Health Testing

FritzFox is dedicated to the health and integrity of the breed! We don't take any risks with the health of our puppies. All of our breeding adults are clear/normal and have been DNA tested. We have raised puppies that are now producing and they are clear by parentage. We test again after one generation of clear by parentage. All results can be found on the PawPrints Genetics website and are made public for you to see. When looking for your next TFT, ask if testing for PLL , DM, CHG, SCA, and Patellas on the parents is done and expect to see certificates on that information prior to purchasing your puppy.

Primary Lens Luxation (PLL)

Primary Lens Luxation (PLL) is a well-recognized, 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, Jagd Terrier, Patterdale Terrier, Rat Terrier, Sealyham Terrier, Tenterfield Terrier, Toy Fox Terrier, Volpino Italiano, Welsh Terrier, Wire-haired 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.

Our scientists have identified a mutation that is associated with the development of PLL in several breeds of dog. The DNA test we are now offering examines the DNA from each dog being tested for the presence or absence of this precise mutation. It is thus a ‘mutation-based test’ and not a ‘linkage-based test’.

Breeders will be sent results identifying their dog as belonging to one of three categories:

CLEAR: these dogs have two normal copies of DNA. Our research has demonstrated clear dogs will not develop PLL as a result of the mutation we are testing for, 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. Our research has demonstrated that carriers 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 currently estimate that between 2% – 20% of carriers will develop the condition, although we believe the true percentage is nearer to 2% than 20%. 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 two, throughout their entire lives.

GENETICALLY AFFECTED: these dogs have two copies of the mutation and will almost certainly develop PLL during their lifetime. We advise that 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.

Breeding Advice

Our research has also demonstrated that the frequency of the PLL mutation is extremely high in the PLL-affected breeds that we have studied in depth. This means that allowing only CLEAR dogs to breed could have a devastating effect on breed diversity and substantially increase the likelihood of new inherited diseases emerging. Therefore, we strongly advise breeders to consider all their dogs for breeding, regardless of their PLL geneotype. GENETICALLY AFFECTED and CARRIER dogs can be bred with, but should only be bred to DNA tested, CLEAR dogs. All puppies from any litter that has at least one CARRIER parent should be DNA tested, so that the CARRIERS can be identified and followed clinically throughout their lives. This practice should be followed for at least one or two generations, to allow the PLL mutation to be slowly eliminated from the population without severely reducing the genetic diversity of breeds at risk.

Canine Spinocerebellar Ataxia (SCA)

Canine spinocerebellar ataxia (SCA) is an inherited disorder occuring in Jack Russell Terrier, Smooth-haired Fox Terrier and Toy Fox Terrier. First time form of hereditary ataxia was reported in Smooth-Haired Fox Terrier in 1957, which was followed by report of a disease with similar symptoms in the Jack Russell Terrier in the 1973. Another form of ataxia is cerebellar ataxia. Cerebellar ataxia, however, is a different disorder than spinocerebellar ataxia and a Jack Russell Terrier can be affected with one of the forms of ataxia, not both. Different forms of ataxia differ from each other in ages at onset, clinical signs, and histopathologic changes.

Jack Russell Terriers, Parson Russell Terrier and Russell Terriers are recognized as separate breeds and it is believed they have common descend, originating from the stock of Parson Jack Russell, a 19th century dog breeder from Great Britain.

Characteristics and Symptoms

Age of onset of canine spinocerebellar ataxia is between 2 months to 9 months of age. At beginning, the dog’s owner may notice lack of coordination, pelvic limb swazing when walking, and difficulties in climbing up-stairs or jumping. SCA is a progressive disorder, and with its progress, ”prancing” type of gaint is noticed, especially in the pelvic limbs. Affected dogs may have difficulties while standing, and may fall frequently, with troubles in attempts of returning to standing position. Neurological examinations have revealed symmetric spinocerebellar ataxia, characterized by hypertermia and spasticity, especially in the pelvic limbs. Postural reactins appear to be delayed and hypertermic, while spinal reflexes are normal to increased. Brain stem auditory-wvoked potentials (BAEPs) identified abnormalities in some but not all SCA affected dogs. These abnormalities include lack of waves III, IV and V.

Post-mortem histopathological examination showed bilateral symmetrical myelopathy, myelin loss, swelling of axons, moderate diffuse gliosis and marked loss of myelinated nerve fibers.

All of the SCA affected Jack Russell Terriers exhibit myokymia. Myokymia is a involuntary tremor of muscles, where muscles become hyperactive and heat is created. The excessive heat causes hyperthermia and can result in a seizure. In SCA affected dogs it usually appears between 2 moths to 3 years of age. Common symptoms of myokymia are stifness of hind limbs and fore limbs, curled paws, facial rubbing and extremly high core body temperature. Myokymia is exhibitedby human patients with voltage-gated potassium channel genes.

Since SCA is an inherited disorder with a progressive nature, with no cure developed, most of SCA affected dogs are euthanized by 2 years of age due to poor quality of life.

Degenerative Myelopathy (DM)

Degenerative Myelopathy is a debilitating disease that causes gradual paralysis in many dog breeds. It is caused by a degeneration of the spinal cord that onsets typically between 8 and 14 years of age. It presents first with the loss of coordination of the hind legs. It will typically worsen over six months to a year, resulting in paralysis of the hind legs. If signs progress for a longer period of time, loss of urinary and fecal continence may occur and eventually, weakness will develop in the front limbs. An important feature of Degenerative Myelopathy is that it is not a painful disease

Congenital hypothyroidism with goiter (CHG) 

Congenital hypothyroidism with goiter was observed to segregate as a simple autosomal recessive trait in Toy Fox Terriers (TFTs). Neonatal affected pups exhibited inactivity, abnormal hair coat, stenotic ear canals, and delayed eye opening. Palpable ventrolateral cervical swellings were evident by 1 week of age. Serum thyroid hormone and thyroid-stimulating hormone concentrations were low and high, respectively. Histologic examination of the cervical masses disclosed cuboidal to columnar follicular epithelial cell hyperplasia with widely varying follicular size, shape, and amount of colloid. Oral thyroid hormone replacement therapy restored near-normal growth and development. At 8 weeks of age, radioiodine uptake and perchlorate discharge testing indicated an iodine organification defect. Biochemical analysis of thyroid tissue from affected dogs demonstrated enzymatic iodine oxidation deficiency and lack of sodium dodecyl sulfate-resistant thyroglobulin dimers, suggesting thyroid peroxidase deficiency. A nonsense mutation in the thyroid peroxidase gene of affected dogs was discovered and demonstrated to segregate with the disease. A DNA-based carrier test was developed and currently is used by TFT breeders to prevent this disorder.

What is Patellar Luxation?

The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position.

Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are eight weeks of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb.

Patellar luxations fall into several categories:

 Medial luxation (toy, miniature, and large breeds)

Lateral luxation (toy and miniature breeds)

Lateral luxation (large and giant breeds)

Luxation resulting from trauma (various breeds, of no importance to the certification process)

Numbers 1-3 are either known to be heritable or strongly suspected.

 Medial Luxation in Toy, Miniature, and Large Breeds

Although the luxation may not be present at birth, the anatomical deformities that cause these luxations are present at that time and are responsible for subsequent recurrent patellar luxation. Patellar luxation should be considered an inherited disease.

Clinical Signs

Three classes of patients are identifiable:

 Neonates and older puppies often show clinical signs of abnormal hind-leg carriage and function from the time they start walking; these present grades 3 and 4 generally.

Young to mature animals with grade 2 to 3 luxations usually have exhibited abnormal or intermittently abnormal gaits all their lives but are presented when the problem symptomatically worsens.

Older animals with grade 1 and 2 luxations may exhibit sudden signs of lameness because of further breakdown of soft tissues as result of minor trauma or because of worsening of degenerative joint disease pain.

Signs vary dramatically with the degree of luxation. In grades 1 and 2, lameness is evident only when the patella is in the luxated position. The leg is carried with the stifle joint flexed but may be touched to the ground every third or fourth step at fast gaits. Grade 3 and 4 animals exhibit a crouching, bowlegged stance (genu varum) with the feet turned inward and with most of the weight transferred to the front legs.