Test #1 - MDR1 A mutation in canine MDR1 gene (multidrug resistance gene) leads to a hypersensitivity to multiple drugs including Ivermectin (antiparasitic drug). Ivermectin hypersensitivity based on MDR1 gene mutation was proved in several breeds including the Australian Shepherd.  Introduction of antiparasitic drug Ivermectin in 1980 revealed new inherited disease in several dog breeds.  Ivermectin potentiates chloride ion channels in peripheral nervous system, causing lethal paralysis of some invertebrates parasites. If administered to defective animals, administering of ivermectin or similar drug can lead to elevated levels of drug in the CNS, resulting in potentially lethal neurotoxic reaction.  These drugs include, but are not limited to:  Acepromazine, Butorphanol, Doramectin, Doxorubicin, Ivermectin, Lopramide, Milbemycin, Moxidectin, Selamectin, Vinblastine, Vincristine. MDR1 related drug hypersensitivity is inherited as an autosomal recessive trait.  That means the disease affects dogs with P/P genotype only.  The dogs with P/N genotype are considered carriers of the disease (heterozygotes).  In offspring of two heterozygous animals following genotype distribution can be expected: 25% N/N (healthy no-carriers), 25% P/P (affected), and 50% N/P (healthy carriers).  Because of high risk of producing affected offspring, mating of two N/P animals (carriers) can not be recommended. Test # 2 - PRCD/PRA PRA -PRCD disease information:  Late form of Progressive Retinal Atrophy, called PRA-prcd (progressive rod-code degeneration), is just one of all retinal defects. Rods degenerate at first. Affected dogs become night-blind.  This is very often the first symptom that dog owners recognize.  Dogs usually have poor sense of directions and they crash into things.  Pupil is widely open even when direct ray of light hits the eye (dogs have shining eyes in pictures).  Later, cones start degenerating.  Final disease symptoms are cataracts and total blindness.  PRA-prcd is a hereditary disease.  Causal mutation G1298A in ninth canine chromosome (CFA9) PRA-prcd was recognized.  This mutation is inherited as an autosomal recessive trait.  That means that disease affects dogs with P/P genotype only.  The dogs with P/N genotype are considered carriers of the disease (heterozygotes).  In offspring of two heterozygous animals following genotype distribution can be expected:  25% N/N (healthy non-carriers), 25% P/P (affected), and 50% N/P (healthy carriers).  Because of high risk of producing affected offspring, mating of two N/P animals (carriers) can not be recommended.  Test # 3 - HC Hereditary cataract (HC) Cataract is an eye disorder affecting the lens transparency.  Cataracts are very often inherited and occur in more than 70 dog breeds.  In connection with the hereditary forms of cataracts in dogs, there have been described several modes of inheritance, the majority being autosomal recessive.  There are also autosomal dominant or polygenic modes of inheritance.  Cataracts are the leading cause of blindness in dogs.  The hereditary cataracts are often called primary cataracts.  Secondary cataracts are forms of a cataract that accompanies other eye disorders, for example, progressive retinal atrophy, glaucoma, retinal dysplasia, metabolic diseases and other disorders.  The cataracts may develop after an eye injury (traumatic cataracts) or are related to aging (senile cataracts). The cataracts are very specific in individual breeds with regard to the affected parts of the lens, age of disease onset, progression rate and the rate of bilateral development of the cataract.  The presence of deletion is significantly associated with the development of binocular cataracts at various ages.  The HC disorder in Australian Shepherds has an autosomal dominant mode of inheritance, however with incomplete penetrance.  It means that the disease may not develop in every carrier of this deletion and effects of other genetic factors or environmental factors are not excluded. The probability that the binocular HC develops in individuals with one copy of deletion (carriers) is approximately 17 times higher than in dogs clear of the deletion mutation.  The carriers of the mutation pass it on to their offspring and therefore, it is necessary to avoid mating two heterozygous dogs as 25% of puppies born will be homozygous.  Test # 4-CEA   Collie Eye Anomoly Collie Eye Anomaly (CEA), also known as choroidal hypoplasia (CH), is an inherited disease affecting several dog breeds. The choroid is the layer of tissue in the eye responsible for supplying blood and nutrients to the Retina. In dogs affected with CEA, the choroid does not develop properly and is therefore thinner than normal. The severity of the condition can vary from dog to dog. In mild cases, affected dogs may only show signs of collie eye anomaly on eye exam between about 5 and 12 weeks of age, just prior to normal, age-related pigmentation of the retina which often masks the characteristic, disease-related changes. After this time period, mildly affected dogs may be impossible to distinguish from normal dogs on eye exam (a phenomenon often referred to as “going normal”) and may not display obvious vision deficits. In more severely affected dogs, clinical signs include malformations of the eye and/or optic nerve (colobomas), retinal detachment, intraocular bleeding, and subsequent blindness. Both mild and severe forms of CEA are associated with the same NHEJ1 gene Mutation. Therefore, predicting the potential severity of the disease in an affected puppy is difficult as mildly affected parents may produce offspring that are severely affected. Test # 5- CD   Cone Degeneration Cone Degeneration is an inherited eye disease affecting dogs. Affected dogs develop day blindness (blindness in bright light) and Photophobia (light sensitivity) between 8 to 12 weeks after birth due to degeneration of cells in the eye called cone photoreceptors which are responsible for vision in bright light. Affected dogs have normal vision in low light and structures of the inner eye appear normal on eye exam. Normal cone cell function can be seen on Electroretinogram (ERG) before six weeks of age, but becomes abnormal between 6 to 12 weeks of age and is completely absent in affected adult dogs signifying complete loss of Cone Cells. The cells responsible for vision in low light called Rod photoreceptors are not affected and thus, affected dogs will still be able to see normally in low light throughout life Test # 6- DM   Degenerative Myelopathy is an inherited neurologic disorder caused by a Mutation of the SOD1 gene in dogs. This mutation is found in many breeds of dog, though it is not clear for some breeds whether all dogs carrying two copies of the mutation will develop the disease. The variable presentation between breeds suggests that there are environmental or other genetic factors responsible for modifying disease expression. The average age of onset for dogs with degenerative myelopathy is approximately nine years of age. Affected dogs usually present in adulthood with gradual muscle Atrophy and loss of coordination typically beginning in the hind limbs due to degeneration of the nerves. The condition is not typically painful for the dog, but will progress until the dog is no longer able to walk. The gait of dogs affected with degenerative myelopathy can be difficult to distinguish from the gait of dogs with hip dysplasia, arthritis of other joints of the hind limbs, or intervertebral disc disease. Late in the progression of disease, dogs may lose fecal and urinary continence and the forelimbs may be affected. Affected dogs may fully lose the ability to walk 6 months to 2 years after the onset of symptoms. Affected small breed dogs often progress more slowly than affected large breed dogs and owners may postpone euthanasia until the dog is paraplegic. Test # 7- Hyperuricosuria is an inherited condition of the urinary system affecting many breeds of dog, including Australian Shepherds. The SLC2A9 gene codes for a protein that allows the kidneys to transport uric acid from the urine. Dogs with mutations in both copies of the SLC2A9 gene are predisposed to have elevated levels of uric acid in the urine, hence the name hyperuricosuria. Uric acid can form crystals and/or stones (uroliths) in the urinary tract. Dogs with hyperuricosuria most commonly present with symptoms of recurrent urinary tract inflammation, which include frequent urination, blood in the urine, and straining to urinate. They may also have loss of appetite, lethargy, weakness, vomiting and pain. Urinary stones in the bladder can cause urinary tract infections or more seriously, blockage of the Urethra. Both male and female dogs can be affected, but obstruction of urine flow is more common in males due to differences in anatomy. Although an x-ray can be used to exclude other types of stones, urate stones cannot typically be seen using x-rays and must be evaluated by ultrasound. Not all dogs with mutations in both copies of the SLC2A9 gene will have symptoms of disease, though they have increased uric acid excretion in the urine. Test # 8- Multifocal Retinopathy 1 is an inherited disorder of the Retina affecting multiple breeds of dog. Affected dogs typically present between 11 and 16 weeks of age with multiple discrete circular areas of retinal detachment with underlying fluid accumulation that are visible on an eye exam performed by a veterinarian. These blister-like lesions are typically found in both eyes and can appear gray, tan, orange, or pink and vary in number, size and location. Progression of retinal changes is usually slow and new lesions are not noted after 6 to 12 months of age. Occasionally as affected dogs age, lesions appear to heal and are no longer visible on an eye exam. Generally the dog’s vision is not affected although vision loss has been described in some cases of multifocal retinopathy 1 Test # 9- Neuronal Ceroid Lipofuscinosis 6 (NCL6) is a lysosomal storage disease affecting dogs. Affected dogs lack a specific Enzyme necessary for normal metabolism. As a result, there is an abnormal accumulation of waste compounds primarily in the cells of the nervous system, leading to a range of nervous system disorders. Affected dogs typically present around 1.5 years of age with progressive neurologic disease. Symptoms include loss of vision, behavioral change, anxiety, lack of muscle coordination and abnormal gait. Affected dogs are often humanely euthanized by 2 years of age due to progression of the disease.  
All of our breeding dogs have been tested for the following genetic diseases below & we guarantee you that any puppy/adult that you purchase from us will not be affected by any of the following:
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Julie Fullerton 12015 Rd 75 Bayard, Nebraska  69334 308-586-3008 email:  fullertontoyaussies@gmail.com