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Genetic Health of Rhodesian Ridgebacks

This information is designed to elucidate the known genetic diseases associated with Rhodesian Ridgebacks to enthusiasts of the breed. The aim is to educate owners and breeders in order to reduce the occurrence of genetically inherited diseases such as Hypothyroidism and Dermoid Sinus among others.

The breeder’s ethical responsibility is to discuss dogs with defects or those that produce defects and to appropriately breed away from such genetic traits. As an owner of a Rhodesian Ridgeback, it is also your responsibility to report the development of any genetic anomaly that presents itself during the course of your dog’s lifetime to the breeder of that dog. The breeders aim is to produce the healthiest and most correct conformation puppy possible. This cannot be achieved successfully without open knowledge of genetic problems that are present within any line of Ridgebacks.

By developing pedigrees to illustrate genetic inheritance the breeder is able to interpret the genetic status of dogs used to produce a litter. This knowledge allows the breeder to more carefully select breeding stock. Every Rhodesian Ridgeback carries genes for approximately 6.6 genetic defects which is similar to the amount of genetic defects you and I carry. By knowing which 6.6 genetic defects are carried by a breeding dog or bitch and breeding away from those defects is the key to controlling genetic disease in Rhodesian Ridgebacks.

Adwera Rhodesian Ridgebacks is committed to the welfare of our beloved breed. We are developing genetic pedigrees and are committed to discuss them with other breeders and to use them to improve the genetic quality of Rhodesian Ridgebacks. If you are interested in beginning a genetic pedigree or would like more information about control of genetic traits Adwera Rhodesian Ridgebacks recommends the book “Control of Canine Genetic Diseases” by Dr. George A. Padgett, DVM

Disease Name
Description

Megaesophagus (Esophageal Achalasia)

Clinical symptoms are regurgitation of undigested food. This occurs due to the failure of esophageal muscles to force swallowed food through to the stomach.
Mode of inheritance is undetermined
Age of onset < 6 mos.

Hypothyroidism (Autoimmune thyroiditis, Hashimoto’s Disease, Lymphocytic thyroiditis)

Destruction of the thyroid gland due to an attack from the animal’s own immune system. Symptoms are rough, scaly skin, hair loss, and weight gain.
Mode of inheritance is recessive
Age of onset is < 2 yrs.

Deafness

Inability to hear, may be unilateral or bilateral.
Mode of inheritance is undetermined
Age of onset is < 6 mos.

Alopecia (Idiopathic Flank Alopecia or Cyclical Flank Alopecia)

Clinical symptoms include hair loss on flanks with little or no scaling or any inflammatory changes. Hyperpigmentation may occur.
Mode of inheritance is undetermined
Age of onset < 5 yrs.

Myotonia

Muscles continue to contract after voluntary movement ceases causing a stiff gait.
Mode of inheritance is recessive
Age of onset < 6 mos.

Dermiod Sinus (Arachnoid cyst, Meningeal cyst)

Cavities or cysts may develop within the meninges separated from the spinal cord by pia mater. They may compress the cord.
Mode of inheritance is undetermined
Age of onset birth.

Rhodesian Ridgeback cerebellar degeneration and color dilution syndrome

All affected puppies show coat color dilution and cerebellar signs, including growth retardation, ataxia, inability to stand and tremors.
Mode of inheritance is recessive
Age of onset < 4 wks.

Cataracts

Lens opacity that obscures vision and may cause blindness.
Mode of inheritance is undetermined
Age of onset varies.

Entropian

Turning in of the eyelids causing the eyelashes to rub the eyeball.
Mode of inheritance is undetermined
Age of onset is < 1 yr.

Eversion of the nicitating membrane (Eversion of the third eyelid)

The cartlidge in the third eyelid is abnormal, causing the third eyelid to roll away from or toward the globe.
Mode of inheritance is undetermined
Age of onset < 3 mos.

Pannus (Superficial Stromal Keratitis)

An epithelial growth over the cornea causing a gray haze that may obscure vision.
Mode of inheritance is undetermined
Age of onset < 1 yr.

Persistent Pupillary Membranes (PPM Mesodermal dygenesis)

A failure of blood vessels in the anterior chamber of the eye to regress normally; there may be impaired vision or blindness.
Mode of inheritance is undetermined
Age of onset < 3 mos.

Progressive Retinal Atrophy (PRA)

Degeneration of the retinal vision cells which progresses to blindness.
Mode of inheritance is undetermined
Age of onset varies

Calcinosis Circumscripta

Abnormal deposits of calcium in the skin and subcutaneous tissue.
Mode of inheritance is undetermined
Age of onset < 1 yr.

Hemivertebra

Abnormal formation of he body of the vertebrae, which can cause posterior ataxia and paralysis.
Mode of inheritance is undetermined
Age of onset < 1 yr.

Hip Dysplasia

Abnormal formation of the hip socket; causes rear-limb lameness.
Mode of inheritance is polygenic
Age of onset < 2 yrs.

Osteochondritis Dessicans (OCD)

Aseptic necrosis of bone under joint cartlidge; causes lameness.
Elbow Joint (Elbow Dysplasia): OCD of the medial humeral condyle, fractured coronoid process and nonfusion of the anconeal process.
Mode of inheritance is polygenic
Age of onset < 1yr.
Shoulder joint Undetermined < 1 yr.
Tarsocrural Joint Undetermined < 1 yr.

Spondylosis Deformans

Abnormal fusion or bridging between vertebrae, may cause pain and/or paralysis.
Mode of inheritance is polygenic
Age of onset > 1 yr.

Transitional Vertebral Segments (Lumbosacral)

Clinical signs associated with this disorder relate to damage to the cauda equina and include paresis, paralysis, denervation, atrophy and atonia.
Mode of inheritance is polygenic
Age of onset varies

Wobbler Syndrome (Cervical Spondylolisthesis, vertebral instability)

Abnormality of the neck vertebrae causing rear leg ataxia that may progress to paralysis. The main vertebrae affected are 5, 6, and 7.
Mode of inheritance is polygenic
Age of onset < 1yr.

Renal Dysplasia

Failure of normal development of the renal parenchyma causing malfunction and death. Clinical signs are those of renal failure.
Mode of inheritance is undetermined
Age of onset < 1 yr.
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