Dietary and Surgical Management of Lipid Keratopathy and Systemic Hyperlipidemia in Captive Moray Eels
Six green moray (Gymnothorax funebris), three spotted moray (G. moringa) and two reticulate moray (Muraena retifera) eels maintained in captivity for variable periods of time received complete ophthalmic exams under MS-222 anesthesia, measurement of serum triglyceride (TG) and cholesterol (CHO) levels, and dietary evaluation as part of routine physical assessment. Seven of eleven eels (63%) were diagnosed with lipid keratopathy due to the presence of crystalline opacification of the cornea and spectacle with variable vascularization.3,4,9,10 Baseline CHO levels (mean 714 mg/dl, range 198-1313 mg/dl) were elevated relative to normal values extrapolated from other species (<150 mg/dl),2,5-8,11 as well as relative to values from four wild-caught green moray eels (mean 370 mg/dl) in all but two eels. Baseline TG levels (mean 712 mg/dl, range 256-1657 mg/dl) were elevated relative to other species (<300 mg/dl)2,5-8,11 and to wild-caught eels (mean 390 mg/dl). The diet in captivity was composed primarily of mackerel (42.3-48.4% fat) and a combination of squid and smelt (12.7-39.5% fat).1 An attempt to lower plasma lipid levels and decrease ocular lipid deposition was made through gradual implementation of dietary modification to primarily lower-fat squid (8.3-11.4% fat) and capelin (7.0-23.3% fat). Due to the severity of the ocular lesions and impact on feeding ability, surgical removal of the superficial spectacle in both eyes (OU) and superficial cornea in the right eye (OD) was performed in one green moray.4 Histopathologic evaluation of the surgical specimens supported lipid infiltration via identification of presumed intrastromal cholesterol clefts and lipid-filled macrophages. The combination of dietary modification and surgery in this individual led to increased ocular clarity and improved feeding behavior for 11 months of follow-up, at which time the eel died following movement to another aquarium. At the time of death, both eyes were clear and histopathologic evaluation did not identify recurrence of lipid keratopathy as identified at the time of surgery. An additional green moray eel was identified as a surgical candidate due to the degree of corneal opacification, however reevaluation following approximately five weeks of dietary modification indicated marked improvement of ocular clarity, and surgery was therefore not performed. Initial CHO values in this eel of 1004 mg/dl were essentially unchanged at 1018 mg/dl at the five-week time point, while serum TG increased from 774 to 1025 mg/dl over that same time period, which is difficult to reconcile with the clinical improvement. In conclusion, captive moray eels have an apparent predisposition to increased serum TG and CHO, and an associated high prevalence of presumed lipid keratopathy. Surgical removal of lipid deposits in the cornea and spectacle may be indicated in severely affected individuals, while dietary lipid reduction may be an appropriate husbandry consideration for all individuals.
We thank the staff at the Fort Fisher Aquarium for their dedication to the care and well-being of the animals examined, and for their expertise in handling the animals. We also wish to thank Brian Gilger, Greg Lewbart, Shane Christian, Damian Launer, and Sandy Machon for assisting in evaluation of individuals at the North Carolina State University College of Veterinary Medicine, and Doug Mader and Kelly Martin at the Marathon Veterinary Hospital, and Scott Moroff at Antech Diagnostics, for processing samples from wild-caught eels.
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