Common condition, variable in presentation: ulcerative/non-ulcerative, vascular/avascular, inflammatory/non-inflammatory, traumatic/non-traumatic.
Cause : secondary vascularization of avascular cornea in response to insult, with or without surface ulceration. Further secondary changes possible, eg pigmentation, edema, alteration in corneal contour, calcium and lipid deposition.
Lack of sensory (V) innervation  punctate keratitis  may progress to ulceration/edema.
Neuroparalytic keratitis.
Facial nerve paralysis  loss of eyelid movement.
Pathophysiology
Classified according to etiology and depth. Broad division into non-ulcerative keratitis (epithelium intact) and ulcerative keratitis (epithelium damaged).
Superficial keratitis involves epithelium and anterior stroma, vascularization from conjunctival vessels. If conjunctiva also involved, called keratoconjunctivitis.
Deep keratitis involves deep stroma +/- Descemet's membrane/endothelium, vascularization arises from ciliary plexus at limbus.
Canine corneal anatomy:
Non-keratinized stratified squamous epithelium, including trilaminar precorneal tear film (lipid, aqueous and mucous phases) with basement membrane (analogous to primate Bowman's membrane).
Stroma, composed of type 1 collagen arranged in lamellae, precisely orientated, in relatively dehydrated glycosaminoglycan ground substance - both important for transparency.
Elastic Descemet's membrane, secreted by endothelium.
Monolayered endothelium, site of Na/K-ATPase-dependent pump, responsible for regulating water content of stroma.
Superficial ulcers - 3 types:
Uncomplicated : rapid healing by epithelial sliding and mitosis (conjunctival sliding/mitosis/metaplasia if all corneal epithelium damaged). Pluripotential limbal stem cells are source of dividing cells.
Progressive : underlying cause must be identified. Eyelids (agenesis, entropion, distichiasis, trichiasis, inflammation, neoplasia, ectopic cilia), nasal folds (trichiasis), precorneal tear film.
Refractory : basement membrane abnormality, specific condition.
Secondary bacterial invasion usually gram-positive (Staph/Strep), some gram-negative ( Pseudomonas, E. coli, Bacillus).
Deep ulcers (>half stromal thickness).
Non-progressive - as for superficial uncomplicated ulcers, healing takes longer because stromal regeneration necessary, scar persists, possibly results in a corneal facet (irregularity in corneal surface).
Progressive - may erode through stroma to elastic Descemet's membrane, which bulges forwards because of intraocular pressure (then called Descemetocoele), perforation a common sequela. Deep ulcers usually associated with uveitis via axon reflex. Gram-negative infection (especially Pseudomonas) produces proteases which, with endogenous collagenases (serina and matrix metalloproteinases) from keratocytes and neutrophils, produce rapid stromal breakdown (liquefaction or 'melting') emergency intensive treatment necessary.
Pigmentary keratitis - usually associated with chronic keratitis, pigment produced in epithelium, anterior stroma and migrates from perilimbal melanocytes, may be secondary to corneal vascularization. Impairs vision when becomes central.
Chronic superficial keratitis (CSK) - immune mediated (cell-mediated immunity to corneal/conjunctival antigems - ultraviolet radiation may alter immunogenicity of antigens) vascular lesion appears at temporal limbus and invades cornea, pigmentation follows vascularization. May also affect nictitating membrane. Epithelium remains intact.
For further information about diagnosis and treatment see specific diseases:
Tolar E L, Hendrix D V H, Rohrbach B W, Plummer C E, Brooks D E & Gelatt K N (2006) Evaluation of clinical characterisitics and bacterial isolates in dogs with bacterial keratitis: 97 cases (1993-2003).JAVMA228 (1), 80-85 PubMed.
Vetstream contributor(s)
Dr Dennis E Brooks DVM PhD DipACVO , College of Veterinary Medicine, 2015 SW 16th Ave, University of Florida, PO Box 100126, Gainesville, FL 32610-0126, USA.
Dr David L Williams MA VetMB CertVOphthal PhD MRCVS , Department of Clinical Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, UK.