Infectious Etiologies
Bacterial infection
See the discussion of endophthalmitis in Chapter 10 in this volume and in BCSC Section 9, Uveitis and Ocular Inflammation.
Viral infection
Multiple viruses may cause retinal infections, including rubella virus, measles virus, human immunodeficiency virus (HIV), herpes simplex virus (HSV), varicella-zoster virus (VZV), and cytomegalovirus (CMV). Two of the most frequent clinical presentations of retinal viral infection, acute retinal necrosis (ARN) and CMV retinitis, are discussed here.
Acute retinal necrosis is a rapidly progressive, necrotizing retinitis caused by infection with HSV types 1 and 2, VZV, or in rare instances, CMV. ARN can occur in healthy or immunocompromised individuals. Histologic findings include robust inflammation in the vitreous and anterior chamber with prominent obliterative retinal vasculitis and retinal necrosis (Fig 11-7). Inflammatory cells include neutrophils, lymphocytes, plasma cells, and epithelioid histiocytes. Electron microscopy has shown viral inclusions in retinal cells. Polymerase chain reaction analysis of aqueous or vitreous samples is the most sensitive and most rapid method for identifying the presence of virus, reducing the need for viral culture, intraocular antibody analysis, immunohistochemistry, or other diagnostic techniques.
CMV retinitis is an opportunistic infection that occurs in immunosuppressed patients (Fig 11-8). Histologically, it is characterized by retinal necrosis that heals with a thin fibroglial scar. Acute lesions show enlarged neurons (20–30 µm) that contain large eosinophilic intranuclear and/or intracytoplasmic inclusion bodies (see Fig 11-8C, D). At the cellular level, CMV may infect vascular endothelial cells, retinal neurons, the RPE, and histiocytes. Because of the immunocompromised status of the infected host, a prominent inflammatory infiltrate is typically not present.
Fungal infection
Fungal infections of the retina are uncommon, occurring most often in immunosuppressed patients and in patients with fungemia (eg, from parenteral nutrition or intravenous drug use). These infections usually begin as single or multiple small foci in the choroid or retina (Fig 11-9). The most common causative fungi are Candida species, particularly C albicans. Less common agents include Aspergillus species and Cryptococcus neoformans.
Histologically, fungal infections are characterized by necrotizing granulomatous inflammation. A central zone of necrosis is typically surrounded by the granulomatous inflammation with an outer layer of lymphocytes. Although histologic examination may reveal the causative agent, a culture and/or molecular studies are required for definitive identification of the organism. With treatment, these lesions heal with a fibroglial scar.
Protozoal infection
Toxoplasmic retinochoroiditis (also called toxoplasmic chorioretinitis, ocular toxoplasmosis) is the most common infectious retinitis. It may be due to reactivation of a congenitally acquired infection or to an acquired Toxoplasma infection in healthy or immunocompromised individuals. In patients with reactivated disease, toxoplasmic retinochoroiditis typically presents as a posterior uveitis or panuveitis with marked vitritis and focal retinochoroiditis adjacent to a pigmented chorioretinal scar. The absence of a preexisting chorioretinal scar suggests newly acquired disease.
Microscopic examination of active toxoplasmic retinochoroiditis reveals necrosis of the retina, a prominent infiltrate of neutrophils and lymphocytes, and Toxoplasma organisms in the form of tissue cysts and tachyzoites (Fig 11-10). There is generally a prominent lymphocytic infiltrate in the vitreous and the anterior segment and granulomatous inflammation in the inner choroid. Healing brings resolution of the inflammatory cell infiltrate with encystment of the organisms in the retina adjacent to the atrophic chorioretinal scar. See also BCSC Section 9, Uveitis and Ocular Inflammation, and Section 12, Retina and Vitreous.
Excerpted from BCSC 2020-2021 series: Section 4 - Ophthalmic Pathology and Intraocular Tumors. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.