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English Springer Spaniel

English Springer Spaniel
Photo: Ratsniffer / CC0 · Wikimedia

118 English Springer Spaniels in the atlas. Every number on this page has a source.

Population-genetic snapshot of English Springer Spaniels in the Sniff Atlas, source-graded Mendelian carrier frequencies from Donner 2023, and nutrition guidance tied to the genetic findings above.

Also known as Spaniel, English Springer, Springer Spaniel, and Springer, English Spaniel.

The plain version

English Springer Spaniels have a moderately varied genetic background. They typically weigh around 49 pounds and live about 13 years. This breed is known for its energetic personality and beautiful, medium-sized build. Some dogs in this breed carry genes related to eye and spine conditions, which is a reflection of the breed’s overall gene pool, so it’s a good idea to talk with your vet or consider genetic testing to keep your dog healthy.

What the atlas says about English Springer Spaniel

In the atlas, the English Springer Spaniel clusters consistently as English Springer Spaniel (100% of the 118 dogs here). At the trait loci, FGF4_retrogene_CFA12 runs lower than average (37% here vs 80%); HMGA2 runs higher than the atlas average (92% here vs 56%).

Genetic dimensions · CanVAS atlas

What the genome says about English Springer Spaniel

Computed from the 18,477 research dogs in the Atlas.

Dogs in the Atlas
118Founders
57 from Shannon, 49 from Hayward2016, 10 from Spatola
Genetic diversity
0.29Moderate
Mean heterozygosity across the breed. Ranks 34th most genetically tight of 107 ranked breeds.
What does genetic diversity mean?

How varied a breed's gene pool is — the share of gene spots where a typical dog of the breed carries two different versions rather than two identical ones.

How to read it: Higher = more diverse. Among well-sampled breeds it ranges roughly 0.22 (least diverse) to 0.33 (most diverse).

Diversity is a strength, not a verdict on any individual dog. Lower diversity means it's worth paying attention to recessive-risk testing — not that a dog is doomed.

Cluster structure
Splits into two genetic sub-populations
Intra-breed RMS distance: 30.63 · likely working/show-line, regional, or kennel lineage split.
What does within-breed variation mean?

How much individual dogs within the breed differ from each other genetically.

How to read it: Higher = more internal variety among individuals of the breed.

Sensitive to how many dogs of the breed we've sampled.

Related breeds
In the Sporting group
Explore the full lineage map →
VBO foundation stock (breeding records) · AKC breed group
Relatedness is documented lineage + kennel family. Genetic-ancestry distance measures diversity, not kinship, so it isn't used here.
How long they live
13.5years (life expectancy)
95% CI 13.4–13.6 · VetCompass, McMillan 2024, n=17,905. source
What does typical lifespan mean?

The median age dogs of the breed tend to reach.

How to read it: Higher = longer-lived. Compare to longevity-for-size to see whether it's just a size effect.

Drawn from population lifespan records; individual dogs vary widely with care, genetics, and luck.

Trait genetics
Allele frequencies at named morphology loci

Frequency of the alternate allele in this breed at each locus's representative SNP.

Body size
IGF163%
HMGA292%
SMAD287%
LCORL78%
STC260%
ADAMTS1744%
Leg length
FGF4·CFA1847%
FGF4·CFA1237%
Coat
RSPO235%
FGF588%
KRT7197%
MC1R32%
Ear set
MSRB394%
Skull shape
BMP367%
SMOC290%
n = 118 dogs · high confidence · CanVAS (Brundage 2026) · Sniff Atlas
Names & origins

Other names

The English Springer Spaniel is also recorded as Spaniel, English Springer, Springer Spaniel, and Springer, English Spaniel.

Identified as English Springer Spaniel (VBO:0200497) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 125 · iDog 97 · VeNom 14884.

What you see when you look at a English Springer Spaniel

What does the genome say about how a English Springer Spaniel looks?

English Springer Spaniels look the way they do because of a small set of fixed and near-fixed morphology genes that, taken together, define the visible breed. Each translation below pairs the gene with the trait an owner actually sees, the breed's allele frequency at that locus, and a one-clause causal phrase.

Where the breed-defining genes act, mapped on a generic dog-body key — and how fixed each marker is in the English Springer Spaniel. The figure is the most-settled marker we read in that region; the full per-locus panel is below. (The silhouette is a shared anatomical guide, not this breed's outline.)

Body sizeHMGA2 · 92%Skull shapeSMOC2 · 90%EarsMSRB3 · 94%Leg lengthFGF4 CFA18 · 47%Coat & colorKRT71 · 97%
CanVAS trait-locus panel (Brundage 2026)
15 morphology markers read across 5 regions. Allele frequency = how fixed a marker is in this breed, not whether your dog carries it.

Size and build

IGF1 sits at 63% for the small-body allele. IGF1 is the gene that sets dog body size from Chihuahua to Great Dane. Intermediate frequencies typically keep a breed in the mid-sized range rather than tipping toward the larger working forms.

IGF1what this gene does

IGF1 is a gene that plays a key role in determining a dog's body size. It influences how much a dog grows, affecting overall stature.

For your dog: Knowing about IGF1 gives you insight into your dog's size traits, but it’s just one part of the bigger picture when it comes to their health and care.

Full IGF1 gene page →

HMGA2 is near-fixed at 92%, reinforcing the breed's size signal through a second locus on chromosome 10.

HMGA2what this gene does

HMGA2 is a gene that influences body size in dogs, helping determine how big or small a dog grows.

For your dog: Knowing about HMGA2 helps you appreciate the genetic factors behind your dog's size, but it doesn't signal any health issues.

Full HMGA2 gene page →

SMAD2 is near-fixed at 87%, a chromosome-7 height locus differentiating small from giant breeds.

SMAD2what this gene does

SMAD2 is a gene involved in regulating body size by influencing how cells grow and develop.

For your dog: Knowing about SMAD2 helps understand your dog's size traits but isn't linked to health issues; no immediate action needed.

Full SMAD2 gene page →

LCORL sits at 78% at the NCAPG/LCORL height locus on chromosome 3.

LCORLwhat this gene does

LCORL is a gene that influences body size in dogs. It helps determine how big or small a dog might grow.

For your dog: Knowing about LCORL helps you appreciate the genetic factors behind your dog's size, but it’s just one piece of the bigger picture when it comes to health and care.

Full LCORL gene page →

STC2 sits at 60%.

ADAMTS17 sits at 44%. ADAMTS17 is a body-size locus also linked to lens disorders.

ADAMTS17what this gene does

ADAMTS17 is a gene that influences body size and also plays a role in certain eye conditions. It affects the structure of tissues in the eye and elsewhere in the body.

For your dog: If your dog belongs to a breed known to carry ADAMTS17 variants, it’s worth discussing genetic testing and eye exams with your vet to stay ahead of potential issues.

Full ADAMTS17 gene page →

Leg length

The FGF4 retrogene on chromosome 18 sits at 47%. This is the leg-length variant. The intermediate frequency means some dogs in this breed carry the short-legged allele and some do not.

The FGF4 retrogene on chromosome 12 sits at 37%, the chondrodystrophic variant.

Coat type, length, and color

RSPO2 sits at 35% for the furnishings variant. Furnishings (the eyebrow-and-mustache pattern seen in Schnauzers and Wheaten Terriers) vary across the population at this intermediate frequency, and visible expression depends on the specific allele combination each dog carries.

RSPO2what this gene does

RSPO2 influences the texture and appearance of a dog's coat, particularly the presence of 'furnishings' like mustaches and eyebrows. It helps determine whether a dog has that distinctive wiry or textured look.

For your dog: If your dog has those wiry eyebrows or a mustache, RSPO2 is part of the reason—no health worries, just a coat feature worth knowing about.

Full RSPO2 gene page →

FGF5 is at 88% for the long-coat variant, which is why the breed's coat sits where it does on the long end of the dog coat-length spectrum.

FGF5what this gene does

FGF5 is a gene that influences the length of a dog's coat. It acts like a natural switch, telling hair follicles when to stop growing longer fur.

For your dog: If your dog has a notably long or short coat, FGF5 is likely part of the reason—no action needed, but it’s a neat genetic detail to know.

Full FGF5 gene page →

KRT71 is near-fixed at 97% for the wavy/curly variant. Coat curl phenotype varies across breeds at this fixation depending on modifier loci, and visible expression is not always curled even when the locus is fixed.

KRT71what this gene does

KRT71 is a gene that influences the curliness of a dog's coat. It helps determine whether a dog's fur is straight or has a distinctive curl.

For your dog: If your dog has a curly coat, KRT71 is likely part of the reason; it’s a natural variation, not a health concern.

Full KRT71 gene page →

MC1R sits at 32% at the representative SNP. MC1R controls the switch between red-to-gold pigment and black-to-brown pigment, with the e/e homozygous genotype producing the gold-to-red spectrum. Substrate frequencies at this SNP depend on the array's polarity, so visible coat color in the breed is a more reliable indicator than this single number.

MC1Rwhat this gene does

MC1R is a gene that influences coat color in dogs, affecting how pigments are produced in the fur.

For your dog: Knowing about MC1R gives insight into your dog's coat color but doesn't relate to health issues.

Full MC1R gene page →

Ears

MSRB3 is at 94% for the drop-ear allele, the genetic basis of the breed's signature dropped ear set.

MSRB3what this gene does

MSRB3 is a gene involved in the development of ear shape and structure in dogs.

For your dog: Understanding MSRB3 helps explain why your dog's ears look the way they do, but it isn't linked to any health issues.

Full MSRB3 gene page →

Skull shape

BMP3 sits at 67%, contributing to the breed's moderate, mesaticephalic head shape rather than the extreme brachycephalic form.

BMP3what this gene does

BMP3 is a gene that influences the shape of a dog's skull, particularly contributing to a shorter, broader head shape known as brachycephaly.

For your dog: If your dog has a broad, short skull, it's worth discussing with your vet how this might impact their health, even though BMP3 isn't directly tied to illness.

Full BMP3 gene page →

SMOC2 is at 90%, the major locus contributing to the breed's brachycephalic face shape.

SMOC2what this gene does

SMOC2 influences the shape of a dog's skull, particularly affecting how flat or short the face appears.

For your dog: If your dog has a short nose, it's worth discussing with your vet how this trait might impact their health over time.

Full SMOC2 gene page →
Mendelian-disease genetics

What genetic diseases do English Springer Spaniels carry?

From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), English Springer Spaniels carry 12 of them at observable frequency. Carrier frequency is not clinical risk. Most recessive variants require two copies for disease expression; many dominant variants show incomplete penetrance. Read this as a population fingerprint of what's in the gene pool, not a per-dog prediction.

Cone-Rod Dystrophy (cord1-PRA/crd4)
Autosomal recessive (Incomplete penetrance)
high 29.9%
n = 750 dogs · 1 variant tested · OMIA:001432-9615 · omia.org →
RPGRIP1what this gene does

RPGRIP1 is a gene involved in the function of photoreceptor cells in the eye, which help dogs see in different light conditions.

For your dog: If your dog belongs to a breed known to carry RPGRIP1 mutations, it’s worth discussing with your vet to understand the risks and monitor eye health.

n = 749 dogs · 1 variant tested · OMIA:000157-9615 · omia.org →
FGF4what this gene does

FGF4 influences leg length by affecting bone growth, leading to shorter legs in certain breeds.

For your dog: If your dog is from a breed known to carry this gene, it's worth discussing spinal health with your vet, but being a carrier doesn’t guarantee problems.

Cystinuria Type I-B (SLC7A9 p.A217T)
Autosomal recessive (Incomplete penetrance)
low 4.4%
n = 751 dogs · 2 variants tested · OMIA:001880-9615 · omia.org →
SLC7A9what this gene does

SLC7A9 is a gene that helps transport certain amino acids in the kidneys. It plays a role in how the body handles cystine, an amino acid that can form crystals.

For your dog: If your dog is a carrier, it’s worth discussing with your vet to monitor urinary health and catch any issues early.

Degenerative Myelopathy (DM)
Autosomal recessive (Incomplete penetrance)
low 3.4%
n = 751 dogs · 1 variant tested · OMIA:000263-9615 · omia.org →
SOD1what this gene does

SOD1 is a gene that helps protect cells from damage caused by harmful molecules called free radicals.

For your dog: If your dog is a carrier of SOD1 variants, it's worth discussing with your vet, but remember carrier status doesn't mean your dog will get the disease.

low 1.6%
n = 751 dogs · 1 variant tested · OMIA:001514-9615 · omia.org →
GDNFwhat this gene does

GDNF is a gene that helps support nerve cells, especially those involved in sensing pain and movement.

For your dog: If your dog is from a breed that can carry this gene change, it’s worth asking your vet about testing to understand any potential risks.

low 0.60%
n = 751 dogs · 1 variant tested · OMIA:001057-9615 · omia.org →
n = 751 dogs · 2 variants tested · OMIA:000710-9615 · omia.org →
Factor VII Deficiency
Autosomal recessive
low 0.13%
n = 751 dogs · 1 variant tested · OMIA:000361-9615 · omia.org →
F7what this gene does

The F7 gene helps produce a protein important for blood clotting, which stops bleeding when dogs get injured.

For your dog: If your dog is from a breed known to carry F7 variants, it's worth mentioning to your vet before any surgery or if you notice unusual bleeding.

n = 751 dogs · 2 variants tested · OMIA:000162-9615 · omia.org →
PDK4what this gene does

PDK4 helps regulate how cells use energy, especially in the heart muscle.

For your dog: If your dog is one of the breeds known to carry this gene, it’s worth discussing heart health with your vet, but being a carrier doesn’t mean your dog will develop disease.

Exercise-Induced Collapse (EIC)
Autosomal recessive (Incomplete penetrance)
low <0.1%
n = 751 dogs · 1 variant tested · OMIA:001466-9615 · omia.org →
DNM1what this gene does

DNM1 is a gene that helps nerve cells communicate properly by managing how they send signals during muscle activity.

For your dog: If your dog belongs to one of the breeds known to carry this gene variant, it's worth discussing EIC with your vet, especially if your dog is very active or shows signs of weakness during exercise.

n = 751 dogs · 1 variant tested · OMIA:001298-9615 · omia.org →
PRCDwhat this gene does

PRCD is a gene involved in the health of a dog's retina, the part of the eye that detects light and helps with vision.

For your dog: If your dog belongs to a breed known to carry PRCD changes, it's worth discussing eye health and potential genetic testing with your vet.

Source: Donner J et al. 2023. Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics 19(2):e1010651 · Evidence: Limited (DTC ascertainment, tag-SNP proxy) · Confounding MEDIUM · License CC-BY-4.0 · Phene IDs from OMIA (Sydney School of Veterinary Science, The University of Sydney; DOI 10.25910/2AMR-PV70).
Sample size in this breed: 751 dogs from the Donner 2023 cohort.

Which Mendelian variants matter most for English Springer Spaniels?

The Mendelian-disease table above lists variants screened in 751 English Springer Spaniels (Donner 2023). Two matter most by carrier frequency and clinical impact.

Cone-Rod Dystrophy (cord1-PRA/crd4)

Cone-rod dystrophy in English Springer Spaniels is a recessive progressive retinal disease caused by the crd4 locus. Affected dogs lose vision gradually, typically beginning with reduced vision in dim light and progressing toward complete blindness. It is incurable and leads to functional blindness by middle age. About 29.9% of English Springer Spaniels in the Donner cohort carry the variant (n=750). Nearly one in three. This is the single most common Mendelian variant in the breed.

The inheritance is autosomal recessive with incomplete penetrance, meaning not every dog with two copies will show symptoms, though the published evidence on penetrance in this breed is limited. Testing is widely available through commercial DNA labs and breed-specific panels. Breed-club health committees generally recommend testing breeding stock to avoid carrier-by-carrier pairings; owners can verify current guidance at the English Springer Spaniel Field Trial Association health pages (essfta.org).

Chondrodystrophy and Intervertebral Disc Disease Risk (CDDY)

Chondrodystrophy in English Springer Spaniels is caused by the FGF4 retrogene at high frequency (23.6% carriers, n=749). The classical chondrodystrophy phenotype is shortened limbs and premature calcification of intervertebral disc material. English Springer Spaniels do not express the visible shortened-limb phenotype; the breed standard shows normal leg proportions. What English Springer Spaniels do express is intervertebral disc disease (IVDD) risk. Carriers are at elevated risk for disc herniation, which can cause back pain, neurological signs, and partial or complete paralysis depending on severity and location.

The variant is dominant, meaning a single copy confers risk. Testing is available. Dogs inheriting the variant benefit from weight management, controlled jumping and diving into water (which is common for gun-dog retrievers), and spinal awareness in training and play.

Cystinuria Type I-B (SLC7A9 p.A217T)

Cystinuria Type I-B in English Springer Spaniels is the autosomal-recessive-with-incomplete-penetrance form of cystinuria. The SLC7A9 variant causes excess urinary cystine excretion and predisposes to bladder stones. About 4.4% of English Springer Spaniels in the Donner cohort carry the variant (n=751). Not every carrier with two copies forms stones. Affected dogs are managed with a low-protein diet, increased water intake to dilute urine, and veterinary monitoring.

Degenerative Myelopathy (DM)

Degenerative myelopathy in English Springer Spaniels is a progressive spinal-cord degeneration caused by a recessive variant with incomplete penetrance. Affected dogs develop hind-limb weakness and progressive paralysis, typically in middle to late life. The carrier frequency is 3.4% (n=751). The published evidence on penetrance in this breed is limited. Testing is available and is useful for breeding decisions.

How should I test my English Springer Spaniel?

A breed-specific panel from a CLIA-accredited lab is the high-yield path. The minimum useful set for English Springer Spaniels is the cone-rod dystrophy panel (crd4), FGF4 retrogene (CDDY), SLC7A9 (cystinuria), DM, and vWD1. This covers the variants with the highest carrier frequencies and clinical significance in the breed.

What should I feed an English Springer Spaniel?

Feeding an English Springer Spaniel well means feeding around the breed’s known genetic vulnerabilities and the breed’s working metabolism. English Springer Spaniels were bred as gun-dog retrievers for long days in the field. A pet English Springer Spaniel eating a maintenance kibble in a suburban home is being fed for a job they aren’t doing, which leads to weight gain. The breed’s CDDY-associated IVDD risk is weight-sensitive, making body condition the first lever an owner pulls; hip dysplasia is also reported in the breed at OFA (ofa.org/breeds/results/?breed=ESS), and excess weight worsens both conditions.

Control weight through the whole life cycle. The atlas-derived median lifespan for English Springer Spaniels is 12.7 years. Hip dysplasia is reported in the breed, and the CDDY variant at 23.6% carrier frequency predisposes to intervertebral disc disease. Both conditions worsen with excess weight. A sporting-breed or medium-breed adult formulation with controlled portions is the right starting point. Portion control guided by body condition score is the practical lever; labels overestimate needs for inactive dogs, and most nutritionists suggest starting 10 to 20% below label recommendations for sedentary pets (NRC, Nutrient Requirements of Dogs and Cats, 2006).

Puppy growth matters because the breed grows steadily from birth to adulthood. A puppy formulation with controlled calcium (target 0.8 to 1.5% on a dry-matter basis) and a calcium-to-phosphorus ratio between 1.1:1 and 2:1 minimizes growth-plate stress. The growth rate is slower than in giant breeds, but rapid enough that a high-calcium free-fed puppy diet can predispose to orthopedic disease later.

Joint support is worth calibrating, not guessing. The breed’s CDDY carrier frequency and IVDD risk mean that spinal health is a concrete priority. Omega-3 supplementation from fish oil supports joint and spinal-cord health; dose guidance for a medium-sized adult dog is available from your veterinarian or the NRC 2006 nutrient guidelines. Glucosamine and chondroitin sulfate are widely used in the breed; peer-reviewed evidence for efficacy is mixed, but the compounds are safe and breed-club health committees often recommend them as adjuncts to weight management.

Grain-free diets carry no breed-specific signal in English Springer Spaniels. English Springer Spaniels were not among the breeds flagged in the FDA’s 2018 and 2022 DCM advisories. A grain-free diet is a valid choice for this breed if it meets AAFCO standards, though the FDA investigation remains open and breed-neutral caution is reasonable. The more important decision is calories and portion control.

What we don’t know

The penetrance of cone-rod dystrophy in English Springer Spaniels is incompletely characterized. We know 29.9% of the breed carries the variant. We do not yet have solid data on what fraction of dogs with two copies actually become symptomatic and at what age. Donner 2023 did not report confirmed phenotype data for this variant in the breed, so the published evidence is limited. Breeders and owners who test positive should discuss risk with their vet and the breed-club health committee.

The long-term functional outcome of CDDY carriers in English Springer Spaniels is also not fully resolved. The variant is at 23.6% frequency, but we do not have good prospective data on how many carriers remain asymptomatic for life versus how many develop IVDD. Weight management, activity modulation, and careful spinal awareness appear to reduce risk, but the exact magnitude of that protection is not published.

Cancer epidemiology in English Springer Spaniels is undercharacterized. The breed is not flagged in the peer-reviewed oncology literature the way Goldens and Bernese Mountain Dogs are, but that may reflect lower enrollment in cancer studies rather than lower actual incidence. We do not have breed-club cancer registry data equivalent to what exists for other sporting breeds.

Frequently asked questions about English Springer Spaniels

What is the most common genetic disease in English Springer Spaniels? Cone-rod dystrophy (crd4). 29.9% of English Springer Spaniels carry the variant (Donner 2023, n=750). It is a progressive retinal disease that leads to vision loss and eventual blindness. Not every carrier with two copies becomes symptomatic, but the risk is real for breeding decisions.

Are English Springer Spaniels prone to back problems? Yes. The FGF4 retrogene (CDDY) is present in 23.6% of the breed. Carriers are at elevated risk for intervertebral disc disease (IVDD), which can cause back pain and neurological signs. Weight management and careful activity modulation reduce risk.

Should I do a DNA test on my English Springer Spaniel? For breeding stock, yes. A breed-specific panel covering cone-rod dystrophy, CDDY, cystinuria, degenerative myelopathy, and von Willebrand’s disease Type 1 is a high-yield starting point; verify current breed-club guidance at essfta.org. For pet dogs, testing is useful if you want to know your dog’s carrier status for planning activity and veterinary monitoring.

How long do English Springer Spaniels live? The atlas-derived median lifespan is 12.7 years. Individual dogs vary based on genetics, weight, health screening, and veterinary care.

What is the best diet for an English Springer Spaniel? A sporting-breed or medium-breed formulation with controlled portions and moderate calories. The breed’s IVDD risk and hip dysplasia susceptibility are weight-sensitive, so body condition is the most important dietary lever. Grain-free diets are not contraindicated in this breed the way they are in Goldens.

Are English Springer Spaniels good with kids? Yes. The breed was developed for hunting and retrieving, traits that select for trainability and biddability. English Springer Spaniels are typically social, eager-to-please, and gentle. Individual temperament varies; early socialization and adult supervision with young children are always best practice.

Do English Springer Spaniels need a lot of exercise? Yes. They are gun-dog retrievers bred for full-day work in the field. A pet English Springer Spaniel needs at least an hour of meaningful exercise per day, walking, retrieving, or structured activity, to stay mentally and physically satisfied.

What is the most common health problem in English Springer Spaniels? Hip dysplasia and intervertebral disc disease are among the orthopedic conditions reported in the breed (OFA data available at ofa.org/breeds/results/?breed=ESS). The breed also carries cone-rod dystrophy at high frequency (29.9%), making vision screening worthwhile in breeding dogs and valuable for planning exercise and veterinary monitoring in carriers.

A gift to human medicine

English Springer Spaniels are a natural model for human disease

Because the same genes cause the same conditions across species, the inherited conditions documented in English Springer Spaniels help researchers understand, and work toward treating, the human diseases they model. This is the dog advancing human medicine. The breed models the human disease; it does not have it, and this is not a prediction for your dog.

Human equivalents via OMIA → Mondo / OMIM. Model-of, not identity.
Documented in OMIA

Every condition recorded in the English Springer Spaniel

Beyond the testable carriers above, OMIA's literature catalogue records 19 genetic conditions in the English Springer Spaniel, 15 of which have a known human equivalent. This is the documented landscape across all English Springer Spaniels ever studied, not a prediction for any one dog.

Plus 1 more conditions recorded in the English Springer Spaniel in OMIA.

Online Mendelian Inheritance in Animals (OMIA); Nicholas, Tammen & Sydney Informatics Hub, DOI 10.25910/2AMR-PV70
Documented in the breed's literature is not carrier status and not a forecast for an individual dog. Human equivalents are mapped via Mondo/OMIM. Carrier frequencies (above) are the separately-measured testable subset (Donner 2023).
The data behind this page

Where every number on this page came from.

This page draws on three primary data sources. Carrier frequencies for the Mendelian section come from Donner et al. 2023 (CC-BY-4.0). We grade these data at evidence Limited because the cohort is a direct-to-consumer ascertainment, which biases toward owners who chose to test their dogs. The panel also uses tag-SNP proxies for some variants rather than direct causal-variant assays. Limited is a study-design grade, not a quality grade: the Donner cohort is the largest open canine-genotype dataset in existence and we are grateful for it. We rate the confounding MEDIUM.

Population-genetic dimensions (heterozygosity, intra-breed PCA distance, nearest neighbors, trait-locus frequencies) come from CanVAS (Brundage 2026), harmonized through the Sniff Atlas. The exact release date and verification commit are pinned at the bottom of the page so a researcher can trace a number back to a specific snapshot. The disease-gene-variant graph comes from OMIA (Online Mendelian Inheritance in Animals; Nicholas, Tammen, and the Sydney Informatics Hub at the Sydney School of Veterinary Science, The University of Sydney; retrieved April 2026, DOI 10.25910/2AMR-PV70).

What this page does not yet have. Inheritance modes and per-disease penetrance evidence from Donner 2023 are now in the structured data for every variant the panel covers. Mondo, OMIM, Ensembl, and HGNC cross-references on gene pages remain pending, they arrive in December 2026 alongside the imputed 9.67M-variant CanVAS dataset via the OMIA SQL dump absorption. Until then, gene IDs carry NCBI Gene and OMIA phene URLs only; the wider human-homolog and disease-ontology cross-reference set fills in with that release.

How to cite this page. The computed dimensions on this page are derived from the open Sniff Atlas v1.0.1 (Gehring 2026, doi:10.5281/zenodo.20566358, CC-BY 4.0). Full citation formats including BibTeX, RIS, and CITATION.cff at sniff.world/cite.

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References
  1. Donner J, Freyer J, Davison S, Anderson H, Blades M, Honkanen L, et al. (2023). Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics 19(2):e1010651. doi:10.1371/journal.pgen.1010651
  2. Brundage J, et al. (2026). CanVAS: a harmonized canine variant atlas. bioRxiv. doi:10.64898/2026.04.13.718238
  3. Nicholas, F.W., Tammen, I., & Sydney Informatics Hub. (2026). Online Mendelian Inheritance in Animals (OMIA) [dataset]. The University of Sydney. https://omia.org. doi:10.25910/2AMR-PV70 (retrieved April 2026).
Last updated
Sources: CanVAS (Brundage 2026) · Donner 2023 · OMIA