Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Ординатура / Офтальмология / Английские материалы / Uveitis Fundamentals and Clinical Practice 4th edition_Nussenblatt, Whitcup_2010.pdf
Скачиваний:
1
Добавлен:
28.03.2026
Размер:
53.26 Mб
Скачать

Part 4 Infectious Uveitic Conditions

Chapter 14 Ocular Toxoplasmosis

right eye, with a white retinal lesion, 1.5 disc diameters, encompassing the vessels of the superior temporal arcade and extending into the posterior pole. The more peripheral portion of the lesion seemed old – that is, less white and raised, with some pigment surrounding the edges – whereas the more active area seemed pointed toward the macula. The left eye also had an old inactive scar in the periphery of the superior portion of the retina. The clinical

impression was that of ocular toxoplasmosis. The toxoplasmosis titer was positive at 1 : 128. The decision was made not to

treat the patient.

The patient returned 1 week later with the same visual acuity. However, the lesion had progressed toward the macula. A decision was then made to initiate anti-Toxoplasma therapy: clindamycin 300 mg by mouth four times daily and sulfadiazine 0.5 g by mouth four times daily. No steroid was given. The patient was followed up weekly, and after 3 weeks of therapy the disease involuted. Therapy was stopped after 4 weeks. By late April 1981 the patient’s visual acuity was 20/15 OU, and the lesion in the right eye was quiet. He had no problems until August 1985, when he noted an increase in floaters in the right eye. An examination at that time showed that there was a small area of active retinitis on the peripheral portion of the old lesion, on the side not facing the macula. It was elected not treat the patient, and the lesion regressed. He has been free of recurrence to date.

Comment 14-1.  We elected to treat the patient despite good vision only after following the clinical course and noting its progression toward the macula. It did not seem reasonable to wait any longer. He has continued to have recurrences, even after clindamycin therapy, and needs to be seen regularly. In passing, it can be argued that a patient presenting today with his or her first attack of ocular toxoplasmosis deserves to be screened for HIV.

Case 14-2

This 43-year-old white man has congenital toxoplasmosis. He has never had good vision in the left eye because of a large atrophic scar in the macula. The right eye has multiple lesions, all compatible with the diagnosis of ocular toxoplasmosis. In the right eye there is a lesion that encroaches on the temporal side of the fovea, but his visual acuity was 20/25 in that eye when he was first seen at the National Eye Institute. Two years later he complained of a ‘haziness’ to his vision in the right eye. Examination of the parafoveal lesion could not detect an area of activity. Despite this, therapy with clindamycin, sulfadiazine, pyrimethamine (Daraprim), folinic acid, and prednisone was begun.

The haziness disappeared over the course of the 3-week therapy period. During the ensuing years his vision in the right eye has varied from 20/25 to 20/32. He has had one episode every 12 to 18 months when he feels there is a change in the quality of his vision. Examination of serial retinal photographs shows greater pigment around the atrophic scars but rarely evidence of activity.

Comment 14-2.  The lack of observable activity on the edge of the old lesion abutting the fovea has not dissuaded us from

treating the patient each time he complains of a change in his vision. A small nidus of infection, enough to alter his vision but not enough for the observer to note, could very well be there. This patient always maintains a supply of his medication and begins the antimicrobial therapy (sulfadiazineand clindamycin) immediately when symptoms appear. He is seen within 24 hours and then pyrimethamine (after a baseline platelet count), folinic acid, and steroid are begun.

Case 14-3

This 36-year-old white man with AIDS-related complex had chronic granulomatous skin disease, chronic hepatitis, thrombocytopenia, and evidence of exposure to both the HIV and human T-cell leukemia/lymphoma-1 virus. We first saw him in November 1984, when he had had uveitis in the right eye for several months. He had active toxoplasmic retinitis in the right eye and an old pigmented lesion in the left eye, also compatible with ocular toxoplasmosis. The left eye also had a dense cataract. He was treated with clindamycin and sulfadiazine, with resolution of his inflammation after a 6-week course of sulfadiazine. The clindamycin was stopped after 3 weeks because of severe gastrointestinal problems, and pyrimethamine with folinic acid was begun for the next 3 weeks. A CT scan of the head showed no evidence of cerebral toxoplasmosis. Under this therapeutic regimen the patient underwent cataract surgery, with a good visual result.

The patient continued to have recurrences of his ocular toxoplasmosis as soon as the specific antimicrobial therapy was discontinued. It was therefore decided to maintain long-term sulfadiazine therapy, but this needed to be stopped because of hives. Pyrimethamine was then used. In August 1985 the cataract in the patient’s right eye significantly reduced his vision and made it difficult to maintain close follow-up of his retinitis. There were now cottonwool spots in both eyes and cells in the left, but the lesion in the right eye seemed to be stable. He therefore underwent lensectomy and vitrectomy in the right eye. HIV was cultured out of the vitreous specimen, his Witmer quotient was markedly elevated, supporting the preoperative diagnosis, and after surgery his right eye revealed 4+ cells

and 3+ haze. These responded only to the addition of sulfadiazine.

Comment 14-3.  This man’s ocular course emphasizes the rapidity of changes and the difficulty of treating them in the immunosuppressed host. The presence of HIV in the vitreous, in addition to his history of chronic hepatitis, emphasizes the great care needed in handling these samples. Further, without an intact cell-mediated immune arm, the disease simply recurred once therapy was discontinued. The only therapeutic option was to ‘juggle’ the available therapeutic agents. He ultimately succumbed to his underlying disease. HAART will certainly change this disease dynamic.

Case 14-4

A 67-year-old white man from Latin America underwent triple coronary artery bypass surgery in his home country. This surgery

204

Соседние файлы в папке Английские материалы