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Can Vet J. 2010 September; 51(9): 1041–1042.
PMCID: PMC2920165

Diagnostic Ophthalmology

History and clinical signs

An 8-year-old, 5-kg, neutered male domestic shorthair cat was examined at the ophthalmology service at the Western College of Veterinary Medicine for evaluation of a pink mass on the left eye. General physical examination was normal except for the ocular abnormalities. The menace responses were present bilaterally. Direct and consensual pupillary light reflexes were present in both eyes. The palpebral, and oculocephalic reflexes were present bilaterally. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were 10 mm/min bilaterally. The intraocular pressures were estimated with a rebound tonometer (Tonvet; Tiolat, Helsinki, Finland) and were 16 mmHg bilaterally. Results from fluorescein staining (Fluorets; Bausch & Lomb Canada, Markham, Ontario) were negative bilaterally. On direct examination the palpebral conjunctiva and third eyelids were hyperaemic and thickened bilaterally and a pink fleshy mass was present in the left lateral cornea extending from the limbus centrally. Biomicroscopic (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) examination following dilation with 0.5% tropicamide (Mydriacyl; Alcon, Canada, Mississauga, Ontario) revealed further abnormalities including bilaterally peripheral corneal vascularization and a white-pink infiltrate in the superficial corneal stroma adjacent to the fleshy mass. Indirect ophthalmoscopic (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) examination was unremarkable. A photograph of both eyes is provided for your assessment (Figure 1).

Figure 1
Photograph of the right (a) and left eye (b) of a 8-year-old domestic shorthair cat.

What are your clinical diagnosis, differential diagnoses, therapeutic plan, and prognosis?


Our clinical diagnosis was bilateral proliferative keratoconjunctivitis. Differential diagnoses for proliferative lesions of the conjunctiva and cornea include eosinophilic keratoconjunctivitis, fungal keratitis, acid-fast granuloma, foreign body granuloma, corneal trauma, and neoplasia. A scraping for cytology was obtained from the left cornea following application of topical anesthetic 0.5% proparacaine hydrochloride (Alcaine; Alcon Canada, Mississauga, Ontario). The smears contained dysplastic epithelial cells, numerous eosinophils, and rare mast cells and a diagnosis of eosinophilic keratoconjunctivitis was made.

Eosinophilic keratoconjunctivitis is a progressive infiltrative disease of the conjunctiva and cornea that typically affects young adult cats. There is no breed or sex predilection and no known relationship between eosinophilic keratoconjunctivitis and dermatologic eosinophilic granuloma complex (1,2). It may be unilateral or bilateral. The most common corneal manifestation is superficial vascularization of the perilimbal region. The cornea may become thickened by a white-pink infiltrate, and white to yellow gritty corneal plaques frequently develop (1). The nasal and temporal limbus are most frequently involved; however, the entire cornea can become involved over time (1,2). Occasionally, corneal ulceration may occur adjacent to the proliferative lesions (1,3). Conjunctival manifestations include hyperemia and chemosis, as well as thickening of the third eyelids (1).

Diagnosis of eosinophilic keratoconjunctivits requires cytologic or histologic confirmation. Cytologic examination of corneal or conjunctival scrapings shows a predominance of eosinophils with variable numbers of mast cells, lymphocytes, and neutrophils (1,3). Histopathologic examination of the affected cornea shows hypertrophy and hyperplasia of the corneal epithelium, as well as, areas of corneal ulceration. There is corneal stromal vascularization and cellular infiltration with numerous eosinophils, plasma cells, mast cells, and infrequent lymphocytes, neutrophils, and macrophages (3). Corneal ulcerations are often associated with excrescences of necrotic debris intermingled with amorphous eosinophilic material and free granules of eosinophils (3).

The pathogenesis of eosinophilic keratoconjunctivitis is thought to be an immune-mediated response to an antigenic stimulus. A type I hypersensitivity reaction mediated by IgE, mast cell degranulation, and subsequent tissue injury from degranulating eosinophils or a type IV reaction mediated by sensitized T lymphocytes, interleukin 5 production, and stimulation of a local eosinophil response have been suggested (3). A possible role for feline herpesvirus type-1 (FHV-1) has also been suggested. Feline herpesvirus type-1 DNA was detected in 76.3% of cytology specimens from cats with eosinophinophilic keratoconjunctivitis compared to 5.9% of corneas from normal cats (4). The exact association of FHV-1 with the eosinophilic infiltration is not clear.

The most common treatment for eosinophilic keratoconjunctivitis includes topical steroid medications and topical antibiotics if corneal ulcerations are present. If FHV-1 infection is confirmed, an antiviral medication such as topical trifluridine 1% or idoxuridine 0.1% should also be used. Recently topical cyclosporine 1.5% has been used as an effective treatment for this condition (5). Oral megestrol acetate has also been used as treatment for eosinophilic keratoconjunctivitis (1,2). Its use should be a last resort as this medication may be associated with numerous systemic side effects such as behavioral changes, adrenocortical suppression, diabetes mellitus, pyometra, mammary hyperplasia, and neoplasia (6).

Many ophthalmologists will continue to use topical corticosteroids even when corneal ulceration is present. This is done under very close observation with frequent follow-up to monitor for complications. In most cases the corneal ulcerations will heal quickly which may support the theory that the ulcerations are due to tissue damage from degranulation of eosinophils (3). Resolution of clinical signs is reported to be from 2 wk to 8 mo with a mean of 2.5 mo (1). The condition commonly recurs (1,2). In one study 19 of 29 cats had recurrence of the lesions; time to recurrence ranged from 1 to 60 mo (1).

Treatment for this cat was initiated with a topical steroid, prednisolone acetate 1% (Sandoz Prednisolone; Sandoz Canada, Boucherville, Quebec), q6h. The cat was re-evaluated 10 d later and the lesions were completely resolved at that time. The frequency of topical steroid application was reduced from q8h to q12h to q24h for 3 wk at a time, and finally, to q48h as an ongoing maintenance therapy. There has been no recurrence of the ocular lesions.

The prognosis for eosinophilic keratoconjunctivitis is good. Resolution of clinical signs is usually achieved with appropriate therapy. The presence of corneal ulceration requires close observation and frequent re-evaluation during treatment. Because recurrence is common, long-term, low-frequency maintenance therapy is required in most cats. Client compliance is, therefore, important in the long-term outcome of eosinophilic keratoconjunctivitis.


Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office (gro.vmca-amvc@nothguorbh) for additional copies or permission to use this material elsewhere.


1. Morgan RV, Abrams KL, Kern TJ. Feline eosinophilic keratitis: A retrospective study of 54 cases: (1989–1994) Vet Comp Ophthalmol. 1996;6:131–134.
2. Paulsen ME, Lavach JD, Severin GA, Eichenbaum JD. Feline eosinophilic keratitis: A review of 15 clinical cases. J Am Animal Hosp Assoc. 1987:2363–2369.
3. Prasse KW, Winston SM. Cytology and histopathology of feline eosinophilic keratitis. Vet Comp Ophthalmol. 1996;6:74–81.
4. Nasisse MP, Glover TL, Moore CP, Wigler BJ. Detection of feline herpesvirus 1 DNA in corneas of cats with eosinophilic keratitis or corneal sequestration. Am J Vet Ophthalmol. 1998;59:856–858. [PubMed]
5. Spiess AK, Sapienza JS, Mayordomo A. Treatment of feline eosinophilic proliferative keratitis with topical cyclosporine: 30 cases. Proc American College of Veterinary Ophthalmologists; Kona Hawaii. October 22–27, 2007; p. 47.
6. Plumb DC. Veterinary Drug Handbook. 5th ed. Ames, Iowa: Blackwell Publ; 2005. pp. 485–487.

Articles from The Canadian Veterinary Journal are provided here courtesy of Canadian Veterinary Medical Association