A study in Austria found over the course of the testing, a total of 154 cases of "Acanthamoeba" keratitis. The age of the positive tests ranged from 8 to 82 years old and 58% of the people were female. The data showed that 89% of the infected patients were contact lens wearers and 19% required a corneal transplant.

CNV causes may be congenital in nature, such as with Aniridia, or acquired. Frequently, inflammatory, infectious, degenerative, traumatic and iatrogenic (from contact lenses) diseases are responsible for acquired CNV.

Some major associated, acquired inflammatory conditions include graft rejection following keratoplasty, graft or host diseases of the new tissue, atopic conjunctivitis, rosacea, ocular pemphigoid, Lyell's syndrome, and Steven's Johnson syndrome.

Infections responsible for CNV range from bacterial (chlamydia, syphilis, pseduomonas), Viral (herpes simplex and herpes zoster viruses), Fungal (candida, asperigillus, fusarium), and parasistic (onchocerca volvolus).

Degenerative diseases such as pterygiums, and terrien's marginal degeneration may be responsible.

Traumas frequently seen with CNV include ulceration, alkali burns, and stem cell deficiency.

One of the most common causes of corneal neovascularization is iastrogenic pathology from contact lens wear. This is especially true of lenses made with older hydrogel materials such as HEMA (2-hydroxyethyl methacrylate) for both daily and extended wear. Such older hydrogel materials have a relatively low oxygen transmissibility so the cornea becomes starved of oxygen leading to the ingress of blood capillaries into the clear cornea to satisfy that oxygen demand. Older estimates have 128,000 to 470,000 cases of lens-induced CNV each year, but this may be decreasing due to the increasing popularity of daily disposable lenses.

The risk for CNV is elevated in certain instances for patients following penetrating keratoplasty without active inflammation or epithelial defects. CNV is more likely to occur in those with active blepharitis, those who receive sutured knots in their host stromas, and those with a large recipient area.

The cornea, an avascular tissue, is among the most densely innervated structures of the human body. Corneal nerves are responsible for maintaining the anatomical and functional integrity of the cornea, conveying tactile, temperature and pain sensations, playing a role in the blink reflex, in wound healing and in the production and secretion of tears.

Most corneal nerve fibres are sensory in origin and are derived from the ophthalmic branch of the trigeminal nerve. Congenital or acquired ocular and systemic diseases can determine a lesion at different levels of the trigeminal nerve, which can lead to a reduction (hypoesthesia) or loss (anesthesia) of sensitivity of the cornea.

The most common causes of loss of corneal sensitivity are viral infections (herpes simplex and herpes zoster ophthalmicus), chemical burns, physical injuries, corneal surgery, neurosurgery, chronic use of topical medications, or chronic use of contact lenses.

Possible causes also include systemic diseases such as diabetes, multiple sclerosis or leprosy.

Other, albeit less frequent, potential causes of the disease are: intracranial space-occupying lesions such as neuroma, meningioma and aneurysms, which may compress the trigeminal nerve and reduce corneal sensitivity.

Conversely, congenital conditions that may lead to this disorder are very rare.

Diffuse lamellar keratitis (DLK) is a sterile inflammation of the cornea which may occur after refractive surgery, such as LASIK. Its incidence has been estimated to be 1 in 500 patients, though this may be as high as 32% in some cases.

DLK is predominantly associated with Lasik, as the creation of a flap creates a potential space for cells to accumulate. Individuals with atopic conditions with pre-existing allergic conjunctivitis, or ocular rosacea, are more prone to developing the condition after surgery. Some authors have reported that moderate to severe eye allergies and chronic allergic conjunctivitis are an absolute contraindication to the LASIK procedure. This is in distinction to findings of earlier studies. Keratitis can also occur after photorefractive keratectomy (PRK), although because it occurs in the setting of infection, it is distinct from the sterile infiltrates of DLK. DLK can also occur following myopic keratomileusis, in which a disc of corneal tissue is removed, shaped and sutured back into place, although this technique is more historical, having been replaced by Lasik and PRK.

The incidence and prevalence of PMD are unknown, and no studies have yet investigated its prevalence or incidence. However, it is generally agreed that PMD is a very rare condition. Some uncertainty regarding the incidence of PMD may be attributed to its confusion with keratoconus. PMD is not linked to race or age, although most cases present early in life, between 20 and 40 years of age. While PMD is usually considered to affect men and women equally, some studies suggest that it may affect men more frequently.

Several diseases have been observed in patients with PMD. However, no causal relationships have been established between any of the associated diseases and the pathogenesis of PMD. Such diseases include: chronic open-angle glaucoma, retinitis pigmentosa, retinal lattice degeneration, scleroderma, kerato-conjunctivitis, eczema, and hyperthyroidism.

Neurotrophic keratitis (NK) is a degenerative disease of the cornea caused by damage of the trigeminal nerve, which results in impairment of corneal sensitivity, spontaneous corneal epithelium breakdown, poor corneal healing and development of corneal ulceration, melting and perforation.

Neurotrophic keratitis is classified as a rare disease, with an estimated prevalence of less than 5 in 10,000 people in Europe. It has been recorded that on average, 6% of herpetic keratitis cases may evolve to this disease, with a peak of 12.8% of cases of keratitis due to herpes zoster virus.

The diagnosis, and particularly the treatment of neurotrophic keratitis are the most complex and challenging aspects of this disease, as a satisfactory therapeutic approach is not yet available.

The Appaloosa has a higher risk of developing ERU than other breeds; this predisposition has a genetic basis. Appaloosas which develop ERU are more likely than other breeds to have ERU in both eyes, and more likely to become blind in one or both eyes.

Several aetiologies are suggested, and any combination of these may be present in any given case.

- Vitamin deficiency (A, B or C)

- Viral infection

- Bacterial infection

- "Leptospira

- "Streptococcus

- "Brucella

- Parasitic infection

- Strongyle

- "Onchocerca cervicalis"

- Autoimmune disease

The disease has been suggested to be primarily autoimmune in nature, being a delayed hypersensitivity reaction to any of the above agents.

The causes of TSPK are currently not yet well known.

However, there seem to be indications that dysfunctioning of the Meibomian gland can cause the condition. Inflammation of the meibomian glands (also known as meibomitis, meibomian gland dysfunction, or posterior blepharitis) causes the glands to be obstructed by thick waxy secretions. Besides leading to dry eyes, the obstructions can be degraded by bacterial lipases, resulting in the formation of free fatty acids, which irritate the eyes and sometimes cause punctate keratopathy.

Scleritis is not a common disease, although the exact prevalence and incidence are unknown. It is somewhat more common in women, and is most common in the fourth to sixth decades of life.

Punctate epithelial erosions may be seen with different disorders:

- Rosacea

- Dry-eye syndrome

- Blepharitis

- Acute bacterial conjunctivitis

- Trauma

- Exposure keratopathy from poor eyelide closure

- Ultraviolet or chemical burn

- Contact lens-related disorder such as toxicity or tight lens syndrome

- Trichiasis

- Entropion or ectropion

- Floppy eyelid syndrome

- Chemotherapy i.e. cytosine arabinoside

- Thygeson's Superficial Punctate Keratopathy

Some infections may scar the cornea to limit vision. Others may result in perforation of the cornea, (an infection inside the eye), or even loss of the eye. With proper medical attention, infections can usually be successfully treated without long-term visual loss.

Corneal neovascularization (CNV) is the in-growth of new blood vessels from the pericorneal plexus into avascular corneal tissue as a result of oxygen deprivation. Maintaining avascularity of the corneal stroma is an important aspect of corneal pathophysiology as it is required for corneal transparency and optimal vision. A decrease in corneal transparency causes visual acuity deterioration. Corneal tissue is avascular in nature and the presence of vascularization, which can be deep or superficial, is always pathologically related.

Corneal neovascularization is a sight-threatening condition that can be caused by inflammation related to infection, chemical injury, autoimmune conditions, post-corneal transplantation, and traumatic conditions among other ocular pathologies. Common causes of CNV within the cornea include trachoma, corneal ulcers, phylctenular keratoconjunctivitis, rosacea keratitis, interstitial keratitis, sclerosing keratitis, chemical burns, and wearing contact lenses for over-extended periods of time. Superficial presentations of CNV are usually associated with contact lens wear, while deep presentations may be caused by chronic inflammatory and anterior segment ocular diseases.

Corneal neovascularization is becoming increasingly common worldwide with an estimated incidence rate of 1.4 million cases per year, according to a 1998 study by the Massachusetts Eye and Ear Infirmary. The same study found that the tissue from twenty percent of corneas examined during corneal transplantations had some degree of neovascularization, negatively impacting the prognosis for individuals undergoing keratoplasty procedures.

Thygeson's superficial punctate keratopathy (TSPK; also "Thygeson Superficial Punctate Keratitis") is a disease of the eyes. The causes of TSPK are not currently known, but details of the disease were first published in the Journal of the American Medical Association in 1950 by the renowned American Ophthalmologist, Phillips Thygeson (1903–2002) - after whom it is named.

By far the most common cause of IK is syphilitic disease. However, there are two possible causes of the corneal inflammatory response: an infection and/or an immunological response, such as a hypersensitivity type reaction, or (rarely) Cogan syndrome. Infectious causes include syphilis (commonest), followed by other bacterial infections (TB, Leprosy and Lyme disease) and parasitic infections (Acanthamoeba, Onchocerciasis or river blindness, Leishmaniasis, Trypanosoma cruzi or "Chagas disease", Trypanosoma brucei or "African sleeping sickness" and microsporidia)

Visual function declines as a result of the irregular corneal shape, resulting in astigmatism, and causing a distortion in vision. Deterioration can become severe over time.

According to the American Optometric Association, the following steps can be taken to prevent "Acanthamoeba" keratitis:

- Always wash and dry your hands before handling contact lenses, ordinary water should never come in contact with your lenses.

- Rub and rinse the surface of the contact lens before storing.

- Use only sterile products recommended by your optometrist to clean and disinfect your lenses. Saline solution and rewetting drops are not designed to disinfect lenses.

- Avoid using tap water to wash or store contact lenses.

- Contact lens solution must be discarded upon opening the case, and fresh solution used each time the lens is placed in the case.

- Replace lenses using your doctor’s prescribed schedule.

- Do not sleep in contact lenses unless prescribed by your doctor and never after swimming.

- Never swap lenses with someone else.

- Never put contact lenses in your mouth.

- See your optometrist regularly for contact lens evaluation.

Vernal keratoconjunctivitis (VKC) or spring catarrh is a recurrent, bilateral, and self-limiting inflammation of conjunctiva, having a periodic seasonal incidence.

Complications are the exception rather than the rule from simple corneal abrasions. It is important that any foreign body be identified and removed, especially if containing iron as rusting will occur.

Occasionally the healed epithelium may be poorly adherent to the underlying basement membrane in which case it may detach at intervals giving rise to recurrent corneal erosions.

Previous long-standing eye infection which possibly during childhood time recalled as being treated with antibiotic and/or hospitalized over long period of time.

Corneal abrasions are generally a result of trauma to the surface of the eye. Common causes include being poked by a finger, walking into a tree branch, and wearing old contact lenses. A foreign body in the eye may also cause a scratch if the eye is rubbed.

Injuries can also be incurred by "hard" or "soft" contact lenses that have been left in too long. Damage may result when the lenses are removed, rather than when the lens is still in contact with the eye. In addition, if the cornea becomes excessively dry, it may become more brittle and easily damaged by movement across the surface. Soft contact lens wear overnight has been extensively linked to gram negative keratitis (infection of the cornea) particularly by a bacterium known as "Pseudomonas aeruginosa" which forms in the eye's biofilm as a result of extended soft contact lens wear. When a corneal abrasion occurs either from the contact lens itself or another source, the injured cornea is much more susceptible to this type of bacterial infection than a non-contact lens user's would be. This is an optical emergency as it is sight (in some cases eye) threatening. Contact lens wearers who present with corneal abrasions should never be pressure patched because it has been shown through clinical studies that patching creates a warm, moist dark environment that can cause the cornea to become infected or cause an existing infection to be greatly accelerated on its destructive path.

Corneal abrasions are also a common and recurrent feature in people who suffer specific types of corneal dystrophy, such as lattice corneal dystrophy. Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma. During an eye examination, the doctor sees these deposits in the stroma as clear, comma-shaped overlapping dots and branching filaments, creating a lattice effect. Over time, the lattice lines will grow opaque and involve more of the stroma. They will also gradually converge, giving the cornea a cloudiness that may also reduce vision. In some people, these abnormal protein fibers can accumulate under the cornea's outer layer—the epithelium. This can cause erosion of the epithelium. This condition is known as recurrent epithelial erosion. These erosions: (1) Alter the cornea's normal curvature, resulting in temporary vision problems; and (2) Expose the nerves that line the cornea, causing severe pain. Even the involuntary act of blinking can be painful.

Boehm Syndrome defines erosion events that occur only during periods of sleep.

Most of the time, scleritis is not caused by an infectious agent. Histopathological changes are that of a chronic granulomatous disorder, characterized by fibrinoid necrosis, infiltration by polymorphonuclear cells, lymphocytes, plasma cells and macrophages. The granuloma is surrounded by multinucleated epitheloid giant cells and new vessels, some of which may show evidence of vasculitis.

Treatment depends on the cause of the keratitis. Infectious keratitis can progress rapidly, and generally requires urgent antibacterial, antifungal, or antiviral therapy to eliminate the pathogen. Antibacterial solutions include levofloxacin, gatifloxacin, moxifloxacin, ofloxacin. It is unclear if steroid eye drops are useful or not.

In addition, contact lens wearers are typically advised to discontinue contact lens wear and replace contaminated contact lenses and contact lens cases. (Contaminated lenses and cases should not be discarded as cultures from these can be used to identify the pathogen).

Aciclovir is the mainstay of treatment for HSV keratitis and steroids should be avoided at all costs in this condition. Application of steroids to a dendritic ulcer caused by HSV will result in rapid and significant worsening of the ulcer to form an 'amoeboid' or 'geographic' ulcer, so named because of the ulcer's map like shape.

Keratoconjunctivitis is inflammation ("-itis") of the cornea and conjunctiva.

When only the cornea is inflamed, it is called "keratitis"; when only the conjunctiva is inflamed, it is called "conjunctivitis".

There are several potential causes of the inflammation:

- Keratoconjunctivitis sicca is used when the inflammation is due to dryness. ("Sicca" means "dryness" in medical contexts.) It occurs with 20% of rheumatoid arthritis patients.

- The term "Vernal keratoconjunctivitis" (VKC) is used to refer to keratoconjunctivitis occurring in spring, and is usually considered to be due to allergens.

- "Atopic keratoconjunctivitis" is one manifestation of atopy.

- "Epidemic keratoconjunctivitis" is caused by an adenovirus infection.

- "Infectious bovine keratoconjunctivitis" (IBK) is a disease affecting cattle caused by the bacteria "Moraxella bovis".

- "Pink eye in sheep and goat" is another infectious keratoconjunctivitis of veterinary concern, mostly caused by "Chlamydophila pecorum"

- "Superior limbic keratoconjunctivitis" is thought to be caused by mechanical trauma.

- "Keratoconjunctivitis photoelectrica" (arc eye) means inflammation caused by photoelectric UV light. It is a type of ultraviolet keratitis. Such UV exposure can be caused by arc welding without wearing protective eye glass, or by high altitude exposure from sunlight reflected from snow ("snow blindness"). The inflammation will only appear after about 6 to 12 hours. It can be treated by rest, as the inflammation usually heals after 24–48 hours. Proper eye protection should be worn to prevent keratoconjunctivitis photoelectrica.