In the primary care setting, lymphadenopathy (LN) is a not an uncommon complaint or finding on physical examination (6
). It may be discovered during routine physical examination or incidentally by the patient and constitute the sole reason for a medical visit. In either setting, because of the wide variety of diseases that cause lymph node enlargement, defining the etiology can present a diagnostic challenge. The cause is frequently obvious, and most patients can be diagnosed on the basis of a careful history and physical examination. In others, diagnosis may require laboratory tests and/or biopsy of the involved node(s).
Infection with Toxoplasma gondii
is a cause of clinically significant, nontender and nonsuppurative LN. Infection with this organism usually causes regional enlargement of lymph nodes (most commonly suboccipital and cervical) rather than generalized LN (11
). Although the diagnosis can be made when the classic histopathologic findings are present on lymph node biopsy (4
), we have continued to seek serologic methods to make the diagnosis so as to avoid biopsy in most cases. In a previous study by our group, it was also demonstrated that the diagnosis of toxoplasmic lymphadenopathy (TL) can be established by the use of a panel of serological tests, i.e., the toxoplasma serological profile (TSP) (13
). Little value has been added by performing isolation procedures (3
) or the PCR (21
The kinetics of the individual tests included in the TSP are unique, and results in these tests are time dependent and vary from the onset of lymphadenopathy to the time of drawing of the serum sample (13
). A TSP consistent with a recently acquired infection (i.e., high titers in the dye test [DT], i.e., >1,024; positive immunoglobulin G [IgM], IgA, and IgE findings; and acute pattern in the AC/HS) is strongly suggestive of TL and is essentially found only in patients whose LN was detected within 2 to 3 months of the sampling of the serum (13
). In these patients a lymph node biopsy is usually not indicated unless the LN persists, other symptoms develop, or some other diagnosis is being considered.
Equivocal results in the TSP (i.e., DT titer of ≤1,024, low-positive or equivocal results in the IgM, IgA, or IgE enzyme-linked immunosorbent assay [ELISA] results, and an equivocal pattern in the AC/HS) are more difficult to interpret. In such cases, T. gondii
should not be ruled out or implicated as the etiological agent of the patient's LN (13
). TSP results consistent with a chronic infection acquired in the distant past—i.e., a DT titer of ≤256, equivocal or negative IgM, IgA, and IgE levels, and a chronic pattern in the AC/HS—essentially excludes T. gondii
as the causative agent of a lymph node detected to be enlarged within the previous 3 months of the drawing of the serum sample (13
The avidity of T. gondii
-specific IgG antibodies (in the patient's serum) for defined toxoplasma antigens (purified and used to capture and bind T. gondii
-specifc IgG antibodies) has been found to gradually increase after primary infection with the parasite (7
). IgG avidity can be measured by the resistance of the antibody-antigen complex to the disrupting force of 6 M urea (7
). Avidity has been primarily studied in the setting of pregnancy (8
). Low or equivocal avidity test results can persist for months to more than 1 year after primary infection (16
). The time of conversion from low or equivocal to high avidity test results is highly variable among different individuals. However, high avidity test results are observed only in individuals infected for at least 3 to 5 months (this time window varies according to the method used to measure avidity antibodies). In studies in pregnant women, high avidity test results by the IgG VIDAS avidity test (VIDAS Toxoplasma IgG Avidity test [bioMérieux, Marcy l'Etoile, France]), for example, have been reported to be present only in individuals who have been infected for at least 4 months (12
The goal of the present study was to attempt to define the kinetics and the clinical utility of the IgG VIDAS test in patients with TL.
(Presented in part at the 40th Annual Meeting of the Infectious Diseases Society of America, Chicago, Ill., in October 2002.)