White band disease (Acroporid white syndrome) is a coral disease that affects acroporid corals and is distinguishable by the white band of dead coral tissue that it forms. The disease completely destroys the coral tissue of Caribbean acroporid corals, specifically elkhorn coral ("Acropora palmata") and staghorn coral ("A. cervicornis"). The disease exhibits a pronounced division between the remaining coral tissue and the exposed coral skeleton. These symptoms are similar to white plague, except that white band disease is only found on acroporid corals, and white plague has not been found on any acroporid corals. It is part of a class of similar disease known as "white syndromes", many of which may be linked to species of "Vibrio" bacteria. While the pathogen for this disease has not been identified, "Vibrio carchariae" may be one of its factors. The degradation of coral tissue usually begins at the base of the coral, working its way up to the branch tips, but it can begin in the middle of a branch.

White band disease causes the affected coral tissue to decorticate off the skeleton in a white uniform band for which the disease was given its name. The band, which can range from a few millimeters to 10 centimeters wide, typically works its way from the base of the coral colony up to the coral branch tips. The band progresses up the coral branch at an approximate rate of 5 millimeters per day, causing tissue loss as it works its way to the branch tips. After the tissue is lost, the bare skeleton of the coral may later by colonized by filamentous algae.

There are two variants of white band disease, type I and type II. In Type I of white band disease, the tissue remaining on the coral branch shows no sign of coral bleaching, although the affected colony may appear lighter in color overall. However, a variant of white band disease, known simply as white band disease Type II, which was found on Staghorn colonies near the Bahamas, does produce a margin of bleached tissue before it is lost. Type II of white band disease can be mistaken for coral bleaching. By examining the remaining living coral tissue for bleaching, one can delineate which type of the disease affects a given coral.

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".

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.

Lethal white syndrome (LWS), also called overo lethal white syndrome (OLWS), lethal white overo (LWO), and overo lethal white foal syndrome (OLWFS), is an autosomal genetic disorder most prevalent in the American Paint Horse. Affected foals are born after the full 11-month gestation and externally appear normal, though they have all-white or nearly all-white coats and blue eyes. However, internally, these foals have a nonfunctioning colon. Within a few hours, signs of colic appear; affected foals die within a few days. Because the death is often painful, such foals often are humanely euthanized once identified. The disease is particularly devastating because foals are born seemingly healthy after being carried to full term.

The disease has a similar cause to Hirschsprung's disease in humans. A mutation in the middle of the endothelin receptor type B (EDNRB) gene causes lethal white syndrome when homozygous. Carriers, which are heterozygous—that is, have one copy of the mutated allele, but themselves are healthy—can now be reliably identified with a DNA test. Both parents must be carriers of one copy of the LWS allele for an affected foal to be born.

Horses that are heterozygous for the gene that causes lethal white syndrome often exhibit a spotted coat color pattern commonly known as "frame" or "frame overo". Coat color alone does not always indicate the presence of LWS or carrier status, however. The frame pattern may be minimally expressed or masked by other spotting patterns. Also, different genetic mechanisms produce healthy white foals and have no connection to LWS, another reason for genetic testing of potential breeding stock. Some confusion also occurs because the term overo is used to describe a number of other non tobiano spotting patterns besides the frame pattern. Though no treatment or cure for LWS foals is known, a white foal without LWS that appears ill may have a treatable condition.

Unlike some coat color dilution lethals, which may result in premature births, stillborn, or weak foals, foals born with lethal white syndrome appear to be fully formed and normal. The coat is entirely or almost entirely pure white with underlying unpigmented pink skin. Pigmented regions may be any color, and if present, are most common around the muzzle, underside of the barrel, and the hindquarters or tail. The eyes are blue. A few lethal white foals have been shown to be deaf.

Healthy foals pass meconium, the first stool, soon after birth, though some healthy foals may require an enema to assist this process, but the meconium of LWS foals is impacted high in the intestine, and never appears, even with the use of enemas. Signs of colic begin to appear within the first day, and all LWS-afflicted foals die within the first few days of life. The painful and inevitable death that follows usually prompts veterinarians and owners to euthanize foals suspected of having lethal white syndrome.

Death is caused by an underdeveloped part of the digestive system. The large intestine of the horse is a complex system where most digestion takes place, and comprises the cecum, the colon, and the rectum. Necropsies on LWS foals reveal a pale, underdeveloped colon and intestinal obstruction (impaction). Samples of affected tissue show a lack of nerves that allow the intestine to move material through the digestive system, a condition called intestinal agangliosis.

Closer examination of the skin and hair shows both to be unpigmented, and most hair follicles are inactive and many are devoid of hair altogether. All LWS foals test homozygous for a genetic abnormality.

Leukonychia (or leuconychia), also known as white nails or milk spots, is a medical term for white discolouration appearing on nails. It is derived from the Greek words "leuko" ("white") and "nychia" ("nails"). The most common cause is injury to the base of the nail (the matrix) where the nail is formed.

It is harmless and most commonly caused by minor injuries, such as nail biting, that occur while the nail is growing. Leukonychia occurs most commonly in healthy individuals, unrelated to any known nutritional or physiological deficiency. When caused by injury the marks will disappear as the nail grows outwards, however a dietary deficiency will cause recurrent leukonychia.

Other possible reasons for this problem with nail colour can be linked to:

- Arsenic poisoning

- Lead poisoning

- Pneumonia

- Heart disease

- Renal failure

- Ill health

- Hypoalbuminemia

- Vitamin deficiency

- Ulcerative colitis

- Hepatic cirrhosis

- Psychogenic stresses

- Onychophagia

- Occupational trauma

- Zinc deficiency

- Protein deficiency

- Psoriasis as well as eczema

- Iron deficiency

Onychomycosis, also known as tinea unguium, is a fungal infection of the nail. This condition may affect toenails or fingernails, but toenail infections are particularly common.

Treatment may be based on the signs. Treatment may be with the medication terbinafine.

It occurs in about 10 percent of the adult population. It is the most common disease of the nails and constitutes about half of all nail abnormalities.

The term is from Ancient Greek ὄνυξ "ónux" "nail", μύκης "múkēs" "fungus" and -ωσις "ōsis" "functional disease."

The most common symptom of a fungal nail infection is the nail becoming thickened and discoloured: white, black, yellow or green. As the infection progresses the nail can become brittle, with pieces breaking off or coming away from the toe or finger completely. If left untreated, the skin underneath and around the nail can become inflamed and painful. There may also be white or yellow patches on the nailbed or scaly skin next to the nail, and a foul smell. There is usually no pain or other bodily symptoms, unless the disease is severe. People with onychomycosis may experience significant psychosocial problems due to the appearance of the nail, particularly when fingers – which are always visible – rather than toenails are affected.

Dermatophytids are fungus-free skin lesions that sometimes form as a result of a fungus infection in another part of the body. This could take the form of a rash or itch in an area of the body that is not infected with the fungus. Dermatophytids can be thought of as an allergic reaction to the fungus.

Longitudinal leukonychia is far less common and features smaller 1mm white longitudinal lines visible under the nail plate. It may be associated with Darier's disease.

People with CHS have light skin and silvery hair (albinism) and frequently complain of solar sensitivity and photophobia. Other signs and symptoms vary considerably, but frequent infections and neuropathy are common. The infections involve mucous membranes, skin, and the respiratory tract. Affected children are susceptible to infection by Gram-positive and gram-negative bacteria and fungi, with "Staphylococcus aureus" being the most common infection cause. Infections in CHS patients tend to be very serious and even life-threatening. Neuropathy often begins in the teenage years and becomes the most prominent problem. Few patients with this condition live to adulthood.

Most children with Chédiak–Higashi syndrome ultimately reach a stage known as the "accelerated phase", or the "lymphoma-like syndrome", in which defective white blood cells divide uncontrollably and invade many of the body's organs. The accelerated phase is associated with fever, episodes of abnormal bleeding, overwhelming infections, and organ failure. These medical problems are usually life-threatening in childhood.

Yunnan sudden death syndrome is a label used to define unexplained cases of cardiac arrest, which afflicted significant numbers of rural villagers in Yunnan province, in southwest China. Cases occurred almost always during the midsummer rainy season (from June to August), at an altitude of . The cause turned out to be a mushroom now blamed for an estimated 400 deaths in the past three decades.

The mysterious fatalities were recorded for decades before researchers from the Chinese Center for Disease Control and Prevention isolated a significant factor common in every case: a tiny unknown mushroom which was unintentionally gathered and consumed during wild mushroom harvests in the region. Previously the syndrome was thought to be caused by Keshan disease, caused by the Coxsackie virus.

The mushroom, "Trogia venenata", is also known as 'Little White'. It has been determined that families collecting fungi to sell have been eating these Little White mushrooms as they have no commercial value. Three amino acids present in the mushrooms have been shown to be toxic. The mushrooms have also been shown to contain very high quantities of barium, and it may be that some of the deaths are simply from barium poisoning.

In the hours before death, about two-thirds of the victims had such symptoms as nausea, dizziness, heart palpitations, seizures and fatigue.

However, in December 2012 it was announced that Dr Xu Jianping (徐建平) has been collecting samples of "Trogia venenata" in Yunnan for the past three years, and his research now shows that barium levels in the wild mushroom are no higher than those of common foods such as poultry and fish. Nonetheless, it appears the mushroom will still likely play a role. Since publication of the widely circulated 2010 "Science" article, no instances of Yunnan sudden death syndrome have been reported.

Erythrokeratodermia with ataxia (also known as "Giroux–Barbeau syndrome") is a condition characterized by erythematous, hyperkeratotic plaques with fine, white, attached scales distributed almost symmetrically on the extremities.

Chédiak–Higashi syndrome is a rare autosomal recessive disorder that arises from a mutation of a lysosomal trafficking regulator protein, which leads to a decrease in phagocytosis. The decrease in phagocytosis results in recurrent pyogenic infections, albinism and peripheral neuropathy. It occurs in humans, cattle, blue Persian cats, Australian blue rats, mice, mink, foxes, and the only known captive white orca.

Excessive exposure to hand arm vibrations can result in various patterns of diseases casually known as HAVS or VWF. This can affect nerves, joints, muscles, blood vessels or connective tissues of the hand and forearm:

- Tingling 'whiteness' or numbness in the fingers (blood vessels and nerves affected): This may not be noticeable at the end of a working day, and in mild cases may affect only the tips of the fingers. As the condition becomes more severe, the whole finger down to the knuckles may become white. Feeling may also be lost.

- Fingers change colour (blood vessels affected): With continued exposure the person may suffer periodic attacks in which the fingers change colour when exposed to the cold. Initially the fingers rapidly become pale and feeling is lost. This phase is followed by an intense red flush (sometimes preceded by a dusky bluish phase) signalling the return of blood circulation to the fingers and is usually accompanied by uncomfortable throbbing.

- Loss of manual dexterity (nerves and muscles affected): In more severe forms, attacks may occur frequently in cold weather, not only at work, but during leisure activities, such as gardening, car washing or even watching outdoor sports and may last up to an hour causing considerable pain and loss of manual dexterity and reduced grip strength.

In extreme cases, the sufferer may lose fingers. The effects are cumulative. When symptoms first appear, they may disappear after a short time. If exposure to vibration continues over months or years, the symptoms can worsen and become permanent.

White dog shaker syndrome (also known as idiopathic steroid responsive shaker syndrome, shaker dog syndrome and "little white shakers" syndrome; Latin name Idiopathic Cerebellitis) causes full body tremors in small dog breeds. It is most common in West Highland White Terriers, Maltese, Bichons, and Poodles, and other small dogs. There is a sudden onset of the disease at one to two years of age. It is more likely to occur, and the symptom is worse during times of stress. Nystagmus, difficulty walking, and seizures may occur in some dogs.

The cause is unknown, but it may be mediated by the immune system. One theory is that there is an autoimmune-induced generalized deficiency of neurotransmitters. Cerebrospinal fluid analysis may reveal an increased number of lymphocytes. Treatment with corticosteroids may put the dog into remission, or diazepam may control the symptoms. Typically the two drugs are used together. There is a good prognosis, and symptoms usually resolve with treatment within a week, although lifelong treatment may be necessary.

The nails are markedly thickened with yellow to yellow-green discoloration of the nails. They grow slowly, at a rate of 0.25 mm/week or less. The nails may have ridges and increased side-to-side curvature, reduction of the white crescent and detachment of the nail from the nailbed. The nail changes may change over time.

Most people with yellow nail syndrome (four fifths) have lymphedema; it is symmetrical and typically affects both legs. It is the first symptom of the condition in about a third. Involvement of the arms and face is more unusual, as is lymphedema of the abdomen with ascites (fluid collection in the abdominal cavity) and fluid collection around the heart.

Various lung problems can occur in people with yellow nail syndrome. Many experience cough and shortness of breath. Forty percent of cases develop pleural effusions, which are collections of fluid in the pleural cavity (the space that contains the lungs and normally only has a minimal amount of fluid in it). About half of all people with yellow nail syndrome have either recurrent chest infections or a chronic lung condition known as bronchiectasis which causes chronic production of sputum with episodes of worsening. Forty percent of people with yellow nail syndrome have chronic sinusitis.

Yellow nail syndrome has been associated with some drugs, "e.g." penicillamine, bucillamine and gold sodium thiomalate.

Reynolds syndrome is a rare secondary laminopathy, consisting of the combination of primary biliary cirrhosis and progressive systemic sclerosis. In some patients this syndrome has also been associated with Sjögren's syndrome and hemolytic anemia. Typical clinical features include jaundice, elevated blood levels of alkaline phosphatase, calcinosis cutis, telangiectasias, and pruritus. This disease may cause white or yellow-ish spots on the arms or legs. The syndrome, a special case of scleroderma, is named after the American physician, Telfer B. Reynolds, MD (1921–2004), who first described it. He is also known for creating one of the world's first hepatology programs at the University of Southern California.

It should not be confused with the more common Raynaud's phenomenon.

Poliosis, also called poliosis circumscripta, is the decrease or absence of melanin (or colour) in head hair, eyebrows, eyelashes or any other hairy area. It is popularly known as white forelock when it affects hair right above the forehead.

This condition can cause single or, less commonly, multiple white patches on the hair. Some mistake these white patches for simple birth marks. In poliosis there is decreased or absent melanin in the hair bulbs of affected hair follicles; the melanocytes of the skin are usually not affected. Poliosis occurs in several genetic syndromes such as piebaldism, Waardenburg syndrome, neurofibromatosis type I, and tuberous sclerosis. It can also occur in conditions such as vitiligo, Vogt–Koyanagi–Harada disease, alopecia areata, sarcoidosis, and in association with neoplasms and some medications.

It can give rise to a "Mallen streak" that can be hereditary. Catherine Cookson wrote a novel and later a TV series called "The Mallen Streak", where a family had the condition. Sports presenter Dickie Davies, runner Sam Brown, and fashion expert Stacy London were famous for their respective Mallen streak.

Cross–McKusick–Breen syndrome (also known as "Cross syndrome", "hypopigmentation and microphthalmia", and "oculocerebral-hypopigmentation syndrome") is an extremely rare disorder characterized by white skin, blond hair with yellow-gray metallic sheen, small eyes with cloudy corneas, jerky nystagmus, gingival fibromatosis and severe mental and physical retardation.

It was characterized in 1967.

The features of this syndrome affect the face, skin, brain and the body.

Face:

- downslanting palpebral fissures

- pointed chin

- prominent forehead

- proptosis

- thin upper lip

- wide nasal bridge

Skin:

- fragile

- hyperelastic

Brain:

- Low IQ

- Periventricular white matter lesions

Body:

The height, lower-segment, hand, and foot length are all greater than usual.

Marshall–White syndrome is a skin condition that consists of Bier spots associated with insomnia and tachycardia.

White dot syndromes are inflammatory diseases characterized by the presence of white dots on the fundus, the interior surface of the eye. The majority of individuals affected with white dot syndromes are younger than fifty years of age. Some symptoms include blurred vision and visual field loss. There are many theories for the etiology of white dot syndromes including infectious, viral, genetics and autoimmune.

Classically recognized white dot syndromes include:

- Acute posterior multifocal placoid pigment epitheliopathy (APMPPE)

- Birdshot chorioretinopathy

- Multiple evanescent white dot syndrome (MEWDS)

- Acute zonal occult outer retinopathy (AZOOR)

- Multifocal choroiditis and panuveitis (MCP)

- Punctate inner choroiditis (PIC)

- Serpiginous choroiditis

The signs and symptoms of "activated PI3K Delta Syndrome" are consistent with the following:

- Immunodeficiency

- Lymphadenopathy

- Sinopulmonary infections

- Bronchiectasis

Vibration white finger (VWF), also known as hand-arm vibration syndrome (HAVS) or dead finger, is a secondary form of Raynaud's syndrome, an industrial injury triggered by continuous use of vibrating hand-held machinery. Use of the term "vibration white finger" has generally been superseded in professional usage by broader concept of HAVS, although it is still used by the general public. The symptoms of vibrating white finger are the vascular component of HAVS.

HAVS is a widespread recognized industrial disease affecting tens of thousands of workers. It is a disorder that affects the blood vessels, nerves, muscles, and joints, of the hand, wrist, and arm. Its best known effect is vibration-induced white finger (VWF), a term introduced by the Industrial Injury Advisory Council in 1970. Injury can occur at frequencies between 5 and 2000Hz but the greatest risk for fingers is between 50 and 300Hz. The total risk exposure for hand and arm is calculated by the use of ISO 5349-1, which stipulates maximum damage between 8-16Hz and a rapidly declining risk at higher frequencies. The ISO 5349-1 frequency risk assessment does not match the estimated risks for vibration-induced white finger well.