Retinitis is inflammation or degeneration of the retina, the thin layer of light-sensitive tissue lining the back of your eye. It can be triggered by infections, inherited genetic mutations, or immune system dysfunction, and without treatment it often leads to progressive vision loss. The term covers several distinct conditions, from infection-driven inflammation to retinitis pigmentosa, a group of inherited diseases affecting more than 1.5 million people worldwide.
How Retinitis Damages Vision
Your retina depends on a precise, layered structure to convert light into signals your brain can interpret. When inflammation disrupts that architecture, the consequences for vision can be severe. In infectious retinitis, invading organisms directly damage retinal cells and blood vessels. Immune cells rush to the site and can cause additional collateral harm, breaking down the tight barriers that normally keep fluid out of retinal tissue. This leads to swelling, leaking blood vessels, and eventually cell death.
In inherited forms like retinitis pigmentosa, the process is different. A genetic mutation causes photoreceptor cells (the rods and cones that detect light) to gradually die off. As damaged cells release their proteins into surrounding tissue, the immune system reacts to those proteins, creating a secondary wave of inflammation that accelerates the destruction. So even though RP starts as a genetic problem, chronic inflammation plays a role in making it worse over time.
Infectious Causes
Several types of microorganisms can infect the retina directly. The most clinically significant include:
- Cytomegalovirus (CMV): The most common opportunistic eye infection in people with advanced HIV. CMV retinitis typically strikes when a specific type of immune cell (CD4+ T-cells) drops below 50 cells per microliter of blood, a sign of severe immune suppression. It can also affect organ transplant recipients on immunosuppressive drugs. Because active CMV retinitis is often painless in its early stages, people at high risk need eye exams at least every three months.
- Herpes viruses: HSV-1, HSV-2, and the varicella-zoster virus (the same virus that causes chickenpox and shingles) can all cause acute retinal necrosis. Unlike CMV retinitis, this form can occur in people with healthy immune systems. It tends to come on suddenly with eye redness, pain, and rapid vision changes.
- Toxoplasma gondii: A widespread single-celled parasite found in undercooked meat and cat feces. Toxoplasma retinitis is one of the most common causes of infectious retinal inflammation globally. It can be acquired during pregnancy and passed to the fetus, or reactivate years after an initial infection.
- Candida: A fungal cause most often seen in people with compromised immune systems or those with long-term intravenous lines.
Retinitis Pigmentosa
Retinitis pigmentosa is the most common inherited retinal disease and the leading cause of visual disability and blindness in people under 60. It affects roughly 1 in 4,000 people. Despite the name, RP is not an infection. It’s a group of genetic disorders caused by mutations in more than 45 different genes, all of which lead to the same outcome: progressive death of photoreceptor cells.
The disease usually begins by killing rod cells, which handle low-light and peripheral vision. Cone cells, responsible for color and central vision, tend to be affected later. This sequence explains the characteristic pattern of symptoms: night blindness first, then a shrinking visual field, and eventually, in many cases, tunnel vision or further central vision loss.
Symptoms and Early Warning Signs
The symptoms of retinitis depend on whether the cause is infectious or inherited, but there is meaningful overlap.
In retinitis pigmentosa, the first sign is almost always night blindness. People notice they can’t see well in dim lighting, or they struggle to adjust when moving from a bright environment into a dark one. Driving at night becomes difficult because oncoming headlights create a blinding effect, and the eyes take much longer to readjust to darkness afterward. These symptoms typically begin around age 20. Peripheral vision narrows so gradually that many people don’t realize it’s happening until the loss becomes significant. Over time, the visual field contracts into tunnel vision.
Infectious retinitis can come on much faster. Acute retinal necrosis from herpes viruses causes eye redness, pain, and rapid vision loss. CMV retinitis, by contrast, is often silent in its early stages. People may notice floaters, flashing lights, or blurry patches, but sometimes there are no symptoms at all until substantial retinal damage has occurred.
How Retinitis Is Diagnosed
Diagnosis relies on a combination of a detailed eye exam, imaging, and functional tests. During a dilated fundus exam, a doctor looks at the retina directly and can often spot characteristic signs: dark pigment deposits in RP, or areas of white, necrotic retina in infectious cases.
Two imaging techniques are particularly useful. Optical coherence tomography (OCT) creates cross-sectional images of the retina’s layers, revealing thinning or loss of the photoreceptor layer. In RP, OCT shows where a critical structural band called the ellipsoid zone has broken down, marking the boundary between functional and degenerated retina. Fundus autofluorescence imaging uses specific wavelengths of light to highlight metabolic activity in retinal cells. In RP patients, this often reveals a glowing ring around the center of the retina. The inside of the ring marks where photoreceptors are still functioning, while the area outside shows degeneration.
Electroretinography, which measures the retina’s electrical response to light, is the gold standard for confirming RP. Reduced or absent electrical signals confirm that photoreceptor function has declined. For infectious retinitis, blood tests and sometimes fluid samples from inside the eye help identify the specific organism responsible.
Treatment for Infectious Retinitis
Treating infectious retinitis means eliminating the invading organism before it destroys more retinal tissue. The approach depends on which pathogen is involved.
CMV retinitis is treated with antiviral medications, typically given both systemically (by mouth or intravenously) and by injection directly into the eye. Treatment continues until the immune system recovers enough to keep the virus suppressed on its own. For people with HIV, that means staying on antiretroviral therapy until immune cell counts rise to safer levels.
Acute retinal necrosis from herpes viruses is treated aggressively with intravenous antivirals for the first one to two weeks, followed by weeks of oral antiviral medication. Injections into the eye may be added. Speed matters here: delays in treatment increase the risk of retinal detachment, a serious complication where the retina peels away from the tissue beneath it.
Toxoplasma retinitis is managed with a combination of antiparasitic and antibiotic medications, often alongside anti-inflammatory drugs to limit immune-mediated damage.
Treatment for Retinitis Pigmentosa
For most forms of RP, there is no cure, and treatment focuses on slowing progression and managing vision loss. Vitamin A supplementation has shown modest benefit in some studies, and specialized low-vision aids, orientation training, and adaptive technology help people maintain independence.
The major breakthrough has been gene therapy. In 2017, the FDA approved the first gene therapy for any genetic disease: a treatment called Luxturna, designed for people whose RP is caused by mutations in a specific gene called RPE65. The therapy delivers a working copy of the gene directly under the retina via injection. In clinical trials, treated patients showed a significant increase in light sensitivity (more than a 100-fold improvement) and meaningful gains in their ability to navigate obstacles in low light. Visual field measurements also improved substantially. These benefits appeared within about 30 days and have held up for at least four years of follow-up so far.
Luxturna works for a specific genetic subtype, so it doesn’t help everyone with RP. But it has opened the door for similar gene therapies targeting other mutations, and dozens of clinical programs are now underway for different forms of inherited retinal disease.
Complications to Watch For
Both infectious and inherited forms of retinitis can lead to serious complications if not monitored. Retinal detachment is one of the most dangerous. In acute retinal necrosis, the inflamed, weakened retina is especially prone to tearing away from its underlying support tissue, which can cause sudden, permanent vision loss without emergency treatment.
Swelling in the central retina (macular edema) is another common complication across several types of retinitis. Because the macula handles your sharpest, most detailed vision, even small amounts of swelling there can cause noticeable blurriness. In RP, cataracts develop earlier and more frequently than in the general population, adding another layer of visual impairment that may need separate treatment.