|Values are valid only on day of printing.|
Aids in the diagnosis of both congenital and acute acquired toxoplasmosis
Toxoplasma gondii is an obligate intracellular protozoan 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 the soil and become infectious.(1) Toxoplasmosis is acquired by humans through ingestion of food or water contaminated with cat feces or through eating undercooked meat containing viable oocysts. Vertical transmission of the parasite through the placenta can also occur, leading to congenital toxoplasmosis. Following primary infection, Toxoplasma gondii can remain latent for the life of the host; the risk for reactivation is highest among immunosuppressed individuals.
Seroprevalence studies performed in the United States indicate that approximately 9% to 11% of individuals between the ages of 6 and 49 have antibodies to Toxoplasma gondii.(2)
Infection of immunocompetent adults is typically asymptomatic. In symptomatic cases, patients most commonly present with lymphadenopathy and other nonspecific constitutional symptoms, making definitive diagnosis difficult to determine.
Severe-to-fatal infections can occur among patients with AIDS or individuals who are otherwise immunosuppressed. These infections are thought to be caused by reactivation of latent infections and commonly involved the central nervous system.(3)
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.(4) 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.
Toxoplasma ANTIBODY, IgM
Toxoplasma IgM VALUE
0.55 to <0.65 (Equivocal)
> or =0.65 (Positive)
Active toxoplasmosis is suggested by the presence of IgM antibodies, but elevated anti-IgM titers are often absent in immunocompromised patients. In addition, elevated IgM can persist from an acute infection that may have occurred as long ago as 1 year.
A suspected diagnosis of acute toxoplasmosis should be confirmed by further testing at a toxoplasmosis reference laboratory or by detection of Toxoplasma gondii DNA by PCR analysis of cerebrospinal fluid or amniotic fluid specimens (PTOX / Toxoplasma gondii, Molecular Detection, PCR).
For confirmation of a diagnosis, the FDA issued a Public Health Advisory (7/25/1997) suggesting that sera found to be positive/equivocal for Toxoplasma gondii IgM antibody be sent to a Toxoplasma reference laboratory; CDC or Jack Remington, MD, Palo Alto Medical Foundation, 860 Bryant Street, Palo Alto, CA 94301, were recommended.(Reviewed 12/2011)
Specimens interpreted as equivocal may contain very low levels of IgM. A second specimen should be drawn and tested.
Negative results do not preclude recent primary Toxoplasma gondii infection. A negative result could indicate either no previous exposure or also could be seen in cases of remote exposure with subsequent loss of detectable antibody. A second specimen drawn at a later point in time may be needed to rule out a recent infection.
Positive serologic results alone are not diagnostic of Toxoplasma gondii infection. For example, infections with Epstein-Barr virus (EBV) have been suspected to elicit antigen-specific IgM responses (eg, false-positive IgM Toxoplasma reactions) in individuals previously sensitized to a variety of non-EBV infectious agents.
Since persisting IgM levels may be detected long after the onset of acquired infection, the use of a single serological test result must be used with caution in those cases when it is critical to establish the time of infection. This applies to the diagnosis of acute Toxoplasma gondii infection acquired during pregnancy. Determination of the date of infection based solely on the results of detectable IgM antibody to Toxoplasma gondii is not recommended. That determination should include clinical history and previous serology, since low levels of IgM antibody may persist for a year or more. The use of a test to determine a rise in IgG antibody to Toxoplasma gondii (TOXGP / Toxoplasma gondii Antibody, IgG, Serum or TOXOP / Toxoplasma gondii Antibody, IgM and IgG [Separate Determinations], Serum) may provide additional information as to the date of infection. Therefore, the FDA has instructed commercial suppliers of Toxoplasma IgM kits to recommend Toxoplasma IgG testing also be performed.
The VIDAS TOXO IgM system was compared to an indirect immunofluorescence (IFA) IgM assay (GenBio, San Diego, CA). Of 125 specimens tested, 45 and 47 were IFA- and VIDAS-positive, respectively. Using the IFA IgM as the gold standard, the sensitivity and specificity of the VIDAS Toxo IgM assay was 98% and 96%, respectively.
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