Feline Corneal Disease

Chapter 248


Feline Corneal Disease



The cornea is the transparent anterior aspect of the outer fibrous layer of the globe. The cornea is composed of five layers: a precorneal tear film over the outer stratified squamous epithelium, epithelial basement membrane, middle stroma, Descemet’s membrane, and inner endothelium. The main functions of the cornea are to contain the intraocular contents and to aid in the refraction and transmission of light due to its curvature and transparency, respectively. The transparency of the cornea is maintained by a number of anatomic features: a lack of blood vessels, lymphatics, or pigmentation; a nonkeratinized surface epithelium maintained by the moisture of the preocular tear film; a unique lattice organization of small-diameter stromal collagen fibrils; and a functioning inner endothelial layer to maintain its relative state of dehydration. It is noteworthy that the feline cornea is only 0.5 mm thick at its periphery and 0.6 mm thick centrally. The cornea is rich in sensory nerve supply derived from the ophthalmic branch of the trigeminal nerve (cranial nerve V). A functional tear film; an intact and healthy corneal epithelium, stroma, endothelium, and nerve supply; and lack of corneal infiltrate are crucial for the overall health and functioning of the cornea. The unique necessity for the cornea to maintain transparency often is compromised because many corneal disorders lead to corneal opacification and impaired vision.


Cats are affected by a variety of nonulcerative and ulcerative corneal diseases. Feline herpesvirus type 1 is known to play a role in many forms of feline keratopathies, including dendritic corneal ulcers, eosinophilic keratitis, and corneal sequestra. Fortunately, many feline corneal diseases are responsive to medical or surgical therapies. The identification of appropriate treatments depends on the clinician’s first establishing an accurate diagnosis. This chapter focuses on the diagnostic approach to feline corneal disease, describes both general and distinguishing clinical characteristics of the most common disorders, and provides an overview of currently available medical and surgical therapies.



Clinical Signs


There are a number of clinical signs associated with corneal disease in the cat. These signs generally are not specific for a type of disease. The most common findings are summarized in Box 248-1.



Box 248-1   Clinical Signs of Feline Corneal Disease




Ocular discharge (serous, mucoid, mucopurulent, serosanguineous, crusty, dark brown or black)


Blepharospasm


Conjunctival or episcleral injection


Chemosis (conjunctival edema)


Corneal opacification due to the following:



Corneal vascularization (superficial branching or straighter deep blood vessels)


Secondary reflex uveitis (miotic or constricted pupil; conjunctival hyperemia; aqueous flare; inflammatory cells in anterior chamber; fibrin in anterior chamber)


Raised pink to white chalky plaques from medial or lateral limbus (most consistent with proliferative eosinophilic keratitis)


Amber to black region of cornea (most consistent with corneal sequestrum)



Feline Herpesvirus 1 Keratoconjunctivitis



Clinical Presentation and Diagnosis


Feline herpesvirus 1 (FHV-1) is a ubiquitous DNA α-herpesvirus that infects and causes necrosis of the epithelial surfaces of the respiratory tract and conjunctiva and, to a lesser extent, the corneal epithelium. Infection with FHV-1 generally causes a self-limiting primary disease. Primary FHV-1 disease is characterized by malaise, pyrexia, inappetence, sneezing or coughing, and nasal as well as ocular discharge. The virus is spread from cat to cat by direct contact, fomites, or aerosolization of the virus. Studies have estimated that over 90% of cats are seropositive for the virus. Approximately 80% of FHV-1–affected cats develop a lifelong latent infection (FHV-1 carriers), and of these cats, approximately 45% develop periodic reactivation of the virus and either asymptomatically shed FHV-1 or have clinical disease.


Many feline ocular diseases are caused directly by or associated with FHV-1, including most commonly conjunctivitis and ulcerative keratitis. FHV-1 produces disease via at least two mechanisms: (1) cytolytic infection during active viral replication resulting in cell rupture such as occurs during primary FHV-1 infection or following viral reactivation from latency, and (2) immune-mediated inflammation. Clinical ophthalmic manifestations of FHV-1 cytolytic infection are numerous and include conjunctivitis characterized by hyperemia, blepharospasm, chemosis, and ocular discharge. Conjunctivitis, unilateral or bilateral, is the most common FHV-1–related ocular disorder in adult cats without active respiratory disease, although some cats have concurrent sneezing or other mild signs of respiratory tract infection. Keratoconjunctivitis sicca (KCS) has been reported in cats with FHV-1–related conjunctivitis as well. FHV-1 is the sole documented viral cause of keratitis in cats; therefore every case of feline ulcerative and nonulcerative keratitis should be considered to be associated with FHV-1 unless proven otherwise. Dendritic or geographic corneal ulcers are a common manifestation of FHV-1 infection. If both the cornea and conjunctiva are ulcerated because of the cytolytic effects of FHV-1, corneal stroma and conjunctival substantia propria become exposed, which facilitates adhesion formation between these tissues (i.e., symblepharon). Neonatal ophthalmia may be caused by FHV-1 infection, either from maternal transmission to the kitten or infection shortly after birth.


Clinical disease caused by the immunopathologic mechanism of FHV-1 is an uncommon response to the viral infection. Stromal keratitis results from an immune-mediated response to viral antigen and is probably the most serious ocular manifestation of FHV-1 infection. Subconjunctival administration of dexamethasone has predisposed experimentally infected cats to develop stromal keratitis. Stromal keratitis, often secondary to chronic ulceration, is characterized by ocular discomfort, deep corneal vascularization, edema, and cellular infiltrates and can lead to significant corneal opacification and fibrosis. Table 248-1 provides a list of the corneal diseases in which FHV-1 infection plays a role and their characteristic clinical signs.



The frequency with which cats are vaccinated against FHV-1 as well as the number of clinically healthy cats that carry and shed FHV-1 make serologic and virus isolation detection methods unhelpful in the diagnosis of FHV-1 keratoconjunctivitis. Therefore, despite the wide availability of diagnostic tests such as virus isolation and fluorescent antibody tests, these are considered relatively insensitive in cats with chronic or recurrent ocular disease. Modern techniques that identify viral DNA, such as the polymerase chain reaction (PCR) assay, are more sensitive for diagnosis. However, several recent studies evaluating the use of PCR for the detection of FHV-1 in feline ocular samples have revealed that a high percentage of cats without clinical signs of ocular disease have detectable levels of FHV-1 DNA in their conjunctiva and corneas. Thus the diagnosis of FHV-1 keratoconjunctivitis typically is made based on detection of characteristic clinical signs such as dendritic corneal ulcers or scars or the finding of symblepharon along with a history of upper respiratory tract disease or a positive response to antiviral therapy.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Feline Corneal Disease

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