Idiopathic Corneal Edema in a Monk Seal Pup Hand Reared From Birth
IAAAM 2009
Gregg Levine1; Robert Braun2; Frances Gulland5; Maya Yamagata3; Carmen Colitz4; Deb Wickham5; David Schofield6; Charles Littnan6; Lizabeth Kashinsky7; Cynthia Kendall8
1Contract Veterinarian, NOAA Fisheries, Pacific Islands Fisheries Science Center, Kailua, HI, USA; 2Contract Veterinarian, Marine Mammal Research Program, Pacific Islands Fisheries Science Center, NOAA Fisheries, Kaneohe, HI, USA; 3Hawaii Veterinary Vision Care, Honolulu, HI, USA; 4Animal Eye Specialty Clinic, West Palm Beach, FL and Aquatic Animal Eye Care, Jupiter, FL, USA; 5The Marine Mammal Center, Sausalito, CA, USA; 6NOAA Fisheries, Pacific Islands Fisheries Science Center, Honolulu, HI, USA; 7Joint Institute for Marine and Atmospheric Research, University of Hawaii, Honolulu, HI, USA; 8Ophthalmic Echography Services, Sacramento, CA, USA


Corneal edema is commonly observed in both captive and wild pinnipeds.3,5-7 It has been suggested that the sensitivity of the eye to light and the narrow iridocorneal angle are important factors in the susceptibility of these animals to ocular disease.7 Since the exact etiology of corneal edema in pinnipeds has not been determined, a variety of husbandry practices have been used to minimize its severity in captive animals. A specific infectious etiology has not been identified to date, although a herpes virus was detected in a case of keratitis in a California sea lion.11 Minimizing exposure to sunlight, use of hyperosmotic saline drops and anti-inflammatory drugs are the most common therapies available at this time. This case of bilateral corneal edema in a hand raised Hawaiian monk seal pup (Monachus schauinslandi) illustrates current diagnostic and therapeutic limitations in this common problem.

An abandoned male neonatal Hawaiian monk seal was rescued from Kauai and transported to the NMFS Kewalo Research Facility on Oahu for rehabilitation. This quarantined area consisted of a 25 x 25 foot dry resting area around a 20-ft diameter, 4-ft deep pool with a constant flow of sea water. The deck was painted white, the pool light blue. There was no shade structure in place. The pup was about 24 hours old at capture, weighed 15.7 kg, and appeared dehydrated with an inflamed umbilicus. Hematology and serum chemistries were within normal limits. Amoxicillin and enrofloxacin were given orally for 10 days to minimize risk of omphalophlebitis and septicemia. Subcutaneous and oral fluids were administered for rehydration. Initially a formula of milk matrix 30/55 (PetAg, Hampshire, IL), vitamins, electrolytes, and salmon oil was tube fed. This formula was discontinued after 6 days due to constipation and gas and was replaced with a simple fish gruel/electrolyte/salmon oil diet. With incremental increases in volume and caloric content, the pup gained about 15 kg by 9 weeks of age. The pup did not eat dead fish, but showed immediate interest when live moi (threadfin fingerlings) were added to his pool. He would chase, kill and attempt to eat the moi, with increasing success.

At 10 weeks of age, the pup appeared less active and displayed signs consistent with back pain. Acute unilateral angioedema and cellulitis of the left muzzle and buccal mucosa were noted on the same day. It was concluded that there were likely two separate problems: myositis secondary to caudal spine venipuncture attempts the previous day; and cellulitis of the oral cavity after a possible bee sting. He was given five days of enrofloxacin and amoxicillin, and two doses of flunixin meglumine and both problems quickly resolved.

At 14 weeks of age, a mild diffuse bilateral corneal edema was noted. Serial ophthalmic examinations were performed by a veterinary ophthalmologist (Dr. Maya Yamagata). Corneal surfaces were smooth and did not retain fluorescein stain. Other structures of the eye appeared normal. To determine the likely etiology (Table 1), serum samples and ocular swabs were taken. Diet, nutritional supplements, and medications were evaluated as potential causative or contributing factors of the corneal edema. A series of therapeutic drugs were tried (Table 2) in an attempt to use response to treatment as an aid to diagnosis. Aggressive therapy with topical antivirals and anti-inflammatories were discouraged because of lack of etiologic evidence of viral or inflammatory disease at the time. The severity of the corneal edema then progressed to include vascularization, corneal surface irregularity, and corneal bullae formation over the next few weeks. Eventually up to 95% of the cornea were involved in both eyes. No improvement in the corneal condition was observed with any topically or orally administered medication. The pup's appetite, behavior, and activity remained normal, but his vision became significantly impaired. Because all tests for pathogens were negative, it was hypothesized that the corneal edema might be due to a combination of environmental factors (i.e., reflected bright sunlight, and water quality issues). To mitigate these potential factors it was decided that the pup should be moved to a shoreline pen on a protected beach. All medical therapies were also discontinued near the time of transfer to the shoreline pen.

Over the next 2-½ months the pup's vision appeared to improve daily. Central/axial dense corneal edema remained in both eyes but the extent was reduced to 30% in both eyes. The corneas appeared smooth with no bullae and no signs of inflammation. At approximately 29 weeks of rehabilitation there was no noticeable vision impairment. At this time, the pup was anesthetized for a detailed examination of the entire eye (by veterinary ophthalmologist Carmen Colitz and ocular ultrasonographer Cynthia Kendall) using high-resolution ophthalmic ultrasound and pachymetry to measure the extent of the corneal edema and evaluate conclusively for signs of cataract formation. Pachymetry was not successful due to the relative flatness of the pinniped cornea.

The corneal edema began approximately 3 mm medial to the axial cornea and extended to 2-3 mm from the temporal limbus forming a horizontal oval area of diffuse corneal edema bilaterally. This edematous area encompassed approximately 1/3 of the total corneal surface. The anterior chamber was easily examined through most of the edema except where it is most severe. At the temporal aspect of the edema, thin branching superficial corneal vascularization extended into the middle of the lesion. In between the dorsal and ventral vessels there was a mild amount of superficial pigmentation (more severe OS) that was seen to be entering at the temporal limbus and swept medially. The pupil was normal in anatomy as was the iris surface with the usual phacoid appearance. Intraocular pressures were measured two separate times with 5% error: OD (23, 25 mmHg) and OS (16, 18 mmHg). The OD has a significantly higher IOP than OS. IOPs in the 20-30'ish range are normal for pinnipeds with a TonoPen. The significance of the OS having a lower IOP without significant intraocular disease is unknown but the difference may be due to the corneal edema. Next, the cornea was sampled for both PCR testing and storage. The conjunctiva was biopsied in 2 separate locations, first temporal bulbar location, then dorsal palpebral location, samples were placed in formalin for evaluation by Dr Dick Dubielzig at University of Wisconsin. Similar sampling was performed OD. Drops given following sample collection included: 100% epinephrine without preservative, atropine, and cyclogel each at 2-3 minute intervals. Pupils dilated to approximately 3-4 mm OD and 4-5 mm OS.

Limited fundic examination was performed following ultrasound evaluation. The fundus appeared normal and no lens opacities were evident. The corneal edema precluded evaluation of the medial aspect of the fundus. In addition, the limited dilation did not allow peripheral evaluation. However, the optic nerve head and the area centralis were normal. High frequency ophthalmic ultrasound confirmed that there were no cataracts at the time of the examination. Histological examination of a conjunctival biopsy revealed conjunctivitis but no viral or bacterial particles. The evaluation did not reveal any pathognomonic characteristic or classical signs of any single etiology.

The pup's eye condition improved, and he gained weight eating live fish and octopus, and it became evident that consideration for reintroduction to the wild was due. Based on the above diagnostics and professional evaluations, it was determined that the pup posed no disease threat to the wild population and release should be attempted to evaluate both the success of re-introduction of a hand raised neonatal Hawaiian monk seal back into the wild, and the effect of environmental change (natural habitat) on the corneal lesions. At approximately 32 weeks of age the pup was released on a remote region of Molokai. Prior to release, the pup was instrumented with a small satellite linked time-depth recorder and a VHF tag. Both tags were affixed to his pelage with epoxy.

Since release on December 15, 2008 the pup's behavior appears normal. He has slowly been venturing further from the release sight and diving deeper as he gains experience. Recently he traveled over 65 km from his release site and successfully found his way back. Body condition remains very good, and the corneal edema (noted in photos from a distance) appears unchanged or improved from the time of release. Recheck ophthalmic examinations are scheduled for 3, 6, 9, and 12 months post release. Data from the 3-month check up (March 15, 2009) will be presented.

The lack of detection of any infectious agent (other than non-specific bacteria) in ocular swabs or evidence of exposure to infectious agents associated with ocular disease in other species via serology, combined with the epidemiological characteristics of this edema (history of isolation from other mammals, gradual onset with progression in one environment followed by regression of lesions in a novel environment) suggest an environmental etiology for the clinical signs observed in this animal. However, other potential etiologies that remain possible include the deposition of antigen-antibody complexes in the cornea (e.g., as a result of the insect sting), viruses that have not been identified to date in animals (e.g., cytomegalovirus recently reported in human corneal endotheliitis9) as well as a combination of factors that increased susceptibility of the cornea to environmental conditions, (e.g., photosensitization following drug usage). From the data available, it cannot be determined whether the etiology of edema in this case is similar to the etiology of progressive ocular disease described in 9 monk seals in 1995.1

Table 1. Etiological Differential Diagnosis for Corneal Edema in KP2


Symptoms in other species

Diagnostic Test


Possible Differential


Not documented





Retinal dz/Uveitis


Present at birth


Immune mediated

Adenovirus infection or vaccination


Bee sting 10 days prior to onset of edema


Vitamin A excess/deficiency

Association of retinal degeneration with corneal

Vitamin A evaluation in fish diet
Retinal/lens exam

Vitamin A consistent with those fed other captive seals

Role of Lutein/ carotenoids in mar. mammals unclear

Vitamin C deficiency

Corneal edema associated with other pathology of eye.

Evaluation of levels in diet

No established standard doses


Diabetic corneal edema


Serum glucose

Serum biochem normal


Eosinophilic keratitis

Keratitis in cats associated with feline Herpesvirus-1


No eosinophilia or keratitis (eosinophilia not a component!)





Unlikely due to age


Idiopathic Corneal



Hypertonic saline treatment ineffective

No. A dystrophy would progress

Toxoplasma gondii


MAT- Negative



Inf. Can. Hepatitis

Diffuse corneal edema




Inf. Can. Hepatitis

Diffuse corneal edema

Serology - Negative



Feline Herpes Virus

Conjunctivitis, ulcerative keratitis

PCR- Negative
ELISA- Negative

Corneal edema noted well before clinical signs of keratitis



Oral ulcers


No ocular disease noted previously with other pinniped species



Ulcerative keratitis or stromal abscessation





Uveitis in horses and dogs


Clin signs not consistent with Uveitis


Bacterial infection


Culture swab

Periodic coliform spikes at KRF



Increased IOP

IOP-not elevated




Retinal damage in cats given enrofloxacin4


KP2 treated with two courses of Baytril.

Possible, but retina normal

UV Light2,8,10,12,13

Hx of exposure

Removal from environment



Chemical irritant. Oxidative damage

Corneal edema with associated keratitis

Removal from environment

Extreme care was taken to minimize risk of exposure to bleach and cleaners


Table 2. Therapeutic Trial for Corneal Edema in KP2




Shade Structure

Decrease UV light

No effect

Hypertonic saline ophthalmic drops

For idiopathic corneal edema

No effect

Doxycycline 200mg PO SID x 10 days

Antibacterial and anti-inflammatory properties

No effect

Neosporin Ophthalmic drops


No effect

Rimadyl 150mg PO SID


Decreased blepharospasm

Voltaren Ophthalmic drops


No effect

Move from pool to beach

Decrease glare UV light and resolve potential water quality issues

Dramatic improvement


1.  Braun R., M. Paulson, et al. 1996. Corneal opacities in Hawaiian monk seals. IAAAM 27th Annual Conference Proceedings, May 1996, Chattanooga, Tennessee: Pp. 105-106.

2.  Doughty M.J., and A.P. Cullen. 2008. Long-term effects of a single dose of ultraviolet-B on albino rabbit cornea-I. In vivo analyses. Photochem Photobiol 49:185-196.

3.  Dunn L., N. Overstrom, et al. 1996. An epidemiologic survey to determine factors associated with corneal and lenticular lesions in captive harbor seals and California sea lions. IAAAM 27th Annual Conference Proceedings, May 1996, Chattanooga, Tennessee; Pp. 108-109.

4.  Gelatt K.N., A. van der Woerdt, Ketring et al. 2001. Enrofloxacin-associated retinal degeneration in cats. Vet Ophthal 4: 99-106

5.  Greenwood, A.G. 1985. Prevalence of ocular anterior segment disease in captive pinnipeds. Aquatic Mammals 1: 13-15.

6.  Haulena M., C. Mcknight, and F. Gulland. 2003. Acute necrotizing keratitis in California sea lions (Zalophus californianus) housed at a rehabilitation facility. IAAAM 34th Annual Conference Proceedings, May 2003, Waikoloa, Hawaii; Pp. 193-194.

7.  Hirst L.W., M. Stoskopf, et al. 1983. Pathologic findings in the anterior segment of the pinniped eye. J Am Vet Med Assoc 183: 1226-1231.

8.  Kennedy M., K.H. Kim, et al. 1997. Ultraviolet irradiation induces the production of multiple cytokines by human corneal cells. Invest Ophthal Vis Sci 38: 2483-2491.

9.  Koizumi N., T. Suzuki, T. Uno, H. Chihara, A. Shiraishi, Y. Hara, T. Inatomi, C. Sotozono, S. Kawasaki, K. Yamasaki, C. Mochida, Y. Ohashi, and S. Kinoshita. 2008. Cytomegalovirus as an etiologic factor in corneal endotheliitis. Ophthal 115(2): 292-297.

10. Newkirk K.M., H.L. Chandler, A.E. Parent, D.C. Young,, C.M.H. Colitz,, D.A. Wilkie, and D.F. Kusewitt. 2007. Ultraviolet radiation-Induced corneal degeneration in 129 Mice. Toxicol Pathol 3: 817-824.

11. Nollens H.H., E.R. Jacobson, F. Gulland, M. Haulena, D. Beusse, and R. Condit. 2005. A novel herpes virus associated with necrotizing keratitis in the California sea lion. National Marine Mammal Stranding Network Conference, April 3-7, 2005, The National Conference Center, Landsdowne, Virginia.

12. Podskochy A.M.D., L. Gan, and M.D. Fagerholm. 2000. Apoptosis in UV-exposed rabbit corneas. Cornea. 19(1): 99-103

13. Sheng Y., and D.L. Birkle. 1995. Release of platelet activating factor (PAF) and eicosanoids in UVC-irradiated corneal stromal cells. Current Eye Research 14: 341-347.

Speaker Information
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Gregg Levine
Dolphin Quest Oahu
Kahala, HI, USA

MAIN : Ophthalmology : Corneal Edema
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