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Editor,—Ocular toxoplasmosis is the most frequent infectious cause of chorioretinal inflammation in immunocompetent individuals.1 Diagnosis is usually made by observing the typical fundus lesion, by detecting the presence of anti-Toxoplasma antibodies in the serum, and by excluding other causes of necrotising fundus lesions.2In unusual cases, invasive procedures may be required to aid diagnosis.3
A 17 year old white male presented complaining of floaters and reduced visual acuity in the left eye. Visual acuity was 6/9 in the left eye, 6/6 in the right. Examination revealed moderate anterior chamber activity, marked vitritis, and an active retinochoroiditis adjacent to an area of old chorioretinal scarring inferonasal to the optic disc. A diagnosis of ocular toxoplasmosis was suspected, and topical and oral steroids, and oral clindamycin were commenced. Peripheral blood anti-Toxoplasma IgG antibodies, measured using the dye test, were positive (16 IU/ml). Despite treatment, the ocular inflammatory signs increased and 5 weeks following initial presentation he developed a confluent area of retinal necrosis in the peripheral retina leading to a superotemporal retinal detachment. This was distinct from the original area of inflammation. The presence of severe vitreous inflammation and peripheral retinal necrosis suggested a unilateral acute retinal necrosis syndrome.4 Three port trans pars plana vitrectomy with perfluorocarbon liquid and fluid/silicone exchange was performed. At vitrectomy, vitreous humour was taken for anti-Toxoplasma and antiviral antibody levels and a retinal biopsy was also obtained. Postoperatively, he was commenced on sulphadiazine, pyrimethamine, and folinic acid and continued on oral steroid medication. Levels of IgG, IgA, and IgM were measured in serum and vitreous aspirate at the same time. The Goldmann–Witmer coefficient using IgG was greater than 59, using IgA greater than 45, and using IgM greater than 65. This is evidence of intraocular antibody production. Samples were negative for antiviral antibodies. Intraocular ToxoplasmaDNA was demonstrated by a polymerase chain reaction (PCR) assay using primers for the P30 gene. PCR testing for viral DNA was negative. Insufficient material was obtained to attempt to isolate the parasite using tissue culture or animal inoculation. Retinal biopsy demonstrated a mixed inflammatory response without a specific infective agent. The patient subsequently responded to treatment and the intraocular inflammatory signs subsided.
Ocular toxoplasmosis is a common cause of retinochoroiditis, and can usually be diagnosed clinically. Rarely is it possible to obtain vitreous and retinal biopsies to aid diagnosis, but in doubtful cases, it may be appropriate to perform anterior or posterior chamber aspirate to confirm the diagnosis. The assessment ofToxoplasma antibodies in serum is of limited use, unless rising titres can be demonstrated, since the incidence ofToxoplasma infection in the general population is high. The demonstration of antibody production within the eye is particularly valuable in the diagnosis of difficult cases. The finding of higher anti-Toxoplasma antibody levels in the aqueous humour than in the serum (the Goldmann–Witmer coefficient) indicates intraocular antibody production.5 A further investigation which is extremely useful is the demonstration of parasite DNA within ocular fluid by PCR.6 With PCR a sequence of DNA is amplified from minuscule amounts of DNA making it amenable to direct analysis.7 8 De Boeret al used a combination of the demonstration of intraocular antibody production and PCR analysis in the diagnosis of a variety of infectious uveitis cases.9In this case we initially made a diagnosis of ocular toxoplasmosis, but the disease progressed clinically and did not respond to treatment. The patient was compliant with prescribed medication, and had no evidence of immunocompromise. Retinal detachment is unusual in ocular toxoplasmosis,10 but is typical of acute retinal necrosis syndrome, suggesting an alternative diagnosis in this case. We were, however, able to confirm the diagnosis of toxoplasmosis by evidence of intraocular antibody production and by positive PCR amplification.
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