Diagnostic Ophthalmology

History and clinical signs

A 7-week-old, male, Labrador retriever was referred to the ophthalmology service at the Western College of Veterinary Medicine. The anterior segments of both eyes were similar and a photograph of the right eye is provided for your assessment (Figure 1). The menace responses and palpebral, oculo-cephalic, and direct and consensual pupillary reflexes were present in both eyes. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were within normal reference ranges in both eyes. The intraocular pressures were estimated with an applanation tonometer (Tonopen XL; Biorad Ophthalmic Division, Santa Clara, California, USA), and they were within normal reference ranges. The pupils were dilated with tropicamide (Mydriacyl; Alcon Canada). Biomicroscopic (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) examination revealed opacities in both eyes within the fetal nucleus of the lenses. Indirect ophthalmoscopy (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) revealed no other detectable abnormalities.

Figure 1. Photograph of the right eye of a 7-week-old, male Labrador retriever.

Discussion

Our diagnoses were bilateral incipient nuclear cataracts. Incipient nuclear cataracts are often congenital and many etiologies may be considered. Without detailed and accurate histories, many nuclear cataracts are designated as idiopathic. Traumatic and toxic etiologies were considered less likely because of their nuclear location and the age of this dog. Most cataracts that develop secondary to trauma and toxins are cortical in location initially (1). Littermates were not available for examination and it was unknown whether similar nuclear cataracts were present in the siblings. No other abnormalities were present. The perinuclear location and appearance were consistent with previous reports of nutritional cataracts that are induced by supplementation of the puppies' diet. However, despite careful review of the history, we were unable to determine accurately whether this puppy had received hand-made or commercial formula or supplements preweaning. The owner had received the puppy from a friend and the original owner of the litter had moved and was unavailable for comment or to provide sibling puppies for examination.

Several nutritionally induced cataracts have been reported in animals. Histidine deficiency has been reported to induce cataracts in rats (2). Several other amino acid deficiencies have also been associated with cataract development, including tryptophan, phenylalanine, and arginine (2). Most nutritionally induced nuclear cataracts are not progressive (1,2,3,4). Sporadically, a specific syndrome of nutritionally induced cataracts is seen in puppies fed milk replacers (5,6). These cataracts often manifest with a perinuclear halo or clover leaf appearance at the anterior and posterior nuclear-cortical junction, similar in appearance to the cataracts noted in Figure 1. These cataracts are linked to an arginine deficiency (1); this was considered as a potential etiology in this dog.

The pathogenesis of nutritional deficiencies and cataracts is poorly understood. Deficiencies of 1 or more essential amino acids may lead to changes in the structure and conformation of the lens' proteins and subsequent lenticular opacities (7). Most nuclear cataracts do not interfere with vision substantially. However, extensive nuclear cataracts will interfere with vision when the pupil is constricted and these cases may benefit from phacoemulsification and intraocular lens implantation. Focal nuclear cataracts that are not interfering significantly with vision are usually left untreated and are reexamined in 6 to 12 mo to confirm a lack of progression. This puppy was reexamined 1 y later and the perinuclear cataracts were unchanged.