Corneal ulcers are open sores on the cornea, the clear front surface of the eye. They’re most often caused by infections, particularly bacterial, but trauma, chronic dry eyes, autoimmune diseases, and even nutritional deficiencies can also break down this tissue. Understanding the specific cause matters because treatment differs significantly depending on what’s driving the damage.
Bacterial Infections Are the Leading Cause
Bacteria account for the majority of infectious corneal ulcers. A global meta-analysis found that Staphylococcus species are responsible for about 41% of bacterial cases, making them the single most common culprit. Pseudomonas species come in second at roughly 17%, followed by Streptococcus at 13%. Over the past few decades, the pattern has shifted: Staphylococcus infections have risen from about 26% of cases in the 1990s to nearly 40% in the 2000s, while Pseudomonas has declined.
Bacteria typically can’t penetrate an intact cornea on their own. They need a way in, usually through a tiny scratch, a contact lens that traps organisms against the eye, or an already compromised surface. Once bacteria gain access, they multiply rapidly in the corneal tissue, triggering inflammation and creating the characteristic ulcer crater.
Herpes Simplex Virus and Viral Ulcers
The herpes simplex virus (HSV-1), the same virus behind cold sores, is the most significant viral cause of corneal ulcers. After an initial infection, the virus retreats into nerve cells near the eye and can reactivate repeatedly throughout life. Triggers for reactivation include fever, physical trauma to the eye, UV exposure, hormonal changes, stress, and anything that suppresses the immune system.
When the virus reactivates, it travels along nerve fibers back to the cornea. It first appears as tiny dot-like spots on the surface, which then merge into branching, tree-shaped lesions called dendritic ulcers. The virus replicates most actively at the edges and tips of these branches. Within the first day of active infection, corneal cells begin to swell and break down, destroying the outer layers of the cornea. If left untreated, dendritic ulcers can spread into larger “geographic” ulcers with significant areas of dead tissue, increasing the risk of scarring and vision loss.
Contact Lenses Are a Major Risk Factor
Contact lenses are the single biggest modifiable risk factor for corneal ulcers in developed countries, and the danger increases dramatically with overnight wear. Sleeping in contact lenses carries an 8-fold increased risk of ulcerative keratitis compared to removing them at night. Researchers have estimated that 49% to 74% of all contact lens-related corneal ulcers could be prevented simply by not sleeping in lenses.
The reasons are straightforward. Contact lenses reduce oxygen flow to the cornea, create a warm moist environment where bacteria thrive, and can cause microscopic abrasions that give organisms a foothold. Overnight wear compounds every one of these problems because the closed eyelid further limits oxygen and traps debris.
Water exposure while wearing contacts introduces additional risks. Swimming, showering, or even washing your face with lenses in can expose the cornea to Acanthamoeba, a microscopic parasite found in tap water, pools, and hot tubs. Using tap water to rinse or store contact lenses is widely recognized as the primary risk factor for Acanthamoeba keratitis. Research has found that tap water in some metropolitan areas contains highly virulent strains of this organism. Acanthamoeba infections are notoriously difficult to treat and can cause severe, prolonged pain. Making matters worse, standard contact lens disinfecting solutions, including multipurpose solutions and one-step hydrogen peroxide systems, are often ineffective at killing the parasite’s dormant cyst form.
Fungal Infections
Fungal corneal ulcers are less common than bacterial ones but tend to be more difficult to treat and slower to heal. They most often occur after the eye is injured by plant material, soil, or organic matter, making them more prevalent in agricultural workers and people in tropical climates. A tree branch scratch, a thorn poke, or dirt blown into the eye can introduce fungal spores directly into the cornea. Fungal ulcers can also develop in people using steroid eye drops for extended periods, since steroids suppress the local immune response that would normally keep fungal growth in check.
Injuries, Burns, and Dry Eyes
Not all corneal ulcers start with an infection. Physical and chemical damage to the cornea can cause ulcers on their own or create the conditions for infection to follow.
- Eye injuries. Scratches (corneal abrasions), cuts, puncture wounds, and burns can all lead to ulcers when they don’t heal properly. Even a small abrasion from a fingernail, makeup brush, or piece of debris can become an ulcer if bacteria colonize the damaged area.
- Chemical burns. Exposure to acids, alkalis, or other caustic substances can destroy corneal tissue directly, creating immediate ulceration.
- Severe dry eyes. When the eye doesn’t produce enough tears or the tear film evaporates too quickly, the cornea loses its protective moisture layer. Over time, chronic dryness breaks down the surface cells, leaving the cornea vulnerable to erosion and ulceration.
- Inability to close the eyelids. A condition called lagophthalmos, where the eyelids can’t fully close during sleep or blinking, leaves the cornea exposed and unprotected for long stretches. This dries out the surface and can lead to ulcer formation.
- Toxic exposure. Certain chemicals or, in rare cases, medications can have toxic effects on the corneal surface that progress to ulceration.
Autoimmune Diseases and the Cornea
Autoimmune conditions, particularly rheumatoid arthritis, can cause a specific type of corneal ulcer called peripheral ulcerative keratitis (PUK). Nearly half of all non-infectious PUK cases are linked to a connective tissue disorder, with rheumatoid arthritis being the most common. In late-stage rheumatoid arthritis, PUK affects both eyes in roughly half of patients.
The mechanism involves the immune system attacking its own corneal tissue. Autoantibodies combine with the body’s own proteins to form immune complexes, which deposit along the tiny blood vessels at the edge of the cornea. This triggers a cascade of inflammation that eats away at the corneal tissue, creating a crescent-shaped area of thinning near the border of the cornea. The peripheral cornea is especially vulnerable because, unlike the central cornea, it has a rich blood supply and a high concentration of immune cells. Other autoimmune conditions associated with PUK include lupus, Sjögren syndrome, and systemic vasculitis.
Vitamin A Deficiency
In developing countries, severe vitamin A deficiency remains a significant cause of corneal ulcers, particularly in children. Vitamin A is essential for maintaining the glands that produce tears and the mucus layer that keeps the cornea moist. Without adequate vitamin A, the cornea dries out in a condition called xerophthalmia. The dryness destroys the protective surface, increases the risk of infection, and if the deficiency isn’t corrected urgently, the cornea can ulcerate and literally melt away.
In the most severe form, called keratomalacia, more than a third of the cornea becomes swollen, then undergoes tissue death as the collagen structure breaks down. The cornea can be destroyed in just a few days. This is rare in countries with adequate nutrition but remains a leading cause of preventable childhood blindness worldwide.
How Corneal Ulcers Are Detected
Corneal ulcers typically announce themselves with a combination of eye pain, redness, tearing, blurred vision, and sensitivity to light. A white or grayish spot may be visible on the cornea. These symptoms can overlap with less serious conditions like conjunctivitis (pink eye), but the presence of significant pain and vision changes distinguishes an ulcer from a routine eye infection.
To confirm the diagnosis, an eye doctor applies fluorescein dye to the surface of the eye. The dye fills any defect in the corneal surface and, under cobalt blue light, the damaged area glows green, clearly outlining the size and shape of the ulcer. A slit-lamp microscope allows the doctor to examine the depth of the ulcer and look for a cloudy infiltrate in the corneal tissue, which signals active infection or inflammation. If an infection is suspected, a small sample may be collected from the ulcer to identify the specific organism and guide treatment.
Long-Term Risks of Corneal Ulcers
The biggest concern with any corneal ulcer is scarring. As the ulcer heals, it often leaves behind opaque scar tissue that permanently reduces vision if it sits over the central cornea. How much vision is affected depends on the ulcer’s size, depth, location, and how quickly treatment begins. Ulcers caused by Pseudomonas bacteria or Acanthamoeba tend to be the most aggressive and carry the highest risk of severe outcomes.
When scarring is dense enough to impair vision significantly, a corneal transplant may be the only option for restoring sight. About 12% of all corneal transplants performed are specifically for managing infectious keratitis. In the worst cases, a deep ulcer can perforate the cornea entirely, which is a medical emergency that threatens the entire eye.