DNA panel specific for the Devon Rex that combines genetic blood group determination with screening for congenital myasthenic syndrome (CMS) and two aesthetic traits: hair length and the wavy or hairless coat characteristic of the Devon Rex and the Sphynx. CMS is a serious inherited neuromuscular disease, although uncommon; the hair variants allow the coat of the litters to be predicted. It is performed from a buccal swab or blood. It is a key tool for the health and morphological planning of the breed.

CMS is now uncommon in the breed thanks to genetic control. A notable frequency of group B has been described in Rex-type breeds, reinforcing the value of its determination. The hair variants are distributed across numerous breeds with frequencies depending on each programme.

- CMS: generalised muscle weakness, exercise intolerance that improves with rest, and risk of aspiration pneumonia in the most severely affected kittens\n- Neonatal isoerythrolysis due to blood group incompatibility\n- Hair length and wavy or hairless coat: purely aesthetic phenotypic traits

The Devon Rex arose in the United Kingdom in the 1960s from a cat with a wavy coat, and its characteristic coat was later associated with variants of the KRT71 gene, shared in its allelic series with the Sphynx. Congenital myasthenic syndrome was described in the breed as an inherited neuromuscular condition and was later associated molecularly with a variant of the COLQ gene, which enabled a DNA test. Determination of hair length is based on variants of the FGF5 gene. The AB blood group system was deciphered in 2007 with the identification of the CMAH gene.

- Never mate two CMS carriers: expectably 25% of the litter would be affected\n- CMS carriers can be mated with clear animals and gradually withdrawn, to preserve the breed's limited genetic base\n- Determine the blood group of the breeding animals: prevent group A kittens from being born to group B mothers or prevent their access to colostrum during the first 16-24 hours\n- Use the KRT71 and FGF5 results to plan the coat of the litters without health implications

CMS must be differentiated from acquired myasthenia gravis (with detectable anti-acetylcholine receptor antibodies) and from other congenital myopathies. In COLQ CMS, acetylcholinesterase inhibitors may be ineffective or aggravate weakness (worsening on the neostigmine test is a diagnostic clue), so they are not the treatment of choice; management relies on β2 agonists and 3,4-diaminopyridine, according to experience in human COLQ CMS. Cats with recurrent weakness require neurological assessment. The genetic blood group predicts the b allele, but cross-matching is recommended before transfusions.

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2. Abitbol M et al. 2015. A COLQ missense mutation in Sphynx and Devon Rex cats with congenital myasthenic syndrome. PLoS One. PMID: 26327126
3. Gandolfi B et al. 2015. COLQ variant associated with Devon Rex and Sphynx feline hereditary myopathy. Anim Genet. PMID: 26374066
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7. Kehler JS et al. 2007. Four independent mutations in the feline fibroblast growth factor 5 gene determine the long-haired phenotype in domestic cats. J Hered. PMID: 17767004
OMIA:001583-9685 (SPH, KRT71); OMIA:001581-9685 (DRX, KRT71); OMIA:000684-9685 (miastenia/SMC); OMIA:000119-9685 (grupo sanguíneo AB).