Lipoidal corneal degeneration in aged falcons.

PubMed ID: 29350449

Author(s): Moore BA, Paul-Murphy JR, Adamson KL, Dubielzig RR, Kern T, Gonzales BJ, Wolff P, Murphy CJ. Lipoidal corneal degeneration in aged falcons. Vet Ophthalmol. 2018 Jul;21(4):332-338. doi: 10.1111/vop.12508. Epub 2018 Jan 19. PMID 29350449

Journal: Veterinary Ophthalmology, Volume 21, Issue 4, Jul 2018

OBJECTIVE To present a case series of idiopathic lipoidal corneal degeneration in falcons.

ANIMALS STUDIED Five falcons including three peregrine falcons (Falco peregrinus), one prairie falcon (Falco mexicanus), and one red-naped shaheen (Falco peregrinus babylonicus) were observed to develop slowly progressive corneal opacification that began at the temporal limbus and extended centripetally across the cornea over a period of years. Four of the birds were over 20 years old.

PROCEDURES All animals underwent complete ophthalmic examinations. A red-naped shaheen underwent ocular imaging via spectral-domain optical coherence tomography. Two peregrine falcons were euthanized due to declining health, and their eyes were examined histologically.

RESULTS The opacities were pale and granular, with frequent vascularization associated perilimbally. Diffuse neutral lipid was observed in stromal cells throughout the corneal stroma of both clear and opaque areas of the cornea, sparing only the acellular anterior limiting lamina. Clusters of cholesterol crystals surrounded by macrophages were present in the mid-stroma. Fibrosis was evident in a subepithelial location, which separated the epithelium from the anterior limiting lamina. Ultrastructurally, diffuse vacuolization of the keratocytes was observed. No other ophthalmic or systemic abnormalities were noted.

CONCLUSIONS Results suggest that lipid degeneration occurs rarely in captive falcons of advanced age. The underlying cause is unclear. Though unsubstantiated, possible contributing factors include dyslipoproteinemia, corneal trauma, diet, and age-related alterations in corneal metabolism. The initiation of pathology at the temporal limbus, as well as slow progression, suggests that exposure contributes to the onset and progression of this unique keratopathy.