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)

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.

Clinical signs may vary, with regurgitation and neurological symptoms being the most prominent in the early and later stages of its progression. In boa constrictors, the first signs may include off-and-on regurgitation, and some develop head tremors. Abnormal shedding may occur. Some develop chronic regurgitation and anorexia (lack of appetite or refusal to feed). However, not all infected snakes may regurgitate. Boas lose weight and may develop clogged nares (nostrils), stomatitis, or secondary pneumonia. The disease can rapidly progress to produce nervous-system disorders, such as disorientation, corkscrewing of the head and neck, holding the head in abnormal and unnatural positions, rolling onto the back, or stargazing. Stomatitis, pneumonia, undifferentiated cutaneous sarcomas, lymphoproliferative disorders, and leukemia have all been observed in affected specimens. Burmese pythons generally show signs of central nervous system disease without manifestation of other clinical signs and regurgitation is seen only in boas. These are symptoms similar to those seen in specimens infected by "Chlamydia"–specifically "Chlamydophila psittaci", the so-called parrot's disease.

Several snakes have been seen with proliferative pneumonia, while inclusions are commonly seen in the liver, kidney, and pancreas. Cases have also been observed where with only very few inclusions. In a few snakes with signs of central nervous system disease, and with a severe encephalitis, no inclusions have been seen in any cells. While the presence of characteristic inclusions is diagnostic for the disease, the absence of such inclusions does not necessarily indicate that the snake is not diseased or is free from the IBD virus. While cells having inclusions may show mild degenerative changes, inflammation is rarely seen in visceral tissues. In the brain, mild to severe encephalitis occurs, with lymphocytic perivascular cuffing. Several snakes with lymphoproliferative disorders have been identified with lymphoid infiltrates in multiple organs.

Symptoms typically begin to appear two months after the fish are transferred from freshwater hatcheries to open net sea cages. Symptoms include mucus build-up on the gills of infected fish and hyper-plastic lesions, causing white spots and eventual deterioration of the gill tissue. Fish will show signs of dyspnoea such as rapid opercular movements and lethargy. Although usually recognised by hyperplastic and proliferative gill lesions, the effects of AGD occur before oxygen transfer across the gill is severely compromised. AGD affected fish show a significant increase in vascular resistance contributing to cardiovascular collapse. Such effects result in compensatory changes in heart shape to improve its efficiency at pumping blood.

Contributing factors are an ambient water temperature above 16 degrees Celsius, crowding and poor water circulation inside the sea pens. Clinical cases are more common in the Summer. The lesions on the gills are highly suggestive of infection. Gill biopsies can be observed under the microscope for amoebas, or tested using fluorescent antibody testing.

Amoebic gill disease (AGD) is a potentially fatal disease of some marine fish. It is caused by "Neoparamoeba perurans", the most important amoeba in cultured fish. It primarily affects farm raised fish of the Salmonidae family, most notably affecting the Tasmanian Atlantic Salmon (Salmo salar) industry, costing the A$20 million a year in treatments and lost productivity. Turbot, bass, bream, sea urchins and crabs have also been infected.

The disease has also been reported affecting the commercial salmon fisheries of the United States, Australia, New Zealand, France, Spain, Ireland and Chile. It was first diagnosed in the summer of 1984/1985 in populations of Atlantic Salmon off the east coast of Tasmania and was found to be caused by the "Neoparamoeba perurans" n.sp.

Digital dermatitis appears as lesions which initially looks like raw, red, oval ulcer on the back of the heel. These lesions develop raised, hair-like projections or wart-like lesions, and some may extend up between the claws or appear on the front of the foot.

A scoring system was developed to classify the different stages of digital dermatitis, the M-stages system, where "M" stands for Mortellaro. The different stages are described as: M0, healthy skin; M1, early stage, skin defect < 2 cm diameter; M2, acute active ulcerative lesion; M3, healing stage, lesion covered with scab-like material; M4, chronic stage, that may be dyskeratotic (mostly thickened epithelium) or proliferative or both.

Diagnosis is principally based on history and clinical signs. It is very rare that attempts are made to isolate the bacteria.

Digital dermatitis is a disease that causes lameness in cattle. It was first discovered in Italy in 1974 by Cheli and Mortellaro. This disease is caused by a mixture of different bacteria. Anaerobic bacteria, including spirochetes of the genus "Treponema", are found in the lesions associated with the infection. Digital dermatitis is different from foot rot in cattle and both conditions may occur concurrently.

Digital dermatitis primarily affects dairy cattle and has been known to lower the quantity of milk produced, but the quality of the milk is unaffected.

Evidence show that risk factors favouring digital dermatitis outbreaks include: poor hygiene and high humidity; introduction of infected animals; no hoof care for heifers and dry cows; high levels of chronically infected animals; insufficient or inadequate hoof trimming; soft hooves and unbalanced nutrition.

Inclusion body disease (IBD) in the boid family of snakes, particularly "Boa constrictor", has been recognized since the mid-1970s. It is so named because of the characteristic intracytoplasmic inclusions which are observed in clinical examinations in epidermal cells, oral mucosal epithelial cells, visceral epithelial cells, and neurons. In the 1970s and 1980s, the disease was most commonly observed in Burmese pythons, "Python bivittatus". From the 1980s till the present day, it has been most commonly observed in boa constrictors from South America.

All boid snakes should be considered susceptible to the disease. Many zoos quarantine boas specifically as a result of this high risk before introducing them into their permanent collections and (breeding) programs. While the disease has not been identified in non-boid snakes, it is yet unknown whether non-boid snakes harbour the virus. The primary host of this virus has not yet been identified, but mites are thought to be primary hosts or at least a contributory factor.

Its distribution is worldwide, specifically in captive boid snakes. Its occurrence in the wild is unknown. Strangely enough, the disease has only been identified in adult and subadult specimens. Even so, all age groups are considered susceptible. Also, anecdotal reports of the infection in neonates have been made. A retro-like virus infection was suspected as the causative agent of IBD, but identification of highly divergent arenavirus sequences from boa constrictors with IBD suggested arenaviruses to be the etiological agent of IBD. Cell culture isolation of several arenaviruses from boid snakes with IBD further solidified, but did not yet confirm, the etiological relationship between IBD and arenaviruses.

Skin disorders are among the most common health problems in dogs, and have many causes. The condition of a dog's skin and coat are also an important indicator of its general health. Skin disorders of dogs vary from acute, self-limiting problems to chronic or long-lasting problems requiring life-time treatment. Skin disorders may be primary or secondary (due to scratching, itch) in nature, making diagnosis complicated.

Skin disease may result from deficiency or overactivity of immune responses. In cases where there is insufficient immune responses the disease is usually described by the secondary disease that results. Examples include increased susceptibility to demodectic mange and recurrent skin infections, such as Malassezia infection or bacterial infections. Increased, but harmful immune responses, can be divided into hypersensitivity disorders such as atopic dermatitis, and autoimmune disorders (autoimmunity), such as pemphigus and discoid lupus erythematosus.

The primary symptoms of contact granuloma include chronic or acute hoarseness of the voice and vocal fatigue. More severe granulomas may result in throat ache or soreness, as well as pain that lateralizes to one or both ears. Smaller granulomas may result in a tickling sensation or slight discomfort.

Signs of contact granulomas are frequent coughing and throat-clearing. Some people may also notice that their pitch range is restricted due to granuloma.

Contact granuloma, also known as a contact ulcer or vocal process granuloma, is a condition that develops due to persistent tissue irritation in the posterior larynx. Benign granulomas, not to be confused with other types of granulomas, occur on the vocal process of the vocal folds, where the vocal ligament attaches. Signs and symptoms may include hoarseness of the voice, or a sensation of having a lump in the throat, but contact granulomas may also be without symptoms. The most common cause of the condition is sustained periods of increased pressure on the vocal folds, and is commonly seen in people who use their voice excessively, such as singers (John Mayer, for example). Treatment typically includes voice therapy and changes to lifestyle factors. Granulomas thought to result secondary to gastroesophageal reflux are controlled through the use of anti-reflux medication.

Proximal enteritis, also known as anterior enteritis or duodenitis-proximal jejunitis (DPJ), is inflammation of the duodenum and upper jejunum. It produces a functional stasis of the affected intestine (ileus) and hypersecretion of fluid into the lumen of that intestine. This leads to large volumes of gastric reflux, dehydration, low blood pressure, and potentially shock. Although the exact cause is not yet definitively known, proximal enteritis requires considerable supportive care.

The portal of entry is the gastrointestinal tract. The organism is acquired usually by insufficiently cooked pork or contaminated water, meat, or milk. Acute "Y. enterocolitica" infections usually lead to mild self-limiting enterocolitis or terminal ileitis and adenitis in humans. Symptoms may include watery or bloody diarrhea and fever, resembling appendicitis or salmonellosis or shigellosis. After oral uptake, "Yersinia" species replicate in the terminal ileum and invade Peyer's patches. From here they can disseminate further to mesenteric lymph nodes causing lymphadenopathy. This condition can be confused with appendicitis, so is called pseudoappendicitis. In immunosuppressed individuals, they can disseminate from the gut to the liver and spleen and form abscesses. Because "Yersinia" species are siderophilic (iron-loving) bacteria, people with hereditary hemochromatosis (a disease resulting in high body iron levels) are more susceptible to infection with "Yersinia" (and other siderophilic bacteria). In fact, the most common contaminant of stored blood is "Y. enterocolitica". See yersiniosis for further details.

In medicine, Aschoff bodies are nodules found in the hearts of individuals with rheumatic fever. They result from inflammation in the heart muscle and are characteristic of rheumatic heart disease. These nodules were discovered independently by Ludwig Aschoff and Paul Rudolf Geipel, and for this reason they are occasionally called Aschoff-Geipel bodies.

Signs and symptoms of enteritis are highly variable and vary based on the specific cause and other factors such as individual variance and stage of disease.

Symptoms may include abdominal pain, cramping, diarrhoea, dehydration, fever, nausea, vomiting and weight loss.

Signs include acute onset of moderate to severe pain, large volumes of gastric reflux (4–20 L per decompression) which is usually orange-brown and fetid, distended small intestine (up to 5–7 cm in diameter) palpable on rectal examination, fever, depression, increased heart rate (>60 bpm), increased respiratory rate, prolonged CRT, and darkened mucous membranes. After gastric decompression, the horse may show signs of malaise and act lethargic, but pain level usually improves.

Abdominocentesis usually reveals a yellow, turbid fluid with an increased white blood cell count (usually 5,000–10,000 cells/microliter) and protein level (>3.5 g/dl), although the fluid may be serosanginous in severe cases. A chemistry panel will often show electrolyte abnormalities (hypokalemia, hyponatremia, hypochloremia) due to electrolyte loss into the lumen of the intestine. Leukocytes may be normal, increased, or decreased. PCV and total protein are usually both increased due to fluid loss, and the horse displays a prerenal azotemia. On the chemistry panel, liver enzymes such as GGT, ALP, AST are increased, likely due to ascending infection from the common bile duct, endotoxin absorption, and hypoperfusion. A metabolic acidosis with a high anion gap is often seen due to loss of bicarbonate in gastric reflux and an increase in lactic acid in the blood, secondary to hypovolemia and decreased tissue perfusion.

Diagnosis may be simple in cases where the patient's signs and symptoms are idiopathic to a specific cause. However this is generally not the case, considering that many pathogens which cause enteritis may exhibit the similar symptoms, especially early in the disease. In particular, "campylobacter, shigella, salmonella" and many other bacteria induce acute self-limited colitis, an inflammation of the lining of the colon which appears similar under the microscope.

A medical history, physical examination and tests such as blood counts, stool cultures, CT scans, MRIs, PCRs, colonoscopies and upper endoscopies may be used in order to perform a differential diagnosis. A biopsy may be required to obtain a sample for histopathology.

Infection with "Y. enterocolitica" can cause a variety of symptoms depending on the age of the person infected, therefore it's often referred to as "monkey of diseases". Common symptoms in children are fever, abdominal pain, and diarrhea, which is often bloody. Symptoms typically develop 4 to 7 days after exposure and may last 1 to 3 weeks or longer. In older children and adults, right-sided abdominal pain and fever may be the predominant symptoms, and may be confused with appendicitis. In a small proportion of cases, complications such as skin rash, joint pains, ileitis, erythema nodosum, and sometimes septicemia, acute arthritis or the spread of bacteria to the bloodstream (bacteremia) can occur.

Enteropathy refers to any pathology of the intestine. Although enteritis specifically refers to an inflammation of the intestine, and is thus a more specific term than "enteropathy", the two phrases are sometimes used interchangeably.

Even though anatomically part of the GI tract, diseases of the mouth are often not considered alongside other gastrointestinal diseases. By far the most common oral conditions are plaque-induced diseases (e.g. gingivitis, periodontitis, dental caries). Some diseases which involve other parts of the GI tract can manifest in the mouth, alone or in combination, including:

- Gastroesophageal reflux disease can cause acid erosion of the teeth and halitosis.

- Gardner's syndrome can be associated with failure of tooth eruption, supernumerary teeth, and dentigerous cysts.

- Peutz–Jeghers syndrome can cause dark spots on the oral mucosa or on the lips or the skin around the mouth.

- Several GI diseases, especially those associated with malabsorption, can cause recurrent mouth ulcers, atrophic glossitis, and angular cheilitis (e.g. Crohn's disease is sometimes termed orofacial granulomatosis when it involves the mouth alone).

- Sideropenic dysphagia can cause glossitis, angular cheilitis.

Oesophageal diseases include a spectrum of disorders affecting the oesophagus. The most common condition of the oesophagus in Western countries is gastroesophageal reflux disease, which in chronic forms is thought to result in changes to the epithelium of the oesophagus, known as Barrett's oesophagus.

Acute disease might include infections such as oesophagitis, trauma caused ingestion of corrosive substances, or rupture of veins such as oesophageal varices, Boerhaave syndrome or Mallory-Weiss tears. Chronic diseases might include congenital diseases such as Zenker's diverticulum and esophageal webbing, and oesophageal motility disorders including the nutcracker oesophagus, achalasia, diffuse oesophageal spasm, and oesophageal stricture.

Oesophageal disease may result in a sore throat, throwing up blood, difficulty swallowing or vomiting. Chronic or congenital diseases might be investigated using barium swallows, endoscopy and biopsy, whereas acute diseases such as reflux may be investigated and diagnosed based on symptoms and a medical history alone.

Yersiniosis is an infectious disease caused by a bacterium of the genus "Yersinia". In the United States, most yersiniosis infections among humans are caused by "Yersinia enterocolitica". The infection by "Y. enterocolitica" is also known as pseudotuberculosis. Yersiniosis is mentioned as a specific zoonotic disease to prevent outbreaks in European Council Directive 92/117/EEC.

Infection with " Y . enterocolitica" occurs most often in young children. The infection is thought to be contracted through the consumption of undercooked meat products, unpasteurized milk, or water contaminated by the bacteria. It has been also sometimes associated with handling raw chitterlings.

Another bacterium of the same genus, "Yersinia pestis", is the cause of Plague.

Specific types of enteropathy include:

- Enteropathy-associated T-cell lymphoma

- Environmental enteropathy

- Eosinophilic enteropathy

- Gluten-sensitive enteropathy (which can progress to coeliac disease)

- Coeliac disease

- Human immunodeficiency virus (HIV) HIV Enteropathy

- Immunodysregulation polyendocrinopathy and enteropathy, X-linked (see FOXP3)

- Protein-losing enteropathy

- Radiation enteropathy

- Tropical enteropathy

If the condition also involves the stomach, it is known as "gastroenteropathy".

In pigs, porcine proliferative enteropathy is a diarrheal disease.

Yersinia enterocolitica is a Gram-negative bacillus-shaped bacterium, belonging to the family Enterobacteriaceae. It is motile at temperatures of 22–29°C, but becomes nonmotile at normal human body temperature"." "Y. enterocolitica" infection causes the disease yersiniosis, which is an animal-borne disease occurring in humans, as well as in a wide array of animals such as cattle, deer, pigs, and birds. Many of these animals recover from the disease and become carriers; these are potential sources of contagion despite showing no signs of disease. The bacterium infects the host by sticking to its cells using trimeric autotransporter adhesins.

The genus "Yersinia" includes 11 species:

"Y. pestis, Y. pseudotuberculosis, Y. enterocolitica, Y. frederiksenii,"

"Y. intermedia, Y. kristensenii, Y. bercovieri," "Y. mollaretii, Y. rohdei, Y. aldovae", and "Y. ruckeri". Among them, only "Y. pestis, Y. pseudotuberculosis", and certain strains of "Y. enterocolitica" are of pathogenic importance for humans and certain warm-blooded animals, whereas the other species are of environmental origin and may, at best, act as opportunists. However, "Yersinia" strains can be isolated from clinical materials, so have to be identified at the species level.

"Y. enterocolitica" is a heterogeneous group of strains, which are traditionally classified by biotyping into six biogroups on the basis of phenotypic characteristics, and by serotyping into more than 57 O serogroups, on the basis of their O (lipopolysaccharide or LPS) surface antigen. Five of the six biogroups (1B and 2–5) are regarded as pathogens. However, only a few of these serogroups have been associated with disease in either humans or animals. Strains that belong to serogroups O:3 (biogroup 4), O:5,27 (biogroups 2 and 3), O:8 (biogroup 1B), and O:9 (biogroup 2) are most frequently isolated worldwide from human samples. However, the most important "Y. enterocolitica" serogroup in many European countries is serogroup O:3 followed by O:9, whereas the serogroup O:8 is mainly detected in the United States.

"Y. enterocolitica" is widespread in nature, occurring in reservoirs ranging from the intestinal tracts of numerous mammals, avian species, cold-blooded species, and even from terrestrial and aquatic niches. Most environmental isolates are avirulent; however, isolates recovered from porcine sources contain human pathogenic serogroups. In addition, dogs, sheep, wild rodents, and environmental water may also be a reservoir of pathogenic "Y. enterocolitica "strains. Human pathogenic

strains are usually confined to the intestinal tract and lead to enteritis/diarrhea.