Necrotic retinal pigment epithelium in toxoplasmic retinochoroiditis

Abstract

Editor, We read with interest Belfort and colleagues’ clinicopathological report on a case of toxoplasmic retinochoroiditis, published in Acta Ophthalmologica (Belfort et al. 2008). The authors describe the histopathological findings of an enucleated globe of a 66-year-old immunosuppressed man with severe bilateral posterior uveitis that had progressed despite antiviral therapy for presumed cytomegalovirus retinitis. This article illustrated well the role of histopathological examination and immunohistochemistry in establishing definitively the aetiology in these challenging cases. However some of the authors’ histopathological observations deserve further comments. The authors stated that, in addition to the necrotizing retinitis and the granulomatous inflammation of the choroid, ‘necrosis of Bruch’s membrane’ might be a distinctive feature of toxoplasmic retinochoroiditis. However, histopathologically such a term is a misnomer. Necrosis is the morphological expression of cell death and is characterized by protein denaturation, loss of energy producing mechanisms, enzymatic cellular digestion and often a secondary inflammatory response (Spencer 1996). Being essentially an acellular structure, made up of the basement membranes of the retinal pigment epithelium (RPE) and of the choriocapillaris in each side, and of a core elastic layer surrounded by two collagenous zones (Garron 1963), Bruch’s membrane may undergo secondary pathological changes but not necrosis, and this term should be avoided. The secondary changes in Bruch’s membrane reflect the involvement of RPE and/or of choriocapillaris endothelium. RPE necrosis is shown nicely in their Fig. 1E (Belfort et al. 2008), and has been recognized not only in cases of toxoplasmic retinochoroiditis (Rao & Font 1977) but also in other necrotizing retinites secondary to mycobacteria, fungi, viruses and even in primary retinal lymphoma (Spencer 1996; Rao et al. 2006). Finally, according to the authors, the involvement and eventual disruption of Bruch’s membrane might justify the occurrence of secondary granulomatous inflammation of the choroid in toxoplasmic retinochoroiditis. Nevertheless this is unlikely, because in many of the entities listed earlier, secondary inflammation of the choroid occurs despite an uninterrupted Bruch’s membrane (Spencer 1996). We congratulate Belfort and colleagues on their interesting article, emphasizing the role of histopathology on the aetiological diagnosis of these complex cases.