Congenital toxoplasmosis acquired from an immune woman.

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Congenital toxoplasmosis is considered a consequence of an acute maternal Toxoplasma infection acquired during pregnancy.1 Primary infection is associated with parasitemia that can infect the placenta and subsequently the fetus. Acute infection is followed by the formation of cysts. This is associated with an immune response that theoretically confers protection against reinfection. This chronic infection is characterized by stable titers of specific IgG. To facilitate early detection of congenital toxoplasmosis, French authorities have implemented determination of the serologic status against Toxoplasma gondii for women at the prenuptial examination and a serologic follow-up for seronegative pregnant women. We report a case of symptomatic congenital toxoplasmosis in a child whose mother had serologic results consistent with chronic infection. To our knowledge only one similar case has been previously described.2 Case report. This 34-year-old woman, a native of Saint Domingue, had been living in French Guyana for 7 years when she became pregnant for the third time. Her first two children were healthy. Clinical examination was normal at 4 weeks of pregnancy. She had no history of exposure or clinical syndrome suggesting primary infection. However, tests for Toxoplasma antibodies, performed at 4 and 10 weeks, were consistent with past infection acquired before pregnancy. Serologic data included moderate and stable specific IgG titers, nonacute pattern with the comparative agglutination test using formalin- and methanol-fixed T. gondii1 and no specific IgM or IgA antibodies detected by the immunosorbent agglutination assay (Table 1). No previous determination was available. Until the end of the pregnancy she had no history of exposure or clinical signs and symptoms suggesting acute toxoplasmosis.TABLE 1: Serologic results of the mother and child Delivery was at term. The newborn infant, otherwise healthy (birth weight, 3.3 kg) was examined because of a dense cataract of the left eye. Fundus examination of the right eye revealed a fresh macular chorioretinitis. Serologic tests for rubella and cytomegalovirus were negative. The infant had high titers of anti-Toxoplasma IgG associated with specific IgM- and IgA-specific antibodies. Cerebral computerized tomography scan and lumbar puncture did not reveal abnormalities. At that time a new test of the mother showed an increased titer of specific IgG and IgA but no specific IgM. Tests for underlying immunosuppression, including a human immunodeficiency virus serologic test and immunoglobulin assays, were negative in this otherwise healthy patient. She was not lymphopenic and had not received corticosteroid therapy. The child was also negative for HIV. He received surgical treatment for the cataract and was treated with pyrimethamine/sulfadiazine. Discussion. The clinical signs and the presence of specific IgM and IgA antibodies confirmed the diagnosis of congenital toxoplasmosis. This was apparently the consequence of an episode of maternal parasitemia that followed either reinfection or reactivation. Congenital toxoplasmosis acquired after prepregnancy acute infection have also been reported.3, 4 But in our case recent primary infection was eliminated on the basis of serologic results. To our knowledge seven cases of fetal contamination with T. gondii have been described in women with previous serologic tests consistent with past infection.2, 5-7 Reactivation resulting from underlying immunosuppression was obvious in six cases.5-7 Because immunosuppression was absent in our case, reinfection seems to be more likely. The serologic data were very similar to those of the case described by Fortier et al.2 for whom specific IgA antibodies were detected without specific IgM. Because IgA synthesis is associated with infection acquired via the oral route,8 our observation suggests that ingestion of cysts occurred late in the pregnancy. Ingestion of a strain with increased virulence or with distinctive phenotypic characteristics can also be considered in our case. Some clinical and biologic data support the hypothesis of strain-specific virulence. Whereas acute toxoplasmosis is mainly asymptomatic or responsible for lymphadenopathy, some family clusters of patients with toxoplasmic chorioretinitis reported in Brazil indicated increased virulence of some strains.9 Differences in the virulence of T. gondii strains have been observed in laboratory animals.10 This was subsequently supported by genotypic analysis with polymerase chain reaction/restriction fragment length polymorphism, which demonstrated a significant correlation between genotype and virulence in humans.11 Further studies should evaluate the cross-protection between strains of different genotypes. The frequency and consequence of reexposure during pregnancy in previously immune women are unknown and perhaps underestimated because of the lack of serologic follow-up. Christophe Hennequin, M.D. Pascal Dureau, M.D. Laurence N'Guyen, M.D. Philippe Thulliez, M.D. Béatrice Gagelin, M.D. Jean Louis Dufier, M.D. Microbiology (CH, LN) and Ophthalmology (PD, JLD) Services; Hôpital Necker-Enfants Malades; Paris, France Toxoplasmosis Laboratory; Institut de Puériculture; Paris, France (PT) Departmental Laboratory of Hygiene and Medical Analyses; Cayenne, France (BG)