Recurrence of ocular toxoplasmosis

The classic description of recurrent active Toxoplasma chorioretinitis is a focus of retinitis appearing at the border of a retinochoroidal scar;

however, there are several reports illustrating the variance in the clinical features of this disease. Active chorioretinitis does resolve without treatment, leaving a hyperpigmented scar, and recurrences develop as 'satellite' lesions. A recurrence is usually symptomatic, with the redness, pain, and light sensitivity and decreased vision that occur with any generalized panuveitis. Recurrence of chorioretinitis can lead to vision loss (Friedmann and Knox, 1969) and blindness.

There is limited understanding regarding the many factors that exist between infection and recurrence of disease. There is a strong pattern of recurrence during the teenage and adult years. Women with ocular toxoplasmosis are at a higher risk of recurrence during pregnancy (O'Connor, 1983b), though the fetus (except for rare reports -Silveira et al., 2003) appears to be at risk only during a mother's initial infection.

Initially it was unclear what recurrence actually was, and it certainly remains unclear why recurrence occurs. Prior to the AIDS epidemic there was controversy as to whether recurrence represents an autoimmune process alone without the presence of active parasites. Histopathology on patients with ocular toxoplasmosis and HIV infection has demonstrated parasites in areas of involved retina. In addition, eyes that have received corticosteroid treatment alone have had very poor outcomes associated with parasites demonstrated on tissue biopsy (Sabates et al., 1981). Frenkel's theory (Frenkel, 1974) that recurrence represents a hyper-sensitivity reaction appears unlikely to be the central cause of recurrent ocular toxoplasmosis. Release of T. gondii antigen into the retina is not associated with a hypersensitivity reaction. Reactivation is thought to represent a shift of T. gondii from the dormant phase known as brady-zoites to the more active phase of tachyzoites. There is no clear understanding of how this shift from bradyzoite to tachyzoite occurs within the eye, or what factors influence or cause the shift.

Evidence of prior recurrence is the presence of inactive satellite lesions, which are local areas of chorioretinal scars. Recurrent lesions usually occur in close proximity to prior areas of choriore-tinitis, as is evident in the usual clusters of scars that exist (Figure 5.1). Recurrent disease occurs

FIGURE 5.1 Toxoplasma gondii chorioretinitis.

(A) Left macula with old scar superior temporal to new active lesion.

(B) Late fluorescein angiogram of (A) demonstrating incompetence of the blood-brain barrier of both the active and the old lesion.

(C) Hypofluorescent lesion where active lesion is on (A) and vascular remodeling of superior temporal old lesion.

(D) Active lesion in (A) within 2 mm of the fovea (red-free photograph).

(E) Old chorioretinal lesion inferior to optic nerve with overlying vitreal condensation.

FIGURE 5.1 Toxoplasma gondii chorioretinitis.

(A) Left macula with old scar superior temporal to new active lesion.

(B) Late fluorescein angiogram of (A) demonstrating incompetence of the blood-brain barrier of both the active and the old lesion.

(C) Hypofluorescent lesion where active lesion is on (A) and vascular remodeling of superior temporal old lesion.

(D) Active lesion in (A) within 2 mm of the fovea (red-free photograph).

(E) Old chorioretinal lesion inferior to optic nerve with overlying vitreal condensation.

FIGURE 5.1, Cont'd Toxoplasma gondii chorioretinitis.

(F) Nasal to optic nerve - there is an active lesion adjacent to old chorioretinal scar. This figure is reproduced in color in the color plate section.

FIGURE 5.1, Cont'd Toxoplasma gondii chorioretinitis.

(F) Nasal to optic nerve - there is an active lesion adjacent to old chorioretinal scar. This figure is reproduced in color in the color plate section.

when new areas of retina are involved in an infectious inflammatory process that results in permanent destruction of involved tissue. Resolution of the inflammatory process will usually occur spontaneously after several weeks. Although the general eye inflammation will resolve, the area of retina with focal chorioretinitis is irreversibly impaired. If the lesion or recurrence is in the peripheral retina, the impact of the recurrence on the infected individual's vision can be minimal or even asymptomatic, because the impaired vision exists in a small area of the peripheral field. Usually the new lesion is a focal chorioretinitis; however, a more generalized vitritis and anterior uveitis usually develops secondarily as a generalized intraocular inflammatory process. This more generalized intraocular inflammatory process is responsible for the complaint of decreased vision in patients with ocular toxoplasmosis. The secondary inflammatory process can lead to retinal detachment or other ocular morbidity, such as epiretinal membranes.

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