Cairn Terrier
Cairn Terriers have a cited life expectancy of 14 years (McMillan 2024 / VetCompass, n=2,585, 95% CI 13.8 to 14.3). The most carried tested variant is Macrothrombocytopenia, in 19% of 183 Cairn Terriers tested (Donner 2023), then Craniomandibular Osteopathy (7.7%) and Von Willebrand's Disease, Type 1 (5.7%).
What genetic diseases do Cairn Terriers carry?
From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Cairn Terriers carry 7 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.
SLC37A2what this gene does
SLC37A2 is a gene involved in how cells manage certain sugar molecules, which can affect bone development.
For your dog: If your dog is from a breed known to carry this gene variant, it's worth discussing with your vet, especially if you notice jaw discomfort or eating issues.
TUBB1what this gene does
TUBB1 is a gene that helps make the building blocks of platelets, which are tiny blood cells important for clotting. It plays a key role in keeping platelet size and number normal.
For your dog: If your dog is from one of the breeds known to carry TUBB1 variants, it’s worth mentioning to your vet, especially before surgeries or if you notice unusual bleeding.
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.
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.
BEST1what this gene does
BEST1 is a gene that helps maintain the health of the retina, the light-sensitive layer at the back of the eye. It plays a role in keeping the cells in the retina functioning properly.
For your dog: If your dog is from a breed known to carry BEST1 variants, it’s worth discussing retinal health with your vet, especially if you notice any vision changes.
What these results mean for a Cairn Terrier
2.7% of Cairn Terriers in the Donner 2023 cohort carried it (n=183).
- DM is a loss of function in the spinal cord that begins in adulthood and progresses to paralysis of the back legs. There is no treatment that stops it.
OMIA 000263-9615
“This is an adult onset degeneration of the spinal cord that progresses to paraplegia and tetraparesis. There is no successful treatment. A genetic test is available.” OMIA 000263-9615
- Two copies of the SOD1 variant mean at risk, not affected. Some dogs with two copies never show signs.
OMIA 000263-9615
“some homozygous mutant dogs had no signs of degenerative myelopathy, which suggests incomplete penetrance or other causative loci” OMIA 000263-9615
- One copy makes a dog a carrier. In the study that found the variant, every affected dog tested had two copies.
OMIA 000263-9615
“All affected dogs tested were homozygous mutant.” OMIA 000263-9615
What to do
A DNA result is not a diagnosis. Take the result, and any change in how the dog walks, to a veterinarian.
No test, or a mix
Without a test nobody can say how many copies a dog has. A breed's carrier frequency describes the breed, not this dog.
SLC7A9 p.A217T (sold as a cystinuria test)
Marker disputed1.9% of Cairn Terriers in the Donner 2023 cohort carried it (n=183).
- The curated record finds no support for this variant causing cystinuria, and the researchers who studied it advise against using it as a test.
OMIA 001880-9615
“there appears to be no support for the variant to be causal” OMIA 001880-9615
“strongly recommend not to use "the variant in SLC7A9 as a test to predict the risk of developing cystinuria in male English bulldogs.” OMIA 001880-9615
What to do
A carrier result for this variant does not predict bladder stones. Straining to urinate or blood in the urine is a reason to see a veterinarian whatever a DNA test says.
No test, or a mix
The curated record gives no reason to test for this variant.
Identified as Cairn Terrier (VBO:0200267) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 4 · iDog 60 · VeNom 14993.
For researchers Population genetics, disease models and every recorded condition Open the research detail for the Cairn Terrier
In the atlas, the Cairn Terrier clusters consistently as Cairn Terrier (100% of the 120 dogs here).
High breed predictability score (1.15), individual dogs of this breed reliably cluster together genetically.
What the atlas genotypes say about Cairn Terrier
Computed from the 14,478 CanVAS dogs in the Atlas, on an imputed genotype backbone: 77,215 directly typed sites per dog, imputed to 9.67 million variants.
The confidence below counts dogs, not reads: it is the size of the sample, and it is separate from how the genotypes were measured.
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.
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.
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.
Cairn Terriers are a natural model for human cancer.
Some cancers appear in Cairn Terriers and in people driven by the same somatically-altered genes, cohort by cohort and cited on both sides. That makes this breed part of how we understand, and one day treat, the human disease. This is not a prediction about your dog, it is a window into the biology we share.
Cairn Terriers are a natural model for human disease
Because the same genes cause the same conditions across species, the inherited conditions documented in Cairn Terriers 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.
- hemophilia B, modeled by the breed's Haemophilia B via F9, the same underlying biology.
- Krabbe disease, modeled by the breed's Krabbe disease via GALC, the same underlying biology.
- OMIM:164980, modeled by the breed's Chondrodysplasia, FGF4 retrogene-related , the same underlying biology.
- Caffey disease, modeled by the breed's Craniomandibular osteopathy, generic , the same underlying biology.
- OMIM:619136, modeled by the breed's Craniomandibular osteopathy, SLC37A2-related , the same underlying biology.
- OMIM:600803, modeled by the breed's Gallbladder mucoceles , the same underlying biology.
Every condition recorded in the Cairn Terrier
Beyond the testable carriers above, OMIA's literature catalogue records 12 genetic conditions in the Cairn Terrier, 11 of which have a known human equivalent. This is the documented landscape across all Cairn Terriers ever studied, not a prediction for any one dog.
- Haemophilia B X-linked recessiveHuman equivalent: hemophilia B
- Krabbe disease Autosomal recessiveHuman equivalent: Krabbe disease
- Chondrodysplasia, FGF4 retrogene-related AutosomalHuman equivalent: OMIM:164980
- Craniomandibular osteopathy, generic MultifactorialHuman equivalent: Caffey disease
- Craniomandibular osteopathy, SLC37A2-related Autosomal dominant with incomplete penetranceHuman equivalent: OMIM:619136
- Human equivalent: OMIM:600803
- Ocular melanosis Autosomal dominantHuman equivalent: OMIM:600510
- Polycystic kidney disease Autosomal dominantHuman equivalent: polycystic kidney disease 1
- Pyruvate kinase deficiency of erythrocyte Autosomal recessiveHuman equivalent: pyruvate kinase deficiency of red cells
- Human equivalent: OMIM:248250
- Thrombocytopenia, TUBB1-related Autosomal recessiveHuman equivalent: macrothrombocytopenia, isolated, 1, autosomal dominant
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 in the structured data for every variant the panel covers. Mondo, OMIM, Ensembl, and HGNC cross-references live on the gene and disease pages this page links to, rather than being repeated here. What is still absent from this breed page is anything not in the cited panel, and each such gap carries its cause where it appears.
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.
Some things about living with a cairn terrier never make it into a database. Add what you know as a Keeper, in your words →
Lived experience, kept beside the science.We have 120 cairn terriers. We do not have yours.
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- 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
- Brundage DM (2026). CanVAS: A Harmonized and Imputed Canine Variant Atlas. bioRxiv. doi:10.64898/2026.04.13.718238
- 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).