by Addi Pittman
Every breeder will produce defects if they breed long enough. Those that profess that they don’t produce defects have either stopped breeding, rarely breed, or aren’t telling the truth. Defects will occur in any breed of dog (or species of animal including man). Sometimes defects can appear with no warning or previous clues that would indicate the defect was within a given line. Breeders and stud owners should collaborate with each other regarding defects each has encountered prior to a planned breeding. If defects occur in a given mating, the breeder should contact the stud owner and explain what the breeding produced. When information is exchanged in this manner, both parties can hope to reduce their chances of producing multiple defects in a litter.
The following health concerns are found in purebred dogs including English Cocker Spaniels. The inheritance of some of these conditions may not be completely understood.
Breeders and owners should incorporate health checks in all English Cockers considered for breeding PRIOR to being bred. Brucella canis “Brucellosis” is a contagious bacterial infection that causes both abortions and sterility. It was first recognized as a serious disease of dogs in 1966. It is especially prevalent in the southern states, but occurs nationwide. Infected dogs can also suffer from other conditions such as uveitis, prostatitis, and testicular atrophy. B. canis can be spread through oral, nasal, conjunctival, and genital secretions (including urination). There is NO known cure.
Each species has its own brucella. All are zoonotic (contagious to humans), but in varying degrees. The Baker Institute suggests that you don’t introduce new dogs into a breeding colony until they have been tested clear of Brucella canis. Bitches should be checked several weeks prior to a planned breeding. Stud dogs should be tested at least annually.
This listing of diseases and defects is not meant to overwhelm you. Many of these things you will not experience in a lifetime of breeding.
CANINE HIP DYSPLASIA
Canine hip dysplasia (CHD) is the most common, heritable orthopedic problem in dogs. It is usually characterized by hip joint instability (laxity) and secondary degenerative joint disease (DJD). Normally, the ball-shaped head of the femur fits snugly into the socket (acetabulum). When the hip doesn’t fit tightly, degenerative joint disease begins. The genetic basis for CHD is thought to be polygenic and multifactorial.
Preliminary hip x-rays should be done on any animal under age 2 if a breeding is anticipated. All dogs over age 2 can be radiographed for certification by the Orthopedic Foundation for Animals (OFA).
In the last 15 years, the incidence of CHD has been greatly reduced in our breed. No doubt, examination and OFA certification have played a significant role in reducing the incidence. Currently, solid color English Cockers have a higher incidence of CHD and “Fair” ratings than parti-colors; however, the disease exists in all colorations.
PROGRESSIVE RETINAL ATROPHY
PRA is a descriptive term applied to retinal diseases that affect all breeds of dogs. The same clinical signs are present in all PRA affected animals. Affected animals will show night blindness and a progressive loss of day vision.
Many PRA affected English Cockers can be diagnosed between three and five years of age. It is during this age period subtle retinal changes can be noted by the experienced ophthalmologist. Even though the same clinical signs will be present in all PRA affected animals, the age of onset of disease differs from breed to breed. The onset period is divided into three approximate age groups: early, middle, and late. The English Cocker falls into the late-onset group (4-7 years old). This late-onset form of the disease is now called Progressive Rod-Cone Degeneration (PRCD). PRCD is inherited RECESSIVELY.
An affected animal can only be produced if both parents are affected, both carry the defective gene, or one parent is affected and the other carries. All the offspring of a PRA affected dog will carry ONE PRA gene. The status of the second parent will determine whether the offspring will be affected or carriers. Statistically, when two carriers are mated a 1:2:1 ratio (25% will be affected-i.e., 1 in 4, 50% will carry, 25% will be genetically clear-1 in 4) will occur.
All breeding stock should have annual eye exams for life. There are other ocular conditions that affect our breed. some of these conditions are: cataracts, entropian, ectropion, distichiasis, dry eye (geriatric), persistent pupillary membranes, and retinal dysplasia.
Congenital sensorineural deafness (present at birth) is currently found in parti-colored English Cockers. Most studies of this defect have been done in Dalmatians dating as early as 1896. Dalmatian studies have shown that they do not go deaf until 3-4 weeks of age. However, degeneration begins as early as one day after birth and is clearly evident histologically by 4 wks. old (Strain). The cause of this degeneration isn’t known; however, there is an observed absence of “melanocytes” (pigment) in the tissue of many deaf animals.
The inheritance of deafness in parti-colored English Cockers isn’t know. It is believed there is a correlation between white coat color and the piebald (spotting) genes. Whatever the inheritance is, it isn’t simple.
Currently, we haven’t had congenital deafness reported in solid colored English Cockers. We are trying to build a data base through the use of BAER TESTING. Solid breeders and owners can contribute to this data base by BAER testing their animals. This procedure can help reduce the frequency of this defect by identifying affected individuals. Statistics for this defect appear in the Health Education Committee’s Annual Report.
SHORT TOE ANOMALY
This trait is formally known as, “Brachydactylia of the 5th metacarpo-pharyngeal radiant. This defect in soundness has been found in this breed for many years. It occurs when the outside toe (less frequently, the inside toe) of the forefoot ceases normal growth at about three months of age, leaving the affected toe shorter than the other three and its toe pad atrophied. The problem may range from mild (and difficult to find) to extreme.
This trait occurs in humans and is an autosomal dominant trait with incomplete penetrance. No formal studies have been done in dogs.
Epilepsy is found in all breeds including those mixed in origin. Our breed generally experiences seizure episodes that are infrequent and many affected animals are not maintained on anticonvulsants. There are exceptions! There are many reasons for seizures; therefore, not all seizure activity is inherited. The average age of onset is between the ages of 4-7 years old. Researchers have suggested that each animal inherits a “genetically determined predisposition to seizures.” Seizures occur when this threshold is exceeded.
Liver disease is any destructive or metabolic disorder involving the liver. It isn’t limited to a particular age or breed. There are also many causes for liver disease.
In recent years our breed has been implicated in several journal articles that have been published in this country and abroad. Unfortunately, it is currently impossible to tell you what is going on in this area. When an animal dies from a liver disorder pathology isn’t done or the results aren’t shared. Be aware that liver disease is surfacing.
This is a disease of dogs in which ” the heart muscle becomes overly distended.” There are numerous journal articles that are reporting this defect in our breed. We have received several reports over the years regarding this defect primarily in solid colors.
The “classic” signs are: weight loss; general debility; weakness; abdominal distention; coughing; syncope (fainting spells); and a rapid heart beat (OFA diagnostic information). Not all patients will show all of these symptoms.
Cardiomyopathy can have a very subtle onset and the dog will often show little or no clinical signs in the early stages.
Diagnosis can be made thorough x-rays and echo cardiography (ultra sound). The prognosis for dogs with this defect is generally poor.
Autoimmune Hemolytic Anemia (AIHA)
Cushings Disease Glomerulonephritis (over age 3)
Hypothyroidism Immune Mediated Thrombocytopenia (IMT)
- Extra teeth-deciduous/permanent
- Deciduous lingual mandibular canines
Young- age renal failure has occurred in this breed since at least 1957. The age of death is approximately between 9 months and 24 months old (some have lived until age 3+). The disease in this instance is inherited recessively.
Swimmers Cleft palate – complete/partial multifactorial/polygenic/environmental
blue eye – type fault-multifactorial/polygenic
Intersexuality – hermaphroditism, all forms.