Feline uveitis:aqueous flare intensity excellent clinical monitor

Q: Please review diagnosis and management of feline uveitis.

A: Dr. Mark P. Nasisse at the 2005 American College of Veterinary Internal Medicine Forum in Baltimore gave a lecture on feline uveitis. Some relevant points in this lecture are provided below.

The most sensitive indicator of intra-ocular inflammation is decreased intraocular pressure that is attributable to decreased aqueous humor production and increased uveoscleral outflow. The clinical sign frequently described is aqueous flare. Changes in iris surface topography and pupil size and shape are seen in uveitis of any cause and represent the accumulation of inflammatory cells or fluid in the iris stroma. Iris color change is a frequent concomitant finding. Chronic uveitis may include focal iridal nodules that represent aggregates of lymphocytes and plasma cells as may the proliferation of small vessels upon the iris surface. Uveitis is typically accompanied by pain that is manifested most commonly by squinting and reflex tearing. Secondary glaucoma, usually attributable to changes in the outflow pathway, is common sequelae to chronic uveitis.

Causes

Although in the strictest sense uveitis may result from any insult that damages the uveal tissues and most cases in the cat are attributable to an infectious agent.

Feline infectious peritonitis virus induces uveitis in primarily young cats (younger than 2 years) with the predominant lesion being a pyogranulomatous inflammatory response in the uveal tract. Although both the anterior and posterior uvea may be affected, anterior segment signs are most often seen clinically. Consistent clinical signs may include aqueous flare, hypopyon, non-specific iridal changes, keratic precipitates and the accumulation of fibrin in the anterior chamber. Posterior segment changes considered highly suggestive of FIP are retinal perivasculitis and pyogranulomatous chorioretinitis. Because systemic infection typically involves the kidneys, liver, spleen, lungs and central nervous system, systemic illness is a common component to the ocular disease.

The feline immuno-deficiency virus is a lentivirus of the Retroviridae family that is increasingly recognized as a cause for chronic immunodeficiency in cats. The ocular manifestations are typically in older cats (older than 5 years), and the most conspicuous changes are seen in the anterior segment. This infection is one of chronic, relatively mild uveitis and abnormalities include aqueous flare, keratic precipitates, incipient cortical cataracts, iridal hyperemia and the formation of iridal lymphocytic-plasmacytic nodules. Because of the clinical subtlety of the ocular diseases, owners often do not notice a problem until glaucoma becomes the presenting complaint.

The accumulation of inflammatory cells in the anterior vitreous humor in close approximation to the ciliary body is a common concomitant finding. The specificity of this lesion for FIV infection is uncertain because cats with this finding test negative for the virus. Cats with FIV-associated uveitis typically develop systemic signs of the infection months to years following the recognition of the ocular disease. It is unknown whether the ocular findings reflect a direct effect of the virus or that of secondary opportunistic pathogens.

The recent demonstration that IgM titers to the Toxoplasma gondii can be found in many uveitis-affected cats has led to heightened interest in Toxoplasma gondii as a cause of feline uveitis. The organism is ubiquitous, and serologic evidence suggests that many cats have been exposed to it. Ocular disease occurs when sporozoites released from sporulated oocysts or ingested cysts hematogenously spread to the eye. Toxoplasmosis causes a granulomatous chorioretinitis and retinal vasculitis. Lymphocytic-plasmacytic anterior uveitis also occurs with clinical signs including aqueous flare, iridal changes and keratic precipitates. Pulmonary and central nervous system infection are the most common systemic manifestations of the disease. The clinical course of Toxoplasma uveitis tends to be chronic and an association with systemic immunosuppression occurs.

Although systemic mycoses are relatively uncommon in cats, depending to some extent on geographic location, most have been reported to produce ocular manifestations, including cryptococcosis (Cryptococcus neoformans), histoplasmosis (Histoplasma capsulatum), blastomycosis (Blastomyces dermatitidis) and coccidioidomycosis (Coccidioides immitis).

While subtle features of these diseases may differ, their ocular manifestations have in common the hematogenous dissemination from a primary pulmonary site of infection to the posterior uvea and the formation of a granulomatous chorio-retinitis. Anterior segment involvement can also occur.

Uveitis of undetermined origin is a cause for uveitis that can often not be found by routine hematologic or serologic tests, especially in older cats in which the uveitis had been present chronically. The typical clinical signs of this idiopathic uveitis are mild to moderate aqueous flare, keratic precipitates, iris color change and iridal nodules representing mono-nuclear inflammatory cell infiltrates (lymphocytes and plasma cells). The uveitis is either unilateral or bilateral, and secondary glaucoma seems to be an inevitable sequelae. Recently, serologic evidence has suggested feline herpesvirus-1 and Bartonella species may be causes of chronic uveitis in cats.

Treatment

Corticosteroids remain the primary treatment of uveal inflammation. Topical therapy is the route of choice in most cases, as effective anterior uveal concentrations are easily achieved. It is imperative that uveitis be treated with cortico-steroids with the ability to penetrate the epithelial barrier of the cornea. 1 percent prednisolone acetate suspension or 0.1 percent dexamethasone is an excellent topical steroid choice. The routine initial frequency in moderately severe cases is four-times daily and then reduced to a maintenance frequency of one to two times daily after the clinical signs have subsided or resolved (usually within two to three weeks). In acute severe anterior uveal inflammation topical therapy as frequent as every one to two hours is sometimes necessary. The intensity of aqueous flare is an excellent clinical monitor of the effectiveness of therapy. Subconjunctival corticosteroids (1-2 mg betamethasone) are also highly effective but are generally reserved for cases in which the uveitis is unusually severe, or when owner compliance with topical therapy cannot be expected. Needless to say, subconjunctival therapy must be used with caution in the face of systemic infectious diseases, particularly mycoses. Systemic corticosteroids are usually not indicated unless the posterior segment is involved, and the cause is non-infectious in nature.

Specific antimicrobial therapy is a critical adjunct to palliative anti-inflammatory therapy in cases in which the uveitis can be attributed to a susceptible organism. For toxoplasmosis, clindamycin hydro-chloride (25 mg/kg daily in divided oral doses) may be beneficial; however, the use of antimicrobial therapy for Toxoplasma-associated uveitis remains controversial. The prognosis for uveitis secondary to systemic mycoses is generally poor. Cures from histoplasmosis and cryptococcosis have been noted with imidazole therapy. Effective specific therapy for FIP and FIV infection has not been reported. On the basis of the serologic information suggesting a role for Bartonella species as a cause of uveitis in cats, azithromycin therapy (10 mg/kg PO daily for 21 days) has been advocated for treating cats with this uveitis.

Cycloplegic therapy is not routinely indicated in feline uveitis because the disease is rarely associated with significant miosis. Atropine solution should be avoided in cats because it invariably travels the short nasolacrimal duct to induce copious salivation. n

Dr. Hoskins is owner of DocuTech Services. He is a diplomate of the American College of Veterinary Internal Medicine with specialities in small animal pediatrics. He can be reached at (225) 955-3252, fax: (214) 242-2200, or e-mail: jdhoskins@mindspring.com