Toxoplasma can infect most warm-blooded animals, both domestic and wild; it is thus the most cosmopolitan of parasites. Approximately 50% of the human population of the United States has been infected. In the overwhelming majority of persons, infection is chronic, asymptomatic, and self-limiting. Clinical disease presents in three major forms: (1) self-limiting febrile lymphadenopathy, (2) highly lethal infection of immunocompromised patients, and (3) congenital infection of infants.
Toxoplasmosis is a cosmopolitan disease that occurs in almost all mammals and many birds. Human infections are found in every region of the globe; in general, the incidence is higher in the tropics and lower in cold and/or arid regions. In the United States, the prevalence of positive serologic evidence for the disease increases with age. By adulthood, approximately 50% of Americans can be shown to have circulating antibodies against T. gondii.
Although it is known that humans may acquire toxoplasmosis in a variety of ways, data on their relative frequency are both meager and conflicting. It is likely that the route of transmission varies from population to population, and perhaps from age to age, within any given area. The most important transmission mechanisms are discussed below.
Felinophobes are inclined to the view that the deposition of oocysts in the feces of cats and their subsequent ingestion by the unsuspecting owner is the most frequent way in which humans acquire this important infection. Disease epidemics associated with ex-posure to infected cats have been reported. Unfortunately, data from studies relating the frequency of feline exposure to the prevalence of positive serologic tests are conflict-ing. Acutely infected cats shed oocysts for only a few weeks. It has been shown, how-ever, that chronically infected felines can occasionally reshed oocysts, and prevalence studies have demonstrated that 1% of domestic cats excrete oocysts at any given time. The large number of these structures passed during active shedding and their prolonged survival in the external environment greatly enhance their chance of transmission. Par-ticularly at risk are individuals such as children at play, who may come in close contact with areas likely to be contaminated with cat feces, and adults responsible for changing a cat’s litter box. It is also possible that insects can mechanically transfer oocysts to hu-man food.
Tissue cysts have been frequently demonstrated in meat produced for human consumption. They are most common in pork (25%) and mutton (10%) and less so in beef and chicken (<1%). Although such cysts are killed at normal (well-done) cooking temperatures, an impressive array of epidemiologic information links the handling and/or ingestion of raw or undercooked meat with serologic and, occasionally, clinical evidence of disease. Confounding these data is an Indian study that demonstrated no difference between meat eaters and vegetarians in the incidence of positive serologic tests.
Approximately 1 of every 500 pregnant women acquires acute toxoplasmosis, and ap-proximately 10 to 20% of the involved women become symptomatic. Regardless of the clinical status of the infected mother, the parasite involves the fetus in 33 to 50% of all acute maternal infections. The risk of transplacental transmission is independent of the clinical severity of the disease in the mother, but does correlate with the stage of gestation at which she is exposed. Fetal involvement occurs in 17% of first-trimester and 65% of third-trimester infections. Conversely, the earlier a fetal infection is acquired, the more severe it is likely to be. Overall, 20% of fetuses experienced severe consequences; a simi-lar proportion develop mild disease. The remainder are asymptomatic.
In addition to causing congenital infection, trophozoites have been responsible for disease transmission in a number of other situations, including laboratory accidents, transfusions of whole blood and leukocytes, and organ transplantation. Because trophozoites may survive for several hours in body fluids or exudates of acutely infected humans, it is possible for infection to occur after contact with such materials.
In the primary infection, the proliferation of trophozoites results in the death of involved host cells, stimulation of a mononuclear inflammatory reaction, and a parasite-specific se-cretory IgA response. In immunodeficient hosts, rapid organism proliferation continues, producing numerous widespread foci of tissue necrosis. The consequences are most seri-ous in organs such as the brain, where the potential for cell regeneration is limited.
In normal hosts, however, acute infection is rapidly controlled with the development of humoral and cellular immunity. Extracellular parasites are destroyed, intracellular multiplication is hindered, and tissue cysts are formed. With the exception of lysis of extracellular parasites by antibody and complement, cell-mediated immunity appears to play
the principal role in this process, mediated in part by IL-2, interferon-_, and cytotoxic T
cells. Immunity appears to be lifelong, possibly because of survival of the parasite in the
tissue cysts. The cysts, which are found most frequently in the brain, retina, heart and skeletal muscle, normally produce little or no tissue reaction. The suppression of cellmediated immunity that accompanies serious illness, or the administration of immunosuppressive agents, may lead to the rupture of a cyst and the release of trophozoites. Their subsequent proliferation and the intense antibody reaction to their presence results in an acute exacerbation of the disease.
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