Uveitis affects approximately 1 in 4500 people and is most common between the ages 20 to 60 with men and women affected equally.

In western countries, anterior uveitis accounts for between 50% and 90% of uveitis cases. In Asian countries the proportion is between 28% and 50%.

Uveitis is estimated to be responsible for approximately 10%-20% of the blindness in the United States.

Uveitis is usually an isolated illness, but can be associated with many other medical conditions.

In anterior uveitis, no associated condition or syndrome is found in approximately one-half of cases. However, anterior uveitis is often one of the syndromes associated with HLA-B27. Presence of this type of HLA allele has a relative risk of evolving this disease by approximately 15%.

The most common form of uveitis is acute anterior uveitis (AAU). It is most commonly associated with HLA-B27, which has important features: HLA-B27 AAU can be associated with ocular inflammation alone or in association with systemic disease. HLA-B27 AAU has characteristic clinical features including male preponderance, unilateral alternating acute onset, a non-granulomatous appearance, and frequent recurrences, whereas HLA-B27 negative AAU has an equivalent male to female onset, bilateral chronic course, and more frequent granulomatous appearance. Rheumatoid arthritis is not uncommon in Asian countries as a significant association of uveitis.

Of the many causes, conjunctivitis is the most common. Others include:

"Usually nonurgent"

- blepharitis - a usually chronic inflammation of the eyelids with scaling, sometimes resolving spontaneously

- subconjunctival hemorrhage - a sometimes dramatic, but usually harmless, bleeding underneath the conjunctiva most often from spontaneous rupture of the small, fragile blood vessels, commonly from a cough or sneeze

- inflamed pterygium - a benign, triangular, horizontal growth of the conjunctiva, arising from the inner side, at the level of contact of the upper and lower eyelids, associated with exposure to sunlight, low humidity and dust. It may be more common in occupations such as farming and welding.

- inflamed pinguecula - a yellow-white deposit close to the junction between the cornea and sclera, on the conjunctiva. It is most prevalent in tropical climates with much UV exposure. Although harmless, it can occasionally become inflamed.

- dry eye syndrome - caused by either decreased tear production or increased tear film evaporation which may lead to irritation and redness

- airborne contaminants or irritants

- tiredness

- drug use including cannabis

"Usually urgent"

- acute angle closure glaucoma - implies injury to the optic nerve with the potential for irreversible vision loss which may be permanent unless treated quickly, as a result of increased pressure within the eyeball. Not all forms of glaucoma are acute, and not all are associated with increased 'intra-ocular' pressure.

- injury

- keratitis - a potentially serious inflammation or injury to the cornea (window), often associated with significant pain, light intolerance, and deterioration in vision. Numerous causes include virus infection. Injury from contact lenses can lead to keratitis.

- iritis - together with the ciliary body and choroid, the iris makes up the uvea, part of the middle, pigmented, structures of the eye. Inflammation of this layer (uveitis) requires urgent control and is estimated to be responsible for 10% of blindness in the United States.

- scleritis - a serious inflammatory condition, often painful, that can result in permanent vision loss, and without an identifiable cause in half of those presenting with it. About 30-40% have an underlying systemic autoimmune condition.

- episcleritis - most often a mild, inflammatory disorder of the 'white' of the eye unassociated with eye complications in contrast to scleritis, and responding to topical medications such as anti-inflammatory drops.

- tick borne illnesses like Rocky Mountain spotted fever - the eye is not primarily involved, but the presence of conjunctivitis, along with fever and rash, may help with the diagnosis in appropriate circumstances.

A red eye is an eye that appears red due to illness or injury. It is usually injection and prominence of the superficial blood vessels of the conjunctiva, or sclera, which may be caused by disorders of these or adjacent structures. Conjunctivitis and subconjunctival hemorrhage are two of the less serious but more common causes.

Management includes assessing whether emergency action (including referral) is needed, or whether treatment can be accomplished without additional resources.

Slit lamp examination is invaluable in diagnosis but initial assessment can be performed using a careful history, testing vision (visual acuity), and carrying out a penlight examination.

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.

According to recent research not a single theory is able to explain the cause fully. However current plausible theories include infection with "Toxoplasma gondii", Herpes simplex virus, Rubella, neurogenic causes, and autoimmune pathology.

Mydriatic/cycloplegic agents, such as topical homatropine, which is similar in action to atropine, are useful in breaking and preventing the formation of posterior synechia by keeping the iris dilated and away from the crystalline lens. Dilation of the pupil in an eye with the synechia can cause the pupil to take an irregular, non-circular shape (Dyscoria) as shown in the photograph. If the pupil can be fully dilated during the treatment of iritis, the prognosis for recovery from synechia is good. This is a treatable status.

To subdue the inflammation, use topical corticosteroids. If the intra-ocular pressure is elevated then use a PGA such as Travatan Z.

A synechia is an eye condition where the iris adheres to either the cornea (i.e. "anterior synechia") or lens (i.e. "posterior synechia"). Synechiae can be caused by ocular trauma, iritis or iridocyclitis and may lead to certain types of glaucoma. It is sometimes visible on careful examination but usually more easily through an ophthalmoscope or slit-lamp.

Anterior synechia causes closed angle glaucoma, which means that the iris closes the drainage way of aqueous humour which in turn raises the intraocular pressure. Posterior synechia also cause glaucoma, but with a different mechanism. In posterior synechia, the iris adheres to the lens, blocking the flow of aqueous humor from the posterior chamber to the anterior chamber. This blocked drainage raises the intraocular pressure.

Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Neovascularisation (growth of new abnormal vessels) is possible and any eye surgery, such as cataract surgery, can cause bleeding from the fragile vessels in the atrophic iris causing accumulation of blood in anterior chamber of the eye, also known as hyphema.

Retinal vasculitis is inflammation of the vascular branches of the retinal artery, caused either by primary ocular disease processes, or as a specific presentation of any systemic form of vasculitis such as Behçet's disease, sarcoidosis, multiple sclerosis, or any form of systemic nectrozing vasculitis such as temporal arteritis, polyarteritis nodosa, and granulomatosis with polyangiitis, or due to lupus erythematosus, or rheumatoid arthritis. Eales disease, pars planitis, birdshot retinochoroidopathy (autoimmune bilateral posterior uveitis), and Fuchs heterochromic iridocyclitis (FHI) can also cause retinal vasculitis. Infectious pathogens such as "Mycobacterium tuberculosis", visceral larva migrans ("Toxocara canis" & "Toxocara cati") can also cause retinal vasculitis.

Retinal vasculitis presents as painless, decrease of visual acuity (blurry vision), visual floaters, scotomas (dark spot in vision), decreased ability to distinguish colors, and metamorphopsia (distortion of images such as linear images).

Herpes zoster ophthalmicus (HZO) and also known as ophthalmic zoster is a disease characterised by reactivation of dormant varicella zoster virus residing within the ophthalmic nerve (the first division of the trigeminal nerve). This condition is an important subtype of shingles, representing 15% of all cases.

Herpes zoster ophthalmicus is transmitted via direct contact or droplets. Varicella zoster virus is a DNA virus which produces acidophilic intranuclear inclusion bodies. The virus is neurotrophic in nature.

The frontal nerve is more commonly affected than the nasociliary nerve or lacrimal nerve.

Any potential ocular involvement should be assessed by an ophthalmologist as complications such as episcleritis and uveitis may occur.

Keratic precipitate (KP) is an inflammatory cellular deposit seen on corneal endothelium. Acute KPs are white and round in shape whereas old KPs are faded and irregular in shape. Mutton-fat KPs are large in shape and are greasy-white in color and are formed from macrophages and epithelioid cell. They are indicative of inflammatory disease. Mutton fat Kps are due to granulomatous iridocyclitis. Another variant called red KPs may be seen in hemorrhagic uveitis.

Many individuals have mild symptoms, which recur infrequently, while others may have persistent problems that become debilitating or life-threatening.

Relapsing polychondritis is an autoimmune disease in which the body's immune system begins to attack and destroy the cartilage tissues in the body. It has been postulated that both cell-mediated immunity and humoral immunity are responsible.

Reasons for disease onset are not known, but there is no evidence of a genetic predisposition to developing relapsing polychondritis. However, there are cases where multiple members of the same family have been diagnosed with this illness. Studies indicate that some genetic contribution to susceptibility is likely.

JIA occurs in both sexes, but like other rheumatological diseases, is more common in females. Symptoms onset is frequently dependent on the subtype of JIA and is from the preschool years to the early teenaged years.

Although it may occur in the absence of other known disease, SS is often associated with hematologic disease (including leukemia), and immunologic disease (rheumatoid arthritis, inflammatory bowel disease, Behçet's syndrome).

A genetic association has been suggested, but no specific genetic link has been identified.

The cause of JIA remains a mystery. However, the disorder is autoimmune — meaning that the body's own immune system starts to attack and destroy cells and tissues (particularly in the joints) for no apparent reason. The immune system is thought to be provoked by changes in the environment, in combination with mutations in many associated genes and/or other causes of differential expression of genes. Experimental studies have shown that certain mutated viruses may be able to trigger JIA. The disease appears to be more common in girls, and the disease is most common in Caucasians.

Associated factors that may worsen or have been linked to rheumatoid arthritis include:

- Genetic predisposition; When one family member has been diagnosed with rheumatoid arthritis or another autoimmune disorder, the chances are higher that other family members or siblings may also develop arthritis.

- Females are more likely to develop rheumatoid arthritis than males at all ages.

- A strong belief is held that psychological stress may worsen the symptoms of rheumatoid arthritis. However, when the emotional stress is under control, the arthritis symptoms do not always disappear, suggesting that the association is not straightforward.

- Though no distinct immune factor has been isolated as a cause of arthritis, some experts believe that the triggering factor may be something like a virus which then disappears from the body after permanent damage is done.

- Because rheumatoid arthritis is more common in women, perhaps sex hormones may play a role in causing or modulating arthritis. Unfortunately, neither sex hormone deficiency nor replacement has been shown to improve or worsen arthritis.

The cause of JIA, as the word "idiopathic" suggests, is unknown and an area of active research. Current understanding of JIA suggests that it arises in a genetically susceptible individual due to environmental factors.

SS is a reactive phenomenon and should be considered a cutaneous marker of systemic disease. Careful systemic evaluation is indicated, especially when cutaneous lesions are severe or hematologic values are abnormal. Approximately 20% of cases are associated with malignancy, predominantly hematological, especially acute myelogenous leukemia (AML). An underlying condition (streptococcal infection, inflammatory bowel disease, nonlymphocytic leukemia and other hematologic malignancies, solid tumors, pregnancy) is found in up to 50% of cases. Attacks of SS may precede the hematologic diagnosis by 3 months to 6 years, so that close evaluation of patients in the “idiopathic” group is required.

There is now good evidence that treatment with hematopoietic growth factors — including granulocyte colony-stimulating factor (G-CSF), which is used to treat AML, and granulocyte-macrophage colony-stimulating factor — can cause SS. Lesions typically occur when the patient has leukocytosis and neutrophilia but not when the patient is neutropenic. However, G-CSF may cause SS in neutropenic patients because of the induction of stem cell proliferation, the differentiation of neutrophils, and the prolongation of neutrophil survival.

Kawasaki disease affects boys more than girls, with people of Asian ethnicity, particularly Japanese and Korean people, most susceptible, as well as people of Afro-Caribbean ethnicity. The disease was rare in Caucasians until the last few decades, and incidence rates fluctuate from country to country.

Currently, Kawasaki disease is the most commonly diagnosed pediatric vasculitis in the world. By far, the highest incidence of Kawasaki disease occurs in Japan, with the most recent study placing the attack rate at 218.6 per 100,000 children <5 years of age (about one in 450 children). At this present attack rate, more than one in 150 children in Japan will develop Kawasaki disease during their lifetimes.

However, its incidence in the United States is increasing. Kawasaki disease is predominantly a disease of young children, with 80% of patients younger than five years of age. About 2,000-4,000 cases are identified in the U.S. each year (9 to 19 per 100,000 children younger than 5 years of age).

In the United Kingdom, estimates of incidence rate vary because of the rarity of Kawasaki disease. However, it is believed to affect fewer than one in every 25,000 people. Incidence of the disease doubled from 1991 to 2000, however, with four cases per 100,000 children in 1991 compared with a rise of eight cases per 100,000 in 2000.

In the continental United States, Kawasaki Disease is more common during the winter and early spring, boys with the disease outnumber girls by ≈1.5–1.7:1, and 76% of affected children are <5 years of age.

With early treatment, rapid recovery from the acute symptoms can be expected, and the risk of coronary artery aneurysms is greatly reduced. Untreated, the acute symptoms of Kawasaki disease are self-limited ("i.e." the patient will recover eventually), but the risk of coronary artery involvement is much greater. Overall, about 2% of patients die from complications of coronary vasculitis. Patients who have had Kawasaki disease should have an echocardiogram initially every few weeks, and then every one or two years to screen for progression of cardiac involvement.

Laboratory evidence of increased inflammation combined with demographic features (male sex, age less than six months or greater than eight years) and incomplete response to IVIG therapy create a profile of a high-risk patient with Kawasaki disease. The likelihood that an aneurysm will resolve appears to be determined in large measure by its initial size, in which the smaller aneurysms have a greater likelihood of regression. Other factors are positively associated with the regression of aneurysms, including being younger than a year old at the onset of Kawasaki disease, fusiform rather than saccular aneurysm morphology, and an aneurysm location in a distal coronary segment. The highest rate of progression to stenosis occurs among those who develop large aneurysms. The worst prognosis occurs in children with giant aneurysms. This severe outcome may require further treatment such as percutaneous transluminal angioplasty, coronary artery stenting, bypass grafting, and even cardiac transplantation.

A relapse of symptoms may occur soon after initial treatment with IVIG. This usually requires rehospitalization and retreatment. Treatment with IVIG can cause allergic and nonallergic acute reactions, aseptic meningitis, fluid overload and, rarely, other serious reactions. Overall, life-threatening complications resulting from therapy for Kawasaki disease are exceedingly rare, especially compared with the risk of nontreatment. Also, evidence indicates Kawasaki disease produces altered lipid metabolism that persists beyond the clinical resolution of the disease.

Blau Syndrome is an autosomal dominant genetic inflammatory disorder which affects the skin, eyes, and joints. It is caused by a mutation in the NOD2 (CARD15) gene. Symptoms usually begin before the age of 4, and the disease manifests as early onset cutaneous sarcoidosis, granulomatous arthritis, and uveitis.

About 37 million people are infected with this parasite; about 300,000 of those had been permanently blinded. As of 2008, about 99% of onchocerciasis cases occurred in Africa. Onchocerciasis is currently endemic in 30 African countries, Yemen, and isolated regions of South America. Over 85 million people live in endemic areas, and half of these reside in Nigeria. Another 120 million people are at risk for contracting the disease. Due to the vector’s breeding habitat, the disease is more severe along the major rivers in the northern and central areas of the continent, and severity declines in villages farther from rivers. Onchocerciasis was eliminated in the northern focus in Chiapas, Mexico, and the focus in Oaxaca, Mexico, where "Onchocerca volvulus" existed, was determined, after several years of treatment with ivermectin, as free of the transmission of the parasite.

According to a 2002 WHO report, onchocerciasis has not caused a single death, but its global burden is 987,000 disability adjusted life years (DALYs). The severe pruritus alone accounts for 60% of the DALYs. Infection reduces the host’s immunity and resistance to other diseases, which results in an estimated reduction in life expectancy of 13 years.