Hereditary Equine Regional Dermal Asthenia (HERDA), or Hyperelastosis Cutis (HC), is a genetic skin disease that primarily affects Quarter Horses.

It’s characterized by a deficiency in collagen production within the skin cells. Collagen is an important protein responsible for maintaining the strength and elasticity of the skin. [1][2]

Horses affected by HERDA typically exhibit extremely fragile skin, which is prone to tearing even with minor pressure or friction. As a result, they may develop chronic wounds, scars and other severe skin abnormalities.

Skin fragility can severely impact the horse’s quality of life, as recurring and non-healing skin wounds require ongoing management and are prone to bacterial infection.

Understanding the genetic inheritance and signs of HERDA are important for accurate diagnosis, effective management, and informed breeding practices to reduce the prevalence of this debilitating condition within horse populations.

HERDA in Horses

Collagen is a protein found abundantly in the body, serving as a key building block for various tissues, including skin, tendons, ligaments, bones, and cartilage. It provides strength, structure, and elasticity to these tissues, contributing to their resilience and flexibility.

Hereditary Equine Regional Dermal Asthenia (HERDA) stems from a genetic mutation that disrupts collagen formation in the horse’s body. [2][3][4]

HERDA is a form of Ehlers-Danlos syndrome (EDS), a group of genetic connective tissue disorders affecting collagen production. EDS affects various species, including humans, cattle, pigs, cats and dogs. [5][6][7]

While genetic skin disorders may be present in other animals, HERDA is specific to equines, notably Quarter Horses.

EDS arises due to mutations in genes related to collagen formation and processing, resulting in a range of clinical effects between affected horses. Researchers are studying HERDA as an animal model to gain insight into EDS in humans. [1][13]

Horses with HERDA typically seem healthy at birth and do not display signs of disease until they mature. Skin lesions typically emerge between 18 and 24 months of age, sometimes as late as 4 or 5 years old. [1]

Signs of HERDA typically emerge when the horse is started under saddle. During this period, lesions manifest along the horse’s back, particularly in areas where the saddle sits and exerts pressure. [2][4][9]


The genetic mutation associated with HERDA impacts the protein structure of collagen produced by skin cells. As a result, collagen folding and secretion are impaired.

This prevents the skin layers from sticking together, causing the top layer to separate easily from the deeper tissues. As the skin separates from the layer underneath, it becomes increasingly fragile. [10][11]

HERDA is inherited in an autosomal recessive manner, meaning that affected horses must inherit the mutated gene from both parents to display symptoms.

Heterozygous carriers of the mutated gene do not exhibit signs of HERDA themselves, but they can pass the gene to their offspring. [6]

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