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Ocular Neovascularization in Endogenous Candida Endophthalmitis: Using Multimodal Imaging to Understand Different Pathogenic Pathways.

Ocular neovascularization is a known complication of uveitis.1 Intraocular inflammation itself can stimulate new vessels (NVs) growth, but NVs’ location may vary according to different pathogenic pathways. Hypoperfusion of the retina is the commonest cause of retinal neovascularization,1 whereas damage to the retinal pigment epithelium–Bruch membrane complex often precedes choroidal neovascularization in uveitis.2 Endogenous candida endophthalmitis has been associated with both retinal neovascularization Fig. 1. Multimodal imaging of a patient affected by endogenous candida endophthalmitis complicated by retinal neovascularization. At baseline, fungal colonies were detectable within the vitreous, with no signs of choroidal infiltration (A). Five days later, fine NVs started growing radially from the disk (B). In the following 4 days, the new vessels kept growing along the posterior hyaloid, heading straight toward the fungal colonies (C), and ending up surrounding them (D). Fluorescein angiography (E) and optical coherence tomography angiography (F) performed on day 9, just before pars plana vitrectomy, allowed the neovascular complex to be clearly visualized, and distinguished from the underlying retinal vasculature (retinal arteries [red arrowhead] or veins [blue arrowhead]). The line-art series (H–K) underlines the NVs growth. Retinal structures are reported in B/W and NVs are highlighted in red. The circumpapillary area where the retinal neovascularization started is marked by a black circle. Small black arrows highlight NVs spreading direction, which we postulate follows the inflammatory mediators’ gradient.