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Toxoplasmosis is the disease caused by infection with the obligate intracellular
parasite Toxoplasma gondii.
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.
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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,
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
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.