External abscesses are the most common form of pigeon fever seen in horses. Abscesses develop on the body, usually in the pectoral region and along the ventral midline of the abdomen. However, abscesses can also develop on other areas of the body such as the prepuce, mammary gland, triceps, limbs and head. The fatality rate for this form infection is very low. The abscess is often drained once it has matured.

This is the least common form of pigeon fever seen in horses. It is characterized by severe limb swelling and cellulitis in one or both hind limbs and can lead to lameness, fever, lethargy and loss of appetite. Antimicrobial and anti-inflammatory treatments are required to prevent further complications such as limb edema, prolonged or recurrent infection, lameness, weakness and weight loss.

In the subgroup of patients where an inoculating event was noted, the mean incubation period of acute melioidosis was 9 days (range 1–21 days). Patients with latent melioidosis may be symptom-free for decades; the longest period between presumed exposure and clinical presentation is 62 years. The potential for prolonged incubation was recognized in US servicemen involved in the Vietnam War, and was referred to as the "Vietnam time-bomb". A wide spectrum of severity exists; in chronic presentations, symptoms may last months, but fulminant infection, particularly associated with near-drowning, may present with severe symptoms over hours.

Symptoms usually appear 2 to 4 weeks after exposure. There are four general types of infection including localized, pulmonary, blood-borne, or disseminated throughout the body. The type and location of the infection usually determines which symptoms appear first as well as which symptoms are more prominent.

Patients with melioidosis usually present with fever. Pain or other symptoms may be suggestive of a clinical focus, which is found in around 75% of patients. Such symptoms include cough or pleuritic chest pain suggestive of pneumonia, bone or joint pain suggestive of osteomyelitis or septic arthritis, or cellulitis. Intra-abdominal infection (including liver and/or splenic abscesses, or prostatic abscesses) do not usually present with focal pain, and imaging of these organs using ultrasound or computed tomography should be performed routinely. In one series of 214 patients, 27.6% had abscesses in the liver or spleen (95% confidence interval, 22.0% to 33.9%). "B. pseudomallei" abscesses may have a characteristic "honeycomb" or "swiss cheese" architecture (hypoechoic, multiseptate, multiloculate) on CT.

Regional variations in disease presentation are seen: parotid abscesses characteristically occur in Thai children, but this presentation has been described only once in Australia. Conversely, prostatic abscesses are found in up to 20% of Australian males, but are rarely described elsewhere. An encephalomyelitis syndrome is recognised in northern Australia.

Patients with melioidosis usually have risk factors for disease, such as diabetes, thalassemia, hazardous alcohol use, or renal disease, and frequently give a history of occupational or recreational exposure to mud or pooled surface water. However, otherwise healthy patients, including children, may also get melioidosis.

In up to 25% of patients, no focus of infection is found and the diagnosis is usually made on blood cultures or throat swab. Melioidosis is said to be able to affect any organ in the body except the heart valves (endocarditis). Although meningitis has been described secondary to ruptured brain abscesses, primary meningitis has not been described. Less common manifestations include intravascular infection, lymph node abscesses (1.2–2.2%), pyopericardium and myocarditis, mediastinal infection, and thyroid and scrotal abscesses and ocular infection.

Strangles (equine distemper) is a contagious upper respiratory tract infection of horses and other equines caused by a gram-positive bacterium, "Streptococcus equi". As a result the lymph nodes swell, compressing the pharynx, larynx and trachea and can cause airway obstruction leading to death, hence the name Strangles. Strangles is enzootic in domesticated horses worldwide. The contagious nature of the infection has at times led to limitations on sporting events.

A horse with strangles will typically develop abscesses in the lymph nodes of the head and neck causing coughing fits and difficulty swallowing. Clinical signs include fever up to 106 °F and yellow coloured nasal discharge from both the nose and eyes.

Abscesses may form in other areas of the body, such as the abdomen, lungs and brain. This is considered a chronic form of strangles called "bastard strangles" and can have serious implications if the abscesses rupture. Horses develop this form of strangles when their immune systems are compromised or if the bacteria rapidly invades the body.

Strangles has a 8.1% mortality rate. Mortality is lower in cases without complications than it is in cases of bastard strangles. The disease is very contagious and morbidity is high. Precautions to limit the spread of the illness are necessary and those affected are normally isolated. An isolation period of 4–6 weeks is usually necessary to ensure that the disease is not still incubating before ending the quarantine.

Chronic melioidosis is usually defined by a duration of symptoms greater than two months and occurs in about 10% of patients. The clinical presentation of chronic melioidosis is protean and includes such presentations as chronic skin infections, chronic lung nodule, and pneumonia. In particular, chronic melioidosis closely mimics tuberculosis, and has sometimes been called "Vietnamese tuberculosis".

In dogs, signs of distemper vary widely from no signs, to mild respiratory signs indistinguishable from kennel cough, to severe pneumonia with vomiting, bloody diarrhea and death.

Commonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. If neurological signs develop, incontinence may ensue. Central nervous system signs include a localized involuntary twitching of muscles or groups of muscles, seizures with salivation and jaw movements commonly described as "chewing gum fits", or more appropriately as "distemper myoclonus". As the condition progresses, the seizures worsen and advance to grand mal convulsions followed by death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly, they may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological signs may not come until several weeks or months later. Those few that survive usually have a small tic or twitch of varying levels of severity. With time, this tic will usually diminish somewhat in its severity.

A dog that survives distemper will continue to have both nonlife-threatening and life-threatening signs throughout its lifespan. The most prevalent nonlife-threatening symptom is hard pad disease. This occurs when a dog experiences the thickening of the skin on the pads of its paws as well as on the end of its nose. Another lasting symptom commonly is enamel hypoplasia. Puppies, especially, will have damage to the enamel of teeth that are not completely formed or those that have not yet grown through the gums. This is a result of the virus's killing the cells responsible for manufacturing the tooth enamel. These affected teeth tend to erode quickly.

Life-threatening signs usually include those due to the degeneration of the nervous system. Dogs that have been infected with distemper tend to suffer a progressive deterioration of mental abilities and motor skills. With time, the dog can acquire more severe seizures, paralysis, reduction in sight and incoordination. These dogs are usually humanely euthanized because of the immense pain and suffering they face.

The incubation period is 5–7 days (with a range of 3–10). Symptoms can include a harsh, dry cough, retching, sneezing, snorting, gagging or vomiting in response to light pressing of the trachea or after excitement or exercise. The presence of a fever varies from case to case.

A lethal infection in mink, the Aleutian disease virus lies dormant in ferrets until stress or injury allows it to surface. While the parvovirus itself causes little or no harm to the ferret host, the large number of antibodies produced in response to the presence of the virus results in a systemic vasculitis, resulting in eventual renal failure, bone marrow suppression and death.

The symptoms are chronic, progressive weight loss, lethargy, splenomegaly (enlarged spleen), anemia, rear leg weakness, seizures and black tarry stool. Additional symptoms include poor reproduction and/or oral bleeding/gastrointestinal bleeding. Lesions can also be found within the pelt depending on the severity of the disease. This virus can unfortunately reduce fitness of wild mink especially, by disturbing both the productivity within adult females and the overall survivor rates of both juveniles and adults. Likewise, in the mink kits that survive, it infects the alveolar cells and ultimately causes respiratory distress, possibly leading to death.

Once symptoms show themselves, the disease progresses rapidly, usually to death within a few months.

Aleutian disease, also known as mink plasmacytosis, is a disease which causes spontaneous abortion and death in minks and ferrets. It is caused by "Carnivore amdoparvovirus 1" (also known as "Aleution diease virus", ADV), a highly contagious parvovirus in the genus "Amdoparvovirus".

The virus has been found as a natural infection in the "Mustelidae" family within mink, ferrets, otters, polecats, stone and pine martens and within other varying carnivores such as skunks, genets, foxes and raccoons. This is most commonly explained as because they all share resources and habitats.

Although kennel cough is considered to be a multifactorial infection, there are two main forms. The first is more mild and is caused by B. bronchiseptica and canine parainfluenza virus infections, without complications from canine distemper virus (CDV) or canine adenovirus (CAV). This form occurs most regularly in autumn, and can be distinguished by symptoms such as a retching cough and vomiting. The second form has a more complex combination of causative organisms including CDV and CAV. It typically occurs in dogs that have not been vaccinated and it is not seasonal. Symptoms are more severe than the first form, and may include rhinitis, conjunctivitis, and fever in addition to a hacking cough.

Lymphoma/lymphosarcoma is the most common malignancy in ferrets. Ferret lymphosarcoma occurs in two forms -- "juvenile lymphosarcoma", a fast-growing type that affects ferrets younger than two years, and "adult lymphosarcoma", a slower-growing form that affects ferrets four to seven years old.

In juvenile ferret lymphosarcoma, large, immature lymphocytes (lymphoblasts) rapidly invade the thymus or the organs of the abdominal cavity, particularly the liver and spleen. In adult ferret lymphosarcoma, the lymph nodes in the limbs and abdominal cavity become swollen early on due to invasion by small, mature lymphocytes. Invasion of organs, such as the liver, kidney, lungs, and spleen, occurs later on, and the disease may be far advanced before symptoms are noticeable.

As in humans, ferret lymphosarcoma can be treated surgically, with radiation therapy, chemotherapy or a combination thereof. The long-term prognosis is rarely bright, however, and this treatment is intended to improve quality of life with the disease.

Epizootic catarrhal enteritis (ECE) is a viral disease that first appeared in the northeastern US in 1994, is an inflammation of the mucous membranes in the intestine. The condition manifests itself as severe diarrhea (often of a bright green color), loss of appetite, and severe weight loss. The virus can be passed via fluids and indirectly between humans. Although it was often fatal when first discovered, ECE is less of a threat today.

Death rates during outbreaks were usually extremely high, approaching 100% in immunologically naïve populations. The disease was mainly spread by direct contact and by drinking contaminated water, although it could also be transmitted by air.

Initial symptoms include fever, loss of appetite, and nasal and eye discharges. Subsequently, irregular erosions appear in the mouth, the lining of the nose, and the genital tract. Acute diarrhea, preceded by constipation, is also a common feature. Most animals die six to twelve days after the onset of these clinical signs.

Rinderpest (also cattle plague or steppe murrain) was an infectious viral disease of cattle, domestic buffalo, and many other species of even-toed ungulates, including buffaloes, large antelope and deer, giraffes, wildebeests, and warthogs. The disease was characterized by fever, oral erosions, diarrhea, lymphoid necrosis, and high mortality. Death rates during outbreaks were usually extremely high, approaching 100% in immunologically naïve populations. Rinderpest was mainly transmitted by direct contact and by drinking contaminated water, although it could also be transmitted by air. After a global eradication campaign, the last confirmed case of rinderpest was diagnosed in 2011.

On 14 October 2010, the United Nations Food and Agriculture Organization (FAO) announced that field activities in the decades-long, worldwide campaign to eradicate the disease were ending, paving the way for a formal declaration in June 2011 of the global eradication of rinderpest. On 25 May 2011, the World Organisation for Animal Health announced the free status of the last eight countries not yet recognized (a total of 198 countries were now free of the disease), officially declaring the eradication of the disease. In June 2011, the United Nations FAO confirmed the disease was eradicated, making rinderpest only the second disease in history to be fully wiped out (outside laboratory stocks), following smallpox.

Rinderpest is believed to have originated in Asia, later spreading through the transport of cattle. The term "Rinderpest" is a German word meaning "cattle-plague". The rinderpest virus (RPV) was closely related to the measles and canine distemper viruses. The measles virus emerged from rinderpest as a zoonotic disease between 1000 and 1100 AD, a period that may have been preceded by limited outbreaks involving a virus not yet fully acclimated to humans.

Granulomatous meningoencephalitis (GME) is an inflammatory disease of the central nervous system (CNS) of dogs and, rarely, cats. It is a form of meningoencephalitis. GME is likely second only to encephalitis caused by "canine distemper virus" as the most common cause of inflammatory disease of the canine CNS. The disease is more common in female toy dogs of young and middle age. It has a rapid onset. The lesions of GME exist mainly in the white matter of the cerebrum, brainstem, cerebellum, and spinal cord. The cause is only known to be noninfectious and is considered at this time to be idiopathic. Because lesions resemble those seen in allergic meningoencephalitis, GME is thought to have an immune-mediated cause, but it is also thought that the disease may be based on an abnormal response to an infectious agent. One study searched for viral DNA from "canine herpesvirus", "canine adenovirus", and "canine parvovirus" in brain tissue from dogs with GME, necrotizing meningoencephalitis, and necrotizing leukoencephalitis (see below for the latter two conditions), but failed to find any.

The severe combined immunodeficiency (SCID) is a severe immunodeficiency genetic disorder that is characterized by the complete inability of the adaptive immune system to mount, coordinate, and sustain an appropriate immune response, usually due to absent or atypical T and B lymphocytes. In humans, SCID is colloquially known as "bubble boy" disease, as victims may require complete clinical isolation to prevent lethal infection from environmental microbes.

Several forms of SCID occur in animal species. Not all forms of SCID have the same cause; different genes and modes of inheritance have been implicated in different species.

In Yorkshire Terriers there can be severe mononuclear inflammation of the brainstem and periventricular cerebral white matter. Because the condition in this breed frequently affects only the white matter, it has been called necrotizing leukoencephalitis. Symptoms of brainstem and central vestibular disease predominate.

Craniomandibular osteopathy, also known as lion's jaw, is a developmental disease in dogs causing extensive bony changes in the mandible and skull. In this disease, a cyclical resorption of normal bone and replacement by immature bone occurs along the inner and outer surfaces of the affected bones. It usually occurs between the ages of 3 and 8 months. Breeds most commonly affected include the West Highland White Terrier, Scottish Terrier, Cairn Terrier, and Boston Terrier. It is rare in large-breed dogs, but it has been reported. Symptoms include firm swelling of the jaw, drooling, pain, and difficulty eating.

It is an inherited disease, especially in Westies, in which it has been recognized as an autosomal recessive trait. Canine distemper has also been indicated as a possible cause, as has "E. coli" infection, which could be why it is seen occasionally in large-breed dogs. Growth of lesions will usually stop around the age of one year, and possibly regress. This timing coincides with the normal completion of endochondral bone growth and ossification. If the disease is extensive, especially around the tympanic bulla (middle ear), then the prognosis is guarded.

A similar disease seen in young Bullmastiffs is known as calvarial hyperostotic syndrome. It is also similar to human infantile cortical hyperostosis. It is characterized by irregular, progressive bony proliferation and thickening of the cortical bone of the calvaria, which is part of the skull. Asymmetry of the lesions may occur, which makes it different from craniomandibular osteopathy. Symptoms include painful swelling of the skull, fever, and lymph node swelling. In most cases it is self-limiting.

African trypanosomiasis symptoms occur in two stages. The first stage, known as the hemolymphatic phase, is characterized by fever, headaches, joint pains, and itching. Fever is intermittent, with attacks lasting from a day to a week, separated by intervals of a few days to a month or longer. Invasion of the circulatory and lymphatic systems by the parasites is associated with severe swelling of lymph nodes, often to tremendous sizes. Winterbottom's sign, the tell-tale swollen lymph nodes along the back of the neck, may appear. Occasionally, a chancre (red sore) will develop at the location of the tsetse fly bite. If left untreated, the disease overcomes the host's defenses and can cause more extensive damage, broadening symptoms to include anemia, endocrine, cardiac, and kidney dysfunctions.

The second phase of the disease, the neurological phase, begins when the parasite invades the central nervous system by passing through the blood–brain barrier. Disruption of the sleep cycle is a leading symptom of this stage and is the one that gave the disease the name 'sleeping sickness.' Infected individuals experience a disorganized and fragmented 24-hour rhythm of the sleep-wake cycle, resulting in daytime sleep episodes and nighttime periods of wakefulness.

Other neurological symptoms include confusion, tremor, general muscle weakness, hemiparesis and paralysis of a limb. Parkinson-like movements might arise due to non-specific movement disorders and speech disorders. Individuals may also exhibit psychiatric symptoms such as irritability, psychotic reactions, aggressive behaviour, or apathy which can sometimes dominate the clinical diagnosis. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma, systemic organ failure, and death. An untreated infection with "T. b. rhodesiense" will cause death within months whereas an untreated infection with "T. b. gambiense" will cause death after several years. Damage caused in the neurological phase is irreversible.

Equine SCID is an autosomal recessive disorder that affects the Arabian horse. Similar to the "bubble boy" condition in humans, an affected foal is born with no immune system, and thus generally dies of an opportunistic infection, usually within the first four to six months of life. There is a DNA test that can detect healthy horses who are carriers of the gene causing SCID, thus testing and careful, planned matings can now eliminate the possibility of an affected foal ever being born.

SCID is one of six genetic diseases known to affect horses of Arabian bloodlines, and the only one of the six for which there is a DNA test to determine if a given horse is a carrier of the allele. There are other genetic diseases that affect other horse breeds, and horses of part-Arabian bloodlines can be carriers of SCID.

Unlike SCID in humans, which can be treated, for horses, to date, the condition remains a fatal disease. When a horse is heterozygous for the gene, it is a carrier, but perfectly healthy and has no symptoms at all. If two carriers are bred together, however, classic Mendelian genetics indicate that there is a 50% chance of any given mating producing a foal that is a carrier heterozygous for the gene, and a 25% risk of producing a foal affected by the disease. If a horse is found to carry the gene, the breeder can choose to geld a male or spay a female horse so that they cannot reproduce, or they can choose to breed the known carrier only to horses that have been tested and found to be "clear" of the gene. In either case, careful breeding practices can avoid ever producing an SCID-affected foal.

Hyperesthesia (or hyperaesthesia) is a condition that involves an abnormal increase in sensitivity to stimuli of the sense. "When a non-noxious stimulus causes the sensation of pain the area will be termed hyperaesthetic". Stimuli of the senses can include sound that one hears, foods that one tastes, textures that one feels, and so forth. Increased touch sensitivity is referred to as "tactile hyperesthesia", and increased sound sensitivity is called "auditory hyperesthesia". Tactile hyperesthesia may be a common symptom of many neurologic disorders such as herpes zoster, peripheral neuropathy and radiculopathies. In 1979, and then in 1994, Merskey, Bogduk, Noordenbos, Devor and others (a subcommittee of International Association for the Study of Pain) proposed, instead of hyperaesthesia, the concept of allodynia, meaning "other pain", defined as a pain resulting from a stimulus that does not normally provoke pain.

In psychology, Jeanne Siaud-Facchin uses the term by defining it as an "exacerbation des sens" that characterizes gifted children (and adults): for them, the sensory information reaches the brain much faster than the average, and the information is processed in a significantly shorter time.

Feline hyperesthesia syndrome is an uncommon but recognized condition in cats, particularly Siamese, Burmese, Himalayan, and Abyssinian cats. It can affect cats of all ages, though it is most prevalent in mature animals. The disease can be somewhat difficult to detect as it is characterized by brief bursts of abnormal behavior, lasting around a minute or two. One of its symptoms is also found in dogs that have canine distemper disease (CD) caused by canine distemper virus (CDV).

Mild or early cases of Pagets are asymptomatic, and so most people are diagnosed with Paget's disease incidentally during medical evaluation for another problem. Approximately 35% of patients with Paget's have symptoms related to the disease when they are first diagnosed. Overall, the most common symptom is bone pain. When symptoms do occur, they may be confused with those of arthritis or other disorders, and so diagnosis may be delayed.

Paget's may first be noticed as an increasing deformity of a person's bones.

Paget's disease affecting the skull may lead to loss of hearing in one or both ears due to compression of the nerves in the inner ear. Rarely, skull involvement may lead to compression of the nerves that supply the eye, leading to vision loss.