Epidemiology and Classification of Uveitis

Uveitis is responsible for over 2.8% of blindness in the United States. Each year, 17.6% of active uveitis patients experience a transient or permanent loss of vision, with 12.5% developing glaucoma [4]. The incidence and prevalence of uveitis has been difficult to determine because the disease is not reportable to the health authorities and is treated in an ambulatory setting. More recently, the epidemiology of the disease in the US has been affected by the aging of the population, racial diversity and an increasing incidence of autoimmune disease. Historically, an incidence rate of 17/100,000 person-years and a prevalence ratio of 204/100,000 over a 10-year period has been reported [5]. However, a recent report from the Northern California Epidemiology of Uveitis Study [6] suggested a higher disease rate for the older population, particularly women, with a higher incidence of chronic disease. Recurrence rates after an initial episode of uveitis in Great Britain showed that 11.3% of patients had at least one recurrence within 5 years, with 2.5% experiencing a second recurrence during this period [7].

In an attempt to more precisely clarify this group of diseases, the International Uveitis Study Group proposed both an anatomic and etiologic classification of uveitis, as well as other descriptive terms of the disease [8]. The location of the primary focus of inflammation, taking into account spillover either to the anterior or posterior segment of the eye, is used to describe the inflammation as anterior (e.g. iritis and iridocyclitis), intermediate (e.g. pars planitis), posterior (e.g. toxoplasmosis) or panuveitis (e.g. diffuse). Other ocular on non-ocular findings do not influence the anatomic classification of uveitis. Important descriptive terms to accurately describe uveitis include the duration of the disease - i.e. acute, <3 months in duration, or chronic, >3 months in duration - and the recurrence of the disease - i.e. with multiple episodes; the term recurrence is used to signal the return of intraocular inflammation after a period of quiescence.

Uveitis is etiologically classified as either infectious or non-infectious. The predominant form of the disease is felt to be non-infectious - specifically, autoimmune for AU. HLA-B27-associated acute AU is the most common form of non-infectious uveitis that occurs in genetically predisposed individuals. This allele is frequently associated with acute AU in conjunction with a spondyloarthropathy, such as anklyosing spondylitis. Although the B27 AU is felt to be autoimmune in origin, there is some evidence that a microbial trigger for the disease may exist - specifically, certain species of Klebsiella, Salmonella, Shigella, Yersinia and Chlamydia trachomatis have been implicated [9]. This has recently focused attention on the role of Toll-like receptors (TLRs) within the eye and the pathogen-associated molecular patterns on these and other microorganisms [10]. For example, the resistance of C3H/HeN mice to endotoxin-induced uveitis (EIU) by lipopolysaccharide (LPS) resides in a point mutation within the coding region of the Tlr4 gene, which results in a functional disruption of Tlr4 signalling [11, 12].

Infectious causes of uveitis include viruses, bacteria, protozoa, parasites and rickettsiae. Typical organisms involve Toxoplasma gondii, Histoplasma capsulatum, Toxocara canis, cytomegalovirus, Borrelia burgdorferi, and Mycobacterium tuberculosis, for example. Most recently, a presumed viral etiology (i.e. rubella) for a form of AU, namely Fuchs heterochromic cyclitis, has been reported [13]. There is a lingering suspicion that many cases of AU are the result of infection with a pathogen that has not been recognized or is difficult to identify.

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