Clinical signs are normally only seen in either piglets less than 3 weeks old or pregnant sows.

Signs in piglets include rhinitis, pneumonia, anaemia, fever and sudden death. Black discoloration around the eyes is often seen and gastrointestinal and neurological signs are also reported.

Signs in pregnant sows include reproductive failure, genital ulceration and agalactia.

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.

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.

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.

Inclusion Body Rhinitis, also known as IBR or Cytomegalic Inclusion Disease, is a pig disease caused by porcine cytomegalovirus, which is a member of the herpesvirus family. It is a notifiable disease that is found worldwide. It is spread both vertically and horizontally and prevalence is high.

It is not a zoonosis but the risk to humans that receive pig organ transplants is currently under investigation.

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)

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.

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.

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.

Truckloads or railcar loads of PSS-susceptible pigs may be found with a higher-than-average percentage dead on arrival after stressful events such as transport.

Initial signs of the onset of PSS are pyrexia, panting, sweating, tachycardia and arrhythmias. Chronic cases may show muscle atrophy.

Under halothane anaesthesia, pigs will suddenly become rigid and pyrexic.

The halothane challenge was the historical method of diagnosis.

Genetic testing via a PCR enables affected and carrier animals to be found.

Psychologist Melanie Joy has likened PSS to post-traumatic stress disorder in humans.

Porcine stress syndrome, also known as malignant hyperthermia or PSS, is a condition in pigs. It is characterised by hyperthermia triggered by stress, anaesthesia with halothane or intense exercise. PSS may appear as sudden death in pigs, often after transport. It is an inherited, autosomal recessive disorder due to a defective ryanodine receptor leading to huge calcium influx, muscle contracture and increase in metabolism.

PSS can manifest itself in the abattoir as the production of Pale, Soft and Exudative meat due to a rapid fall in muscle pH and degradation of muscle proteins and structure. This meat is usually rejected after inspection.

This disorder is most common in Landrace, Piétrain and crossbreeds of these breeds of pig. The genes may have been favoured in the past due to a larger muscle bulk in these breeds. However this is not standard protocol in developed countries these days.

Leiner's disease is a systemic disease, a skin disorder and extends to erythroderma, typically diagnosed in early infancy. Leiner’s disease is characterized by a long-lasting seborrhea dermatitis associated with increased likelihood to infection. Other characterizations found on newborns with Leiner’s disease are a patch or a large patch of red skin normally on the bottom and spreads to the rest of the body.

This disease is also listed as a "rare disease", meaning that a small percent of the population, fewer than 200,000 people in the United States, will have this disorder.

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.

Affected male and carrier female dogs generally begin to show signs of the disease at two to three months of age, with proteinuria. By three to four months of age, symptoms include for affected male dogs: bodily wasting and loss of weight, proteinuria & hypoalbuminemia. Past nine months of age, hypercholesterolemia may be seen. In the final stages of the disease, at around 15 months of age for affected males, symptoms are reported as being renal failure, hearing loss and death. Since the condition is genetically dominant, diagnosis would also include analysis of the health of the sire and dam of the suspected affected progeny if available.

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.

After an incubation period of up to seven days, the signs associated with swine vesicular disease occur. The first sign is a transient mild fever. Other signs include:

- Vesicles in the mouth and on the snout and feet

- Lameness and an unsteady gait, shivering and jerking–type leg movements

- Ruptured vesicles can cause ulcers on limbs and feet, and foot pads may be loosened.

Young animals are more severely affected. Recovery often occurs within a week. There is no mortality.

Swine vesicular disease has the same clinical signs as foot-and-mouth disease, and can only be diagnosed by laboratory testing.

Onset occurs in infancy or early childhood, usually before 3 years of age. Progression is slow until the teenage years at which point it may accelerate, resulting in severe disability.

Symptoms are usually more severe and rapidly progressive than in the other more common Charcot–Marie–Tooth diseases. Some patients may never walk and solely use wheelchairs by the end of their first decade, while others may need only a cane (walking stick) or similar support through life.

Dejerine–Sottas disease is characterized by moderate to severe lower and upper extremity weakness and loss of sensation, which occur mainly in the lower legs, forearms, feet and hands. Loss of muscle mass and reduced muscle tone can occur as the disease progresses. Other symptoms may include pain in the extremities, curvature of the spine, clawed hands, foot deformities, ataxia, peripheral areflexia, and slow acquisition of motor skills in childhood. Symptoms that are less common can include limitation of eye movements, other eye problems such as nystagmus or anisocoria, or mild hearing loss.

Swine vesicular disease (SVD) is an acute, contagious viral disease of swine caused by the swine vesicular disease virus, an enterovirus. It is characterized by fever and vesicles with subsequent ulcers in the mouth and on the snout, feet, and teats. The pathogen is relatively resistant to heat, and can persist for a long time in salted, dried, and smoked meat products. Swine vesicular disease does not cause economically-important disease, but is important due to its similarity to foot-and-mouth disease.

Symptoms of the Roussy–Lévy syndrome mainly stem from nerve damage and the resulting progressive muscle atrophy. Neurological damage may result in absent tendon reflexes (areflexia), some distal sensory loss and decreased excitability of muscles to galvanic and faradic stimulation. Progressive muscle wasting results in weakness of distal limb muscles (especially the peronei), gait ataxia, pes cavus, postural tremors and static tremor of the upper limbs, kyphoscoliosis, and foot deformity.

These symptoms frequently translate into delayed onset of ability to walk, loss of coordination and balance, foot drop, and foot-bone deformities. They are usually first observed during infancy or early childhood, and slowly progress until about age 30, at which point progression may stop in some individuals, or symptoms may continue to slowly progress.

Some early signs of HIBMs includes:

- Difficulty walking on heels, and difficulty running;

- Weak index finger;

- Frequent loss of balance.

- On muscle biopsy, the typical finding includes inclusion bodies, rimmed vacuoles and accumulation of aberrant proteins similar to those found in senile plaques of Alzheimer's disease (amyloid beta, hyperphosphorylated tau, amongst others)

Porcine enzootic pneumonia is caused by "Mycoplasma hyopneumoniae" and describes an important respiratory disease of pigs.

It is part of the Porcine Respiratory Disease Complex along with Swine Influenza, PRRS and Porcine circovirus 2, and even though on its own it is quite a mild disease, it predisposes to secondary infections with organisms such as "Pasteurella multocida".

Clinical signs are most commonly seen in pigs over 8 weeks of age, and the disease occurs worldwide. Transmission is horizontal and vertical from sows.

Samoyed hereditary glomerulopathy [glo-mer″u-lop´ah-the] (SHG) is an hereditary noninflammatory disease of the renal glomeruli, occurring in the Samoyed breed of dog. The disease has been shown to be a model for hereditary nephritis (HN) in humans in that the disease resembles that of the human disease. Because of this, it is sometimes referred to by the name given to the disease in humans when referring to the conditions in Samoyed dogs. Alternatively, it may also be known as X-linked hereditary nephritis. Genetically, the trait is inherited as a sex-linked, genetically dominant disease, and thus affects male dogs to a greater degree than female dogs, since males only have one X chromosome.

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.

Hereditary inclusion body myopathies (HIBM) are a heterogeneous group of very rare genetic disorders which have different symptoms. Generally, they are neuromuscular disorders characterized by muscle weakness developing in young adults. Hereditary inclusion body myopathies comprise both autosomal recessive and autosomal dominant muscle disorders that have a variable expression (phenotype) in individuals, but all share similar structural features in the muscles.

HIBMs are a group of muscle wasting disorders, which are uncommon in the general world population. One autosomal recessive form of HIBM is known as IBM2 or GNE myopathy, which is a common genetic disorder amongst people of Iranian Jewish descent. IBM2 has also been identified in other minorities throughout the world, including people of Asian (Japanese and others), European, and South American origin, as well as Muslim people in the Middle Eastern, Palestinian, and Iranian origin. In Japan and many East Asian countries, this disorder is known as Distal Myopathy with Rimmed Vacuoles (DMRV).

IBM2 causes progressive muscle weakness and wasting. Muscle wasting usually starts around the age of 20 – 30 years, although young onset at 17 and old onset at 52 has been recorded. As such, it affects the most productive times of our lives. It can progress to marked disability within 10 – 15 years, confining many people with IBM2 to a wheelchair. The weakness and severity can vary from person to person. In some, weakness in the legs is noticed first. In few others, the hands are weakened more rapidly than the legs. Weakness is progressive, which means the muscle becomes weaker over time. IBM2 does not seem to affect the brain, internal organs or sensation. The quadriceps are relatively spared, and remain strong until the late stages of disease, which is the reason IBM2 is often referred to as Quadriceps Sparing Myopathy (QSM).