Abstract

From May to September 2002, an epizootic of corneal lesions occurred in California sea lions in rehabilitation in The Marine Mammal Center in California. Clinical signs included unilateral corneal opacities to severe bilateral corneal edema, conjunctivitis, blepharospasm, bullous keratopathy, corneal ulceration and temporary blindness. The eye lesions were histologically characterized by superficial stromal scarring, post-necrotic epithelial dysplasia, edema, fibrosis, keratomalacia and necrotizing keratitis. No infectious agent was initially detected, and the lesions were believed to be associated with changes in water quality parameters. DNA was extracted from corneal swabs and necropsy specimens and, using polymerase chain reaction (PCR), the presence of herpesviral DNA was detected in several of these eye lesions. Preliminary results suggest that herpesviral DNA sequences can be detected in corneal samples collected within 3 weeks of onset of clinical signs. However, sequences can no longer be detected in corneal samples collected later than 3 weeks after the onset of clinical signs. Based on partial sequencing of the DNA polymerase gene, the virus was tentatively identified as a novel alphaherpesvirus, distinct from the alphaherpesvirus PhHV-1 from seals and the gammaherpesvirus OtHV-1 from California sea lions. This novel herpesvirus was tentatively named OtHV-2. Attempts to cultivate OtHV-2 are ongoing. This preliminary study suggests that OtHV-2 may be a factor in the causation of necrotizing keratitis in California sea lions. Similar keratitis syndromes in humans and cats are caused by the alphaherpesviruses HSV-1 and FeHV respectively. Alphaherpesviruses are characterized by their ability to become latent. Adverse water conditions may therefore trigger recrudescence and cause clinical disease. Additional research is underway to further classify OtHV-2 and clarify its role in the causation of necrotizing keratitis in California sea lions.