Typically the first symptom of starfish wasting disease is white lesions that appear on the surface of the starfish and spread rapidly, followed by decay of tissue surrounding the lesions. Next the animal becomes limp as the water vascular system fails and it is no longer able to maintain its internal hydrostatic balance. The body structure begins to break down, signs of stretching appear between the arms which may twist and fall off, and the animal dies. The arms may continue to crawl around for a while after being shed. Progression of these events can be rapid, leading to death within a few days.

A deflated appearance can precede other morphological signs of the disease. All of these symptoms are also associated with ordinary attributes of unhealthy stars and can arise when an individual is stranded too high in the intertidal zone (for example) and simply desiccates. "True" wasting disease will be present in individuals that are found in suitable habitat, often in the midst of other individuals that might also be affected.

The final result is a white, mushy blob, which no longer seems to be a sea star.

Sea star wasting disease or starfish wasting syndrome is a disease of starfish and several other echinoderms that appears sporadically, causing mass mortality of affected starfish. There are around 40 different species of sea stars that have been affected by this disease. The disease seems to be associated with raised water temperatures. It starts with the emergence of lesions, followed by body fragmentation and death. In 2014 it was shown that the disease is associated with a densovirus now known as the sea star-associated densovirus (SSaDV).

Both PMWS and porcine dermatitis and nephropathy syndrome (PDNS) are associated to PCV-2. Many pigs affected by the circovirus also seem to develop secondary bacterial infections, like Glässer disease ("Haemophilus parasuis"), pulmonary pasteurellosis, colibacilosis, salmonellosis and others. Postmortem lesions occur in multiple organs, especially in lymphoid tissues and lung, giving rise to the term "multisystemic". Lesions may also affect the skin, kidney, reproductive tissue, brain, or blood vessels.

Wasting pigs is the most common sign of PMWS infection, increasing the mortality rate significantly.

Paratuberculosis or Johne's disease is a contagious, chronic and sometimes fatal infection that primarily affects the small intestine of ruminants. It is caused by the bacterium "Mycobacterium avium" subspecies "paratuberculosis". Infections normally affect ruminants (mammals that have four compartments of their stomachs, of which the rumen is one), but have also been seen in a variety of nonruminant species, including rabbits, foxes, and birds. Horses, dogs, and nonhuman primates have been infected experimentally. Paratuberculosis is found worldwide, with some states in Australia (where it is usually called bovine Johne's disease or BJD) as the only areas proven to be free of the disease.

Some sources define "paratuberculosis" by the lack of "Mycobacterium tuberculosis", rather than the presence of any specific infectious agent, leaving ambiguous the appropriateness of the term to describe Buruli ulcer or Lady Windermere syndrome.

Porcine circoviral disease (PCVD) and Porcine circovirus associated disease (PCVAD), is a disease seen in domestic pigs. This disease causes illness in piglets, with clinical signs including progressive loss of body condition, visibly enlarged lymph nodes, difficulty in breathing, and sometimes diarrhea, pale skin, and jaundice. PCVD is very damaging to the pig-producing industry and has been reported worldwide. PCVD is caused by porcine circovirus type 2 (PCV-2).

The North American industry endorses "PCVAD" and European use "PCVD" to describe this disease.

Cutoff points may vary, but <80% (close to −2 Z-score) is often used.

- Adults:

- Body Mass Index (BMI) is the quotient between weight and height squared (kg/m). An individual with a BMI < 18.5 is regarded as a case of wasting.

- Percent of body weight lost (At Tufts, an unintentional loss of 6% or more in 6 months is regarded as wasting)

Wasting can be caused by an extremely low energy intake (e.g., caused by famine), nutrient losses due to infection, or a combination of low intake and high loss. Infections and conditions associated with wasting include tuberculosis, chronic diarrhea, AIDS, and superior mesenteric artery syndrome. The mechanism may involve cachectin – also called tumor necrosis factor, a macrophage-secreted cytokine. Caretakers and health providers can sometimes contribute to wasting if the patient is placed on an improper diet. Voluntary weight loss and eating disorders are excluded as causes of wasting.

In cattle, the main signs of paratuberculosis are diarrhea and wasting. Most cases are seen in 2- to 6-year-old animals. The initial signs can be subtle, and may be limited to weight loss, decreased milk production, or roughening of the hair coat. The diarrhea is usually thick, without blood, mucus, or epithelial debris, and may be intermittent. Several weeks after the onset of diarrhea, a soft swelling may occur under the jaw. Known as "bottle jaw" or intermandibular edema, this symptom is due to protein loss from the bloodstream into the digestive tract. Paratuberculosis is progressive; affected animals become increasingly emaciated and usually die as the result of dehydration and severe cachexia.

Signs are rarely evident until two or more years after the initial infection, which usually occurs shortly after birth. Animals are most susceptible to the infection in the first year of life. Newborns most often become infected by swallowing small amounts of infected manure from the birthing environment or udder of the mother. In addition, newborns may become infected while in the uterus or by swallowing bacteria passed in milk and colostrum. Animals exposed at an older age, or exposed to a very small dose of bacteria at a young age, are not likely to develop clinical disease until they are much older than two years.

The clinical signs are similar in other ruminants. In sheep and goats, the wool or hair is often damaged and easily shed, and diarrhea is uncommon. In deer, paratuberculosis can progress rapidly. Intestinal disease has also been reported in rabbits and nonhuman primates.

Unlike cattle and sheep, infections in deer often present with clinical illness in animals under one year of age.

The clinical presentation of this disease varies with the individual as well as in severity of those symptoms. Often the symptoms include a gastrointestinal component, but many times birds suffering from this disease will present with neurologic signs as well, or in lieu of digestive anomalies.

Gastrointestinal signs may include: Regurgitation, crop impaction, poor appetite, weight loss, or passage of undigested food in the feces.

Neurologic symptoms may include: Weakness, ataxia, paresis, proprioceptive deficits, head tremors, and rarely seizures.

Muscle wasting and a generalized poor body condition is usually found as well. The virus can also affect the Purkinje cells of the heart, the adrenal medulla, the brain, and the spinal cord.

On necropsy the affected organs appear dilated and may include the crop, proventriculus, ventriculus, and small intestine. On histopathological examination the tissues will contain a lymphoplasmacytic infiltration in the peripheral and central nervous tissue. The causative virus is believed to commonly affect the myenteric plexuses which will also lead to the presentation of atrophied smooth muscle within the affected gastrointestinal organs. It is this atrophy and loss of tone in the organs that causes the dilation and subsequent gastrointestinal symptoms which are commonly the first sign of disease for the owners.

Most cases of CWD occur in adult animals; the youngest animal diagnosed with natural CWD was 17 months. The disease is progressive and always fatal. The first signs are difficulties in movement. The most obvious and consistent clinical sign of CWD is weight loss over time. Behavioral changes also occur in the majority of cases, including decreased interactions with other animals, listlessness, lowering of the head, tremors, repetitive walking in set patterns, and nervousness. Excessive salivation and grinding of the teeth also are observed. Most deer show increased drinking and urination; the increased drinking and salivation may contribute to the spread of the disease.

The ICD-10 Clinical Modification (ICD-10-CM), which is the United States' national adaptation of ICD-10, classifies sarcopenia to code M62.84. (This is an enhancement over the base ICD-10 classification, which only uses the 5th character position within Chapter XVII to identify the anatomical site of occurrence.)

The European Working Group on Sarcopenia in Older People (EWGSOP) developed a clinical definition and consensus diagnostic criteria for age-related sarcopenia, using the presence of low muscle mass and either low muscular strength or low physical performance. Severe sarcopenia requires the presence of all three conditions.

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of mule deer, white-tailed deer, elk (or "wapiti"), moose, and reindeer. As of 2016, CWD had only been found in members of the deer family. First recognized as a clinical "wasting" syndrome in 1967 in mule deer in a wildlife research facility in northern Colorado, USA, it was identified as a TSE in 1978 and has spread to free-ranging and captive populations in 23 US states and two Canadian provinces. CWD is typified by chronic weight loss leading to death. No relationship is known between CWD and any other TSE of animals or people.

Although reports in the popular press have been made of humans being affected by CWD, a study by the Centers for Disease Control and Prevention suggests, "[m]ore epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions".

The epidemiological study further concluded, "[a]s a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified".

Sarcopenia is characterized first by a muscle atrophy (a decrease in the size of the muscle), along with a reduction in muscle tissue quality, characterized by such factors as replacement of muscle fibres with fat, an increase in fibrosis, changes in muscle metabolism, oxidative stress, and degeneration of the neuromuscular junction and leading to progressive loss of muscle function and frailty. Sarcopenia is determined by two factors: initial amount of muscle mass and rate at which aging decreases muscle mass. Due to the loss of independence associated with loss of muscle strength, the threshold at which muscle wasting becomes a disease is different pathologically from person to person.

Simple circumference measurement does not provide enough data to determine whether or not an individual is suffering from severe sarcopenia. Sarcopenia is also marked by a decrease in the circumference of distinct types of muscle fibers. Skeletal muscle has different fiber-types, which are characterized by expression of distinct myosin variants. During sarcopenia, there is a decrease in "type 2" fiber circumference (Type II), with little to no decrease in "type I" fiber circumference (Type I), and deinervated type 2 fibers are often converted to type 1 fibers by reinnervation by slow type 1 fiber motor nerves.

Proventricular dilatation disease (PDD) is a disease affecting psittacines (parrots). It was first recognized and described in 1978 by Dr. Hannis L. Stoddard. Since the first reported cases were involving species of macaw, the condition was termed macaw wasting syndrome.

Starvation is a severe deficiency in caloric energy intake, below the level needed to maintain an organism's life. It is the most extreme form of malnutrition. In humans, prolonged starvation can cause permanent organ damage and eventually, death. The term inanition refers to the symptoms and effects of starvation. Starvation may also be used as a means of torture or execution.

According to the World Health Organization, hunger is the single gravest threat to the world's public health. The WHO also states that malnutrition is by far the biggest contributor to child mortality, present in half of all cases. Undernutrition is a contributory factor in the death of 3.1 million children under five every year. Figures on actual starvation are difficult to come by, but according to the Food and Agriculture Organization, the less severe condition of undernourishment currently affects about 842 million people, or about one in eight (12.5%) people in the world population.

The bloated stomach, as seen in the adjacent picture, represents a form of malnutrition called kwashiorkor which is caused by insufficient protein despite a sufficient caloric intake. Better medicine will prevent the pictured symptoms in which included is weight loss and muscle wasting from further taking form.

About 50% of all cancer patients suffer from cachexia. Those with upper gastrointestinal and pancreatic cancers have the highest frequency of developing a cachexic symptom. This figure rises to 80% in terminal cancer patients. In addition to increasing morbidity and mortality, aggravating the side effects of chemotherapy, and reducing quality of life, cachexia is considered the immediate cause of death of a large proportion of cancer patients, ranging from 22% to 40% of the patients.

Symptoms of cancer cachexia include progressive weight loss and depletion of host reserves of adipose tissue and skeletal muscle. Cachexia should be suspected if involuntary weight loss of greater than 5% of premorbid weight occurs within a six-month period. Traditional treatment approaches, such as appetite stimulants, 5-HT antagonists, nutrient supplementation, and COX-2 inhibitor, have failed to demonstrate success in reversing the metabolic abnormalities seen in cancer cachexia.

Cachexia is often seen in end-stage cancer, and in that context is called "cancer cachexia". Patients with congestive heart failure can have a cachectic syndrome. Also, a cachexia comorbidity is seen in patients who have any of the range of illnesses classified as chronic obstructive pulmonary disease. Cachexia is also associated with advanced stages of chronic kidney disease, cystic fibrosis, multiple sclerosis, motor neuron disease, Parkinson's disease, dementia, HIV/AIDS and other progressive illnesses.

Early symptoms include impulsivity, irritability, and hyperactivity. Atrophy (wasting away) of the stomach weakens the perception of hunger, since the perception is controlled by the percentage of the stomach that is empty. Individuals experiencing starvation lose substantial fat (adipose tissue) and muscle mass as the body breaks down these tissues for energy. "Catabolysis" is the process of a body breaking down its own muscles and other tissues in order to keep vital systems such as the nervous system and heart muscle (myocardium) functioning. The energy deficiency inherent in starvation causes fatigue and renders the victim more apathetic over time. As the starving person becomes too weak to move or even eat, their interaction with the surrounding world diminishes. In females, menstruation ceases when the body fat percentage is too low to support a fetus.

Victims of starvation are often too weak to sense thirst, and therefore become dehydrated. All movements become painful due to muscle atrophy and dry, cracked skin that is caused by severe dehydration. With a weakened body, diseases are commonplace. Fungi, for example, often grow under the esophagus, making swallowing painful. Vitamin deficiency is also a common result of starvation, often leading to anemia, beriberi, pellagra, and scurvy. These diseases collectively can also cause diarrhea, skin rashes, edema, and heart failure. Individuals are often irritable and lethargic as a result.

There is insufficient scientific data on exactly how long people can live without food. Although the length of time varies with an individual's percentage of body fat and general health, one medical study estimates that in adults complete starvation leads to death within 8 to 12 weeks. There are isolated cases of individuals living up to 25 weeks without food. Starvation begins when an individual has lost about 30% of their normal body weight. Once the loss reaches 40% death is almost inevitable.

One of the reasons a cat may stop eating is separation anxiety and the emotional stress that results. Moving, gaining or losing housemates or pets, going on vacation, or prolonged boarding are all common situations that pet owners report just prior to the onset of the disease, but it may develop without these conditions existing. Obesity is known to increase the risk of hepatic lipidosis; however, there is no known "official" cause of the disease. Severe anorexia usually precedes the onset of the disease. When the cat has no energy from eating, the liver must metabolize fat deposits in the body into usable energy to sustain life. The cat liver, however, is poor at metabolizing fat, causing a buildup of fat in the cells of the liver, leading to fatty liver. At this point the disease can be diagnosed; however, it will often not be diagnosed, and many animals are euthanized due to improper or no diagnosis.

Marasmus is commonly represented by a shrunken, wasted appearance, loss of muscle mass and subcutaneous fat mass. Buttocks and upper limb muscle groups are usually more affected than others. Edema is not a sign of marasmus and is only present in kwashiorkor, and marasmic kwashiorkor. Other symptoms of marasmus include unusual body temperature (hypothermia, pyrexia), anemia, dehydration (as characterized with consistent thirst and shrunken eyes), hypovolemic shock (weak radial pulse, cold extremities, decreased consciousness), tachypnea (pneumonia, heart failure), abdominal manifestations (distension, decreased or metallic bowel sounds, large or small liver, blood or mucus in the stools), ocular manifestations (corneal lesions associated with vitamin A deficiency), dermal manifestations (evidence of infection, purpura, and ear, nose, and throat symptoms (otitis, rhinitis). Dry skin and brittle hair are also symptoms of marasmus. Marasmus can also make children short-tempered and irritable.

Microsporidiosis is an opportunistic intestinal infection that causes diarrhea and wasting in immunocompromised individuals (HIV, for example). It results from different species of microsporidia, a group of microbial (unicellular) fungi.

In HIV infected individuals, microsporidiosis generally occurs when CD4+ T cell counts fall below 150.

Symptoms include severe seborrheic dermatitis of the scalp, severe diarrhea, recurrent local and systemic infection, central nervous system problems, and failure to thrive. Other symptoms also include scaling on the trunk and limbs, red patches of skin on parts of the body that bend, fevers, reduced blood protein levels, thick red skin patches, peeling of the skin, itching, corneal ulcers. wasting of the lymph nodes, underdeveloped lymphatics, anemia, wasting, and nervous system deficiency. The disease may then spread to the rest of the epidermis with the appearance of crusty, dry, moist or greasy scaling on the scalp. Scaling could also appear behind the ears, nose or eyebrows, or around the mouth; peeling of the skin may also happen in these areas. If left untreated, the skin infections will cause loss of protein or electrolytes. Leiner’s Disease may also be accompanied by a systemic reaction that is most evident in its gastrointestinal manifestation.

It is caused by a deficit of the complement protein, C5; however, case reports have described it in relation to deficits in either C3 or C4.

Marasmus is caused by a severe deficiency of nearly all nutrients, especially protein, carbohydrates, and lipids, usually due to poverty and scarcity of food. Viral, bacterial, and parasitic infections can cause children to absorb too few nutrients, even when consumption is adequate. Marasmus can develop in children who suffer from weakening conditions such as chronic diarrhea.

Feline hepatic lipidosis shares similar symptoms to other problems, including liver disease, renal failure, feline leukemia, Feline infectious peritonitis and some cancers. Diagnosis requires tests that target the liver to make an accurate diagnosis. Jaundice is highly indicative of the disease. Blood tests and a liver biopsy will confirm the presence of the disease.

Usually manifesting itself between 20 and 40 years of age, it is characterized by pain, paresthesia, muscular weakness and autonomic dysfunction. In its terminal state, the kidneys and the heart are affected. FAP is characterized by the systemic deposition of amyloidogenic variants of the transthyretin protein, especially in the peripheral nervous system, causing a progressive sensory and motor polyneuropathy.