Known and Suspected Factors Contributing to Chronic Corneal Lesions in Captive Pinnipeds
Laurie J. Gage, DVM, DACZM
Captive pinnipeds appear to have a disproportionally high incidence of chronic corneal problems when compared to the incidence of similar eye diseases in other captive mammalian species. Known or suspected causes include one or a combination of the following: trauma, periodic or persistent excessive chemical, oxidant, or noxious byproduct levels in the water, osmolality of the water, pathogens, excessive UV light exposure, and nutritional imbalances.
Common corneal problems seen in pinnipeds are edema, opacities, and chronic keratitis. When trauma and infections can be ruled out as the cause, water quality is often to blame. Checking the water quality records for chemical spikes or imbalances over the course of a year may help to identify the problem. When pinnipeds housed at a facility develop chronic eye problems, outside of a typical ophthalmic exam, a thorough evaluation of oxidant levels, coliform counts, pool color, availability of shade, salinity, nutritional supplements, or exposure to pathogens is warranted.
The following outlines some probable causes of corneal lesions in pinnipeds:
Punctures of the cornea may occur from vibrissae or from negative social interactions. Eye trauma may also occur from excessive debris in the water, such as pine needles, or other plant materials. Fragments of fiberglass material have been found in pools where residual ozone was causing the lining of some of the filtration system components to disintegrate, causing bits of fiberglass to be introduced into animal pools.
Excessive Chemicals, Oxidants, or Noxious Byproducts in the Water
Most modern filtration systems utilize oxidants such as chlorine, bromine, or ozone to control pathogen levels in the water. Measurements of these chemicals should be done daily and recorded. Total chlorine levels may spike on occasion; however, if these spikes occur repeatedly, the chlorine or its byproducts could cause damage to the cornea. If the makeup water is from a municipal source, levels of chlorine should routinely be measured to ensure the chlorine levels going into the pool out of the tap do not exceed 1–1.5 mg/L (PPM). In many cities in the United States, the total chlorine levels in municipal water measure over 2–3 PPM. The chlorine in some cities fluctuates seasonally between acceptable levels that may be used for source water for marine mammal pools, to levels of chlorine that are unacceptable. Optimally total chlorine levels in the water should not exceed 1 PPM. If the chlorine levels in the source water are too high, methods to dechlorinate should be employed before the water is placed in the animal’s pools. Byproducts of disinfection, such as chloramines or trihalomethanes, may also be irritating to the eye and screening for these compounds may be warranted. Ozone systems must have an efficient method to degas the water. Ozone is a powerful oxidant, and there should be no measurable residual ozone in the animal pools. Simple, inexpensive test kits are available commercially to test for the presence of ozone in the water where the animals live. While these tests are not quantitative, they will adequately determine the presence of ozone in the water. If the test is positive, measures must be taken to eliminate residual ozone from entering water that is in contact with the animals.
While pinnipeds typically come from a bright and sunny environment, they are not adapted to dealing with bright, reflective surfaces when diving. Noting that clear water absorbs very little UVA light and UVA light energy is very effectively reflected by light blue or light green surfaces, it stands to reason that pinnipeds housed in pools painted with these reflective colors will be exposed to a higher daily ocular level of potentially damaging UVA light than their wild counterparts. Over time, this exposure could lead to cumulative oxidative damage to the cornea or the endothelial layer of the cornea. Animals that are trained to accept fish at a set station may be forced to look directly into the sun at certain times of the day to accept their food. Keepers and trainers should be aware of this issue and either alter the feeding locations based on the position of the sun or provide shade to prevent discomfort and potential eye damage during feeds.
It appears there are more cases of corneal damage in pinnipeds housed in fresh water; however, there are some facilities utilizing fresh water (including those with no chemical additives) where few eye problems are observed. It should be noted that these facilities also have dark-colored, non-reflective pool surfaces. The eyes of pinnipeds housed in saltwater systems seem better able to withstand occasional oxidative insults than those housed in freshwater systems. Saltwater pools are optimal for these marine mammals; however, a well-managed freshwater system may be adequate.
Corneal problems in pinnipeds may have fungal, bacterial, or viral etiologies. Both bacterial and fungal etiologies have been diagnosed in captive pinnipeds with eye lesions. Herpesvirus has been suspected when other factors have been ruled out and because of the similarity of the appearance of some corneal opacities to herpesvirus-induced corneal lesions in other species. Herpesvirus has never been proven to cause corneal disease in captive pinnipeds.
Free radicals produced from biologic processes or in response to exogenous stimuli are controlled by various enzymes and antioxidants in the body. Antioxidants such as vitamin E, vitamin A, or vitamin C may aid in mitigating oxidative damage to the cornea and other eye structures.
1. Greenwood, A.G. 1985. Prevalence of ocular disease in captive pinnipeds. Aquatic Mammals. 1:13–15.
2. Dunn, J.L., N. Overstrom, D. St. Alibis, D. Abt. 1996. An epidemiologic survey to determine factors associated with corneal and lenticular lesions in captive harbor seals and California sea lions. Proceedings IAAAM.
3. Svobodova, A., D. Walterova, J. Vostalova. 2006. Ultraviolet light induced alteration to the skin. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 150(1):25–38.