The purpose is to describe three consistent, possibly progressive, presentations of keratitis in Zalophus californianus. Animals underwent slit lamp evaluation; some were stained with fluorescein. All eyes were photographed. Signalment for all animals and facility where located, were noted. All animals were at facilities where shade was available but not always used by the animal. A total of 112 eyes from 56 animals (42 males/14 females) were examined. The average age of all animals was fourteen years. Nineteen animals had the mildest form of keratitis (category one). These lesions were located dorsotemporal to the axial cornea (paraxial) and were small, white and focal, and may have been superficially ulcerated (fluorescein positive). Four were fluorescein positive. Four were unilateral and thirteen were bilateral. Seven animals (5 males/2 females) had more diffuse white corneal opacities that encompassed approximately 5 to 15 % of the dorsotemporal paraxial cornea but were still considered superficial (category two). One eye was fluorescein positive. Six were unilateral and one was bilateral; the bilateral case had been in category one 19 months earlier. Eleven animals had the most severe form of keratitis (category three) encompassing over 20% of the cornea with the primary densest opacity evident in the dorsotemporal paraxial cornea in most. The lesion extended deeper through the corneal stroma. Most of these cases had been treated for bacterial and/or fungal keratitis, which resulted in progression of the fibrosis. Three were unilateral and eight were bilateral; one case had been in category one 2 years previously. The initial cause of the focal lesion located consistently at the dorsotemporal paraxial cornea is unknown. Traumatic and viral etiologies have been suggested; one other possibility is exposure to ultraviolet radiation (sunlight). The consistent location would make a traumatic cause less likely. Viral origin is still considered but further testing to prove this hypothesis is in development. Exposure to sunlight is known to cause and promote keratitis in other species; this may be a component of the disease. The more extensive lesions in category two are probably due to recurrence or exacerbation of the initial cause resulting in progressive scarring. The final and most devastating, often sight impairing, lesion appears to be due to secondary opportunistic infections including bacterial and fungal organisms. This suggests that the recurrent focal initial lesion causes the cornea to become weakened, possibly exacerbated by excessive sun exposure, and more susceptible to secondary infections.