There are no mandatory requirements for any health testing of Rhodesian Ridgebacks in Australia and not one of the Australian RR clubs, nor the National RR Council, recommends anything other than xrays of hips and elbows.

We strive to breed healthy ridgebacks so, to be on the safe side, we have decided to take advantage of the tests currently available.

Testing is a tool which allows us to be aware of inherited diseases prior to breeding and so, if these conditions appear, they can be prevented from passing unknown from one generation to the next.  Most of the following conditions have been found in ridgebacks in this country.  

In Queensland now there is a requirement for all dogs conceived after 1 January 2018 to have a DNA profile and for any dog used for breeding, to also have a DNA profile.  This is not a health test. This is simply an individual identification and every puppy in every litter must be profiled before they are registered to ensure that the parents are who they are supposed to be. This has come about mainly because of the extraordinary amount of breeding of French Bulldogs and the very dubious ethics of a few breeders.

In Australia, in addition to DNA profiling, the following DNA tests are available for Rhodesian Ridgebacks through the Orivet laboratory.  

A Locus (Fawn/Sable;Tri/Tan Points)
Black Hair Follicular Dysplasia
Brown Coat Colour Profile
D (Dilute) Locus
E Locus - (Cream/Red/Yellow)
K Locus (Dominant Black)
Coat Colour Dilution Alopecia
Degenerative Myelopathy

With the exception of Coat Colour Dilution Alopecia and Degenerative Myelopathy, Orivet state that each test listed above is:

"Scale 1 has a very low degree of severity.  It is a trait and so is tested based on preference, not usually for health concerns."

The two conditions in the above list which affect the health of the individual dog are:

Category: Dermatologic (Associated with Skin)

Severity: Scale 3 has a moderate degree of severity, as it is not a fatal disease, though it can decrease the quality of life.

Mode of Inheritance: Autosomal Recessive

Test Overview:
This condition is seen in dogs with a dilute coloured coat and occurs in up to 90% of blue Dobermanns, and 75% of fawns. This condition also occurs in other breeds where breeding for colour dilute individuals occurs, although it does not tend to be seen at such high rates as in the Dobermann, and prevalence rates can vary depending on the breed. Colour dilute Weimeraners do not seem to be affected at all. The reason for the amount of variation between colour dilute animals of different breeds is not known. The main breeds affected (other than the Dobermann) include the Boston terrier, the Chihuahua (blue), Great Dane (blue), Dachshund (blue), Miniature Schnauzer, Miniature Pinscher (blue), Shetland Sheepdog (blue), Whippet (blue), Standard Poodle (blue), Yorkshire Terrier (grey/blue), Irish Setter (fawn) and the Bernese Mountain Dog. Colour dilution alopecia is a type of follicular dysplasia, and only occurs when colour dilution is present. A blue coloured animal is the colour dilute form of the normal black and tan colouration, and fawn is the colour dilute form of the normal red colouration. It is thought that there is a defect in the regulation of melanisation (pigmentation) and the structure of the hair cortex, although the underlying genetic defect is not fully understood. Affected animals are born with normal hair coats, but usually signs will be seen between 6 months and 2 years of age, when the hair will begin to break, and patchy alopecia (hair loss) occurs. This usually starts on the back, and will progress to widespread hair loss wherever there is light coloured hair. The skin becomes dry and scaly, and is prone to infections. Hair that is lost will not grow back. Affected dogs are also susceptible to sunburn and cold. There is no cure for this condition. Diagnosis is confirmed with skin biopsy, which will show characteristic changes when assessed by an experienced veterinary dermatopathologist. Treatment is symptomatic, using antiseborrhoeic shampoos and oil rinses, moisturisers and antibiotic therapy or antiseptics for secondary infections.

Category: Neurologic (Associated with the Brain, Spinal and Nerves)

Severity: Scale 4 has a high degree of severity. It generally causes a decreased quality of life and may also decrease the life expectancy.

Mode of Inheritance: Autosomal Recessive with Incomplete Penetrance

Test Overview:
Degenerative myelopathy is most commonly seen in the German Shepherd Dog, although other breeds are also predisposed, including the boxer, Cardigan and Pembroke Welsh Corgi, Siberian husky and the Rhodesian ridgeback. This disease is normally seen around middle age, and in general diagnosis can only be confirmed at post mortem examination. Breed surveys of some predisposed breeds indicate a fairly low occurrence rate, but most experts think this rate is actually much higher, due to the lack of post mortem follow up of the majority of suspected cases. Signs are due to the immune-mediated destruction of a part of the nerves in the spinal cord, leading to loss of these nerve fibres. The first sign is knuckling of the hind feet, and hind limb ataxia. Once the spinal cord damage progresses past this initial stage (termed proprioceptive deficits), the effectiveness (if any) of treatment is much diminished. Hence early diagnosis is vital. Following this initial stage, hind limb reflexes are affected, then weakness in the hind limbs develops, progressing to total paralysis. Once a dog shows these signs it will almost always respond poorly to therapy. Eventually destruction progresses from the middle of the spinal cord to the upper cord and brain stem, leading to forelimb weakness and eventually interference with the muscles of breathing, causing death. Most dogs are euthanased for humane reasons before this happens. Treatment is with specific supplements and drugs aimed at interfering with the immune destruction in the spinal cord, to slow further nerve damage. The effectiveness of this treatment is variable, but is only of benefit if started as early as possible. Once nerves are lost, they will not be replaced. Degenerative myelopathy cannot be cured. A DNA test is available for predisposed pure breeds to carry out screening of breeding animals.

This test is not yet available in Australia and samples from individual dogs must be sent to the UC Davis research facility in California.

An inherited deafness has previously been clinically documented among purebred dogs of the Rhodesian Ridgeback breed. Affected dogs appear to show normal hearing early in post-natal development, but ultimately these dogs lose their hearing, with complete loss by 1 year of age. Anecdotal observations from breeders and owners suggest that hearing loss occurs as early as 4 months in some affected dogs, and that males exhibit an earlier onset deafness than affected females. Over many years, breeders and owners of affected dogs have submitted cheek, saliva, and blood samples to the Laboratory of Dr Mark Neff in support of a genetic study. Research in Dr Neff's lab at UC Davis established that this defect is indeed genetic, and that the mode of transmission from parent to offspring follows a simple Mendelian autosomal recessive pattern of inheritance. This means that any sire or dam that has previously produced affected progeny must be a carrier of the causal mutation.

The UC Davis research further showed that the defect maps to a single chromosomal region, and that all carriers and affected dogs have inherited exactly the same DNA sequence in this region. This means that the mutation that causes the deafness occurred once and only once, and that all affected dogs are descendants of a single common ancestor. It is not known how long ago this ancestor lived, and it is possible that the mutation occurred prior to the development of the breed in the late nineteenth century.

As research into this condition is ongoing, test results are divided into two classes:

The first class will be those that are high confidence outcomes -- highly likely to be affected, highly likely to be a carrier, or highly likely to be clear.
The second class will be results that will be uniquely informative to the research, but difficult to interpret for the breeder/owner. These outcomes will represent test results where some but not all the candidate mutations are found in a given dog. Researchers will follow up with the owners of these dogs to help explain the uncertainty of the outcome, and to have the dog tracked for health and breeding outcome. These rare exceptional dogs hold the key for pinpointing the truly causal mutation.

Once enough dogs like this have been studied, test results can be re-interpreted. It is hoped that all participants will ultimately be provided with a definitive result.

Finally, Dr Neff has indicated that the gene responsible for adult onset deafness in the Ridgeback is highly likely to be responsible for a similar deafness in humans. Specifically, human genetics literature suggests that this human deafness affects infants before they learn how to speak, thus sentencing these children to a lifetime of challenges in communicating. It is hoped that a successful conclusion of this research will enable Rhodesian Ridgeback breeders to improve the health of future generations of dogs, and beyond this, have important implications for improving human health as well.  Dr Neff and his team have expressed deep appreciation for the long term commitment and patience by the Ridgeback community, and for the continued support of this important research.

This test is not yet available in Australia and samples from individual dogs are sent to Laboklin Laboratory, Manchester UK.

JME is an inherited disease in the Rhodesian Ridgeback breed. Affected dogs start showing symptoms between the age of 6 weeks and 18 months. Symptoms include frequent myoclonic jerks or twitches especially when the dogs are sleeping or resting. Photo sensitivity has also been noticed in affected dogs. Most affected dogs will also develop more severe generalized and tonic clonic (grand mal) seizures.

Due to the recessive mode of inheritance, affected dogs must inherit two copies of the mutation, one from each parents.

The test will tell you if your dog has 0, 1 or 2 copies of the mutation. Clear (N/N) and carriers (N/ JME) are healthy dogs and will not develop the specific symptoms associated with the JME mutation, however carriers should only be bred to clear dogs to avoid having affected puppies.

Please note that there are other forms of epilepsy that cannot be eliminated by this test.

Inheritance: Autosomal recessive trait

There are several conditions that can affect Ridgebacks as well as other breeds:

CHF Canine Congestive Heart Failure
Valvular Disease
DCM Dilated Cardiomyopathy
Canine Heart Murmurs

The vast majority of heart disease cases in dogs are considered "acquired" heart disease. Typically, the result of normal wear and tear or they can also be caused by injury or infection. They are most often seen in middle-aged and older dogs. Some of the most common types of acquired heart disease are:

Chronic valvular disease: when the valves of the heart weaken with age and begin to leak.
Myocardial disease:  when the heart muscle weakens, causing it to enlarge.
Arrhythmias: when there is a problem with the body's electrical system, which tells the heart how to beat.
Pericardial disease: when the protective sac that surrounds the heart fills with fluid, preventing normal beating of the heart.
Heart murmurs: caused by a defect in the heart that disrupts blood flow, creating a "whooshing" sound that can be heard through a stethoscope

Dogs can be born with congenital defects and while these are not particularly common, it is certainly not unusual these days to hear of a Ridgeback with one of the above conditions.  Murmurs may be heard at 6 weeks of age when puppies are vaccinated and may not necessarily be anything to worry about.  The condition may clear up on its own by four to six months of age.  There is no guarantee of this, however, so puppies that present with murmurs at the time of vaccination, are cause for concern.

Other congenital defects often involve the improper development of a specific part of the heart, or a small hole in one of the chambers. There are many different types, but the results are the same: the heart cannot function properly. Such defects can limit a dog's lifespan and make him more susceptible to other problems. Very mild cases, however, may have little effect.

Because heart disease has so many causes, there is little that can be done to prevent it. Unfortunately, with the exception of the RR IVA test, there are no DNA tests which can determine the exact cause and identify carriers so the only way to be certain that a dog or bitch does not suffer any heart condition prior to breeding is to perform an ECG and this will only tell you that your dog is clear on the day of the ECG.  There is no guarantee the dog will not develop a heart condition at a later date.  

This is not yet available in Australia and samples from individual dogs must be sent to North Carolina State College of Veterinary Medicine, USA.  This is a very newly recognised condition and as at December 2017 less than 100 Ridgebacks have been tested.  The condition came to light following the sudden death of several young ridgebacks and the DNA test is in its infancy.

This is an inherited disease that results in an abnormality of the cardiac electrical system leading to the development of abnormal heart beats (ventricular premature beats (VPCs). In some cases these abnormal heart beats can result in sudden death.  It appears that the most severe disease may be present between 6 and 30 months of age and many dogs appear to outgrow the problem.

A genetic test can be performed to determine if your dog has the DNA mutation that will put him/her at risk for the disease.

At this time we recommend that dogs that have the DNA mutation have a Holter monitor performed occasionally between 6 and 30 months of age to determine if they are having abnormal heart beats that should be more closely monitored or may indicate a need for treatment.

Additionally, breeding decisions about dogs that have the mutation should be made carefully and with planning to help gradually reduce the prevalence of the mutation in the breed.

by E. Clough, V.M.D.
1010 Daniel Webster Highway
Merrimack, New Hampshire 03054

Dermoid sinus (D.S.) was first used to describe the Rhodesian Ridgeback skin anomaly by Steyn, et al. This skin condition has also been called trichiasis spiralis, dermoid cyst, dermoid inclusion cyst and epidermal inclusion cyst. All of these terms have some applications; however, Dermoid, skin-like sinus, channel or fistula; (cyst means sac, i.e., not open to the surface) is most applicable. The Rhodesian Ridgeback Club of the U.S., Inc. prefers to use D.S. to describe the condition.

No reports have been located which substantiate the author's impression that D.S. has been found in other breeds. Dermoid sinus included in the ridge has been reported only once. They also occur in the sacral (rump) area and in this location are sometimes connected to the dura (spinal cord covering). This is not the case in the more common cervical (neck area) D.S. which connects the skin to the dorsal spinous ligament (the ligament which connects the top parts of the vertebrae). One or more D.S. may occur in the same animal. These sinuses are congenital (present at birth) and can be palpated (felt) as cords running between the skin and the spine. They form a small external opening which can be readily seen once the hair has been shaved.

Histologically (microscopically) the sinus is a thick-walled tube composed chiefly of fibrous tissue and lined with stratified squamous epithelium (skin cells). The surrounding connective tissue may or may not contain hair follicles, sebaceous glands and sweat glands which open into the lumen (hollow center) of the sinus. In uncomplicated cases the sinus is filled with sebum (oil), skin debris and hair. Once infected with bacteria the resulting inflammation and abscessation can lead to myelitis and encephalitis (swelling and infection of the spinal cord, its covering, and the brain). The reason for discrimination against animals with D.S. is the almost inevitable abscess which forms.

Although not well understood, transmission of D.S. seems to be a dominant, polygenic problem with inconstant penetration. Another geneticist thinks that D.S. is due to a single completely recessive autosomal gene. This is not likely because normal parents do produce pups affected with D.S. Because of the genetic complexity and the difficulty in arranging, coordinating and collating the breeding studies necessary to prove the heredity of D.S., it is unlikely that we will be able to substantiate the exact mechanism of genetic transmission. There is a widely held belief that breeding Ridgebacks with D.S. produces an increased prevalence of pups with D.S. The R.R. Club of the U.S., Inc. believes that this could be substantiated if breeders had accurate records which could be collated and computed. It is our belief that careful controlled breeding studies would prove the inheritance of D.S. to be not only complex but also inter-related with other characteristics. Therefore, the likelihood seems to be remote that we will ever have Ridgebacks which are entirely free of D.S.

Because selective breeding will unquestionably reduce the prevalence of D.S., but probably not eliminate its occurrence, and because the condition results in difficult to treat abscesses unless surgically removed, it is our opinion and strong recommendation that dogs which have D.S. not be acceptable as show or breeding candidates. Surgical correction can be accomplished; however, culling at birth is a more humane way to handle the affected pups.

Elbow dysplasia is a disease with a high inherited component, which primarily affects intermediate and large breed dogs.   A high incidence of occurrence has been noted in some terrier breeds. Typically, both elbows are affected. However, unilateral elbow dysplasia is not uncommon.
The elbow joint is composed of three bones (radius, ulna, and humerus) which must all grow together and fit perfectly. The radius and ulna are paired bones with the radius being the main weight bearing bone. The normal elbow joint is characterized by a smooth transition from the ulnar articular surface to the radial surface.  In a dysplastic elbow the edge of the ulnar surface lies above the level of the adjoining radius, creating a step between the radius and ulna and causing incongruity of the joint. The height of the step may vary from barely noticeable to 4 mm or more. When this occurs the weight bearing force on the ulna is increased, resulting in excessive pressure on the medial coronoid process. This leads to fragmentation of the coronoid process. This usually occurs between 5 and 7 months of age. A superficial to deeply grooved "kissing lesion" is often present on the humeral articular surface opposite the fragment. A cartilage flap or OCD (osteochondritis dissecans) lesion may also develop. Secondary arthritis becomes evident at 6-7 months. Compensatory adjustments during growth may occur in some dogs, tending to minimize unequal growth rates between the three bones and moving the ulna distally to better conform to the radius. However, excessive force is then placed on the anconeal process at the top of the ulnar articular surface. This force will cause a failure of ossification, leading to an unnitedanconeal process. (UAP)

The routine monitoring for the presence of elbow dysplasia is carried out from a lateral x-ray of the flexed elbow joint taken when the dog is over 12 months of age.  Correct radiograph technique is critical for making the diagnosis. The grade is derived by measuring the amount of new bone that has developed as a result of arthritis.  Unlike the grading systems for hip dysplasia the system for elbow dysplasia is used internationally.             

It is generally considered that dogs with grade 3 elbow dysplasia should not be used for breeding and that dogs with grade 2 should be considered a serious risk.

Hip dysplasia is not a congenital defect ie  it is not present at birth. Multiple studies have demonstrated that all normal puppies are born with "perfect" hips.  That is, they are "normal" for a newborn with no signs of dysplasia. The structures of the hip joint are cartilage at birth and only become bone as the puppy grows.

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. This is one reason why decades of strong selection has resulted in only modest reductions in hip dysplasia in some breeds. At the current rate of progress and selecting only by phenotype, it could take decades to achieve a meaningful reduction in the incidence of hip dysplasia (Lewis et al 2013).

The top three environmental factors that have been found to play a significant role in the development of dysplastic hips are: a) joint laxity, b) weight, and c) exercise.

Dogs should be xrayed for hip and elbows any time after they reach 12 months of age in Australia.  In the USA, it is 2 years of age.  Xrays are sent to one of three experts in Australia who then score and grade each dog.  

Hip Score
Norberg Angle
Cranial acetabular edge
Dorsal acetabular edge
Cranial eff. acet. rim
Acetabular fossa
Caudal acetabular edge
Fem neck exostosis
Fem head recon touring
The 9 items listed on the scoring sheet are all details of the anatomy of the hip joint that can be seen on an x-ray film.  Of these features 8 are scored out of 6 with 0 being normal. One of these, the Caudal Acetabular Edge, is scored out of 5.  Therefore the worst possible score for each hip is 53 with the worst combined score being 106.  

There is not a direct relationship between scoring and grading which causes considerable confusion.  The grading is done on the worst hip only. Because of differences in the assessment methods it is possible, though uncommon, for a dog with a relatively low score to have a relatively high grade.   Generally speaking it is considered acceptable to breed from dogs with grades 0, 1, 2, and 3 and not from grades 4, 5, and 6.  It is probable that the grading system will stop being used sometime in the near future


After 40+ years of breeding Ridgebacks, we have never bred a blue puppy or one suffering from Alopecia so we have chosen not to test for this condition.

We started to xray for hips in 1982 and elbows soon after and continue to do so.

All our dogs are now tested for DM, EOAD and JME. To date all our dogs are clear of these conditions.  

Because the RR IVA test is so new and because we have never had a puppy or adult die a sudden death, we have decided not to use this test until more research has been done and the results are more conclusive.    

Because of the lack of DNA test for various heart conditions and because most of our dogs live to between 10 and 15 years so obviously do not suffer from any heart conditions, we are also holding off on ECGs for the time being.

Should we have a puppy born with dermoid sinus, we have it surgically removed at about 6 weeks of age and to date every operation has been successful and the puppy goes on to live a normal, healthy life.


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