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Canine Mendelian disease record

Canine Leukocyte Adhesion Deficiency (CLAD), Type III

Canine Leukocyte Adhesion Deficiency (CLAD), Type III. Autosomal recessive. Observed in 1 of 266 breeds tested in the Sniff Atlas, with measured carrier frequencies drawn from 242,658 dogs (Donner 2023). Per-dog phenotype outcome depends on penetrance, modifiers, and environment; the carrier frequencies below describe variant prevalence, not disease incidence.

OMIA identifier
OMIA:001525-9615
Autosomal recessive
Source dataset
Sniff Atlas v1.0.1 / DOI
The human connection

A model of human leukocyte adhesion deficiency 3

This is the canine counterpart of leukocyte adhesion deficiency 3 in people. That makes affected dogs a naturally-occurring model of the human disease, and it is part of why studying dogs moves medicine forward for everyone. It does not mean your dog has the human disease. It means the two share an underlying biology.

In people, the disease is described as: Leukocyte adhesion deficiency type III (LAD-III) is a form of LAD characterized by both severe bacterial infections and a severe bleeding disorder.

In humans it is also called: IADD, LAD-III, lad-III, LAD1V, LAD3.

MONDO:0013016 OMIM 612840

Mapped from OMIA via the human disease's OMIM entry to the Mondo Disease Ontology (Monarch Initiative, CC-BY 4.0). Sniff renders this as a model-of link; the canine disease remains the subject of this page.

About this disease

From OMIA's curated record

Documented in OMIA (Online Mendelian Inheritance in Animals). This describes the disease as recorded in the published literature, not a prediction for any individual dog. As of 2026-06-03.

Clinical features

Key clinical signs include pyrexia, bleeding diathesis, and dental disease (Hugo & Heading, 2014; Boudreaux et al.,2010). Other signs may include joint effusions (Hugo & Heading, 2014), lameness, and infections, such as pododermatitis, deep pyoderma, and cellulitis (Boudreaux et al., 2010). Bleeding diathesis has been noted to occur following injury or surgery (Boudreaux et al., 2010; Hugo and Heading, 2014). Affected dogs have persistent leukocytosis and neutrophilia (Hugo & Heading, 2014; Boudreaux et al., 2010). Assays of haemostasis may yield variable results, including prolonged buccal mucosal bleeding times, normal coagulation screening assays and vWF antigen concentration, and delayed platelet aggregation and clot retraction (Hugo & Heading, 2014; Boudreaux et al., 2010). IT thanks DVM student Mulan Zhong, who provided the basis of this contribution in May 2023.

Molecular genetics

By sequencing a likely candidate gene (based on clinical signs and pathology) in a single German Shepherd Dog that had been euthanased five years previously), Boudreaux et al. (2010) reported that a "12-base pair insertion was identified in the coding region for KINDLIN3 in the affected dog but not in the canine genome sequence or the control dog sequences. This mutation is predicted to result in the insertion of amino acids RRLP within an alpha helix located in the Kindlin-3 pleckstrin-homology domain of the F2 band 4.1, ezrin, radixin, moesin (FERM) subdomain". The KINDLIN3 gene is now known as FERMT3 (fermitin family member 3).

Human analog

OMIA links this condition to its human counterpart in OMIM (Mendelian Inheritance in Man), the place to read across to the deeper human literature for the same biology.

Disease · OMIM 612840 Gene · OMIM 607901

Source: OMIA (Nicholas, Tammen & the Sydney Informatics Hub), entry OMIA:001525-9615, doi:10.25910/2AMR-PV70 (CC-BY 4.0).

Signs & cross-references

How it presents

Catalogued in the Mondo disease ontology (the cross-species disease identity used by the Monarch Initiative) as leukocyte adhesion deficiency 3 (MONDO:0013016).

Phenotype terms: Human Phenotype Ontology + Mammalian Phenotype Ontology; disease terms: Mondo (Monarch Initiative). Cross-references curated by OMIA (doi:10.25910/2AMR-PV70, CC-BY 4.0).

The evidence

Published references

The peer-reviewed papers behind this disease, curated by OMIA. Starred entries are OMIA-designated landmark papers.

  2. Leucocyte adhesion deficiency III in a mixed-breed dog. · Aust Vet J · 2014 · PMID 24954630

References curated by OMIA (Nicholas, Tammen & the Sydney Informatics Hub), doi:10.25910/2AMR-PV70 (CC-BY 4.0). Full list at the OMIA entry.

Predict a litter

Set each parent's status for Canine Leukocyte Adhesion Deficiency (CLAD), Type III and see the odds for their puppies. Single recessive variant, exact Mendelian math.

Parent A
Parent B
NNClear
NmCarrier
NmCarrier
mmAffected
Clear25%
Carrier50%
Affected25%

These are the genetic odds for one known variant, not a promise: a real litter varies around them, and penetrance or other genes can change whether the condition ever appears. Use it to avoid pairing two carriers and to keep a line healthy, not to engineer a dog. Inheritance mode per OMIA.
Your breed

See what Canine Leukocyte Adhesion Deficiency (CLAD), Type III looks like in your dog's breed.
Carrier frequency by breed

Top 1 well-sampled breeds (n ≥ 50)

Maximum per breed across variants in the Donner 2023 cohort, with . The list below is split into well-sampled breeds (n ≥ 50 tested) and small-sample breeds (n < 50, where the Wilson CI typically spans more than 20 percentage points and frequencies should not be compared directly to the well-sampled entries). Frequencies are population-level, not per-litter or per-line.

0%1%2%
German Shepherd0.22% · n 15,648
n = 15,648 dogs · Donner et al. 2023 carrier-screening cohort · Sniff Atlas
Each bar is one well-sampled breed; the whisker is its Wilson 95% CI, and fainter bars have wider intervals. Frequencies are population-level, not per-litter. Carrier status for Canine Leukocyte Adhesion Deficiency (CLAD), Type III is measured; phenotype outcome depends on penetrance and modifiers.
▸ Full table with Wilson 95% confidence intervals
Breed Carrier frequency n tested
German Shepherd 0.22% 15,648

265 additional breeds in the Donner 2023 cohort were tested but showed no carriers.

Penetrance

From genotype to phenotype

Carrier status is not the same as disease status. Penetrance is the fraction of at-risk dogs that develop the phenotype. The Donner 2023 S4 table tracks this for 1 variant(s) underlying this disease in the cohort.

At-risk dogs evaluated
3
Phenotype confirmed
3
Penetrance range
not yet quantifiable

Fewer than 20 at-risk dogs evaluated; too few to state a penetrance figure.

Predicted disease relevance at the per-dog level is UNPROVEN. The carrier frequency is measured; phenotype outcome is governed by penetrance, environment, and modifier loci. Consult a veterinarian for clinical interpretation.

How to cite this record

Citations

If you use this record in published work, cite the Sniff Atlas (the published dataset that carries the breed-level carrier frequencies) and the upstream sources:

  • Sniff Atlas v1.0.1 for the per-breed carrier frequencies:

    Gehring, M. (2026). Sniff Atlas v1.0.1. Zenodo. https://doi.org/10.5281/zenodo.20566358. CC-BY 4.0.

  • OMIA for the disease definition, inheritance, and gene assignment:

    Nicholas, F. W., & Tammen, I. (2024). OMIA. Sydney Informatics Hub, The University of Sydney. https://doi.org/10.25910/2AMR-PV70. Entry: OMIA:001525-9615.

  • Donner et al. 2023 for the breed × variant carrier-frequency cohort:

    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. https://doi.org/10.1371/journal.pgen.1010651.

Full citation formats (BibTeX, RIS, CITATION.cff) at sniff.world/cite.

Related

Related

Last updated
Sources: Sniff Atlas v1.0.1 · OMIA OMIA:001525-9615 · Donner et al. 2023