Cytomegalovirus (CMV) retinitis is a serious viral infection causing inflammation within the retina, the light-sensing layer at the back of the eye. This condition is a progressive disease that can lead to permanent damage of the retinal cells, making it a significant cause of vision loss if not addressed promptly. It primarily manifests in individuals whose body defenses are substantially weakened.
How Cytomegalovirus Causes Retinitis
Cytomegalovirus is a common virus that belongs to the herpesvirus family. The majority of adults have been exposed to CMV, but in people with healthy immune systems, the virus remains inactive or “latent” and causes no symptoms. T-cells keep this dormant virus in check, preventing it from replicating uncontrollably.
The retinitis develops when the immune system becomes severely compromised, allowing the latent virus to reactivate and spread to the eye. Individuals with advanced Human Immunodeficiency Virus (HIV) or Acquired Immunodeficiency Syndrome (AIDS) are at high risk, particularly when their CD4+ T-cell counts drop below 50 cells per microliter of blood. Other populations susceptible to CMV retinitis include recipients of organ or bone marrow transplants who must take immunosuppressive medications.
The virus infects the cells of the retina, causing tissue destruction called necrosis. This damage typically begins in the peripheral retina before advancing toward the center of the eye. As the infection progresses, it can create a distinctive appearance, sometimes described as resembling “pizza pie” due to the combination of retinal whitening and hemorrhage.
Recognizing the Signs of Active Infection
Patients frequently notice an increase in floaters, which are small specks or cloud-like shapes that drift across the field of vision. These floaters are caused by inflammatory cells and debris released into the vitreous gel inside the eye.
As the infection expands across the retina, it can lead to blurred or distorted vision. A person may also begin to experience blind spots, known as scotomas, where segments of their vision are missing or dark. Because the disease often starts in the outer edges of the retina, loss of peripheral vision is a common early sign.
The condition is not usually associated with eye pain. Since the retina lacks pain receptors, tissue damage can occur silently. If left unchecked, the progressive destruction of the retina will eventually reach the macula, the central part responsible for sharp, detailed vision, leading to visual impairment.
Confirming the Diagnosis and Treatment Options
Diagnosis requires a comprehensive eye examination performed by an ophthalmologist. After dilating the pupils, the doctor uses an ophthalmoscope to visualize the retina directly. The presence of the characteristic retinal whitening and hemorrhage pattern is usually enough to confirm the diagnosis in a high-risk patient.
In some cases, the physician may take a small fluid sample from the eye, known as a vitreous tap, to perform a polymerase chain reaction (PCR) test to confirm the presence of CMV DNA. Blood tests, particularly checking the CD4+ T-cell count and the systemic CMV viral load, help to guide the overall management of the patient’s underlying immune status.
Treatment involves antiviral medications aimed at stopping the virus from replicating. Standard first-line drugs include oral valganciclovir, and ganciclovir and foscarnet, which can be administered intravenously or through direct injection into the eye. Intravitreal injections deliver a concentrated dose of the drug directly to the infected area, minimizing systemic side effects.
Valganciclovir is often used for maintenance therapy after the initial infection is controlled, while the more potent intravenous or injected forms are reserved for the acute phase or for cases that are sight-threatening. A time-release ganciclovir implant may be surgically placed in the eye to provide a steady local drug dose over several months.
Long-Term Outlook and Preventing Recurrence
The prognosis for CMV retinitis depends on how quickly the condition is diagnosed and whether the patient’s underlying immune function can be restored. Any vision lost due to retinal necrosis is permanent, as the damaged retinal tissue cannot regenerate. Retinal detachment is a complication that occurs when the damaged, thinned retina tears and peels away from the back of the eye.
The primary goal of long-term management is to prevent the virus from reactivating and causing further damage. For patients with HIV, this means strict adherence to Highly Active Antiretroviral Therapy (HAART) to elevate the CD4+ T-cell count above 100 cells/µL. Immune recovery is a reliable indicator that the body can control the virus without the need for lifelong antiviral medication.
Patients who have achieved immune recovery can often discontinue maintenance antiviral therapy, but they require ongoing monitoring for potential relapse. For individuals who cannot achieve sufficient immune recovery, continuous suppressive antiviral medication is necessary to prevent recurrent outbreaks of retinitis. Regular, dilated eye examinations remain a necessary part of care for all high-risk patients.