One of the biggest risks factors faced by the affected foals is susceptibility to secondary infection. Within three to eight days after birth, the foal may die from infection or is euthanized for welfare reasons.

JEB also affects the human population. Symptoms are closely related to those that are seen in horses. Blisters occur over a large portion of the body and are very susceptible to agitation. There are other symptoms associated, such as alopecia (hair loss), abnormalities of fingernails and toenails, and joint deformities.

Children born with JEB may not live past the first year of age if the condition is severe enough. Other children that have a less severe case of JEB may live a normal lifespan.

An estimated 20 per million live births are diagnosed with EB, and 9 per million people in the general population have the condition. Of these cases, approximately 92% are epidermolysis bullosa simplex (EBS), 5% are dystrophic epidermolysis bullosa (DEB), 1% are junctional epidermolysis bullosa (JEB), and 2% are unclassified. Carrier frequency ranges from 1 in 333 for JEB, to 1 in 450 for DEB; the carrier frequency for EBS is presumed to be much higher than JEB or DEB.

The disorder occurs in every racial and ethnic group and affects both sexes.

A 2014 study classified cases into three types—epidermolysis bullosa simplex (EBS), junctional epidermolysis bullosa (JEB), and dystrophic epidermolysis bullosa (DEB) -- and reviewed their times of death. The first two types tended to die in infancy and the last in early adulthood.

IBS is an autosomal dominant genetic condition caused by a mutation in the gene for keratin 2e on chromosome 12.

This means an affected person has a 50% chance of passing the condition on to their child. Around half of cases of IBS, however, have no parent with the condition and have the genetic fault due to a spontaneous mutation.

Lethal acantholytic epidermolysis bullosa is a fatal genetic skin disorder caused by mutations in DSP

Epidermolysis bullosa dystrophica or dystrophic EB (DEB) is an inherited disease affecting the skin and other organs.

"Butterfly child" is the colloquial name for a child born with the disease, as their skin is seen to be as delicate and fragile as that of a butterfly.

A keratin disease (or keratinopathy) is a genetic disorder of one of the keratin genes.

An example is monilethrix.

The first to be identified was epidermolysis bullosa simplex.

"Junctional epidermolysis bullosa with pyloric atresia" is a rare autosomal recessive form of junctional epidermolysis bullosa that presents at birth with severe mucocutaneous fragility and gastric outlet obstruction. It can be associated with "ITGB4" or "ITGA6".

"Junctional epidermolysis bullosa gravis" (also known as "Herlitz disease," "Herlitz syndrome," and "Lethal junctional epidermolysis bullosa") is the most lethal type of epidermolysis bullosa, a skin condition in which most patients do not survive infancy, characterized by blistering at birth with severe and clinically distinctive perorificial granulation tissue.

JEB-H is generally caused by mutations in one of the three laminin-332 coding genes: LAMA3 (18q11.2), LAMB3 (1q32) and LAMC2 (1q25-q31).

This is rare and is usually due to mutations in the R-spondin 4 (RSPO4) gene which is located on the short arm of chromosome 20 (20p13). Clinically it is manifest by the absence (anonychia) or hypoplasia (hyponuchia) of finger- and/or toenails.

Usually, a common form of treatment for the condition is a type of hand cream which moisturises the hard skin. However, currently the condition is incurable.

Epidermolysis bullosa simplex (EBS),is a disorder resulting from mutations in the genes encoding keratin 5 or keratin 14.

Blister formation of EBS occurs at the dermoepidermal junction. Sometimes EBS is called "epidermolytic".

Bart syndrome is a genetic disorder characterized by the association of congenital localized absence of skin, epidermolysis bullosa, lesions of the mouth mucosa, and dystrophic nails.

Anonychia is the absence of nails, an anomaly, which may be the result of a congenital ectodermal defect, ichthyosis, severe infection, severe allergic contact dermatitis, self-inflicted trauma, Raynaud phenomenon, lichen planus, epidermolysis bullosa, or severe exfoliative diseases.

Epidermolysis bullosa simplex may be divided into multiple types:

The deficiency in anchoring fibrils impairs the adherence between the epidermis and the underlying dermis. The skin of DEB patients is thus highly susceptible to severe blistering.Collagen VII is also associated with the epithelium of the esophageal lining, and DEB patients may suffer from chronic scarring, webbing, and obstruction of the esophagus. Affected individuals are often severely malnourished due to trauma to the oral and esophageal mucosa and require feeding tubes for nutrition. They also suffer from iron-deficiency anemia of uncertain origin, which leads to chronic fatigue.

Open wounds on the skin heal slowly or not at all, often scarring extensively, and are particularly susceptible to infection. Many individuals bathe in a bleach and water mixture to fight off these infectionsThe chronic inflammation leads to errors in the DNA of the affected skin cells, which in turn causes squamous cell carcinoma (SCC). The majority of these patients die before the age of 30, either of SCC or complications related to DEB.

The chronic inflammatory state seen in recessive dystrophic epidermolysis bullosa (RDEB) may cause Small fiber peripheral neuropathy (SFN).; RDEB patients have reported the sensation of pain in line with neuropathic pain qualities.

Ichthyosis bullosa of Siemens is a type of familial, autosomal dominant ichthyosis, a rare skin disorder. It is also known as bullous congenital ichthyosiform erythroderma of Siemens or ichthyosis exfoliativa. It is a genetic disorder with no known cure which is estimated to affect about 1 in 500,000 people.

Some systemic diseases can become symptomatic as a skin disorder. These include many endocrine (hormonal) abnormalities, such as hypothyroidism, Cushing's Syndrome (hyperadrenalcorticism), and tumors of the ovaries or testicles.

Vitamins are one of many of the nutritional factors that change the outward appearance of a dog. The fat soluble vitamins A and E play a critical role in maintaining skin health. Vitamin A, which can also be supplemented as beta-carotene, prevents the deterioration of epithelial tissues associated with chronic skin diseases and aging. A deficiency in vitamin A can lead to scaly of skin and other dermatisis related issues like alopecia Vitamin E is an antioxidant. Vitamin E neutralizes free radicals that accumulate in highly proliferative cells like skin and prevent the deterioration of fibrous tissue caused by these ionized molecules. There are also a couple of water-soluble vitamins that contribute to skin health. Riboflavin (B2) is a cofactor to the metabolism of carbohydrates and when deficient in the diet leads to cracked, brittle skin. Biotin (B7) is another B vitamin that, when deficient, leads to alopecia.

The disease is inherited by autosomal dominant transmission with complete penetrance but variable expression. This means that children of an affected parent that carries the gene have a 50% chance of developing the disorder, although the extent to which they are affected is variable.

Bart syndrome is caused by ultrastructural abnormalities in the anchoring fibrils. Genetic linkage of the inheritance of the disease points to the region of chromosome 3 near the collagen, type VII, alpha 1 gene (COL7A1).

Ultraviolet light from the sun causes premature aging of the skin and skin damage that can lead to melanoma. Some scientists hypothesize that overexposure to UV, including excessive sunlight, may play a role in the formation of acquired moles. However, more research is needed to determine the complex interaction between genetic makeup and overall exposure to ultraviolet light. Some strong indications that this is so (but falling short of proof), are:

- The relative lack of moles on the buttocks of people with dysplastic nevi.

- Freckles (spots of melanin on the skin, and distinct from moles) are known to be influenced by sunlight.

Studies have found that sunburns and too much time in the sun can increase the risk factors for melanoma. This is "in addition to" those who have dysplastic nevi being at higher risk of this cancer (the uncertainty is in regard to acquiring "benign" moles). To prevent and reduce the risk of melanoma caused by UV radiation, the American Academy of Dermatology and the National Cancer Institute recommends staying out of the sun between 10 a.m. and 4 p.m. standard time (or whenever one's shadow is shorter than one's height). The National Cancer Institute also recommends wearing long sleeves and trousers, hats with a wide brim, sunscreens, and sunglasses that have UV-deflecting lenses.

The disease is an autosomal recessive condition,

which means that both parents of the foal must carry the gene in order for the disease to hit their offspring. The disease has been found in animals with a frameshift mutation variety of the protein Serpin B11.

Palmoplantar keratodermas are a heterogeneous group of disorders characterized by abnormal thickening of the palms and soles.

Autosomal recessive and dominant, X-linked, and acquired forms have all been described.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.