Panel of five hereditary equine diseases with molecular testing, applicable to stock breeds and to horses with Quarter Horse ancestry. It brings together glycogen branching enzyme deficiency (GBED), hereditary equine regional dermal asthenia (HERDA), hyperkalaemic periodic paralysis (HYPP), type 1 polysaccharide storage myopathy (PSSM1) and equine malignant hyperthermia (EMH). GBED and HERDA are recessive and lethal or severely debilitating in homozygosity; HYPP, PSSM1 and EMH are dominant with incomplete penetrance and present with muscular episodes. Each test reports the clear, carrier or affected genotype and allows matings to be planned. The panel does not replace clinical examination or biopsy when the clinical picture does not fit.

Applicable to stock breeds and to horses with Quarter Horse ancestry. GBED, HERDA, HYPP, PSSM1 and EMH are documented in those populations; frequencies depend on the line and are not consolidated (limited data).

The signs depend on the condition:\n- GBED: abortions and stillbirths, weak foals with hypoglycaemia, tremors, seizures, contractures and neonatal death.\n- HERDA: hyperextensible and fragile skin, with tears and seromas on the back and withers when training begins.\n- HYPP: episodes of tremors, sudden weakness, prolapse of the nictitating membrane, sweating and recumbency, triggered by dietary potassium, fasting, stress, transport or anaesthesia.\n- PSSM1: stiffness and muscle pain (tying-up), dark urine and elevation of CK/AST, especially after rest and resumption of exercise.\n- EMH: rapid hyperthermia, tachycardia, stiffness, acidosis and rhabdomyolysis during anaesthesia or in response to stress/intense exercise.

GBED was characterised in the early 2000s and its mutation in GBE1 was identified in 2004. HERDA was recognised in cutting lines and its mutation in PPIB was described in 2007. HYPP was recognised in the 1980s in halter lines linked to the stallion Impressive and was linked to SCN4A in the 1990s. PSSM1 was defined in the 1990s and its mutation in GYS1 (R309H) was identified in 2008. EMH was described in the horse in the early 2000s and in 2004 the RYR1 C7360G variant was identified; its coexistence with PSSM1 was later confirmed.

Genotype breeding animals before mating, especially in stock lines or those with ancestry from the stallion Impressive.\n- Recessive (GBED, HERDA): do not cross carrier with carrier (25 % affected); carrier with clear produces 50 % carriers and no affected animals.\n- Dominant (HYPP, PSSM1, EMH): every carrier transmits the allele to 50 % of the offspring; breed preferentially with N/N and avoid carrier x carrier because of the 25 % more severely affected homozygotes. Deliberate breeding of HYPP H/H foals is incompatible with welfare.\n- Do not breed affected animals.\n- Communicate the status to the veterinarian before anaesthetising, castrating or transporting and to the buyer; monitor lines with a history of tying-up or anaesthetic reactions.

Equine rhabdomyolysis has multiple causes: PSSM1, PSSM2, atypical myopathy due to hypoglycin A, HYPP and infectious, traumatic or nutritional causes. The coexistence of PSSM1 and EMH (or HYPP) aggravates the muscular picture. In the face of an anaesthetic reaction, EMH must be considered, but also heat stroke, sepsis and anaphylaxis; in at-risk animals, use non-triggering agents and have dantrolene available. A negative test does not rule out myopathy of another origin. The skin fragility of HERDA can be confused with photosensitisation or deep pyodermas.

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