Treatment of Corneal Opacities in a Northern Fur Seal (Callorhinus ursinus)
IAAAM 2009
Tatyana G. Romanova; Vasily V. Romanov; Maria B. Chelysheva
Utrish Dolphinarium Ltd, Moscow, Russian Federation


Due to its high prevalence in several species of captive pinnipeds, ocular pathology continues to attract the close attention of veterinarians. The relationship between the occurrence of corneal opacities and poor maintenance conditions (poor water quality, decreased salinity, excessive use of different water disinfectants, inefficient protection against sun exposure, high water and air temperature, deficient animal nutrition, and unbalanced vitamin A, E, and C supplementation) was suggested by a number of previous investigations.4-6,8 Usually, improvement of husbandry conditions and removal of an etiological agent result in regression of ophthalmic disease. However, occasionally a pathological process emerges on the cornea that progresses and gets complicated by the development of persistent ulcers, in spite of optimal maintenance conditions and proper treatment. This calls for new ideas and approaches to the problem. Our views on the possible origin of corneal opacities in pinnipeds, as well as the suitable approaches to the treatment of affected animals are the subjects of the present communication.

A female northern fur seal (Callorhinus ursinus) was captured in 1993 near the Commander Islands (Russian Federation) and was kept in different facilities of the Utrish Dolphinarium Ltd. The appearance of lenticular opacities (complete in the right eye and partial in the left eye) was noted in early 2004. Development of mature bilateral cataracts was recorded a year later. The animal has managed to adapt with residual eyesight, probably limited to photosensitivity. It confidently orientates in the enclosure and takes part in public shows following the trainer's hand and voice. Since March 2005, the animal has been housed in an open air enclosure supplied with a sea water pool (salinity 14-16 ppt) and sun protecting shelter. In August 2007, the animal began to experience irritation of the left eye: excessive epiphora, blepharospasm, and photophobia. Two shallow round epithelial defects (central - up to 4 mm in diameter, and medial - up to 2 mm) were viewed on the cornea through a highly narrowed palpebral fissure. The edges and the bottom of the defects appeared thickened and opaque, and the cornea surrounding the ulcerous zones appeared cloudy and rough. Taking into account the antibiotic sensitivity of gram-negative microflora cultured from the smears, a topical antibacterial therapy with different eye drops (ocular solutions of gentamicin, amikacin, ciprofloxacin, polymixin, sulfacyl-sodium) and ointments (tetracycline, erythromycin) was administered. In addition, fish oil, vitamin A oily solution, 20% glucose, Citral solution with vitamins, ocular actovegin jelly, and solcoseryl ophthalmic gel were administered topically to improve the trophic conditions of the cornea.

Despite the therapy, the clinical course persisted, with exacerbations and remissions. During acute periods of eye irritation, an increase in corneal edema and opacity, vesicle and bullae formation, expansion and deepening of earlier formed ulcers, and white opaque cord formation in the upper stroma of the cornea was visualized. The remissions were characterized by desorbing of corneal opacification, and decrease in the area and depth of the ulcer surfaces.

Increasing pool water salinity to 30 ppt in late October 2007 decreased the severity of the disease but did not solve the problem completely. Moreover, by the end of November, a few round opaque zones (up to 2 mm in diameter) developed in the central area of the previously intact right cornea. Detailed analysis (at a high magnification) of the fur seal's photographs taken before the beginning of the disease (July 2007) revealed an identical central opacity in the cornea of the left eye. The symmetry of the pathological process, similar initial manifestations in both eyes, ineffectiveness of antibacterial therapy, and presence of bilateral cataracts supported diagnosis of a dystrophic process. The previous therapy was canceled, and dexpanthenol solution ("Siccaprotect", Ursapharm Arzneimittel Gmbh & Co Kg,TID) in combination with dexpanthenol gel ("Corneregel", Bausch & Lomb, OID, in the evening), were prescribed. Both medications contain a derivative of Vitamin B5, which stimulates regeneration of corneal epithelium, and different polymeric systems (polyvinyl alcohol in Siccaprotect and carbomer in Corneregel) forming the lubricating and moistening film on the ocular surface.

During the subsequent 2 weeks, the ulcerous surfaces healed, and the edema and rough corneal opacity resolved. The soft, central, sub-epithelial corneal opacity and irregular pattern of the corneal surface remained without signs of eye irritation. Attempts to discontinue or change the therapy (substitution of Siccaprotect eye drops with tauphon (taurine) or emoxipine, and use of Actovegin jelly instead of Corneregel) resulted in the recurrence of corneal edema, opacity, and erosions with manifestation of ocular irritation. The total course of treatment with Siccaprotect eye drops and Corneregel lasted for 3 months. The initial salinity of water in the pool was gradually restored in April 2008 (no complications to the animal's health were noted). Since then, in summer and long haul-out periods, the course of treatment is renewed as a prophylactic measure.

The avascular pinnipedian cornea obtains nutrition through the aqueous humor, the tear film (TF), and the limbal capillary arcade. In humans and terrestrial mammals, the later consists of three layers: the mucin-rich inner, the aqueous middle, and the lipid outer.3 In spite of the lack of available data on the TF structure in pinnipeds, it is possible that the lachrymal and Harderian glands (excretes lipidic-mucous secretion), as well as the small conjunctival glands, may contribute to film formation in these animals. Tear film covers, moistens and protects the cornea, and supplies it with oxygen and nutritive substances. Under the effect of different unfavorable factors (decrease in TF component production, direct damage as a result of osmotic and chemical impact, intensive solar radiation, or other exogenous influences), the TF stability may be disturbed. It can become thinner, and some of the layers may be destroyed, giving the appearance of dry zones on the corneal surface. Dystrophic and degenerative changes in the corneal epithelium may develop as a result of these changes (Brjesskiy & Somov 2003, Pflugfelder 2004).2,7 The morphological peculiarities of the pinniped eye (large cornea and prominent globe) may be considered as predisposing factors of corneal pathology.8 Because of their location, the central areas of the cornea depend on the TF trophic function to a greater extent, and appear to be more vulnerable than in most other mammals. The development of corneal edema manifests in progressive opacification, and vesicles merging into larger vacuoles (up to bulla). This results in the formation of eroded surfaces transforming into long-lasting unhealing ulcers indifferent (or even negatively reacting) to antibacterial therapy. Prescription of medications stabilizing TF and improving nutrition and regeneration of corneal epithelium ("artificial tears"), may lead to healing of the ulcers and resolution of the opacities.


 The impairment of TF stability and associated degeneration of the corneal epithelium (condition similar to "dry eye" syndrome in humans) may be a cause of the origin and development of corneal opacities in captive pinnipeds.

 Topical use of medicines that stabilize TF and ensure reparative processes of the corneal epithelium, should be used in the therapy of pinnipeds with corneal opacities, along with elimination of known unfavorable exogenous and endogenous factors involved in the development of ocular pathology.



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4.  Dunn L.J., N.A. Overstrom, D.J. Alibis, and D.A. Abt. 1996. An epidemiologic survey to determine factors associated with corneal and lenticular lesions in captive harbor seals and California sea lions. Proc Int Assoc Aquat Anim Med 27: 100-102.

5.  Haulena M., C. McKnight, and F.M.D. Gulland. 2003. Acute necrotizing keratitis in California sea lions (Zalophus californianus) housed at a rehabilitation facility. Proc Int Assoc Aquat Anim Med 34: 193-194.

6.  Lair S., G.J. Crawshaw, K.G. Mehren, and S.J.F. Young. 2001. Environmental aspects of corneal opacities in captive South African fur seals (Arctocephalus pussilus pussilus). Proc Int Assoc Aquat Anim Med 32: 93.

7.  Pflugfelder S.C., R.W. Beuerman, and M.E. Stern (eds). 2004. Dry eye and ocular surface disorders. London: Taylor & Francis, Inc., 440 pp.

8.  Stoskopf M.K., S. Zimmerman, L.W. Hirst, and R. Green. 1985. Ocular anterior segment disease in northern fur seals. J An Vet Med Assoc 187: 1141-1144.


Speaker Information
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Tatyana G. Romanova
Utrish Dolphinarium Ltd
Moscow, Russian Federation

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