Since I got my first breeding girl, Sky,  I've read almost everything I could about Rough Collie. I've learnt a lot about temperament, health, I've talked to various successful breeders. And when I decided to open my own kennel, I promised myself I will aim at breeding only top quality puppies here. So instead of having many puppies I will rather breed my girls just one of two times and with the best stud dogs I could find.

My first concern is the character. I want to breed collies that are open, friendly and brave, that love people, children and animals and are first and furthermost great family companions. I also like active collies, that are not only show dogs but could be used also for various dog sports, sheepdog, maybe even rescue dogs. People have forgotten collies used to be great sheepdogs, very active, strong, full of energy. With over breeding them they have lost some of this active character, but I still think Rough Collies are great working dogs if you teach them things from young age and socialize them well. I know a lot of collies that are competing in agility, are great obedience dogs, sheepdogs and some even train rescue. So my goal is definitely breeding collies great to work with!

       Secondly, there is health. Rough Collies are generally resilient and healthy, but there are some health issues that can affect the breed. In my opinion, the healthy hips are very important so we check the hips of our collies and are very careful young dogs don't start practicing any sports too soon.

Another health problem is a mdr1 gene that causes the sensitivity to some drugs. The gene is responsible for pumping drug and toxins out of the brain but dogs that carry the mdr1 gene cannot do this and that can result in serious health problems that can include death if given the wrong drugs.

Another possible health problem is DM - Degenerative Myelopathy which is a progressive disease of the spinal cord that causes weakness, and eventually inability to walk in the rear legs. In its early stages DM is commonly mistaken for “arthritis”, “old age”, “hip dysplasia” or “spine problems”. (Nancy Kelso, I believe it is important to test for DM and try to breed out this disease.

And lastly, there are some eye diseases affecting collies, like CEA and PRA. But that will be more difficult to solve since more than 95% of collies are CEA affected. Fortunately, the dogs with mild CEA will most probably live all their lives without any problems, so for now it's just important we examine the puppies clinically for this disease. But in the future I would like to follow the footsteps of the breeder I admire the most - Angela Harvey from Wicani kennel who is doing her best to help eradicate this problem and is using the dogs brought from America, who are genetically clear.

And last but not least, there is appearance. I don't like collies who have been bred only for showing, have tons of hair, and can't even move properly...Most of such collies have lots of flaws, from stop being too big, necks and bodies being too short, wrong tail carriage...I want to breed elegant collies whose look is according to standard, with as less visual errors as possible, and that can, most importantly, be your lively and active companions.


Canine Hip Dysplasia is a malformation of the hip joint where the ball or head of the femur does not fit snugly within the hip socket.

Multiple studies have demonstrated that all normal puppies are born with "perfect" hips,  due to the environmental factors, the soft tissues surrounding the hip joints may develop abnormally as the puppy grows with an accompanying laxity or looseness in the muscles, cartilage, connective tissue and ligaments. As the joint is not supported, the femoral head and the socket move apart producing an unstable joint. It is this instability that causes all subsequent problems.

Genes that are associated with hip dysplasia have been identified in some breeds, but they are breed-specific; that is, the assortment of genes is different in every breed. (For example, see studies on the German Shepherd dog (Marschall & Distl 2007, Fells & Distl 2014, and Fels et al 2014), Bernese Mountain Dog (Pfahler & Distl 2012), and Labrador Retriever (Phavaphutanon et al 2008). Genes that could cause hip dysplasia have not been found in any breed.

Environmental factors are very important

Although there is a genetic influence on hip dysplasia, the heritability of the trait is rather low. Many studies have shown that genetic variation accounts for only a modest fraction of the variation in hip scores, usually 15-40%. This means that some fraction of the variation in the quality of the hips is the result of non-genetic, or "environmental" influences.

The top three environmental factors that have been found to play a significant role in the develop of dysplastic hips are:

a) Joint laxity occurs when the head of the femur does not fit snugly into the acetabulum. This could be the result of traumatic injury, overloading of the joint by weight, lack of muscle strength, or adductor forces (e.g., bringing the legs together). Joint laxity is the primary factor that predisposes a dog to the development of hip dysplasia.

b) Body weight is a MAJOR environmental factor. Puppies that weigh more at birth as well as those with higher growth rates (so they get heavier sooner) have a higher risk of degenerative changes in the hip joint (Vanden Berg-Foels et al 2006).

c) Exercise: Puppies raised on slippery surfaces or with access to stairs when they are less than 3 months old have a higher risk of hip dysplasia,while those who are allowed off-lead exercise on soft, uneven ground (such as in a park) have a lower risk (Krontveit et al 2012)Dogs born in summer have a lower risk of hip dysplasia, presumably because they have more opportunity for exercise outdoors (Ktontveit et al 2012). On the other hand, dogs from 12-24 months old that regularly chase a ball or stick thrown by the owner have an higher risk of developing dysplastic hips (Sallander et al 2006). 

The most critical period for proper growth and development of the hip in dogs is from birth to 8 weeks old, so the type of exercise the puppies are exposed to is most important during this time.

 There are a number of dysplastic dogs with severe arthritis, that can run, jump and play as if nothing were wrong, and some dogs with minimal radiographic changes that show severe lameness.

Even if Slovenian club for British Sheepdog doesn’t require hip-scores I think a responsible breeder would check their dogs.

MDR 1 

It is now widely accepted that some Collies appear to be hypersensitive to certain toxins (natural or drug-induced) and are more prone to stress-related problems.

The problem first came to light in 1983 when several Collies died from Ivermectin poisoning and, since then, the veterinary profession has accepted this drug should never be given to Collies. More recently a Rough Collie died from eating horse faeces (Ivermectin is used for worming horses and any excess drug passes out with their faeces).

Researchers have since found that approximately 60% of Rough and Smooth Collies appear to be susceptible not only to Ivermectin, but to a wide range of other drug substances. The MDR1 (multi-drug resistant) gene is responsible for ensuring the body’s natural P-glycoprotein functions normally by protecting the body from both environmental toxins and administered toxins eg drugs, and acting as a transport mechanism moving substances from cell to cell. P-glycoproteins are normally extensively distributed in the blood-brain and blood-testes barriers as well as major organs such as the liver, kidneys, intestines and placenta. When they are present in the intestinal tract three things normally happen – the substance may be metabolised; it may enter the circulatory system; or it may be passed out of the large intestine with the faeces.

In MDR1-affected dogs the function of the P-glycoprotein is compromised and so toxins may leak into the major organs. If these compounds leak across the blood-brain barrier, they enter the central nervous system causing toxic reactions such as excessive salivation, Ataxia, blindness, coma, respiratory problems and even death.

An Affected dog (-/-) receives a defective or mutant MDR1 gene from both its parents, so such dogs are double recessive and will display toxic reactions to a wide range of drug compounds (see list below). In 2007 a genetic test was made available for MDR1 and so It is extremely important that breeders try and use Normal (+/+) dogs in their breeding programmes so as to eliminate the defective MDR1 genes as soon as possible.

The table here shows three classes of drug compounds: Class A includes substances that have been proven to pass through the blood-brain barrier in MDR1-affected dogs and cause problems; Class B lists substances which have shown interactions in animal tests, whereas Class C substances can be given without problems, even to affected dogs:

Class A

DO NOT USE in dogs with MDR1 defect (-/-)

Anti-Parasitic Drugs
Ivermectine substances: Diapec®, Ecomectin®, Equimax®,Eqvalan®, Ivomec®, Noromectin®, Paramectin®, Qualimec®, Sumex® & Virbamec®

Doramectine substances: Dectomax®

Moxidectine substances: Cydectin® & Equest®

(EU scientists commonly find residues of the above drugs in animal products – milk, cows, sheep, pigs & salmon).

Loperamide substances: Immodium® [anti-diarrhoeal]

Class B

Use only under close supervision of your vet.

Cytostatics:(Cancer treatment) Vinblastine, Doxorubicine, Paclitaxel, Docetaxel, Methotrexat & Vincristine

Glucocorticoids (Steroids commonly used to treat auto-immune diseases): Dexamethason

Immuno-suppressives: Cyclosporine A

Heart glycosides: Digoxine & Methyldigoxine

Antiarrhythmics: Verapamil, Diltiazem & Chinidine [Heart problems]

Pain control: Morphine & Butorphenol

Anti-emetics: Ondansetron & Domperidon [sickness/vomiting]

Antibiotics: Sparfloxacin, Grepafloxacin; Erythromycin

Antihistamines: Ebastin 

Tranquillisers & pre-anaesthetic agents: Acepromazine 

Analgesic & pre-anaesthetic agent: Butorphanol

Other drugs; Etoposide; Mitoxantrone; Ondansetron; Paclitaxel;Rifampicin.

Class C

Can be used

Stronghold®, Advocate® & Milbemax® can be used safely, but only in the recommended application form and dosage.

*In dogs with an MDR1 mutant gene [-], Acepromazine and Butorphanol tend to cause deeper and more prolonged sedation. Vets are recommended to reduce the dosage by 25% in MDR1 carriers [+/-] and by 30 -50% in MDR1 affected dogs [-/-]



 Degenerative Myelopathy is a progressive disease of the spinal cord that causes weakness, and eventually inability to walk in the rear legs. It has long been know to exist in German Shepherds, Corgis and over 50 breeds. It has long been suspected in collies, and this last year has been confirmed in a collie by Collie Health Foundation and University of Missouri, after confirmatory autopsy of a collie believed to be affected.

In its early stages DM is commonly mistaken for “arthritis”, “old age”, “hip dysplasia” or “spine problems”.

Signs of Degenerative Myelopathy: Degenerative myelopathy typically occurs in older dogs, 7 to 14 years of age. It is a relentlessly progressive disease of the spinal cord. The first signs are loss of coordination (ataxia) and weakness in the hind legs. One rear leg is often worse then the other. The disease starts as trouble rising in the rear legs and weakness, and progresses to wobbly rear legs. Over time the rear legs become weaker, buckle, and have trouble standing or walking. Eventually, the disease progresses, over months to a couple years, to complete paraplegic. Lastly, fecal and urinary incontinence occurs, with front leg weakness. Amazingly this disease is not painful.

 The genetic mutation discovered is equivalent to the most common inherited form of the human disease, ALS (Amyotrophic Lateral Sclerosis), also known as Lou Gehrig’s Disease. Diagnosis of Degenerative Myelopathy: Unfortunately there is no single test to confirm DM in a live patient. The genetic test developed by University of Missouri can only confirm if a dog is at risk for the disease. Not all dogs with the affected genes will develop the disease. The test can be most valuable to rule in or out DM. If the test is negative, the dog does NOT have DM. If it is positive for both mutations, the dog is at risk, and further testing needs to be done to diagnose the disease.

(Nancy Kelso)



     Collie Eye Anomaly (CEA)

CEA is the most common form of eye problem found in the Collie, both rough and smooth variety. It is also found in the Border Collie, Shetland Sheepdog and Australian Shepherds. Those dogs with minor anomaly make fine pets and usually do not lose their eyesight.

CEA is a non-progressive congenital eye disease. Is an abnormality of the choroid layer of the eye, so is technically referred to as Choroidal Hypoplasia (CH). It presents itself as a pale patch (due to a localised lack of retinal and choroidal pigment) in the dorso-lateral region of the choroid, near the optic disc.

Since CEA was first made public in the 1960’s the only way of detecting the disease has been by ophthalmic examination, with dogs being diagnosed as either ‘clear’ or ‘affected’ (mild to severe). Abnormalities of the choroid can be diagnosed in puppies as young as six to seven weeks of age so it is recommended that puppies are clinically examined for CEA at 6-7 weeks.

The majority of Collies with CEA suffer no ill-effects and appear to show no visual defects, neither does the disease progress. In rare cases of CEA the Collie may suffer retinal detachment and in very mild cases clinically ‘affected’ puppies may ‘go normal’ before they reach one year of age.

     Progressive Retinal Atrophy (PRA)

PRA will result in blindness. A well known and widely used stud dog in the '70s was found to be a carrier and did produce blind puppies. While the breeder now test-breeds all their stock available for stud services, PRA is present in a number of lines. Most reputable breeders who know or suspect that PRA is in their lines do test-breed. Since PRA in Collies is a simple recessive, it has been easier to control than CEA.




Nancy Kelso,