Cytomegalovirus (CMV) retinitis is a serious vision-threatening eye condition that is seen in patients who are immunosuppressed.^1,2 Classically it was an AIDS-related opportunistic infection that occurred in high frequency prior to the advent of antiretroviral therapy, more commonly when CD4 counts are less than 50. Its incidence has been decreasing in the developed world, although it still remains prevalent in the developing world. It is also seen in severe immunosuppression from chemotherapy or in the context of immune modulating therapy for autoimmune conditions. It is caused by cytomegalovirus, a double stranded DNA virus in the herpesviridae family, which reaches the retina hematogenously. Immunosuppression permits uncontrolled CMV replication. It may mimic ARN as it presents as with vitritis (inflammation of the vitreous), retinial vasculitis (inflammation of the retinal vessels which clinically appears as sheathing) and peripheral retinitis (inflammation of the retina which clinically appears as retinal whitening). However, it differs, principally from ARN, in that it exclusively affects the immunocompromised (ARN primarily affects the immunocompetent), has less vitritis, mainly periphebitis (mostly affects retinal venules where ARN affects arterioles), more posterior retinitis, and hemorrhages are very prominent (pizza pie appearance). Compared to ARN and PORN, CMV typically progresses more slowly. Viral PCR is often performed to confirm the diagnosis. Previously, CMV retinitis was treated with intravenous induction therapy with ganciclovir followed by maintenance therapy. Due to the cost, risk of sepsis, and the quality of life associated with an indwelling catheter, the oral formulation of valgancyclovir was developed. A randomly controlled trial was performed in 2002 which demonstrated oral valganciclovir was non-inferior to intravenous ganciclovir for induction treatment.³

Progressive outer retinal necrosis (PORN) is a rapidly progressive herpetic retinopathy with features that make it its own distinct entity from ARN.⁴ As with ARN, PORN represents a reactivation of a latent herpes (VZV) infection. PORN differs principally from ARN in that it is a disease of the immunocompromised, particularly HIV infected patients. This difference leads to the distinct clinical presentation of a minimal inflammatory retinitis (with minimal or no vitritis) in PORN, compared to the exuberant response in ARN as the immunosuppressed individuals with PORN are unable to mount a significant immune response.Thus, patients with PORN are typically asymptomatic. Additionally, PORN typically presents as retinitis in the posterior pole of the retina, whereas ARN affects the anterior peripheral retina. PORN is treated similarly to ARN with antiviral therapy until the immune system is reconstituted.

Toxoplasma choroiditis is the most common cause of posterior uveitis (inflammation affecting the “back” of the uvea, called the choroid) worldwide.⁵ The causative agent is toxoplasma gondii, a parasitic protozoon that exists in an oocyte form (filled with sporozoites) or cyst form (filled with bradyzoites). Sporozoites and bradyzoites can then transform into actively dividing tachyzoites which may proliferate in nucleated cells, thus protecting them from the host immune system. These organisms may lay dormant for years before stress prompts recurrent activity; this typically presents in the retina as an area of retinitis adjacent to an old scar. Most cases are acquired congenitally due to a pregnant woman being exposed to contaminated uncooked meat, or cat feces. Toxoplasma chorioretinitis may mimic ARN in that the host is immunocompromised, there is significant vitritis, and an area of retinitis. Toxoplasma chorioretinitis differs, however, as the retinitis typically presents adjacent to an old chorioretinal scar. Serum serology or aqueous PCR can be performed to support the diagnosis. The classic antibiotic triple therapy involves oral pyrimethamine, sulfadiazine, and folinic acid, however other antibiotics can be used with success.