Reliability of immunoglobulin G antitoxoplasma avidity test and effects of treatment on avidity indexes of infants and pregnant women

Abstract

The immunoglobulin G antitoxoplasma avidity test (Vidas; BioMérieux) is an immunoenzymatic test useful for excluding acute infection after the onset of pregnancy. The avidity index (AI) is the ratio of the signal in a test sample washed with urea, which disrupts low-avidity complexes, to that washed without urea. An AI of >0.3 is taken to mean that infection had occurred more than 4 months ago. The increase of the AI with time and the influence of the different treatments given to pregnant women and their newborns were evaluated. A total of 59 pregnant women (271 sera) and their 60 neonates (199 sera) were tested from 1998 to 2002. There were five groups of women based on the type and duration of treatment given. Thirteen pregnant women (group 1) did not receive any treatment, 15 (group 2), 11 (group 3), and 17 (group 4) women received treatment with spiramycin (9 MIU/day) for 0.5 to 2, 2.5 to 5, and 5.5 to 8 months, respectively, and the last 3 women (group 5) received tritherapy (pyrimethamine-sulfonamide and spiramycin alternatively) for 1.5 to 2.5 months. All of the maternal sera collected in the first 6 months had an AI of <0.30, with a mean of 0.07 (range, 0.01 to 0.21). The increase was slow (0.02/month), and there was no significant difference when comparisons were made between the treatment groups. Neonates with proven maternofetal transmission had an increasing AI, unlike those without transmission. However, long-term therapy with pyrimethamine-sulfonamide, as opposed to treatment with spiramycin alone, was found to slow down the progression of the AI. An AI of >0.2 is sufficient to exclude acute infection in pregnant women. In neonates, it is not of major use to diagnose congenital infection; however, it could be a good indicator of compliance and efficacy of treatment of infected infants.

FIG. 1.

Increase of the AI in 59 pregnant women followed up after accurately dated seroconversion (total number of avidity tests, 215; correlation coefficient of Spearman, r = 0.85, y = 0.020x + 0.010). (A) Infection had occurred between the two samples (real seroconversion) (37 patients); (B) infection had occurred at most 1 month before the first sample (positive IgM and negative or weakly positive IgG followed by a twofold or greater increase) (22 patients) (no difference between the two groups).

FIG. 2.

Increase of the AI in pregnant women followed up as a function of the duration and type of antitoxoplasma treatment. Group 1, no treatment (13 patients, 46 sera); group 2, spiramycin (9 MIU/day) for 0.5 to 2 months (15 patients, 59 sera); group 3, spiramycin (9 MIU/day) for 2.5 to 5 months (11 patients, 40 sera); group 4, spiramycin (9 MIU/day) for 5.5 to 8 months (17 patients, 60 sera); group 5, tritherapy for 1.5 to 2.5 months (sulfadiazine [3 g/day], pyrimethamine [50 mg/day], and folinic acid [50 mg/7 days]) alternated with 3-week courses of spiramycin (9 MIU/day) (3 patients, 10 sera) (for cutoff value of 0.2, P = 0.19 [ANOVA Fisher Snedecor test]; for cutoff value of 0.3, P = 0.72 [ANOVA Fisher Snedecor test]).

FIG. 3.

Increase of the AI in 60 neonates followed up for congenital toxoplasmosis. (a) 49 neonates (59 sera) in whom maternofetal transmission was either negative or indeterminate; (b) 11 neonates (46 sera) in whom maternofetal transmission was proven. Dotted lines indicate neonates treated with tritherapy. Solid lines indicate neonates treated with spiramycin alone.