SURVEY RESULTS
January 2000 - December 2001

This is the raw data from the NA/MAS Health Survey conducted from January 2000 - December 2001.  You may click on any of the highlighted diseases for a brief description of the disorder, it's heritability (if known) and recommendations for breeders.

Total number of dogs submitted: 358

Healthy dogs with no known genetic problems: 281

Average age: 1.8 years

Deafness related to Excess White: 3 (the only reported cause of deafness)

Number of dogs  CERF’d: 74

Number of dogs  OFA’d:  35

Why should I do hip and eye certifications? (A commentary)

Spayed or Neutered: 41
Estrus varied from 6-24 months old at onset with the majority beginning estrus cycles between 8-12 months.
Litter sizes average litter size for a first litter was 4.8, second litter 4, third litter 6, fourth litter 5.5. There are only two reported neonatal deaths although in several surveys the number of pups surviving to weaning age was not reported.


Genetic Diseases Reported

Iris Coloboma 8 "IC found in right blue eye, left amber eye is normal"
"IC in right eye"
Atypical coloboma not detected at 6 or 8 wk exams. Dx at 1 yr by 2 vets
Distichiasis 10 "A few hairs in 4 lids"
"single eyelash in one eye"
"2 eyelashes in one eye"
"one eye lash each eye no problems so far as irritation or [cornea] scraping"
"several lashes, no problems so far"
"Distichiasis is asymptomatic"
8 eyelashes had to be removed at a cost of $840.00
Persistent Pupillary Membranes 3 "Very small, diagnosed at 7 weeks; has probably disappeared and I will have him examined in the next few months to confirm this."
Undershot Bite 4 Bite was normal before adult teeth came in
Overshot Bite 2
Level Bite

 

6

 

"Bite changed to level at 3 yrs. old"

"Was scissors til 3 then changed to level"

Missing Teeth 2
Teeth (other) 1 Baby canine tooth did not fall out and permanent tooth was coming in; baby tooth extracted when she was spayed
Pituitary Dwarfism (Diagnosed) 1
Elbow Dysplasia 1 Puppy started limping, on and off, from age 9 weeks
Luxated Patella(s) 3 "Bilateral bowed tibias"
"Onset 12-24 months. "... was just diagnosed with 2 luxated patellas. One is bad enough to require surgery.."
Epilepsy (of unknown cause) 6 "mild seizures started at 4 mos. she has had 3 that we have seen"
She has only had one seizure so far about one mo.ago. On no meds at this time.
Onset at 15 months
On phenobarbital since 10/13. No seizures since.
[Epilepsy] onset at 15 months
[epilepsy] first seen at about 2 1/2 years total of 3 we know of.
Aggression
12
Dog Aggressive... 2 litters born to him. Puppies are all normal. no IC in litters no sign of aggression"
"We euthanized this bitch at not quite 2 years of age. We spent thousands on blood work and training, but it seems we were fighting her genetic makeup. At least one of her littermates was put down for aggression as well."
"Does not like children or strangers. Very protective of me and our home. Will snap if provoked by child"
"Very strong "Prey drive" chases and will nip at joggers, bicyclists, people walking by without dogs. Very assertive, and unlike my other mini."
"very aggressive toward other dogs"
"aggressive toward other dogs and some people; generally great with everyone, but when walking is aggressive toward people who seem to be afraid of him."
"may attack other dogs"
Fear aggression, restraint (on-leash)aggression, territorial aggression (as diagnosed by a certified veterinary behaviorist from NC State Vet School)
Other Behavioral Problems 4 "Very Territorial , more out of being unsure."
"Can be food aggressive, I think more to past environmental causes rather than genetic aggression"
Very shy, tends to be a worrier
Severe separation anxiety
Benign Tumors 1 "Benign cysts have been removed and grown back."
Thyroiditis 2 Self-limiting during pregnancy and resolved upon delivering 15 puppies!
Single Allergy 5 Food allergy: very reactive to wheat, somewhat reactive to beef
Multiple Allergies 5 "Allergy to fleas and certain grasses"
seasonal [allergies] fall and spring
Demodectic Mange 1 Localized mange

OTHER COMMENTS:

"[unaffected female] Has produced IC's w/clear male"

"[unaffected female] 2nd litter resulted in 3 puppies that were put down due to double IC's, one was kept up with a small IC-the remaining three were unaffected"

"One pup died at birth in her first litter. It was perfectly formed, just was too small to survive apparently"

"Dog had chronic bouts of diarrhea for years. No meds from vet gave long term relief. I went from good dog food to premium to super premium with no improvement. I now home cook with supplements and acidophilus added and stool is usually normal."

"Elbows x-rayed "normal"

"Nervous, no known reason, especially with men. Positive training only."

"Very sensitive nose, sneezes somewhat often"

"Two deaf female pups in litter [due to excess white].

"Very sweet and angelic!"

"Our girl is very sweet."

Diagnosed with weak hocks

Shy of strangers, friendly when with people he knows

Friendly outgoing little girl

very shy...may have been abused before I got him

7 weeks old and already has herding instinct

Suspicious/fearful of strangers but warms up with time; fearful of some dogs

towards animals and people. spooky temperment. sometimes she's fine; nervousness flighty


Why Should I do Hip and Eye Certifications?

Below is a question I received from a survey respondent. Based on the number of dogs being reported who are not certified, but are being bred, I thought the answer might be worth reprinting here!

My dogs have not been x-rayed or eye certified, as I know of no problems at least three generations back.  Can you give me a good reason to certify?  It seems expensive if there are no known problems.

Hip dysplasia is a polygenic disease. That is to say that it is not a single gene that is either recessive or dominant. Rather it is more of a conformational combination that is affected by the size and shape of the head of the femur and the size, depth and shape of the hip socket. If one of your dogs were to have a somewhat shallow socket which the femur head did not fit into quite correctly the muscles, etc., could easily adapt to compensate and hold the joint together to the point that you would never guess he actually had hip dysplasia. If one of your females had a similarly shallow socket, or a femur head that was not quite rounded enough, the breeding of the two dogs could then produce dysplastic puppies.

As a breeder you are not only responsible for looking out for your dog's health, but also the breed's health. Only through the cooperative effort of all breeders's doing hip certifications can the incidence of hip dysplasia be reduced throughout the minis!

OFA will rate the hips as Excellent, Good, Fair or dysplastic. In order to reduce the risk of producing dysplasia, you would avoid breeding Fair to Fair. Neither "Fair" rated dog would be dysplastic, but due to the irregularities in the conformation of their joints, the combination has a fairly high risk of producing dysplastic puppies.

Now, I personally have a "fair" rated dog and you would never ever guess that her hip conformation was any less than perfect. My "fair" dog is the fastest runner, the highest jumper, can execute amazing maneuvers -- turning, spinning, etc. I am so glad that I had her x-rayed because now I know that to reduce any risk of producing hip dysplasia, I should not breed her to any dog with less than a "good" rating. These types of decisions can not be made without x-rays and certifications.

As far as expense, hip certification is a one shot deal. The most expensive I have seen was $120 for both hips and elbows. To do both parents at this price is less than 1/2 the cost of a single puppy for most breeders!

Regarding eye certs: based on the health survey, I would say the minis are fairly free of genetic eye diseases. The big one is iris coloboma. Some colobomas are visible to the naked eye, most are not detectable except by ophthalmic exam. While this is not a devastating problem right now, if we are not vigilant and do not keep track of what combination of lines are producing this we may find ourselves in a few years with such a prevalence that it becomes impossible NOT to produce! Then the disease becomes worse breed-wide. We don't know how IC's are inherited yet, so for now we must be careful not to breed a dog with an IC, or breed two dogs who both had littermates with IC's.

As far as expense, yes, eye exams are expensive, about $40/dog. It is important for your breeding program to not only have the parents examined, but also the puppies.  In 2000 I had 2 litters at the same time - 13 puppies. I made one trip to the ophthalmologist with 13 puppies and 4 adults, which cost me a little over $300 (volume discount!). My total bill for hip and eye testing then for those two litters was just over $600 (hip certs on 2 girls and one sire, plus all the eye exams). This total was made up for by the sale of a single puppy.

Finally, breeding rarely makes a profit. That is why most good breeders classify themselves as "hobby breeders." Breeding is done because you are passionate about your breed and want to produce the best possible dogs that are not only a credit to the breed, but who will also give and receive years of love and companionship to the people who love them. You want your dogs to be a part of 'something special', not just a means to earn a dollar. With this in mind, hip and eye testing on all breeding dogs in a single kennel is far less expensive than the treatment of a single dysplastic puppy, and saves you the heartache and the puppy the physical pain that goes along with it.

Links to read more about dysplasia and it's control:
OFA
Penn-Hip

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REPORTED DISEASES IN THE NORTH AMERICAN/MINIATURE AUSTRALIAN SHEPHERD


Deafness related to Excess White

Deafness in dogs has many causes; all cases of deafness in the North American/Miniature Australian Shepherd however are due to the relationship between excess whiteness and inner ear pigmentation. 

In order for the inner ear to work properly it must be pigmented. Lack of or decreased pigmentation in the inner ear leads to various levels of hearing loss or complete deafness. Early in fetal development only certain areas of the body are pigmented. The pigmentation then migrates throughout the body during the fetal period and for several weeks after birth. Studies have shown that when pigment is not present around the eyes or the ears (the sites of pigmentation origin for the inner ear) hearing loss can occur.

Deafness due to lack of pigmentation is part of color inheritance.   The genes that control the white that appears in Miniature Australian Shepherds is located on the S locus of the chromosomes. These genes are the Irish Spotting Gene (si) which produces the sought after white collar, socks, muzzle, and forehead and chest blazes. The Piebald Gene (sp) produces white body splashes (unacceptable in the MAS breed standard), and the Extreme Piebald Gene (sw) which produces an almost all-white dog with very little color. 

The genes described above are all recessive to the gene for no white (S).  Therefore, in order for a dog to inherit si, both parents must carry the gene for it. Modifier genes, of which relatively little is known, also affect the degree of expression of the genes. Plus modifiers increase the amount of color, decreasing the amount of white expressed, while Minus modifiers decrease the amount of color, increasing the amount of white. The Merle gene (M) seems to also act as a minus modifier on the S-locus genes.

It is important that breeders realize that there may be more genes affecting the expression and distribution of white, especially on the head, that have yet to be discovered.  Per Sue Ann Bowling (site link below): "It is not clear to what extent the S series affects head pigment. Color-headed white shelties, for instance (swsw), can have completely colored heads - not even a forehead star or white nose. On the other hand, relatively conservatively marked dogs can appear with half white or all white heads. There is probably at least one other gene series that affects head markings. It is at least possible that the plus and minus modifiers affect head and body markings simultaneously."

Links:  Color Genetics
             Inheritance of Coat Color in the Australian Shepherd
             Color Genetics 101

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Iris Coloboma

Iris Coloboma is a condition in which the iris, or colored portion of the eye has a "hole" in it.  In the normal eye, the pupil appears round and black.  The black color of the pupil is because the pupil is an opening through which light is admitted into the eye.  The pupil has the ability to constrict to restrict the amount of light entering the eye, or dilate to admit more light.  When an iris coloboma is present, extra light is continually admitted.  The most common complications from the presence of an iris coloboma is squinting in bright sunlight. Iris coloboma does not progress nor lead to blindness and can be detected by ophthalmic examination very early.  Large colobomas are detectable with the naked eye, but small ones may escape detection unless a professional exam is performed by a certified veterinary ophthalmologist.  Screening for iris coloboma is part of a normal CERF exam.

Mode of inheritance is not known at this time.  Current CERF recommendations are to exclude affected animals from breeding, but does not exclude unaffected parents or siblings of an affected dog.

Links:     Canine Eye Registration Foundation
                Hereditary Eye Defects

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Distichiasis

In this condition of the eyelid, one or several eyelashes may be found growing on the lower eyelid, which is typically without lashes. They are typically painless and cause no lasting damage.

Trichiasis is a similar condition referring to lashes growing in an abnormal direction. This is a hereditary defect that can cause chronic corneal irritation through constant contact of the lash with the cornea. The only treatment is removal of the errant hairs through surgical excision or a local freezing procedure known as cryosurgery.

Distichiasis and Trichiasis are thought to be a dominantly inherited condition but large scale studies are lacking. Therefore, in order to avoid producing these conditions, affected dogs should not be bred.

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Persistent Pupillary Membrane

A pupillary membrane covers the anterior (forward facing) surface of the eye during fetal development and normally disappears before birth. In PPM, small strands of the membrane remain.  Those that are attached to the lens or to the cornea are known to cause cataracts or corneal opacities. If blindness due to cataract formation is imminent, the strands may be surgically removed. The vast majority of PPM's disappear without intervention during the puppies first year with no long lasting deficits. There are conflicting reports on the heritability of this disorder, however the fact that some breeds are affected and others are not certainly points to a genetic contribution. In the Miniature Australian Shepherd no cases of "attached" PPM's have been reported and are therefore considered a minor defect that does not exclude a previously affected dog from breeding.

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Bites

"Bite" refers to the relationship of the lower teeth to the upper teeth.  A "scissors" bite is correct in that the front teeth close just in front of the bottom teeth and when viewed from the side, the teeth come together like the teeth of pinking shears.

In an UNDERSHOT bite the bottom teeth close in front of the upper teeth, while in an OVERSHOT bite the upper teeth protrude more than 1/8" in front of the lower teeth.  A LEVEL bite then refers to condition in which the upper and lower teeth meet evenly.  A WRY mouth is almost non-sensical in that the right and left sides of the mouth are completely different and teeth have no order to their placement or relationship to each other.  A PARROT mouth is a severely undershot bite.

The bite is determined by the sizes of the upper and lower jaws.   The size and formation of the upper jaw is inherited independent of the lower jaw.   Therefore it makes sense that breeding dogs with vary disparate jaw sizes can lead to the formation of bite problems.  Most bite problems, unless severe, do not cause problems.

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Pituitary Dwarfism

Dwarfism is an autosomal recessive trait that affects the amount of the growth hormone somatatrophin secreted from the pituitary gland. Dwarfs may appear normal at birth but are significantly smaller than their unaffected litter mates by six weeks of age. In dwarfism, body proportions remain normal. The pituitary gland also secretes the hormone TSH (thyroid stimulating hormone). Pituitary dwarfism is often accompanied by hypothyroidism that results from the low levels of TSH. This leads to cretinism which causes retention of the fuzzy puppy coat, hair loss along the sides of the body and bone deformities. They often have reproductive difficulties, scaly skin, weight gain, exercise intolerance and mental dullness. Cretin dogs often appear disproportionate with large broad heads, wide square trunks and short limbs.

  • Achondroplasia - this a separate form of dwarfism that is defined as "a failure of endochondral bone growth, usually caused by a Mendelian dominant defect, that results in shortened extremities." Translated, this means that Achondroplasia is the abnormal lack of growth in the long bones (leg bones) due to premature closure or calcification of the growth plate.  This results in a dog with a normal body size, but abnormally small extremities.  Often the skull appears larger than the limbs and the leg bones themselves are short and wide.   Achondroplasia is inherited via a simple dominant gene, meaning that dogs who have the disorder will exhibit it and will pass the gene on to 50% of their offspring when bred to an unaffected dog.  The other 50% will be normal.  Dogs who do not exhibit achondroplasia do not carry the gene.  Homozygosity (both parents affected) for achondroplasia is almost always lethal, however heterozygotes (one parent affected) do not have related health problems.  ** Achondroplasia is being added to the Health Survey effective June 1, 2000 **

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Luxated Patellas

The patella is the kneecap of the dog and sits within a groove of the femur called the trochlea. If the groove is too shallow the patella will shift out of place and become dislocated (luxated). This causes the muscles holding the patella to also be shifted out of place. The dislocation of the patella is painless. The dog may suddenly refuse to put weight on the affected leg or may even show no signs of the dislocation. The patella can shift back into position on its own or it may be manipulated back into position, but will typically dislocate again at some time. Surgical treatment can be performed to fix the patella in the correct position.

This condition is more frequently seen in smaller breeds and has been suggested to result from dwarfism although no proof of that claim exists. It has also been suggested that it's occurrence in smaller breeds is due to the smaller size of the trochlea leaving less "margin for error."  It is actually very similar to hip dysplasia except affecting a different joint.  It is most likely polygenic in inheritance and therefore affected dogs should not be considered for breeding.

Links:    OFA - Patella Luxation

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Epilepsy

Epilepsy is a neurological condition. It is of utmost importance that any dog observed to have seizure activity be tested for an environmental cause before a ruling of a epilepsy is established. Environmental causes of seizures can include exposure or ingestion of plant or chemical toxins, head injury, heat stroke, hypoglycemia (low blood sugar), hypoxia (lack of oxygen), liver diseases, kidney diseases, Vitamin D malabsorption, teething distress, infections (most often distemper) and parasitic or malignant brain tumors. Most cases of environmentally induced seizures resolve once the underlying problem has been treated.

A diagnosis of Idiopathic or Primary Epilepsy is made only after all known environmental causes of the seizure activity has been definitively ruled out. The term idiopathic literally means "of unknown cause." Epilepsy is not well understood. We know that seizure activity is caused by a misfiring or over-active firing of nerve impulses in the brain, but we do not know why this occurs. There is considerable evidence of a familial tendency, but studies have been inconclusive in determining the mode of inheritance. For this reason, dogs with Idiopathic Epilepsy should not be bred. This seems simple, but most reported cases of Idiopathic Epilepsy begin between 1-3 years of age, while others may not develop until 4 years of age or older. Many affected dogs have already produced offspring by the time epilepsy has declared itself. In these cases, the offspring should be closely monitored and careful breeding to unaffected lines be strictly enforced.

Links: Canine Epilepsy Network

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Aggression

Aggression is all too often in the eyes and expectations of the beholder.   There are numerous forms of aggression including food aggression, on-leash aggression, dog aggression, etc.  Most causes of aggression are environmental, or learned by the dog due to bad experiences.  Even with environmentally caused aggression, the question remains as to why some dogs develop aggressive tendencies after a negative exposure and other do not.  Obviously, their underlying personality has a relationship.

Unprovoked viciousness with no known environmental background to explain it is the type of aggression most worrisome.  Most behaviorists find that viscious/aggressive animals have a very dominant personality - that is they seem to have a need to be in control and will overreact aggressively to a perceived threat or challenge.   This is still a personality trait.  Scientists, behaviorists, psychologists and sociologists have pondered the origin of personality traits for centuries with no definitive or simple answers yet gained.  There is certainly a familial trend seen in the inheritance of personality disorders, though the mode of inheritance is unclear.   Therefore, aggressive dogs should not be utilized in a breeding program.

Links: A Behavioral View on Dog Aggression
            Preventing Dog Aggression
            Understanding Aggressive Behavior in Dogs

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Allergies

Allergies are a form of auto-immune disease.  The immune system exists to protect the body from foreign "antigens" invading the body and causing illness.   It accomplishes this purpose by first trying to remove the antigen through increased mucous production in the airways and GI tract, increased movement through the bowels, sneezing, coughing and scratching.  When that fails, the immune system produces and sends out antibodies to attack the antigen.  This is all well and good unless the immune system "overreacts" causing an all-out assault on a relatively harmless allergen, or on a substance that is actually not harmful at all.

Allergies are just that, the overreaction of the immune system which causes an exaggerated immune response.  Allergies are included as a heritable disorder because they cause extreme discomfort in affected animals and worry and expense to the owner. There is certainly a familial tendency to reproduce allergies, especially allergies to pollens, although the exact mode of inheritance is not known.  The fact that some breeds of dogs are more plagued with allergies than others also suggests a heritable cause.  Dogs with multiple allergies should not be included in a breeding program.  

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Demodectic Mange

DM is an over-infestation of the mite Demodex canis. These mites are present on every animal but in cases of generalized mange the individual's immune system is too weak to control their numbers sufficiently. Therefore, DM is considered an auto-immune disorder.  Common sites for the scaly lesions and itching caused by the mites include the face, muzzle and forelegs. DM is not diagnosed until at least one year of age as many young puppies whose immune systems are immature may exhibit localized or generalized mange. By one year of age the immune system has developed enough to control the mite population and end the disease process. Therefore, dogs over the age of 12 months and in good health who develop DM are not used for breeding.

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References:

Padgett, George A: Control of Canine Genetic Diseases, 1998.
Giffin, James M., Carlson, Liisa D: Dog Owner's Home Veterinary Handbook, 3rd ed., 2000.
Siegal, Mordecai (editor): UC Davis School of Veterinary Medicine Book of Dogs, 1995.
Willis, Malcolm B: Genetics of the Dog, 1989.

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