The principal stage in the life cycle of the parasite takes place in the cat (the definitive host) and its prey. The parasite's sexual phase is defined by the formation of oocysts within the cat. The oocyst envelops itself in a rigid wall and is secreted in the feces as an unsporulated oocyst. After 2 to 3 days of exposure to air at ambient temperature, the noninfectious oocyst sporulates to produce eight sporozoite progeny. The sporulated oocyst can be ingested by an intermediate host, such as a person emptying a cat's litter box, a pig rummaging in a barnyard, or perhaps a mouse.
Oral Transmission The principal source of human Toxoplasma infection remains uncertain. Transmission usually takes place by the oral route and can be attributable to ingestion of either sporulated oocysts from contaminated soil or bradyzoites from undercooked meat.
In addition to oral transmission, direct transmission of the parasite by blood or organ products during transplantation takes place at a low rate. Transplacental Transmission may also take place.
Toxoplasmosis in the immunocompetent patient: In persons whose immune systems are intact, acute toxoplasmosis is usually asymptomatic and self-limited. The most common manifestation of acute toxoplasmosis is cervical lymphadenopathy (enlargement of the lymph glands of the neck). A smaller proportion of symptomatic individuals have myalgia, sore throat, abdominal pain, maculopapular rash, meningoencephalitis, and confusion.
Toxoplasmosis in the immunocompromised patient: Patients with AIDS and those receiving immunosuppressive therapy for lymphoproliferative disorders such as leukemia or lymphoma are at greatest risk for developing acute toxoplasmosis. Toxoplasmosis is a principal opportunistic infection of the CNS in persons with AIDS. More than 50% of patients with clinical manifestations have intracerebral involvement. Clinical findings at the time of presentation range from nonfocal to focal dysfunction. These findings include encephalopathy, meningoencephalitis, and mass lesions. Patients may present with altered mental status, fever, seizures, headaches, and focal neurologic findings, including motor deficits, cranial nerve palsies, movement disorders, dysmetria, visual-field loss, and aphasia.
Congenital toxoplasmosis: Clinical manifestations in congenitally infected children includes severe neurologic complications such as hydrocephalus, microcephaly, mental retardation, and chorioretinitis. If prenatal infection is severe, multiorgan failure and subsequent intrauterine fetal death can occur.
Occular toxoplasmosis: Infection with T. gondii is estimated to cause 35% of all cases of chorioretinitis in the United States and Europe. Most ocular involvement is believed to be due to congenital infection, with a very low incidence following acquired infection.
Diagnosis of acute infection with T. gondii can be established by detection of the simultaneous presence of IgG and IgM antibody to Toxoplasma in serum. The presence of circulating IgA favors the diagnosis of an acute infection. The diagnosis of acute toxoplasmosis can also be made by isolation of the parasite from blood or other body fluids after subinoculation of the sample into the peritoneal cavity of mice.
Immunologically competent adults and older children who have only lymphadenopathy do not require specific therapy unless they have persistent and severe symptoms.
Pyrimethamine and trimethoprim inhibit the enzyme dihydrofolate reductase. Inhibitors of protein synthesis, including clindamycin, chlortetracycline, and azithromycin, affect growth of the parasite. Inhibitors of purine synthesis, such as arprinocid, may prove to be important. Atovaquone, which blocks pyrimidine salvage, has demonstrated activity against both T. gondii and P. carinii.