependyma, and in nerve cells. There may also be tissue cysts. Patients with encephalitis show large areas of focal necrosis contain cysts and tachyzoites. The tachyzoites radiate from a single center and later extend into arterioles, causing occlusive hypertrophic arteritis. The end result may be infarction: within the infarct there may be central necrosis and the appearance may suggest an abscess, but histopathologically there is no pus.

The placenta is grossly normal but histopathologically there may be tachyzoites and cysts with bradyzoites in both the chorion and the umbilical cord: there are seldom any necrotic lesions. In spite of this, the fetus is often infected.
In the neonate it is the ventricular system which is mostly affected. Foci occur in the ependyma and subependyma. Inflammatory obstruction causes internal hydrocephalus of the lateral and third ventricles; the fourth ventricle is not distended. The necrosis and vasculitis in the lateral and third ventricles is probably a local antigen-antibody reaction. As the intracerebral pressure increases, there may be hypothalamic destruction. Necrotic areas of brain often calcify and are seen on imaging. Congenital toxoplasmosis may also cause cellular necrosis and glial nodules; tissue necrosis occurs when a cyst has disintegrated and following infection when a blood vessel is involved.

Infected lymph nodes usually show follicular hyperplasia with a histiocytic reaction and distended sinuses but no eosinophilia or necrosis. Fibrosis is unusual and the normal architecture of the lymph node is usually maintained.

Acute Toxoplasma infection may cause myocarditis, particularly in those who are immunodeficient. Pericardial effusions and pericarditis may occur. Myositis is rare.
Retinal infections can occur at any age with toxoplasmosis, but the majority occur in congenital infections. The organisms are found in the retina and this infection should be considered whenever there is retinochoroiditis. Histopathologically there may be focal retinitis with scarring and inflammation or a more diffuse infection which is often clinically more progressive. The choroid will be heavily infiltrated with plasma cells, lymphocytes and mononuclear cells. In the immunodeficient patients, as in AIDS, the lesions become confluent and there is retinal detachment.

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