Corneal ulcers are a common human eye disease. They are caused by trauma, particularly with vegetable matter, as well as chemical injury, contact lenses and infections. Other eye conditions can cause corneal ulcers, such as entropion, distichiasis, corneal dystrophy, and keratoconjunctivitis sicca (dry eye).

Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa, and chlamydia:

- Bacterial keratitis is caused by "Staphylococcus aureus", "Streptococcus viridans", "Escherichia coli", "Enterococci", "Pseudomonas", "Nocardia", "N. Gonorrhoea" and many other bacteria.

- Fungal keratitis causes deep and severe corneal ulcer. It is caused by "Aspergillus" sp., "Fusarium" sp., "Candida" sp., as also "Rhizopus", "Mucor", and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and hypopyon is usually seen.

- Viral keratitis causes corneal ulceration. It is caused most commonly by Herpes simplex, Herpes zoster and Adenoviruses. Also it can be caused by coronaviruses & many other viruses. Herpes virus cause a dendritic ulcer, which can recur and relapse over the lifetime of an individual.

- Protozoa infection like "Acanthamoeba keratitis" is characterized by severe pain and is associated with contact lens users swimming in pools.

- "Chlamydia trachomatis" can also contribute to development of corneal ulcer.

Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially dangerous and can rapidly result in corneal perforation, if not treated in time.

The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Entropion, severe dry eye and trichiasis (inturning of eyelashes) may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include Rheumatoid arthritis, rosacea, systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a circumferential crater like depression of the cornea, just inside the limbus, usually with an overhanging edge.

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

Prevention of trauma with vegetable / organic matter, particularly in agricultural workers while harvesting can reduce the incidence of fungal keratitis. Wearing of broad protective glasses with side shields is recommended for people at risk for such injuries.

Primary infection most commonly manifests as blepharoconjunctivitis i.e. infection of lids and conjunctiva that heals without scarring. Lid vesicles and conjunctivitis are seen in primary infection. Corneal involvement is rarely seen in primary infection.

Herpetic simplex keratitis, also known as herpetic keratoconjunctivitis and herpesviral keratitis, is a form of keratitis caused by recurrent herpes simplex virus (HSV) infection in the cornea.

It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving the cornea. Primary infection typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis), accompanied by small white itchy lesions on the corneal surface. The effect of the lesions varies, from minor damage to the epithelium (superficial punctate keratitis), to more serious consequences such as the formation of dendritic ulcers. Infection is unilateral, affecting one eye at a time. Additional symptoms include dull pain deep inside the eye, mild to acute dryness, and sinusitis. Most primary infections resolve spontaneously in a few weeks. Healing can be aided by the use of oral and topical antivirals.

Subsequent recurrences may be more severe, with infected epithelial cells showing larger dendritic ulceration, and lesions forming white plaques. The epithelial layer is sloughed off as the dendritic ulcer grows, and mild inflammation (iritis) may occur in the underlying stroma of iris. Sensation loss occurs in lesional areas, producing generalised corneal anaesthesia with repeated recurrences. Recurrence can be accompanied by chronic dry eye, low grade intermittent conjunctivitis, or chronic unexplained sinusitis. Following persistent infection the concentration of viral DNA reaches a critical limit. Antibody responses against the viral antigen expression in the stroma can trigger a massive immune response in the eye. The response may result in the destruction of the corneal stroma, resulting in loss of vision due to opacification of the cornea. This is known as immune-mediated stromal keratitis.

HSV infection is very common in humans. It has been estimated that one third of the world population have recurrent infection. Keratitis caused by HSV is the most common cause of cornea-derived blindness in developed nations. Therefore, HSV infections are a large and worldwide public health problem. The global incidence (rate of new disease) of herpes keratitis is roughly 1.5 million, including 40,000 new cases of severe monocular visual impairment or blindness each year.

Filamentous fungi

- Aspergillus flavus

- Aspergillus fumigatus

- Fusarium spp.

- Alternaria spp.

- Curvularia

- Acremonium

Yeasts

- Candida

Fusarium spp. is most common then Aspergillus spp. and thirdly Dematitious fungi causing fungal keratitis in India.

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.

Corneal ulcer, or ulcerative keratitis, is an inflammatory or more seriously, infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and the agrarian societies. In developing countries, children afflicted by Vitamin A deficiency are at high risk for corneal ulcer and may become blind in both eyes, which may persist lifelong. In ophthalmology, a corneal ulcer usually refers to having an infectious cause while the term corneal abrasion refers more to physical abrasions.

Due to the different underlying causes, proper diagnosis, treatment, and prognosis can only be determined by an eye care professional. Punctate epithelial erosions may be treated with artificial tears. In some disorders, topical antibiotic is added to the treatment. Patients should discontinue contact lens wear until recovery.

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.

A study conducted in November of 2017, conveyed a correlation between blepharitis and early onset metabolic syndrome (MetS). To investigate the relationship between blepharitis and MetS, researchers used the Longitudinal Health Insurance Database in Taiwan. Results indicated that hyperlipidaemia and coronary artery disease were significantly correlated with the prior development of blepharitis. Therefore, blepharitis was shown to be significantly related to MetS and can serve as an early indication of the condition.

In another recent study, the presence of Demodex has been unveiled as a common cause of blepharitis. However, the pathogenesis of demodicosis is still unclear. In this study, researchers provide a diagnosis of the disease and propose diagnostic criteria of Demodex blepharitis.

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.

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.

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.

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.

Interstitial keratitis (IK) is corneal scarring due to chronic inflammation of the corneal stroma. Interstitial means space between cells i.e. corneal stroma which lies between the epithelium and the endothelium. Keratitis means corneal inflammation.

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.

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)

The mechanism by which the bacteria causes symptoms of blepharitis is not fully understood and may include direct irritation of bacterial toxins and/or enhanced cell-mediated immunity to S. aureus.

Staphylococcal blepharitis is caused by an infection of the anterior portion of the eyelid by Staphylococcal bacteria. In a study of ocular flora, 46% to 51% of those diagnosed with staphylococcal blepharitis had cultures positive for Staphylococcus aureus in comparison to 8% of normal patients. Staphylococcal blepharitis may start in childhood and continue into adulthood. It is commonly recurrent and it requires special medical care. The prevalence of Staphylococcus aureus in the conjunctival sac and on the lid margin varies among countries, likely due to differences in climate and environment. Seborrheic blepharitis is characterized by less inflammation than Staphylococcal blepharitis; however, it causes more excess oil or greasy scaling. Meibomian Gland Dysfunction is a result of abnormalities of the meibomian glands and altered secretion meibum, which plays an imperative role in lagging the evaporation of tear films and smoothing of the tear film to produce an even optical surface. Posterior blepharitis is an inflammation of the eyelids, secondary to dysfunction of the meibomian glands. Like anterior blepharitis, it is a bilateral chronic condition and may be associated with skin rosacea. There is growing evidence that, in some cases, it is caused by Demodex mites.

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.

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.

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.

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.

There are a number of different treatments to deal with TSPK. Symptoms may disappear if untreated, but treatment may decrease both the healing time and the chances of remission.

- PRK laser eye surgery may cure this disease (NOTE: A full clinical study has not been done, but a case study of one person was reported in 2002 PRK-pTK as a treatment).

- Artificial tear eye-drops or ointments may be a suitable treatment for mild cases.

- Low-dosage steroidal eye-drops, such as prednisone, fluorometholone, loteprednol (Lotemax 0.5%) or rimexolone. Steroidal drops should be used with caution and the eye pressure should be regularly checked during treatment.

- Soft contact lenses.

- Ciclosporin is an experimental treatment for TSPK. It is usually used during transplants as it reduces the immune system response.

- Tacrolimus (Protopic 0.03% ointment) is also an experimental treatment.

- Laser eye treatment.

- Amniotic membrane (Case Study)

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.