Whaten terrier is a mostly healthy dog. However, in order to preserve the health of a dog, we need to be fully aware of all the risks that can arise in breeding. The breed’s popularity will always result in a large number of legumes and reduced health control. Fortunately, what a terrier is not a popular dog for now.
If you want to have a wheaten terrier, always ask the breeder for health tests or make them yourself.
The first thing to look at in what is a terrier is a skeleton: hips, elbows and patel. Then, test the clinical eye test.
Genetic tests ISCWT are divided into divisions of the group:
Hereditary diseases: Nephropathy with the loss of proteins, protein-losing enteropathy, as with (PLE) and Renal Dysplasia (RD); Paroxysmal dyskinesia in Soft Coated Wheaten Terrier (PxD); Microphthalmia Soft Coated Wheaten Terrier (RBP4); Hyperuricosuria (HUU); Degenerative myelopathy; Malignant hyperthermia (MH).
Inherited traits dogs – Coat colours and quality: A LOCUS (BLACK & TAN); B LOCUS (BROWN NOSE); E LOCUS (BLONDE GENE); K LOCUS Ky/Ky (HOMOZIGOEUS WHEAT); Cu Locus (Curly Coat)
Nephropathy with the loss of proteins (PLN) – Hereditary diseases most typical for the wheat Terriers (Nephropathy with the loss of proteins, protein-losing enteropathy, as with (PLE) and Renal Dysplasia (RD))
Nephropathy with loss of protein in ISCWT (PLN) – is a form of broader set of diseases known as nephropathy with the loss of protein, dDisorders of glomerular state characterized by loss of protein in the urine. The group of diseases including glomerulonephritis (inflammation of the glomeruli of kidney), inherited glomerulopathy (non-inflammatory disease of the glomerulus), and amyloidosis (expressed by protein deposits in the kidneys). The disorder usually affects larger breeds of dogs, such as ISCWT, Bernese mountain dog, Labrador retriever and golden retriever, but diseases in these breeds differ in the causal mutation. It was observed that females are at greater risk of developing symptoms than males.
Genetics – Nephropathy with loss of protein in the wheat softcoated terrier (PLN) is caused by mutations in NPHS1 and KIRREL2 genes which encode for proteins nefrin and Neph3. The mode of inheritance of this disease is complex, some sick dogs show autosomal recessive inheritance, while some dogs, mongrels with one parent who is ill Soft Coated Wheaten Terrier showed dominant inheritance. The greatest risk of contracting the disease are homozygous dogs, with a 95% chance of developing symptoms of the disease. Studies have shown that 10 to 15% ISCWT are sick.
Protein-losing enteropathy with PLE -is a condition in which a protein is excessively lost in the intestine and may pose a number of abnormalities, resulting in the loss of plasma protein from the gastrointestinal tract. The loss of healthy mucous membranes leads to leaking vital fluids rich in protein. Mechanisms of gastrointestinal protein loss include obstruction of the lymph, mucosal disease with erosions or ulcerations .. PLE is probably associated with the immune defenses of the intestinal tract, and liver and other cleaning systems cannot compensate for the loss. This can be a late disease, which means that the dog develops in adulthood.
Renal Dysplasia is a developmental defect or a genetic kidney. Dogs who are affected by renal dysplasia have kidneys that are not properly developed when the fetus was growing in the womb and so are born with the problem. Unhealthy or unformed nephrons in the kidneys are replaced by fibrous tissue and microscopic cystic lesions in the kidney and reducing immature glomeruli and glomerular cysts. At the end, the kidney cannot do its job of cleaning the blood. Dogs with renal displasia often need to drink and drink. They cannot concentrate their urine, making it a very dilute and pale blue. There are different levels of arrested development in affected puppies. Therefore, some pups show symptoms of kidney disease, or shortly after birth, while other symptoms occur later in life. The disease is genetic and is considered to be the mode of inheritance caused by a recessive mutation. This means that both parents must carry the gene to a puppy might be affected (Refers to a recessive gene inheritance).
Paroxysmal dyskinesia (PxD) is an inherited disorder which affects the Soft Coated Wheaten Terrier breed. The disorder is characterized by episodic involuntary movements in the form of focal motor seizures. Other names of paroxysmal dyskinesia are atypical epilepsy or episodic dyskinesia. Paroxysmal dyskinesia has been diagnosed also in human patients, where unlike the canine form of the disorder, PxD is inherited autosomal dominant.
Paroxysmal dyskinesia in Soft Coated Wheaten Terrier (PxD) is caused by a mutation in PIGN gene. The disorder is inherited in an autosomal recessive pattern. A dog can be clear, carrier or affected. Carriers of the gene are heterozygous and do not develop the disease’s symptoms. When mating two carrier dogs, each future cub has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier.
Kolicheski, A. L., Johnson, G. S., Mhlanga-Mutangadura, T., Taylor, J. F., Schnabel, R. D., Kinoshita, T., … O’Brien, D. P. (2017). A homozygous PIGNmissense mutation in Soft-Coated Wheaten Terriers with a canine paroxysmal dyskinesia. Neurogenetics, 18(1), 39–47. http://doi.org/10.1007/s10048-016-0502-4
Microphthalmia (RBP4) Soft Coated Wheaten Terrier type is an inherited disorder of the eyes whose causative mutation has been identified in this dog breed. In humans, microphtalmia is part od spectrum of congenital eye diseases which are a known cause of childhood blindness. The disorder has been recognized in many dog breeds, however, until now the causative mutation has been confirmed only in Soft Coated Wheaten Terrier dog.
Microphthalmia Soft Coated Wheaten Terrier (RBP4) is caused by the deletion mutation within the retinol-binding protein gene (RBP4). Role of the RBP4 is to carry vitamin A (retinol) from hepatic stores to peripheral tissues, including eye, where is participates in the synthesis of retinoic acid. Deficiency of vitamin A during the pregnancy is well-recognized risk factor for ocular birth defects. Mentioned deletion mutation causes decreased vitamin A secretion from hepatocytes to serum.
The disorder is inherited ina n autosomal recessive pattern with penetrance dependent on maternal genotype. For the disorder to appear in puppies, puppies and mother must be homozygous for the mutation (affected). The dependence on maternal genotype arises from the obstructed transfer of retinol across the placenta.
Kaukonen, M., Woods, S., Ahonen, S., Lemberg, S., Hellman, M., Hytönen, M. K., … Lohi, H. (2018). Maternal Inheritance of a Recessive RBP4 Defect in Canine Congenital Eye Disease. Cell Reports, 23(9), 2643–2652. doi:10.1016/j.celrep.2018.04.118
Crook A et al. 2011. Canine Inherited Disorders Database (CIDD).
Hyperuricosuria (HUU) Dogs with this genetic mutation metabolize waste products as uric acid in their urine. The uric acid forms into hard stones in the bladder, causing pain and inflammation as the stone moves through the urinary tract.
A dog that has difficulty urinating or appears to have an inflamed bladder may have HUU. Other signs can include blood in the urine and frequent urination. If the dog is unable to pass the urate stones without medical intervention, surgery may be required to remove them. And if the urinary tract is blocked, the condition can be life-threatening. Even in the best-case scenario, HUU is uncomfortable and painful for the dog.
The mutation is autosomal recessive. Both parents will need to be carriers of the mutation to pass it on to their offspring. Carriers will not show any symptoms of HUU and even affected dogs may not show any signs, so it is important to test dogs for HUU prior to breeding
Animal Genetics offers DNA testing for Hyperuricosuria. The genetic test verifies the presence of the Hyperuricosuria mutation and presents results as one of the following:
|The dog carries two copies of the mutant gene and is homozygous for Hyperuricosuria. The dog is likely to be affected by Hyperuricosuria and will always pass a copy of the mutation to its offspring.
|Both the normal and mutant copies of the gene detected. Dog is a carrier for the Hyperuricosuria mutation and can pass on a copy of the defective gene to its offspring.
|Dog tested negative for the Hyperuricosuria mutation and will not pass on the defective gene to its offspring.
Bannasch D, N Safra, A Young, N Karmi, RS Schaible and GV Ling. 2008. Mutations in the SLC2A9 Gene Cause Hyperuricosuria and Hyperuricemia in the Dog. PLoS Genetics 4(11): e1000246. [PubMed 18989453]
Karmi N, EA Brown, SS Hughes, B McLaughlin, CS Mellersh, V Biourge, and DL Bannasch. 2010. Estimated Frequency of the Canine Hyperuricosuria Mutation in Different Dog Breeds. J Vet Intern Med 24(6):1337–1342. [PubMed 21054540]
Karmi N, Safra N, Young A, Bannasch DL. 2010. Validation of a urine test and characterization of the putative genetic mutation for hyperuricosuria in Bulldogs and Black Russian Terriers. Am J Vet Res 71(8):909-914. [PubMed 20673090]
Degenerative myelopathy (DM) – Degenerative myelopathy is a progressive neurodegenerative disease of spinal cord injury whose symptoms manifest late, usually not until the age of 8. The first symptoms include a general asymmetric proprioceptive ataxia and spastic paralysis of the hind limbs. At this stage, the presence of spinal reflex is indicative of a loss of function (paralysis) of the upper motor neurons. Dogs after the appearance of symptoms can live for up to 3 years, or progression of the disease is relentless and dog owners often opt to euthanize dogs after becoming paraplegic. In cases where euthanasia is postponed, the weakness may extend to the front limbs and affect the lower motor neurons with signs of mild tetraplegia, expanding areas of muscle atrophy, difficulty in feeding and inability to bark.
Degenerative myelopathy may occur in any breed, but some breeds are more prone to developing the disease which is associated with a mutation. Breeds that are particularly susceptible to developing this disease are Pembroke Welsh Corgi, Boxer, Rhodesian Ridgeback, Chesapeake Bay Retriever. The frequency of these breeds of dogs suffering associated with mutation of genes varies from 30 to as high as 90%, mainly depending on the geographical location. Mutation of the gene responsible for the development of degenerative myelopathy is possible to identify DNA testing, which is very important for the early detection and prevention of disease as well as to eliminate the mutation of a specific breed of controlled mating.
Awano, T., Johnson, G.S., Wade, C.M., Katz, M.L., Johnson, G.C., Taylor, J.F., Perloski, M., Biagi, T., Baranowska, I., Long, S., et al. (2009). Genome-wide association analysis reveals a SOD1 mutation in canine degenerative myelopathy that resembles amyotrophic lateral sclerosis. PNAS 106, 2794–2799.
Holder, A.L., Price, J.A., Adams, J.P., Volk, H.A., and Catchpole, B. (2014). A retrospective study of the prevalence of the canine degenerative myelopathy associated superoxide dismutase 1 mutation (SOD1:c.118G > A) in a referral population of German Shepherd dogs from the UK. Canine Genetics and Epidemiology 1, 10
Malignant hyperthermia (MH) – is a hereditary disorder characterized by skeletal muscle hypercarbia, rabdomieloza, the general contraction of skeletal muscle, cardiac arrhythmias, and renal disorder caused by the aggressive exposure to anesthetics and depolarizing muscle relaxants. Dogs in patients, these drugs also cause tachycardia, hyperthermia, increased production of carbon dioxide and death in the case when anesthesia is not terminated. The disease is inherited autosomal dominant.
Roberts, M.C., Mickelson, J.R., Patterson, E.E., Nelson, T.E., Armstrong, P.J., Brunson, D.B., and Hogan, K. (2001). Autosomal Dominant Canine Malignant Hyperthermia Is Caused by a Mutation in the Gene Encoding the Skeletal Muscle Calcium Release Channel (RYR1 ). Anesthesiology 95, 716–725 – 716–725.
Inherited traits dogs – Coat colours and quality
A LOCUS (BLACK & TAN)
Agouti signal peptide (ASIP) or A locus is responsible for many different colour patterns in dogs. Specific A locus allele products can interact with functional MC1R and thus interfere with production of black melanin. Dogs have four different ASIP gene alleles with following dominance hierarchy: Ay > aw > at > a, meaning that the most dominant allele present will be expressed.
Ay/Ay: the dog carries two copies of the dominant Ay allele for fawn/sable; the offspring will always inherit one Ay allele.
Kerns, J.A., Newton, J., Berryere, T.G., Rubin, E.M., Cheng, J.-F., Schmutz, S.M., and Barsh, G.S. (2004). Characterization of the dog Agouti gene and a nonagoutimutation in German Shepherd Dogs. Mamm Genome 15, 798–808.
B LOCUS (BROWN NOSE)
Gene TYRP1 (Tyrosinase related protein 1) is responsible for chocolate/liver brown colour in dogs. This coat colour is inherited recessively. There are 4 different alleles on B locus: normal B allele (dominant), and three recessive alleles bc, bs and bd. Combination of any two recessive alleles will result in chocolate/liver brown colour (for example two bc alleles or one bc and one bs allele).
Because TYRP1 gene is related to eumelanin production, it only affects dogs which have genotype E/E or E/e on E locus. B locus also affects colour of the nose, eyes and pads. Dogs with genotype e/e produce only pheomelanin in coat but production of eumelanin in the nose, eyes and pads is not affected and therefore totally controlled by B locus. Depending on genotypes of E and B loci dog can have yellow coat and brown nose/eyes (e/e, b/b) or chocolate coat and brown nose/eyes (E/e or E/E and b/b).
E LOCUS (BLONDE GENE)
D locus is responsible for coat colour dilution. Mutation of the MLPH gene (melanophilin) is responsible for most cases of diluted colours. While all mutations and genes causing colour dilution has not been discovered yet, all cases of dilution cannot be explained by genetic testing. MLPH gene encodes a protein melanophilin, a key component in the hair and skin pigment formation. A mutation in the gene causes the improper distribution of melanosomes and coat colour dilution. The mutation has an effect on the formation of black eumelanin as well as red-yellow pheomelanin, though in lesser extent. The dilution of black pigment results in blue or grey coat colour, and dilution of brown pigment results light brown or isabella. D locus is not responsible only for coat pigment dilution but also dilutes pigment of the nose, pads and eyes.
K LOCUS Ky/Ky (HOMOZIGOEUS WHEAT)
The symbol K was chosen to denote the locus causing black dog coat color which is inherited as a dominant. The identification of dominant black (formally, an allele of the “K locus”) relied on two major advances in dog genetics: the sequencing of the dog genome and recognition that the distinctive genetic structure of dog breeds allows for efficient gene mapping. The K locus is identified as b-defensin 103 (CBD103). Its protein product binds with high affinity to the Mc1r and has a simple and strong effect on pigment type-switching in domestic dogs.
The K locus has three alleles with a simple dominance order: Black (KB) > brindle (kbr) > yellow (ky)
In the vast majority of dog breeds, in order for solid eumelanin coat colour (black, brown and grey) to occur the dog must have at least one E or EM allele at MC1R and at least one dominant allele at the K locus.
A single copy of the kbr allele in the presence of a ky allele is sufficient to cause the dog to express the phenotype known as brindle. Brindle in dogs consists of alternate stripes of phaeomelanin and eumelanin of various shades. In some dogs, there is such a preponderance of eumelanin that the dog appears virtually black whereas in other individuals the eumelanin stripes are very thin. Brindle occurs over the entire body in dogs with an ay allele but only on the ventral surfaces in dogs with an at/at genotype.
Dogs with a ky/ky genotype at this locus could be fawn, wolf sable or eumelanin-and-tan depending on their genotype at ASIP.
K locus DNA test identifies presence of KB allele. Allele kbr cannot be detected with this test.
Kerns, J.A., Cargill, E.J., Clark, L.A., Candille, S.I., Berryere, T.G., Olivier, M., Lust, G., Todhunter, R.J., Schmutz, S.M., Murphy, K.E., et al. (2007). Linkage and Segregation Analysis of Black and Brindle Coat Color in Domestic Dogs. Genetics 176, 1679–1689.
Cu Locus (Curly Coat)
Hair shape, or curl, in dogs is a complex trait that is difficult to classify, especially when comparing phenotypes across breeds. Extreme differences in phenotype are exemplified by the long, relatively straight hair of the Afghan Hound and the long, tightly curled hair of the Poodle. This locus is called Cu, and the two alleles CuC and Cu+, for straight and curly coat, respectively. The curly hair is known to be recessive. Intermediate phenotypes between these two extremes, such as the loose, spiral-shaped hair characteristic of Irish Water Spaniels, are described as kinky or wavy.
Genome-wide mapping identified association between KRT71 coding alteration and curly coat. Analysis across breeds indicates that the variant allele, KRT71151W, is uncommon in straight coated breeds, but fixed in several curly- and wavycoated breeds. Inheritence of curly coat is non-Mendelian, and the KRT71151W allele is not found in some curly-coated breeds, such as the Curly Coated Retrievers.
Cadieu, E., Neff, M.W., Quignon, P., Walsh, K., Chase, K., Parker, H.G., Vonholdt, B.M., Rhue, A., Boyko, A., Byers, A., et al. (2009). Coat variation in the domestic dog is governed by variants in three genes. Science 326, 150–153. Airedale Terrier, the Kerry Blue Terrier etc.
Furnishings refers to the longer mustache and eyebrows seen in wire-haired dogs and other breeds. A dominant variant (167bp in the 3’-UTR sequence) of the R-spondin-2 (RSPO2) gene, produces this desired texture and growth pattern of fur.
Improper Coat: The breed standard for Labradoodle, Goldendoodles and Portuguese Water Dog requires “furnishings”. In these dog breeds, lack of the dominant RSPO2 variant (IC) causes Improper Coat which is characterized by short hair on the head, face and legs.
Furnishings results reported as:
|The dog does not have furnishings.
|The dog has furnishings and carries 1 copy of the non-furnishing gene.
|The dog has furnishings. All offspring will have furnishings.
Improper Coat results reported as:
|Improper Coat (RSPO2)
|No copies of Improper Coat, normal, dog will have longer hair on the muzzle and eyebrows.
|1 copy of Improper Coat, carrier, dog will have longer hair on the muzzle and eyebrows.
|2 copies of Improper Coat, dog has Improper Coat, dog will NOT have longer hair on the muzzle and eyebrows.
Cadieu E, Neff MW, Quignon P, Walsh K, Chase K, Parker HG, Vonholdt BM, Rhue A, Boyko A, Byers A, Wong A, Mosher DS, Elkahloun AG, Spady TC, André C, Lark KG, Cargill M, Bustamante CD, Wayne RK, Ostrander EA. Coat variation in the domestic dog is governed by variants in three genes. Science 326:150-153, 2009.