An odd-eyed cat is a cat with one blue eye and one eye either green, yellow, or brown. This is a feline form of complete heterochromia, a condition that occurs in some other animals. The condition most commonly affects white-colored cats, but may be found in a cat of any color, provided that it possesses the white spotting gene.

The odd-eyed coloring is caused when either the epistatic (dominant) white gene (which masks any other color genes and turns a cat completely white) or the white spotting gene (which is the gene responsible for bicolor and tuxedo cats) prevents melanin (pigment) granules from reaching one eye during development, resulting in a cat with one blue eye and one green, yellow, or brown eye. The condition only rarely occurs in cats that lack both the dominant white and the white spotting gene.

In segmental heterochromia, sometimes referred to as sectoral heterochromia, areas of the same iris contains two completely different colors.

Segmental heterochromia is rare in humans; it is estimated that only about 1% of the population have it.

Heterochromia is classified primarily by onset: as either genetic or acquired.

Although a distinction is frequently made between heterochromia that affects an eye completely or only partially (segmental heterochromia), it is often classified as either genetic (due to mosaicism or congenital) or acquired, with mention as to whether the affected iris or portion of the iris is darker or lighter. Most cases of heterochromia are hereditary, caused by certain diseases and syndromes. Sometimes one eye may change color following disease or injury.

The appropriate treatment for binocular diplopia will depend upon the cause of the condition producing the symptoms. Efforts must first be made to identify and treat the underlying cause of the problem. Treatment options include eye exercises, wearing an eye patch on alternative eyes, prism correction, and in more extreme situations, surgery or botulinum toxin.

If diplopia turns out to be intractable, it can be managed as last resort by obscuring part of the patient's field of view. This approach is outlined in the article on diplopia occurring in association with a condition called "horror fusionis".

Diplopia has a diverse range of ophthalmologic, infectious, autoimmune, neurological, and neoplastic causes.

Photopsia is the presence of perceived flashes of light. It is most commonly associated with posterior vitreous detachment, migraine with aura, migraine aura without headache, retinal break or detachment, occipital lobe infarction, and sensory deprivation (ophthalmo"pathic" hallucinations). Vitreous shrinkage or liquefaction, which are the most common causes of photopsia, cause a pull in vitreoretinal attachments, irritating the retina and causing it to discharge electrical impulses. These impulses are interpreted by the brain as 'flashes'.

This condition has also been identified as a common initial symptom of Punctate inner choroiditis (PIC), a rare retinal autoimmune disease believed to be caused by the immune system mistakenly attacking and destroying the retina. During pregnancy, new-onset photopsia is concerning for severe preeclampsia.

Photopsia can present as retinal detachment when examined by an optometrist or ophthalmologist. However, it can also be a sign of Uveal melanoma. This condition is extremely rare (5–7 per 1 million people will be affected, typically fair-skinned, blue-eyed northern Europeans). Photopsia should be investigated immediately.

Melanism is a development of the dark-colored pigment melanin in the skin or its appendages and is the opposite of albinism. The word "melanism" is derived from the ("black pigment").

Pseudo-melanism, also called abundism, is another variant of pigmentation, characterized by dark spots or enlarged stripes, which cover a large part of the body of the animal, making it appear melanistic.

A deficiency in or total absence of melanin pigments is called amelanism.

The morbid deposition of black matter, often of a malignant character causing pigmented tumors, is called melanosis. For a description of melanin-related disorders, see melanin and ocular melanosis.

Patients with optic disc drusen should be monitored periodically for ophthalmoscopy, Snellen acuity, contrast sensitivity, color vision, intraocular pressure and threshold visual fields. For those with visual field defects optical coherence tomography has been recommended for follow up of nerve fiber layer thickness. Associated conditions such as angioid streaks and retinitis pigmentosa should be screened for. Both the severity of optic disc drusen and the degree of intraocular pressure elevation have been associated with visual field loss. There is no widely accepted treatment for ODD, although some clinicians will prescribe eye drops designed to decrease the intra-ocular pressure and theoretically relieve mechanical stress on fibers of the optic disc. Rarely choroidal neovascular membranes may develop adjacent to the optic disc threatening bleeding and retinal scarring. Laser treatment or photodynamic therapy or other evolving therapies may prevent this complication.

The term squitten is generally used to refer to cats with the condition radial hypoplasia (underdeveloped radius bones) or foreleg micromelia (small forelegs) and related conditions known as radial aplasia (absent radius bones), radial agenesis (failure of radius bones to form) that produces stunted forelegs. The mutation sometimes occurs in the random-breeding population, particularly in inbred populations where recessive genes may be exhibited. Such cats have also been called twisty cats; In the late 1990s, several were deliberately bred at Karma Farms, a horse farm and cattery in Marshall, Texas, resulting in a public outcry against the operators of the farm.

Radial hypoplasia is related to one form of polydactyly, sometimes called patty feet or hamburger feet by cat lovers to distinguish them from thumb cat polydactyls. Ordinary mitten cat polydactyls are not affected.

Cats with radial hypoplasia or similar mutations often sit on their rump with their forelegs unable to touch the floor; this gives them a resemblance to a squirrel or kangaroo. This raises special care considerations for owners of affected cats. Kittens may be unable to knead effectively with their short forelegs; kneading is required to stimulate milk flow in the mother. The short or twisted forelegs cause mobility problems and such cats may adapt by using their hindlegs in a hopping gait.

A corresponding condition affecting the hind legs is called femoral hypoplasia and has only been reported three times in cats.

Typical characteristics of a squitten are short forelegs, with a short radius and ulna which may be twisted or absent, extra front toes, and normal-length hind legs.

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.

In most instances, the diagnosis of toxoplasmic retinochoroiditis is made clinically on the basis of the appearance of the characteristic lesion on eye examination.

Seropositivity (positive blood test result) for Toxoplasma is very common and therefore not useful in diagnosis; however, a negative result i.e. absence of antibodies is often used to rule out disease. Others believe that serology is useful to confirm active toxoplasmic retinochoroiditis, not only by showing positivity but by also showing a significant elevation of titers: The mean IgG values were 147.7 ± 25.9 IU/ml for patients with active disease versus 18.3 ± 20.8 IU/ml for normal individuals.

Antibodies against Toxoplasma:

- IgG : appear within the first 2 weeks after infection, typically remain detectable for life, albeit at low levels;and may cross the placenta.

- IgM : rise early during the acute phase of the infection, typically remain detectable for less than 1 year, and do not cross the placenta.

- IgA : Measurement of IgA antibody titers may also be useful in a diagnosis of congenital toxoplasmosis in a fetus or newborn because IgM production is often weak during this period and the presence of IgG antibodies may indicate passive transfer of maternal antibodies in utero. IgA antibodies however usually disappear by 7 months.

In atypical cases, ocular fluid testing to detect parasite DNA by polymerase chain reaction or to determine intraocular production of specific antibody may be helpful for establishing etiology.

Neuroimaging is warranted in AIDS patients presenting with these findings because intracranial toxoplasmic lesions have been reported in up to 29% of these patients who have toxoplasmic chorioretinitis.

Melanism, meaning a mutation that results in completely dark skin, does not exist in humans. Melanin is the primary determinant of the degree of skin pigmentation and protects the body from harmful ultraviolet radiation. The same ultraviolet radiation is essential for the synthesis of vitamin D in skin, so lighter color of skin - less melanin - is an adaptation for the prehistoric movement of humans away from equatorial regions, as there is less exposure to sunlight at higher latitudes. People from parts of Africa have very dark skin, but this is not melanism.

Not all white, blue-eyed foals are affected with LWS. Other genes can produce healthy pink-skinned, blue-eyed horses with a white or very light cream-colored coat. For a time, some of these completely white horses were called "living lethals", but this is a misnomer. Before reliable information and the DNA test were available to breeders, perfectly healthy, white-coated, blue-eyed foals were sometimes euthanized for fear they were lethal whites, an outcome which can be avoided today with testing and a better understanding of coat color genetics or even waiting 12 hours or so for the foal to develop clinical signs. The availability of testing also allows a breeder to determine if a white-coated, blue-eyed foal that becomes ill is an LWS foal that requires euthanasia or a non-LWS foal with a simple illness that may be successfully treated.

- Double-cream dilutes such as cremello, perlinos, and smoky creams, have cream-colored coats, blue eyes, and pink skin. The faint cream pigmentation of their coats can be distinguished from the unpigmented white markings and underlying unpigmented pink skin. A similar-looking "pseudo double dilute" can be produced with help from the pearl gene or "barlink factor" or the champagne gene.

- The combination of tobiano with other white spotting patterns can produce white or nearly white horses, which may have blue eyes.

- Sabino horses that are homozygous for the sabino-1 ("Sb-1") gene are often called "sabino-white", and are all- or nearly all-white. Not all sabino horses carry "Sb-1".

- Dominant white genetics are not thoroughly understood, but are characterized by all- or nearly all-white coats.

In most patients, optic disc drusen are an incidental finding. It is important to differentiate them from other conditions that present with optic disc elevation, especially papilledema, which could imply raised intracranial pressure or tumors. True papilledema may present with exudates or cotton-wool spots, unlike ODD. The optic disc margins are characteristically irregular in ODD but not blurred as there is no swelling of the retinal nerve fibers. Spontaneous venous pulsations are present in about 80 percent of patients with ODD, but absent in cases of true disc edema. Other causes of disc elevation clinicians must exclude may be: hyaloid traction, epipapillary glial tissue, myelinated nerve fibres, scleral infiltration, vitreopapillary traction and high hyperopia. Disorders associated with disc elevation include: Alagille syndrome, Down syndrome, Kenny-Caffey syndrome, Leber Hereditary Optic Neuropathy and linear nevus sebaceous syndrome.

Amelanism (also known as amelanosis) is a pigmentation abnormality characterized by the lack of pigments called melanins, commonly associated with a genetic loss of tyrosinase function. Amelanism can affect fish, amphibians, reptiles, birds, and mammals including humans. The appearance of an amelanistic animal depends on the remaining non-melanin pigments. The opposite of amelanism is melanism, a higher percentage of melanin.

A similar condition, albinism, is a hereditary condition characterised in animals by the absence of pigment in the eyes, skin, hair, scales, feathers or cuticle. This results in an all white animal, usually with pink or red eyes.

"Toxoplasma" infection can be prevented in large part by:

- cooking meat to a safe temperature (i.e., one sufficient to kill "Toxoplasma")

- peeling or thoroughly washing fruits and vegetables before eating

- cleaning cooking surfaces and utensils after they have contacted raw meat, poultry, seafood, or unwashed fruits or vegetables

- pregnant women avoiding changing cat litter or, if no one else is available to change the cat litter, using gloves, then washing hands thoroughly

- not feeding raw or undercooked meat to cats to prevent acquisition of "Toxoplasma"

Prolonged and intense rainfall periods are significantly associated with the reactivation of toxoplasmic retinochoroiditis. Changes promoted by this climatic condition concern both the parasite survival in the soil as well as a putative effect on the host immune response due to other comorbidities.

The cat should be taken to a veterinarian. The most suspected cause of skin problems in cats will be fleas. Other causes of over-grooming are not as easily ascertained. As household antiseptics are known to be toxic to cats, veterinary antiseptics for cats can be used to treat open sores, if they do occur. Sores can also be treated with cream, oral or injected anti-inflammatories, however if the problem continues to recur it may be more cost effective to subject the cat to laboratory testing early on. It may be difficult to keep a clean dressing on a cat's belly, and an anti-lick collar is adequate to let the wound heal. If an anti lick collar is used, a soft anti-lick collar is less cumbersome, although they are less durable. If the cat wears a plastic anti-lick collar, it may use the edge of the collar to grind against existing wounds, making them worse. A soft anti lick collar will become less effective as it is kicked out of the shape by the cat's hind leg, and will need prompt replacement. The cat can sanitize the wound if the collar is removed for daily short periods of time, also giving the cat an opportunity for an overall grooming. Scratches and wounds can heal completely using this method. When the cat stops wearing the collar, thinned hair, redness of skin or cracked nipples on the cat are early indicators that the cat has started to over-groom again.

Antidepressants for cats may be suggested by a vet.

Aphaeomelanism is the abnormal absence of phaeomelanin from the integumentary system and/or eyes. Phaeomelanin is produced by melanocytes in the absence of melanocortin 1 receptor. This absence is mediated by agouti signalling protein, which antagonizes melanocortin 1 receptor. Loss of function of agouti signalling protein can permit unmediated eumelanin production, producing a uniformly black-to-brown coat color. This condition can be observed in dogs, cats, and horses. The appearance of mammals with recessive agouti mutations is typically dense black. As with aeumelanism, the difference between lack of phaeomelanin and abundance of eumelanin is one of words. Some agouti alleles in mice are associated with health defects, but this is not the case in dogs, cats, or horses.

The cat must have a supply of niacin, as cats cannot convert tryptophan into niacin like dogs. However, diets high in corn and low in protein can result in skin lesions and scaly, dry, greasy skin, with hair loss. Another B vitamin, biotin, if deficient causes hair loss around the eyes and face. A lack of B vitamins can be corrected by supplementing with a vitamin B complex, and brewers yeast.

Angel wing, also known as airplane wing, slipped wing, crooked wing, and drooped wing, is a syndrome that affects primarily aquatic birds, such as geese and ducks, in which the last joint of the wing is twisted with the wing feathers pointing out laterally, instead of lying against the body. Males develop it more frequently than females. It has also been reported in goshawks, bustard chicks, and psittacine birds (budgerigars, macaws, and conures).

The syndrome is acquired in young birds. Due to a high-calorie diet, especially one high in proteins and/or low in vitamin D, vitamin E, and manganese, one or both carpus (wrist) joints are retarded in their development relative to the rest of the wing; for reasons unknown, if only one wing is affected, it is usually the left one. The result is a wrist which is twisted outwards and unable to perform its usual function. Angel wing symptoms include stripped remiges (flight feathers) in the wrist area, or remiges protruding from wings at odd angles. In extreme cases, the stripped feathers may resemble sickly blue straws protruding from wings. In adult birds, the disease is incurable and usually leads to an early death, as affected birds are rendered effectively or totally flightless. In young birds, wrapping the wing and binding it against the bird's flank, together with feeding the bird a more nutritionally balanced diet, can reverse the damage.

The theorized causes of angel wing are genetics, the excessive intake of carbohydrates and proteins, together with insufficient intake of vitamin E, low dietary calcium and manganese deficiency. Angel wing is occasionally observed in waterfowl residing near humans, (including domestic fowl), and the disease can sometimes be observed in areas where geese or ducks are excessively fed bread. Duck seed is an alternative for duck feeders.

A squitten is a cat with unusually short forelegs and/or unusually long hind legs that resembles a squirrel. It is an example of a cat body type genetic mutation. The word is a portmanteau of squirrel and kitten.

The term kangaroo cat is also, rarely, used; this derives from a 1953 specimen known as the Stalingrad Kangaroo Cat.

Ear mites of dogs and cats can be treated with any of the spot-on preparations available from veterinary surgeons as well as over the counter at many pet stores and online. If the chosen solution does not destroy mite eggs, treatment should be repeated after one month, to catch the next generation of mites that will have hatched by then. Relief, in terms of the cat or dog no longer scratching at his or her ears, will be noticeable within a few hours. However, since mite irritation is partly allergic (see scabies), symptoms may also outlive mites by weeks. Moreover, it may take topical antibiotics and several weeks to clear infected external wounds caused by scratching on the exterior surfaces of cat and dog ears.

Common home remedy treatment options include household ingredients such as isopropyl alcohol, acetic acid (vinegar), boric acid, tea tree oil, coconut oil, and many other plant based extracts, in varying proportions.

Option for treating ear mites in rabbits are the related antiparasitics ivermectin and selamectin. Both of these antiparasitics have also been used with good effect in cats and dogs. A topical preparation of 0.01% ivermectin (Acarexx) can be used directly as an oil in cat ears, and the related new generation drug selamectin (brand name "Revolution") is available as a once-per-month skin treatment for both dogs and cats, which will prevent new mite infestation as well as a number of other parasitic diseases. As with ivermectin, selamectin must be used with caution in collies and herder breeds with the possibility for homozygous MDR1 mutations. A single treatment with a topical formulation containing fipronil, (S)-methoprene, eprinomectin and praziquantel was shown to be efficient for the prevention of "Otodectes cynotis" infestation in cats.

Cats cannot synthesize vitamin A from plant beta-carotene, and therefore must be supplemented with retinol from meat. A deficiency in vitamin A will result in a poor coat, with hair loss, with scaly and thickened skin. However an excess of vitamin A, called hypervitaminosis A, can result from over feeding cod liver oil, and large amounts of liver. Signs of hypervitaminosis A are overly sensitive skin, and neck pain causing the cat to be unwilling to groom its self, resulting in a poor coat. Supplementing vitamin A with retinol to a deficient cat, and feeding a balanced diet to a cat with hypervitaminosis A will treat the underlying nutritional disorder.

There is currently no treatment or cure for Waardenburg syndrome. The symptom most likely to be of practical importance is deafness, and this is treated as any other irreversible deafness would be. In marked cases there may be cosmetic issues. Other abnormalities (neurological, structural, Hirschsprung disease) associated with the syndrome are treated symptomatically.