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Toxoplasmic retinochoroiditis (TRC) is an infectious disease caused by the protozoan Toxoplasma gondii. This infection affects many organs including the eyes. Most of the time ocular involvement occurs after a transplacental transmission, throughout pregnancy, but the infection can also be acquired. In immunocompetent patients, TRC is the most common cause of infection affecting the posterior segment. Clinically, the lesion appears as a white focal necrosis involving the full thickness of the retina, at the margin of an old pigmented chorioretinal scar. A vitreous inflammation is usually present and occasionally vasculitis is observed.1
We report the case of a healthy patient who developed a unilateral haemorrhagic retinochoroiditis (RC). The investigations performed were positive for a TRC.
A 45 year old African man was referred with a 10 day history of a painless progressive visual loss affecting the left eye. No other ophthalmological or systemic complaints were present. His past medical history was unremarkable.
Ophthalmological examination disclosed a vision of 20/20 in the right eye without correction and in the left eye the best visual acuity was 20/200. Anterior segment examination was normal in the right eye but revealed a mild inflammation in the left. Intraocular pressure was within the normal limits in both eyes. Left eye fundus examination showed a vitreous inflammation (cells: ++) and a whitish retinochoroidal lesion surrounded by a large preretinal haemorrhage. Hard exudates were present in the macular area as well as a retinal oedema (Fig 1).
Investigations revealed an erythrocyte sedimentation rate of 6 mm in the first hour (reference range 1–12), and a normal white blood count. Serological testing for toxoplasmosis gave negative results for IgM but IgG titres were 40 IU/ml (reference range >3). Serology tests for Borrelia burgdorferi, Treponema pallidum, and HIV were normal. An acute infection was suspected and we decided to perform an anterior chamber tap. Polymerase chain reaction (PCR) (toxoplasmosis, CMV, HSV, VZV) gave negative results, but the Goldmann-Wittmer coefficient was 13.64 (reference range <4), revealing a local production of anti-toxoplasmic immunoglobulins. Tests for sarcoidosis and for connective tissue disorders were negative. Immunoglobulin electrophoresis, quantitative immunoglobulin levels, CD4-CD8 lymphocyte count, C3-C4 and CH50 examination were within the normal range. PPD skin test was just positive (7 mm). Chest x ray was normal.
Based on these findings, a TRC was diagnosed. The patient was treated with sulphadiazine (4 × 1 g/day), pyrimethamine (2 × 25 mg/day) and folinic acid, during 6 weeks. Topical steroids and mydriatic drops were also prescribed. Prednisone (1 mg/kg) was introduced, at tapering doses, during the treatment.
After 3 months, visual acuity returned to 20/20 without a correction in the left eye. Anterior segment examination was normal. Left eye posterior segment examination disclosed a regression of the haemorrhages and a white chorioretinal scar with hard exudates located around the fovea. Kyrieleis’s plaque were observed along the inferior papillary arterial vessel (Fig 2).
The patient was followed during 2 years and no reactivation of the RC was observed. Moreover, tests to exclude an immune disease were still within the normal limits (HIV, immunoglobulin electrophoresis, quantitative immunoglobulin levels, PPD skin test, CD4-CD8 lymphocytes count, C3-C4, and CH50).
The most classic clinical presentation of an active toxoplasmic lesion is that of a whitish and oedematous necrotising RC close to an old pigmented scar. A severe vitreous inflammatory reaction is usually associated, appearing as a “headlight in the fog.” Lesions can occur anywhere in the posterior segment but most of the time, they are located in the macular area, affecting one or both eyes. Associated findings include the presence of an inflammatory sheathing of retinal vessels.1
However, a variety of clinical presentations have been reported in the past; Friedmann et al2 described the presence grey-white fine punctuate lesions affecting the deep retina with a mild vitreous inflammation. Direct optic nerve involvement by the protozoan was described by Zimmermann in 1956.3 More recently, various clinical aspects of TCR were described in immunocompromised hosts, appearing as diffuse areas of retinal necrosis4 or as a bilateral military retinitis.5
Ocular occlusive vasculitis can be observed in inflammatory diseases including Behçet’s syndrome, sarcoidosis and systemic lupus erythematosus, in infectious disorders (syphilis, acute retinal necrosis), and in TCR. Branch artery obstruction has been reported when a vessel passes through an acute TCR,6,6a as well as retinal vein occlusion.7,8
The case reported here was diagnostically challenging as the fundus appearance was not characteristic of classic TCR. In fact, haemorrhages are more frequently found in viral infections such as cytomegalovirus retinitis. This feature could be explained by damage to the vascular wall passing through the RC, without signs of a vascular obstruction.
This case demonstrates the importance of including toxoplasmosis in the differential diagnosis of unilateral haemorrhagic RC in immunocompetent patients.