Congenital forms of hypertrichosis are caused by genetic mutations, and are extremely rare, unlike acquired forms. Congenital hypertrichosis is always present at birth.

- Hypertrichosis lanuginosa

Congenital hypertrichosis lanuginosa is noticeable at birth, with the infant completely covered in thin lanugo hair. In normal circumstances, lanugo hair is shed before birth and replaced by vellus hair; however, in a person with congenital hypertrichosis lanuginosa, the lanugo hair remains after birth. The palms of the hands, soles of the feet, and mucous membranes are not affected. As the person ages, the lanugo hair may thin, leaving only limited areas of hypertrichosis.

- Generalized hypertrichosis

Congenital generalized hypertrichosis causes males to exhibit excessive facial and upper body hair, whereas women exhibit less severe asymmetrical hair distribution. The palms, soles, and mucous membranes are not affected.

- Terminal hypertrichosis

Congenital terminal hypertrichosis is characterized by the presence of fully pigmented terminal hair that covers the entire body. This condition is usually accompanied by gingival hyperplasia. This form is most responsible for the term "werewolf syndrome" because of the thick, dark hair that appears. People with this condition are sometimes performers at circuses because of their unusual appearance.

- Circumscribed hypertrichosis

Congenital circumscribed hypertrichosis is associated with the presence of thick vellus hair on the upper extremities. Circumscribed signifies this type of hypertrichosis is restricted to certain parts of the body, in this case, the extensor surfaces of the upper extremities. Hairy elbow syndrome, a type of congenital circumscribed hypertrichosis, shows excessive growth on and around the elbows. This type of hypertrichosis is present at birth, becomes more prominent during aging, and regresses at puberty.

- Localized hypertrichosis

Congenital localized hypertrichosis is a localized increase in hair density and length.

- Nevoid hypertrichosis

Nevoid hypertrichosis may be present at birth or appear later in life. It features an isolated area of excessive terminal hair and is usually not related to any other diseases.

Midphalangeal hair, or the presence/absence of hair on the middle phalanx of the ring finger, is one of the most widely studied markers in classical genetics of human populations. Although this polymorphism was observed at other fingers as well, for this kind of research, the fourth finger of the hand has been conventionally selected.

Acquired hypertrichosis appears after birth. The multiple causes include the side effects of drugs, associations with cancer, and possible links with eating disorders. Acquired forms can usually be reduced with various treatments.

- Hypertrichosis lanuginosa

Acquired hypertrichosis lanuginosa is characterized by rapid growth of lanugo hair, particularly on the face. Hair also appears on the trunk and armpits, while palms and soles are unaffected. The excess hair is commonly referred to as malignant down. This hair is very fine and unpigmented.

- Generalized hypertrichosis

Acquired generalized hypertrichosis commonly affects the cheeks, upper lip, and chin. This form also affects the forearms and legs, but is less common in these areas. Another deformity associated with acquired generalized hypertrichosis is multiple hairs occupying the same follicle. It may also include abnormal hair growth patterns as what happens to the eyelashes in a condition known as trichiasis. Oral minoxidil treatments for hypertension are known to cause this condition. Topical minoxidil used for alopecia causes hair growth in the areas where it is applied, however this hair disappears shortly after discontinuing the use of topical minoxidil.

- Patterned hypertrichosis

Acquired patterned hypertrichosis is an increase in hair growth in a pattern formation. It is similar to acquired generalized hypertrichosis and is a sign of internal malignancy.

- Localized hypertrichosis

Acquired localized hypertrichosis is an increase in hair density and length often secondary to irritation or trauma. This form is restricted to certain areas of the body.

In humans, hair is commonly present on all the basal segments of the digits and invariably absent from all the terminal ones. On the middle segments, there is wide fluctuation with apparent familial and racial tendencies. Hair is present on the middle segment of the fingers more frequently than on the middle segment of the toes. Hair is most often found on the middle segment of the fourth finger.

The presentation may be of alopecia (baldness). Individuals vary in severity of symptoms. Nail deformities may also be present as well as hair follicle keratosis and follicular hyperkeratosis.

The hair is normal in quantity and is usually silvery-blond or straw-colored. It is disorderly, it stands out from the scalp, and cannot be combed flat. The underlying structural anomaly is longitudinal grooving of the hair shaft, which appears triangular in cross section. This is caused by mutations in one of three possible genes; "PADI3", "TGM" or "TCHH3." The characteristic hair shaft anomaly can be demonstrated in asymptomatic family members by scanning electron microscopy. To be noticeable, 50% of hairs must be affected by the structural abnormality. Improvement often occurs in later childhood. An autosomal dominant mode of inheritance has been suggested though an autosomal recessive pattern with varying degrees of penetrance has also been noted. The stiffness of the uncombable hair has been reasoned to be due to the triangular form of the hair shaft in cross section. It has been suggested that the condition may result from premature keratinization of the inner root sheath.

Hypotrichosis ("" + "" + "") is a condition of abnormal hair patterns, predominantly loss or reduction. It occurs, most frequently, by the growth of vellus hair in areas of the body that normally produce terminal hair. Typically, the individual's hair growth is normal after birth, but shortly thereafter the hair is shed and replaced with sparse, abnormal hair growth. The new hair is typically fine, short and brittle, and may lack pigmentation. Baldness may be present by the time the subject is 25 years old.

Hypotrichosis is a common feature of Hallermann–Streiff syndrome as well as others. It can also be used to describe the lack of hair growth due to chemotherapy.

The opposite of hypotrichosis is hypertrichosis, where terminal hair (thick) grows in areas that would otherwise normally have vellus hair (thin), for example abnormally thick facial hair growth in women.

Other syndromes with hair abnormalities may also show features of uncombable hair syndrome such as Rapp–Hodgkin ectodermal dysplasia syndrome, loose anagen syndrome, EEC syndrome (ectodermal dysplasia, ectrodactyly and cleft lip/palate) and familial tricho-odonto-onychial ectodermal dysplasia with syndactyly. However, unlike these conditions, uncombable hair syndrome alone is not associated with physical, neurologic, or mental abnormalities.

Woolly hair nevus (alternatively spelled "Wooly hair nevus") is a congenital condition in which hair in a circumscribed area of the scalp is kinked or woolly.

Trichorrhexis invaginata (also known as "Bamboo hair" ) is a distinctive hair shaft abnormality that may occur sporadically, either in normal hair or with other hair shaft abnormalities, or regularly as a marker for Netherton's syndrome. The primary defect appears to be abnormal keratinization of the hair shaft in the keratogenous zone, allowing for intussusception of the fully keratinized and hard distal shaft into the incompletely keratinized and soft proximal portion of the shaft.

In 1937, Touraine and Solente first noted the association between hair-shaft defects (bamboo node) and ichthyosiform erythroderma. Còme first coined the term ichthyosis linearis circumflexa in 1949, although Rille had previously recorded the distinctive features of ichthyosis linearis circumflexa by 1922. In 1958, Netherton described a young girl with generalized scaly dermatitis and fragile nodular hair-shaft deformities, which he termed trichorrhexis nodosa. Later, this was more appropriately renamed as trichorrhexis invaginata (bamboo hair) for a ball-and-socket–type hair-shaft deformity at the suggestion of Wilkinson et al.

In 1974, Mevorah et al. established the clinical relationship between ichthyosis linearis circumflexa and Netherton syndrome, and an atopic diathesis was found to occur in approximately 75% of patients with Netherton syndrome.

Monilethrix (also referred to as beaded hair) is a rare autosomal dominant hair disease that results in short, fragile, broken hair that appears beaded. It comes from the Latin word for necklace ("monile") and the Greek word for hair ("thrix").

The condition gets its name because most, though not all, affected foals are born with a unique coat color dilution that lightens the tips of the coat hairs, or even the entire hair shaft. The color has variously been described as a silver sheen, a dull lavender, a pale, dull pinkish-gray, or pale chestnut. This dilution differs from gray foals because grays are born a dark color and lighten with age. It is also different from roan, because the hair is of a uniform shade, not of intermingled light and dark hairs.

Foals with LFS are unable to stand, and sometimes cannot even attain sternal recumbency (to roll from their side to lie upright, resting on the sternum, a precursor position to standing). They may lie with their necks arched back (Opisthotonos), make paddling motions with their legs, and often have seizures. extensor rigidity and seizure activity are also common signs. Apparent blindness may also be a clinical sign of the disorder, but is not seen in every case. Although they do have a sucking reflex, they cannot stand to nurse, and affected foals are usually euthanized within a few days of birth. There is no cure. In some cases, the mare may also have difficulty foaling, though foaling difficulties are not the cause of the condition. In some cases, LFS-affected foals may be larger than usual.

LFS is distinguishable from Neonatal Maladjustment Syndrome (NMS) or "Dummy Foal Syndrome".

Affected babies are born in a collodion membrane, a shiny, waxy-appearing outer layer to the skin. This is shed 10–14 days after birth, revealing the main symptom of the disease, extensive scaling of the skin caused by hyperkeratosis.

With increasing age, the scaling tends to be concentrated around joints in areas such as the groin, the armpits, the inside of the elbow and the neck. The scales often tile the skin and may resemble fish scales.

In medicine, the term collodion baby applies to newborns who appear to have an extra layer of skin (known as a "collodion membrane") that has a collodion-like quality. It is a descriptive term, not a specific diagnosis or disorder (as such, it is a syndrome).

Junctional epidermolysis bullosa (JEB) is an inherited disorder that is also known as red foot disease or hairless foal syndrome. JEB is the result of a genetic mutation that inhibits protein production that is essential for skin adhesion. Therefore, tissues, such as skin and mouth epithelia, are affected. As a result, blisters form over the entire body causing pain and discomfort. Also, the open sores leave the newborn foal highly susceptible to secondary infection. The condition can be categorized into two types of mutations: JEB1 and JEB2. JEB1 is found in Belgian Draft horses, as well as other related Draft breeds. In contrast, JEB2 is found in American Saddlebred horses.

Genetic forms of localized autosomal recessive hypotrichosis include:

JEB has documented in Belgian drafts, American Cream Draft, Breton drafts, Comtois, and American Saddlebreds. Of these horses, 12% of Belgians and 4% of Saddlebreds are thought to carry the disorder.

There are two expressions of this condition, one for long or double coated breeds and one for short coated breeds, both with differing presentations.

- For long- or double-coated breeds such as Poodles, Akitas and Samoyeds, the condition often presents itself with silvery dandruff which adheres to the coat, hair loss (not to be confused with moulting or "blowing coat"), a dull and brittle coat, and later on skin lesions along the back and ears as well as thickened skin and a musty or rancid odour.

- For short-coated breeds such as Vizslas, the condition causes facial swellings, nodular skin lesions, fine dandruff which does not adhere to the coat, and a general "moth-eaten" appearance to the coat.

Sabinas brittle hair syndrome, also called Sabinas syndrome or brittle hair-mental deficit syndrome, is an autosomal recessive congenital disorder affecting the integumentary system.

Sebaceous adenitis in an uncommon skin disease found in some breeds of dog, and more rarely in cats, rabbits and horses. characterised by an inflammatory response against the dog's sebaceous glands (glands found in the hair follicles in the skin dermis), which can lead to the destruction of the gland. It was first described in veterinary literature in the 1980s.

Symptoms include brittle hair, mild mental retardation and nail dysplasia. The syndrome was first observed in Sabinas, a small community in northern Mexico.

The principal biochemical features of the illness are reduced hair cystine levels, increased copper/zinc ratio, and presence of arginosuccinic acid in the blood and urine.

The key finding is brittle hair with low sulfur content, but alternating dark and light bands under polarizing microscopy, trichoschisis, and absent or defective cuticle are additional important clues for the diagnosis of trichothiodystrophy. Review of literature reveals extensive associated findings in trichothiodystrophy. Amino acid analyses of control hair when compared with those of patients with the Sabinas syndrome showed very striking differences with regard to content of sulphur amino acids. As in previous descriptions of amino acid abnormalities in the trichorrhexis nodosa of arginosuccinicaciduria, there were increases in lysine, aspartic acid, alanine, leucine, isoleucine, and tyrosine.

Trichothiodystrophy represents a central pathologic feature of a specific hair dysplasia associated with several disorders in organs derived from ectoderm and neuroectoderm. Trichothiodystrophy or TTD is a heterogeneous group of autosomal recessive disorders, characterized by abnormally sulfur deficient brittle hair and accompanied by ichthyosis and other manifestations.

Patients with trichothiodystrophy should have a thorough evaluation for other associated manifestations, including investigation of photosensitivity and DNA repair defects. Because the disease appears to be inherited in an autosomal recessive pattern, detection of low-sulfur brittle hair syndrome is also important for genetic counseling.

Peeling skin syndrome (also known as "Acral peeling skin syndrome," "Continual peeling skin syndrome," "Familial continual skin peeling," "Idiopathic deciduous skin," and "Keratolysis exfoliativa congenita") is an autosomal recessive disorder characterized by lifelong peeling of the stratum corneum, and may be associated with pruritus, short stature, and easily removed anagen hair.

The acral form can be associated with "TGM5".

Lavender foal syndrome (LFS), also called coat color dilution lethal (CCDL), is an autosomal recessive genetic disease that affects newborn foals of certain Arabian horse bloodlines. Affected LFS foals have severe neurological abnormalities, cannot stand, and require euthanasia shortly after birth. The popular name originates due to a diluted color of the foals coat, that in some cases appears to have a purple or lavender hue. However, not all foals possess the lavender coat colour, colouring can range from silver to light chestnut to a pale pink. Carrier horses have no clinical signs and DNA testing can determine if a horse carries the gene.

The first visible sign of a beech scale insect infestation is a woolly, white, waxy covering that the insect secretes. This sign can be observed covering small areas or most of the tree. The amount of waxy material observed depends on the population of the beech scale insect on that tree. The "Neonectria" fungi also show signs of its presence. An early sign is what looks like a bleeding spot on the tree. A reddish-brown fluid will ooze from the wound site, giving it this appearance. Later, perithecia will form around the dead spot, which is another sign of the disease.

Symptoms of beech bark disease can be observed in the foliage and on the bole of the tree. Foliage may become small, sparse and yellowed. Trees that display a thin, weak crown may persist for several years but may also die without displaying any symptoms. Noticeable symptoms on the bole are the cracking of the bark, the formation of cankers, and beech snap. Beech snap is a result of the fungi and insect weakening the wood, which makes it susceptible to being blown over by wind.