The following is just a synopsis of the various genetic health problems associated with Border Collies.
CEROID LIPOFUSCINOSIS (CL)As of 1 July 2005 a DNA Test is available, so now a very avoidable desease.
Ceroid lipofuscinosis is a broad term describing a group of incompletely understood diseases caused by an abnormal accumulation of metabolic by-products within cellular lysosomes of neural and visceral organs. The disease is reported as an inherited cause of progressive nervous system disfunction in humans, nonhuman primates, dogs. cats, cattle, sheep, and goats. Clinical signs of disease include impairment of motor function, conscious proprioceptive deficits, ataxia. progressive blindness, behavior changes, hypersensitivity to stimuli, and seizures. The disease is variable in rate of progression, irreversible, and fatal. CL is a storage disease (commonly called storage) characterised by the accumulation of cytoplasmic autofluorescent lipopigments, predominantly in neurons. It occurs in humans - known as Battens disease and has been reported in several breeds of dogs.
The onset of clinical signs occur at around sixteen to twenty-three months of age and usually leading to death by euthanasia one to six months later, at eighteen to twenty-eight months of age.
Behavioural changes, motor abnormalities and blindness are the major clinical signs in all affected dogs. Hyperactivity, with compulsive running or aimless wandering, is commonly the first abnormality observed. Abnormal behaviour, sometimes episodic, is also an early feature that increases in frequency and severity as the disease progresses. This includes uncharacteristic fearfulness, snapping or biting, exaggerated responses to auditory, visual or tactile stimuli, continuous barking, agitation, disorientation, frenzy, mania and rage. The dogs often appear to have visual and auditory hallucinations, snapping at nonexistent objects, biting and growling at inanimate objects such as food dishes. There was a loss of learned behaviour. Trained dogs seem easily confused and unable to concentrate Loss of house training was also a common complaint. As the disease progresses, dogs become ataxic and some have minor proprioceptive deficits, hypermetria, intermittent head tilt and coarse tremors. Many dogs have difficulty in eating and drinking, mainly due to ineffective prehension. Blindness, or some degree of visual loss, is more often than not at a later development.
COLLIE EYE ANOMALY (CEA)As of January 2005 a DNA test is available for this eye problem.
This disease is congenital, and so can be detected at around six to eight weeks of age. The inheritance pattern is a simple autosomal recessive trait. It is desirable to examine the eyes as soon as possible, as in Border Collies, there may be secondary pigmentation as the dog develops. The secondary pigmentation could obscure the opthalmoscopically visible signs of mild forms of CEA.
Characterised by the presence of choroidal hypoplasia lateral to the optic disk. There is a lack of retinal and choroidal pigmentation in the affected area, and the tapetum is absent locally. Colobomas are present in some individuals, visible in the optic disk or inferior to it. These colobomas can be extensive, four to five times the diameter of the normal optic disk. Some retinal detachments that can occur, cause visual difficulties, and defects in the central vision have been associated with the presence of large colobomas.
Treatment: The condition is generally benign, and the dogs retain vision unless complete retinal detachment occures.
PROGRESSIVE RETINAL ATROPHY (PRA)
Occurs in dogs 2 years and over, symptoms in early stages, Hyperreflective band at or near the tapetal-nontapetal junction in all areas, but the most evident and important area is the horizonatal juntional zone. The location and appearance should not be confused with the impression of the long posterior ciliary artery in the fundus. As the disease prgresses the hyper-reflectives zones advance centripetally, until the only opthalmoscopically normal area is a narrow band superior to the optic disk parallel to the horizontal tapetal-nontapetal junction. At this stage day vision remains good, although some dogs exhibit tunnel vision as a result of the loss of all cells at the periphery of the fundus. Affected dogs will lose vision completely, although day vision may be retained for a variable time. No treatment is available. The condition is not associated with pain or discomfort. There have been no investigations into the genetic mechanisms in this breed, but the presumption is that the condition, as in other breeds, is recessively transmitted. Opthalmological testing should be done at six to eight weeks.
CENTRAL PROGRESSIVE RETINAL ATROPHY (CPRA)
Occurs primarily in dogs between 1 and 2 years of age. Outward signs for the owner are usually not visual until you start seeing the affects on the vision. The dog starts going blind. Ocular examinations is where the physical symptoms are seen. Characterised by brown pigment spots in the tapetal fundus, these spots vary greatly in size, number, shape and density. They may appear as small clouds of cystic areas with clear centres. Sometimes they are regular, forming a network often appearing along the course of blood vessels. In other dogs the spots are quite irregular and join with others to form a network of pigment in the tapetal zone. The two eyes are generally identically affected and occasionally there is a secondary cataract. Most affected dogs do not become completely blind. Peripheral vision can be enhanced by maintaing dogs on topical mydriatics such as 1% atropine once every second or third day.
RETINAL FOLDS (Multifocal Retinal Dysplasia)
Usually seen in young, still growing dogs up to about 2 and a half years. As the dog grows the condition improves, with folds lessening, in mild cases, disappearing altogether. The retinal folds are usually multiple, vermiform or slightly branched, and usually located in the vertical meridian and ferolateral and inferonasal nontapetal zones. Border Collies also have severe retinal dysplasia similar to that seen in English Springer Spaniels, according to Garvin. The retinal damage in these dogs is extensive, although instances of retinal detachment or other sequelae are not known. It is not known whether the severe type and the multifocal type are separate entities or interrelated.
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