Revised from 6th edition of Veterinary Ophthalmology, Chapter 28: Feline Ophthalmology, by Mary Belle Glaze, David J. Maggs, and Caryn E. Plummer Cats are the most popular household pet in the United States and Europe, with populations numbering 94 million and 100 million, respectively. This growth has increased interest in feline well‐being, the evolution of veterinary practices devoted exclusively to their care, and a demand for increasingly sophisticated healthcare that includes management of their ocular disease. Inherited disorders of the eye are infrequent in cats, but systemic infectious diseases often affecting the eyes are common. Kittens are born with their eyelids fused (physiological ankyloblepharon), with opening generally predicted between 10 and 14 days of age. In the majority of kittens, both eyes open on the same day, with separation usually beginning at the medial canthus. In the normal feline eye, the lid margins should just cover the upper and lower limbal arcs of the cornea. Limited conjunctiva is visible within the palpebral fissure, with the exception of a small portion of the third eyelid medially and a small area of bulbar conjunctiva laterally. Brachycephalic breeds tend to have slightly longer eyelids, a factor that may explain their predilection for surface diseases such as entropion and corneal sequestration. The cat has no eyelashes, but a row of thicker facial hairs serves as rudimentary lashes along the upper lid. On the rare occasion that the eyelids separate prematurely, a neonatal kitten’s tear production may not be sufficient to prevent desiccation of the ocular surface. Frequent lubrication using a topical artificial tear or prophylactic antibacterial ointment is necessary to discourage secondary progressive ulceration until the lacrimal system matures. Eyelid opening is more likely to be delayed than early (pathological ankyloblepharon) (Figure 14.1). Delayed separation occurs in Persian cats. If the lids remain fused beyond the usual 10–14 days of age with no evidence of eyelid swelling or discomfort, conservative therapy with warm compresses may encourage natural separation. If the eyelids are distended to any degree by trapped secretions, if the site is painful, or if any purulent exudate is evident, it is imperative to rule out neonatal conjunctivitis (also known as ophthalmia neonatorum) and treat promptly. Primary infectious pathogens in kittens include feline herpesvirus (FHV) and Chlamydia felis as well as secondary bacteria that include Staphylococcus spp. or Gram‐negative bacteria of fecal origin. The eyelids should be gently pried apart with firm digital pressure over the medial canthus, or the closed tip of a small mosquito hemostat may be inserted at the medial canthus where a small gap often exists, sometimes identified by a drop of exudate. The hemostat is carefully opened to separate the lids, followed by liberal flushing of the ocular surface with sterile saline or dilute aqueous (1:50) povidone–iodine solution until all exudate is removed. Sharp instruments are best avoided since inadvertent damage to the lid margins or meibomian glands could predispose to chronic keratitis. Topical therapy is directed at the most likely bacteria, notably C. felis, applying tetracycline, erythromycin, or a fluroquinolone several times daily for 7–10 days until signs of infection resolve. Tear production and the blink reflex may be inadequate in these very young kittens, so consideration should also be given to supplemental lubrication. Failure to promptly address an infection beneath the fused eyelids can lead to permanent corneal scarring, symblepharon, and even corneal perforation. Figure 14.1 Ankyloblepharon and neonatal ophthalmia in a 2.5‐week‐old domestic shorthair kitten. Exudate is trapped beneath the left fused lids but seeps from the partially opened right palpebral fissure. Eyelid agenesis or coloboma is the most common congenital eyelid abnormality in the cat. Although this developmental defect occurs sporadically in any breed, agenesis has been reported in the domestic shorthair, Burmese, and Persian. Embryologically, the defect may be linked to inadequate induction of the surface ectoderm by an abnormally oriented optic vesicle. In affected cats, thorough ocular examinations should be performed to rule out concurrent colobomas of the iris, choroid, and optic nerve. The effect of this developmental defect ranges from a small notch in the lid margin to complete absence of two‐thirds or more of the upper eyelid and its conjunctival lining (Figure 14.2). The temporal aspect of the superior lid is most commonly affected; medial canthal involvement is rare. Lesions are typically bilateral but may not be symmetrical. Mildly affected animals may be asymptomatic but patients more often exhibit secondary corneal disease and discomfort resulting from corneal contact with adjacent facial hair, failure of the eyelid to close, or both. Figure 14.2 Eyelid agenesis. The normal pink margin is missing in the temporal third of the upper eyelid, calling attention to this subtle example of agenesis. Treatment is dictated by the severity of the agenesis. Mild deformities may require only supplemental lubrication with a topical artificial tear ointment. Cryoepilation of misdirected hairs or correction of the trichiasis using a Hotz–Celsus or Stades technique may suffice if the eyelid retains sufficient mobility and bulk to protect the cornea. Otherwise, the choice of surgical technique is governed by the extent of the coloboma. Defects involving one‐fourth to one‐third of the lid margin may be closed directly by converting to a simple wedge, with a releasing incision at the lateral canthus to create an advancement flap if needed to minimize wound tension. The majority of lesions are too large for primary apposition. Reparative techniques utilize a rotational pedicle of lower eyelid skin and orbicularis muscle, anchored at the lateral canthus, sutured into the upper defect, and lined by neighboring conjunctiva undermined and mobilized at the site (Roberts–Bistner technique). The most common complication, related to corneal irritation and absence of the lid margin, is the downward angle of hairs within the grafted skin, often requiring a second procedure such as cryoepilation to correct the trichiasis. A modification of the rotational technique includes conjunctiva transposed from the anterior surface of the third eyelid to line the newly created upper eyelid. A buccal mucosal island graft has also been used in conjunction with a single pedicle advancement flap from the dorsolateral forehead skin to recreate a rudimentary superior fornix. Sliding skin grafts, Z‐plasty skin flaps, and semicircular skin grafts can also be used for correction. Traditionally used to repair extensive lower lid defects, the lip‐to‐lid reconstruction technique can be modified to reconstruct the upper lid with skin, muscle, and mucus membrane of the commissure of the lip, which provides a stable upper lid and lateral canthal margins, and avoids the problem of trichiasis frequently encountered with other techniques. Alternative multistage techniques used for extensive defects include the Cutler–Beard or bucket handle technique, borrowing skin, orbicularis muscle, and conjunctiva from the lower eyelid, a modification of the Mustardé cross‐lid technique using the full‐thickness lower eyelid to reconstruct the upper lid and a technique using injectable subdermal collagen to replace the eyelid stroma, combined with a modified Stades technique to remove misdirected hairs. Inversion of the eyelid is less common in cats than in dogs. Primary entropion occurs most often in the Persian and other brachycephalic breeds, usually involving the medial aspect of the lower eyelid. Pronounced facial “jowls” in the intact male Maine Coon cat are implicated as a predisposing breed‐related factor. The same facial conformation may accompany entropion in the occasional feral tomcat as well. Cats with entropion tend to be either (i) young cats with chronic surface irritation from conjunctivitis, corneal ulceration, or corneal sequestration, or (ii) older cats with eyelid laxity or enophthalmos from reduced orbital tissue volume. These observations suggest feline entropion is more likely a consequence of chronic, painful ocular disease rather than faulty conformation (Figure 14.3). Surgical correction of entropion in cats must eliminate the cause of eyelid spasm that leads to recurrence and the amount of eyelid tissue that must be resected to sufficiently evert the lid is often surprisingly greater than that required in a similarly entropic dog. If the entropion resolves following application of a topical anesthetic, definitive surgical correction should be postponed until the underlying cause of the blepharospasm is identified and treated. Vertical mattress sutures or staples may be used to temporarily evert or “tack” the eyelids, limiting damage to the ocular surface in the interim. Subdermal injection of a hyaluronic acid filler (Restylane® Silk, Galderma Laboratories LP, Fort Worth, TX, USA) may be used to correct entropion of senile, primary, and cicatricial origin. Using only manual restraint, 0.1–0.3 ml of filler is injected into the subdermal space 1–2 mm ventral to the eyelid margin using a 27‐ or 30‐gauge needle. Figure 14.3 (a and b) Chronic bilateral entropion in a two‐year‐old Persian with secondary keratitis. (c) Entropion of the lower eyelid in a six‐year‐old domestic shorthair with a history of chronic conjunctivitis. (d) Postoperative appearance of the same eye following a modified Hotz–Celsus technique combined with lateral canthal closure. Most cases of feline entropion can be successfully corrected using a Hotz–Celsus procedure, but recurrences are possible. To correct medial entropion and properly position the lower nasolacrimal (NL) punctum in brachycephalic cats, the Hotz–Celsus technique can be modified by excising a triangular rather than elliptical section of skin, with the tip of the triangle opposite the lower lacrimal punctum. In some cats, it may be necessary to also address excess lid length to successfully correct the entropion. Success rates of 88.6% are seen when the Hotz–Celsus procedure is combined with a lateral wedge resection, shortening the lower eyelid by as much as 5 mm. A dermoid is a congenital malformation in which fully differentiated tissue develops in an aberrant location. An ocular dermoid contains elements of normal skin, including keratinized epithelium, hair, glandular tissue, and fat. Ocular dermoids are considered rare in cats. The anomaly may develop spontaneously in any breed, although a multifactorial mode of inheritance has been proposed in the Birman breed. Locations vary, but dermoids have been noted in the temporal perilimbal conjunctiva and cornea as well as the skin and conjunctiva of the lateral canthus. Surgical excision is advisable in most cases of dermoid, but the proper technique must be determined on an individual basis. A lateral canthal dermoid may simply require a wedge‐shaped excision and two‐layer closure, with a figure‐of‐eight suture at the margin to ensure perfect apposition. Patients with concurrent conjunctival and/or corneal involvement are best referred to an ophthalmologist to ensure complete excision and restoration of normal anatomical relationships during repair of the operative site. Surgical excision is curative. Inflammation of the eyelids may occur as an isolated problem or as part of generalized dermatological disease. The causes of blepharitis are as varied as the causes of dermatitis in general and in the cat are usually infectious, allergic, or immune‐mediated in origin. Cats presenting with blepharitis should be examined carefully to identify accompanying dermatological lesions. If concurrent skin lesions are present and the eye itself is spared, consultation with a veterinary dermatologist is advisable. Dermatophytosis is a common cutaneous fungal infection in cats, colloquially referred to as “ringworm.” Over 90% of feline cases are caused by Microsporum canis, with Microsporum gypseum and Trichophyton mentagrophytes accounting for the remainder. Infection results from contact with another affected cat or from environmental contamination. There is indirect evidence that Persian cats are predisposed to infection. Lesions occur most commonly on the face, ears, and muzzle, and then progress to the paws. Eyelid lesions include variably shaped areas of alopecia, erythematous patches, and crusted plaques. Pruritus is minimal to absent. Although dermatophytosis in most healthy animals is self‐limiting within four months of onset, topical and systemic treatment is recommended to shorten the disease course as well as limit spread to other animals and their human caretakers. Spot treatment of only visible lesions is not recommended in cats. Twice‐weekly lime sulfur dips or miconazole–chlorhexidine shampoos remain the most effective choices for topical therapy in the United States; enilconazole is recommended in other parts of the world. Topical therapy is combined with noncompounded itraconazole (5–10 mg/kg p.o. q 24 h with food) or terbinafine (20–30 mg/kg q 24 h). A pulsed regimen of oral 10% itraconazole solution administered for seven days at 5 mg/kg q 24 h on alternate weeks over a five‐week period produced a clinical cure in 97.5% of infected cats. Treatment should be continued until diagnostic testing confirms a cure. Systemic mycotic infections are relatively uncommon in cats. Cryptococcus neoformans and Histoplasma capsulatum infections are more often diagnosed than those of Blastomyces dermatitidis or Coccidioides immitis. The predominant ocular manifestations of these deep mycoses are chorioretinitis and anterior uveitis, but papules and nodules can develop on the face, nose, pinnae, and eyelids. In endemic areas (Figure 14.4), these pathogens should be considered in any cat exhibiting raised erythematous nodules of the eyelid and palpebral conjunctiva. Facial nodules and ulcers commonly associated with the subcutaneous fungus Sporothrix schenckii can also extend to the eyelids. Figure 14.4 Mycotic blepharitis. A three‐year‐old DSH exhibits multiple erythematous nodules of the eyelid and conjunctiva associated with systemic histoplasmosis. Feline demodicosis is an uncommon dermatological disease caused by the mites Demodex cati, Demodex gatoi, and a third unnamed Demodex sp. Localized disease affects the eyelids, periocular area, head, and neck, with patchy alopecia, erythema, scaling, and crusting (Figure 14.5). Demodex gatoi is contagious to other cats and infestation is distinguished by moderate to severe pruritus. Generalized demodicosis is usually associated with underlying systemic diseases, including diabetes mellitus, or infection with feline leukemia virus (FeLV) or feline immunodeficiency virus (FIV). Even in generalized disease, lesions predominate on the face and head. Diagnosis is based on the presence of mites in skin scrapings, hair plucks, or acetate tape preparations (Figure 14.5). Localized D. cati lesions are typically self‐limiting but can be treated with topical rotenone ointment, lime sulfur, pyrethrin‐containing ear medications, or amitraz in mineral oil (1:9). For generalized D. cati infestations, alternatives to weekly 2% lime sulfur dips include oral aqueous ivermectin (0.2–0.3 mg/kg q 24–48 h, oral milbemycin oxime (1–2 mg/kg q 24 h), injectable doramectin (600 μg/kg subcutaneously once weekly), topical imidacloprid–moxidectin applied q 7–14 days, or oral fluralaner (single 28 mg/kg oral dose). Treatment of choice for D. gatoi consists of at least four weekly 2% lime sulfur dips. Treatment of either mite should continue until two consecutive skin scrapings, taken two weeks apart from the same site, are negative. Figure 14.5 Demodicosis. Periocular skin scrapings were positive for Demodex spp. in this 13‐year‐old diabetic DLH with periocular alopecia, erosion, and crusting. Notoedric mange or feline scabies is a highly contagious yet uncommon disorder caused by Notoedres cati. Affected animals typically have large numbers of mites that are easily found on skin scrapings or acetate tape impressions. Lesions first appear on the proximal edge of the ear, and then spread rapidly to the face, eyelids, and neck. The infestation is intensely pruritic, accompanied by heavy crusts, thickened skin, and hair loss. Lime sulfur dips, topical selamectin (6–12 mg/kg once or twice at a 14‐ or 30‐day interval), topical imidacloprid/moxidectin (Advantage Multi®, Bayer, 0.1 ml/kg once), subcutaneous doramectin (0.2–0.3 mg/kg once), oral ivermectin (0.2 mg/kg twice weekly for four doses), or subcutaneous ivermectin (0.2–0.3 mg/kg at 14‐day intervals) are treatment options. FHV has been identified as a cause of dermatological lesions, particularly those involving facial skin of domestic and wild Felidae. Feline herpetic dermatitis typically but not always involves facial skin and is both proliferative and ulcerative with papules, crusts, and ulcers. Concurrent or preceding upper respiratory or ocular signs can be noted. Skin biopsy is critical for diagnosis and will reveal a markedly destructive eosinophilic furunculosis. The likelihood of an etiological diagnosis will be improved if the pathologist is provided with the clinical suspicion and directed to look for pathognomonic intranuclear inclusion bodies. Failing that, polymerase chain reaction (PCR) assessment of fresh or paraffin‐embedded biopsy samples for the presence of FHV‐1 DNA is very helpful. Unlike ocular disease, where the high rate of viral shedding seen in normal cats dramatically reduces the diagnostic utility of PCR, FHV‐1 PCR appears to be extremely useful for herpetic dermatitis. Treatment can be challenging; in fact, lack of response to empirical therapy for dermatitis should encourage consideration of the diagnosis of herpetic dermatitis. Twice‐daily administration of famciclovir at 90 mg/kg per os is recommended for control of herpetic dermatitis. Lower doses appear less successful, and a protracted course may be necessary. Corticosteroids are contraindicated. Recurrence seems common. Five species within the genus Leishmania have been identified in cats. Leishmania infantum is the predominant pathogen in the Mediterranean Basin, Middle East, and China, but only Leishmania mexicana is established in North America (specifically Texas). In addition to L. infantum, there are regionally endemic Leishmania species in South America. The disease is transmitted by phlebotomine sand flies. Tissue damage is due to granulomatous inflammation and immune complex deposition. Although uveitis is the most common ocular lesion, blepharitis and conjunctivitis have been described. Cutaneous papules, nodules, exudative crusts, and ulcers often develop on the head and may affect the periocular skin. The most common histopathological feature is diffuse granulomatous inflammation with macrophages that contain Leishmania amastigotes. The most frequently used treatment regimen is either long‐term oral administration of allopurinol (10 mg/kg q 12 h or 20 mg/kg q 24 h) as monotherapy or allopurinol as maintenance treatment after a course of subcutaneous injections of meglumine antimoniate. Bacterial infections occur most commonly as a consequence of cat fight injuries. Pasteurella multocida is the most common organism cultured from cat bite wounds. Other isolates include Staphylococcus pseudintermedius, β‐hemolytic Streptococcus, and various anaerobic species. The treatment of choice for a discrete abscess is surgical drainage, flushing the site thoroughly with sterile saline, balanced electrolyte solution, or dilute (1:50) povidone–iodine solution. Pyoderma and bacterial folliculitis are considered rare in cats and usually occur as a consequence of an underlying primary dermatosis, of which hypersensitivities are most common. Periocular involvement occurs in roughly half of cats with facial lesions. Diagnosis is based on cytological examination of adhesive tape preparations, with neutrophils and intracellular bacterial cocci almost always present. Cutaneous nodules are characteristic of mycobacterial infections in cats including feline tuberculosis, caused almost exclusively by Mycobacterium microti or Mycobacterium bovis, and feline leprosy syndrome, attributed to various mycobacteria including Mycobacterium lepraemurium. Single or multiple ulcerated or fistulated nodules have been described on the face and in the eyelids of cats infected with M. lepraemurium. Diagnosis is based on detection of acid‐fast bacilli in smears from fine‐needle aspirates, crush preparations of biopsy specimens, or histological sections. Wide surgical excision of solitary nodules is the treatment of choice, with pre‐ and postoperative antimicrobial therapy using clofazimine, combined with clarithromycin or rifampin. Treatment must be continued for several months or at least two months beyond lesion resolution. Of the various generalized autoimmune dermatoses that may involve the eyelids, pemphigus foliaceus is most common in the cat (Figure 14.6). The disorder develops at any age and often presents with bilaterally symmetrical focal crusting lesions on the head, face, and ears, with periocular involvement. Lesions often appear first in the preauricular skin, accompanied by changes across the bridge of the nose and nasal planum. Claw folds are also commonly affected as the disease progresses. Diagnosis is based on histopathology. Prognosis is favorable when treated with triamcinolone, prednisolone, prednisolone plus chlorambucil, or cyclosporine. Immunosuppressive therapy is usually continued indefinitely at the lowest possible dosage needed to maintain disease remission. Figure 14.6 Pemphigus erythematosus in an adult domestic longhair. Erythematous macular dermatitis and excoriations affect the eyelids, nose, muzzle, and pinnae. Localized and regional erythema, edema, and pain can develop rapidly following stings by bees, wasps, and other hymenopteran insects. The majority of insect stings are self‐limiting events that resolve in a few hours without treatment. Conservative therapy consists of systemic antihistamines, cold compresses, and occasionally topical corticosteroid ointment. Patients should be monitored in the early stages for progressive signs suggestive of anaphylaxis. Facial and periocular edema developed in 5.7% of cats following vaccination. Young adult cats that received multiple vaccines per visit are at greatest risk. Although acute hypersensitivity to a topical medication can produce immediate, transient conjunctival and eyelid swelling, the disorder is more often a delayed lymphocyte‐mediated reaction, the result of repeated or prolonged drug application (Figure 14.7). The telltale eyelid abnormalities include marginal erythema, swelling, and depigmentation, often exaggerating the meibomian gland orifices. A wider zone of periocular alopecia may develop. Conjunctivitis invariably accompanies the lid changes. Commonly implicated medications include neomycin, gentamicin, tetracycline, trifluridine, atropine, and dorzolamide. Blepharitis also occurs with topical cyclosporine, though the reaction more likely reflects the type of oil used to compound the product rather than the cyclosporine itself. Figure 14.7 Blepharitis attributed to adverse drug reaction. Repeated application of topical trifluridine inflamed the eyelids and conjunctiva of this two‐year‐old DSH. The marginal depigmentation is a reliable feature of drug‐related blepharitis. Clinically, feline atopic dermatitis and food allergy appear to be indistinguishable. Young cats appear predisposed to atopic dermatitis, with the majority showing clinical signs between 6 and 24 months of age. The mean age of onset of adverse food reactions was 3.5 years, thought to reflect the prolonged sensitization period before clinical signs develop. The Siamese and its crosses may be predisposed to food allergy. Signs tend to be nonseasonal in either hypersensitivity disorder. The most common and consistent clinical sign of both is pruritus, often localized to the face and neck. Crusted, erythematous papules, self‐induced excoriations, and patchy alopecia often develop in the preauricular area and may extend into the eyelids. Some cats also develop lesions of the eosinophilic granuloma complex, especially eosinophilic plaques. Cytology of skin scrapings revealed eosinophils, while histological sections of affected skin contained eosinophils, mast cells, and plasma cells. In a multicenter study of feline hypersensitivity dermatoses, conjunctivitis occurred in 19% of cats with non‐flea‐associated pruritic dermatitis. The only way to definitively diagnose food allergy is through a food elimination trial. Symptomatic treatment of pruritus with oral or injectable glucocorticoids, cyclosporine, antihistamines, or serotonin antagonists is used in conjunction with allergen‐specific immunotherapy to manage feline atopy. Avoidance of the offending food is required to effectively manage food hypersensitivity. Solar dermatitis is a consequence of chronic sun exposure occurring in white‐ or orange‐faced cats. Lesions first appear on the margins of the ear pinna, but the eyelids (particularly the lower lids) may also be affected. Erythema and fine scaling are followed by skin peeling and crusts, consistent with sunburn. The actinic dermatitis may be a precursor to squamous cell carcinoma (SCC), since cancerous lesions appear at a younger age if preceded by solar damage. Affected cats should be kept indoors from 11 a.m. to 2 p.m., when solar intensity and ultraviolet exposure are greatest, and should not be allowed to sunbathe by open doors or windows. The potential for ocular irritation limits the use of periocular topical sunscreens. Named for its characteristic conjunctival reaction rather than its meibomian gland association (Figure 14.8), lipogranulomatous conjunctivitis is a distinctive inflammatory disorder concentrated within the palpebral conjunctiva adjacent to the eyelid margin and meibomian glands. It occurs in older cats, with a mean age of 11 years (range 6–16 years), and in predominantly white or white‐faced cats or those with limited pigmentation of the eyelid margins. Lesions occur unilaterally or bilaterally but are usually more extensive in the upper eyelid. Increased tearing, mucoid discharge, and blepharospasm are common presenting signs. Smooth, nonulcerated, cream‐ or white‐colored 2–3 mm conjunctival nodules are found adjacent to the eyelid margin, usually numerous and closely packed but occasionally coalescing into much larger nodules that extend the length of the lid. On rare occasion, the nodules may distort the overlying eyelid skin (Figure 14.9). Histological features include variably sized lipid lakes within the submucosal connective tissue, surrounded by macrophages, multinucleated giant cells, and low numbers of plasma cells and lymphocytes, and periglandular fibrosis. Figure 14.8 Meibomitis is less conspicuous in cats than dogs, appearing in this six‐month‐old Persian as a roughened lid margin, with caseous material plugging the meibomian gland orifices. Lipogranulomatous conjunctivitis may respond to a combined oral regimen of doxycycline and prednisolone. Doxycycline provides an inherent anti‐inflammatory benefit as well as a restorative effect on lipid quality within meibomian gland secretions. Warm compresses may also be of benefit. In poorly responsive or severely affected patients, surgical excision of the conjunctival nodules may be considered. Apocrine hidrocystomas arise from modified sweat glands (of Moll) within the skin near the eyelid margin. These benign, cystic tumors have also been referred to as cystadenomas. Persian cats represent over 80% of reported cases, with rare instances in the Himalayan and the domestic shorthair. Older cats are typically affected, with reported cases ranging in age from 3 to 15 years, for a mean of 9.6 years. No sex predisposition is seen. Early lesions appear flat, but typical hidrocystomas are raised, reddish‐brown to black cystic nodules distributed in the skin along the eyelids, especially around the medial canthus. Aspirates of the fluid help differentiate the cysts from melanoma, with macrophages of variable reactivity, phagocytosis of black‐colored debris, and numerous cholesterol clefts. The color of the thick, cell‐poor fluid within the cyst lumen is attributed to hemosiderin and ceroid pigments. Definitive diagnosis requires excisional biopsy and histopathology characterized by multiple cystic structures of various sizes expanding the dermis, with intraluminal hyaline to granular material. Figure 14.9 Lipogranulomatous conjunctivitis. (a) Lipid‐laden macrophages and retained lipid secretions create multifocal conjunctival nodules overlying the meibomian glands in this 12‐year‐old DSH. (b) Secretions may also coalesce to create larger lobules that protrude beyond the lid margin, as in this 13‐year‐old DSH. Treatment is determined by the number and size of the lesions and their effect on eyelid function. Small and random cysts may be monitored without treatment. Individual cysts may be drained by fine‐needle aspirate, but recurrence is common within a matter of weeks to months. Surgical excision can be considered for individual lesions, but new cysts may appear subsequently in some cases. Following incision and drainage of the cyst, the residual tissue can be treated cryosurgically using either liquid nitrogen or nitrous oxide or photoablated using a 1450‐nm diode laser. Anecdotal reports suggest that 1% polidocanol is an effective alternative sclerosing agent for cyst ablation. Eyelid tumors are less common in cats than dogs but more likely to be malignant. Histologically malignant or potentially malignant tumors accounted for 91% of the eyelid masses in one study. Cats older than 10 years of age are most frequently affected, but no sex or breed predilections for eyelid neoplasms have been identified (Table 14.1). SCC is the most common eyelid neoplasm of the cat, occurring most frequently in older cats and in white cats (Figure 14.10). White cats of any haircoat length have a 13 times greater risk of developing SCC than cats of other colors. The Siamese cat’s coloration reportedly decreases its risk of SCC. Solar dermatitis often precedes development of SCC and likely increases the odds of lower eyelid involvement. The tumor occurs at or adjacent to the eyelid margin, appearing erythematous, either slightly raised or depressed, and commonly ulcerated, often with a crusted surface. Local invasion can be extensive, with orbital and regional lymph node involvement, but metastasis is rare until late in the disease. Tumor recurrence is common. In one retrospective study, seven of nine cats with SCC for which follow‐up was available were euthanized, with an average survival time of 7.4 months. SCC is best managed by complete excision with wide, 4–5 mm surgical margins. This approach is most likely to be curative, but excision of larger lesions will require reconstructive techniques to maintain a functional eyelid – or may even dictate enucleation of a visual eye. A variety of techniques have been described for eyelid reconstruction or wound closure following “en bloc” tumor excision in companion animals, including lip‐to‐lid subdermal plexus flaps, local transposition flaps combined with third eyelid advancement, and others. Figure 14.10 Squamous cell carcinoma. The most frequent eyelid neoplasm in cats can appear (a) erosive, as in this localized lower eyelid lesion in a 12‐year‐old DSH; (b) multifocal, involving the medial canthus and lower eyelid in an 11‐year‐old DSH; or (c) nodular, infiltrating the lower eyelid, conjunctiva and nictitans in a 17‐year‐old DSH. Reports of nonsurgical options generally refer to sites other than the eyelid, including the pinnae and nasal planum. Cryosurgery may be an option for superficial tumors. Brachytherapy with radioactive gold‐198 seeds, accelerated, hypofractionated electron beam radiation, and photodynamic therapy have also been reported for treatment of eyelid SCC in cats with varying successes. Beta radiation using strontium‐90 can be used for superficial SCC lesions of 3 mm or less in depth. Intralesional chemotherapy has rarely been reported in the cat, but electrochemotherapy is advocated to improve response of SCC to systemic chemotherapeutic agents. Complete tumor regression occurred in 21/26 (81%) cats (including 12 cats with periocular SCC) treated with intravenous bleomycin and permeabilizing electric pulses delivered across the tumor by modified caliper electrodes. Basal cell carcinoma usually appears round and well circumscribed, but its tendency to ulcerate can make it difficult to clinically distinguish from SCC. The tumor may also appear melanotic, cystic, and alopecic. This carcinoma is generally benign, with slow, indolent growth and very rare metastasis from nonocular sites. Most are small and singular and can be successfully treated by surgical excision or cryotherapy. However, large expansive basal cell tumors may require radical excision and reconstruction. Table 14.1 Frequency of feline eyelid tumors. a Four tumors reported as “undetermined” are omitted from the original data. In the eyelid, mast cell tumors often appear as single, pink, hairless, slightly raised, and sometimes ulcerated masses, near to but typically sparing the lid margin (Figure 14.11). Appearance does vary in the lid as in other cutaneous sites, ranging from clustered, ulcerated masses to large subcutaneous tumors. The age of onset tends to be significantly younger (6.5 years) than the average age of cats with all other types of tumors (11.7 years). One study suggests an increased susceptibility to cutaneous mast cell tumors in the Siamese, Burmese, Russian Blue, and Ragdoll breeds. Mast cell tumors generally have one of the more favorable prognoses of the common eyelid neoplasms in the cat. Eyelid fibrosarcomas in older cats (average age of onset 10.4 years) are generally solitary, nodular, alopecic, and may be ulcerated. This tumor is typically well differentiated, slow growing, and characterized histopathologically by immature fibroblasts interspersed among bundles of collagen. Wide surgical excision is the treatment of choice, with prognosis correlated with the tumor’s mitotic index. The feline eyelid appears particularly prone to peripheral nerve sheath tumors. Characterized as a low‐grade spindle cell tumor, it is locally infiltrative but unlikely to metastasize. Recurrence after excision occurs in nearly all cases treated conservatively. The NL drainage system consists of the upper and lower lacrimal puncta, the lacrimal canaliculi, the lacrimal sac, and the NL ducts that terminate distally in the nasal cavity vestibule beneath the ventral concha. From its origin at the lacrimal sac, the cat’s NL duct descends vertically toward the second premolar and there, at an angle of approximately 90°, changes to a horizontal course that parallels the hard palate. In one area, the NL duct and the canine tooth are separated by only a thin alveolar socket, explaining why tooth extraction in this area may be problematic. In brachycephalic cats, the upper canine teeth are displaced dorsally, forcing the NL ducts to adopt a V‐shaped course that adversely alters tear drainage. Figure 14.11 Mast cell tumors range from small, lightly pigmented, alopecic nodules adjacent to the lid margin (a), seen in this five‐year‐old DSH, to extensive subcutaneous masses (b), involving the entire upper eyelid in this eight‐year‐old DSH. NL disorders occur infrequently in cats and are usually characterized by epiphora. Epiphora due to NL disease must be differentiated from excessive lacrimation secondary to surface irritation or ocular pain. Congenitally imperforate lacrimal puncta are rare and involve the upper punctum more often than the lower in the cats, as is dacryocystitis. In most cases, NL blockage is difficult, if not impossible, to resolve. Irrigation of the NL system produces only temporary improvement in most brachycephalic cats. The rare congenitally imperforate punctum is corrected by carefully excising the overlying mucus membrane, identified by the transient bleb that forms when the system is flushed through the opposite punctum. Restoration of punctal patency in cases of symblepharon is unlikely. Surgical conjunctivorhinostomy has been used with variable success to circumvent the obstructed system and divert tears into the nasal cavity. The third eyelid, also called the nictitating membrane, membrana nictitans, or haw, consists of a semilunar fold of conjunctiva supported by a T‐shaped piece of elastic cartilage curved to conform to the shape of the underlying globe. Its serous gland surrounds the base of the cartilage and contributes to the cat’s aqueous tear film. The epithelium overlying the third eyelid contains numerous goblet cells on the palpebral surface, while aggregates of lymphoid tissue are present on both the inner (bulbar) and outer (palpebral) surfaces of the nictitans. The third eyelid is normally unobtrusive in the cat, visible only with changes in position of the globe, e.g., enophthalmos or exophthalmos, or following loss of the sympathetic tone required to maintain its tonic retraction. Third eyelid protrusion is commonly seen in association with painful ocular disease. Gross thickening or swelling accompanying neoplasia or inflammation may also increase third eyelid visibility. The normal membrane sweeps diagonally across the cornea from its inferonasal location, refreshing the tear film and physically protecting the cornea. There is conflicting information in the literature regarding movement of the third eyelid in cats. Some describe a mechanism for active protrusion effected by abducens‐innervated striated muscle fibers from the levator palpebrae superioris and lateral rectus muscles that attach to the third eyelid. Horner’s syndrome results from the interruption of the efferent sympathetic nervous system to the eye anywhere along its three‐neuron pathway, from the hypothalamus and midbrain to the globe. First‐order Horner’s syndrome is invariably associated with additional neurological deficits that may include ataxia, paresis, postural deficits, altered mental status, and involvement of other cranial nerves. Horner’s syndrome can be the sole neurological abnormality when either second‐ or third‐order neurons are affected. In the cat, protrusion of the third eyelid and miosis are the most consistent features, with variable ptosis and enophthalmos (Figure 14.12). Causes of Horner’s syndrome in the cat include trauma (both exogenous and iatrogenic), neoplasia, and inflammation (especially of the middle ear). Horner’s syndrome is a common complication following surgery for middle ear disease, especially ventral bulla osteotomy, occurring in 53% of cases in one study. Prognosis for spontaneous recovery is generally favorable in cases of trauma, infection, and inflammation, but not so in neoplastic disease. Figure 14.12 Horner’s syndrome. Enophthalmos, ptosis, third eyelid protrusion, and miosis characterize the sympathetic defect in this six‐year‐old DLH with a mediastinal mass. Idiopathic third eyelid protrusion without other ocular is known as “haws syndrome”; the condition is always bilateral, of acute onset, and without any age, breed, or sex predilection. Increased peristalsis, soft stools, and/or diarrhea are present in some cats, suggesting a more generalized sympathetic neuropathy or dysautonomia. Spontaneous resolution is likely but clinical signs may persist for several weeks to even a few months. Prolapse of the gland of the third eyelid is uncommon in cats compared with dogs. The Burmese breed predominates in reports of this disorder, but it has also been documented in the Persian and domestic shorthaired cat. While glandular prolapse in dogs typically occurs during the first one to two years of life, cats tend to be older at presentation (Figure 14.13). The gland should be surgically repositioned in order to preserve its substantial contribution to the cat’s tear volume, with reported success similar to that for the dog. Figure 14.13 Prolapse of the third eyelid gland in a three‐year‐old Burmese. The gland in the opposite eye prolapsed four years later. Both were successfully corrected using a pocket technique. Although third eyelid neoplasia is uncommon in cats, a variety of tumors have been described that affect either the surface tissues and substantia propria or the gland of the third eyelid. Differentials for third eyelid masses include eosinophilic conjunctivitis, epitheliotropic mastocytic conjunctivitis, and adnexal cryptococcosis. Hemangiomas involving the leading edge of the third eyelid, mast cell tumors, and SCCs have all been described in the third eyelid of cats. Lymphoma has also been reported to affect the conjunctiva and the third eyelid of cats, often as a periocular manifestation of generalized disease. Compared to third eyelid gland neoplasms in dogs, those in cats are more likely to metastasize, recur, and substantially shorten patient survival times. With the exception of severe, irreparable trauma, the only indication for third eyelid removal is advanced and invasive neoplasia. Ocular surface disease is common in cats. Owing to the frequency with which bacterial and viral pathogens have been documented in cats with conjunctivitis and corneal disease, it is prudent to consider feline surface disease infectious until proven otherwise. Unlike the dog, in which most surface infections are linked with predisposing abnormalities of the adnexa and tear film, several primary pathogens are implicated in diseases of the feline conjunctiva and cornea. The most important of these are C. felis, a conjunctival pathogen, and FHV‐1, a causative agent of conjunctival or corneal disease (or both). While initial clinical signs reflect a direct cytopathic effect on ocular surface epithelium, and less commonly and less severely pathology within the underlying corneal stroma or conjunctival lamina propria, long‐term consequences of these infections may include altered surface anatomy, tear film deficiency and dysfunction, persistent or recurrent immunological reactions, altered corneal clarity, and diminished tissue viability. Conjunctivitis is arguably the most common ocular complaint in cats. Feline conjunctivitis should be considered infectious until proven otherwise. The most commonly implicated primary pathogens are C. felis and FHV‐1; the latter is also capable of infecting the feline cornea. Based on the volume of experimental and clinical data substantiating the role of these two pathogens in feline ocular surface disease, a practical clinical approach is to first eliminate keratitis, uveitis, or glaucoma as the primary diagnosis, and then to rule out less common causes of conjunctivitis in cats, such as foreign body, neoplasia, eyelid or cilia disorders, tear film dysfunction, or allergy. Conjunctivitis can then be considered most likely caused by C. felis or FHV‐1, with chlamydial conjunctivitis being nonulcerative, seen in the absence of keratitis, and more likely dominated by chemosis than intense hyperemia. In contrast, herpetic conjunctivitis often has more intense hyperemia than it does chemosis and can be ulcerative, especially in primary infections. There is often coincident keratitis. Other conjunctival pathogens include Mycoplasma spp., feline calicivirus (FCV), and Bordetella bronchiseptica. Chlamydiae are obligate intracellular Gram‐negative bacteria that demonstrate a predilection for conjunctival epithelial cells. The most significant feline pathogen is C. felis. This organism also persistently infects respiratory, gastrointestinal, and genitourinary epithelial cells, a factor that likely accounts for the relapse of clinical signs following topical therapy. Chlamydia felis infection occurs primarily through close contact with other infected cats and their ocular secretions, or less commonly via aerosol transmission. The organism can also be spread by contaminated fomites, but survives only a few days at room temperature and is inactivated by most disinfectants. Following exposure, infectious elementary bodies attach to and enter epithelial cells, and then differentiate into reticulate bodies that undergo binary fission within a cytoplasmic vacuole or inclusion. Organisms mature into elementary bodies, infecting adjacent conjunctival epithelial cells following cell lysis. Chlamydia felis also spreads via the bloodstream to other tissues, including the tonsil, lung, liver, spleen, gastrointestinal tract, and kidney. The incubation period is approximately 3–5 days following experimental infection, but clinical signs may take 5–14 days to appear following natural infection. Infection with C. felis is more common in young cats, especially those 2–12 months of age. Although maternal antibody is thought to protect most kittens less than 12 weeks of age, they may be infected by the queen at birth based on occasional isolation of C. felis from cats with neonatal conjunctivitis. Clinically normal cats with high Chlamydiae‐specific antibody titers can shed and transmit Chlamydiae. Cats older than five years of age are less likely to be infected with C. felis. Clinical signs of acute chlamydial infection often develop unilaterally, and then appear in the second eye a few days later. Characteristics include blepharospasm, serous ocular discharge, and chemosis, the latter often masking the intensity of concurrent conjunctival hyperemia (Figure 14.14). The discharge may become purulent with chronicity or coinfection by opportunistic resident flora. Conjunctival follicle formation has been described, but lymphoid hyperplasia is more likely a nonspecific sign of chronic antigenic stimulation rather than a reliable indicator of C. felis infection. Upper respiratory signs are mild to absent. Following initial infection, signs usually regress spontaneously within two to six weeks, and may improve more rapidly in older cats than kittens. Conjunctivitis may persist in milder form for many months, alternate between active and quiescent phases, or resolve completely. It is unclear whether chronic conjunctivitis is the result of reinfection from infected in‐contact cats or recrudescence stemming from persistence of the organism in nonocular tissues. Treatment of the affected as well as all in‐contact cats would therefore appear to be the most successful approach to managing feline chlamydiosis. A variety of diagnostic tests have been used to confirm infection with C. felis, each with limitations. Basophilic intracytoplasmic inclusions, often located adjacent to the nucleus, may be identified by light microscopy in conjunctival scrapings collected two to nine days after onset of clinical signs; however, this method is relatively insensitive due to the transient nature of the inclusions and the improbability of finding inclusions in chronically infected cats. If available, direct fluorescent antibody or immunocytochemical stains may increase sensitivity and specificity of this method. Assays utilizing the PCR are the preferred method for confirming active chlamydial infection. Chlamydial DNA can be detected in conjunctival swabs, scrapings, or biopsies, although no significant difference was found in the C. felis detection rate between samples collected from the oropharynx, conjunctiva, nose, or tongue of cats with upper respiratory disease. Vigorous swabbing is recommended to ensure adequate numbers of epithelial cells are collected. Since healthy cats can be PCR‐positive on occasion, results must always be interpreted in light of the patient’s history and clinical signs. Other diagnostic methods such as ELISA to detect chlamydial antigen in conjunctival swabs or serology to detect circulating chlamydial antibodies are considered inferior to PCR or culture as diagnostic tools. When limitations of all available tests are considered, some simply rely on clinical signs and response to therapy as a means of diagnosis. Figure 14.14 PCR‐positive Chlamydia felis conjunctivitis in a six‐year‐old DSH. (a) Initial presentation with conjunctival hyperemia and chemosis. (b) Following a 30‐day regimen of oral doxycycline. Systemically administered doxycycline is the drug of choice for feline chlamydial infections, producing rapid improvement in clinical signs and likely clearing the organism from ocular as well as systemic sites. Both the hyclate and monohydrate salts are effective. Kittens over four weeks of age can be treated with doxycycline without enamel discoloration. Oral administration of doxycycline at 5–10 mg/kg q 12 h for three to four weeks results in clinical resolution in most cats. Clinical signs diminish within 24–72 h of the start of treatment. Client compliance may improve using a once‐daily regimen of oral doxycycline (10 mg/kg q 24 h), but treatment must then be continued for at least 28 days to eliminate the organism. Since some group‐housed cats require treatment for as long as six to eight weeks to clear the infection, a general rule is to treat for a minimum of three weeks and at least two weeks beyond resolution of clinical signs. Oral pradofloxacin suspension (5–7.5 mg/kg q 24 h for six weeks) is an acceptable alternative in cats unable to tolerate doxycycline. Topical therapy is not recommended as a sole route for treatment of cats with chlamydiosis. Treatment with tetracycline or erythromycin ointment two to four times daily for as long as 60 days can improve clinical signs but will not eliminate infection. Therefore, these formulations are probably best used in conjunction with systemic therapy to promote therapeutic drug concentrations at the ocular surface, control secondary infections not susceptible to doxycycline, and lubricate the inflamed tissues. Other common topical antibacterial agents such as gentamicin, triple antibiotic, chloramphenicol, and fusidic acid are ineffective against C. felis. Maternal antibodies usually protect kittens from infection by C. felis until seven to nine weeks of age. Natural infection confers little protection against reinfection, although there may be an age‐related resistance based on the lower prevalence of chlamydiosis in older cats. Both inactivated and attenuated live chlamydial vaccines may reduce the severity of clinical signs by decreasing C. felis replication, but they do not completely prevent infection or shedding of the organism after challenge. Mycoplasma spp. have traditionally been considered causative agents of feline conjunctivitis, but their role as primary pathogens has been difficult to substantiate since they may also be found as apparently commensal organisms of the feline conjunctiva and upper respiratory tract. Mycoplasma felis and Mycoplasma gateae are the species most often mentioned in association with feline conjunctivitis, but one study utilizing PCR also detected Maianthemum canadense, Mycoplasma cynos, Mycoplasma lipophilum, and Mycoplasma hyopharyngis in affected cats. Clinical signs ascribed to infection with Mycoplasma spp. are nonspecific and include unilateral or bilateral conjunctivitis, accompanied by serous to mucopurulent discharge, conjunctival hyperemia, and chemosis (Figure 14.15). In one experimental study, conjunctival hyperemia developed two to three days after inoculation and disappeared without treatment within seven days. Papillary hypertrophy lends a velvety texture to the conjunctival surface. An adherent conjunctival pseudomembrane may be misinterpreted as a thick white exudate. Corneal stromal ulcers with neutrophilic cellular infiltrates and keratomalacia have been seen in association with Mycoplasma spp. infection, but predisposing factors such as coinfection with FHV‐1 are probably required for mycoplasmal invasion of the cornea to occur. Figure 14.15 PCR‐positive Mycoplasma spp. conjunctivitis in a two‐year‐old DSH. (a) Initial presentation with conjunctival hyperemia and chemosis. (b) Day 16 of an oral azithromycin regimen. Although cytology of conjunctival scrapings has been suggested as a diagnostic tool, Mycoplasma spp. are not dependably visible by light microscopy because of their small size. When found, the organisms appear as multiple punctate, darkly staining coccoid inclusions within the cytoplasm of conjunctival epithelial cells. Culture of this commensal organism does not necessarily substantiate its role in a patient’s clinical disease. Although PCR assays provide more rapid detection of Mycoplasma spp., the clinical significance of positive results is still unclear. Tetracyclines and fluoroquinolones are active against most Mycoplasma spp. isolates. Treatment should be continued for at least two weeks, although the optimal duration of therapy in systemic infections is unknown. FCV is a nonenveloped RNA virus, widespread in the feline population. Between them, FCV and FHV‐1 are estimated to account for up to 90% of upper respiratory tract infections in domestic cats. Infection occurs through direct contact of oral or nasal secretions from infected animals with conjunctival, oral, or nasal mucosa. The oropharynx is the primary site of viral replication. Most cats shed virus for at least 30 days following infection, but some may become lifelong carriers, infecting naïve cats through chronic intermittent shedding. Clinical findings depend on the virulence of the FCV strain, the age of the affected cat, and elements of the animal’s husbandry. Acute oral and upper respiratory disease occurs mainly in kittens following an incubation period of 2–10 days, with transient viremia occurring three to four days after infection. The virus induces necrosis of epithelial cells, creating vesicles on the margin of the tongue that coalesce into geographic, map‐shaped ulcers, considered the hallmark of FCV infection. These erosive or ulcerative lesions typically heal within two to three weeks. Mild upper respiratory disease with sneezing and serous nasal discharge accompanies oral ulceration. Less common manifestations of FCV include pneumonia, lameness secondary to acute synovitis, and chronic stomatitis. Despite its ability to induce epithelial cell necrosis, FCV has been considered a rather inconsequential ocular pathogen, causing ocular discharge and only mild, if any, conjunctivitis in experimentally infected cats. More significant ocular surface disease has been described in recent reports, including moderate to severe erosive conjunctivitis and conjunctivitis sufficiently severe to obscure the corneal surface. Detection of FCV is optimized using combinations of quantitative reverse transcription PCR (RT‐qPCR) or by combining RT‐qPCR with cell culture to confirm the presence of replicating virus. Calicivirus RNA can be detected in conjunctival and oral swabs, cutaneous scrapings, and blood by use of PCR. Since seroprevalence of FCV is high due to natural infection and vaccination, evidence of FCV antibodies by virus neutralization or ELISA does not reliably indicate infection. Therapeutic options are limited. Contemporary topical and systemic antiviral agents used to treat FHV‐1 inhibit DNA synthesis and are therefore ineffective against FCV, an RNA virus. All healthy cats should be vaccinated against FCV. Modified live virus vaccines, particularly those administered intranasally, are preferred in shelters due to rapid seroconversion. While vaccination provides protection against acute oral and upper respiratory tract diseases, it does not prevent cats from becoming infected or from subsequently shedding FCV. Although B. bronchiseptica is considered an important cause of respiratory disease in cats, this aerobic Gram‐negative coccobacillus is likely to cause only mild ocular discharge and conjunctivitis. This highly contagious organism is shed in oral and nasal secretions and also grows in natural water sources. Strains that infect dogs can be transmitted to cats, and vice versa. Once inhaled, the bacteria adhere to respiratory cilia and secrete toxins damaging to the underlying respiratory epithelium. The incubation period ranges from 2 to 10 days. Clinical signs vary in severity, but sneezing is a conspicuous feature of feline infection, in contrast to the paroxysmal cough exhibited by dogs. Disease is usually confined to the upper respiratory tract, but fatal bronchopneumonia does occur in kittens. Ocular signs consist of conjunctivitis accompanied by serous to mucopurulent ocular discharge. Bordetellosis is confirmed by aerobic bacterial culture and PCR assays performed on nasal and oropharyngeal swabs. Dacron or rayon swabs are preferred for culture, since growth may be inhibited by cotton swabs. Positive PCR results can occur for at least three weeks after intranasal vaccination. Serology is of limited value for diagnosis because of the high prevalence of antibodies in the feline population. Many infections are mild or self‐limiting. Systemic antibacterial treatment is usually reserved for kittens less than six to eight weeks of age, patients with respiratory disease lasting longer than 7–10 days, or those with signs of bronchopneumonia. Doxycycline is the antibiotic of choice, dosed at 5 mg/kg orally every 12 h for 21 days. Specific treatment of the conjunctivitis is not required, since the organism does not colonize the ocular surface. Supportive care can be provided with a topical mucinomimetic such as sodium hyaluronate. Routine vaccination against B. bronchiseptica is not recommended in pet cats but should be considered in animals group‐housed in facilities with a record of confirmed bordetellosis. Eosinophilic conjunctivitis appears as an autonomous clinical entity, without signs of the keratitis that shares its name – and likely its etiopathogenesis. One or both eyes may be affected in cats ranging in age from 1 to 15 years. The conjunctival surface often has a distinctive velvety texture, with concurrent swelling and hyperemia that also extends to the third eyelid (Figure 14.16). Mucoid to mucopurulent discharge is common, as is depigmentation, thickening, and erosion of the lower eyelid margin and medial canthus. Conjunctival scrapings are characterized by a preponderance of eosinophils and mast cells. Eosinophils, lymphocytes, plasma cells, mast cells, and macrophages are seen histologically. The same type I and IV hypersensitivity reactions proposed for eosinophilic keratitis could explain the cellular profile of eosinophilic conjunctivitis. Topical or systemic anti‐inflammatory drugs resolve clinical signs in as little as three to six weeks, but most cats require indefinite maintenance therapy to prevent relapse, similar to that subsequently described in detail for eosinophilic keratitis. Figure 14.16 Eosinophilic conjunctivitis in a seven‐year‐old DSH with a three‐year history of ocular disease. Generalized conjunctival thickening and a suede‐like surface texture obscure the underlying keratitis. A conjunctival scraping contained eosinophils, lymphocytes, and plasma cells. Clinical signs of epitheliotropic mastocytic conjunctivitis resemble those of eosinophilic conjunctivitis, albeit in an uncommonly severe proliferative form, with conjunctival hyperemia, thickening, and mucoid ocular discharge. Third eyelid abnormalities feature prominently, with either solitary nodules that expand the third eyelid or smaller, sometimes ulcerated nodules proliferating within the third eyelid conjunctiva. Its proliferative character may be clinically misinterpreted as SCC. Topical treatment with tacrolimus or corticosteroid is effective in controlling clinical signs, but some cats required long‐term therapy to prevent relapse. Feline conjunctivitis has been associated with the nematode Thelazia californiensis, particularly in the western United States, while Thelazia callipaeda is considered an emerging pathogen in Europe. Fannia spp. flies serve as vectors of T. californiensis; T. callipaeda is transmitted by the fruit fly Phortica variegata. Transmission of the parasite occurs when flies feed on lacrimal secretions, depositing third‐stage larvae that develop into adult worms within the conjunctival cul‐de‐sac. Cases are often diagnosed in the late summer and autumn when the fly vectors are most active. Clinical signs include serous to purulent discharge, blepharospasm, conjunctival hyperemia, and chemosis, although an occasional cat is asymptomatic. The threadlike, motile whitish worms are physically removed from the conjunctival cul‐de‐sac using forceps. Monthly administration of milbemycin oxime has been suggested to prevent reinfection. The larvae of Cuterebra spp. may be deposited within the conjunctival tissue, leading to severe inflammation. Treatment consists of manual removal of the larva, followed by application of a topical antibiotic coupled with a topical or systemic anti‐inflammatory drug until the conjunctivitis has resolved. Feline conjunctival melanoma is an invasive tumor that may involve the bulbar and the palpebral conjunctiva as well as that of the third eyelid (Figure 14.17). Most tumors are heavily pigmented; only five amelanotic tumors have been described. This tumor exhibits a slightly higher metastatic risk (14% versus 10%) and a decidedly higher mortality rate (61% versus 5%) than affected dogs. Prognosis is guarded to poor, but aggressive surgical intervention may improve outcome. Enucleation or exenteration are generally recommended. Feline conjunctival lymphoma is an uncommon isolated tumor, but it has been reported with both bilateral and unilateral presentations of the palpebral or third eyelid conjunctiva with either B‐cell or T‐cell predominance (Figure 14.18). A marked lobulated thickening of the conjunctiva may be appreciated. Prognosis is guarded since subsequent development of generalized disease is typical. Figure 14.17 Malignant melanoma of the conjunctiva in an 11‐year‐old DSH. A darkly pigmented third eyelid is accompanied by bulbar and palpebral conjunctival pigmentation and thickening. Conjunctival vascular tumors of endothelial origin tend to be superficial exophytic masses, red to reddish‐brown in color, and either smooth or multilobulated in character. Hemangiomas or hemangiosarcomas may develop along the leading edge of the third eyelid, the temporal bulbar conjunctiva, or the inferior palpebral conjunctiva. Hemangiosarcomas tend to have a more chronic course, existing 10.5 months prior to presentation versus 3.5 months for hemangiomas. Conjunctival vascular tumors have a favorable prognosis. Treatment of choice is surgical excision with adjunctive cryotherapy. Squamous Cell Carcinoma SCC is most likely to affect the palpebral conjunctiva and third eyelid as a consequence of eyelid tumor expansion. SCC has not been reported as a primary conjunctival tumor in cats, with the exception of a single case report of a 14‐year‐old domestic shorthair (DSH) in which SCC and hemangioma developed on the cornea and conjunctiva without apparent eyelid involvement. Figure 14.18 Conjunctival lymphoma was diagnosed in a nine‐year‐old DSH based on biopsy of a mass that distended the superior palpebral and bulbar conjunctiva. Adenocarcinoma of the conjunctival surface occurs in cats of various breeds with a mean of 10.7 years. The conjunctiva overlying the third eyelid is the most frequent location, but tumor cells can also infiltrate the perilimbal cornea and third eyelid gland. Local recurrence is frequent; enucleation or exenteration may be required. Although corneal and conjunctival disease can occur independently of each other, it is more common, especially with inflammatory disorders, to see coincident involvement of both tissues (i.e., keratoconjunctivitis), albeit with one tissue sometimes more affected than the other. As with conjunctivitis, feline keratoconjunctivitis is typically infectious in nature, with the most important primary corneal pathogen in cats being FHV‐1. While many other pathogens worsen corneal ulceration, FHV‐1 is the only organism known to initiate ulcers in cats. FHV‐1 is a DNA virus and member of the alphaherpesvirus subfamily of herpesviruses. Typical of members of this subfamily, the hallmark biological features of FHV‐1 are “tight” host species specificity, rapid intracellular replication within epithelial cells, and establishment of lifelong latency within neural cells. Because of FHV‐1 short environmental survival, the major route of infection is via direct transfer of virus‐containing macrodroplets between oral, nasal, and conjunctival mucosal surfaces of cats. An estimated 75–97% of the world’s cat population is seropositive, and the virus is considered to be responsible for 45% of all upper respiratory infections and the majority of corneal ulcers in cats. Viral replication occurs primarily within epithelium of the upper respiratory tract and eye, principally the conjunctiva, nasal turbinates, and nasopharynx, with more limited replication in corneal epithelium. Like species specificity, tissue specificity is likely mediated by virus–host cell surface receptor interactions. Cell damage occurs through lysis or rupture of the cell membrane at the time of viral release, a phase of infection called “productive” or “cytolytic,” causing erosion and ulceration of mucosal epithelium. During acute replication within peripheral epithelial cells, some viral particles ascend neural axons to the nucleus where they may establish lifelong latency (Figure 14.19). Latency is defined as a state where virus cannot be cultured (i.e., nonproductive infection), viral transcription is limited to only latency‐associated transcripts (LATs), and there is no clinical disease. Viral DNA has been identified in the trigeminal ganglion, the autonomic ganglia, optic nerve, olfactory bulb, vestibular ganglia, conjunctiva, and cornea. Periodic reactivation of latent FHV‐1 occurs after physiological stresses such as rehousing, transport, parturition, and lactation, or following systemic administration of corticosteroids or epinephrine. Indeed, corticosteroid administration has been advocated as a method of detecting carriers in endemic populations. Once reactivation occurs, the virus is believed to descend the same sensory nerve axons it ascended during primary infection, and thereby reach the peripheral epithelial tissues again. Viral reactivation may occur in the absence of clinical signs or with a diverse range of recrudescent ocular, dermatological, or upper respiratory signs associated with recurrence of cytolytic (productive) replication in the mucosal epithelia. Figure 14.19 A common sequela of neonatal FHV‐1 infection, symblepharon can restrict eyelid mobility, obliterate the conjunctival cul‐de‐sac, limit tear drainage, and impact corneal clarity and vision. (a) This young Maine Coon illustrates a reduced palpebral fissure and gross corneal opacity OS. (b) The temporal limbus is obscured in a young DSH, with an accompanying inclusion cyst and focal sequestrum. (c) Diffuse corneal adhesions hide intraocular detail in this four‐month‐old DSH. In addition to the latent and cytolytic phases of the FHV‐1 life cycle, a “persistent” state is also proposed. Persistency mimics some aspects of latency, especially the inability to culture viable (virulent) virus. However, persistent virus is distinct from latent virus because (i) genes in addition to LATs are expressed and (ii) it is associated with (and likely induces) a chronic, often low‐grade, inflammatory response. Persistency is the purported mechanism for chronic, typically nonulcerative, immunopathological diseases such as herpetic stromal keratitis, lymphocytic/plasmacytic conjunctivitis, and potentially eosinophilic keratoconjunctivitis, herpetic dermatitis, and herpetic uveitis. Finally, there is a growing appreciation that FHV‐1 may cause disease through an additional mechanism – so‐called metaherpetic disease. Metaherpetic disease arises from permanent or semipermanent anatomical changes as a result of cytolytic and/or immunopathological disease. Some examples of suggested metaherpetic disease include (i) symblepharon following exposure of corneal and/or conjunctival stroma due to ulcerative herpetic disease, (ii) chronic conjunctival goblet cell depletion and tear film dysfunction following apparent clinical recovery from primary herpetic disease, (iii) neurogenic dry eye as a result of corneal anesthesia secondary to herpetic injury to the trigeminal nerve, and (iv) band keratopathy or corneal sequestra as a result of exposure and structural alteration of the anterior stroma following chronic herpetic corneal ulceration. There appears to be a real but relatively minor relationship between chronic herpetic diseases and coinfection with FeLV and FIV. Cats with chronic FHV‐1 infection are more likely to be infected with FeLV or FIV than normal cats. Coinfection rates of FHV‐1 with other agents of upper respiratory disease such as FCV, C. felis, B. bronchiseptica, and Mycoplasma spp. range widely and the likely clinical significance of coinfections is not known. Clinical signs of infection with FHV‐1 vary greatly depending on the cat’s age, viral inoculum, and immune status. Following primary infection of FHV‐1‐naïve kittens, there is widespread and rapid viral replication in epithelium of nasal mucosa and conjunctiva, marked upper respiratory and conjunctival inflammation, fever, anorexia, and lethargy. Morbidity is high but mortality is uncommon, especially with supportive care. Tissue damage is due to viral cytolysis with subsequent ulceration of these mucosal surfaces, and sometimes symblepharon formation. In contrast, FHV‐1 replicates to a more limited extent in corneal epithelium; however, it can cause ulceration, notably dendritic lesions. The cause of the branching pattern of these ulcers is unknown, but is considered to be pathognomonic for herpetic infections of all species. Dendritic corneal lesions occur in a biphasic pattern on days 3 and 12 of primary infection, the latter peak likely reflecting virus released from replication within and rupture of conjunctival epithelium. Little, if any, viral replication occurs within the corneal stroma. Primary disease is usually self‐limiting within 10–20 days. Recrudescent disease is seen in some latently infected cats following periods of viral reactivation. The severity of disease and the tissues involved in these recrudescent episodes range widely among individuals and even among disease episodes. Disease may result from cytolytic, immunopathological, or metaherpetic mechanisms. Conjunctivitis is usually milder and less ulcerative than seen in the acute infection. However, substantial conjunctival thickening and hyperemia can occur secondary to inflammatory cell infiltration. Corneal infections may again involve epithelial tissues, in which case dendritic and later geographic corneal ulceration may be seen, as in primary infections. Stromal keratitis may occur and is likely immunopathological, i.e., immune‐mediated but not necessarily autoimmune in origin. The events surrounding experimental FHV‐1 stromal keratitis are most compatible with a delayed type hypersensitivity response (Th1 cell‐mediated, macrophage effector cells). A major paradox exists with respect to the diagnosis of FHV‐1. Cats experiencing primary FHV‐1 infection shed virus in sufficient quantities that viral detection is relatively easy. However, clinical signs during this phase of infection tend to be characteristic and self‐limiting, making definitive diagnosis less necessary. In contrast, during the more chronic FHV‐1‐associated syndromes, the diversity and ambiguity of clinical signs make viral identification more desirable, especially if specific antiviral therapy is being considered. However, the elusive nature of the virus in these chronic syndromes makes this difficult. Indeed, the diagnosis of FHV‐1 in individual cats represents one of the greatest challenges in the management of chronic FHV‐1‐related diseases. Although the specificity and extreme sensitivity of PCR has improved detection of virus, it has also confirmed that virus can be demonstrated in a large minority of apparently normal cats. Currently available tests rely on demonstration of an immunological response (usually in serum) to the organism, or detection of whole, cultivable virus by virus isolation (VI), its antigens by immunofluorescent antibody (IFA) test, or its DNA by PCR. Treatment of herpetic disease in cats inevitably involves the use of supportive care (e.g., topical antibiotics if secondary infection or corneal ulceration is present, artificial tears if lacrimal insufficiency exists, etc.) but may also require antiviral therapy. In cytolytic disease, where cell rupture occurs as a direct result of viral replication, and virus can often be cultured from diseased tissue, antiviral drugs are recommended and immunomodulatory therapy is generally contraindicated. In immunopathological disease, where the host’s reaction to viral antigens or altered autoantigens is believed to be the major cause of disease, virus is less reliably isolated (but can sometimes still be detected by PCR), and ulceration is less common. Here, antiviral drugs are typically ineffective when used alone, and concurrent immunomodulatory therapy is often required. However, if used without the “backdrop” of an antiviral agent, immunomodulatory therapy may encourage cytolytic disease. With metaherpetic disease, antiviral or immunomodulatory therapies alone or together are typically ineffective, and therapy specific to the anatomical and/or physiological disruption is required. Although opinions vary as to when and why antiviral therapy should be instituted in cats believed to be experiencing herpetic diseases, it appears reasonable that antiviral agents should be considered when signs are severe, persistent, or recurrent, particularly when there is corneal involvement, and especially ulceration. Because epithelial replication, latency and reactivation, and persistence are such interdependent and sequential phases of herpetic disease, interruption of any one of them is expected to limit the virus’ abilities to cause subsequent disease. Therefore, aggressive treatment of FHV‐1‐associated disease may limit disease progression and minimize frequency and severity of recurrences. Idoxuridine has been used as a 0.1% ophthalmic solution or 0.5% ophthalmic ointment. This drug is reasonably well tolerated by most cats and seems efficacious in many. It should be applied to the affected eye at least five to six times daily. Vidarabine is available as a 3% ophthalmic ointment and may be better tolerated than many of the other topical antiviral preparations but should be applied to the affected eye at least five to six times daily. Trifluridine is too toxic to be administered systemically, but topically administered trifluridine is considered one of the most effective drugs for treating HSV‐1 keratitis. This is in part due to its superior corneal epithelial penetration. This makes it the preferred topical agent from stromal keratitis (although the systemic agent – famciclovir – may be even more effective). A 1% ophthalmic solution is used in human herpetic keratitis at least five to six times daily. Unfortunately, it often causes marked ocular irritation in cats. Cidofovir dissolved in artificial tears to form a 0.5% or 1.0% solution and applied is equally effective when administered only twice daily as trifluridine administered four to nine times daily. This is believed to be due to the long tissue half‐lives of the metabolites of this drug. The efficacy of a 0.5% solution compounded in methylcellulose artificial tears and applied topically twice daily to cats experimentally infected with FHV‐1 was associated with reduced viral shedding and clinical disease. Acyclovir has poor bioavailability and is potentially toxic when systemically administered to cats. With the advent of the apparently safer and more effective famciclovir, systemic administration of acyclovir seems difficult to justify. However, acyclovir is available in some countries as an ophthalmic ointment that reduces systemic toxicity concerns but not necessarily questions of antiviral efficacy against FHV‐1. Regardless, a 0.5% ointment used five times daily in naturally infected cats was associated with a median time to resolution of clinical signs of 10 days. Valacyclovir is a prodrug of acyclovir and should never be administered to cats. Famciclovir is a highly bioavailable prodrug of penciclovir that is effective against FHV‐1 in vitro. While some debate continues regarding the optimum dose of famciclovir in cats, 90 mg famciclovir/kg twice daily has been shown to achieve adequate plasma levels and a reduction in clinical signs. Lysine’s antiviral effect is believed to arise because arginine is an essential amino acid for FHV‐1 replication, and assumes that lysine antagonizes arginine availability to or utilization by these viruses during protein synthesis. Studies suggest that lysine is safe when orally administered to cats and, provided that it is administered as a bolus (250 mg [kittens] or 500 mg [adult cats] once or twice daily), may reduce viral shedding in latently infected cats and clinical signs in cats undergoing primary exposure to the virus. However, improvement in clinical signs or their duration is unpredictable and study results vary. The interferons (IFNs) are a group of cytokines that have diverse immunological and antiviral functions. The IFNs are divided into four groups; α, β, γ, and ω IFNs, and numerous subtypes. Viral infection stimulates cells to secrete IFN into the extracellular space where it binds to specific receptors on neighboring cells and, through mechanisms not fully understood, prevents or limits the spread of infection (i.e., it is not virucidal). The few peer‐reviewed in vivo studies do not lend strong support to use of these drugs. Adhesion of the palpebral, bulbar, and/or third eyelid conjunctiva to itself or to the cornea is termed symblepharon. The epithelial ulceration that predisposes to the adhesions is most often a consequence of neonatal herpetic keratoconjunctivitis, but symblepharon could follow any severe conjunctivitis that effaces the epithelial surface, including chemical or thermal burns. Clinical signs are determined by the severity and location of the symblepharon and range from subtle alterations in depth of the conjunctival cul‐de‐sac to blinding corneal opacification. Common signs include a reduced palpebral fissure, a prominent third eyelid, and epiphora due to NL punctal occlusion. The conjunctival vessels that overlie the corneal surface may be misinterpreted as a refractory keratitis, since conventional therapy will not alter these permanently transposed vessels. Symblepharon is not painful, once the causative inflammation resolves. Symblepharon is easier to prevent than to treat. Early recognition and appropriate treatment of neonatal conjunctivitis are essential. In cases of acute conjunctival damage, the raw surfaces must be separated until re‐epithelialization occurs. Soft contact lenses and methyl methacrylate conformers have been used for that purpose following chemical injury in people. Otherwise, the opposing tissues must be pried apart, sometimes several times daily, using a sterile cotton swab or forceps inserted between the topically anesthetized layers. Surgical treatment of chronic symblepharon is usually reserved for patients with impaired vision or altered eyelid function, since success of surgery is often disappointing. Eosinophilic keratitis is a gradually progressive, infiltrative disease that derives its name from the eosinophils found in cytological and histopathological samples of the affected cornea and adjacent conjunctiva. The age of affected cats ranges from 7 months to 17 years, with a trend toward young adult males of ≤4–6 years of age (Figure 14.20). Figure 14.20 Eosinophilic keratitis. (a) Raised white plaques and vascularization in the temporal cornea of a two‐year‐old DSH. (b) Distinctive temporal plaque formation with mild vascularization in a six‐year‐old DSH. (c) Generalized stromal infiltration with widespread yet indistinct surface plaques and prominent vascularization in a two‐year‐old DSH. The disorder is more often unilateral than bilateral, affecting only one eye approximately 75% of the time. The classical lesion appears commonly in the dorsolateral cornea, but any and all corneal quadrants may be affected. Pinpoint cream‐colored nodules in the perilimbal conjunctiva and subtle superficial vascularization in the adjacent cornea may be overlooked at the onset. As the infiltrative process progresses, an irregular pink to flesh‐colored vascularized corneal mass develops, bordered by a zone of corneal edema. Perhaps, the most distinguishing feature of eosinophilic keratitis are the raised, variably sized, friable white plaques that develop atop the corneal infiltrate and adjacent bulbar conjunctiva, described as cheesy or cottage cheese‐like. Corneal ulcerations may be present as well. Blepharospasm, ocular discharge, and conjunctival hyperemia are variable, usually intensifying over time. The nictitating membrane may appear thickened. Diagnosis of eosinophilic keratitis is confirmed by cytological examination of superficial corneal scrapings. Smears often contain epithelial cells, eosinophils, mast cells, neutrophils, and lymphocytes, along with nuclear debris and eosinophilic granules from disrupted cells. Eosinophils may not be the predominant cell type, but a single eosinophil is considered diagnostic. The etiopathogenesis of eosinophilic keratoconjunctivitis is unknown, although there is a suspected association with FHV‐1 infection based on positive IFA or PCR assays. The presence of eosinophils in cytological specimens of cats with conjunctival and corneal lesions also correlates highly with detection of FHV‐1 DNA. Eosinophilic keratoconjunctivitis is more likely controllable rather than curable, based on a 65.5% recurrence rate once treatment is discontinued. Local immunosuppression remains the mainstay of treatment. Traditionally, topical corticosteroids such as 1% prednisolone acetate or 0.1% dexamethasone are applied q 6–12 h in a gradually tapering regimen, dictated by clinical response. Treatment is recommended for several weeks beyond resolution of clinical signs. A low‐frequency maintenance regimen may be required, e.g., application three times weekly, should clinical signs relapse following cessation of therapy. In cats with a history of corneal ulceration, documented FHV‐1 infection, or concurrent ulceration, topical or systemic antiviral therapy is a prudent addition to any immunosuppressive regimen. Other immunomodulatory or anti‐inflammatory drugs have also been used to manage eosinophilic keratoconjunctivitis. Topical cyclosporine of varying concentrations has been used successfully either alone or in combination with corticosteroids. Cyclosporine may be better suited for long‐term maintenance once the keratoconjunctivitis has been initially controlled with steroids. Early reports of eosinophilic keratitis relied almost exclusively on oral megestrol acetate to control clinical signs. This oral progestogen should be used with caution, since its glucocorticoid activity at high or prolonged doses can cause adrenocortical suppression and impaired glucose metabolism leading to diabetes mellitus. Following an induction regimen of 5 mg daily for five days, and then 5 mg every other day for five doses, dosage is quickly tapered to the lowest level needed to sustain clinical remission. Only 2.5–5 mg megestrol acetate as infrequently as once monthly may prevent relapses once clinical signs are controlled. A topical regimen of megestrol acetate 0.5% applied q 8–12 h also appears to successfully control eosinophilic keratitis while limiting the risk of systemic side effects. Unlike dogs, tear film dysfunction and dry eye disease in cats is less commonly recognized, remains very poorly understood, and seems to be associated with more subtle clinical signs and often poorly responsive to therapies typically effective in dogs. In dogs, dry eye disease carries with it strong connotations of aqueous tear film deficiency consequent to immune‐mediated destruction of the lacrimal glands and typically responsive to cyclosporine. In contrast, this appears to be a very rare syndrome in cats. Rather, those cases of dry eye disease in cats in which an etiopathogenic diagnosis is made appear more likely to result from dysfunction of the meibomian glands, goblet cells, or trigeminal nerve, and it appears that this dysfunction may result from metaherpetic (anatomical/physiological postherpetic) damage. Of particular relevance is a specific metaherpetic syndrome in which virally induced damage to the trigeminal nerve axons and their ganglion is believed to reduce corneal sensation and thus reduce reflex tearing. Neurogenic keratoconjunctivitis sicca may occur secondary to diseases disrupting parasympathetic innervation of the lacrimal glands, such as dysautonomia. When neurogenic dry eye disease is suspected in cats, it appears, in addition to a very thorough clinical exam, as well as Schirmer tear test‐1 (STT‐1) and tear film break up time (TFBUT) measurements, that assessment of corneal touch threshold and a stimulated STT (similar in intent to the originally described STT‐3) may be useful. The goal of this revised STT‐3 is to cause reflex tearing by stimulation of a nerve other than the trigeminal nerve while a STT strip is in place in the conjunctival fornix. One described way of doing this is to place a cotton ball soaked in alcohol in front of but not touching the cat’s nose for 1 min prior to and during performance of an otherwise standard STT‐1. Cats with a functional lacrimal gland and intact efferent sympathetic and parasympathetic pathways, and therefore capable of tear production and secretion but lacking the normal trigeminal reflex to initiate or promote such tearing, have dramatic increases in their STT result in response to this olfactory stimulation. It may be that the percentage increase in tearing that occurs in affected eyes is of more interest and potentially more diagnostic than is the absolute STT result achieved. Given the permanent anatomical, likely metaherpetic, changes associated with tear film dysfunction in cats, therapy at present is extremely limited and largely focused upon tear film supplementation. There is some evidence that hyaluronate will not only increase tear film stability in the short term but also cause/facilitate goblet cell regeneration. The feline cornea is almost circular in shape, with a mean horizontal diameter of 16.5 ± 0.6 mm and a mean vertical diameter of 16.2 ± 0.61 mm. Values reported for the adult cat’s central corneal thickness range from 546 μm using ultrasonic pachymetry to 767 μm measured histologically. Corneal curvature also changes over the first 12–15 months of life, decreasing from a steeply curved, astigmatic state in the young kitten to a roughly spherical shape with 39 D of refractive power in the adult. Normal endothelial cell density in cats ranges from 2668 ± 211 to 2846 ± 403 cells/mm2. With age, endothelial cell density decreases, while endothelial cell size and pleomorphism increase. The central cornea is less sensitive in brachycephalic than domestic shorthair cats and corneal subepithelial/subbasal nerve fiber densities measured in mm/mm2 are higher in domestic cats compared to Persian cats and mesocephalic and brachycephalic dogs. Until proven otherwise, it is fair to assume a cat’s superficial corneal ulcer is a consequence of FHV‐1 infection. Poorly adherent epithelial margins are also common in herpetic ulcers. The indolent‐type ulcer or SCCED of middle‐aged and older dogs, characterized by failure of epithelial adherence to the underlying stroma, seldom, if ever, occurs in cats. Accordingly, keratotomies with a needle have little place in the management of feline ulceration and have been implicated in sequestrum formation when performed. Management of stromal ulcers in cats is not unlike that in dogs (see Chapter 9). Keep in mind that herpetic ulcers involve loss of only corneal epithelium. Stromal involvement implies persistence of another inciting cause or opportunistic infection by bacteria or fungi that adhere to damaged tissue. Corneal “melting” occurs when an imbalance between endogenous matrix metalloproteinases, bacterial proteolytic enzymes, and the proteinases present in the cornea and precorneal tear film leads to destruction of corneal collagen (Figure 14.21). Figure 14.21 Mycoplasma spp. was cultured from the axial cornea of this 16‐year‐old cat with diffuse keratomalacia and corneal vascularization. Other potential causes of ulceration include eyelid abnormalities, quantitative or qualitative tear deficiencies, foreign bodies, neurological deficits that alter eyelid function or corneal sensitivity, and trauma. With perhaps the exception of trauma, these precipitating factors appear less frequently in cats than in dogs A normal STT measures 14.3 ± 4.7 mm/min; TFBUT in young, healthy cats is 16.7 ± 4.5 s. Surgical grafting may be indicated if an ulcer is rapidly progressing, if >66% of the corneal thickness has been lost, or when medical therapy fails to resolve the ulcer. Mycotic keratitis is rare in cats, although the presence of fungi in conjunctival swabs has been demonstrated in 40% of healthy cats. In general, predisposing factors for fungal keratitis include tear film insufficiency, treatment of corneal ulceration with topical antimicrobials and/or corticosteroids, exposure to environmental vegetative material, and the presence of fungal organisms within the normal conjunctival flora. Clinical signs often include unusually severe blepharospasm, with conjunctival hyperemia and variable discharge. Corneal ulceration may be accompanied by a raised, opaque surface plaque with irregular margins and multifocal satellite lesions of gray‐white stromal infiltrates. A pigmented plaque suggests infection by dematiaceous fungi. Keratomalacia can lead to rapid stromal loss. Secondary corneal vascularization and anterior uveitis are common (Figure 14.22). Figure 14.22 Mycotic keratitis in a seven‐year‐old DSH with a raised, dull corneal plaque composed of mats of fungal hyphae, masking the underlying stromal ulcer. Rapid confirmation is based on cytological evidence of fungal hyphae in corneal scrapings. The specific fungus is ideally identified by culture, but samples may require prolonged incubation. PCR is an emerging option for faster and thus clinically relevant fungal identification. Topical 1% voriconazole, 1% miconazole, or silver sulfadiazine has been used successfully to treat fungal keratitis in the cat. A seemingly benign corneal disease referred to as Florida spots or tropical keratopathy has long been recognized in cats in the southeastern United States, the Caribbean Basin, and Brazil. The disorder is characterized by singular or multiple gray to white corneal opacities located within the anterior stroma of one or both eyes (Figure 14.23). The lesions are variably sized, from 1 to 8 mm in diameter, round to irregular in shape, and often appear most dense at their center. The cornea is otherwise unremarkable, with no signs of vascularization or inflammation, and the affected cats show no discomfort. The cause of the keratopathy is unknown; however, affected cats suffer no discomfort or changes in visual behavior. Figure 14.23 Tropical keratopathy (Florida spots). (a) Multiple opacities in the cornea of a 5.5‐year‐old DSH appear pale against the medial iris and dark against the tapetal reflection. (b) Multiple pale stromal infiltrates with typically denser centers are present in the dorsal cornea of an otherwise asymptomatic feline eye. A sequestrum is characterized histologically by stromal collagen degeneration and distinguished clinically by discoloration of the affected corneal stroma, its color progressing from subtle amber and bronze to jet black over time. The unmistakable stromal discoloration is seldom, if ever, seen in these other species (Figure 14.24). Corneal sequestration occurs in cats of all ages, with the apparent exception of neonates, and exhibits no gender predilection. Brachycephalic breeds appear predisposed to sequestrum formation. Persian cats have the highest reported incidence, followed by Siamese, Burmese, Himalayan, and domestic shorthair breeds. The clinical appearance of a corneal sequestrum is unmistakable. The lesion usually develops unilaterally. Bilateral lesions can arise simultaneously or sequentially but tend to occur most often in Persians or other brachycephalic breeds. An oval to circular pigmented lesion commonly develops in the central or paracentral cornea, its color progressing from translucent amber to darker bronze, and then to an impervious jet black with chronicity. Depth of the lesion varies and can extend from the superficial stroma to Descemet’s membrane. As the sequestrum progresses and opacifies, lesion depth becomes increasingly difficult to determine without benefit of advanced imaging modalities such as ultrahigh‐resolution ultrasound. The lesion may appear raised above the surrounding cornea as corneal epithelium migrates beneath the sequestrum, separating it from the deeper stroma. Accompanying clinical signs include blepharospasm, ocular discharge, and conjunctival hyperemia. The corneal epithelium is usually absent over and immediately surrounding the sequestrum, but uptake of fluorescein may be limited by the stromal necrosis or may be difficult to visualize over the sequestrum itself. Corneal vascularization varies from mild to severe, with no clear relationship to duration of the sequestrum. Histopathologically, the epithelium overlying the sequestrum is usually absent and poorly adherent at the lesion margins. The sequestrum itself is characterized by coagulation necrosis and lacks keratocytes, inflammatory cells, and blood vessels. Vascularization or granulation tissue commonly encompasses or undermines the sequestrum. The etiopathogenesis of sequestrum formation remains speculative, although some form of chronic corneal insult is thought to initiate the process. Brachycephalic breed‐related adnexal abnormalities, including lagophthalmos, entropion, and medial canthal trichiasis, are repetitively linked with corneal sequestration. Tear film abnormalities have also been described as potential initiators of sequestra formation. Chemical cauterization has also been incriminated as an iatrogenic stimulus. FHV‐1 is implicated as a factor in sequestrum formation. Chronic corneal ulceration precedes sequestration in some cats and FHV‐1 DNA has been identified in experimentally induced and naturally occurring sequestra. Interestingly, the prevalence of FHV‐1 DNA is greater in sequestra from domestic breeds than in Persians or Himalayans, lending support to the fundamental role of conformation in sequestrum formation in the brachycephalic breeds of cat. Figure 14.24 Corneal sequestrum. (a) Early stromal bronzing associated with a central corneal ulcer in an adult Persian. (b) Temporal sequestrum secondary to chronic entropion in an eight‐year‐old DSH. Treatment must address causative factors as well as the sequestrum itself. Because a superficial sequestrum may eventually slough as the corneal epithelium undermines the necrotic tissue, some clinicians advocate a conservative medical approach that combines a topical prophylactic antibiotic, a topical hyaluronan‐based lubricant, and a topical or oral antiviral if herpesvirus is suspected. Spontaneous healing is often a prolonged process and less likely to occur with deep stromal lesions. Definitive removal of the sequestrum is indicated in persistent or deep lesions, especially as corneal inflammation progresses and pain increases. Lamellar keratectomy is the technique of choice for definitive surgical excision, removing the sequestrum in its entirety while preserving as much healthy cornea as possible (Figure 14.25). Time to healing is significantly shorter following surgical removal (3.8 weeks) than with medical therapy alone (11.2 weeks). Recurrence may be prevented using a conjunctival graft over the keratectomy site. Acute bullous keratopathy (ABK) is a rare but distinctive feline disorder characterized by sudden onset of profound but relatively well‐circumscribed corneal edema, with coalescing fluid bullae that disrupt and weaken the stroma’s lamellar structure and dramatically alter corneal contour. Synonyms include eruptive bullous keratopathy and acute corneal hydrops. The disorder tends to present unilaterally in young adult cats; however, both eyes may be involved concurrently or sequentially, and cats as old as 15 years of age have been affected. Nonspecific findings accompanying the acute corneal change include excessive tearing, blepharospasm, and conjunctival hyperemia. The extremely edematous stromal bulla develops within hours and without warning. The lesion may vary from only a few millimeters in diameter to one that encompasses the entire corneal surface (Figure 14.26). There is typically a distinct junction between the lesion and the normal cornea that surrounds it. The underlying cause of ABK is unknown. Proposed etiologies include a defect of Descemet’s membrane and the adjacent endothelium, a primary or inherited stromal dystrophy, or endothelial dysfunction. Figure 14.25 Corneal sequestrum of one‐year duration in a six‐year‐old DSH. (a) Preoperative appearance. At surgery, the lesion extended to Descemet’s membrane. (b) Eight weeks after, deep lamellar keratectomy and fresh lamellar corneal graft. Figure 14.26 ABK characterized by a well‐defined protrusion of markedly edematous, structurally compromised corneal stroma in (a) a three‐year‐old DSH and (b) a six‐year‐old DSH. Both cats were treated successfully using a third eyelid flap. Some instances of feline ABK have responded to medical treatment using topical 5% sodium chloride and/or antibacterials (oxytetracycline, neomycin–polymyxin B–bacitracin, and/or tobramycin) administered for weeks to months. Smaller lesions are realistically the only candidates for medical management alone. For more extensive lesions, surgical options are generally grouped into those that provide tectonic support, including conjunctival pedicle and corneal grafts, and those that tamponade the bullous tissue, including nictitating membrane flaps and tarsorrhaphies. Resolution of ABK occurred in 90.5% of eyes treated with nictitating membrane flap. Corneal dystrophy is defined as a primary inherited, bilaterally symmetrical corneal disease, unassociated with prior inflammation or systemic disease. The only reports of dystrophy in cats describe endothelial dysfunction and secondary stromal edema (Figure 14.27). A recessive mode of inheritance has been proposed in the Manx cat. The disease inevitably progresses over a two‐year period, culminating in bullous keratopathy. Endothelial dystrophy also occurs in domestic shorthair cats, with stromal edema beginning in the central cornea at three to four weeks of age, progressing peripherally but ultimately sparing the perilimbal cornea. Bullous keratopathy and epithelial thinning are late complications. There is no specific treatment, although penetrating keratoplasty may be a viable alternative in cats. Lipid keratopathy/degeneration is also rare in the cat and almost always associated with prior damage to the cornea (Figure 14.27b). Lipid and/or mineral deposition accompanies corneal inflammation and vascularization. The infiltrate can develop without concurrent systemic lipid abnormalities, but hyperlipidemia may modify the appearance and progression of the keratopathy. Corneal cloudiness is a common feature in cats with lysosomal storage diseases, including GM1 and GM2 gangliosidoses, α‐mannosidosis, and mucopolysaccharidoses I and VI. Each of these recessively inherited inborn errors of metabolism is linked to a specific enzymatic deficiency that causes accumulation of a substrate – lipid, glycoprotein, or mucopolysaccharide – within the lysosomes. Figure 14.27 Corneal dystrophy/degeneration. (a) Presumed endothelial dystrophy in a three‐year‐old DSH with bilateral progressive corneal edema beginning at four months of age. (b) Corneal degeneration with lipid deposition and vascularization following corneal ulceration in a three‐year‐old Siberian cat. Although the lateral canthus may be the most common location for feline ocular dermoids, corneal dermoids have been described in the domestic shorthair and Birman breeds and lateral limbal dermoids have been seen in Burmese and domestic shorthair cats. Lamellar keratectomy is the treatment of choice. Neoplasia of the feline cornea is rare. Expansion of a conjunctival, limbal, or intraocular tumor into the cornea is considered far more likely than development of a primary neoplasm in this normally avascular tissue. Feline corneal tumors resulting from extension of ocular or periocular tumors include SCC, limbal melanoma, lymphoma, anterior uveal melanoma, and post‐traumatic ocular sarcoma (Figure 14.28). The neonatal feline iris appears blue to blue‐gray, developing its adult coloration around eight weeks of age. The mature feline iris is lightly colored, with a spectrum that includes blue, green, yellow, and gold, or combinations thereof. The overall lighter coloration may reflect a greater proportion of pheomelanin to eumelanin within the iris stroma. The colored feline iris also lacks a pigmented cell layer in the anterior iris stroma typical of brown‐eyed dogs and has less pigmentation surrounding its iridal vessels. The serpentine character of the major arterial circle in the peripheral iris is also easily appreciated in these lightly colored eyes. The cat’s vertically elliptical pupil is regulated by two autonomically innervated antagonistic muscles. The iris sphincter is parasympathetically controlled via the oculomotor and short ciliary nerves. The cat has only two short ciliary nerves that exit the ciliary ganglion, the nasal nerve that innervates the medial half of the sphincter and the malar nerve that supplies the lateral half. A lesion affecting a single short ciliary nerve produces a hemidilated pupil with a D‐ or reverse‐D shape, determined by the nerve and the eye affected. Blue‐eyed white cats lack pigment in their iris and choroidal stroma due to absence of pigmented cells normally derived from the embryonic neural crest (Figure 14.29). Presumably, the progenitor cells fail to migrate to the ocular tissue, fail to differentiate into uveal pigment cells, or fail to survive. The Siamese cat is also deficient in ocular pigment, but its blue eyes are the result of defective pigment production. Pigment cells within the Siamese iris and choroid contain little to no pigment. Figure 14.28 (a) A subconjunctival limbal melanocytoma extends into the deep cornea in a fan‐shaped pattern. (b) The same eye following excision and repair using a full‐thickness scleral homograft. (Image courtesy of Dr Caryn Plummer.) Figure 14.29 Iris heterochromia in a white domestic shorthair cat. (Image courtesy of Dr Caryn Plummer.) The presence of blue irides in cats is often linked with other functional abnormalities. The white (W) pigment gene in cats is autosomal dominant over color but distinct from albinism. Unlike dogs homozygous for the merle gene, homozygous blue‐eyed white cats do not typically have visual deficits but are instead prone to deafness. The prevalence of deafness is greater when blue eyes are bilateral than if unilateral. While white coat color is clearly a dominant trait, inheritance of blue eyes and deafness is described as autosomal non‐Mendelian, with incomplete penetrance. Neuroanatomical abnormalities in the visual pathways of blue‐eyed Siamese cats give rise to crossed eyes (convergent strabismus or esotropia), nystagmus, and decreased stereopsis. Part of the temporal retina that normally projects to the ipsilateral lateral geniculate nucleus (LGN) instead projects to the contralateral LGN. While abnormal retinogeniculate pathways exist in every Siamese cat, the degree of involvement varies. The abnormal contralateral projection creates a mirror or inverted image of the normal representation. While this misalignment would be expected to create substantial visual impairment in the Siamese, adjustments in the cortex reduce the behavioral impact of the misdirected projections. The cats either suppress a portion of the input to the visual cortex (i.e., the Midwest cat) or rearrange the relay of the abnormal projections in the visual cortex (i.e., the Boston cat). Most Siamese cats probably possess a mixed pattern of cortical organization that combines both mechanisms. Nevertheless, Siamese cats lack both binocular vision and stereoscopic depth perception and are virtually blind in the nasal hemifield when they view the world with only one eye. Esotropia or convergent strabismus may accompany these neuroanatomical abnormalities, developing during the third month of age (Figure 14.30). Since the patterns of visual activation by each eye are independent and lack binocular interaction in the visual cortex, there is no advantage to normal ocular alignment. The convergent strabismus may in fact be beneficial, providing an overlapping, albeit independent, view of a few degrees of frontal vision. Surgical correction of the strabismus is neither indicated nor recommended. Nystagmus may be more common than strabismus. Figure 14.30 Esotropia in a feral DSH cat of unknown age. Persistent pupillary membranes (PPMs) are relatively uncommon in cats when compared to dogs. There is no apparent breed or sex predisposition. Normally, the pupillary membrane regresses during late fetal development and into the immediate postnatal period. PPMs are vestiges of this embryonic vascular network, originating at the iris collarette, a region of the iris face midway between the pupillary margin and peripheral iris base. The point of origin helps differentiate PPMs from postinflammatory adhesions (synechia) that typically incorporate the pupillary margin. PPMs are either confined to the iris surface or extend from the iris face to the posterior cornea or to the anterior lens capsule where they produce nonprogressive opacities at the attachment site (Figure 14.31). The residual strands are variably pigmented, thick or thin, singular or multiple, and may even appear as a fiber web spanning the pupil. Thin, lightly pigmented iris face PPMs may continue to regress in kittens up to three to four months of age but are permanent thereafter. Those PPMs with corneal or lens attachments do not regress. Treatment of PPMs is seldom indicated. Figure 14.31 A network of PPMs originates at the iris collarette and spans the pupil in this adult DSH. Rare instances of anterior segment dysgenesis have been described in cats, with broad adherence of the iris to the posterior cornea. Synonyms include anterior segment cleavage syndrome and Peters’ anomaly. The space normally representing the anterior chamber is narrowed or nonexistent. Notable corneal opacification is associated with segmental histological defects in Descemet’s membrane and the corneal endothelium, where the uveal and corneal tissues blend. Iris colobomas are characterized by a notch‐like defect in the pupil (Figure 14.32), most often occurring in the ventromedial iris. The iris defect may be full or partial thickness, the latter not only altering the pupil shape but also exposing the posterior pigmented layers of the iris. Though rare in cats, iris colobomas may be associated with other colobomatous defects of the eyelid, choroid/sclera, and optic disc. Iris atrophy occurs in cats less frequently than in dogs. The problem is generally one of older cats, but iris thinning and loss of surface texture can also follow chronic uveitis or glaucoma. Blue‐eyed cats may be more commonly affected. Iris atrophy may be focal or diffuse, recognized by an irregular pupillary margin, by distinct defects in the iris stroma, or by thinning that simply permits visualization of the tapetal reflection through the stroma. Acquired iris cysts are more common than those that occur congenitally (Figure 14.33). The pigmented epithelium of the iris (or, less commonly, the ciliary body’s inner epithelium) may undergo spontaneous cystic hyperplasia in the absence of inflammation or other predisposing factors. Cysts are also a consistent finding in cats with a history of blunt ocular trauma. In contrast to canine iris cysts, those in cats tend to be bilateral, multiple, elongate, or ovoid in shape, more darkly pigmented, and seldom, if ever, free‐floating. Treatment is seldom necessary. Figure 14.32 The left pupil tilts along its vertical axis and is offset nasally in this four‐month‐old Burmese with bilateral corectopia. Figure 14.33 (a) A single darkly pigmented iris cyst remains attached within the posterior chamber. (b) A shallow anterior chamber resulted from multiple, dark‐walled iris cysts within the posterior chamber, seen only after pupillary dilation in this adult DSH. Inflammation of the iris and ciliary body, i.e., anterior uveitis, is one of the most common and significant ocular diseases in cats, with an immediate impact on ocular function and patient comfort. Uveitis can be a stand‐alone condition affecting the eye only, or can be part of a more generalized systemic syndrome in which the eye is one of several organs involved. In order to return the eye’s vascular tunic to normal, the attending clinician is obligated to recognize the clinical signs of uveitis in timely fashion and treat the uveal inflammation to its conclusive resolution. With few pathognomonic signs, documenting the cause of feline uveitis may be the most daunting task. Even with extensive diagnostics, a cause may not be discovered in as many as 70% of cats with uveitis, leaving only symptomatic therapy to combat the inflammation, without eliminating its underlying stimulus. Reduced but not resolved, the inflammation may ultimately lead to complications such as glaucoma that compel the enucleation of a blind, painful eye. The clinical signs of anterior uveitis are similar regardless of the species of animal or underlying cause. The most reliable indicators of intraocular inflammation are the presence of aqueous flare, signaling breakdown of the blood–aqueous barrier, and decreased intraocular pressure (IOP), a consequence of ciliary body dysfunction: Hyperemia results from vasodilation of conjunctival and episcleral vessels. Ciliary flush refers to a rose‐red coloration of the perilimbal sclera that reflects dilation and congestion of the deeper uveal vasculature. Corneal opacification results from edema produced when toxins, inflammatory mediators, and cellular precipitates damage the endothelium. Vessels may invade the deeper corneal layers, while inflammatory cells (keratic precipitates) often settle on the cornea’s inner surface. As noted previously, conjunctival hyperemia and corneal edema are typically more subtle in cats compared to dogs with anterior uveitis. Although many diseases are known to cause uveitis in the cat, idiopathic uveitis remains the most common diagnosis in clinical practice and an etiological conclusion substantiated by reviews of feline uveitis throughout the years. Other considerations include the principal part of the uveal tract involved, the duration of the inflammation, and whether the problem is unilateral or bilateral. Cats with systemic disease are generally younger, with a mean age of 7.6 years compared to 9.6 years for cats with idiopathic uveitis. Two‐thirds of cats with systemic disease have bilateral ocular involvement, while only half of cats with idiopathic disease are bilaterally affected. A thorough physical examination should be performed to assess the cat’s general health and to direct subsequent testing. A minimum database that includes a complete blood count (CBC), serum biochemistry profile, urinalysis, and serology for FeLV and FIV is indicated in patients with systemic signs of illness, those with bilateral endogenous uveitis characterized by cells and fibrin in the anterior chamber and/or concurrent posterior segment inflammation, and those with uveitis that fails to respond as expected to symptomatic therapy. Ultimately thoracic and abdominal radiography, abdominal ultrasound, and aspirates of lymph nodes, masses, and draining tracts for cytological examination may be performed. Serology to confirm or eliminate infectious disease is dictated by systemic signs of illness, abnormalities in the minimum database, or likelihood of exposure based on geographical location, as with systemic mycoses. Aqueous cytopathology is primarily useful in the diagnosis of lymphoma. Cats infected with FeLV have a twofold greater risk of developing eye disease than noninfected cats. However, FeLV causes no primary eye disease, metastatic lymphoma is the apparent cause of anterior uveal infiltration seen in FeLV‐positive cats, and retinal lesions observed in anemic FeLV‐infected cats are secondary to pancytopenia rather than a direct effect of the virus. Perhaps, the most clinically important consequence of FeLV infection is immunosuppression that predisposes to secondary infectious disease and increases tumor risk by altering inherent tumor surveillance mechanisms. Testing for FeLV should be performed in any cat with a new diagnosis of uveitis, even if the cat has tested negative in the past (Box 14.1 ). The early stages of uveal lymphoma may appear similar to any other uveitis, although the iris generally appears increasingly thickened and irregular as the disease progresses. Lesions usually appear flesh‐colored and may have a velvety texture (Figure 14.34). Dyscoria or anisocoria develops as neoplastic infiltration restricts pupil mobility or as a consequence of FeLV‐related neurological effects.
14
Feline Ophthalmology
Introduction
Diseases of the Eyelids
Congenital Eyelid Abnormalities
Abnormalities of Eyelid Opening
Eyelid Agenesis
Structural Eyelid Abnormalities
Entropion
Dermoid
Blepharitis
Fungal Blepharitis
Parasitic Blepharitis
Viral Blepharitis
Protozoal Blepharitis
Bacterial Blepharitis
Immune‐Mediated Blepharitis
Allergic Blepharitis
Miscellaneous Blepharitis
Lipogranulomatous Conjunctivitis
Eyelid Cysts and Nodules
Eyelid Neoplasia
McLaughlin et al. (1993) Total No. (%)
McLaughlin et al. (1993) Total No. (%)
Newkirk and Rohrbach (2009) Total No. (%)
Martins and Barros (2014) Total No. (%)
Tumor type
Veterinary medical data program a
Purdue comparative oncology program
Squamous cell carcinoma
56 (65%)
13 (36%)
12 (28%)
14 (54%)
Mast cell tumor
3 (4%)
4 (11%)
11 (26%)
0
Hemangiosarcoma
2 (2%)
0
6 (14%)
6 (23%)
Carcinoma/adenocarcinoma
5 (6%)
0
4 (9%)
0
Apocrine hidrocystoma
0
1 (3%)
3 (7%)
0
Peripheral nerve sheath tumor
0
0
3 (7%)
0
Lymphoma
0
4 (11%)
3 (7%)
0
Hemangioma
1 (1%)
0
1 (2%)
0
Melanoma
2 (2%)
3 (8%)
0
0
Fibrosarcoma
4 (5%)
3 (8%)
0
3 (12%)
Squamous papilloma
0
3 (8%)
0
0
Basal cell carcinoma
2 (2%)
0
0
1 (4%)
Basal cell epithelioma
0
2 (6%)
0
0
Sebaceous adenoma/epithelioma
3 (4%)
2 (6%)
0
1 (4%)
Histiocytic sarcoma
0
0
0
1 (4%)
Histiocytoma
0
1 (3%)
0
0
Neurofibroma
1 (1%)
0
0
0
Fibroma
2 (2%)
0
0
0
Trichoepithelioma
1 (1%)
0
0
0
Total benign
8 (10%)
9 (25%)
4 (9%)
2 (8%)
Total malignant
74 (90%)
27 (75%)
39 (91%)
24 (92%)
Diseases of the Nasolacrimal System
Diseases of the Third Eyelid
Horner’s Syndrome
Idiopathic Third Eyelid Protrusion
Prolapsed Third Eyelid Gland
Neoplasia
Ocular Surface Disease
Conjunctival Disease
Chlamydia felis
Mycoplasma felis
Feline Calicivirus
Bordetella bronchiseptica
Eosinophilic Conjunctivitis
Epitheliotropic Mastocytic Conjunctivitis
Parasitic Conjunctivitis
Conjunctival Neoplasia
Melanoma
Lymphoma
Vascular Tumors
Conjunctival Surface Adenocarcinoma
Keratoconjunctival Disease
Feline Herpesvirus Type 1
Treatment
Antiviral Therapy
Lysine Therapy
Interferons
Symblepharon
Eosinophilic Keratitis/Proliferative Keratoconjunctivitis
Dry Eye Disease Syndromes
Corneal Disease
Normal Cornea
Corneal Ulceration
Fungal Keratitis
Florida Spots
Corneal Sequestrum
Acute Bullous Keratopathy
Corneal Dystrophies and Degenerations
Corneal Dermoids
Corneal Neoplasia
Diseases of the Anterior Uvea
Developmental or Structural Disorders
Uveal Pigmentation in White and Siamese Cats
Congenital Iris Anomalies
Acquired Iris Abnormalities
Iris Atrophy
Iris Cysts
Anterior Uveitis
Clinical Features of Feline Uveitis
Classification of Uveitis
Systemic Evaluation
Causes of Anterior Uveitis
Feline Leukemia Virus
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