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Overt chorioretinitis after patient acquired toxoplasmosis in an immunocompetent subject
  1. C MARX-CHEMLA,
  2. I VILLENA,
  3. F FOUDRINIER,
  4. J M PINON
  1. Reims Toxoplasmosis Group, Laboratoire Parasitologie, Hôpital Maison Blanche (UPRESEA 2070, IFR 53), CHU, Reims Cedex France
  2. Reims Toxoplasmosis Group, Services Ophtalmologie, Hôpital Robert Debré, CHU, Reims Cedex France
  1. A GOTZAMANIS,
  2. F HAMON,
  3. A DUCASSE
  1. Reims Toxoplasmosis Group, Laboratoire Parasitologie, Hôpital Maison Blanche (UPRESEA 2070, IFR 53), CHU, Reims Cedex France
  2. Reims Toxoplasmosis Group, Services Ophtalmologie, Hôpital Robert Debré, CHU, Reims Cedex France
  1. C Marx-Chemla, Laboratoire de Parasitologie, Hôpital Maison Blanche, 45 rue Cognacq Jay, 51092 Reims Cedex France.

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Editor,—Acquired Toxoplasma gondiiinfection is usually asymptomatic and uncomplicated unless it occurs in severely immunodepressed patients or in particular epidemiological settings.1 2

We report a case of toxoplasmic chorioretinitis (CR) occurring 15 months after patent primary infection with cervical adenopathies in an immunocompetent woman.

CASE REPORT

VK, a 31 year old woman, presented with blurred vision in the left eye, which had started a few days previously. Visual acuity on this side was preserved at 16/20. Split lamp examination showed a negative Tyndall in the anterior chamber. Ocular pressure was 10 mm Hg. Retinal examination with the three mirror method revealed a fresh and strictly peripheral chorioretinal lesion at 10 o’clock, suggestive of toxoplasmosis, with no evidence of previous scarring. Peripapillar haemorrhage and a moderate vitreal reaction were also noted. The right eye was strictly normal. Two small cervical adenopathies could be felt.

Fifteen months previously this nulliparous woman had developed cervical adenopathies, with serum anti-toxoplasmic antibody kinetics typical of very recent seroconversion (Table 1).3 Specific IgA antibodies persisted 8 months after seroconversion and the woman, who wished to become pregnant, was referred to the Reims Toxoplasmosis Group to assess the risk of maternofetal transmission.4 5

Table 1

Kinetics of anti-toxoplasmic IgG, IgM and IgA antibodies (months) from the first serological tests at the time of onset of cervical adenopathies (T0). T8 months corresponds to the first immunological study in parasitological laboratory and T15 months to the onset of chorioretinitis. Note that the first serological tests (undertaken in another laboratory) were based only on immunoenzymatic methodology (IgG and IgM (MEIA))

Eight days after onset of the visual disorders the anterior chamber was sampled by puncture. Aqueous humour and peripheral blood were tested for toxoplasmic DNA by polymerase chain reaction (PCR)6and/or blood circulating T gondii research, and for specific IgG, IgM, and IgA antibodies by immunocapture tests; the Witmer–Desmonts coefficient (C) was calculated.6 7Serological tests for viral and other parasitic infections were also done, and her immune status was thoroughly investigated (Table 2). Anti-toxoplasma chemotherapy was started immediately, with a combination of pyrimethamine-sulphadiazine and calcium folinate for 1 month. The visual disorders improved and the chorioretinal lesion healed rapidly.

Table 2

Results of the different tests performed on serum and aqueous humour

COMMENT

This case is unusual in that a chorioretinal toxoplasmic lesion occurred 15 months after seroconversion in a healthy adult.

The precise date of infection was deduced from clinical arguments and the results of biological tests. The first battery of serological tests, at the onset of cervical adenopathies (T0), was carried out because the patient was intending to have children. Eight months later the persistence of specific IgA antibodies pointed to active toxoplasmosis. As we had previously observed cases of congenital transmission after preconceptional seroconversion with adenopathies, the patient was advised not to become pregnant yet.3-5This position was borne out by the onset of chorioretinitis some months later. The ocular involvement was confirmed by sampling the anterior chamber (positive Witmer–Desmonts coefficient, and local synthesis of specific IgA) less than 8 days after the onset of visual disorders.

Ocular lesions were long considered to be a sometimes very late complication of congenital toxoplasmosis, except in case of immunodepression (human immunodeficiency virus, organ transplantation, etc).1 2 8 Our patient’s immune status was strictly normal; she was not on immunosuppressive drugs and had no intercurrent infections. The persistence of two small cervical adenopathies and specific IgA antibodies 15 months after the primary infection illustrates the long duration of the active phase of infection in this case complicated by secondary chorioretinitis.1 9 With a well defined interval before onset, this case of chorioretinal involvement (isolated, unilateral, and without pre-existing lesions) differs from other reported cases in which the date of seroconversion was less precise and the chorioretinitis was often associated with neurological manifestations.1 8 10

This case of secondary toxoplasmic chorioretinitis in an immunocompetent woman suggests that all patients with persistent adenopathies and serological markers of active T gondii infection should have regular ocular monitoring.

Acknowledgments

Financial support was provided by the Programme Hospitalier de Recherche Clinique (1994), Direction des Hôpitaux, Ministère des Affaires Sociales, de la Santé et de la Ville, Paris, France.

References

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