|Year : 1979 | Volume
| Issue : 2 | Page : 17-25
Leyla Atmaca, Kanpolat
Eye Clinic, Faculty of Medicine, University of Ankara, Ankara, Turkey
Eye Clinic, Faculty of Medicine, University of Ankara, Ankara
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Atmaca L, Kanpolat. Ocular toxoplasmosis. Indian J Ophthalmol 1979;27:17-25
Ocular toxoplasmosis was first reported in 1923 by Janku, who described a boy who became blind at the age of three months and died with hydrocephalus and whose postmortem examination showed granulomatous intraocular inflammation with protozoa in the retinal, Wilder first found organisms morphologically identical with toxoplasma in adult eye enucleated with uveitis. Toxoplasmosis presents as a sub-clinical disease in most people, with ocular lesions being present in a few. Chorioretinitis is usually bilateral in congenital cases and unilateral in acquired ones. It is located at the posterior pole and the macula; a peripheral scar may not be noticed before adult age. Recurrences are common as satellite lesions adjacent to an old scar. Infection tends to involve also the central nervous system and the retina,.
| Material And Methods|| |
29 cases of toxoplasmosis chorioretinitis were observed in the Eye Clinic, Faculty of Medicine, Ankara University, between 1972-1978 [Table - 1],[Table - 2]. Of these 22 were congenital and 7 acquired. The lesion was unilateral in all of the acquired, and bilateral in 13 and unilateral in 9 of the congenital cases. The following examinations were carried out on all of the patients visual acuity, biomicroscopy, direct ophthalmoscopy, coloured fundus photography, fluorescein angiography, serological Sabin-Feldman dye test, haemagglutination test, and other systemic examination. Fluorescein angiography was carried out with a Zeiss fundus camera using 5 cc of 20% sodium fluorescein. All patients were treated with pyremethamine, sulphadiazine, prednisone, and folinic acid, with weekly blood checks.
A 44-year-old female with decreased visual acuity in the right eye 4 months prior to the examination, complained of positive central scotoma. She had no previous history of ocular disease. Other systemic examinations were normal. On examination, her visual acuity was 6/ 18 with correction in the right eye and 6/6 in the left eye. Direct ophthalmoscopy showed a normal fundus in the left eye and an elevated intraretinal exudative haemorrhagic macular lesion of 1.5 disc diameter in the right eye. The periphery of the eye was normal. Visual field examination showed central scotoma. Fluorescein angiography showed a subretinal neovascular membrane [Figure l]a with dye leaking progressively from the neovascular membrane info the subretinal space [Figure - 1]b. The Sabin-Feldman dye test titre was 1/64. She was treated with pyremethamine, sulphadiazine, and prednisone. 2 months later, her visual acuity was 6/60 with correction in the right eye and the dye titre 1/16. 3 months later her visual acuity was counting fingers at 1 m. Flourescein angiography showed enlargement in the lesion [Figure - 2]), with pooling of dye in the late phase [Figure - 2]b. Six months later, there was a white, oval scar in the macula [Figure - 3].
A 34-year-old male with a history of blurred vision in the left eye 8 months was seen with no other previous complaints. Other systemic findings were normal. Visual acuity was 6/6 in the right eye and counting fingers at 10 cm. in the left eye. Visual field examination showed central scotoma in the left eye. Direct ophthalmoscopy showed a normal fundus in the right eye. An elevated, haemorrhagic intraretinal, exudative lesion of the macula was present in the left eye. The periphery of the left eye was normal. The arterial phase of fluorescein angiography showed a subretinal neovascular membrane and detachment of the pigment epithelium [Figure - 4]a. The arterio-venous phase of angiography showed dye pooling in the lesion [Figure - 4]b. The Sabin-Feldman dye titre was 1/256. The patient was given medical treatment. Two momhe later the dye titre was 1/16. Fluorescein angiography showed a decrease in leakage of dye in the lesion and enlagement in the subretinal haemorrhage [Figure - 5]. 5 months later a white scar was formed in the macula.
A 26-year-old female with decreased visual acuity in the right eye 2 months prior to the examination. Systemic examinations were normal. Visual acuity was 6/60 in the right eye and 6/6 in the left eye. The fundus examination demonstrated a normal fundus in the left eye. A lesion of macular chorioretinitis of 1/2 disc diameter and a small satellite lesion of 1/4 disc diameter located Just inferotemporally to the macular lesion were present in the right eye. There was disc oedema and sheathing or the retinal vessels. The fluorescein angiogram showed dye leakage from both lesions. In the late phase the optic disc was completely obscured by fluorescein leakage [Figure - 6]. There was leakage of dye from the sheathed retinal vessels [Figure - 7]. The SabinFeldman dye titre was 1/256. The patient was given medical treatment. 2 months later the dye titre was 1/1000. There was p gmentation around the macular and satellite lesion. F:uorescein angiography demonstrated dye leakage from the margin of satellite lesion [Figure - 8]. Argon laser photo-coagulation was applied circumferentially along the margin of the satellite lesion. 4 months later, both lesions were found to have turned into atrophic scars with visual acuity being 6/30 in the right eye and 6/6 in the left eye.
A 26-year-old female complained of blurred vision in the left eye for a week. All systemic examinations were normal. Visual acuity was 6/6 in the right eye and counting fingers at 1 m. in the left eye. The SabinFeldman dye titre was 1/64. Direct ophthalmoscopy showed a normal fundus in the right eye, and a lesion of macular chorioretinitis of 1 disc diameter with retinal striae extending nasally and temporally from lesion in the left eye. There were tortuous and anastomosed retinal vessels superio temporally to the lesion. Fluorescein angiography showed typically increased tortuousity and anastomosis in the retinal vessels in this region [Figure - 9]. The patient was given medical treatment.
| Discussion|| |
Our report comprises 29 patients with toxoplasmosis chorioretinitis. The patients came to our clinic with complaints of blurred vision. Examination revealed characteristic chorioretinal lesions of toxoplasmosis, which was follow by Sabin-Feldman dye test, complement fixation test and haemagglutination test. 22 out of 29 cases were considered congenital and 7 acquired [Table - 1][Table - 2]. 2 out of 22 congenital cases were recurrences of a previous congenital infection. Both of them had an old atrophic scar in either the same or the other eye. Two congenital cases had a dye titre of 1/ 1000 and the others 1/256 or less. A Sabin-Feldman dye titre of 1/16 or greater was considered positive (after Hogan et al. Scott,). Hogan and his associates reported that 201 out of 240 cases of toxoplasmic uveitis had dye test titres of 1/256 or less.
Perkins suggests that, cases of focal chorioretinitis with positive serological evidence of toxoplasmosis be considered to result from congenital infection unless there is a clear history of recent systemic signs and symptoms of toxoplasmosis. Although 7 cases of this series had no recent systemic signs or symptoms of toxoplasmosis, they were considered acquired on the basis of the absence of any other findings pointing to a congenital origin. These 7 cases were considered acquired on absence of any previous systemic or ocular complaints, absence of any old scars in all but one case, and fluctuating dye test titres. On the other hand, in one case with an old scar, a history of miscarriage following two healthy parturitions and appearence thereafter of ocular lesions, suggested the possibility of acquired infection.
Of acquired cases, in case 1, an acute lesion was observed involving the macula and a subretinal neovascular membrane was noticed on fluorescein angiography. The patient's age and detection of a subretinal neovascular membrane suggested senile macular degeneration. However, with a positive dye test titre and absence from the other eye of lesions such as drusen and pigment epithelial defects indicating macular degeneration, and variable titres led to our diagnosis of toxoplasmosis chorioretinitis. The authors are of the opinion that in cases with haemorrhagic and serous detachment and neovascular membranes the posibility of toxoplasmosis chorioretinitis should be considered besides macular degeneration.
In the second case, also there was an acute lesion involving the macula with a subretinal neovascular membrane. However, this patient was younger than the first one. So far in the literature only one case has been reported with a neovascular frond.
In the third case there was optic disc oedema, a macular lesion with a satellite lesion immediately below it, and sheathing in the retinal vessels. With toxoplasmosis an active lesion is rare in the optic disc. Cranial nerve involvement has been reported with papilloedema developing secondarily. We feel that in this case papilloedema was secondary to periphlebitis. This was the only case presenting periphlebitis. In previous publications, retinal vascular lesions, periphlebitis, and periarteritis have been reported to be associated with toxoplasmosis,. Xenon-arc and argon laser photo-coagulation have been used in cases of toxoplasmosis chorioretinitis in an effort to prevent recurrences. L'Espirance suggested that the choroidal and retinal neovascularisation at the edges of the toxoplasmic scar should be coagulated. Accordingly the satellite lesion in this case was photocoagulated.
In the fourth case fluorescein leakage was not observed in the macular lesion. The vascular lesion and anastomosis had become prominent superio-temporally to the lesion [Figure - 9]. Retinal vascular lesions though reported in association with toxoplasmosis, earlier the retinal vascular anastomoses was not. This case differed from the others in that retinal vascular lesions were present and fluorescein leakage was absent.
In the fifth case there were three foci of active lesions at, and immediately below the macula.
In the sixth case, despite the presence of a peripheral scar the case was considered as acquired due to the fact that the patient had a miscarriage after two normal parturitions with subsequent appearance of the ocular lesion. It is quite pos,ible`that the patient became infected after two normal parturitions, had the miscarriage, and the ocular lesion developed at the periphery. Subsequently uveitis resulted as an instance of recurrence and an active lesion developed adjacent to the old atrophic scar [Figure - 10].
In the seventh case, as in the first one, there was a haemorrhagic acute lesion at the macula. The fact that the patient was 38 years old might suggest the possibility of senile macular degeneration. Yet, variation of dye test as 1/256 and 1/64, coupled with the absence from the other eye of any pathologic signs of senile macular degeneration led to the diagnosis of toxoplasmosis.
| Summary|| |
29 patients with toxoplasmosis chorioretinitis are reported. 22 cases were congenital and 7 acquired. All of the patients received medical treatment and one acquired case argon laser photocoagulatien was performed. Recurrences were observed in 3 of the acquired and 2 of the congenital cases. A subretinal neovascular frond was present in 2 acquired cases, disc oedema and periphlebitis in 1 case, a retinal vascular lesion in one, three separate lesions in and around the macula in one case; in 1 case a quite large acute lesion was present adjacent to an old atrophic peripheral scar, and in another case there was a localised intraretinal haemorrhage and an acute macular lesion. Due to rarity in the literature of the reports concerning the above-mentioned ocular lesions in association with toxoplasmosis, the authors feel that it would be appropriate to consider toxoplasmosis in the differential diagnosis of such cases.
| References|| |
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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10]
[Table - 1], [Table - 2]