Health of Jack Russell Terriers

The Jack Russell Terrier is by nature a robust and healthy breed. However, there are a couple of hereditary health issues which you need to be aware of if you are considering buying a new puppy.

Late Onset Ataxia (LTA)
Late onset ataxia (LOA) in the Parson Russell terrier (PRT) and Jack Russell terrier (JRT) is a disease of incoordination of gait and lack of balance. The onset age for the disease is usually between 6 months and 1 year of age, when owners may start to notice that their dog is showing changes in gait pattern (often weaving of the hind limbs) and some difficulty balancing. The disease is progressive and affected dogs become increasingly uncoordinated with difficulty balancing, which makes moving around and everyday tasks such as going up and down stairs difficult. There is no treatment or cure for LOA and affected dogs are often euthanized, typically around two years after onset, on humane grounds as their quality of life diminishes.

DNA testing
CLEAR: These dogs have two normal copies of DNA and are likely to be clear of LOA. The results of our research suggest that there may be other causes of ataxia in the breed so we cannot exclude the formal possibility that clear dogs could develop a genetically different form of ataxia due to other mutations that are not detected by this test.
CARRIER: These dogs have one copy of the LOA associated mutation and one normal copy of DNA. These dogs will not develop LOA themselves as a result of the LOA mutation, but they will pass the mutation on to approximately 50% of their offspring. The results of our research suggest that there may be other causes of ataxia in the breed so we cannot exclude the formal possibility that carriers could develop a genetically different form of ataxia due to other mutations that are not detected by this test.
AFFECTED: These dogs have two copies of the LOA associated mutation and have a very high chance of developing LOA.

Primary Lens Luxation (PLL)
Primary Lens Luxation (PLL) is a well-recognised, painful and blinding inherited eye condition that affects many breeds of dog, particularly terrier and terrier-type breeds including (but not restricted to) Miniature bull terriers, Tibetan terriers, Jack and Parson Russell terriers, Lancashire Heelers and Chinese Crested dogs, also the Australian Cattle Dog, Sealyham Terrier, Welsh Terrier, Wire Fox Terrier and Yorkshire Terrier.
In affected dogs the zonular fibres which support the lens breakdown or disintegrate, causing the lens to fall into the wrong position within the eye. If the lens falls into the anterior chamber of the eye glaucoma and loss of vision can quickly result.

DNA testing
CLEAR: these dogs have two normal copies of DNA. Research has demonstrated clear dogs will not develop PLL as a result of the mutation, although we cannot exclude the possibility, they might develop PLL due to other causes, such as trauma or the effects of other, unidentified mutations.
CARRIER: these dogs have one copy of the mutation and one normal copy of DNA. Research has demonstrated that carriers from some breeds have a very low risk of developing PLL. The majority of carriers do not develop PLL during their lives, but a small percentage do.
We do not currently know why some carriers develop the condition whereas the majority do not, and we advise that all carriers have their eyes examined by a veterinary ophthalmologist every 6- 12 months, from the age of 2, throughout their entire lives.
GENETICALLY AFFECTED: these dogs have two copies of the mutation and will almost certainly develop PLL during their lifetime. All genetically affected dogs have their eyes examined by a veterinary ophthalmologist every 6 months, from the age of 18 months, so the clinical signs of PLL are detected as early as possible.

Spinocerebellar Ataxia (SCA)
The mutation for Spinocerebellar Ataxia with or without Myokymia and Seizures (SCA) was identified by the University of Missouri and a DNA test is available. Affected dogs show signs of cerebellar ataxia as early as 2-6 months of age. At post-mortem examinations, degeneration can be found in the areas of the spinal cord that carry information to the cerebellum, hence the term spino-cerebellar ataxia. The coordination difficulties progress, but in addition other signs can develop. Most cases also develop myokymia, an involuntary twitching of the muscles. The myokymia also becomes progressively worse with age and can result in episodes of generalized muscle spasms and over-heating. In addition, a small percentage of dogs with SCA have true epileptic seizures, some as young as 10 weeks of age. Most dogs with SCA are also euthanized young due to poor quality of life.


DNA testing
CLEAR: these dogs have no copies of the mutant gene responsible for the condition and will neither develop the condition nor pass the gene on to their offspring.
CARRIER: these dogs have one copy of the normal gene and one copy of the mutant gene; they will not develop the condition, but will pass a mutant gene on to approximately half of their offspring.
AFFECTED: these dogs have two copies of the mutant gene that causes the condition and will develop the disease.