Diagnosis includes dilated fundus examination to rule out posterior uveitis, which presents with white spots across the retina along with retinitis and vasculitis.

Laboratory testing is usually used to diagnose specific underlying diseases, including rheumatologic tests (e.g. antinuclear antibody, rheumatoid factor, angiotensin converting enzyme inhibitor <-- error) and serology for infectious diseases (Syphilis, Toxoplasmosis, Tuberculosis).

Major histocompatibility antigen testing may be performed to investigate genetic susceptibility to uveitis. The most common antigens include HLA-B27, HLA-A29 (in birdshot chorioretinopathy) and HLA-B51 (in Behçet disease).

Radiology X-ray may be used to show coexisting arthritis and chest X-ray may be helpful in sarcoidosis.

Intraocular pressure should be measured as part of the routine eye examination.

It is usually only elevated by iridocyclitis or acute-closure glaucoma, but not by relatively benign conditions.

In iritis and traumatic perforating ocular injuries, the intraocular pressure is usually low.

The prognosis is generally good for those who receive prompt diagnosis and treatment, but serious complication including cataracts, glaucoma, band keratopathy, macular edema and permanent vision loss may result if left untreated. The type of uveitis, as well as its severity, duration, and responsiveness to treatment or any associated illnesses, all factor into the outlook.

In an eye with iridocyclitis, (inflammation of both the iris and ciliary body), the involved pupil will be smaller than the uninvolved, due to reflex muscle spasm of the sphincter muscle of the iris.

Generally, conjunctivitis does not affect the pupils.

With acute angle-closure glaucoma, the pupil is generally fixed in mid-position, oval, and responds sluggishly to light, if at all.

Shallow anterior chamber depth may indicate a predisposition to one form of glaucoma (narrow angle) but requires slit-lamp examination or other special techniques to determine it.

In the presence of a "red eye", a shallow anterior chamber may indicate acute glaucoma, which requires immediate attention.

The cornerstone of diagnosis is an accurate history, and a good clinical examination of the eye, to eliminate traumatic uveitis. Ultrasonography is a useful tool, as it can detect a thickened iris, but only in the hands of an expert.

Diagnosis is made by an ophthalmologist or optometrist based on the clinical presentation. One indication can be the Amsler sign, which is the presence of blood (hyphema) in the aspirated vitreous fluid, in paracentesis of the anterior chamber. This is caused due to iris atrophy usually seen in FHI and exposure of the fragile iris vasculature to the vitreous fluid. The sudden change of pressure in the anterior chamber upon suction induced by the paracentesis, or during a cataract surgery, causes bursting of the fragile superficial iris capillaries resultsing in micro-bleeding. This is one clinical diagnostic sign of FHI slit lamp examination shows stringy keratic precipitates

Patients usually do not require treatment due to benign nature of the disease. In case cataract develops patients generally do well with cataract surgery.

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.

During an acute flare-up, therapy is targeted at reducing the inflammation present, and dilating the pupil. Mydriasis is important, as pupillary constriction is the primary reason for pain. Anti-inflammatory therapy is usually given both systemically, often in the form of flunixin meglumine, and topically, as prednisolone acetate. The mydriatic of choice is atropine. In the periods between acute attacks, no therapy has been shown to be beneficial.

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.

Ophthalmic examination may reveal neovascularization (creation of new vessels in the retina), retinal vessel narrowing, retinal vessel cuffing, retinal hemorrhage, or possible vitritis (inflammation of the vitreous body) or choroiditis (inflammation of the choroid).

Retinal vasculitis is very rare as the only presenting symptom. Often there is sufficient systemic evidence to help the physician decide between any one of the aforementioned possible systemic diseases. For those patients who present with only vasculitis of the retinal vessels, great investigative effort (Chest X-ray, blood test, urinary analysis, vascular biopsy, ophthalmology assessment, etc.) should be undertaken to ensure that a systemic disease is not the hidden culprit.

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

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.

FDG positron emission tomography (PET) may be useful to detect the condition early. Other imaging studies including MRI, CT scans, and X-rays may reveal inflammation and/or damaged cartilage facilitating diagnosis.

A differential diagnosis should be taken into account with the following main RP manifestations.

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.

Studies show a moderate neutrophilia (less than 50%), elevated ESR (greater than 30 mm/h) (90%), and a slight increase in alkaline phosphatase (83%). Skin biopsy shows a papillary and mid-dermal mixed infiltrate of polymorphonuclear leukocytes with nuclear fragmentation and histiocytic cells. The infiltrate is predominantly perivascular with endothelial-cell swelling in some vessels, but vasculitic changes (blood clots; deposition of fibrin, complement, or immunoglobulins within the vessel walls; red blood cell extravasation;inflammatory infiltration of vascular walls) are absent in early lesions.

Perivasculitis occurs secondarily, because of cytokines released by the lesional neutrophils. True transmural vasculitis is not an expected finding histopathologically in SS.

A physical examination will demonstrate many of the features listed above.

Blood tests

- Complete blood count may reveal normocytic anemia and eventually thrombocytosis.

- Erythrocyte sedimentation rate will be elevated.

- C-reactive protein will be elevated.

- Liver function tests may show evidence of hepatic inflammation and low serum albumin levels.

Other optional tests include:

- Electrocardiogram may show evidence of ventricular dysfunction or, occasionally, arrhythmia due to myocarditis.

- Echocardiogram may show subtle coronary artery changes or, later, true aneurysms.

- Ultrasound or computerized tomography may show hydrops (enlargement) of the gallbladder.

- Urinalysis may show white blood cells and protein in the urine (pyuria and proteinuria) without evidence of bacterial growth.

- Lumbar puncture may show evidence of aseptic meningitis.

- Angiography was historically used to detect coronary artery aneurysms, and remains the gold standard for their detection, but is rarely used today unless coronary artery aneurysms have already been detected by echocardiography.

- Temporal artery biopsy

Kawasaki disease can only be diagnosed clinically (i.e., by medical signs and symptoms). No specific laboratory test exists for this condition. It is difficult to establish the diagnosis, especially early in the course of the illness, and frequently children are not diagnosed until they have seen several health-care providers. Many other serious illnesses can cause similar symptoms, and must be considered in the differential diagnosis, including scarlet fever, toxic shock syndrome, juvenile idiopathic arthritis, and childhood mercury poisoning (infantile acrodynia).

Classically, five days of fever plus four of five diagnostic criteria must be met to establish the diagnosis. The criteria are:

1. erythema of the lips or oral cavity or cracking of the lips

2. rash on the trunk

3. swelling or erythema of the hands or feet

4. red eyes (conjunctival injection)

5. swollen lymph node in the neck of at least 15 mm

Many children, especially infants, eventually diagnosed with Kawasaki disease, do not exhibit all of the above criteria. In fact, many experts now recommend treating for Kawasaki disease even if only three days of fever have passed and at least three diagnostic criteria are present, especially if other tests reveal abnormalities consistent with Kawasaki disease. In addition, the diagnosis can be made purely by the detection of coronary artery aneurysms in the proper clinical setting.

The clinical differential diagnosis includes pyoderma gangrenosum, infection, erythema multiforme, adverse drug reactions, and urticaria. Recurrences are common and affect up to one third of patients.

Diagnosis of JIA is difficult because joint pain in children can be from many other causes. No single test can confirm the diagnosis, and most physicians use a combination of blood tests, X-rays, and clinical presentation to make an initial diagnosis of JIA. The blood tests measure antibodies and the rheumatoid factor. Unfortunately, the rheumatoid factor is not present in all children with JIA. Moreover, in some cases, the blood work is somewhat normal. X-rays are obtained to ensure that the joint pain is not from a fracture, cancer, infection, or congenital abnormality.

In most cases, fluid from the joint is aspirated and analyzed. This test often helps in making a diagnosis of JIA by ruling out other causes of joint pain.

New research shows that identifying what type of JIA a child has can help target treatment and lead to more positive outcomes. Identifying the specific biomarkers related to each type of JIA can help form more personalized treatment plans and decrease remission rates.

Children with JIA are more susceptible to cardiovascular disease, depression, sleep disturbance, anxiety and fatigue than healthy individuals. There is also limited information that suggests that children with JIA are at increased risk for malignancies when being treated with TNF blockers.

Prognosis is more positive when gene testing is undergone to identify what subtype of JIA is present in the child. Standardized treatment protocols are in place specific to each subtype of JIA. Treatment is more successful when targeted to the specific subtype of JIA.

Various control programs aim to stop onchocerciasis from being a public health problem. The first was the Onchocerciasis Control Programme (OCP), which was launched in 1974, and at its peak, covered 30 million people in 11 countries. Through the use of larvicide spraying of fast-flowing rivers to control black fly populations, and from 1988 onwards, the use of ivermectin to treat infected people, the OCP eliminated onchocerciasis as a public health problem. The OCP, a joint effort of the World Health Organisation, the World Bank, the United Nations Development Programme, and the UN Food and Agriculture Organization, was considered to be a success, and came to an end in 2002. Continued monitoring ensures onchocerciasis cannot reinvade the area of the OCP.

In 1995, the African Programme for Onchocerciasis Control began covering another 19 countries, mainly relying upon the use of ivermectin. Its goal is to set up a community-directed supply of ivermectin for those who are infected. In these ways, transmission has declined. In 2015, WHO was facilitating launch of an elimination program in Yemen.

In 1992, the Onchocerciasis Elimination Programme for the Americas, which also relies on ivermectin, was launched. On July 29, 2013, the Pan American Health Organization (PAHO) announced that after 16 years of efforts, Colombia had become the first country in the world to eliminate the parasitic disease onchocerciasis. In September 2015, the Onchocerciasis Elimination Program for the Americas announced that onchocerciasis only remained in a remote region on the border of Brazil and Venezuela. The area is home to the Yanomami indigenous people. The first countries to receive verification of elimination were Colombia in 2013, Ecuador in 2014, and Mexico in 2015. Guatemala has submitted a request for verification. The key factor in elimination is mass administration of the antiparasitic drug ivermectin. The initial projection was that the disease would be eliminated from remaining foci in the Americas by 2012.

No vaccine to prevent onchocerciasis infection in humans is available. A vaccine to prevent onchocerciasis infection for cattle is in phase three trials. Cattle injected with a modified and weakened form of "O. ochengi" larvae have developed very high levels of protection against infection. The findings suggest that it could be possible to develop a vaccine that protects people against river blindness using a similar approach. Unfortunately, a vaccine to protect humans is still many years off.

The clinical definition of smallpox is an illness with acute onset of fever equal to or greater than followed by a rash characterized by firm, deep seated vesicles or pustules in the same stage of development without other apparent cause. If a clinical case is observed, smallpox is confirmed using laboratory tests.

Microscopically, poxviruses produce characteristic cytoplasmic inclusions, the most important of which are known as Guarnieri bodies, and are the sites of viral replication. Guarnieri bodies are readily identified in skin biopsies stained with hematoxylin and eosin, and appear as pink blobs. They are found in virtually all poxvirus infections but the absence of Guarnieri bodies cannot be used to rule out smallpox. The diagnosis of an orthopoxvirus infection can also be made rapidly by electron microscopic examination of pustular fluid or scabs. All orthopoxviruses exhibit identical brick-shaped virions by electron microscopy. If particles with the characteristic morphology of herpesviruses are seen this will eliminate smallpox and other orthopoxvirus infections.

Definitive laboratory identification of variola virus involves growing the virus on chorioallantoic membrane (part of a chicken embryo) and examining the resulting pock lesions under defined temperature conditions. Strains may be characterized by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Serologic tests and enzyme linked immunosorbent assays (ELISA), which measure variola virus-specific immunoglobulin and antigen have also been developed to assist in the diagnosis of infection.

Chickenpox was commonly confused with smallpox in the immediate post-eradication era. Chickenpox and smallpox can be distinguished by several methods. Unlike smallpox, chickenpox does not usually affect the palms and soles. Additionally, chickenpox pustules are of varying size due to variations in the timing of pustule eruption: smallpox pustules are all very nearly the same size since the viral effect progresses more uniformly. A variety of laboratory methods are available for detecting chickenpox in evaluation of suspected smallpox cases.