Panel of five hereditary equine diseases with a molecular test available, intended for Quarab breed breeders (a cross of Quarter Horse and Arabian). It brings together conditions from the two founding breeds: cerebellar abiotrophy (CA) and severe combined immunodeficiency (SCID), specific to the Arabian horse, and glycogen branching enzyme deficiency (GBED), hereditary equine regional dermal asthenia (HERDA) and type 1 polysaccharide storage myopathy (PSSM1), described in the Quarter Horse and derived breeds. Each test reports clear, carrier or affected status and allows breeding to be planned while avoiding affected offspring. There are no frequency studies specific to the Quarab: applicability is inferred from the founding breeds (limited data). The panel does not replace clinical examination or veterinary advice.

Applicable breed: Quarab. Panel of 5 hereditary equine diseases with a molecular test available.

Signs depend on the condition and may appear alone or in combination in the offspring of a risk mating:
- CA: cerebellar ataxia, hypermetria and intention tremor from the first weeks or months, with general condition preserved.
- GBED: abortions and stillbirths, weak foals with hypoglycaemia, tremors, seizures, contractures and neonatal death.
- HERDA: hyperextensible and fragile skin, with tears and seromas on the back and withers when training begins (18-24 months).
- PSSM1: stiffness and muscle pain (tying-up), dark urine, elevated CK/AST and poor performance, especially after rest and resumption of exercise.
- SCID: severe and recurrent infections (diarrhoea, pneumonia) from 2-8 weeks of age, lymphopenia and death in the first months.

The five tests were developed independently. Arabian cerebellar abiotrophy has been known for decades; in 2011 it was mapped to ECA2 and a candidate variant in TOE1/MUTYH was proposed, still not confirmed as causal. SCID of the Arabian foal was described in the 1970s and in the 1990s the DNA repair defect (DNA-PK, PRKDC gene) was identified. GBED was characterised in the early 2000s in Quarter Horse foals and its mutation in GBE1 was identified in 2004. HERDA was recognised in cutting lines and its mutation in PPIB was described in 2007. PSSM1 was defined in the 1990s and its mutation in GYS1 (R309H) was identified in 2008. Systematic carrier screening has reduced the incidence of GBED, HERDA and SCID.

Genotype all breeding animals before the breeding season and classify them as clear, carrier or affected.
- Recessive conditions (CA, GBED, HERDA, SCID): do not mate carrier with carrier (25 % affected offspring); carrier with clear produces 50 % carriers and no affected animals, and allows valuable lines to be preserved by selecting clear offspring.
- PSSM1 (dominant): every carrier transmits the allele to 50 % of the offspring; preferably breed with N/N and avoid the P1 x P1 mating because of the 25 % risk of more severely affected homozygotes.
- Do not breed affected animals (GBED, HERDA and SCID are incompatible with breeding; CA has no treatment).
- Record results and communicate the status to the buyer and the veterinarian; monitor lineages with recurrent cases.

The panel covers five variants, but not all equine myopathies or ataxias. Foal ataxia includes traumatic, compressive, infectious (EPM) and toxic causes, in addition to lavender foal syndrome; the definitive diagnosis of CA is neuropathological. PSSM1 does not exclude PSSM2 or atypical myopathy due to hypoglycin A. In a foal with recurrent infections, failure of colostrum transfer (IgG in the first 24 h) must first be ruled out before attributing it to SCID. The skin fragility of HERDA can be confused with photosensitisation or deep pyodermas. The PSSM1 test does not replace biopsy when the clinical picture does not fit.

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