HEALTH

 

Conditions that can affect the Border Collie:
 

CEA
CL
TNS
cPRA
OCD
HD

CDA

 

Collie Eye Anomaly (CEA)

Very briefly, CEA is a condition that affects the normal anatomy of the retina and other deeper structures of the eye, this can be irregularity in structure or even holes/pockets. In it's mildest form it will not affect the dog, in it's severest it will cause detached retina's/complete blindness.

CEA is caused by a recessive gene which both parents must carry to produce affected pups.

An animal will have 2 copies of every gene, one coming from the sire and one from the dam.

If an animal has two normal copies of the gene, it is classed as 'normal' and cannot ever produce affected pups.

If an animal has one normal gene and one defective gene it is classed as a 'carrier', mated to another animal with the defective gene it could produce affected pups. If mated to a 'normal' animal it will at worst produce more carriers but may also produce some 'normals'
(Note: A carrier DOES NOT have the disease)

If an animal had two copies of the defective gene it is classed as 'Affected' and will actually have the disease. If bred from, this animal can only produce carrier and/or affected pups.

The results shown in grey are what everyone wants to avoid...nobody wants to produce affected pups so these are the matings to avoid - carrier to carrier, carrier to affected, affected to affected.

Prior to the introduction of a DNA test; eye testing was first carried out on pups at around the age of 6 weeks by one of only 30 BVA approved veterinarians around the country. This initial test is for CEA only and this period between 5 and 8 weeks of age is the best time for diagnosis of this condition. If a puppy is affected it is an indication that both of it’s parents are carriers of the CEA gene. While the Kennel club does not impose any breeding restrictions from affected dogs or carriers the International Sheepdog Society (ISDS) does not allow the registration of affected pups or their progeny and does not allow the registration of puppies by parents that have produced a CEA/PRA affected pup on more than one occasion (they allow one due to the possibility of a mis-mating). The ISDS is striving to eradicate this disease from the breed. Puppies that successfully pass this eye test are issued with a litter certificate.

Passing an eye examinination at 6 weeks indicates the puppy is not AFFECTED by the disease but the physical examination cannot tell you which puppies are carriers of the gene. The recent introduction of DNA testing for the CEA gene by American laboratory, OptiGen has revolutionised breeding of border collies to a certain extent...although it can be quite expensive, we can now DNA test all breeding stock to see which animals are affected, which are carriers of the gene and which are DNA 'normal'. This means there need never be any more affected puppies produced...we can ensure that by breeding carrier/affected animals to 'normal' animals the puppies cannot ever be affected by the disease. Since this test first became available in January 2005, ALL our dogs used for breeding are DNA tested in this way.
 

 

Ceroid Lipofucinosis (CL)

Also known as 'Storage Disease' (or 'Battens Disease' when it occurs in humans)

CL is a fatal congenital disease which affects the nerve cells of the body, it has been found in a number of dog breeds and is fortunately rare in border collies.

Symptoms do not usually occur until the affected animal reaches around 12-18 months old but the disease progresses rapidly once the initial signs appear and euthanisia is usually the kindest option, there have been no reported cases surviving past 2 half years of age.

The clinical signs of the disease are:

Unreasonable apprehension or fear of familar objects/surroundings or slight disturbances.
An abnormal gait, the animal may be unsteady on it's feet and have difficulty jumping, climbing or placing feet correctly.
Dementend behaviour, characterised by manic hyperactivity and outburts of rage.

Prior to the recent introduction of a DNA test, cases could only be confirmed by a brain biopsy during post mortem examination to give an accurate diagnosis. Thankfully this is no longer the case and DNA testing is available via OptiGen or Dr Alan Wilton at the University of New South Wales.

As with CEA and TNS, the genetic inheritence of CL is via a recessive gene so animals will fall into three categories of genetic status:

CLEAR has not inherited a defective gene.
CARRIER has inherited the defective gene from a parent.
AFFECTED has inherited the defective gene from both parents and has, or will develop, the disease

Using the DNA test, it is now therefore possible to ensure that no more affected puppies are born.

 

Trapped Neutrophil Syndrome (TNS)

TNS was recognised in Border Collies about 8 years ago in New Zealand and Australia and is becoming more apparent. Inheritance patterns and percentage of affected pups in litters indicate that TNS is inherited in a recessive manner (like CL) with both parents having to be carriers of the disease to produce an affected pup. But overall, very little is known about this disease.

Symptoms may be seen in puppies as young as 2 weeks or as old as 7 months of age. Affected puppies are usually smaller, have slower growth rates, and can appear to have a 'ferret like' head and a poor hair coat. Other symptoms of disease include lameness, inappetence, diarrhoea and a high temperature. Some puppies are not obviously different until they become ill which can mean a breeder may send home a seemingly healthy puppy that may get sick very soon after. This is distressing for both breeder and new owner. TNS is a disease which ultimately causes a deficiency of the immune system, so symptoms can vary between pups but ultimately, all affected animals will have to be euthanased on humane grounds.

Diagnosis of TNS currently requires three criteria. Firstly, the pups need to show clinical symptoms consistent with the TNS. Secondly, blood tests which confirm a low neutrophil count are suspicious of TNS but do not provide a diagnosis. Puppies will occasionally develop low neutrophil counts for other reasons, eg. viral or bacterial infections, and should not be condemned on this basis. The third criteriabone marrow biopsywill give accurate diagnosis. Unfortunately, this disease is quite rare and new and further research into its causes, diagnosis, management and its impact on the breed need to be done.

Prospective buyers of Border Collies should be aware of the need to check that their prospective breeder is DNA testing all breeding dogs for TNS and not breeding known carriers together. Note that as more and more dogs are tested (and return Clear results) many dogs will not need to be tested due to having Clear parentage. Make sure you ask for copies of the DNA reports for all dogs that are claimed clear in the pedigree of your prospective pup so that YOU are SURE your pup will be Clear via parentage. A dog that is a Carrier of TNS will not suffer any symptoms and will lead a normal life and would make a fine pet.

 

Centralised Progressive Retinal Atrophy (cPRA)

As the name suggests, cPRA is a form of blindness affecting the light sensitive portion of the eye, this blindness becomes gradually worse over time (hence progressive).

Due to the progressive nature of the disease, PRA cannot be diagnosed until a dog is around 18 months old which is when they usually have their first adult eye test, dogs used for breeding should be tested regularly thereafter.

Puppies registered with the ISDS cannot be ‘pink papered’ until both their parents have successfully passed their 2 year eye test, the society then issues a pink coloured registration paper, indicating that the pup is from fully eye tested stock.

cPRA has been something of a success story in border collies and is now EXTREMELY rare; much of this is thought to be down to the improvement in dogs nutrition with the introduction of complete foods, since cPRA is thought to be mainly down to a defeciency in Vitamin A.

 

Osteochondritis Dissecans (OCD)

What is OCD?

OCD is a condition that occurs in growing puppies of larger breeds, primarily between the ages of 4-9 months, but can occur as late as 12 months or older. It is most commonly seen in the shoulder joint but can be seen in stifles, elbows, hocks or other joints. In approximately one third of the cases of OCD, the disease is bilateral (in both joints). Occasionally, it is present in several different joints in the same individual. It is seen twice as often in males as in females.

OCD is thought to be caused by a problem in the growth rate of the joint cartilage relative to the underlying subchondral bone. The cartilage over the bone in the joint becomes thickened and the growth of the underlying bone is altered. Because the joint is an area of movement and stress, this thickened cartilage is at risk of being torn, especially in the areas most subjected to trauma, stress and movement, such as the caudal area of the shoulder joint. When repeated trauma causes a flap of cartilage to tear away from the underlying bone, the condition becomes OCD. Because of the tear, the joint fluid can come in direct contact with sensitive areas of the now-exposed underlying bone and can cause pain. Lameness will usually be present in the dog at this time. If the cartilage flap remains attached, it will not re-attach and heal back into its original position. If the cartilage flap tears completely loose from the adjoining cartilage, it becomes a loose body in the joint called a "joint mouse". Once the flap has detached, the torn area where the flap originated usually heals when the lesion is filled in with fibrocartilage, a type of "scar" cartilage. Joint mice may float around in the joint, eventually being broken down and absorbed, or they may be nourished by the joint fluid and grow to a larger size than the original loose cartilage body. Possible complications arise when joint mice attach themselves to other areas in the joint or become entrapped it the bicipital tendon sheath, causing irritation, obstruction of movement and pain. The breakdown of cartilage from these various processes may cause inflammation, pain and the eventual development of secondary osteoarthritis in the affected joint.

Is it inherited?

OCD is a considered to be a common disease in large and rapidly growing breeds of dogs, with most affected breeds averaging over 60 lbs. However, some medium breeds, such as the Brittany spaniel, bull terrier, greyhound and border collie, also have a high incidence of this disease. Although the factors that cause OCD are not completely resolved, direct factors considered to be involved in the development of OCD are rapid growth and trauma to the joint. Indirect factors affecting rapid growth include nutrition, hormones, and genetic predisposition to rapid growth and large size. Indirect influences that may lead to increased trauma to the joint include conformation and behavior, which are also influenced by heredity. Therefore, the genetic link for most types of OCD is considered to be indirect, that is, an inherited tendency. Certain sites for OCD lesions, such as the elbow, appear to have a greater direct genetic contribution and a higher heritability than other sites, such as the shoulder. The most important contributing factor in OCD of the shoulder, the most common site, is thought to be trauma.

Border collies have a higher incidence of OCD than might be expected for their size and the weight bearing stress on their joints. It would seem likely that behavioral characteristics common to border collies could contribute to the increased occurrence of OCD in this breed. The high energy levels, athletic ability, stamina and quick reflexes for fast turns and speed changes many border collies possess could predispose them to trauma and stress in joints that most other breeds of similar size would not commonly experience. The overall increased incidence in males for this disease is thought to be due to the increased growth spurt in the male around the susceptible time period for OCD development. As well, it is tempting to speculate that behavioral factors common to males might also be involved in this increased susceptibility.

How can it be prevented?

As in many other developmental skeletal problems, an imbalance of calories, protein and nutrients can increase the occurrence of OCD. In general, rapid weight gain in puppies at the critical time period between 4-9 months predisposes larger breed dogs to OCD. High intake of calcium and protein has been implicated in the development of this condition. Therefore, care must be taken in feeding young puppies special "growth formula" puppy foods or high protein diets. Puppies need extra calcium and protein but free choice or overfeeding of these diets can be harmful. It is of interest to note that some dog food manufacturers have recently responded to health concerns of dog breeders and owners by formulating puppy foods specifically for large breed dogs.

Since trauma is a contributing factor to the development of OCD, it would be reasonable to monitor exercise in puppies, especially between the ages of 4-9 months. Activities such as excessive running and roughhousing with people or other dogs should be avoided. In addition, puppies shouldn't engage in intense activities that encourage abrupt, fast turns, quick stops, or jumping, especially jumping from heights. Of course puppies need exercise and should be allowed to be reasonably active, but they should also be watched carefully so that they don't do too much or do things that might cause injury.

article by C. Denise Wall, Ph.D and quoted from American Border Collie magazine



Hip Dysplasia

Hip Dysplasia (HD) is caused by the abnormal formation of the hip ball and socket joint. Normally the ball should fit snugly into the hip socket, forming a pivot point. Some dogs are born with a genetic predisposition for hip dysplasia; at birth their hips are normal but as they grow, the hip joint becomes a malformed structure so that the ball no longer fits snugly into the socket and cannot rotate smoothly.

HD is a relatively common problem in most breeds of dog and can be a very painful and terribly debilitating disease, in bad cases requiring surgery and in the worst euthanasia.

The Kennel Club and BVA have a testing scheme in an attempt to avoid having puppies born with this genetic predisposition. This scheme involves dogs over 12 months of age having their hips x-rayed and sent to the BVA panel of experts for ‘scoring’; they produce a score for the joints and angles on each hip to give a score for left and right. The higher the score, the worse the dogs hips are, the lowest possible score is 0:0 = 0 and the highest 53:53 = 106.

The BVA publish an annual list of all KC breeds with the average score although in many people’s opinion this average is artificially low as many people will not send off poor x-rays and dogs diagnosed with HD will also not be scored. In most other European countries, the breed clubs make it obligatory that a dog be hip scored before it is bred from and only those with acceptable hips are allowed, this is in my view, a much better system.

The current UK average for border collies is 13. This system of scoring varies around the world
.

 

Colour Dilution Alopecia (CDA)

Alopecia (hair loss) related to dilute coat colour (Blue or Lilac in Border Collies) is a recognized condition in dogs called "Colour Dilution Alopecia". This condition develops in some, but not all dogs with the dilution gene. Affected dogs have a poor, patchy haircoat progressing to widespread permanent hair loss. At the cellular level, there are abnormalities of the hair follicles and uneven clumping of pigment (melanin) granules in the hair shafts in affected areas.

CDA is characterized by loss of hair from the dilutely pigmented areas (so any white or tan areas on your Border Collie will not be affected). Coats are normal at birth, and onset of hair loss usually begins between six months and three years of age. Hair loss usually begins along the spine and often spares the head, tail and limbs.

It has been suggested that richer coloured dogs are less likely to be affected, may be less severely affected or may start to lose hair later in life than lighter colored dogs. The hair loss may be total or partial and any remaining hairs are usually sparse, rough and easily broken or removed. The skin in the affected areas is usually scaly and may occasionally develop bacterial infections. Itching is usually absent, unless a bacterial infection has set in. An affected dogs skin is highly susceptible to sunburn or extreme cold, so should be kept inside as much as possible, but your dog's health is not otherwise affected.

Diagnosis of CDA requires first ruling out other causes of hair loss. Diagnostic tests should include fungal cultures, skin scrapings to check for parasitic mites, etc. CDA often closely resembles endocrine (hormone related) hair loss and the dog should be carefully examined for any other abnormalities, and tested for normal thyroid function. Presence of dilute pigment and a characteristic course of disease also aid in making the diagnosis. Microscopic examination of hairs and\or skin biopsies can be used to confirm the diagnosis. There is no cure for CDA. Treatment is limited to controlling the scaliness and any associated itching with various shampoos or topical treatments.

Since this condition is hereditary but little more is known about it's causes, Arktulu Border Collies will not be breeding specifically for Blue or Lilac coat colour, but puppys of this colour, may at times occur.

 


 

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