--- license: permission_granted topic_id: companion_breed_health_greyhound_omia1191_dog category: companion-breed-health title: "Greyhound — Malignant hyperthermia (hereditary; OMIA-verified breed predisposition)" lang: en source: "OMIA (Online Mendelian Inheritance in Animals, University of Sydney) breed-specific hereditary-disorder record, saved verbatim to source_file; C1 substring-verified. Pulled 2026-08-02 from local OMIA database dump." source_file: pdf-raw/breed-health/greyhound_omia1191_1191.txt date_parsed: 2026-08-02 tokens_estimated: 845 verification: method: substring_match claims: 9 passed: 9 date: 2026-08-02 recovered: false path: companion-breed-health/companion_breed_health_greyhound_omia1191_dog/01_companion_breed_health_greyhound_omia1191_dog.md source_document: "OMIA — Online Mendelian Inheritance in Animals (University of Sydney)" citation: authority: "OMIA — Online Mendelian Inheritance in Animals (University of Sydney)" title: "Greyhound — Malignant hyperthermia (hereditary; OMIA-verified breed predisposition)" url: "https://omia.org/OMIA000621/9615/" retrieved: "2026-08-02" ref: "OMIA breed-specific hereditary-disorder records (omia.org), derived from local OMIA database dump; dataset: https://doi.org/10.25910/2AMR-PV70" doc_type: "academic animal-genetics database (breed-specific disorder entries)" needs_review: false
Greyhound — Malignant hyperthermia (hereditary; OMIA-verified breed predisposition)
Source: first-hand OMIA (University of Sydney) breed-specific hereditary-disorder record, saved verbatim to source_file; every claim below is a C1 byte-substring of it.
Claims
Breed: Greyhound (Dog)Disorder:Mode of inheritance: Autosomal dominantSummary: Malignant hyperthermia is a disorder of skeletal muscle characterized by hypercapnea, tachycardia, and hyperthermia in response to a chemical trigger, and can be fatal. It is an autosomal dominant trait caused by a mutation in the skeletal muscle ryanodine receptor. The omia.variant:54 variant has been identified in several breeds. Affected dogs show no clinical signs until exposed to chemical triggers, which are common anesthetic agents. Edited by Vicki N. Meyers-Wallen, VMD, PhD, Dipl. ACTClin feat: MH is a pharmacogenetic clinical syndrome that affects multiple species. Dogs with malignant hyperthermia present as an outwardly healthy dog, but develop hypercapnea, tachycardia, and hyperthermia during general anesthesia. Signs can progress to cardiac dysrhythmia, rhabdomyolysis, renal failure, and death if the anesthetic is not discontinued. Common triggers of clinical signs include volatile inhalants (halothane, isoflurane, desflurane and sevoflurane) and depolarizing muscle relaxants such as succinylcholine (Roberts et al., 2001, Brunson and Hogan, 2004). Treatment involves cessation of the causative anesthetic, supportive care, cooling, and dantrolene administration. Dantrolene is a muscle relaxant that blocks calcium release inside myocytes (Brunson and Hogan, 2004). Unlike affected humans or pigs (Nelson et al., 2002), affected dogs develop signs primarily in response to chemical triggers and exhibit less severe metabolic acidosis and muscle rigidity during a clinical episode (Roberts et al., 2001). Alternative anesthetic protocols for affected dogs can include nitrous oxide, benzodiazepines, phenothiazines, barbiturates, etomidate, propofol, dissociative agents, opioids, nondepolarizing neuromuscular blockers, or a combination of intravenous and local or regional anesthesia. Sufficient premedication is important, since stress can be a contributing factor to development of clinical signs (Brunson and Hogan, 2004). [IT thanks DVM student Jianjian Gong for suggested changes in April 2022]Defect: yesPathology: A missense mutation in the RYR1 gene causes the function alteration in the ryanodine receptors (a part of the calcium releasing channel in skeletal muscle) in affected dogs and leads to defects in the calcium release channel located in the sarcoplasmic reticulum (Roberts et al., 2001). The calcium channels present prolonged opening when being stimulated by the triggering factors (such as certain general anaesthesia agents). This increases muscle contraction and muscle metabolism, resulting in hyperthermia (Brunson and Hogan, 2004), and eventually can lead to a life-threatening hypermetabolic state (the MH episodes). [IT thanks DVM student Jianjian Gong for suggested changes in April 2022]Prevalence: Although prevalence is thought to be low, it is difficult to estimate because affected dogs appear normal unless they are exposed to a trigger, and some may die before diagnosis is achieved.Control: Relatives of affected dogs should be tested. Breeding of affected dogs is discouraged. Because dogs with this mutation are often not identified before undergoing anesthesia, it is recommended that dantrolene be stocked in the surgical suite.
Associated gene(s)
Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.
- Gene: Entrez Gene ID 3538631 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene
- OMIA molecular-genetics note: By cloning and sequencing a very likely comparative candidate gene (based on the known molecular cause of the same disorder in pigs and humans, and reinforced by showing the candidate gene to be very tightly linked to MHS in dogs), Roberts et al. (2001) identified the causative mutation as a T to C substitution (omia.variant:54) that changes an amino acid codon from valine to alanine (V547A) in a …
Evidence (references)
Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.
- 1990. Canine stress syndrome malignant hyperthermia susceptibility - calcium-homeostasis defect in muscle and lymphocytes. Res Vet Sci — PubMed:PMID2300706 — OMIA Phene_Article / Article
- 1992. Evaluation of Greyhound susceptibility to malignant hyperthermia using halothane-succinylcholine anesthesia and caffeine-halothane muscle contractures. Lab Anim Sci — PubMed:PMID1460848 — OMIA Phene_Article / Article
- 1997. Malignant hyperthermia-like reaction secondary to ingestion of hops in five dogs. J Am Vet Med Assoc — PubMed:PMID8977648 — OMIA Phene_Article / Article
- 1997. Changes in ryanodine-induced contractures by stimulus frequency in malignant hyperthermia susceptible and malignant hyperthermia nonsusceptible dog skeletal muscle. Journal of Pharmacology & Experimental Therapeutics — OMIA Phene_Article / Article
- 1998. Activation of the cardiac calcium release channel (ryanodine receptor) by poly-s-nitrosylation. Science — PubMed:PMID9422697 — OMIA Phene_Article / Article
- 2001. Autosomal dominant canine malignant hyperthermia is caused by a mutation in the gene encoding the skeletal muscle calcium release channel (RYR1). Anesthesiology — PubMed:PMID11575546 — OMIA Phene_Article / Article
- 2004. Malignant hyperthermia: a syndrome not a disease. Vet Clin North Am Small Anim Pract — PubMed:PMID15474681 | DOI:10.1016/j.cvsm.2004.05.010 — OMIA Phene_Article / Article
- 2002. Malignant hyperthermia: a pharmacogenetic disease of Ca++ regulating proteins. Curr Mol Med — PubMed:PMID12108947 — OMIA Phene_Article / Article
- 1973. Letter: Malignant hyperthermia in the dog. Anesthesiology — PubMed:PMID4758363 — OMIA Phene_Article / Article
- 1978. Malignant hyperthermia in a Greyhound. J Am Vet Med Assoc — PubMed:PMID624662 — OMIA Phene_Article / Article
- 1978. Malignant hyperthermia in a greyhound. J Am Vet Med Assoc — PubMed:PMID659305 — OMIA Phene_Article / Article
- 1983. Recurrent malignant hyperthermia in a Greyhound. J Am Vet Med Assoc — PubMed:PMID6833093 — OMIA Phene_Article / Article
- (20 additional references in OMIA)
Comparative medicine (human OMIM)
Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.
- OMIM:145600 (type: trait) — OMIA Group_OMIM (via OMIA_ID)
- OMIM:180901 (type: gene) — OMIA Group_OMIM (via OMIA_ID)
verification_derived: method: derived_from_dataset source: "OMIA database dump (omia.xml, local); fields Gene/Variant/Article/OMIM" note: "Structured fields (gene, variant rsID/protein change, PubMed/DOI references, OMIM cross-link) extracted from OMIA dump and presented with first-hand values; not verbatim prose."