Bit & Bridle

Equine Hyperelastosis Cutis (HERDA)

Other Names

  • Hereditary Equine Regional Dermal Asthenia (HERDA)
  • Hyperelastosis Cutis (HC)
  • Cutaneous asthenia

What is HERDA?

Hereditary Equine Regional Dermal Asthenia (HERDA), also known as Hyperelastosis Cutis (HC), is a severe inherited skin disease affecting primarily American Quarter Horses and closely related breeds including American Paint Horses and Appaloosas. The condition is characterised by an abnormal deficiency in collagen — the structural protein that gives skin its strength and integrity — resulting in skin that is extraordinarily fragile, hyperextensible (excessively stretchy), and unable to heal normally.

HERDA is often described as one of the most distressing genetic conditions in horses because affected animals develop severe, painful skin lesions under routine conditions — simply from wearing a saddle or being ridden. The skin tears and seromas (fluid-filled pockets) form beneath the skin surface, particularly over the back and saddle region. These lesions fail to heal properly, forming fragile scar tissue that breaks down repeatedly.

The disease is inherited as an autosomal recessive trait, meaning two copies of the faulty gene must be inherited — one from each parent — for a horse to be clinically affected. Carriers (horses with one copy) appear entirely normal.

Causes

HERDA is caused by a missense mutation in the PPIB gene (encoding cyclophilin B), which disrupts the normal function of cyclophilin B — a protein involved in the post-translational processing and folding of collagen molecules. Without properly formed collagen, the dermal layer of the skin (the dermis) lacks structural integrity and mechanical strength.

The result is a skin that:

  • Separates easily at the dermo-epidermal junction (the boundary between the outer and inner skin layers)
  • Tears with minimal trauma — even the pressure of a saddle pad or girth
  • Heals abnormally, forming thin, fragile scar tissue prone to re-tearing
  • Is hyperextensible — it can be stretched to an abnormal degree before returning to normal position

The mutation has been identified in the Quarter Horse gene pool with a carrier frequency estimated at around 3.5% in the general population, and considerably higher in certain bloodlines — particularly those descending from the influential cutting horse sire Poco Bueno, though the mutation predates him.

Symptoms and Signs

  • Skin lesions over the back and withers: The most characteristic manifestation. Seromas, open sores, lacerations, and wounds appear in the saddle area — sometimes with minimal or no apparent trauma. Wounds may look disproportionately severe relative to the apparent cause.
  • Hyperextensible skin: The skin can be stretched far beyond what is normal, and when released, returns slowly and incompletely to its original position. This is most easily assessed on the neck or shoulder.
  • Seromas: Fluid-filled pockets beneath the skin surface, particularly along the back.
  • Scarring: Accumulation of thin, fragile scar tissue over time, particularly in areas subject to repeated trauma.
  • Delayed wound healing: All wounds heal poorly and slowly. Even minor cuts or abrasions may take weeks to close.
  • Secondary infections: Open lesions are vulnerable to bacterial infection, adding to the horse’s discomfort.

Signs are rarely apparent at birth or in very young foals. They typically become visible when the horse begins training, usually at 1.5–2 years of age, when a saddle is first used. This makes it a particularly heartbreaking discovery for owners who have invested significantly in the horse’s early development.

Diagnosis

  • Genetic testing: Definitive diagnosis is made through a DNA test detecting the PPIB mutation. Testing requires a blood sample or mane/tail hair with intact follicles. Results identify horses as normal (N/N), carrier (N/HRD), or affected (HRD/HRD). This test is offered by the UC Davis Veterinary Genetics Laboratory and other equine genetic testing services.
  • Clinical signs: The characteristic pattern of skin fragility, hyperextensibility, and back lesions in a young Quarter Horse or related breed is strongly suggestive.
  • Skin biopsy: Histopathological examination of skin biopsies reveals characteristic changes in collagen fibre organisation and density, supporting the diagnosis.
  • The American Quarter Horse Association (AQHA) 5-panel genetic test: HERDA is included in the mandatory 5-panel test required for all AQHA breeding stallions. This test screens for HERDA, GBED, HYPP, MH, and PSSM simultaneously.

Treatment

There is no cure for HERDA. All treatment is palliative and supportive:

  • Wound management: Meticulous care of open lesions including regular cleaning, appropriate dressings, and topical antimicrobials to prevent secondary infection. Wounds should be protected from flies and further trauma.
  • Environmental management: Affected horses should be kept away from rough surfaces, sharp objects, and other horses that may cause fighting injuries. Shade from direct sunlight is important, as UV light worsens skin fragility.
  • No riding or saddle work: Any saddle or tack work is contraindicated in affected horses, as saddle pressure invariably causes devastating skin damage. HERDA horses cannot be ridden safely.
  • Fly control: Flies feeding on open wounds worsen lesions and introduce infection. Comprehensive fly control measures are essential.
  • Pain management: NSAIDs may help manage discomfort during acute lesion flare-ups.
  • Nutritional support: Adequate protein and micronutrients support skin health to the extent possible. Supplementation with biotin and omega-3 fatty acids may be beneficial, though evidence specifically in HERDA horses is limited.

Most affected horses are humanely euthanised, either shortly after diagnosis or once quality of life deteriorates. A small number of mildly affected horses live for years as pasture companions with intensive ongoing management.

Prevention

  • Test all Quarter Horses, Paint Horses, and Appaloosas intended for breeding using the HERDA genetic test before making breeding decisions.
  • Never breed two carrier (N/HRD) horses together — this creates a 25% risk of producing affected offspring with each foal.
  • Carriers can be bred to genetically normal (N/N) horses without risk of producing affected foals — though 50% of offspring will be carriers.
  • Request genetic testing certificates from sellers when purchasing breeding stock — particularly when buying young horses that may not yet have been under saddle.
  • The AQHA’s mandatory 5-panel stallion testing programme has helped reduce the prevalence of this and other genetic diseases, but the mutation remains present in the population.

Prognosis

The prognosis for HERDA-affected horses is very poor. The condition is progressive in the sense that repeated trauma causes cumulative skin damage and scarring. There is no effective treatment that halts the underlying defect. Most affected horses are euthanised within a few years of diagnosis, and virtually none can be used for ridden work. Early genetic identification before training begins allows owners and breeders to make informed decisions and avoid investing time and resources in training horses that cannot be ridden.

When to Call the Vet

If a young Quarter Horse or related breed develops unexplained skin lesions over the back or saddle area — particularly if wounds appear disproportionately severe, fail to heal, or recur repeatedly — contact your veterinarian for assessment. Skin that appears unusually stretchy or elastic is another red flag. Request a HERDA genetic test if you are buying a young horse of relevant breeding or if you are planning to breed a mare or stallion of Quarter Horse, Paint Horse, or Appaloosa breeding. For related reading, see our entry on Equine Exertional Myopathies and the American Quarter Horse breed profile. The British Equine Veterinary Association can assist in sourcing specialist dermatology expertise.

Frequently Asked Questions

Can a HERDA horse be ridden at all?

No. Riding a HERDA-affected horse is not safe or humane. Saddle and girth pressure causes the skin to separate, blister, and tear — even at walk. The damage compounds with each ride. Any form of back-loading work, including driving harness work, is similarly contraindicated. HERDA horses can only live safely as unridden companion animals.

How do I know if my horse is a HERDA carrier?

Carriers are clinically indistinguishable from normal horses — they have no skin fragility or other signs of the disease. The only way to identify a carrier is through genetic testing. A simple blood test or hair sample with follicles (30–40 hairs) sent to an equine genetics laboratory will provide a definitive result. This is a routine, affordable test that all breeders of relevant breeds should consider.

Is HERDA the same as Ehlers-Danlos syndrome?

HERDA shares similarities with Ehlers-Danlos syndrome (EDS) in humans — both involve defective collagen leading to skin fragility and hyperextensibility. However, they are caused by different genetic mutations and are not the same condition. The mechanisms overlap in concept (collagen structural defects) but differ in the specific protein affected and the clinical manifestations.

Does HERDA affect all Quarter Horses?

No. HERDA is a recessive condition and most Quarter Horses are either normal (N/N) or carriers (N/HRD) with no clinical signs. Only horses inheriting two copies (HRD/HRD) develop the disease. The carrier frequency in the general Quarter Horse population is estimated at around 3.5%, with some bloodlines carrying higher frequencies. Routine genetic testing of breeding stock is the most effective way to reduce prevalence over time.