Toxoplasma Antibody, IgG, Serum
Indication of past or recent infection with Toxoplasma gondii
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Toxoplasma gondii is an obligate intracellular parasite that is capable of infecting a variety of intermediate hosts including humans. Infected definitive hosts (cats) shed oocysts in feces that rapidly mature in soil and become infectious. Toxoplasmosis is acquired by humans via ingestion of food or water contaminated with cat feces or undercooked meats containing oocysts.
Infection of the normal adult is commonly asymptomatic. In cases with clinical manifestations, the most common symptom is lymphadenopathy that may be accompanied by an array of other symptoms making differential diagnosis difficult.
Severe-to-fatal infections do occur in adults immunocompromised by cancer chemotherapy or other immunosuppressive treatment and in patients with AIDS. These infections are thought to be caused by reactivation of latent infections and often involve the central nervous system.
Transplacental transmission of the parasites resulting in congenital toxoplasmosis can occur during the acute phase of acquired maternal infection. The risk of fetal infection is a function of the time at which acute maternal infection occurs during gestation. The incidence of congenital toxoplasmosis increases as pregnancy progresses; conversely, the severity of congenital toxoplasmosis is greatest when maternal infection is acquired early during pregnancy. A majority of infants infected in utero are asymptomatic at birth, particularly if maternal infection occurs during the third trimester, with sequelae appearing later in life. Congenital toxoplasmosis results in severe generalized or neurologic disease in about 20% to 30% of the infants infected in utero; approximately 10% exhibit ocular involvement only and the remainder are asymptomatic at birth. Subclinical infection may result in premature delivery and subsequent neurologic, intellectual, and audiologic defects.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
<4 IU/mL (negative)
4-7 IU/mL (equivocal)
> or =8 IU/mL (positive)
Diagnosis of acute central nervous system, intrauterine, or congenital toxoplasmosis is difficult by routine serological methods. A single positive IgG result is only indicative of exposure to toxoplasma at some point in time (past or recent) and is present in up to 70% of the adult United States population.
The absence of IgG is helpful in that it usually indicates the absence of infection. However, a negative result could mean either no previous exposure or could also be seen in cases of remote exposure with subsequent loss of detectable antibody.
Seroconversion from negative to positive IgG is indicative of recent Toxoplasma gondii infection. Seroconversion indicates infection subsequent to the first negative specimen.
Specimens interpreted as equivocal may contain very low levels of IgG. A second specimen should be drawn and tested.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
IgG is not useful for diagnosing infection in infants <6 months of age. IgG antibodies in that age group, are usually the result of passive transfer from the mother. A single Toxoplasma IgG antibody assay cannot be used to diagnose recent infection.
The IgM assay TOXOM/8865 Toxoplasma Antibody, IgM, Serum should be used to diagnose an acute infection with Toxoplasma gondii.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Luft BJ, Remington JS: Toxoplasmic encephalitis in AIDS. Clin Infect Dis 1992 August;15(2):211-222
2. Wong SY, Remington JS: Toxoplasmosis in pregnancy. Clin Infect Dis 1994 June;18(6):853-862