Limber tail syndrome, or acute caudal myopathy, is a disorder of the muscles in the tail, usually affecting working dogs.

It is an injury occurring mostly in sporting or working dogs such as English Pointers, English Setters, Foxhounds, Beagles, and Labrador Retrievers. Limber tail syndrome is also known as swimmer's tail, cold water tail, broken tail, dead tail, "happy tail" or broken wag.

It has been said by many dog owners that limber tail had been caused shortly (24 hours) after swimming in water that is too cold or on rare occasions too warm and indeed this has certainly produced this very condition. The actual cause is unknown but it may be caused by the narrowing of the space through which the spinal cord passes, typically due to degenerative change to the intervertebral disk spaces. These underlying changes may not lead to visible change until the problem is suddenly exacerbated, such as during physical activity, after trauma, etc. Occasionally other changes are seen prior to or in conjunction with limber tail disease, such as urinary or fecal incontinence, postural abnormalities in the pelvic limb, or pain in response to touching the lower back.

Feather duster budgerigars ("Melopsittacus undulatus"), sometimes called budgerigar mops, are budgerigars that have a condition characterised by overly long feathers that do not stop growing at usual periods, giving the bird the appearance of a feather duster. This condition is sometimes known as chrysanthemum feathering. The contour, tail and flight feathers do not stop growing, and they do not have the necessary barbs and barbules for the feather's structure to interlock. The shaft (calamus) is also curved, and so the feathers appear deformed and fluffed out. Individuals with this condition often appear less alert than nest mates. In addition, they are small and some have other defects such as microphthalmia. They lack vigour, often cannot fly and die within a year of hatching. There is no treatment for the condition; birds are often euthanized in the nest.

The condition may be a genetic disorder, caused by a herpesvirus, or perhaps caused by both.

The symptoms may not appear for several days. The main symptom is the animal has a wet tail, matted with faeces. Other signs of the disease are:

- Smell/ foul odor

- Diarrhea

- Lethargy

- Lack of appetite

- Excess sleeping

- Walking with a hunched back

- Folded ears

- Unusual temper(biting or nipping)

During an episode cats show a number of typical signs, including skin rolling or twitching, compulsive self-grooming, self-directed pouncing, or aggressive behaviour such as biting or attacking the tail. There may also be pupil dilation, vocalisation and a general increase in activity.

Wet-tail or proliferative ileitis, is a disease of hamsters. It is precipitated by stress. Even with treatment, the animal can die within 48–72 hours. Baby hamsters are much more likely to get the disease than older hamsters. It commonly is found when the hamster is being weaned at about four weeks of age.

Ringtail, also known as tail necrosis, is an epidermal disease that may occur in rats, mice, hamsters and other rodents.

In affected individuals, the tail swells as a consequence of annular constrictions along its length (hence the name "ringtail") and subsequent dehydration; in the most severe cases, the process may end up in the tail becoming gangrenous and dropping off. Feet may also swell and redden.

Ringtail is traditionally attributed to low environmental humidity and high temperature, although a number of other possible causes have been suggested, from dietary deficiencies (low levels of fatty acids) to genetic predisposition. For lab and pet rodents, poor bedding (i.e., overly absorbent bedding) or repeated blood draws from tail veins have also been identified as possible causes of ringtail.

The cause of feline hyperesthesia syndrome is unknown. Some experts believe FHS to be a form of epilepsy, while others believe it is a behavioural disorder triggered by trauma. Noting that affected cats tend to be dominating rather than submissive, some research argues that FHS is conflict displacement in which the cat acts out thwarted territorial disputes on its own body.

Although any age, breed, or sex of cat can develop feline hyperesthesia syndrome, those most susceptible include the Siamese, Burmese, and Himalayan breeds.

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.

Foals appear normal immediately after birth. JEB affects tissues including mucous membranes, so one of the first signs is blistering of the gingiva and tongue after the first attempt at nursing. Within the next few days, the foal develops lesions all over the body, especially over pressure points. The proteins affected by the gene mutations are also present in the hooves, causing hooves to slough.

Other symptoms that occur in JEB:

- Corneal lesions

- Dental dysplasia

- Depression

- Oral ulcers

- Suppressed appetite

- Incisors present at birth

Many medical causes underlying the development of feather-plucking have been proposed including allergies (contact/inhalation/food), endoparasites, ectoparasites, skin irritation (e.g. by toxic substances, low humidity levels), skin desiccation, hypothyroidism, obesity, pain, reproductive disease, systemic illness (in particular liver and renal disease), hypocalcaemia, psittacine beak and feather disease (PBFD), proventricular dilatation syndrome, colic, giardiasis, psittacosis, airsacculitis, heavy metal toxicosis, bacterial or fungal folliculitis, genetic feather abnormalities, nutritional deficiencies (in particular vitamin A) and/or dietary imbalances, and neoplasia. For many of the above-mentioned factors, a causative relationship or correlation has not been established and may therefore merely be the result of coincidental findings.

Approximately 50% of parrots exhibiting feather damaging behaviour have been diagnosed as having inflammatory skin disease based on paired skin and feather biopsies. The birds try to relieve itching by grooming their feathers, but this often leads to over-grooming and eventually feather-plucking.

Feather-plucking is generally regarded as a multifactorial disorder, although three main aspects of bird keeping may be related to the problem: (1) cage size often restricts the bird’s movements; (2) cage design and barrenness of the environment often do not provide sufficient behavioural opportunities to meet the bird's sensitivity, intelligence and behavioural needs; and (3) solitary housing, which fails to meet the high social needs of the bird.

Swim bladder disease, also called swim bladder disorder or flipover, is a common ailment in aquarium fish. The swim bladder is an internal gas-filled organ that contributes to the ability of a fish to control its buoyancy, and thus to stay at the current water depth without having to waste energy in swimming. A fish with swim bladder disorder can float nose down tail up, or can float to the top or sink to the bottom of the aquarium.

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.

Sirenomelia, alternatively known as Mermaid syndrome, is a rare congenital deformity in which the legs are fused together, giving them the appearance of a mermaid's tail as the nickname suggests.

This condition is found in approximately one out of every 100,000 live births (about as rare as conjoined twins) and is usually fatal within a day or two of birth because of complications associated with abnormal kidney and urinary bladder development and function. More than half the cases of sirenomelia result in stillbirth and this condition is 100 times more likely to occur in identical twins than in single births or fraternal twins. It results from a failure of normal vascular supply from the lower aorta in utero. Maternal diabetes has been associated with caudal regression syndrome and sirenomelia, although a few sources question this association.

VACTERL-H is an expanded form of the VACTERL association that concludes that this diagnosis is a less severe form of sirenomelia. The disorder was formerly thought to be an extreme case of caudal regression syndrome; however, it was reclassified to be considered a separate condition.

Fancy goldfish are among the fish most commonly affected by this disorder. The disease may be caused by intestinal parasites or by constipation induced by high nitrate levels from over feeding.

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.

Coccydynia is also known as coccygodynia, coccygeal pain, coccyx pain, or coccalgia.

One way of classifying coccydynia is whether the onset was traumatic versus non-traumatic. In many cases the exact cause is unknown and is referred to as idiopathic coccydynia.

Coccydynia is a fairly common injury which can often result from falls, particularly in leisure activities such as cycling and skateboarding.

Coccydynia is often reported following a fall or after childbirth. In some cases, persistent pressure from activities like bicycling may cause the onset of coccyx pain. Coccydynia due to these causes usually is not permanent, but it may become very persistent and chronic if not controlled. Coccydynia may also be caused by sitting improperly thereby straining the coccyx.

Rarely, coccydynia is due to the undiagnosed presence of a sacrococcygeal teratoma or other tumor in the vicinity of the coccyx.

This condition exists in a variety of forms, ranging from partial absence of the tail bone regions of the spine to absence of the lower vertebrae, pelvis and parts of the thoracic and/or lumbar areas of the spine. In some cases where only a small part of the spine is absent, there may be no outward sign of the condition. In cases where more substantial areas of the spine are absent, there may be fused, webbed, or smaller lower extremities and paralysis. Bowel and bladder control is usually affected.

In medicine, heterotopia is the presence of a particular tissue type at a non-physiological site, but usually co-existing with original tissue in its correct anatomical location. In other words, it implies ectopic tissue, in addition to retention of the original tissue type. In neuropathology, for example, gray matter heterotopia is the presence of gray matter within the cerebral white matter or ventricles. Heterotopia within the brain is often divided into three groups: subependymal heterotopia, focal cortical heterotopia and band heterotopia. Another example is a Meckel's diverticulum, which may contain heterotopic gastric or pancreatic tissue.

In biology specifically, "heterotopy" refers to an altered location of trait expression. In her book "Developmental Plasticity and Evolution", Mary-Jane West Eberhard has a cover art of the sulphur crested cockatoo and comments on the back cover "Did long crest[head] feathers evolve by gradual modification of ancestral head feathers? Or are they descendants of wing feathers, developmentally transplanted onto the head". This idea sets the tone for the rest of her book which goes into depth about developmental novelties and their relation to evolution. Heterotopy is a somewhat obscure but well demonstrated example of how developmental change can lead to novel forms. The central concept is that a feature seen in one area of an organism has had its location changed in evolutionary lineages.

Trichophagia is characterized by the person eating hair, usually their own; primarily after pulling it out. Most often, hair is pulled out and then the ends of the root bulb are eaten, or occasionally the hair shaft itself. The hair eventually collects in the gastrointestinal tract (on occasion, and depending upon severity of symptoms) causing indigestion and stomach pain. Ritual is a strong factor, and may involve touching the root bulb to the lips, tasting the hair, and occasionally chewing it. Sometimes those with the disorder may even eat the hair of others. In the psychiatric field it is considered a compulsive psychological disorder.

Rapunzel syndrome, an extreme form of trichobezoar in which the "tail" of the hair ball extends into the intestines, can be fatal if misdiagnosed. In some cases, surgery may be required to remove the mass; a trichobezoar weighing was removed from the stomach of an 18-year-old woman with trichophagia.

Adrenal disease, a growth of the adrenal glands that can be either hyperplasia or cancer, is most often diagnosed by signs like unusual hair loss, increased aggression, constant grooming of owner or other ferrets as well as themselves, difficulty urinating (caused by an enlarged prostate) or defecating, or agitation when urinating, and (in the case of females) an enlarged vulva. Signs of an enlarged prostate should be considered an emergency; even if the growth is benign, it can still cause a hormonal imbalance which can have devastating effects on the ferret's health.

Treatment options include surgery or cryosurgery to excise the affected glands, melatonin or deslorelin implants, which treat the symptoms but not the disease itself, and/or hormone therapy. The causes of adrenal disease are as yet uncertain, but speculated triggers include unnatural light cycles, diets based around processed ferret foods, and prepubescent neutering. It has also been suggested that there may be a hereditary component to adrenal disease.

Adrenal disease is usually detected during the spring or fall, as it affects the hormones that make the fur grow. When affected ferrets shed their winter coat, the fur does not grow back. The hair loss pattern is usually very specific for adrenal disease. It begins at the base of the tail and then continues up the back. Ferrets treated for adrenal disease may temporarily have severe hair loss as their bodies recover.

LRBA deficiency presents as a syndrome of autoimmunity, lymphoproliferation, and humoral immune deficiency. Predominant clinical problems include idiopathic thrombocytopenic purpura (ITP), autoimmune hemolytic anemia (AIHA), and an autoimmune enteropathy. Before the discovery of these gene mutations, patients were diagnosed with common variable immune deficiency (CVID), which is characterized by low antibody levels and recurrent infections. Infections mostly affect the respiratory tract, as many patients suffer from chronic lung disease, pneumonias, and bronchiectasis. Lymphocytic interstitial lung disease (ILD) is also observed, which complicates breathing and leads to impairment of lung function and mortality. Infections can also occur at other sites, such as the eyes, skin and gastrointestinal tract. Many patients suffer from chronic diarrhea and inflammatory bowel disease. Other clinical features can include hepatosplenomegaly, reoccurring warts, growth retardation, allergic dermatitis, and arthritis. Notably, LRBA deficiency has also been associated with type 1 diabetes mellitus. There is significant clinical phenotypic overlap with disease caused by CTLA4 haploinsufficiency. Since LRBA loss results in a loss of CTLA4 protein, the immune dysregulation syndrome of LRBA deficient patients can be attributed to the secondary loss of CTLA4. Because the predominant features of the disease include autoantibody-mediated disease (AIHA, ITP), Treg defects (resembling those found in CTLA4 haploinsufficient patients), autoimmune infiltration (of non-lymphoid organs, also resembling that found in CTLA4 haploinsufficient patients), and enteropathy, the disease has been termed LATAIE for LRBA deficiency with autoantibodies, Treg defects, autoimmune infiltration, and enteropathy.