Breeding & Health Testing

Breeding & Health Testing

Our Boston Terrier breeding program is currently in a period of rebuilding (we got our first Bostons starting in 2001) and refinement. Our current focus is on our bloodlines, extensive health testing and keeping current with cutting edge research and genetic testing. Our focus continues to be on quality and not quantity. Once further along with our plans and breeding scheme, we will be showing again in the near future.

Our Boston Terriers are a blend of Canadian, American and European bloodlines. We have imported from reputable breeders in the United States and from many European countries. We do so, in order to promote genetic variability in our bloodlines. More specifically, to prevent homozygosity. Homozygosity is having two identical alleles of a particular gene/genes. While breeding related animals produces more consistent and predictable traits (as a result of homozygosity), loss in vitality and vigor is also the result (Beuchat, 2015). Breeding related animals also reduces fertility, produces smaller offspring, early death and a shorter lifespan (Beuchat, 2015). That is, the higher level of inbreeding, the greater the detrimental effects (Beuchat, 2015). All things considered and weighing the benefits and risks, we aim to breed puppies/dogs with inbreeding coefficients (ICs) as close to zero as possible. It is recommended that ICs are calculated over at least 8-10 generations (the more the better though!) and preferably 5% and under (Beuchat, 2015). Our ICs are calculated on TEN GENERATIONS and therefore reflect higher than they would otherwise (i.e. if calculated over 8 generations). In the past, we have always regarded 6.8% inbreeding coefficient to be an upper limit (again, trying to keep as low as possible), as suggested in the agricultural research available to us at that time. With advancements in genetics in the Veterinary field however, we now consider 5% over 8-10 generations to be an upper limit. In addition to taking into consideration our dogs' ICs when breeding, we also consider and compare these percentages to their Genetic Diversity/Heterozygosity percentage, as determined by DNA. Interestingly, one dog can have a low IC and higher homozygosity percentage and another dog can have a high relative IC and have a lower homozygosity percentage. Cool, right??!! A breeder must consider ALL!! The typical range of heterozygosity percentage of Boston Terriers is 31 - 37% (Wisdom Panel™). The higher the percentage, the greater the heterozygosity.

As per Our Story page, we breed for the "total dog", with an emphasis on health and temperament, while breeding to standard. Given the pitfalls of "breeding for show titles" (i.e. breeding dogs closely related to achieve consistency and predictability) and that breeds are created by inbreeding to begin with, our focus remains on health and temperament first and foremost. Yes, one must also breed to standard and we feel that showing is important in maintaining the integrity of the breed standard and the breed as a whole. However, this isn't our sole focus. Indeed, we enjoy showing and try to get to shows when our family life allows.

"The fewer generations used in calculating the inbreeding coefficient, the "better" (i.e. lower) it will appear to be. But this isn't an accurate assessment of the true degree of homozygosity in a dog, so it does not reflect the true level inbreeding depression and risk of genetic disease" (Beuchat, 2015).

Inbreeding Coefficient

The inbreeding coefficient is the estimated level of inbreeding/homozygosity of a particular mating/breeding. The inbreeding coefficient is the probability of inheriting the same allele from an ancestor on both sides of the pedigree and the fraction of all of the genes of a dog that are homozygous (Beuchat, 2015). A low inbreeding coefficient has a lower risk, but supposedly also lower benefits, as it relates to consistency in type. A high inbreeding coefficient would produce more consistency and prepotency in the puppies produced, but there would also be a significant loss of vigor and health (Beuchat, 2015). The detrimental effects of inbreeding start to become evident at 5%, with a significant loss of vitality and an increase in the expression of detrimental recessive mutations in puppies at 10% (Beuchat, 2015). An inbreeding coefficient of 10% is considered to be the "extinction vortex", in which smaller litters, higher mortality, and expression of genetic defects have a negative effect on the size of the population (Beuchat, 2015). Further, as the population gets smaller, the incidence of inbreeding goes up, culminating in a "negative feedback loop" that eventually drives a population to extinction (Beuchat, 2015).

Again, in terms of health, an inbreeding coefficient of 5% or less is most ideal, as above that, there are detrimental effects and risks. Thus, a breeder needs to weigh these against anticipated benefits gained (Beuchat, 2015). Inbreeding coefficients of 5-10% supposedly will have modest detrimental effects on the offspring, while levels above 10% will yield significant effects - not just on the quality of the offspring, but on the breed as a whole (Beuchat, 2015).

Health Testing

A breeder can use the inbreeding coefficient to reduce the risk of genetic disorders in their puppies, as it's an estimate of the predicted loss of vigor and general health expected as a repercussion of the expression of recessive mutations (Beuchat, 2015). However, the inbreeding coefficient is NOT a measure of health. Rather, it's a measure of RISK, and with or without DNA tests, it's the best way to ascertain the level of genetic risk one takes when breeding (Beuchat, 2015).

However, every dog has many mutations, and one has no way of knowing about them if the dog has only one copy and it's not expressed. Thus, if one breeds two dogs with some of the same mutations, one can expect that the puppies will be homozygous for 25% of them (Beuchat, 2015). Many of these mutations may only have very few effects and one may not recognize these as a "disease". It's the accumulation of these few effects that causes the loss of vigor and vitality in inbred animals (referred to as "inbreeding depression") (Beuchat, 2015). DNA tests tell you only about one particular gene, which is known as a risk for a particular disease (Beuchat, 2015).

To breed healthy animals, one needs to consider ALL of the potential risks, and there are many more recessive mutations than the ones we have DNA tests for (Beuchat, 2015). This is why we're now running (now that the tests are available) Optimal Selection™ panels on our dogs. In the past, we have always at least certified patellas, heart (by auscultation) and Juvenile Hereditary Cataracts and then Degenerative Myelopathy and Hyperuricosuria when the tests came out. We have also tested for the piebald gene in the past (and continue to do so) as well, as it's been hypothesized to be the cause of congenital deafness in related breeds and progenitors of the breed (Bulldogs, Bull Terriers, etc.). Please note, there is no genetic marker for breed specific congenital deafness in the Boston Terrier to date, but we do test for Deafness and Vestibular Dysfunction in this panel. Indeed, there are many reasons for deafness, genetics aside.However, we will continue to follow research and test for all possible causes. The tests in the Optimal Selection™ panel are:

  • 2,8-dihydroxyadenine (DHA) Urolithiasis
  • Acral Mutilation Syndrome
  • Acute Respiratory Distress Syndrome
  • Alaskan Husky Encephalopathy
  • Alexander Disease
  • Amelogenesis Imperfecta
  • Bandera's Neonatal Ataxia
  • Benign Familial Juvenile Epilepsy
  • Canine Leukocyte Adhesion Deficiency (CLAD), type III
  • Canine Multifocal Retinopathy 1
  • Canine Multifocal Retinopathy 2
  • Canine Multifocal Retinopathy 3
  • Canine Scott Syndrome
  • Centronuclear Myopathy (Discovered in the Great Dane)
  • Centronuclear Myopathy (Discovered in the Labrador Retriever)
  • Cerebellar Ataxia
  • Cerebellar Cortical Degeneration
  • Cerebellar Hypoplasia
  • Cerebral Dysfunction
  • Chondrodysplasia
  • Cleft Lip & Palate with Syndactyly
  • Cleft Palate
  • Collie Eye Anomaly (CEA)
  • Complement 3 Deficiency
  • Cone Degeneration (Discovered in the Alaskan Malamute)
  • Cone Degeneration (Discovered in the German Shepherd Dog)
  • Cone Degeneration (Discovered in the German Shorthaired Pointer)
  • Cone-Rod Dystrophy
  • Cone-Rod Dystrophy 1
  • Cone-Rod Dystrophy 2
  • Congenital Dyshormonogenic Hypothyroidism with Goiter (Discovered in the Shih Tzu)
  • Congenital Hypothyroidism (Discovered in the Tenterfield Terrier)
  • Congenital Hypothyroidism (Discovered in the Toy Fox and Rat Terrier)
  • Congenital Myasthenic Syndrome (Discovered in the Golden Retriever)
  • Congenital Myasthenic Syndrome (Discovered in the Jack Russell Terrier)
  • Congenital Myasthenic Syndrome (Discovered in the Labrador Retriever)
  • Congenital Myasthenic Syndrome (Discovered in the Old Danish Pointing Dog)
  • Congenital Stationary Night Blindness (CSNB)
  • Craniomandibular Osteopathy
  • Cystic Renal Dysplasia and Hepatic Fibrosis
  • Cystinuria Type I-A
  • Cystinuria Type II-A
  • Deafness and Vestibular Dysfunction (Discovered in Doberman Pinscher)
  • Degenerative Myelopathy
  • Demyelinating Neuropathy
  • Dental Hypomineralization
  • Dilated Cardiomyopathy (Discovered in the Schnauzer)
  • Dominant Progressive Retinal Atrophy
  • Dystrophic Epidermolysis Bullosa (Discovered in the Central Asian Ovcharka)
  • Dystrophic Epidermolysis Bullosa (Discovered in the Golden Retriever)
  • Early Adult Onset Deafness For Border Collies only (Linkage test)
  • Early Retinal Degeneration (Discovered in the Norwegian Elkhound)
  • Early-onset PRA (Discovered in the Portuguese Water Dog)
  • Early-Onset Progressive Polyneuropathy (Discovered in the Alaskan Malamute)
  • Early-Onset Progressive Polyneuropathy (Discovered in the Greyhound)
  • Enamel Hypoplasia (Discovered in the Parson Russell Terrier)
  • Epidermolytic Hyperkeratosis
  • Episodic Falling Syndrome
  • Exercise-Induced Collapse
  • Factor VII Deficiency
  • Factor XI Deficiency
  • Fanconi Syndrome
  • Fetal Onset Neuroaxonal Dystrophy
  • Focal Non-Epidermolytic Palmoplantar Keratoderma
  • Generalized Progressive Retinal Atrophy (Discovered in the Schapendoes)
  • Glanzmann Thrombasthenia Type I
  • Glanzmann Thrombasthenia Type I (Discovered in Great Pyrenees)
  • Globoid Cell Leukodystrophy (Discovered in Terriers)
  • Globoid Cell Leukodystrophy (Discovered in the Irish Setter)
  • Glycogen Storage Disease Type Ia
  • Glycogen Storage Disease Type IIIa, (GSD IIIa)
  • GM1 Gangliosidosis (Discovered in the Portuguese Water Dog)
  • GM1 Gangliosidosis (Discovered in the Shiba)
  • GM2 Gangliosidosis (Discovered in the Japanese Chin)
  • GM2 Gangliosidosis (Discovered in the Toy Poodle)
  • Hemophilia A (Discovered in Old English Sheepdog)
  • Hemophilia A (Discovered in the Boxer)
  • Hemophilia A (Discovered in the German Shepherd Dog - Variant 1)
  • Hemophilia A (Discovered in the German Shepherd Dog - Variant 2)
  • Hemophilia A (Discovered in the Havanese)
  • Hemophilia B
  • Hemophilia B (Discovered in the Airedale Terrier)
  • Hemophilia B (Discovered in the Lhasa Apso)
  • Hereditary Ataxia (Discovered in the Norwegian Buhund)
  • Hereditary Elliptocytosis
  • Hereditary Footpad Hyperkeratosis
  • Hereditary Nasal Parakeratosis (Discovered in the Greyhound)
  • Hereditary Nasal Parakeratosis (Discovered in the Labrador Retriever)
  • Hereditary Vitamin D-Resistant Rickets Type II
  • Hyperekplexia or Startle Disease
  • Hyperuricosuria
  • Hypocatalasia
  • Hypomyelination
  • Hypophosphatemia
  • Ichthyosis (Discovered in the American Bulldog)
  • Ichthyosis (Discovered in the Great Dane)
  • Intestinal Cobalamin Malabsorption (Discovered in the Beagle)
  • Intestinal Cobalamin Malabsorption (Discovered in the Border Collie)
  • Intestinal Cobalamin Malabsorption (Discovered in the Komondor)
  • Juvenile Encephalopathy (Discovered in the Parson Russell Terrier)
  • Juvenile Laryngeal Paralysis and Polyneuropathy
  • Juvenile Myoclonic Epilepsy
  • L-2-Hydroxyglutaric Aciduria
  • L-2-Hydroxyglutaric Aciduria (Discovered in the Westie)
  • Lagotto Storage Disease
  • Lamellar Ichthyosis
  • Lethal Acrodermatitis (Discovered in the Bull Terrier)
  • Ligneous Membranitis
  • Lung Developmental Disease (Discovered in the Airedale Terrier)
  • Macrothrombocytopenia
  • May-Hegglin Anomaly
  • MDR1 Medication Sensitivity
  • Microphthalmia (Discovered in the Soft-Coated Wheaten Terrier)
  • Mucopolysaccharidosis Type IIIA (Discovered in the Dachshund)
  • Mucopolysaccharidosis Type IIIA (Discovered in the New Zealand Huntaway)
  • Mucopolysaccharidosis Type VII (Discovered in the Brazilian Terrier)
  • Mucopolysaccharidosis Type VII (Discovered in the German Shepherd Dog)
  • Muscular Dystrophy (Discovered in the Cavalier King Charles Spaniel)
  • Muscular Dystrophy (Discovered in the Golden Retriever)
  • Muscular Dystrophy (Discovered in the Landseer)
  • Muscular Dystrophy (Discovered in the Norfolk Terrier)
  • Muscular Hypertrophy (Double Muscling)
  • Musladin-Lueke Syndrome
  • Myeloperoxidase Deficiency
  • Myotonia Congenita
  • Myotonia Congenita (Discovered in the Labrador Retriever)
  • Myotonia Congenita (Discovered in the Miniature Schnauzer)
  • Myotubular Myopathy
  • Narcolepsy (Discovered in the Dachshund)
  • Narcolepsy (Discovered in the Labrador Retriever)
  • Nemaline Myopathy
  • Neonatal Cerebellar Cortical Degeneration
  • Neonatal Encephalopathy with Seizures
  • Neuroaxonal Dystrophy
  • Neuroaxonal Dystrophy (Discovered in the Papillon)
  • Neuroaxonal Dystrophy (Discovered in the Rottweiler)
  • Neuronal Ceroid Lipofuscinosis 1
  • Neuronal Ceroid Lipofuscinosis 7
  • Neuronal Ceroid Lipofuscinosis 8 (Discovered in the Alpine Dachsbracke)
  • Neuronal Ceroid Lipofuscinosis 8 (Discovered in the Australian Shepherd)
  • Neuronal Ceroid Lipofuscinosis 8 (Discovered in the English Setter)
  • Neuronal Ceroid Lipofuscinosis 8 (Discovered in the Saluki)
  • Neuronal Ceroid Lipofuscinosis 12 (Discovered in the Australian Cattle Dog)
  • Obesity risk (POMC)
  • Osteochondrodysplasia
  • Osteochondromatosis (Discovered in the American Staffordshire Terrier)
  • Osteogenesis Imperfecta (Discovered in the Beagle)
  • Osteogenesis Imperfecta (Discovered in the Dachshund)
  • P2RY12-associated Bleeding Disorder
  • Paroxysmal Dyskinesia
  • Persistent Müllerian Duct Syndrome
  • Phosphofructokinase Deficiency
  • Polycystic Kidney Disease
  • Prekallikrein Deficiency
  • Primary Ciliary Dyskinesia
  • Primary Ciliary Dyskinesia (Discovered in the Alaskan Malamute)
  • Primary Lens Luxation
  • Primary Open Angle Glaucoma (Discovered in Basset Fauve de Bretagne)
  • Primary Open Angle Glaucoma (Discovered in Petit Basset Griffon Vendeen)
  • Primary Open Angle Glaucoma and Lens Luxation (Discovered in Chinese Shar-Pei)
  • Progressive Early-Onset Cerebellar Ataxia
  • Progressive Retinal Atrophy (Discovered in the Swedish Vallhund)
  • Progressive Retinal Atrophy (Discovered in the Basenji)
  • Progressive Retinal Atrophy (Discovered in the Golden Retriever - GR-PRA1 variant)
  • Progressive Retinal Atrophy (Discovered in the Lhasa Apso)
  • Progressive Retinal Atrophy (Discovered in the Papillon and Phalène)
  • Progressive Retinal Atrophy (Discovered in the Shetland Sheepdog - BBS2 variant)
  • Progressive Retinal Atrophy (Discovered in the Shetland Sheepdog - CNGA1 variant)
  • Progressive Retinal Atrophy 1 (Discovered in the Italian Greyhound)
  • Progressive Retinal Atrophy Type III
  • Progressive Rod Cone Degeneration (prcd-PRA)
  • Protein Losing Nephropathy
  • Pyruvate Dehydrogenase Phosphatase 1 Deficiency
  • Pyruvate Kinase Deficiency (Discovered in the Basenji)
  • Pyruvate Kinase Deficiency (Discovered in the Beagle)
  • Pyruvate Kinase Deficiency (Discovered in the Pug)
  • Pyruvate Kinase Deficiency (Discovered in the West Highland White Terrier)
  • QT Syndrome
  • Renal Cystadenocarcinoma and Nodular Dermatofibrosis
  • Rod-Cone Dysplasia 1
  • Rod-Cone Dysplasia 1a
  • Rod-Cone Dysplasia 3
  • Sensory Ataxic Neuropathy
  • Sensory Neuropathy
  • Severe Combined Immunodeficiency
  • Severe Combined Immunodeficiency (Discovered in Frisian Water Dogs)
  • Shaking Puppy Syndrome (Discovered in the Border Terrier)
  • Skeletal Dysplasia 2
  • Spinocerebellar Ataxia (Late-Onset Ataxia)
  • Spinocerebellar Ataxia with Myokymia and/or Seizures
  • Spondylocostal Dysostosis
  • Spongy Degeneration with Cerebellar Ataxia
  • Spongy Degeneration with Cerebellar Ataxia (Discovered in Belgian Malinois)
  • Stargardt Disease (Discovered in the Labrador Retriever)
  • Trapped Neutrophil Syndrome
  • Van den Ende-Gupta Syndrome
  • von Willebrand's Disease, type 1
  • von Willebrand's Disease, type 2
  • von Willebrand's Disease, type 3 (Discovered in the Kooiker Hound)
  • von Willebrand's Disease, type 3 (Discovered in the Scottish Terrier)
  • von Willebrand's Disease, type 3 (Discovered in the Shetland Sheepdog)
  • X-Linked Ectodermal Dysplasia
  • X-Linked Hereditary Nephropathy (Discovered in the Navasota Dog)
  • X-Linked Hereditary Nephropathy (Discovered in the Samoyed)
  • X-Linked Myotubular Myopathy
  • X-Linked Progressive Retinal Atrophy 1
  • X-Linked Progressive Retinal Atrophy 2
  • X-Linked Severe Combined Immunodeficiency (Discovered in the Basset Hound)
  • X-Linked Severe Combined Immunodeficiency (Discovered in the Cardigan Welsh Corgi)
  • X-Linked Tremors
  • Xanthinuria (Discovered in a mixed breed dog)
  • Xanthinuria (Discovered in the Cavalier King Charles Spaniel)
  • Xanthinuria (Discovered in the Toy Manchester Terrier)