The lens develops rapidly in the early stages of embryogenesis, during which time it is nourished by the hyaloid vessel. The fully developed lens is avascular; by the second week of life, no remnants of the hyaloid system should remain. The normal lens often exhibits minor imperfections that can be easily detected with magnification in dogs and cats younger than 1 year. These include prominent anterior and posterior Y sutures and minute granules in its nucleus and cortex. A mosaic of brown pigment spots is occasionally seen on the anterior lens capsule near the center of the pupil, representing remnants of embryonic mesoderm. Disease of the vitreous would be expected to influence the lens or retina because of its attachments at the posterior lens surface and the optic disc.
Congenital lens abnormalities include alterations in size or shape. Congenital absence of the lens (aphakia) is uncommon. In microphakia, the margin of the abnormally small lens along with elongated ciliary processes may be observed after pupillary dilation. Microphakia occurs along with other ocular defects in the Saint Bernard and beagle and in cats. Luxation of the microphakic lens may cause glaucoma. Lenticonus is a cone-like anterior or posterior protrusion of the lens. Abnormally shaped lenses occur in many dog breeds, with or without associated opacities, and in Persian cats.
The most common vitreous abnormality is the retention of varying amounts of the hyaloid system. Hyaloid remnants are usually bloodless, appearing as a white vermiform structure that extends a short distance into the vitreous from the optic disc or from the posterior lens capsule. Such remnants are not associated with any recognizable visual deficits. Persistent hyperplastic primary vitreous is a congenital abnormality characterized by the presence of a fibrovascular membrane on the posterior lens surface. It usually is manifested by a congenital pupillary opacity (leukocoria), a fibrovascular sheath on the back of the lens with an attached hyaloid stalk, elongated ciliary processes, and secondary cataract (). A hereditary basis for persistent hyperplastic primary vitreous is established in Doberman pinschers, Staffordshire bull terriers, Bouvier des Flandres, and possibly standard schnauzers.
Cataracts in dogs and cats younger than 6 months are usually congenital or juvenile cataracts. Congenital cataracts are present at birth, although they may be unnoticed until 6 to 8 weeks of age. They may be inherited or secondary to in utero influences, so it is important to question the owner regarding the presence of cataracts in the sire, dam, their previous litters, or their pedigrees. Congenital cataracts occur in Persian cats and are associated with multiple ocular defects in beagles, cocker spaniels, Old English sheepdogs, Australian shepherds, Bedlington terriers, and Sealyham terriers. Cataracts also occur in Labrador retrievers and Sa-moyeds with retinal dysplasia/detachment and skeletal abnormalities.
Juvenile cataracts can develop from birth until 6 years of age. Although inflammatory, metabolic, nutritional, toxic, and traumatic events are considered to cause juvenile cataracts, heredity is the major cause. The development of juvenile cataracts is usually progressive, but their rate of progression varies. Complete opacification of the lens may occur in less than 1 year after recognition. Capsular and nuclear cataracts are usually nonprogressive, whereas cortical and equatorial cataracts are expected to progress.
Uveitis of any cause may precipitate juvenile cataract formation, as inflammatory adhesions disrupt the lens capsule and changes in aqueous humor affect lens metabolism. Metabolic cataracts secondary to diabetes mellitus may occur. Nutritional cataracts may occur in orphaned puppies and kittens fed a commercial milk re-placer, presumably due to an imbalance in essential amino acids in the milk replacer. In most instances, the lens opacification is mild and decreases with eating a growth diet. Juvenile cataracts can be caused by various toxic influences, including chemicals, radiation, and electrical shock. Cataracts may occur in dogs given dimethyl sulfoxide. Traumatic insult to the lens may disrupt lens fibers or initiate an inflammatory response that leads to lens opacities. Traumatic insult is the most common cause of cataract in the young cat.
Inherited juvenile cataracts are known to occur in several breeds of dogs and cats (). Early recognition of cataracts is essential in eliminating affected animals from a breeding program (Table Selected Inherited Cataracts of Young Dogs). Congenital or juvenile cataracts are best managed by temporization if functional vision is present because a high percentage may undergo spontaneous resorption within the first year. If uveitis develops, topical mydriatics and corticosteroids are indicated. Surgical lens extraction may be elected, but the effect of the lens opacities on visual pathway development should first be determined. Inadequate light stimulation from the time the eyelids open until approximately 12 weeks of age produces irreversible functional and structural abnormalities in the visual cortex. It is then possible for a successful lens extraction to be performed without improvement in the animal’s visual capabilities.
Table Selected Inherited Cataracts of Young Dogs
|BREED||MODE OF INHERITANCE||LOCATION||PROGRESSION|
|Afghan hound||Not defined||Equatorial||Progressive|
|Akita||Not defined||Nuclear and cortical||Variable progression|
|Alaskan malamute||Not defined||Posterior subcapsular||Variable progression|
|American cocker spaniel||Autosomal recessive||Cortical||Progression|
|Australian shepherd||Not defined||Nuclear and cortical||Nonprogressive|
|Basenji||Not defined||Anterior capsular||Nonprogressive|
|Beagle||Not defined||Anterior capsular||Nonprogressive|
|Boston terrier||Not defined||Nuclear and cortical||Progressive|
|King Charles Cavalier spaniel||Not defined||Nuclear and cortical||Progressive|
|Chesapeake Bay retriever||Not defined||Posterior subcapsular||Variable progression|
|Chow chow||Not defined||Nuclear and cortical||Variable progression|
|Collie||Not defined||Nuclear and cortical||Unknown|
|Doberman pinscher||Dominant with incomplete penetrance||Posterior subcapsular||Variable progression|
|English cocker spaniel||Not defined||Anterior capsular||Nonprogressive|
|Flat coated retriever||Not defined||Posterior subcapsular||Nonprogressive|
|German shepherd||Autosomal dominant||Nuclear||Nonprogressive|
|Golden retriever||Not defined||Perinuclear||Progressive|
|Labrador retriever||Incomplete dominance||Nuclear and cortical||Variable progression|
|Miniature schnauzer||Autosomal recessive||Nuclear and cortical||Variable progression|
|Old English sheepdog||Not defined||Nuclear and cortical||Progressive|
|Poodle, toy and miniature||Not defined||Cortical||Progressive|
|Poodle, standard||Not defined||Equatorial||Progressive|
|Rottweiler||Not defined||Posterior subcapsular and cortical||Nonprogressive|
|Samoyed||Autosomal recessive||Nuclear and cortical||Variable progression|
|Siberian husky||Not defined||Posterior subcapsular equatorial||Variable progression|
|Staffordshire terrier||Not defined||Nuclear and cortical||Progressive|
|Welsh springer spaniel||Autosomal recessive||Cortical||Progressive|
|West Highland white terrier||Autosomal recessive||Nuclear and cortical||Progressive|
|Not defined||Posterior Y suture||Nonprogressive|
Selections from the book: “Veterinary pediatrics: dogs and cats from birth to six months”. Johnny D. Hoskins. (2001)