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Canine Anterior Uveitis

Canine Anterior Uveitis

3 CE CE Article CREDITS

Canine Anterior

Brett Wasik, DVM, DACVIM-SAIM VCA Animal Diagnostic Clinic Dallas, Texas

Elizabeth Adkins, DVM, MS, DACVOa Hope Center for Advanced Veterinary Medicine Vienna, Virginia

Abstract: Canine anterior uveitis can be a debilitating, painful, vision-threatening disease. Several local and systemic diseases can cause anterior uveitis. Because the is limited in its ability to respond to injury, different diseases produce similar clinical signs, making an etiologic diagnosis difficult but imperative to improve the likelihood of a successful outcome. A thorough his- tory and complete ocular and physical evaluations are necessary to ensure timely and accurate diagnosis. This article reviews the pathophysiology, most common causes, diagnostic recommendations, current therapeutic options, potential complications, and prognosis for canine anterior uveitis.

nterior uveitis is a painful, inflammatory disorder endothelium of the iridal blood vessels. Tight junctions join- that is one of the most frequently observed ocular ing these cells maintain the continuity of the barrier. When diseases in dogs.1 Intrinsic ocular abnormalities and the BAB is breached as a result of uveal , pro- A 2 multiple systemic diseases can trigger its development. tein and blood cells leak into the fluid medium of the eye, Establishing the etiology is essential because inappropriate resulting in aqueous flare. therapy may result in loss of vision. Appropriate therapy can be curative but sometimes is, at best, long term and pallia- Pathophysiology of Ocular Inflammation tive. Complications are common. Anterior uveitis develops as a result of injury to the ante- rior uveal tract. Pathophysiologic mechanisms responsible Anatomy of the Uveal Tract for this tissue injury include damage by organisms or neo- The is the highly vascular middle layer of the eye, plastic cells spread through the bloodstream from distant located immediately beneath the . It comprises the , anatomic sites or directly to the from adjacent tissues , and . The iris and ciliary body make (e.g., meninges, , upper respiratory tract), tis- up the anterior uveal tract, and the choroid composes the sue damage from exposure to environmental or microbial posterior uveal tract. Uveitis is any inflammatory condition involving all or a portion of these tracts. Iritis and cyclitis FIGURE 1 refer to inflammation of the iris and ciliary body, respectively. Anterior uveitis, or iridocyclitis, is present when both the iris and ciliary body are inflamed. Posterior uveitis denotes inflammation of the ciliary body and choroid. Further clas- sification is based on duration (acute, chronic, recurrent), pathology (e.g., granulomatous, suppurative), and cause (e.g., traumatic, infectious, neoplastic, immune-mediated).3 The blood–aqueous barrier (BAB) plays an important ana- tomic role in the development of anterior uveitis. Normally, this selectively permeable barrier prevents the influx of blood and proteins into the aqueous humor. It is formed by

the nonpigmented epithelium of the ciliary body and the Multifocal iridal hemorrhages and in the right aDr. Adkins discloses that she has served as a consultant for eye of a young, mixed-breed dog with immune-mediated ­Covance Inc. hemolytic anemia. Flash artifact present.

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table 1 Differential Diagnosis of Canine Anterior Uveitis

Intraocular Aqueous Fluorescein Condition Ocular Redness Miosis/ Pain Discharge Pressure Flare Dye Uptake

Uveitis Intense ciliary flush just posterior Miosis of affected eye Present in Thin to no Decreased Present Absent to the limbus affected discharge eye Diffuse congestion of large, Mydriasis of affected eye Present in Thin to no Elevated Present Absent deep episcleral vessels; some affected discharge congestion of superficial eye conjunctival vessels Ulcerative Similar to pattern described for Normal if simple; Present in Profuse, Normal to Can be Present uveitis miosis if severe and affected thick decreased if present if secondary uveitis is eye discharge severe keratitis is present; mydriasis if severe secondary glaucoma is present Diffuse reddening of the Normal pupil size Present in Profuse, Normal Absent Absent between small affected thick superficial vessels with thickening eye discharge and folding of conjunctiva; small superficial vessels move with conjunctival manipulation; vessels blanch with topical epinephrine Horner’s Superficial conjunctival hyperemia Miosis, , Absent Absent Normal Absent Absent syndrome may be present , prolapsed third Hyperemia localized to inflamed Normal pupil size Present in Excessive Normal Absent Absent area with local thickening of affected lacrimation episclera and congestion of eye vessels deep to conjunctiva

toxins, immune-mediated mechanisms (FIGURE 1), primary tion, polymorphonuclear cell chemotaxis, increased vascular intraocular neoplasms, trauma, corneal ulceration, and cata- permeability, and smooth-muscle contraction with subse- ract formation.4–6 Tissue injury and the continued presence quent miosis.7 Histamine, prostaglandins, and kinins further of bacteria or viruses or their genetic material results in increase vascular permeability.8 Prostaglandins are power- inflammation. This inflammation, if left unresolved, can ful mediators of intraocular inflammation and can cause damage delicate ocular tissues. miosis, hyperemia, and alterations in IOP.5 Inflammatory The inflammatory mediators that can incite classic ocu- mediators (particularly prostaglandins) cause miosis by their lar changes associated with anterior uveitis (i.e., aqueous direct effects on the iris sphincter.5,7,8 Leukocyte chemotaxis, flare, , hyperemia, miosis, decreased intraoc- phagocytosis, and degranulation are stimulated by comple- ular pressure [IOP]) are the arachidonic acid metabo- ment, the clotting/fibrinolytic systems, and, most impor- lites—prostaglandins, thromboxanes, and leukotrienes. tantly, leukotrienes.8 Tissue destruction is further enhanced Arachidonic acid is released from cell membrane phospho- by release of leukocyte granules and enzymes.9

lipids through the action of phospholipase A2 after tissue injury. Cyclooxygenase converts arachidonic acid to pros- Clinical Signs taglandins, thromboxanes, and prostacyclins, whereas Clinical signs of ocular pain (photophobia, blepharospasm, lipoxygenase converts arachidonic acid into leukotrienes elevation of the nictitating membrane, ) are fre- and hydroperoxy and hydroxyeicosatetraenoic acids.5 In quently observed with anterior uveitis. Aqueous flare, mio- response to the release of these metabolites from cell mem- sis, corneal edema, conjunctival hyperemia, and scleral brane phospholipids, inflammatory cells infiltrate the uveal blood vessel congestion are also commonly documented.6 tract. Platelet-activating factor (PAF) released from damaged The presence of protein and cells in the aqueous humor cells, leukocytes, and mast cells results in platelet aggrega- (flare) is pathognomonic for anterior uveitis.10 Other acute

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FREE Canine Anterior Uveitis CE signs include keratic precipitates, iridal swelling, , Box 1 and .1 Chronic anterior uveitis results in accumulation of toxic Noninfectious Causes of Canine wastes and inflammatory mediators within the aqueous Anterior Uveitis1,6,14–16 humor. These substances damage corneal endothelial cells and disrupt the normal metabolism of the corneal stroma, • -induced uveitis leading to corneal edema.1 Inflammatory debris can accumu- • Trauma late in the aqueous humor drainage channels and increase IOP, predisposing the patient to glaucoma.1 Preiridal fibro- • Idiopathic uveitis vascular membrane formation also contributes to secondary • Primary ocular neoplasia glaucoma. These membranes originate as endothelial buds — Melanocytic tumors from anterior iridal stroma that mature into fibrous or fibro- — Ciliary body tumors vascular membranes and can result in hyphema and glau- coma.11 They are rarely detected clinically and likely form • Secondary ocular neoplasia in response to angiogenic factors released by an ischemic — , neoplasms, or leukocytes involved in ocular inflam- — Hemangiosarcoma — Mammary carcinoma mation.11 As the pupillary margin becomes adhesive due to — Oral malignant chronic inflammation, anterior and posterior synechiae may form. Iris hyperpigmentation, , and deep corneal • Corneal ulceration vascularization can also be consequences of chronic inflam- • Pigmentary uveitis of golden retrievers mation of the anterior uvea.1 Ocular redness, miosis, pain, and discharge can have • Uveodermatologic syndrome many other causes, including glaucoma, ulcerative keratitis, conjunctivitis, Horner’s syndrome, and episcleritis. Therefore, a thorough ocular examination consisting of a Schirmer tear eye with active inflammation, as it may further exacerbate test (STT), fluorescein dye application, tonometry, pupillary inflammation. Aqueous humor obtained by aqueocentesis dilation (if IOP is not elevated), biomicroscopy, can be used for cytologic examination, microbial culture and and funduscopy is necessary to distinguish between these sensitivity testing, genetic evaluation with polymerase chain diseases and anterior uveitis. Reductions in IOP can be an reaction (PCR), and antibody titer determination.13 early but subtle indication of anterior uveitis.6 The decrease in IOP results from reduced production of aqueous humor Etiology due to cyclitis. Concomitantly, increases in uveoscleral aque- Causes of anterior uveitis can be noninfectious or infec- ous humor outflow further decrease IOP. The type of ves- tious1,6,14–16 (BOXES 1 and 2). Noninfectious disease processes sels involved (superficial, mobile conjunctival versus deeper, account for most known causes of anterior uveitis.1 Lens- immobile scleral), magnitude of increase or decrease of IOP induced uveitis (LIU), trauma, idiopathic anterior uveitis, from the normal range, presence of fluorescein dye uptake intraocular neoplasia, corneal ulceration, pigmentary uveitis on the , presence of aqueous flare, presence or of golden retrievers, and uveodermatologic syndrome are absence and consistency of ocular discharge, and presence examples of noninfectious causes of anterior uveitis. Many or absence of photophobia (pain) all aid in differentiating of these etiologies can be identified by evaluation of signal- anterior uveitis from the other diseases8 (TABLE 1). ment, history, and results of thorough physical and ocular examination. Diagnostic Testing Investigation into possible infectious causes can be frus- In addition to performing a complete physical and ocular trating because it is difficult to make an etiologic diagnosis examination, clinicians must obtain a detailed and thorough by ocular examination alone. Appropriate diagnostic test- history.12 The client should be asked about the patient’s travel ing can be performed based on the most likely diseases or history, vaccination status, tick exposure/prophylaxis, trauma, syndromes for each case. Geographic location should also and heartworm prophylaxis. Appropriate tests include hemog- be considered when ranking etiologies, as some infectious raphy, a serum biochemistry panel, urinalysis, and serologic diseases are more prevalent in certain areas. For example, testing (if infectious disease is suspected) as dictated by the blastomycosis is more common in young adult dogs in the history, physical and ocular findings, geographic location, Mississippi and Ohio River valleys, whereas coccidioidomy- and travel history.12 Aqueocentesis may be considered as a cosis is more prevalent in the desert regions of the south- final diagnostic option after exhausting other testing modali- western United States and in the southeastern ties. This is a low-yield test that is contraindicated in a sighted coastal regions.17

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Box 2 FIGURE 2 Infectious Causes of Canine Anterior Uveitis1,6,14–16

Rickettsial • Ehrlichia canis • Rickettsia rickettsii

Mycotic • Blastomyces dermatitidis • Histoplasma capsulatum • Coccidioides immitis • Cryptococcus neoformans • Aspergillus spp Late immature in a young mastiff resulting in Algal lens-induced uveitis. Note the diffuse conjunctival hyperemia, • Prototheca zopfii epiphora, and miosis. There is a 360° at the limbus. • Prototheca wickerhamii 1+ aqueous flare (not seen in this photo) was detected via slit-lamp microscopy. Flash artifact can be seen. Bacterial • Leptospira spp Anterior uveitis secondary to cataract formation can occur • Borrellia burgdorferi in patients with diabetes mellitus. These cataracts are bilat- • Brucella canis erally symmetrical and result from well-described alterations • Bartonella vinsonii subsp berkhoffi in the lens metabolic pathways.6 Due to their osmotic activ- • Bacteremia/septicemia6 ity and rapidly progressive nature, canine diabetic cataracts result in lens intumescence and subsequent leakage of lens Parasitic protein, leading to anterior uveitis.6 • Dirofilaria immitis14 In phacoclastic LIU, zonal inflammation involving intra­ • Leishmania spp15,16 lenticular and perilenticular fibroplasia develops • Toxocara spp1,6 following rupture of the lens capsule.19 Eyes examined early in the onset of clinical signs are likely to have fibrinopuru- Viral lent anterior uveitis; older lesions are dominated by fibro- • Infectious canine hepatitis1 plasia. Phacoclastic uveitis is resistant to antiinflammatory therapy but does respond to early removal of the injured lens.20 Features that may aid in the clinical diagnosis of pha- Noninfectious Causes of Anterior Uveitis coclastic uveitis include historical or physical evidence of Lens-Induced Uveitis ocular penetration, poor response to symptomatic therapy, LIU is an inflammatory response of the ocular uvea to lens and patient age (more prevalent in young dogs, some <1 protein. Under normal conditions, a low concentration of year of age).19 Histopathology can aid in diagnosis because circulating lens protein is chronically present in the eye to the zonal, perilenticular nature of inflammation, intralen- maintain immunologic tolerance to lens antigen by T cells.18 ticular leukocytes, and magnitude of fibroplasia are specific Two distinct types of LIU exist in dogs, phacolytic and to uveitis secondary to lens capsular rupture.19 phacoclastic.8,19 Phacolytic uveitis involves slow leakage of Spontaneous lens capsule rupture has been documented. small amounts of lens protein through an intact lens cap- Rupture is usually equatorial with varying degrees of associ- sule of a resorbing cataract (FIGURE 2).8,19 This incites a mild ated phacoclastic uveitis in diabetic dogs with intumescent lymphocytic–plasmacytic anterior uveitis that can clinically cataracts.21 Spontaneous posterior lens capsule rupture has resemble idiopathic uveitis.19 A presumptive etiologic diag- also been observed in nondiabetic patients with cataracts.22 nosis can be made by considering the history of cataract formation with subsequent development of anterior uveitis. Trauma This type of LIU is frequently observed in dogs presenting Uveal contusion and may occur sec- for cataract surgery and often responds well to antiinflam- ondary to blunt or penetrating ocular trauma. Additional matory therapy.19 lesions include conjunctival hyperemia, corneal edema, iris

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FREE Canine Anterior Uveitis CE vascular congestion, miosis, fibrin and table 2 Drugs Used to Treat Canine Anterior cellular debris in the anterior chamber, Uveitis5,13,59,66 and hypotony.6 The physical and ophthal- mologic examination, a detailed history, Drug Class Drug Dose and ultrasonographic imaging (if avail- Topical drugs able) can aid in establishing the extent of acetate q1–12h ocular trauma. (1% suspension) Idiopathic NSAIDs Flurbiprofen q6–12h Idiopathic uveitis is diagnosed in almost (0.03% solution) 60% of dogs evaluated for anterior uveitis Suprofen (1% solution) q6–12h unrelated to trauma, hypermature cata- ract, neoplasia, or infectious disease.23 Ketorolac (0.5% solution) q6–12h These dogs are generally middle-aged, Diclofenac (0.1% solution) q6–12h spayed or neutered, and have no evi- dence of systemic disease. Unilateral Mydriatic/cycloplegic drugs sulfate (0.5% and q8–24h 1% solution and ointment) ocular involvement is more likely with idiopathic anterior uveitis than with neo- Oral drugs plastic or infectious causes.23 Corticosteroids or 0.5 to 1 mg/kg bid Idiopathic anterior uveitis with concur- prednisolone rent exudative has also been documented in dogs.24 This syn- Immunosuppressive drugs Cyclosporine 5 mg/kg bid; adjust dose pending drome results in blindness; acute, severe 12-h whole blood trough level 48 h after initiation of therapy bilateral choroiditis; and variable anterior uveitis with exudative retinal detachment. Azathioprine 2 mg/kg q12h for 2 weeks, then The etiopathogenesis of this syndrome every other day for 2 weeks, then is unknown, but it has been successfully taper to 1 mg/kg every other day treated with high dosages of corticoster- NSAIDs Carprofen ≤2.2 mg/kg q12–24h PRN oids. Ultimately, many patients require additional immunosuppressive therapy Meloxicam ≤0.2 mg/kg once, then ≤0.1 mg/kg such as azathioprine or cyclosporine in q24h thereafter combination with corticosteroids to con- Etodolac ≤15 mg/kg q24h trol clinical signs (TABLE 2). A thorough diagnostic evaluation is necessary before Deracoxib ≤4 mg/kg q24h initiating /immunosuppres- sive treatment to prevent exacerbation of an underlying retrievers.6 Recent evidence has suggested that limbal mela- infectious etiology or neoplastic process. nomas, caudal anterior uveal , and ocular mel- anosis in golden retrievers may also be partly heritable, with Neoplasia the same genetic mutation(s) causally associated with mel- In one study, almost 25% of dogs evaluated for uveitis from anocytic disease at different ocular sites.26 Uveal melanomas, 1989 to 2000 were diagnosed with neoplasia-associated whether benign or malignant, almost always arise from the uveitis.23 Older dogs make up this population; rottweilers anterior uveal tract and have a low incidence of metasta- are most commonly affected, followed by golden retrievers, sis.6,25 Iridal and ciliary body neoplasms are usually heavily Labrador retrievers, German shepherds, and mixed breeds. pigmented and have a low risk of metastasis.27,28 Ocular inflammation is a possible sequela of any is the most common secondary neoplasm23,25 neoplasm.6 Aqueous flare was the most common clinical of the canine , followed by hemangiosarcoma, mam- sign observed in the study, but corneal edema, hyphema, mary carcinoma, and oral malignant melanoma.25 Lymphoma and keratic precipitates were also documented.23 may cause inflammation, iridal thickening, hypopyon, Although relatively rare, primary and secondary ocular hyphema, and glaucoma.4 Cytologic samples for diagno- neoplasms can cause anterior uveitis. Tumors of melano- sis may be procured via aqueocentesis or hyalocentesis if cytic origin are the most common primary ocular tumors in thorough staging or peripheral lymph node aspiration does dogs, followed by epithelial tumors of the ciliary body.6,25 not suffice. Alternatively, tissue may be submitted for histo- Melanocytic tumors may have a heritable basis in Labrador pathologic evaluation following enucleation. Other tumors

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known to metastasize to the eye include seminoma, transi- Some patients develop generalized vitiligo and/or poliosis. tional cell carcinoma of the urinary bladder and/or urethra, Rapidly depigmenting areas tend to become ulcerated and transmissible venereal tumor, anaplastic fibrosarcoma, neu- crusted. Ocular histopathology primarily reveals panuveitis, rogenic sarcoma, rhabdomyosarcoma, and pheochromocy- retinal separation, and prominent pigment-containing mac- toma.6 Bilateral ocular involvement may occur, and varying rophages.6 Skin histopathology reveals interface dermatitis degrees of anterior uveitis and its sequelae may be the pre- with a primarily lichenoid pattern, large histiocytic cells, senting signs.6 One case of intraocular osteosarcoma caus- plasma cells, and small mononuclear cells.6 ing anterior uveitis in a 10-year-old German shepherd has Treatment involves topical or subconjunctival cortico­ been documented.29 steroids, cycloplegics (atropine), and systemic corticoster- oids (prednisone, 1 to 2 mg/kg/d PO) to treat inflammation Corneal Ulceration and dermatologic signs.34 Recurrence is common, and com- Anterior uveitis may occur as an extension of a local process bination therapy consisting of oral corticosteroids and other such as or keratitis.8 It has been proposed that an immunosuppressive drugs (e.g., azathioprine, 2 mg/kg/d) axonal reflex mechanism may be responsible for vasodilata- may be necessary.6 Oral cyclosporine is a reasonable alter- tion and inflammation of the uvea when ulcerative keratitis native to azathioprine when combined with corticosteroids is present.8 to control inflammation TABL( E 2). Topical administration of cyclosporine can be considered, but this drug cannot pen- Breed-Specific Uveitis etrate an intact cornea. Pigmentary uveitis of golden retrievers is presumed to be an inherited form of anterior uveitis. It presents as adhe- Infectious Causes of Anterior Uveitis sions between the iris and lens or peripheral iris and cornea, In a recent retrospective study23 of dogs with anterior uveitis, with pigment dispersion across the anterior lens capsule.30 17.6% were diagnosed with an infectious etiology. In gen- This form of anterior uveitis is not associated with any sys- eral, tick-borne, fungal, algal, and bacterial agents should be temic disorder or infectious etiology.31 The most frequently suspected when evaluating a patient for infectious causes of observed early clinical sign is pigment on the anterior lens anterior uveitis.23 Other systemic signs may accompany ocu- capsule.32 Other clinical signs associated with this disorder lar manifestations, such as generalized lymphadenopathy, include aqueous flare, uveal cysts, fibrin in the anterior pancytopenia, thrombocytopenia, diarrhea, and draining chamber, posterior synechiae, secondary glaucoma, corneal skin lesions.23 Standard-of-care therapy for these etiologic ulcer, hyphema, iris bombé, , retinal degen- agents is briefly discussed here; a more thorough discussion eration or detachment, and uveal neoplasia.32 Diagnosis is of treatment can be found in veterinary internal medicine or based on exclusion of other underlying etiologies. The prog- canine infectious disease texts. nosis is guarded because this disease is progressive and predisposes to secondary glaucoma.32 Tick-Borne Disease Canine monocytic ehrlichiosis is a tick-borne disease caused Uveodermatologic Syndrome by the rickettsial pathogen Ehrlichia canis. E. canis is trans- Uveodermatologic syndrome is a debilitating disease result- mitted primarily by the brown dog tick (Rhipicephalus ing in blindness in many affected dogs.33 Due to its similari- sanguineus) and the American dog tick (Dermacentor vari- ties to Vogt-Koyanagi-Harada (VKH) syndrome in humans, abilis). Ocular lesions are common, and the severity of signs this disease is commonly known as VKH-like disease.6 The varies.35 Ocular signs include conjunctivitis, conjunctival/ cause is unknown, but an immune-mediated etiology is iridal petechiae and ecchymoses, corneal edema, panuveitis, strongly suspected.33 A slightly greater incidence in males hyphema, secondary glaucoma, , and retinal has been suggested, with a likely immunogenetic predis- hemorrhage with detachment.36 Diagnosis of ehrlichiosis position, evidenced by occurrence of this disease in Akitas, requires visualization of morulae, detection of E. canis anti- Samoyeds, Siberian huskies, and Shetland sheepdogs.6 bodies, or PCR amplification of E. canis DNA.37 Ocular signs are usually the first abnormality noted, with Ocular manifestations can also occur with Rocky Mountain most patients being referred for acute-onset blindness or spotted fever (RMSF). RMSF is caused by Rickettsia rick- chronic anterior uveitis.34 Ocular findings range from bilat- ettsii, a gram-negative, obligate intracellular coccobacillus eral anterior uveitis to severe panuveitis, retinal detachment, transmitted primarily by the D. variabilis tick in the eastern posterior synechiae, secondary glaucoma, cataract, and United States and Dermacentor andersonii in the western vision loss.34 Depigmentation of the hair and skin usually United States and Canada. Ocular involvement occurs sec- follows the onset of ocular signs. The , nasal pla- ondary to .38 Clinical signs include conjunctival num, lips, scrotum, and footpads are often affected; depig- vascular injection, anterior uveitis, petechial hemorrhages of mented areas can be generalized or restricted to the face.34 the iris stroma, and bilateral hyphema.39

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An immunofluorescence assay (IFA) detects IgM and IgG and is the “gold standard” in the diagnosis of RMSF. A single Key Facts IFA titer of 1:64 or higher for IgM with concurrent clini- • Canine anterior uveitis is a common ocular disorder that cal signs is considered diagnostic.38 A fourfold rise in IgG is usually idiopathic but can be associated with multiple, between acute and convalescent specimens acquired 3 to 4 serious systemic diseases. weeks apart is also considered diagnostic.38 Standard therapy of ehrlichiosis and RMSF consists of • It can be difficult to distinguish among the various routine supportive care and doxycycline at a minimum dose etiologies of canine anterior uveitis because the eye is of 10 mg/kg/d for 28 days, but 7 days of administration has limited in its ability to respond to injury. 37,40 been shown to be sufficient for RMSF. Tetracyclines and • A thorough history, physical and ocular examinations, 38 fluoroquinolones are also effective in treating RMSF. and routine database (complete blood cell count, serum chemistry analyses, urinalysis) should be obtained to Fungal Disease direct subsequent diagnostic testing and establish a Systemic mycoses can cause anterior or posterior uveitis definitive diagnosis. or panuveitis. Infection with Blastomycosis dermatitidis • Immediate, aggressive therapy is necessary to stop is the systemic mycosis most commonly associated with inflammation, prevent and control complications ocular lesions.12 Approximately 30% to 43% of dogs with secondary to inflammation (glaucoma, cataract systemic blastomycosis have clinical signs of ocular involve- 41 formation, retinal degeneration), relieve pain, and ment. Common ocular abnormalities include conjunctival preserve vision. hyperemia, corneal edema, aqueous flare, iritis, iridocycli- tis, vitritis, , , serous or granulomatous retinal separation, optic neuritis, secondary glaucoma, and rhagic enteritis as the most common clinical sign.46 However, blindness.42 Other fungal organisms proved or suspected to canine protothecosis can present with acute blindness as cause anterior uveitis in dogs include Coccidioides immi- the only sign.47 tis, Cryptococcus neoformans, Aspergillus fumigatus, and In one study, ocular involvement was present in 77% of Histoplasma capsulatum.6,43 All disseminated mycoses result cases of systemic protothecosis.46 Aqueous flare, iritis, epis- in posterior segment disease, but coccidioidomycosis and cleral injection, epiphora, conjunctival hyperemia, low IOP, cryptococcosis predominantly cause posterior segment dis- and hyphema have also been documented.47 Diagnosis is ease without anterior segment involvement.12 confirmed by direct visualization of the organism, cytologic Organisms can be detected by cytopathology of body examination of rectal scrapings, aqueocentesis, or histo- fluids, lymph node aspirates, vitreous humor, or impression pathologic examination of tissue specimens from the colon smears of skin lesions or by histopathologic examination of or regional lymph nodes.46 various tissues, including enucleated eyes.44 Direct visualiza- Successful therapy has yet to be discovered for proto­ tion of the organism remains the gold standard for diagnosis, thecosis.46 Amphotericin B has been successful in slowing but serology may be useful to aid in supporting a diagnosis disease progression but has not been curative.45 Amphotericin when organisms cannot be identified. B (1 mg/kg IV three times weekly to a cumulative dose of Systemic blastomycosis with ocular involvement is treated 12 mg/kg) used in combination with ketoconazole, flucon- with itraconazole at a dose of 5 mg/kg/d PO for a minimum azole, or itraconazole (5 to 10 mg/kg/d PO) is an option for of 60 to 90 days or at least 30 days beyond resolution of long-term therapy of P. zopfii infection, but the prognosis clinical signs.44 Treatment durations of 6 to 12 months are remains grave.46 not unusual. Enucleation may be necessary if severe sec- ondary glaucoma develops.42 can be treated Bacterial and Protozoal Disease with itraconazole (10 mg/kg/d PO) or with amphotericin B.44 has been documented as a cause of panuveitis Fluconazole is the initial drug of choice for coccidioidomy- in one case, with mild hyphema, aqueous flare, and partial cosis (10 mg/kg PO bid) and cryptococcosis (2.5 to 5 mg/kg serous retinal detachments bilaterally.48 Diagnosis can be PO or IV daily or bid).44,45 obtained by evaluation of acute and convalescent micro- scopic agglutination titers (MATs) for the various Leptospira Protothecosis serovarieties. PCR can be performed on blood and urine to Prototheca spp are colorless algae related to the green algae detect leptospiral genetic material. Appropriate clinical signs of the genus Chlorella. Of the four recognized or proposed with elevated serum MATs are the gold standard in diagno- species, Prototheca zopfii and Prototheca wickerhamii have sis.49 Penicillin (25,000 to 40,000 U/kg q12–24h IV or IM for been found to be pathogenic.46 In dogs, protothecosis usu- 14 days), ampicillin (22 mg/kg PO, SC, or IV q8–12h for 14 ally presents as a systemic infection, with protracted hemor- days), or amoxicillin (22 mg/kg PO q8h for 14 days) is given

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to eliminate leptospiremia, followed by doxycycline (5 to 10 secondary glaucoma, and analgesia.8,12 Specific therapies mg/kg PO bid) for 14 days to eliminate the organism from address etiologic agents or contributing factors (e.g., con- the renal tubular cells.50,51 Appropriate therapy is essential junctival or corneal foreign body, , anterior or because infected animals pose a zoonotic threat to human posterior lens luxation) discovered during the initial diag- caretakers.50 nostic evaluation. Nonspecific therapy comprises decreas- Animals infected with Borrelia burgdorferi can present ing intraocular inflammation, inducing mydriasis to prevent with anterior uveitis.52 Uveal inflammation should therefore formation, and initiating to alleviate prompt the clinician to evaluate for borreliosis if other com- pain (TABLE 2). mon causes are eliminated. Brucella canis, a gram-negative Antiinflammatory drug therapy (corticosteroids and coccobacillus found in the vaginal fluid or urine of infected NSAIDs) is an extremely important consideration in treat- dogs, can also produce anterior uveitis.53 Serology can be ing anterior uveitis regardless of its cause because failure to employed in the diagnosis of either borreliosis or brucel- control inflammation leads to serious complications. Topical losis. Doxycycline (10 mg/kg q24h PO for 21 to 28 days) or or systemic administration depends on drug formulation, β-lactam antibiotics such as amoxicillin (22 mg/kg q12h PO severity of clinical signs, and location of inflammation.13 for 21 to 28 days) are effective treatments.54 Anterior uveitis is initially treated topically, but if the inflam- Bartonella spp have been implicated in causing anterior mation remains poorly controlled by topical treatment alone, uveitis.55 In one case, a 2-year-old, spayed spaniel mix was systemic therapy may be required.58 evaluated for bilateral anterior uveitis. All infectious dis- Corticosteroids are the drugs most commonly used to ease titers were normal, except for a 1:512 antibody titer control ocular inflammation, but they are contraindicated to Bartonella vinsonii subsp berkhoffi. Ocular changes in the presence of ulcerative or infectious keratitis.59 Topical attributable to bartonellosis include optic neuritis, anterior corticosteroids can be used to treat anterior uveitis asso- uveitis, vitritis, pars planitis, focal and multifocal retinal ciated with systemic infectious disease without significant vasculitis, retinal white dot syndrome, branch retinal arte- exacerbation of the infectious process.59 Prednisolone ace- riolar or venous occlusions, focal choroiditis, serous reti- tate achieves a high intraocular concentration and is the drug nal detachments, papillitis, and peripapillary angiomatous of choice for anterior uveitis.60 Topically, it is administered lesions.55 Clinical improvement was linked with a posttreat- as a 1% suspension. Frequency of administration depends ment decrease in B. vinsonii subsp berkhoffi seroreactivity. on the severity, location, and etiology of the disease pro- Long-term antibiotic administration (4 to 6 weeks) may be cess. One to six times daily up to hourly administration has necessary to eliminate infection.56 Macrolides (erythromycin, been advocated for the suspension.5,13,59 Effective treatment azithromycin), fluoroquinolones (alone or in combination results in normalization of IOP and decreased photophobia, with amoxicillin), and doxycycline are the initial drugs of blepharospasm, discharge, keratitis, and aqueous flare.59 choice for treating B. vinsonii subsp berkhoffi infection in Systemic corticosteroids may be necessary to supple- dogs.56 ment topical therapy when treating severe cases of anterior Bacteremia or septicemia from any local or generalized uveitis. These drugs have minimal effects on most forms infectious process may result in anterior uveitis. Common of keratitis and control intraocular inflammation when topi- etiologies of ocular inflammation include pyometra, pros- cal corticosteroids are contraindicated.61 Although not pre- tatitis, neonatal umbilical infections, abscesses, bacterial viously reported, I (E. A.) have observed several cases of endocarditis, dental/oral infections, and pyelonephritis.6,12 melting corneal ulcers in dogs receiving immunosuppres- Ocular leishmaniasis, although rare in the United States, sive doses of systemic corticosteroids. These patients should is known to cause anterior uveitis.12,57 Cases have been be monitored for the development of ulcerative keratitis. reported in Texas, Maryland, and Oklahoma, and anti- Therapy is instituted at a higher dose to suppress inflamma- leishmanial antibodies have been detected in asymptom- tion, followed by drug tapering for long-term maintenance. atic animals in Alabama and Michigan.16 Although ocular The recommended initial dose is 0.5 mg/kg PO bid for leishmaniasis is infrequently diagnosed in the United States, antiinflammatory effects, up to 1 mg/kg PO bid for immu- active military dogs or dogs with travel history to or from nosuppressive effects.59 The dose can then be decreased endemic areas such as Europe, Africa, Asia, and Central and incrementally based on patient response. When an infec- South America should be screened for this disease.12 tious disease is suspected, systemic corticosteroids should be used with caution because of their immunosuppressive Treatment effects. Appropriate antimicrobial therapy is recommended Primary therapeutic objectives for treatment of anterior if systemic corticosteroid administration is required in the uveitis should include treatment or elimination of any spe- presence of a bacterial infection. cific etiology, reduction and control of inflammation, pres- Available topical ophthalmic NSAIDs include suprofen ervation of a functional pupil, prevention or treatment of (1%), diclofenac (0.1%), flurbiprofen (0.03%), and ketorolac

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(0.5%). Flurbiprofen and suprofen are similar in their abil- cations; and timeliness/adequacy of treatment.12 Chances ity to reduce ocular inflammation.62 Flurbiprofen is well of recovery are greatest when the inflammation is mild to absorbed into ocular tissues, concentrates in the cornea, and moderate and a treatable underlying cause can be found. has low systemic absorption.63 It can be used in conjunction Severe, recurrent anterior uveitis typically carries the poor- with topical corticosteroids. Adverse effects include topical est long-term prognosis.12 Systemic spirochetal and rickett- irritation and possible hemorrhage as a result of interference sial infections have a good prognosis if treated promptly and with platelet aggregation.64 aggressively, whereas the prognosis for systemic mycotic/ Choices for injectable or oral NSAIDs include aspirin, algal infections and uveodermatologic syndrome is guarded acetaminophen, piroxicam, ketoprofen, meloxicam, carpro- to poor.12 The prognosis is good for most canine primary fen, etodolac, and deracoxib. These drugs are commonly intraocular neoplasms because they are usually benign, used for treatment of anterior uveitis when corticosteroids whereas the outlook for multicentric or metastatic intraocu- are contraindicated.65 Gastrointestinal effects and hepatopa- lar neoplasia remains guarded.6,12 thy are the most significant adverse effects of their use.66 sicca has been reported in dogs receiv- Conclusion ing oral etodolac.67 Canine anterior uveitis is a complex ocular disorder with Cycloplegic drugs relieve pain by preventing ciliary body several etiologies. Understanding the pathophysiology, clini- and iris muscle spasms, whereas mydriatic drugs prevent cal signs, and potential etiologies can guide clinicians to a or break down posterior synechiae by dilating the pupil prompt, accurate diagnosis and appropriate therapy. Proper and decreasing iris–lens contact.13 Cycloplegia and mydria- treatment is essential to alleviate patient discomfort, pro- sis can be accomplished by using a parasympatholytic agent duce rapid recovery, and prevent secondary complications such as atropine sulfate. Atropine is a direct-acting parasym- and permanent undesirable sequelae that may result in patholytic agent that blocks the postganglionic cholinergic blindness or enucleation. receptor response, resulting in mydriasis, cycloplegia, and References 59 decreased tear production. It is often the drug of choice 1. Gwinn RM. Anterior uveitis: diagnosis and treatment. Semin Vet Med Surg (Small in management of inflammation of the anterior segment.59 Anim) 1988;3(1):33-39. Much of the pain associated with anterior uveitis is a result 2. Glaze MB. Ocular manifestations of systemic disease. In: Bonagura JD, ed. Kirk’s Current Veterinary Therapy XI. Philadelphia: WB Saunders; 1992:1061-1070. of inflammation and subsequent spasm of the iridal and cili- 3. Powell CC, Lappin MR. Causes of feline uveitis. Compend Contin Educ Pract Vet ary body musculature.59 Atropine paralyzes these muscles, 2001;23(2):128-141. 5,60 4. Swanson JF. Ocular manifestations of systemic disease in the dog and cat. Vet Clin decreasing discomfort. Atropine also stabilizes the BAB. North Am Small Anim Pract 1990;20(3):849-867. Topical atropine sulfate is formulated in a 1% ointment or 5. Van der Woerdt A. Management of intraocular inflammatory disease. Clin Tech solution. Duration and frequency of application depend Small Anim Pract 2001;16(1):58-61. 6. Diseases and surgery of the canine anterior uvea. In: Gelatt KN. Essentials of Vet- on the severity of inflammation. Mild inflammation may erinary . Philadelphia: Lippincott Williams & Wilkins; 2000:197-225. require once-daily administration, whereas severe inflam- 7. Millichamp NJ, Dziezyc J. Mediators of ocular inflammation. Prog Vet Comp Oph- 13 thalmol 1991;1(1):41-58. mation may require treatment three to four times a day. 8. Hakanson N, Forrester S. Uveitis in the dog and cat. Vet Clin North Am Small Anim Atropine is contraindicated in glaucoma; therefore, IOP Pract 1990;20(3):715-735. should be measured during the course of atropine therapy 9. Howes EL Jr. Basic mechanisms of pathology. In: Spencer WH, ed. Ophthalmic Pa- thology, an Atlas and Textbook. 3rd ed. Philadelphia: WB Saunders; 1985:Vol. 1:1-108. and immediately discontinued if evidence of glaucoma is 10. Hendrix DVH. Differential diagnosis of the . In: Bonagura JD, ed. Kirk’s Cur- observed.5,59 rent Veterinary Therapy XIII. Philadelphia: WB Saunders; 2000:1042-1045. 11. Peiffer RL Jr, Wilcock BP, Yin H. The pathogenesis and significance of pre-iridal fibrovascular membrane in domestic animals.Vet Pathol 1990;27(1):41-45. Complications and Prognosis 12. Kern TJ. Canine uveitis. In: Bonagura JD, ed. Kirk’s Current Veterinary Therapy XII. Intraocular inflammation can have many deleterious seque- Philadelphia: WB Saunders; 1995:1248-1253. 13. Powell CC, Lappin MR. Diagnosis and treatment of feline uveitis. Compend Contin lae; therefore, treatment should be prompt, aggressive, and Educ Pract Vet 2001;23(3):258-266. appropriate. Synechiae formation can lead to glaucoma by 14. Carastro SM, Dugan SJ, Paul AJ. Intraocular dirofilariasis in dogs. Compend Con- tin Educ Pract Vet 1992;14(2):209-215. obstructing aqueous humor flow through the pupil or irido- 15. Torrent E, Leiva M, Segales J, et al. Myocarditis and generalized vasculitis associ- corneal angle. Development of secondary glaucoma should ated with leishmaniosis in a dog. J Small Anim Pract 2005;46:549-552. be suspected when IOP is >10 mm Hg in eyes with ante- 16. Ciaramella P, Corona M. Canine leishmaniasis: clinical and diagnostic aspects. 13 Compend Contin Educ Pract Vet 2003;25(5):358-368. rior uveitis. Anterior uveitis may cause cataracts, the extent 17. Gilger BC. Ocular manifestations of systemic infectious diseases. In: Bonagura JD, of which depends on the severity and duration of inflam- ed. Kirk’s Current Veterinary Therapy XIII. Philadelphia: WB Saunders; 2000:276-279. mation. Corneal endothelial damage from chronic anterior 18. Woerdt A, Nasisse MP, Davidson MG. Lens-induced uveitis in dogs: 151 cases (1985-1990). JAVMA 1992;201(6):921-926. uveitis can cause corneal edema, often followed by deep 19. Wilcock BP, Peiffer RL Jr. The pathology of lens-induced uveitis in dogs. Vet Pathol corneal vascularization and scarring.8 1987;24:549-553. 20. Slatter DH. Fundamentals of Veterinary Ophthalmology. Philadelphia: WB Saun- The prognosis depends on the location, extent, and dura- ders; 1981:439. tion of inflammation; underlying cause; secondary compli- 21. Wilkie DA, Gemensky-Metzler AJ, Colitz CMH, et al. Canine cataracts, diabetes

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mellitus and spontaneous lens capsule rupture: a retrospective study of 18 dogs. Vet a dog. JAAHA 1991;27:427-431. Ophthalmol 2006;9:328-334. 44. Legendre AM, Toal RL. Diagnosis and treatment of fungal disease of the respira- 22. Davidson MG, Nelms SR. Diseases of the canine lens and cataract formation. In: tory system. In: Bonagura JD, ed. Kirk’s Current Veterinary Therapy XIII. Philadelphia: Gelatt KN, ed. Veterinary Ophthalmology. Ames, Iowa: Blackwell Publishing; 2007:859- WB Saunders; 2000:815-819. 881. 45. Cryptococcosis. In: Greene CE, ed. Infectious Diseases of the Dog and Cat. 3rd ed. 23. Massa KL, Gilger BC, Miller TL, et al. Causes of uveitis in dogs: 102 cases (1989- St. Louis: Elsevier Saunders; 2006:584-598. 2000). Vet Ophthalmol 2002;5(2):93-98. 46. Strunck E, Billups L, Avgeris S. Canine protothecosis. Compend Contin Educ Pract 24. Gwin RM, Wyman M, Ketring K, et al. Idiopathic uveitis and exudative retinal de- Vet 2004;26(2):96-102. tachment in the dog. JAAHA 1980;16:163-170. 47. Schultze AE, Ring RD, Morgan RV, et al. Clinical, cytologic and histopathologic 25. Dubielzig RR. Ocular neoplasia in small animals. Vet Clin North Am Small Anim manifestations of protothecosis in two dogs. Vet Ophthalmol 1998;1:239-243. Pract 1990;20(3):837-848. 48. Townsend WM, Stiles J, Krohne SG. Leptospirosis and panuveitis in a dog. Vet 26. Donaldson D, Sansom J, Scase T, et al. Canine limbal melanoma: 30 cases (1992- Ophthalmol 2006;9(3):169-173. 2004). Part 1. signalment, clinical and histological features and pedigree analysis. Vet 49. Sessions JK, Greene CG. Canine leptospirosis: epidemiology, pathogenesis, and Ophthalmol 2006;9(2):115-119. diagnosis. Compend Contin Educ Pract Vet 2004;26(8):606-622. 27. Diters RW, Dubielzig RR, Aguirre GD, et al. Primary ocular melanoma in dogs. Vet 50. Ross LA, Rentko V. Leptospirosis. In: Bonagura JD, ed. Kirk’s Current Veterinary Pathol 1983;20:379-395. Therapy XIII. Philadelphia: WB Saunders; 2000:308-310. 28. Wilcock BP, Peiffer RL. Morphology and behavior of primary ocular melanomas in 51. Sessions JK, Greene CE. Canine leptospirosis: treatment, prevention, and zoono- 91 dogs. Vet Pathol 1986;23:418-424. sis. Compend Contin Educ Pract Vet 2004;26(9):700-706. 29. Van de Sandt RROM, Boeve MH, Stades FC, et al. Intraocular osteosarcoma in a 52. Munger RJ. Uveitis as a manifestation of Borrelia burgdorferi infection in dogs. dog. J Small Anim Pract 2004;45:372-374. JAVMA 1990;197(7):811. 30. Ocular Disorders Presumed to be Inherited in Purebred Dogs. 2nd ed. Phoenix, AZ: 53. Wanke MM. Canine . Anim Reprod Sci 2004;82-83:195-207. Genetic Committee of the American College of Veterinary Ophthalmologists; 1996. 54. Appel MJG, Jacobson RH. CVT update: canine . In: Bonagura JD, ed. 31. Sapienza JS. Pigmentary uveitis in golden retrievers: 43 cases. Proc Annu Meet Kirk’s Current Veterinary Therapy XII. Philadelphia: WB Saunders; 1995:303-309. ECVO 1998:33. 55. 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Ocular manifestations of systemic disease. In: Gelatt KN, ed. Veterinary 58. Collins, BK, Moore CP. Diseases and surgery of the canine anterior uvea. In: Ge- Ophthalmology. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 1999:1401-1504. latt KN, ed. Veterinary Ophthalmology. Philadelphia: Lippincott Williams & Wilkins; 36. Leiva M, Naranjo C, Pena MT. Ocular signs of canine monocytic ehrlichiosis: a ret- 1999:755-795. rospective study in dogs from Barcelona, Spain. Vet Ophthalmol 2005;8(6):387-393. 59. Wilkie DA. Control of ocular inflammation. Vet Clin North Am Small Anim Pract 37. Neer TM, Harrus S. Canine monocytic ehrlichiosis and neorickettsiosis (E. canis, E. 1990;20(3):693-713. chaffeensis, E. ruminatium, N. sennetsu, and Risticii infections). In: Greene CE, ed. In- 60. Corticosteroid therapy. In: Havener WH. Ocular Pharmacology. 5th ed. St. Louis: fectious Diseases of the Dog and Cat. 3rd ed. St. Louis: Saunders Elsevier; 2006:203- CV Mosby; 1983:223-235, 333-334, 433-500. 217. 61. Slatter DH. Fundamentals of Veterinary Ophthalmology. Philadelphia: WB Saun- 38. Low RM, Holm JL. Canine rocky mountain spotted fever. Compend Contin Educ ders; 1981. Pract Vet 2005;27(7):530-538. 62. Stark WJ, Fagadau WR, Stewart RH, et al. Reduction of pupillary constriction dur- 39. Davidson MG, Breitschwerdt EB, Nasisse MP, et al. Ocular manifestations of RMSF ing cataract surgery using suprofen. Arch Ophthalmol 1986;104:364-366. in dogs. JAVMA 1998;194(6):777-781. 63. Anderson JA, Chen CC, Vita JB, et al. Disposition of topical flurbiprofen in normal 40. Neer TM, Breitschwerst EB, Greene RT, Lappin MR. 2002 Consensus statement on and aphakic rabbit eyes. Arch Ophthalmol 1982;100:642-645. ehrlichial disease of small animals from the Infectious Disease Study Group of the AC- 64. Feinstein NC, Rubin B. Toxicity of flurbiprofen sodium. Arch Ophthalmol VIM. American College of Veterinary Internal Medicine. J Vet Intern Med 2002;16:309- 1988;106:311. 315. 65. Miller TR. Anti-inflammatory therapy of the eye. In: Bonagura JD, ed. Kirk’s Cur- 41. Hendrix DVH, Rohrbach BW, Bochsler PN, et al. Comparison of histologic lesions rent Veterinary Therapy XII. Philadelphia: WB Saunders; 1995:1218-1222. of induced by Blastomyces dermatitidis in untreated and treated 66. Giuliano EA. Nonsteroidal anti-inflammatory drugs in veterinary ophthalmology. dogs: 36 cases (1986-2001). JAVMA 2004;224(8):1317-1322. Vet Clin North Am Small Anim Pract 2004;34(3):707-723. 42. Bloom JD, Hamor RE, Gerding PA. Ocular blastomycosis in dogs: 73 cases, 108 67. Klauss G, Giuliano EA, Moore CP, et al. Keratoconjunctivitis sicca associated with eyes (1985-1993). JAVMA 1996;209(7):1271-1274. administration of etodolac in dogs: 211 cases (1992-2002). JAVMA 2007;230(4):541- 43. Gelatt KN, Chrisman CL, Samuelson DA, et al. Ocular and systemic aspergillosis in 547.

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1. Canine anterior uveitis 5. Which statement regarding aqueous c. Oral corticosteroids are preferred over a. presents with distinctive clinical signs. flare is true? topical corticosteroid administration. b. is almost always associated with a sys- a. It is caused by increased protein and/or d. Atropine is always recommended to temic infectious disease. cells in the aqueous humor as a result relieve ocular discomfort. c. is commonly idiopathic. of a disrupted BAB and is pathogno- d. can be treated effectively, easily, and monic for anterior uveitis. 9. Which statement regarding topical drug with a low risk of complications. b. It does not occur in dogs. therapy for treating canine anterior c. It is caused by BAB breakdown in the uveitis is false? 2. The BAB iridocorneal angle. a. Prednisolone acetate suspension (1%) a. is impermeable to constituents within d. It occurs only when glaucoma is is a potent topical corticosteroid used blood and plasma. present. in the treatment of canine anterior b. is not affected in patients with anterior uveitis. uveitis. 6. The most common secondary ocular b. Topical NSAIDs can be used in conjunc- c. is composed of loosely adherent cells neoplasm in dogs is tion with topical corticosteroids. of the ciliary body and iridal blood a. hemangiosarcoma. c. Atropine relieves ocular pain by relax- vessels. b. osteosarcoma. ing uveal muscle spasm. d. leaks fluid, protein, and cells into the c. malignant melanoma. d. Hemorrhage due to interference with aqueous humor when compromised d. lymphoma. platelet aggregation is not a side effect by inflammation, resulting in aqueous of topical NSAID application. flare. 7. Ocular blastomycosis a. can be ruled out by serology. 10. Which statement regarding complica- 3. Which of the following is not a common b. can be treated inexpensively and tions of anterior uveitis is true? mechanism responsible for ocular tissue rapidly. a. Anterior uveitis rarely results in the injury resulting in anterior uveitis? c. is best diagnosed by direct visualization development of glaucoma. a. damage to ocular tissue by infectious of fungal organisms. b. Development of secondary glaucoma organisms d. always results in enucleation of the should be suspected when IOP is >10 b. topical drug administration affected eye. mm Hg in eyes with anterior uveitis. c. immune-mediated mechanisms c. Anterior uveitis does not cause d. neoplastic invasion 8. Which statement regarding treating cataracts. uveitis is true? d. Development of blindness is a concern 4. ______is not a diagnostic differential a. Nonspecific therapy should never be only with chorioretinitis, not anterior for anterior uveitis. employed until a definitive diagnosis is uveitis. a. Endothelial dystrophy made. b. Glaucoma b. The primary goal should be to stop c. Ulcerative keratitis inflammation, relieve pain, and prevent d. Conjunctivitis or control complications.

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