obserVaTions in Peer reviewed answers to What, Where, Why, & When? CORNEAL OPACITIES IN DOGS & CATS Ann R. Strom, DVM, MS, and David J. Maggs, BVSc, Diplomate ACVO University of California–Davis

Welcome to Observations in Ophthalmology, 1 of 2 new columns in this issue of Today’s Veterinary Practice. The articles in this column will provide succinct nuggets of knowledge about common (and sometimes uncommon) ophthalmic conditions seen in general practice. Authors will share clinical tools, including their own approaches to diagnosis and treatment, that practitioners can use to better care for their patients.

The is transparent, densely innervated, appropriate diagnostic tests and prompt initiation of avascular, and the major refractive structure of optimal therapy are required to maximize the chance the eye. a healthy cornea achieves and maintains of saving vision, producing a comfortable and, transparency due to the organization of constituent occasionally, saving the patient’s life. cells and fi bers, as well as its relatively The following questions should be asked when dehydrated state. anything that alters this a patient with a is presented for Tools for organization or deturgescence leads to development evaluation. of a corneal opacity.1 Ophthalmic as the outer and most exposed structure of the QUESTION 1. WHAT IS THE Examinations globe, the cornea is not only at risk for trauma, but APPEARANCE OF THE OPACITY? Fortunately, also often receives close attention from clients. as causes of corneal opacities, which are often seen diagnosis of such, a presenting complaint of corneal opacity is 2 in various combinations, are listed in Table 1. corneal opacities common in veterinary practice. each of these pathologic changes is associated with is possible with correct interpretation of corneal changes is critical a specifi c appearance—especially color. however, just a few pieces for diagnosing corneal disease as well as many of inexpensive other ocular and some systemic diseases. Therefore, equipment. Among these, a dark room, TABLE 1. magnifi cation, and a bright and Causes of Corneal Opacity & Appearance focal light source CAUSES OF CORNEAL APPEARANCE are key for a CORNEAL good ophthalmic OPACITY examination.2 Edema Blue “cobblestoned” appearance Infl ammatory Yellow, green, or tan corneal cell infi ltration stromal opacity Lipid/mineral Silvery white, crystalline, sparkly FIGURE 1. Focal corneal edema secondary deposition opacities; sometimes coalescing to corneal ulceration in a dog. The has creamy or shiny opacities been pharmacologically dilated. Note the loose epithelial edges of the suggestive Fibrosis Grayish white, sometimes feathery or wispy opacity of a superfi cial chronic corneal epithelial defect (SCCED). Resolution was achieved by Melanosis Dark brown to black, variable debridement (using a sterile cotton-tipped density; often with blood vessels applicator) and topically applied antibiotics and Vascularization Variably perfused blood vessels atropine. Courtesy University of California–Davis extending from corneoscleral limbus Comparative Ophthalmology Service

tvpjournal.com | May/June 2015 | Today’s VeTerinary PracTice 105 Peer reviewed obserVaTions in oPhThalMology

assessment of texture, depth, location, pattern, shape, and outline of the region of opacifi cation is also important as some colors can look similar.

Edema a blue, “cobblestoned” appearance of the cornea— whether focal or diffuse—is indicative of corneal stromal edema, and results from loss of corneal epithelial or endothelial cell function. Focal Edema. specifi c causes of focal edema include focal corneal epithelial dysfunction (due to corneal ulceration), or focal endothelial cell damage FIGURE 2. Diffuse corneal edema in a dog with a (due to blunt corneal trauma, luxation, or penetrating corneal cat claw injury and secondary keratic precipitates) (Figure 1, page 105).2 . The wound from the cat claw can be Diffuse Edema. diffuse corneal edema (Figure seen on the ventromedial paraxial cornea. Courtesy University of California–Davis Comparative 2) is more consistent with intraocular disease, Ophthalmology Service such as or uveitis, but may also indicate breed-related endothelial dystrophy or age-related endothelial degeneration. These conditions can usually be differentiated by assessing for signs of pain or infl ammation: the latter 2 conditions are nonpainful and noninfl ammatory, whereas glaucoma and uveitis are painful and associated with other signs of infl ammation. Whenever possible, treatment for diffuse corneal edema should always be directed at the underlying disease process, especially since both glaucoma and uveitis are vision-threatening diseases, and some causes of uveitis can even be life-threatening.2,3 FIGURE 3. Feline acute bullous keratopathy. When no cause is found or the underlying disease is Note the large corneal stromal bulla protruding untreatable, symptomatic treatment with hypertonic outwards. The lack of corneal vascularization sodium chloride (nacl) ophthalmic ointment may confi rms the acute nature of the disease. be attempted, but it often has little to no effect, may Mucous discharge covers some of the irritate the eye, and requires administration at least 4 dorsomedial cornea and bulla. Courtesy University of California–Davis Comparative Ophthalmology Service to 6 times daily. Diffuse Edema in Cats. cats are rarely affected with endothelial dystrophy or senile endothelial degeneration. instead, severe, diffuse corneal edema in cats is typically seen with acute bullous keratopathy (Figure 3). This condition, which is more common in younger cats, has no recognized predisposing cause and an extremely acute onset that leads to massive stromal edema and, sometimes, corneal rupture. The dysfunction may involve the stroma itself rather than the endothelium or epithelium. Treatment involves emergency surgical support—either conjunctival grafting or placement FIGURE 4. Infectious with of a third fl ap.4,5 keratomalacia (“melting”) and stromal loss in a dog. The patient also has an eyelid tumor on the lateral aspect of the superior eyelid. In ammatory Cell In ltration Courtesy University of California–Davis Comparative a yellow, green, or tan corneal stromal opacity Ophthalmology Service suggests white blood cell (Wbc) infi ltration, which

106 Today’s VeTerinary PracTice | May/June 2015 | tvpjournal.com obserVaTions in oPhThalMology Peer reviewed

• Frequent (up to Q 2 h) topical application of broad-spectrum bactericidal antibiotics and serum. (serum contains anticollagenases that reduce keratomalacia.) • systemically administered analgesics (nonsteroidal anti-inflammatory drugs and/or opiates) • application of an e-collar. if more than 50% of the corneal stroma is lost, conjunctival graft surgery is often recommended to provide immediate tectonic support and promote healing.2 FIGURE 5. Feline eosinophilic keratitis. Note in some disease processes infi ltration of the the dense superfi cial corneal vessels and raised corneal stroma by Wbcs is evident as excrescences white corneal plaques. Diagnosis is made by above the corneal surface. examples include feline cytology, and treatment consists of antiviral and eosinophilic keratitis (FeK; Figure 5) and chronic immunomodulatory drugs. Courtesy University of superfi cial keratitis (csK, or “pannus”; Figure 6) in California–Davis Comparative Ophthalmology Service dogs, or neoplastic keratitis (typically lymphoma). in these instances, the cornea typically becomes heavily vascularized due to chronicity of the process. For the immune-mediated keratitides, it is important to treat any underlying conditions. For example, feline herpesvirus type 1 (FhV-1) is believed to cause FeK in many cats; in dogs, ultraviolet (UV) light exposure is a risk factor for development and progression of csK. These immune-mediated diseases must be controlled with topical application of steroids and/or calcineurin inhibitors, such as cyclosporine or tacrolimus.7,8 Keratic Precipitates. Wbcs, typically in FIGURE 6. Chronic superfi cial keratitis (CSK) or association with fi brin, can also form keratic “pannus” in a German shepherd dog. Note the precipitates (KPs)—more discrete clumps located dense lateral paraxial corneal plaque. This is an on the inner that appear as immune-mediated condition in which ultraviolet (UV) light exposure is a cofactor. Treatment focal tan spots (sometimes likened to mutton fat includes topical immunomodulatory drugs and because of their greasy appearance; Figure 7). due decreased UV exposure. Courtesy University of California–Davis Comparative Ophthalmology Service is most frequently caused by bacterial infection of the cornea, often Pseudomonas or beta-hemolytic Streptococcus species (Figure 4). Melting of the corneal stroma (keratomalacia), sometimes with associated stromal loss, often is seen in conjunction with Wbc infi ltration. Keratomalacia is evident as loss of normal corneal curvature and architecture with “oozing” of softened sections of the cornea over the more dependent regions (Figure 4). it FIGURE 7. Keratic precipitates (KPs) in a cat occurs as a result of enzymatic breakdown of corneal with uveitis. (neovascularization collagen by collagenases of Wbc and bacterial of the ) is also present. The brown KPs are origin, especially Pseudomonas species.6 located on the inner aspect of the corneal Therapeutic Approach. cytology, aerobic bacterial endothelium, predominantly ventrally. KPs are a pathognomonic sign of anterior uveitis. culture, and sometimes fungal culture are strongly Courtesy University of California–Davis Comparative recommended to help guide therapy. infected Ophthalmology Service require intensive medical therapy, including:

tvpjournal.com | May/June 2015 | Today’s VeTerinary PracTice 107 Peer reviewed obserVaTions in oPhThalMology

• be a breed-related • appear secondary to chronic topical corticosteroid therapy (steroid lipid keratopathy) or systemic lipid or possibly mineral imbalances. Identi cation of Causes. The most likely of these causes can be identifi ed based on a thorough history and characterization of the lipid/mineral deposition pattern. lesions secondary to age or chronic keratitis are typically irregular, often unilateral, and accompanied by other signs of keratitis, such as fi brosis, edema, or vascularization. FIGURE 8. Canine corneal lipid/mineral dystrophy. Note the white, sparkly, well- inherited dystrophic lesions are typically central defi ned corneal deposits. This lesion was or paracentral, circular or elliptical, and bilaterally bilateral, symmetrical, and uninfl amed. Lipid/ symmetrical (Figure 8). They are common in many mineral corneal dystrophy has minimal effect dog breeds, including siberian huskies and beagles, on vision and does not require treatment. but are very rarely seen in cats. Courtesy University of California–Davis Comparative steroid keratopathy can appear very similar Ophthalmology Service to corneal lipid dystrophy but is associated with chronic topical steroid use rather than breed-associated, and appears unilaterally unless corticosteroid use has been bilateral. Therapeutic Approach. corneal dystrophy and steroid lipid keratopathy are slowly progressive or static, have minimal effect on vision, and require no therapy (although some recommend replacement of topically applied corticosteroids with topical nonsteroidal anti-infl ammatory agents). by contrast, corneal degeneration can cause recurrent corneal ulceration and, in severe cases, corneal FIGURE 9. Focal corneal fi brosis in a dog. Note rupture, if areas of mineral “chip” off the cornea or the gray appearance and crisp edges of the reduce corneal epithelial adhesion. if extensive or lesion. Some superfi cial corneal blood vessels progressive corneal mineral deposition is present, are also apparent. This lesion has minimal effect topical chelation therapy and debridement, or even on vision and does not require any treatment. keratectomy, may be required.2 Courtesy University of California–Davis Comparative Ophthalmology Service Fibrosis to gravity, KPs tend to be deposited most densely if the cornea has a grayish white, sometimes feathery or wispy opacity, it is most likely fi brosed on the ventral corneal endothelium, and can be (Figure 9). hypoperfused (or “ghost”) corneal overlooked if the patient’s nose is not directed blood vessels may be seen in association with ventrally, which causes the eye to roll upward. KPs resolving or inactive corneal fi brosis, but well- are a pathognomonic sign of uveitis, and a thorough perfused vessels indicate more active keratitis. diagnostic workup is usually warranted.9 in most cases, corneal scarring is permanent, but can decrease over time if the underlying cause of Lipid/Mineral Deposition corneal damage is removed, especially in younger silvery white, crystalline, sparkly opacities (or animals. corneal scars do not retain fl uorescein sometimes coalescing creamy or shiny opacities) stain and require no further treatment.9 however, typically located in the anterior stroma, immediately if extensive scarring causes vision loss, corneal under the corneal epithelium, represent lipid transplantation may be considered. (typically cholesterol) or mineral (typically calcium) deposits.9 These can:2,10 QUESTION 2. WHERE IS THE OPACITY • occur secondary to chronic keratitis or senile LOCATED? degeneration (also known as corneal or calcareous as seen with the examples provided in Question 1, degeneration or calcific ) location, depth, and extent of corneal opacity can be

108 Today’s VeTerinary PracTice | May/June 2015 | tvpjournal.com obserVaTions in oPhThalMology Peer reviewed

diagnostically critical (Table 2). dichotomously to form “tree-shaped” patterns accurate judgment of lesion depth within the on the cornea, and can usually be seen crossing cornea requires use of magnifi cation and a slit lamp; the limbus (Figure 10). These vessels typically however, corneal vessels can also be useful clinical indicate superficial ocular surface disease. guides: • Vessels that arise from under or within the scleral shelf • Superficial corneal blood vessels arise from the are located deeper in the cornea, where they form at the limbus and are fine, branching a more “hedge-shaped” pattern (Figure 11). They are characteristic of deeper, more serious, vision-threatening diseases, such as deep keratitis, TABLE 2. uveitis, and glaucoma.9 Location & Cause of Corneal Opacities

CORNEAL OPACITY LIKELY CAUSE & LOCATION RECOMMENDATIONS Paraxial corneal Adnexal region closest ulcer to corneal ulcer should be investigated for abnormalities, such as distichia, ectopic cilia, or foreign bodies (often associated with intense blepharospasm), or / Lateral perilimbal Typical of age-related to paraxial corneal corneal endothelial edema of both eyes degeneration; edema FIGURE 10. Superfi cial corneal vessels in a progresses medially until it covers entire cornea causing dog with superfi cial nonulcerative keratitis. vision impairment2 Note that the vessels are arising from the conjunctival vasculature and form a branching Circumferential Can indicate diffuse “tree-like” pattern. Schirmer’s tear testing, perilimbal corneal or lymphoma2 edema, cellular fl uorescein staining, and careful examination infi ltrates, and/or for underlying causes are essential whenever vessels superfi cial corneal blood vessels are noted. Courtesy University of California–Davis Comparative Corneal ulcer and In a young dog, warrants Ophthalmology Service focal edema near thorough examination 12 o’clock position for ectopic cilia (certain on dorsal paraxial breeds, such as Shih Tzu, are cornea predisposed) Diffuse corneal Typically indicates intraocu- edema lar disease (Figure 2) Diffuse superfi cial Suggests chronic, diffuse corneal vessels superfi cial irritation, such as sicca (KCS or dry eye); when associated with mucoid to mucopurulent ocular discharge, a Schirmer’s tear test (STT) should be performed FIGURE 11. Deep corneal vessels in a dog Focal corneal edema Often indicates corneal with uveitis and glaucoma. Note that the surface (epithelial) disease (Figure 1) vessels are “hedge-like.” In this patient, vessels were present for 360 degrees around Lateral perilimbal Most common location for the limbus. Deep corneal vessels should cornea; raised dense cellular infi ltrate and plaque stimulate a thorough intraocular examination, corneal vascularization seen including measurement of intraocular pressure. in CSK and FEK; in more Courtesy University of California–Davis Comparative advanced cases, will spread medially Ophthalmology Service

tvpjournal.com | May/June 2015 | Today’s VeTerinary PracTice 109 Peer reviewed obserVaTions in oPhThalMology

QUESTION 3. WHY DID THE CORNEAL Ophthalmic Diagnostic Tests OPACITY OCCUR? Tonometry & Ultrasound. diffuse corneal edema, given the wide variety of causes of corneal opacities deep corneal vessels, or episcleral injection are each and the knowledge that treatment for one cause can indications of intraocular disease, and tonometry be contraindicated for other conditions, it is critical (measurement of intraocular pressure) and ocular to determine the etiology of all corneal lesions. ultrasound (if a complete intraocular examination For example, topical steroids often are required is not possible) are recommended to assess for to control immune-mediated keratopathies, but evidence of glaucoma, uveitis, intraocular masses, they are contraindicated for corneal ulcers because , or lens luxation. steroids slow healing, worsen keratomalacia, and Schirmer’s Tear Test. Presence of predispose to infection. and mucoid discharge combined with superfi cial in some instances, the appearance or location corneal blood vessels, fi brosis, or melanin (in of a corneal opacity is pathognomonic or highly various combinations) are strongly suggestive of diagnostic. For example: Kcs, and a schirmer’s tear test (sTT) should always • dendritic ulcers are considered be performed. pathognomonic for herpesviral infections, Palpebral Re ex. an absent or decreased while circular translucent or “lacy” collections palpebral refl ex predisposes to corneal exposure; of dark brown-black melanin on the corneal a full neurologic examination, especially of cranial endothelial surface are highly suggestive of a nerves, is warranted. ruptured uveal cyst. Fluorescein Stain. any patient with corneal • dogs that blink poorly or sleep with their opacity should have fl uorescein stain applied slightly open often have axial corneal topically to assess for corneal ulceration. This fibrosis, vascularization, and melanosis, which are Algorithm evaluation should be performed after all other characteristic of exposure keratitis. Turn to page assessments are fi nished since it masks many other in other patients, systemic signs may also 112 to view examination fi ndings, and affects results of other provide useful hints regarding the cause of ocular the algorithm tests, such as the sTT, corneal cultures, and cytology. signs; therefore, a thorough history is essential. Diagnosis & When fl uorescein is retained by the cornea, the For example, recent upper respiratory signs, stress, Treatment of character of the fl uorescein staining pattern should Corneal Lesions or immunosuppression in cats with keratitis, be assessed because some patterns are highly that accompanies conjunctivitis, or both raises suspicion of an suggestive of etiopathogenesis. For example: this article. infectious cause, such as FhV-1. • Superficial chronic corneal epithelial defects and in other patients, historical data are critical; (scceds)—also known as indolent or Boxer for example, worsening of a chronic keratitis during summer months might suggest UV involvement ulcers—classically leak fluorescein stain under and a diagnosis of csK.9 nonadherent ulcer edges creating a “halo” effect. • Herpetic ulcers sometimes have a pathognomonic Ophthalmic Examination dendritic pattern. a complete ophthalmic examination (and general • Deep ulcers have staining of both their walls and physical examination, if systemic causes are floor. suspected) is essential to identify related ocular and • Descemetoceles stain only around the wall, creating 2 systemic abnormalities that may have led to the a “donut” pattern of stain retention. corneal opacity. in particular, anatomic or functional eyelid abnormalities, such as , QUESTION 4. WHEN DID THE CORNEAL distichiasis, eyelid tumors, , facial nerve OPACITY OCCUR? paralysis, or conjunctival foreign bodies, should be naturally, history is one of the most valuable tools carefully ruled in or out. to establish the duration of a corneal opacity, but other clues are available through examination. For Cytology example: samples for cytologic assessment—obtained using • Acute corneal opacities (< 3–5 days) do not have the blunt end of a scalpel blade, Kimura spatula, or corneal vessels unless the vessels were present cytobrush—and aerobic bacterial ± fungal culture prior to the current lesion. it is estimated that are excellent means to differentiate immune-mediated corneal vessels first appear approximately 4 from infectious processes, and form the minimum days after the initial corneal injury; then grow database for investigation of corneal disease. approximately 1 mm per day.

110 Today’s VeTerinary PracTice | May/June 2015 | tvpjournal.com obserVaTions in oPhThalMology Peer reviewed

• Active lesions usually have more irregular, or fuzzy, intraocular disease include diffuse TABLE 3. outlines due to corneal edema and/or cellular corneal edema and deep corneal Determining Whether a Corneal infiltrates. vessels; often in association with Ulcer Is Complicated • Chronic, inactive lesions, such as corneal fibrosis or episcleral injection. melanosis, often have more distinct borders with referral to a veterinary A corneal ulcer is considered complicated if one or more of the the surrounding cornea. ophthalmologist should take place following is noted: as early as possible, in order to • Corneal blood vessels QUESTION 5. WHEN SHOULD YOU increase the chance of saving the • Corneal stromal loss (If > 50% is REFER A PATIENT WITH A CORNEAL eye, including its vision. lost, surgical stabilization is typically OPACITY TO A VETERINARY recommended.) • Corneal WBC infi ltration (greenish OPHTHALMOLOGIST? csK = chronic superfi cial keratitis; yellow cornea) although individual practitioners have different FeK = feline eosinophilic keratitis; • Failure to heal within 1 week comfort levels regarding diagnosis and treatment of FhV-1 = feline herpesvirus type 1; • Indolent ulcers (ie, SCCEDs) ocular conditions, certain conditions warrant referral Kcs = keratoconjunctivitis sicca; • Infection • Keratomalacia (“melting”) to a veterinary ophthalmologist. Veterinarians KP = keratic precipitates; • Marked or persistent corneal edema should refer patients when: scced = superfi cial chronic 1. They do not feel comfortable managing the corneal epithelial defect; sTT = schirmer’s tear test; ophthalmic condition UV = ultraviolet; Wbc = white blood cell 2. referral is specifi cally requested by clients 3. intraocular disease, a complicated (deep or References chronic) corneal ulcer (Table 3), or vision 1. Torricelli aa, Wilson se. cellular and extracellular matrix impairment is present2 modulation of corneal stromal opacity. Exp Eye Res 2014; 129c:151-160. 4. Patients require corneal microsurgery. 2. gelatt Kn, gilger bc, Kern TJ (eds). Veterinary Ophthalmology, corneal opacities that are suggestive of 5th ed. Wiley-blackwell, 2013.

tvpjournal.com | May/June 2015 | Today’s VeTerinary PracTice 111 Peer Reviewed Observations in Ophthalmology

Diagnosis & Treatment of Corneal Lesions

Ann R. Strom, DVM, MS, and David J. Maggs, BVSc, Diplomate ACVO University of California–Davis

What color Creamy or sparkly white Gray is the Yellow/green (WBCs) Blue (stromal edema) (lipid/mineral) (fibrosis) lesion?

Unilateral Bilateral, or bilateral, Diffuse, marked Focal, mild symmetric, asymmetric, not inflamed inflamed

• Cytology & aerobic bacterial • Check for pain, • Apply flu- • Apply fluores- • Monitor for • Check for other What cultures flare, redness, or orescein cein stain secondary ocular abnor- ± Fungal cultures lens luxation stain • Consider ulceration malities test(s) to ± Viral PCR • Measure IOP • Perform systemic hy- with fluores- • Perform STT perform? • Fluorescein stain • Apply fluorescein STT perlipidemia, cein stain • Apply • Identify causes of corneal stain hypercalce- • Rule out fluorescein ulcers & perform STT • Consider mia, & pri- chronic top- stain US if unable mary corneal ical steroid to examine disease use intraocular structures

If cornea Negative Positive Nonpainful, Painful, ulcerated, Corneal Corneal Prior corneal Why is cultures/no cultures/ no inflam- inflamed, look for degeneration lipid/mineral damage the lesion organisms cytology: mation or flare, cause, dystrophy there? on cytology: Support flare, abnormal such as Immune- diagnosis normal IOP: eyelid ab- mediated or of IOP: Glaucoma, normalities viral (herpetic) infection Endothelial uveitis, or dysfunc- keratitis degener- or lens tion, tear ation or luxation film defi- dystrophy ciencies, foreign body, trauma, or SCCED Treat with • Intensively treat Consider • Treat Monitor for • No treatment antivirals with topical treating underlying ulceration required unless Treatment or anti-in- antimicrobials with Treat with systemic underlying flamma- (guided by hypertonic prophylac- disease and/ cause found tories cytology and (5%) NaCl tic topical or primary • Monitor C/S results) ointment ≥ antibiotics keratitis • If keratomalacia Q 6 H and atro- • Monitor for present, use pine ulceration serum topically • If > 50% stro- mal loss, con- sider surgical stabilization

When to Refer Refer if progres- Refer if Refer as Refer if • Refer for keratectomy or Referral usually refer to a if poor sive, recurrent, or bullae or soon as progressive, chelation if opacity is marked not needed veterinary response notable stromal secondary possible recurrent, • Refer if ulcer is progressive, ophthal- to loss ulceration or notable recurrent, or involves notable therapy occur stromal loss stromal loss mologist?

The corneal opacities described in this diagram are often seen in various combinations, sometimes with other corneal color changes (such as black, tan, or red). As such, the flowchart is simplified. If the reader has doubts about management of an ophthalmic case, they should consult with a veterinary ophthalmologist. C/S = culture & sensitivity; IOP = intraocular pressure; NaCl = sodium chloride; PCR = polymerase chain reaction; SCCED = superficial chronic corneal epithelial defect; STT = Schirmer’s tear test; US = ultrasound; WBC = white blood cell

112 Today’s Veterinary Practice | May/June 2015 | tvpjournal.com obserVaTions in oPhThalMology Peer reviewed

ANN R. STROM DAVID J. MAGGS Ann Strom, DVM, MS, is a staff veteri- David Maggs, BVSc, Diplomate ACVO, is a narian in the University of California– professor in the University of California–Da- Davis Comparative Ophthalmology vis Comparative Ophthalmology Service. Dr. Service. Her professional interests Maggs’ special interests include ophthalmic include all aspects of ophthalmic surgery and ocular surface disease, partic- disease and surgery, advanced di- ularly feline herpesvirus. He is the author of agnostic imaging, and comparative Slatter’s Fundamentals of Veterinary Ophthal- vision research. Dr. Strom received mology, serves on the editorial board of the her DVM from University of Co- Journal of Feline Medicine and Surgery, and penhagen, Denmark, and complet- is president elect of the International Society ed her MS at University of Zurich, of Veterinary Ophthalmology. Dr. Maggs re- Switzerland, a 1-year internship in ceived his veterinary degree from University small animal medicine and surgery of Melbourne, Australia, and completed small at University of Saskatchewan, and animal and equine internships at Colorado a 3-year residency in comparative State University and a research fellowship and ophthalmology at University of Cal- comparative ophthalmology residency at Uni- ifornia–Davis. versity of Missouri.

3. Townsend WM. canine and feline uveitis. Vet Clin North Am feline eosinophilic keratitis with topical 1.5% cyclosporine: 35 Small Anim Pract 2008; 38(2):323-346, vii. cases. Vet Ophthalmol 2009; 12(2):132-137. 4. Moore Pa. Feline corneal disease. Clin Tech Small Anim Pract 8. barrientos ls, Zapata g, crespi Ja, et al. a study of 2005; 20(2):83-93. the association between chronic superfi cial keratitis and 5. glover T, nasisse MP, davidson Mg. acute bullous keratopathy polymorphisms in the upstream regulatory regions of in the cat. Vet Comp Ophthalmol 1994; 4(2):66-70. dla-drb1, dla-dQb1 and dla-dQa1. Vet Immunol 6. Wang l, Pan Q, Xue Q, et al. evaluation of matrix Immunopathol 2013; 156(3-4):205-210. metalloproteinase concentrations in precorneal tear fi lm from 9. Maggs dJ, Miller P, ofri r. Slatter’s Fundamentals of Veterinary dogs with Pseudomonas aeruginosa-associated keratitis. Am J Vet Ophthalmology, 5th ed. elsevier, 2013. Res 2008; 69(10):1341-1345. 10. sansom J, blunden T. calcareous degeneration of the canine 7. spiess aK, sapienza Js, Mayordomo a. Treatment of proliferative cornea. Vet Ophthalmol 2010; 13(4):238-243.

tvpjournal.com | May/June 2015 | Today’s VeTerinary PracTice 113