Unfortunately sometimes problems occur in the breed, below are a list of the few problems the breed encounters.  All responsible breeders (ourselves included) will take every opportunity to have the relevant tests done to try and prevent this occuring in their stock.

 

We DNA test all our stock for PLL and CEA and breed responsibly.  All our puppies are

litter screened (eye test)  at 8 weeks before going to their new homes.

 

Primary Lens Luxation (PLL) is a well-recognised, painful and blinding inherited eye condition that affects many breeds of dog, particularly terrier and terrier-type breeds including (but not restricted to) Miniature bull terriers, Tibetan terriers, Jack and Parson Russell terriers, Lancashire Heelers and Chinese Crested dogs, also the Australian Cattle Dog, Jagd Terrier, Patterdale Terrier, Rat Terrier, Sealyham Terrier, Tenterfield Terrier, Toy Fox Terrier, Volpino Italiano, Welsh Terrier, Wire-haired Fox Terrier and Yorkshire Terrier.

 

In affected dogs the zonular fibres which support the lens breakdown or disintegrate, causing the lens to fall into the wrong position within the eye. If the lens falls into the anterior chamber of the eye glaucoma and loss of vision can quickly result.

 

Scientists have identified a mutation that is associated with the development of PLL in several breeds of dog. The DNA test now being offered examines the DNA from each dog being tested for the presence or absence of this precise mutation. It is thus a ‘mutation-based test’ and not a ‘linkage-based test’.

 

Breeders will be sent results identifying their dog as belonging to one of three categories:

 

CLEAR: these dogs have two normal copies of DNA. Our research has demonstrated clear dogs will not develop PLL as a result of the mutation we are testing for, although we cannot exclude the possibility they might develop PLL due to other causes, such as trauma or the effects of other, unidentified mutations.

 

CARRIER: these dogs have one copy of the mutation and one normal copy of DNA. Our research has demonstrated that carriers have a very low risk of developing PLL. The majority of carriers do not develop PLL during their lives but a small percentage do. We currently estimate that between 2% – 20% of carriers will develop the condition, although we believe the true percentage is nearer to 2% than 20%. We do not currently know why some carriers develop the condition whereas the majority do not, and we advise that all carriers have their eyes examined by a veterinary ophthalmologist every 6- 12 months, from the age of two, throughout their entire lives.

 

GENETICALLY AFFECTED: these dogs have two copies of the mutation and will almost certainly develop PLL during their lifetime. We advise that all genetically affected dogs have their eyes examined by a veterinary ophthalmologist every 6 months, from the age of 18 months, so the clinical signs of PLL are detected as early as possible.

 

Breeding Advice

Our research has also demonstrated that the frequency of the PLL mutation is extremely high in the PLL-affected breeds that we have studied in depth. This means that allowing only CLEAR dogs to breed could have a devastating effect on breed diversity and substantially increase the likelihood of new inherited diseases emerging. Therefore, we strongly advise breeders to consider all their dogs for breeding, regardless of their PLL genotype. GENETICALLY AFFECTED and CARRIER dogs can be bred with, but should only be bred to DNA tested, CLEAR dogs. All puppies from any litter that has at least one CARRIER parent should be DNA tested, so that the CARRIERS can be identified and followed clinically throughout their lives. This practise should be followed for at least one or two generations, to allow the PLL mutation to be slowly eliminated from the population without severely reducing the genetic diversity of breeds at risk.

 

Collie Eye Anomaly in Dogs

 Collie eye anomaly, also referred to as collie eye defect, is an inherited congenital condition. The chromosomes that determine the development of the eyes are mutated, so that the choroid (the collection of blood vessels that absorb scattered light and nourish the retina) is underdeveloped. The mutation can also result in other defects in the eye with more severe consequences, such as retinal detachment. When this mutation does occur, it is always in both eyes, although it might be more severe in one eye than the other. Approximately 70 to 97 percent of rough and smooth collies in the United States and Great Britain are affected, and approximately 68 percent of rough collies in Sweden are affected. Border Collies are also affected, but at a much lower two to three percent. It is also seen in Australian Shepherds, Shetland Sheepdogs, Lancashire Heelers, and other herding dogs.

 

Symptoms and Types

 While a veterinarian can determine through genetic analysis whether your dog has this defect, there may be no symptoms, until the onset of blindness signals you to the problem. There are stages of this disease, some more obvious that others, that lead up to the final outcome. Some associated conditions that may occur with this defect are microphthalmia, where the eyeballs are noticeably smaller than normal; enophthalmia, where the eyeballs are abnormally sunken in their sockets; anterior corneal stromal mineralization -- that is, the connective tissue of the cornea (the transparent coat at the front of the eye) has become mineralized, and shows as a cloud over the eyes; and an effect that is less obvious on inspection, retinal folds, where two layers of the retina do not form together properly.

 

Causes

•  The cause of collie eye anomaly is a defect in chromosome 37. It only occurs in animals that have a parent, or parents, that carry the genetic mutation. The parents may not be affected by the mutation, and may therefore not have been diagnosed with the abnormality, but offspring can be affected, especially when both parents carry the mutation. It is also suspected that other genes may be involved, which would explain why the disorder is severe in some collies and so mild that it causes no symptoms in another.

 

Patellar Luxation

What is patellar luxation?

The patella is a small bone at the front of the knee (stifle joint). In people it is referred to as the ‘knee-cap’. It is positioned between the quadriceps muscle and a tendon that attaches to the shin bone (tibia). This is termed the quadriceps mechanism. The patella glides in a groove at the end of the thigh bone (femur) as the knee flexes and extends.

Occasionally the patella slips out of the groove. This is called luxation, or dislocation, of the patella. Most commonly the luxation is towards the inside (medial aspect) of the knee, however, it can also dislocate towards the outside (lateral aspect) of the joint.

Patellar luxation can affect dogs and cats.

 

Why does the patella luxate?

The patella luxates because it (and the quadriceps mechanism in general) is not aligned properly with the underlying groove (trochlea). The resultant abnormal tracking or movement of the patella causes it to slip out of the groove.

The cause of the abnormal alignment is often quite complex, involving varying degrees of deformity of the thigh bone (femur) and shin bone (tibia). In severe cases in dogs, the thigh bone (femur) is bowed at the end due to abnormal growth. These dogs often have either a bow-legged or knock-kneed appearance.

Patellar luxation is most common in certain breeds of dogs, such as Poodles, Yorkshire Terriers, Staffordshire Bull Terriers and Labrador Retrievers. Both knees (stifles) are often affected. These features suggest the condition may be genetic.

Luxation of the patella due to injury (trauma) is uncommon.

 

What are the signs of patellar luxation?

The signs of patellar luxation can be quite variable. A ‘skipping’ action with the hind leg being carried for a few steps is typical. This occurs when the patella slips out of the groove and resolves when it goes back in again.

 

How is patellar luxation diagnosed?

Examination may reveal muscle wastage (atrophy), especially over the front of the thigh (the quadriceps muscles), although this is often minimal. Manipulation of the knee (stifle joint) may enable the detection of instability of the patella as it slips in and out of the groove. In some dogs the patella is permanently out of the groove. The severity of the luxation is graded from 1 to 4, with a grade 4 being the most severe.

X-rays (radiographs) provide additional information, especially regarding the presence and severity of osteoarthritis. Specific views may be necessary to assess the shape of the thigh bone (femur) and shin bone (tibia).

 

How can patellar luxation be treated?

Some dogs with patellar luxation can be managed satisfactorily without the need for surgery. The smaller the dog and the milder the grade of luxation (e.g. grade 1 out of 4), the more likely it is that this approach will be successful. Exercise may need to be restricted. Hydrotherapy is often beneficial. Dogs that are overweight benefit from being placed on a diet. Tit-bits may need to be withdrawn and food portions reduced in size. Regular monitoring of weight may be necessary.

Many dogs with patellar luxation benefit from surgery. The key types of surgery, which are described below, are (1) quadriceps mechanism realignment (2) trochlea deepening and (3) femoral osteotomy.

(1) Quadriceps realignment surgery
The aim of this surgery is to move a small piece of bone (the tibial tuberosity) at the top of the shin (tibia) that is attached to the patella and reposition it so that the patella is correctly aligned with the groove in the thigh (femur) bone. This procedure is called a tibial tuberosity transposition. The transposed piece of bone is re-attached with one or two small pins, with or without additional support with a figure-of-8 wire.

Exercise following quadriceps realignment surgery must be very restricted for the first few weeks until the cut bone and soft tissues heal. It must be on a lead or harness to prevent strenuous activity, such as chasing a cat or squirrel. At other times, confinement to a pen or a small room in the house is necessary. Jumping and climbing should be avoided. After a few weeks, exercise may be gradually increased in a controlled manner (still on a lead). Hydrotherapy may be recommended.