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Ординатура / Офтальмология / Английские материалы / Uveitis Fundamentals and Clinical Practice 4th edition_Nussenblatt, Whitcup_2010.pdf
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Part 4 Infectious Uveitic Conditions

Chapter 14 Ocular Toxoplasmosis

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Figure 14-11. Subretinal neovascularization 8 months after acute attack of ocular toxoplasmosis. A, Nasal portion of lesion that stains corresponds to area of old scarred lesion. B, In the late-stage angiogram nasal hyperfluorescence has not increased in size; however, temporal subretinal neovascular lesion can be seen. (Courtesy of Prof. G. Coscas. Reproduced with permission from Journal Francais d’Ophtalmologie 7: 211–218, 1984 © Masson.)

Figure 14-12. Fundus photograph of eye with congenital toxoplasmosis, with retinochoroidal shunt. (Courtesy of J. Melamed, MD, Porto Alegre, Brazil.)

A curious association between Fuchs’ heterochromia and ocular toxoplasmosis was initially made by Toledo de Abreu and coworkers.58 They studied 13 patients with Fuchs’ syndrome who had focal necrotizing chorioretinal toxoplasmic lesions; none of these patients had ciliary injection or posterior synechiae but most had keratitic precipitates, anterior chamber reactions, and cataracts. Six of the 13 had iris transillumination. La Hey and colleagues59 evaluated this possible association in a series of 88 patients with Fuchs’ heterochromia, comparing them with control subjects and other patients with uveitis. Although nine of these patients (10.2%) with Fuchs’ heterochromia had scars compatible with toxoplasmosis, the authors were unable to establish a special relationship between the two entities. Others have confirmed these observations60. Schwab,61 in an interesting review, also looked for a relationship between toxoplasmosis and Fuchs’ heterochromic iridocyclitis. In his review he found that 13 of 25 patients with Fuchs’ heterochromic iridocyclitis had scars typical of toxoplasmosis and serologic evidence of the organism. This result was compared with results for 590 patients seen in the retina clinic at West Virginia University, with only 24 of these patients (4%) having retinal lesions typical of toxoplasmosis. Schwab concluded that a causal relationship between the two entities appears to exist, at least for a subgroup of patients with Fuchs’ heterochromia.

Effects in immunocompromised host

Special mention seems appropriate for ocular toxoplasmosis in the immunocompromised host, particularly the patient with AIDS not being treated with HAART (see Chapter 11). In these patients the development of ocular toxoplasmosis does not meet the criteria for an opportunistic infection but can indicate to the clinician that a change in the patient’s immune state has occurred. Indeed, we have seen active ocular toxoplasmosis in a patient with the AIDS-related complex in whom the full-blown picture of AIDS soon developed. In the patient with AIDS the degree of inflammatory disease associated with a toxoplasmic retinitis is usually far greater than that seen with cytomegalovirus (CMV) retinitis, perhaps indicating that reactivation (or acquisition) of the disease occurs earlier in the course of AIDS than in CMV retinitis, when the immune system is still capable of mustering a significant inflammatory response. In the United States, toxoplasmic retinitis is still a relatively uncommon disorder in patients with AIDS. Often in toxoplasmic retinitis numerous lesions will appear to be active at the same time, a most unusual finding in the immunocompetent patient.

The diagnosis of ocular toxoplasmosis in a patient with AIDS should initiate an evaluation of possible CNS disease as well. CNS toxoplasmosis has become a problem frequently seen in this patient population. The reason for the CNS and the eye incidence disparity is not known. The therapeutic management of these ocular lesions can be difficult. Despite therapy, disease can progress. Moorthy and colleagues62 reported two patients in whom a severe necrotizing retinitis was seen, with one developing a panophthalmitis and orbital cellulitis despite sulfadiazine, pyrimethamine, and folinic acid therapy. Whether the ocular manifestations of this disease represent reactivation or acquired disease is not known. One could conjecture that

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