White dot syndromes

[2] There are many theories for the etiology of white dot syndromes including infectious, viral, genetics and autoimmune.

The cause is generally unknown, but a viral illness has been reported prior to multiple evanescent white dot syndrom in one-third of cases.

[1][3][4] Some discrepancy exists as to whether acute zonal occult outer retinopathy is considered a white dot syndrome.

Acute zonal occult outer retinopathy occurs in young to middle age adults and may eventually progress to retinal cell death.

The fundus presents with yellow or gray lesions (white dots) at the level of the choroid and retinal pigment epithelium.

Unlike multiple evanescent white dot syndrome, multifocal choroiditis is a chronic disorder and macular scarring contributes to severe visual loss.

Theories regarding the cause include an exogenous pathogen sensitizing an individual to antigens within photoreceptors, retinal pigment epithelium, or choroid.

Serpiginous choroiditis, also known as geographic or helicoid choroidopathy, is an uncommon chronic progressive inflammatory condition affecting adult men and women equally in the second to seventh decades of life.

[7] In contrast, white dots appear later in the disease stages of birdshot choroidopathy, serpiginous choroiditis, and acute posterior multifocal placoid pigment epitheliopathy.

The white dots in these diseases may be present throughout the entire fundus, larger (50 to 500 μm), and tend to clump together.

Benezra has theorized that a large amount of CD8+ T suppressor cells are observed in the later stages of the disease in order to down regulate the inflammatory immune reaction.

[6] One cause of the White Dot Syndromes as suggested by Gass involves viral or infectious agents.

Specifically pertaining to the 'AZOOR complex,' Gass has postulated that a virus may enter the retina at the optic head and the infection may spread from one photoreceptor to another.

"[11] An important aspect of this hypothesis pertains to the existence of common non-disease genes that predispose patients to autoimmune diseases.

Jampol and Becker insinuate that 'common susceptibility genes' are present in patients affected by white dot syndromes.

The presence of environmental triggers, such as viral infections, immunizations, and stress, and interactions with other genes contribute to the development of the white dot syndromes.

This is supported by the difficulty in detecting "retinal autoantibodies" in patients with acute zonal occult outer retinopathy.