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Guidelines For Breeding And Purchasing Cocker Spaniels

Revised October, 1996 - Revised from April, 1989 A release from the A.S.C. Health Registry Committee - Judy Iby, R.V.T., Chairman, and Kerry L. Ketring, D.V.M. Diplomate American College of Veterinary Ophthalmologists


In April of 1989, Elizabeth H. Durland and Thomas J. Kern, D.V.M., offered the first guidelines for breeding and purchasing cocker spaniels. Since that time, genetics of cocker spaniels have advanced with the discovery of new disorders, further understanding of some disorders, and identification of some disorders at least thought to be inherited. The current editors have graciously put together a large number of these changes. With the recent emphasis placed on genetic defects by the American Kennel Club, changes will continue to come at a more rapid rate and further revision of the guidelines will be necessary. Probably some changes have already occurred prior to the publication of this revision. This, however, can serve as a guideline to those people interested in breeding cocker spaniels and purchasing cocker spaniels. If these recommendations are followed substantial progress can be made in improving the overall health quality of our breed.


Many cocker spaniel breeders are justifiably concerned about the problems posed by certain hereditary defects to the future of their breed. Their requests for information on how best to handle these problems in their breeding programs prompted the preparation of these guidelines.

These recommendations will stress eight different categories:
  1. eye defects;
  2. blood disorders;
  3. endocrine disorders;
  4. skeletal defects;
  5. metabolic disorders;
  6. heart disorders,
  7. skin disorders,
  8. neuromuscular disorders.
These guidelines will in no way de-emphasize the importance of breed type and basic soundness. In fact, by reducing the incidences of debilitating and life-threatening defects, we should improve type, soundness, and the general health of our cockers.

There is much concern and disagreement over the precise way in which the various defects are inherited. Two modes of inheritance are probably responsible for most genetic defects:
  1. SIMPLE AUTOSOMAL (simple dominant/recessive): a specific pair of genes on matching chromosomes control the expression of a particular trait.
  2. POLYGENIC AUTOSOMAL (multiple gene influences): more than one pair of genes controls the expression of a particular trait.
In autosomal inheritance, the ability to selectively eliminate a defect is possible by planned breedings, but even in this mode of inheritance individual variation as well as environmental factors may affect expression of the causative gene. In both modes of inheritance the prevalence of these defects can be reduced by selective breeding. The key to reducing the frequency of heritable defects is the accurate identification of unaffected dogs from lines of dogs in which these defects are uncommon. The chance of even apparently unaffected dogs developing one or more of the important genetic defects is potentially predictable based upon knowledge of the numbers of affected related dogs. Therefore, a database of information derived from examination of every cocker spaniel (active and retired breeding dogs, show dogs, and their pet littermates) must be developed--and used--to make accurate predictions.

The ASC Health Registry is an invaluable aid because it provides this type of information. The ASC Health Registry currently lists dogs that are certified as unaffected with cataracts, progressive retinal atrophy (PRA), Von Willebrand’s disease (vWD), Factor X, hypothyroidism, and/or hip dysplasia. Several other eye defects of potential concern are not as yet listed in the Registry. Many of these problems do not have a definitive clearance test. Unaffected dogs are determined by the following:
  1. Examination by veterinarians who are diplomates of the American College of Veterinary Ophthalmologists (ACVO) for cataracts, PRA, retinal dysplasia/folds, and other eye defects
  2. Blood test results reported in percentages of normal levels provided from diagnostic laboratories for von Willebrand’s and Factor X levels
  3. Normal thyroid function
  4. A certification number from the Orthopedic Foundation for Animals (OFA) for hip dysplasia.
Eye Defects

I. Cataract By definition a cataract is an opacity of any portion of the lens (capsules, cortex, nucleus), regardless of size, age of onset, or progression. Cataracts may be categorized by:
  1. Age of onset (congenital, juvenile, senile)
  2. Location within the lens (capsular, cortical, nuclear)
  3. Stage of maturation (incipient-beginning, immature, mature and hypermature).
Causes of cataract include: (1) genetic influences; (2) trauma; (3) metabolic disorders (diabetes mellitus); (4) nutritional deficiency; and (5) severe internal inflammation of the eye.

Genetic cataracts in the cocker spaniel develop most commonly in young adult and middle-aged dogs, less than 8 years old (juvenile onset). The cortex (outer layers of the lens) is usually involved first, though the specific location (anterior, posterior, peripheral) varies. These opacities usually, though not always, progress to some degree in affected eyes, often to blindness. Genetic cataract may eventually affect both eyes, though frequently at different times. Nonetheless, even unilateral cataract (afflicting only one eye) should be considered potentially heritable. The mode of inheritance of cataract is not certain but is presumed autosomal recessive.[1] [2] The breed may be afflicted with more than one type of genetic cataract, which further complicates plans to eliminate the problem. There is a common syndrome of acute cataract formation in cockers less than 1 year of age and severe anterior uveitis. Environmental factors might trigger genetic cataract development in some dogs.

II. Progressive Retinal Atrophy

Retinal atrophy is degeneration of all parts of the retina, the light-sensitive layer which lines the back of the eye. Progressive retinal atrophy (PRA) refers to retinal degeneration which is genetically determined and occurs in both eyes. The age of PRA diagnosis by eye examination in cocker spaniels is usually 3-6 years of age. Diagnosis by electroretinography (ERG) may be confirmed earlier (12-18 months of age). The mode of inheritance is thought to be autosomal recessive.

III. Retinal Dysplasia (Folds)

Retinal dysplasia is defined as abnormal development of one or more layers of the retina which may involve the entire retina or only limited areas. Both eyes may be affected but not symmetrically. In the dog the retina is structurally and functionally mature by 7-8 weeks of age. Influences that cause retinal dysplasia theoretically can produce it until at least this age. Possible causes of retinal dysplasia include genetic influences (most significant) as well as illness, modified live virus vaccination, or medication administration to the pregnant dam. An autosomal recessive mode of inheritance is presumed. Not a vision threatening disease in cockers and may not be apparent in adults.[3]

IV. Keratoconjunctivitis Sicca (KCS, Dry Eye Syndrome)

Keratoconjunctivitis Sicca is defined as the degenerative changes in the cornea and conjunctiva that occur following severe reduction in the volume of tears produced and delivered to the eye. Either one or both eyes may be affected. Most dogs with KCS develop thick green or yellow eye discharge, followed by blindness due to scarring and pigmentation of the normally transparent cornea. The condition afflicts dogs of any age. The causes of KCS are thought to include:
  1. genetic influences (most significant, though the mode of inheritance is unknown)
  2. drug toxicity (certain sulfa drugs)
  3. canine distemper virus infection
  4. injury
In some dogs, surgical removal of a prolapsed third eyelid gland (“cherry-eye”, “haw”) may predispose to early development of KCS. The “dry eye” condition is diagnosed simply by measuring a dog’s tear production with a standardized strip of filter paper (Schirmer tear test).

V. Primary Glaucoma

Glaucoma is defined as increased pressure within the eye associated with vision loss. Primary glaucoma is an inherited condition that eventually afflicts both eyes. Age of onset is usually 5-8 years of age. Eyes with glaucoma become intensely red and cloudy and rapidly develop permanent blindness. The mode of inheritance is unknown.

VI. Prolapsed Gland of the Third Eyelid (“Cherry Eye”, “haw”)

The gland of the third eyelid, which produces about one-third of the volume of tears in the dog, may protrude from the underside of the third eyelid. A smooth pink swelling develops, usually suddenly, at the inside corner of one or both eyes in pups and young adult dogs. If gently replaced in normal position soon after protrusion, the glands will often remain in place. If manual replacement is unsuccessful, the protruding gland may be surgically replaced or removed. Removal of the gland in some dogs promotes the development of the dry eye syndrome, though this procedure is not the most important cause of KCS, nor do all dogs that undergo gland removal develop dry eyes. The mode of inheritance is not known.

VII. Distichiasis

Distichia are misplaced eyelid hairs that grow along the margin of the eyelids instead of external to it. They may be present in small or large numbers in one or both eyes. In most dogs they cause little or no discomfort, though they may contribute to eye irritation from other causes. Distichia occasionally cause corneal scratches or severe irritation and must be surgically removed. At least a few distichia may be found in most cocker spaniels. Distichiasis is seldom the primary cause of ocular disease. The mode of inheritance is unknown.

VIII. Ectropion

Ectropion refers to excessive droopiness of the eyelids, usually associated with excessive facial skin. Rarely a problem which requires treatment, it may occasionally predispose dogs to chronic eye infections from dust, grass, etc. The mode of inheritance is unknown.

IX. Entropion

Entropion is defined as inversion of the eyelid margin. Most affected dogs have eye irritation; frequently, corneal scratches result. Most dogs with Entropion require surgical correction. The mode of inheritance is unknown.

X. Imperforate Lacrimal Punctum (unopened lacrimal duct)

Inferior lacrimal puncta fail to open. This is a common problem in cocker spaniels and is a nuisance since there may be unilateral or bilateral severe epiphora (overflow of tears) with or without mucopurulent (infectious) discharge. The puncta may need to be opened. The mode of inheritance is unknown.

XI. Episcleritis (inflammation of the loose tissue between the sclera and conjunctiva)

Swelling and increased vascularization (blood vessel proliferation) of the sclera in one or both eyes. Could cause corneal vascularization, retinal disease, and blindness. May result in anterior uveitis (inflammation of the uvea) and severe ocular (eye) pain. Often misdiagnosed as glaucoma and requires life long treatment. The mode of inheritance is unknown.

XII. Optic Nerve Coloboma

Lack of normal development of the optic nerve or sclera resulting in a notch like defect on optic nerve. Unilateral or bilateral but no vision loss. The mode of inheritance is unknown.

XIII. Persistent Pupillary Membrane

Persistent blood vessel remnants in the anterior chamber of the eye thah fail to regress normally in the neonatal period. These strands may bridge from iris to iris, iris to cornea, iris to lens, or form sheets of tissue in the anterior chamber. The last three forms pose the greatest threat to vision and when severe, vision impairment and blindness may rarely occur in the cocker. The mode of inheritance is unknown.

XIV. Corneal Dystrophy

A non-inflammatory corneal opacity (white to gray) present in one or more of the corneal layers; usually inherited and bilateral. Not a major problem or threat to vision. The mode of inheritance is unknown.

Examination For Eye Defects

The ASC Health Registry accepts for listing only examination results made by members of American College of Veterinary Ophthalmologists (ACVO). Complete eye examinations are performed with specialized equipment, including ophthalmoscopes and the slit lamp biomicroscope, following pupil dilation with a drug. The eyelids and front portions of the eye are examined with both instruments, while the back of eye (retinal, optic nerve) are only examined with the ophthalmoscope. The slit lamp biomicroscope allows careful examination under high magnification of the external eye, the cornea, and the lens. With it, cataracts invisible to the ophthalmoscope or the naked eye can be identified and localized. Thus, potentially genetic cataracts can be discovered long before they become easily visible or impair vision.

Recommendations For Testing And Breeding
  1. Because genetic eye defects may develop at any age, regular eye examinations should be performed throughout a dog’s life. Young dogs and bitches involved in breeding programs and dogs of any age offered at public stud should be examined every six months; older dogs should be examined annually at least through eight years of age. In addition, dogs and bitches that have not been examined within six months prior to planned breeding should be retested prior to being mated. Littermates of breeding stock sold as pets should be examined several times throughout their lifetimes (for example, at 2, 5, and 8 years of age).
  2. Breed or purchase only unaffected dogs. Do not purchase or use for breeding any dog which has not been examined and reported to be free of major inherited eye defects during the previous year by an ACVO diplomate. We highly recommend that proof be provided that the dog’s sire, dam and grandparents are also free of these defects.
  3. Breeding Recommendations:
    • Never breed an individual dog that has a cataract of suspicious genetic origin regardless of its age or the stage of cataract development.
    • Do not use for breeding an offspring of a dog that has a proven or suspect genetic cataract.
    • Full brothers and sisters or grandchildren of an afflicted dog should be considered possible genetic carriers of future afflicted dogs. If used as breeding stock at all, these dogs should be bred with care; wait until the dog is at least 3 years of age and remains unaffected, then breed only to an unaffected older dog from a line with a low incidence of defects. The progeny of these breedings should also be used for breeding with care, mating them as suggested above. The careless use of these dogs, while young, could prove disastrous to a breeding program. If no further problems appear among their progeny over a period of time, then the “suspect” designation could eventually be removed.
    • If there is evidence that a dog, even though not affected itself, is producing more than a rare offspring with cataracts when bred to multiple lines, it should be removed from breeding programs.
    • Dogs affected with PRA or their offspring should not be bred. Parents should be considered to be at least carriers of the defect, if not affected. Some grandparents are also at least carriers, though confirmation is difficult.
    • Dogs with retinal dysplasia/folds can be identified as early as a few months of age. Breeders should consider this when selecting pups to retain for breeding. Ideally, dogs with retinal dysplasia should be bred to dogs without them. Dogs in which retinal dysplasia/folds have been identified in examinations as young dogs but not identified on subsequent examinations should be considered to be affected dogs.
    • Dogs with serious dry eye syndrome should probably be removed from breeding programs. At least, affected dogs should be bred only to dogs without KCS. This is very likely to be a genetic defect, though the mode of inheritance is currently unknown.
    • Dogs with primary glaucoma should not be bred. Offspring of affected dogs may be carriers.
    • Dogs which have required surgical treatment for distichiasis, ectropion, or entropion should probably not be bred.
Although the ASC Health Registry is an invaluable aid for general information, breeders should request a copy of the most recent eye examination sheet from owners of stud dogs and bitches sent for breeding. The ASC Health Registry only lists for cataracts and PRA and does not include any other ocular information. In order to minimize the risk of introducing a dog ultimately affected with one or more serious ocular defects into a breeding program, fanciers should select older unaffected dogs for breeding. Using unaffected dogs and bitches under 3 years of age greatly increase the risk that a program will be based on dogs which are actually affected with serious defects that are not yet apparent.

Blood Disorders

I. von Willebrand’s Disease

von Willebrand’s Disease may be screened by a blood screening test. The disease is found in cocker spaniels and is characterized by moderate to severe bleeding, which is controlled by blood transfusions from normal dogs. vWD is frequently seen in conjunction with hypothyroidism. It is recommended that all cockers be checked and if found to be affected the dog should not be bred. Ideally a carrier should not be bred, but if it is an outstanding dog, free of other inherited problems and “necessary” to a breeding program, then it should be mated to a dog with normal levels and the offspring tested.[4] The mode of inheritance in the cocker spaniel is incomplete dominant (with variable penetrance).

II. Factor X Deficiency

Factor X Deficiency is marked by severe bleeding in newborn and young adults and mild bleeding in mature animals. There is a blood-screening test available. The mode of inheritance is highly penetrant autosomal recessive.

III. Immune-Mediated Blood Disease

Cocker spaniels are predisposed to immune-mediated blood disease although the disease is acquired. No dog should be used for breeding purposes that is affected and caution should be used when breeding related dogs. Pedigree research is important. It is important to identify cocker spaniels with these problems. The veterinarian should be asked to contact veterinary research areas that are interested in this problem, or breeders should contact a member of the Health Committee of the American Spaniel Club to identify laboratories that might offer help for this problem.

Endocrine Disorders

Hypothyroidism is the most common endocrine disorder in the cocker. Autoimmune (Hashimoto’s) thyroiditis (inflammation of the thyroid) is a common cause of hypothyroidism in dogs. The disease has a variable onset, but clinical signs often appear at 2 to 5 years of age. The disease has a genetic component, and available data suggest that the trait is recessive. Screening should begin at 2 years of age and be continued annually or bi-annually through 8 years of age.[5] Ideally hypothyroid dogs should not be bred. OFA now offers a Thyroid Registry as does ASC. Laboratory studies should be done for certification from certified labs only. [6]

Skeletal Defects

I. Hip Dysplasia

Hip Dysplasia is common to the cocker and should be ruled out before breeding. OFA will not issue a permanent number before two years of age, but this should not deter one from performing preliminary radiographs. Every cocker used for breeding should have this examination and receive OFA certification.

II. Patellar luxation (slipped stifle)

Patellar luxation (slipped stifle) (medial or lateral) is common in the cocker. Breeding stock should be free of this disorder. OFA offers a patellar registry.

III. Intervertebral disc disease

Intervertebral disc disease may be the result of conformation or other factors. Cockers are predisposed to this disorder. It can be an emergency. When considering breeding an afflicted dog, you should determine the prevalence within the line and if the dog has enough merit to offset this deficit.

Metabolic Disorders

Liver disease - chronic active hepatitis (inflammation of the liver) and copper toxicosis (poisoning) - is becoming more prevalent in the cocker. At this time pedigree research is an important tool. There may be two disorders – copper toxicosis and an autoimmune chronic hepatitis. Research in both is needed. Both may be genetic, but the mode of inheritance is unclear.


I. Dilative cardiomyopathy

Dilative cardiomyopathy, a disease of the heart muscle, is found in the cocker. It may be taurine/carnitine responsive. A blood test for taurine levels is available. The dog should not be bred and close relatives should be evaluated before breeding.[7]

II. Sick Sinus Syndrome

Sick sinus syndrome is a complex of arrhythmias (abnormal heart rate) that predispose the dog to hypotension (low blood pressure), weakness and syncope (fainting). The dog should not be bred. NOTE: OFA now offers a Heart Registry. Animals may be seen by a veterinary cardiologist or a veterinarian with interest in cardiology.[8]

Skin Disorders

Too little thought is given to breeding dogs that are afflicted with skin disorders and this contributes to giving the cocker spaniel a poor reputation and being labeled a high maintenance

I. Seborrhea

Seborrhea may be primary or secondary. A dog affected with primary seborrhea should never be bred. Affected dogs are born with this cellular defect. The skin cells and sebum are being over produced. Again, pedigree research is important. The mode of inheritance is uncertain.

II. Allergies

Allergies - food and inhalant - are prevalent in the cocker and should be taken into consideration when planning a breeding. If your dog is affected, it is best to breed to a line with a low incidence of this problem. Allergies are the number one cause of otitis externa (inflammation of the outer ear).


Idiopathic epilepsy (seizures of unknown cause) is common in the breed. Afflicted dogs should not be bred. To date there is still no way to identify carriers. The mode of inheritance is uncertain.

Breeders’ Responsibilities

All breeders of cocker spaniels should feel a responsibility for the future of the breed that they have chosen to use for their own enjoyment. One of their obvious goals is not only to improve their stock’s performance in conformation, obedience, or field endeavors but to improve the quality of their pet puppies. Too often little or no attention is paid to elimination of hereditary defects, although this is changing in a positive manner.

As responsible breeders and members of the American Spaniel Club, we owe it to the cocker spaniel to make a serious effort to reduce the incidence of hereditary defects. We need to be aware of all the health problems within our breed. These guidelines cover only a few of the more common and more serous faults. At this time our Health Registry lists all flushing spaniels that are submitted and free of defects that we are able to validate by standardized testing.

When planning a breeding we need to evaluate our stock not only for conformation, type, attitude and temperament, but also for health defects. Cockers with genetic traits, those that are painful or those that require life long treatment or surgery for survival, should not be bred. When considering breeding cockers with lesser faults, we need to give thought to what the dog can contribute to the breed. Are there enough assets to overcome the deficits?

One of the important contributions we can all make is to communicate honestly with one another. If a dog develops a defect, all purchasers of offspring that might be used for breeding, and, in the case of a stud dog, the owners of bitches bred to him should be notified. In so doing, other breeders are provided with the information they must have for their breeding programs. In this way, a major contribution towards the future of the breed will be made.

Finally, some may feel that the recommendations presented here are too restrictive. However, the incidence of hereditary defects has reached such proportions in cocker spaniels that only strict adherence to proven principles of genetic selection will reduce their frequency. By following these guidelines, increasing honest communications between breeders, and educating and guiding new breeders, we can reduce the incidence of these defects that threaten the future of the cocker spaniel.


1. Yakely W L: “Familial cataracts in the American Cocker Spaniel.” J Am Anim Hosp Assoc 7:127, 1971.

2. Yakely W L: “A study of heritability of cataracts in the American Cocker Spaniel.” J Am Vet Med Assoc 172:814, 1978.

3. Macmillan A D Lipton DE: “Heritability of multifocal retinal dysplasia in the American Cocker Spaniel.” J Am Vet Med Assoc 172:568, 1978.

4. Dodds J: “Inherited and acquired von Willebrand’s Disease.” Cocker Spaniel Leader 51, 5/96.

5. Nachreiner R: “Canine Thyroid Registry.” Veterinary Diagnostic Newsletter Vol 13, No. 1, 1996.

6. Nachreiner R: “OFA Canine Thyroid Registry.” Cocker Spaniel Leader, March: 44, 1996.

7. Kittleson M: “Dilated Cardiomyopathy in American Cocker Spaniels.” Cocker Spaniel Leader, December, 1993.

8. “OFA Congenital Heart Disease Registry.” Cocker Spaniel Leader, March: 42, 1996.


Lanting F L: Canine Hip Dysplasia and Other Orthopedic Problems. Alpine Publications. Loveland, Colorado (1981).

Willis M B: Genetics Of The Dog. Howell Book House. New York, New York (1989).

Birchard S J and Sherding R G: Saunders Manual of Small Animal Practice. W B Saunders Company. Philadelphia, Pennsylvania (1994).

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