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===Laboratory Tests===
 
===Laboratory Tests===
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The diagnosis is usually based on blood tests that detect antibodies against the parasite. However, if the person's immune system is impaired by AIDS, the blood test may be falsely negative. To determine whether a fetus has been infected, a doctor usually takes a sample of the fluid around the fetus (amniotic fluid) to be analyzed.
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Changes in routine haematology and biochemistry may be seen in acute toxoplasmosis. These can include a mild anaemia and leukopenia, as well as increases in liver enzymes.
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acute Atypical lymphocytosis, mild anemia, leukopenia, and slightly elevated liver enzymes are common. The syndrome may persist for weeks but is almost always self-limited.
      
The diagnosis is usually made serologically using an indirect fluorescent antibody (IFA) test or enzyme immunoassay (EIA) for IgG and IgM antibodies. Specific IgM antibodies appear during the first 2 wk of acute illness, peak within 4 to 8 wk, and eventually become undetectable, but they may be present for as long as 18 mo after acute infection. IgG antibodies arise more slowly, peak in 1 to 2 mo, and may remain high and stable for months to years. Specific IgM antibodies with low IgG are consistent with recent infection in immunocompetent patients. Acute infection should also be suspected if the IgG is positive in an immunocompromised host with encephalitis. Toxoplasma-specific IgG antibody levels in AIDS patients with Toxoplasma encephalitis are usually low to moderate but may be absent; IgM antibodies are not present. Past infection in a healthy person typically produces a negative IgM test, and a positive IgG test. In patients with retinochoroiditis, low titers of IgG antibodies are usually present, but IgM antibodies are not detected.
 
The diagnosis is usually made serologically using an indirect fluorescent antibody (IFA) test or enzyme immunoassay (EIA) for IgG and IgM antibodies. Specific IgM antibodies appear during the first 2 wk of acute illness, peak within 4 to 8 wk, and eventually become undetectable, but they may be present for as long as 18 mo after acute infection. IgG antibodies arise more slowly, peak in 1 to 2 mo, and may remain high and stable for months to years. Specific IgM antibodies with low IgG are consistent with recent infection in immunocompetent patients. Acute infection should also be suspected if the IgG is positive in an immunocompromised host with encephalitis. Toxoplasma-specific IgG antibody levels in AIDS patients with Toxoplasma encephalitis are usually low to moderate but may be absent; IgM antibodies are not present. Past infection in a healthy person typically produces a negative IgM test, and a positive IgG test. In patients with retinochoroiditis, low titers of IgG antibodies are usually present, but IgM antibodies are not detected.
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