Researchers at the Veterinary Genetics Laboratory of the University of California, Davis, Veterinary School have identified the gene mutation responsible for the skin disease HERDA, hereditary equine regional dermal asthenia. Horses with HERDA have an inability to resist skin tearing or heal normally because of defective connective tissue production or orientation in the junction between the deep and upper layers of skin.
The Davis studies have traced this to a mutation in a gene that codes for cyclophilin B. Cyclophilin B is a protein critical in the early stages of connective tissue collagen formation. It is primarily a problem in Quarter Horse bloodlines.
In HERDA, the horses appear normal at birth, and skin biopsies can’t distinguish between a young horse with HERDA and a normal one. By the age of 2, they usually start to develop lesions along the skin of their back. This coincides with introduction to saddles. Something as simple as a longeing surcingle could start the process. The point of the hock is another fairly common area for the lesions to show up. In both cases, trauma, pressure or friction are what start the process. These lesions break open to leave large open wounds that eventually heal by granulation and leave extensive scars.
Once healed, old HERDA lesions don’t cause any pain, but most afflicted horses are destroyed because they can’t be used for riding and shouldn’t be used for breeding since they will pass on the gene to 100% of their offspring.
Mares and stallions are equally involved in transmitting HERDA. HERDA is a recessive trait, which means that a parent carrying only one gene for the disease won’t have symptoms but will pass the gene on to 50% of the foals. If both dam and sire are apparently normal but carrying the gene, there is a 25% chance of producing a completely normal foal (not a carrier), 50% will be carriers and 25% will actually have the disease. Now that the gene has been identified, breeders can test mares and stallions to exclude carriers from their breeding program.
