Connecticut Uveitis Foundation

Etiology can be divided into idiopathic, infectious, and noninfectious causes. Infecting organisms include herpes simplex virus (HSV), herpes zoster virus, CMV, HIV, Lyme disease, toxoplasmosis, TB, syphilis, and histoplasmosis. Noninfectious causes include seronegative arthropathies, inflammatory bowel disease, autoimmune disorders, sarcoidosis, multiple sclerosis, and eye trauma.

Acute anterior uveitis may be idiopathic, or associated with HLA-B27-related disease or viral eye disease. One study found that 49.4% of patients with anterior uveitis tested positive for the HLA-B27 antigen. [9] Posterior uveitis is associated with localized infections or systemic infection, or systemic inflammatory disease. Rarely, uveitis can be caused by a previous eye injury or underlying neoplasm.

 

Insults to ocular structures, such as trauma or infection, lead to an inflammatory response within the uvea. Traumatic eye injury results in ocular inflammation due to a breakdown of the blood-brain barrier. Release of potent inflammatory mediators (prostaglandins and leukotrienes) leads to vascular leakage and the influx of inflammatory cells. Uveitis may also result from infectious disease. Micro-organisms cause intraocular damage either by direct lysis of host cells or by producing endotoxins or exotoxins toxic to the ocular microenvironment. These breakdown products induce the recruitment of host inflammatory cells (neutrophils and macrophages) and associated production of free radicals and enzymes to eliminate the infectious organism. In the process, further tissue damage occurs. Ocular inflammation is also associated with immunologic disorders. An autoimmune attack begins with an antigen-specific immune response (T cells and B cells) to ocular antigens. Autoantibodies may bind specific antigens, as in peripheral ulcerative keratitis and ocular cicatricial pemphigoid, and complement is activated and macrophages are recruited to the site. This leads to direct tissue damage. In contrast, an autoimmune response may lead to immune complex formation and deposition in the blood vessels and activation of the immune response. Immune complexes appear to be involved in SLE, Wegener granulomatosis, and other vasculitides. Finally, an autoimmune uveitis can occur via a cell-mediated mechanism in which autoreactive T-cells recognize self-antigen and lead to tissue damage by direct infiltration and production of cytokines, amplifying the immune response.