Use of a slow-release intravitreal clindamycin implant for the management of ocular toxoplasmosis

Abstract

Purpose: To report the first patient with ocular toxoplasmosis treated with a slow-release biodegradable intravitreal clindamycin implant.

Observations: A 39-year-old human immunodeficiency virus (HIV)-positive woman with recurrent toxoplasmic retinochoroiditis and vitritis for whom oral medication was medically contraindicated was treated with an intravitreal slow-release clindamycin implant and three monthly intravitreal injections of clindamycin and dexamethasone. Serial ophthalmologic examinations demonstrated gradual, complete resolution of posterior uveitis and healing of the retinochoroidal lesion with cicatricial changes, as well as gradual improvement of cells in the anterior chamber. There was no significant change in electroretinography waves after treatment with the implant. The presence of the implant, or part of it, was detectable in the vitreous cavity for 4 months. To date, the patient has been monitored for 30 months, and there has been no reactivation of ocular toxoplasmosis.

Conclusion: The slow-release clindamycin implant was safe for intravitreal use in this patient and may have contributed to the long-term control of toxoplasmosis chorioretinitis.

Keywords: Clindamycin; Implant; Intravitreal; Toxoplasmosis; Uveitis.

Fig. 1

Multimodal evaluation of the left eye before treatment with intravitreal implant. A– Vitritis; exudative lesion with ill-defined margins in the macula. B- OCT shows thickened homogeneous hyperreflectivity within the retinal layers consistent with full-thickness retinal involvement of the active lesion. Multimodal evaluation after treatment with a clindamycin implant C- Healed lesion in the macula. D- OCT shows reduction of retinal edema and of cells, atrophy and disorganization of the retinal layers, and loss of the foveal contour.

Fig. 2

Multifocal electroretinogram in left eye. A- Before treatment with intravitreal implant, there is a decreased foveal response, secondary to macular inflammatory changes. B- After treatment, there is still a reduced foveal wave amplitude response, but with higher amplitudes compared to baseline in the perifoveal area.