This paper reports a case of recurrent toxoplasmic chorioretinitis in a patient with cellular immunodeficiency. A 37-year-old male presented to an ophthalmologist with complaints of reduced visual acuity and discomfort in his left eye. He had a history of at least two episodes of acute posterior uveitis without identifying the cause of inflammation. An ophthalmoscopic evaluation revealed a scar in the right retina and signs of acute vitritis and chorioretintis surrounding a scar in the left retina. Paired serology confirmed a diagnosis of toxoplasmosis. A deficiency of NK T-cells and cytotoxic СD8+ T-cells was noted, but there was no evidence of secondary immunosuppression. The Primary Immunodeficiency (PID) panel providing sequencing of 208 genes did not find a disease. A test for genetic folate cycle deficiency was conducted due to persistent hyperhomocysteinemia. The genetic testing identified two pathogenic polymorphisms in the genes coding for folic acid cycle enzymes (heterozygous MTHFR A1298C and homozygous MTRR A66G), which was believed to be associated with a cellular immunity, taking into account the data on immunosuppression and opportunistic infections in the presence of a genetic folate cycle deficiency.The following treatment was administered: spiramycin, 3.0 mln units orally daily for 14 days, to inhibit toxoplasma; recombinant human alpha2 interferon (3.0 mln units intramuscularly every other day for a month) and oxodihydroacridinylacetate sodium 2.0 mln units intramuscularly every other day for a month, with switching between this agent and interferon, to compensate for a deficiency of NK T-cells and СD8+ T-cells; and daily peribulbar injection of betamethasone 4 mg/mL for 3 days. The first signs of improved visual acuity were seen at day 8, and a complete restoration of vision in the left eye was achieved by the end of one month of combination therapy. In addition, the patient received three one-month courses of alpha2 interferon for compensation of cellular immunodeficiency over two years which prevented a recurrence of toxoplasmosis.
This article describes a case study of recurrent Toxoplasma chorioretinitis in a young patient with cell immunodeficiency. Patient K., 37 years old, was admitted to ophthalmologist with complaints of decreased visual acuity and discomfort in the left eye. The history of the disease evidenced that he had suffered at least 2 episodes of acute posterior uveitis in the past without finding out the etiological factor. Ophthalmological examination revealed an old scar on the retina of the right eye and signs of acute vitreous and chorioretinitis around the old scar on the retina of the left eye. By applying the method of paired sera, it was possible to establish the etiological factor of ophthalmic lesions — Toxoplasma gondii. Assessment of immune status demonstrated selective deficiency of CD8+ cytotoxic T lymphocytes and NKT cells. Obvious causes of secondary immunosuppression, including HIV, were ruled out. The Genetic Panel «Primary Immunodeficiencies» with sequencing of more than 400 genes of known primary human immunodeficiencies did not reveal pathology. However, persistent hyperhomocysteinemia was noted, and a genetic test for folate deficiency was performed. MTHFR A1298C in the heterozygous state and MTRR A66G in the homozygous state were detected, which was associated with the detected cell immunodeficiency, taking into account the results of studies on immune status in folic acid metabolism disorders and reports of severe opportunistic infections in humans with genetic deficiency of folate cycle. Treatment included spiramycin at a dose of 3 million IU orally three times a day for 14 consecutive days (to inhibit Toxoplasma), recombinant human a2b interferon at a dose of 3 million IU i/m every other day at night №15 (to compensate for the deficiency of NKT cells and CD8+ cytotoxic T lymphocytes), oxodihydroacridinylacetate sodium 2 mL i/m every other day at night №15, alternating with interferon (to compensate for the deficiency of NKT cells and CD8+ cytotoxic T lymphocytes) and local peribulbar injections of betamethasone № 3 (to eliminate the inflammation in the left eye). Improvement in visual acuity was observed on day 8 of treatment, and recovery of left eye function was observed at the end of the month of therapy. Due to the additional three‑month courses of recombinant human alpha2b‑interferon to compensate cell immunodeficiency, which were carried out during the next 2 years of follow‑up, it was possible to prevent further recurrence of toxoplasma invasion.
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