Cats can be born with or may inherit several different kinds of skin abnormalities. Most of these conditions are uncommon to rare. Some occur with greater frequency in particular breeds of cats.
Congenital Skin Disorders
Epitheliogenesis imperfecta, also called aplasia cutis, might be described as missing or absent skin. It is a congenital condition of unknown cause and is rare in cats. Animals with epitheliogenesis imperfecta have failed to develop part or all of the layers of the skin. As a result, the animal is born with ulcers, or areas lacking any skin covering. The condition can be fatal if it involves large portions of the skin. Small defects can be surgically corrected.
Hereditary Hair Loss (Alopecia)
Animals can be born either totally or partially without hair. Hairlessness can also develop later in life. These defects can be associated with abnormal teeth, claws, and eyes, or with skeletal and other developmental defects. Hairless breeds of cats, such as the Sphinx, have been bred for these defects. All animals with abnormal hair development are prone to hair follicle infections, and inflammation caused by foreign objects in the hair follicles.
In cats, hair growth abnormalities known as follicular dysplasia have been reported in the Devon Rex. Hair shaft structural abnormalities called pili torti are known to occur in the American Wirehaired Cat.
Some skin color abnormalities may be acquired, while others are hereditary. Abnormalities in skin and coat color are sometimes related. Some of the associations are mentioned in hereditary hair loss (see Skin Disorders of Cats: Hereditary Hair Loss (Alopecia)).
Albinism is rare in cats. True albinism is always associated with pink or pale irises and with visual defects and increased risk of skin damage from sunlight. Albinism is different from extreme white spotting. Some animals with extreme piebaldism (spotted or blotched with black and white) or dominant white have associated nervous system abnormalities or deafness in one or both ears. About 75% of white cats with 2 blue eyes are deaf. Albino and white skin on piebald cats is subject to solar damage and sun-induced skin cancer, especially where the hair is short or thin (such as on the ears).
Lentigo occurs in orange and orange-faced male cats. It is marked by the development of pigmented spots. Marks are first seen on the lips and eyelids at 1 year of age. Marks later develop on the nose and lips. Lentigo spots are not precancerous and have no medical consequence.
Vitiligo is hereditary but not noticeable at birth. The onset is usually in young adulthood. Affected cats develop bleached areas of skin that occasionally also involve the hair coat and claws. Most patches are on the face, especially the bridge of the nose or around the eyes. Color loss may wax and wane. Complete remission may occur but is rare. Vitiligo causes no other health problems. No treatment is available. Treatments used in people with vitiligo are unlikely to help animals.
Defects of Structural Integrity
Some skin diseases are genetic defects that affect the structural integrity of the skin. Cutaneous asthenia (also known as dermatosparaxis or Ehlers–Danlos syndrome) is a group of syndromes characterized by defects in collagen production. Affected animals develop loose, unusually elastic, fragile skin along with loose joints and other connective tissue dysfunctions. These syndromes have been seen in Himalayan and domestic shorthair cats. For Himalayan cats, the disease is a recessive characteristic. In some families of domestic shorthair cats, the disease is a dominant characteristic.
The signs of these syndromes include fragile skin (present from birth), wounds that heal with thin scars, delayed wound healing, hanging skin, and the formation of blood clots (hematomas) and sacs or cysts filled with fluid (hygromas).
Diagnosis in cats includes assessment of signs, measurement of skin elasticity, and laboratory tests on the collagen structure of skin samples. Prior to diagnosing cutaneous asthenia, your veterinarian will want to eliminate other disorders of acquired rather than hereditary skin fragility as a cause of the skin problems. Cutaneous asthenia is not usually fatal in cats, although older animals develop hanging folds of skin and often have extensive scarring.
Epidermolysis bullosa syndromes are a group of hereditary congenital defects in the zone between the dermis and epidermis. Minor skin trauma results in separation of the dermal and epidermal skin layers and blisters that soon rupture, leaving glistening, flat ulcers. Skin damage may be present at birth or develop within the first weeks of life. The most severe damage occurs on the feet, mouth, face, and genitals. Most occurrences of this disease are fatal.
This disease has been seen in Siamese, domestic shorthair, and Persian cats. (For more information about Epidermolysis Bullosa Syndromes, see Skin Disorders of Dogs: Defects of Structural Integrity.)
Multisystem Disorders that Affect the Skin
Porphyria is an inherited defect in the metabolism of hemoglobin (a blood component) and its byproducts. Signs in cats include photodermatitis (inflammation of the skin brought on by exposure to light); a reddish brown discoloration of the teeth, bones, and urine; anemia; and stunted growth. The abnormal fear and avoidance of light that is a sign of this disease in other animals does not occur in cats. Laboratory tests on urine samples are commonly used to confirm the presence of porphyria, although skin biopsies are also used.
Congenital and Inherited Tumors
Abnormal growth and spread of mast cells in the skin (benign familial cutaneous mastocytosis) has been reported in young Siamese cats. This rare, inherited condition causes skin to thicken and have a leathery, bark-like appearance. Intense itching is evident. Treatment includes medication to control itching and prevent self-inflicted skin damage.
Last full review/revision July 2011 by Karen A. Moriello, DVM, DACVD; Thomas R. Klei, PhD; David Stiller, MS, PhD; Stephen D. White, DVM, DACVD; Michael W. Dryden, DVM, PhD; Carol S. Foil, DVM, MS, DACVD; Paul Gibbs, BVSc, PhD, FRCVS; John E. Lloyd, BS, PhD; Bernard Mignon, DVM, PhD, DEVPC; Wayne Rosenkrantz, DVM, DACVD; Patricia A. Talcott, MS, DVM, PhD, DABVT; Alice E. Villalobos, DVM, DPNAP; Patricia D. White, DVM, MS, DACVD