Treatment depends on many factors, such as the age of horse, severity of symptoms and duration of infection. As long a horse is eating and drinking, the infection must run its course, much like a common cold virus. Over time a horse will build up enough antibodies to overtake and fight the disease. Other treatment options can be applying heat packs to abscesses to help draw it to the surface and using drawing salves such as Ichthammol. A blood test or bacterial cultures can be taken to confirm the horse is fighting Pigeon Fever. Anti-inflammatory such as phenylbutazone can be used to ease pain and help control swelling. Treating Pigeon Fever with antibiotics is not normally recommended for external abscesses since it is a strong bacterium that takes extended treatment to kill off and to ensure it does not return stronger. However, if the abscesses are internal then antibiotics may be needed. Consulting a veterinarian for treatment is recommended. Making the horse comfortable, ensuring the horse has good food supply and quality hay will help the horse keep their immune system strong to fight off the infection. Once the abscess breaks or pops, it will drain for a week or two. During this time keeping the area clean, applying hot packs or drawing salves will help remove the pus that has gathered in the abscess.

As with many streptococcal infections, penicillin or penicillin-derivative antibiotics are the most effective treatments. However, some authorities are of the opinion that use of antibiotics is contra-indicated once abscesses have begun to form, as they pre-dispose to lymphatic spread of the infection (so-called bastard strangles) which has a much higher mortality rate.

After an abscess has burst, it is very important to keep the wound clean. A diluted povidone-iodine solution has been used with good results to disinfect the open hole, flushing the inside with a syringe tipped catheter or with a teat cannula, followed by gentle scrubbing to keep the surrounding area clean.

Symptomatic therapy is an alternative treatment, and is where warm packs are used to mature the abscesses so making it less painful and more comfortable for the horse itself; but once the abscesses have been matured they must be kept clean to prevent further infections.This treatment for "S.equi" only helps to reduce pain for the horse rather than curing the infection.

This bacterium is present in soil and is transmitted to horses through open wounds, abrasions or mucous membranes.

Surgical drainage is usually indicated for prostatic abscesses and septic arthritis, may be indicated for parotid abscesses, and is not usually indicated for hepatosplenic abscesses. In bacteraemic melioidosis unresponsive to intravenous antibiotic therapy, splenectomy has been attempted, but only anecdotal evidence supports this practice.

Prior to 1989, the standard treatment for acute melioidosis was a three-drug combination of chloramphenicol, co-trimoxazole and doxycycline; this regimen is associated with a mortality rate of 80% and is no longer be used unless no other alternatives are available. All three drugs are bacteriostatic (they stop the bacterium from growing, but do not kill it) and the action of co-trimoxazole antagonizes both chloramphenicol and doxycycline.

Both intramuscular and intranasal vaccines are available. Isolation of new horses for 4 to 6 weeks, immediate isolation of infected horses, and disinfection of stalls, water buckets, feed troughs, and other equipment will help prevent the spread of strangles. As with any contagious disease, handwashing is a simple and effective tool.

There is no specific treatment for the canine distemper. As with measles, the treatment is symptomatic and supportive. The supportive care is geared towards treating fluid/electrolyte imbalances, neurological symptoms, and preventing any secondary bacterial infections. Examples include administering fluids, electrolyte solutions, analgesics, anticonvulsants, broad spectrum antibiotics, antipyretics, parenteral nutrition and nursing care.

Antibiotics are given to treat any bacterial infection present. Cough suppressants are used if the cough is not productive. NSAIDs are often given to reduce fever and upper respiratory inflammation. Prevention is by vaccinating for canine adenovirus, distemper, parainfluenza, and "Bordetella". In kennels, the best prevention is to keep all the cages disinfected. In some cases, such as "doggie daycares" or nontraditional playcare-type boarding environments, it is usually not a cleaning or disinfecting issue, but rather an airborne issue, as the dogs are in contact with each other's saliva and breath. Although most kennels require proof of vaccination, the vaccination is not a fail-safe preventative. Just like human influenza, even after receiving the vaccination, a dog can still contract mutated strains or less severe cases.

To increase their effectiveness, vaccines should be administered as soon as possible after a dog enters a high-risk area, such as a shelter. 10 to 14 days are required for partial immunity to develop. Administration of B. bronchiseptica and canine-parainfluenza vaccines may then be continued routinely, especially during outbreaks of kennel cough. There are several methods of administration, including parenteral and intranasal. However, the intranasal method has been recommended when exposure is imminent, due to a more rapid and localized protection. Several intranasal vaccines have been developed that contain canine adenovirus in addition to B bronchiseptica and canine-parainfluenza virus antigens. Studies have thus far not been able to determine which formula of vaccination is the most efficient. Adverse effects of vaccinations are mild, but the most common effect observed up to 30 days after administration is nasal discharge. Vaccinations are not always effective. In one study it was found that 43.3% of all dogs in the study population with respiratory disease had in fact been vaccinated.

A number of vaccines against canine distemper exist for dogs (ATCvet code: and combinations) and domestic ferrets (), which in many jurisdictions are mandatory for pets. Infected animals should be quarantined from other dogs for several months owing to the length of time the animal may shed the virus. The virus is destroyed in the environment by routine cleaning with disinfectants, detergents, or drying. It does not survive in the environment for more than a few hours at room temperature (20–25 °C), but can survive for a few weeks in shady environments at temperatures slightly above freezing. It, along with other labile viruses, can also persist longer in serum and tissue debris.

Despite extensive vaccination in many regions, it remains a major disease of dogs.

To prevent canine distemper, puppies should begin vaccination at six to eight weeks of age and then continue getting the “booster shot” every two to four weeks until they are 16 weeks of age. Without the full series of shots, the vaccination will not provide protection against the virus. Since puppies are typically sold at the age of eight to ten weeks, they typically receive the first shot while still with their breeder, but the new owner often does not finish the series. These dogs are not protected against the virus and so are susceptible to canine distemper infection, continuing the downward spiral that leads to outbreaks throughout the country.

There is currently no known treatment for Aleutian virus. When evidence of ADV shows in a ferret, it is strongly recommended that a CEP (counterimmunoelectrophoresis) blood test or an IFA (immunoflourescent antibody) test be done. The CEP test is usually faster and less expensive than the IFA test, but the IFA test is more sensitive and can detect the disease in borderline cases.

Additionally modern methods such as Real-Time PCR allow for rapid and accurate detection as well as determination of the amount of viron present.

Prevention is best accomplished by stopping the spread of ADV. Any new ferret, or those who have been confirmed as serum positive for the virus should be perpetually isolated from other ferrets. All items that may have come into contact with the infected ferret should be cleaned with a 10% bleach solution.

This is a growing concern within mink producers as it is the most crucial infectious disease which affects farmed mink worldwide.

The coronavirus which causes ECE has a counterpart strain that has more systemic effects with a higher mortality rate. This systemic syndrome has been compared to Feline infectious peritonitis in cats.

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.

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.

For "T. b. gambiense" the combination of nifurtimox and eflornithine (NECT) or eflornithine alone appear to be more effective and result in fewer side effects. These treatments may replace melarsoprol when available with the combination being first line. NECT has the benefit of requiring less injections of eflornithine.

Intravenous melarsoprol was previously the standard treatment for second-stage (neurological phase) disease and is effective for both types. Melarsoprol is the only treatment for second stage "T. b. rhodesiense"; however, it causes death in 5% of people who take it. Resistance to melarsoprol can occur.

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.

The current treatment for first-stage disease is intravenous or intramuscular pentamidine for "T. b. gambiense" or intravenous suramin for "T. b. rhodesiense".

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.

Five bisphosphonates are currently available. In general, the most commonly prescribed are risedronic acid, alendronic acid, and pamidronic acid. Etidronic acid and other bisphosphonates may be appropriate therapies for selected patients but are less commonly used. None of these drugs should be used by people with severe kidney disease.

- Etidronate disodium The approved regimen is once daily for six months; a higher dose is more commonly used. No food, beverage, or medications should be consumed for two hours before and after taking. The course should not exceed six months, but repeat courses can be given after rest periods, preferably of three to six months duration.

- Pamidronate disodium in intravenous form: the approved regimen uses an infusion over four hours on each of three consecutive days, but a more commonly used regimen is over two to four hours for two or more consecutive or nonconsecutive days.

- Alendronate sodium is given as tablets once daily for six months; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any medication, or lying down (patient may sit).

- Tiludronate disodium are taken once daily for three months; they may be taken any time of day, as long as there is a period of two hours before and after resuming food, beverages, and medications.

- Risedronate sodium tablet taken once daily for 2 months is the prescribed regimen; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any medication, or lying down (patient may sit).

- Zoledronic acid is given as an intravenous infusion; a single dose is effective for two years. This is recommended for most people at high risk with active disease.

Calcitonin, also called calcitonin-salmon, is a synthetic copy of a polypeptide hormone secreted by the ultimobranchial gland of salmon. Miacalcin is administered by injection, three times per week or daily, for 6–18 months. Repeat courses can be given after brief rest periods. Miacalcin may be appropriate for certain patients, but is seldom used. Calcitonin is also linked to increased chance of cancer. Due to the increased risk of cancer, the European Medicines Agency (EMA) recommended that calcitonin be used only on a short-term basis for 3 conditions for which it had previously been approved in the European Union: Paget's disease, acute bone loss resulting from sudden immobilization, and hypercalcemia caused by cancer.

The EMA said it based its recommendations on a review of the benefits and risks of calcitonin-containing medicines. Conducted by the agency's Committee for Medicinal Products for Human Use (CHMP), the review encompassed available data from the companies that market these drugs, postmarketing safety data, randomized controlled studies, 2 studies of unlicensed oral calcitonin drugs, and experimental cancer studies, among other sources.

CHMP found that "a higher proportion of patients treated with calcitonin for long periods of time develop cancer of various types, compared with patients taking placebo." The increase in cancer rates ranged from 0.7% for oral formulations to 2.4% for the nasal formulation. CHMP concluded that the benefits of calcitonin for osteoporosis did not exceed the risks. The nasal spray's only indication is for osteoporosis, thus justifying the drug's removal from the market.

As a solution for injection or infusion, calcitonin should be administered for no more than 4 weeks to prevent acute bone loss resulting from sudden immobilization, and normally for no more than 3 months to treat Paget's disease, the EMA said. The agency did not specify a time frame for the short-term use of calcitonin for treating hypercalcemia caused by cancer.

Topical ciclosporin (topical ciclosporin A, tCSA) 0.05% ophthalmic emulsion is an immunosuppressant. The drug decreases surface inflammation. In a trial involving 1200 people, Restasis increased tear production in 15% of people, compared to 5% with placebo.

It should not be used while wearing contact lenses, during eye infections or in people with a history of herpes virus infections. Side effects include burning sensation (common), redness, discharge, watery eyes, eye pain, foreign body sensation, itching, stinging, and blurred vision. Long term use of ciclosporin at high doses is associated with an increased risk of cancer.

Cheaper generic alternatives are available in some countries.

Inflammation occurring in response to tears film hypertonicity can be suppressed by mild topical steroids or with topical immunosuppressants such as ciclosporin (Restasis). Elevated levels of tear NGF can be decreased with 0.1% prednisolone.

Diquafosol, an agonist of the P2Y2 purinogenic receptor, is approved in Japan for managing dry eye disease by promoting tear secretion.

Lifitegrast is a new drug that was approved by the FDA for the treatment of the condition in 2016.

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.

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.

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.