The disease is spread by an infected horse when nasal discharge or pus from the draining lymph nodes contaminate pastures, feed troughs, brushes, bedding, tack etc.

Equines of any age may contract the disease, although younger and elderly equines are more susceptible. Young equines may lack immunity to the disease because they have not had prior exposure. Geriatric equines may have a weaker immune system.

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.

Only 8% of infected horses have this form of pigeon fever, however, it has a 30-40% fatality rate. Organs that are commonly affected are the liver, spleen, and lungs. For a successful recovery, long-term antimicrobial therapy is essential.

The disease can occur in horses of any age, breed or gender. In the US, it occurs throughout the country and at any time of year. The disease was traditionally thought to occur mainly in dry, arid regions, but from at least 2005, its range has been increasing into areas where it was not previously seen, such as the Midwestern US, and Western Canada. Environmental risk factors include over 7 days of a weekly average land surface temperatures above 35 °C, and drier soils; these factors were implicated in an outbreak in Kansas in 2012.

Coccidiosis is a significant disease for chickens, especially affecting the young chicks. It can be fatal or leave the bird with compromised digestion. There are chick feed mixes that contain a coccidiostat to manage exposure levels and control disease. In an outbreak, coccidiocidal medications are given. Examples are toltrazuril (Baycox) or amprolium. After multiple infections, surviving chickens become resistant to the coccidia.

"Campylobacter" is one of the most common causes of human bacterial gastroenteritis. For instance, an estimated 2 million cases of "Campylobacter" enteritis occur annually in the U.S., accounting for 5–7% of cases of gastroenteritis. Furthermore, in the United Kingdom during 2000, "Campylobacter jejuni" was involved in 77.3% in all cases of laboratory confirmed foodborne illness. About 15 of every 100,000 people are diagnosed with campylobacteriosis every year, and with many cases going unreported, up to 0.5% of the general population may unknowingly harbor "Campylobacter" in their gut.

A large animal reservoir is present as well, with up to 100% of poultry, including chickens, turkeys, and waterfowl, having asymptomatic infections in their intestinal tracts. Infected chicken feces may contain up to 10 bacteria per 25 grams, and due to the installations, the bacteria are rapidly spread to other chickens. This vastly exceeds the infectious dose of 1000–10,000 bacteria for humans.

In January 2013, the UK's Food Standards Agency warned that two-thirds of all raw chicken bought from UK shops was contaminated with campylobacter, affecting an estimated half a million people annually and killing approximately 100.

Campylobacteriosis is usually self-limited without any mortality (assuming proper hydration is maintained). However, there are several possible complications.

Purpura hemorrhagica may be prevented by proper management during an outbreak of strangles. This includes isolation of infected horses, disinfection of fomites, and good hygiene by caretakers. Affected horses should be isolated at least one month following infection. Exposed horses should have their temperature taken daily and should be quarantined if it becomes elevated. Prophylactic antimicrobial treatment is not recommended.

Vaccination can reduce the incidence and severity of the disease. However, horses with high SeM antibody titers are more likely to develop purpura hemorrhagica following vaccination and so these horses should not be vaccinated. Titers may be measured by ELISA.

The most common medications used to treat coccidian infections are in the sulfonamide antibiotic family.

Depending on the pathogen and the condition of the animal, untreated coccidiosis may clear of its own accord, or become severe and damaging, and sometimes cause death.

In addition to vaccine-specific factors, vets and owners should also consider pet-specific factors that have been shown to increase the risk of adverse reactions in both dogs and cats. Examples of such factors include:

- age,

- number of vaccinations per office visit,

- size,

- general health of the animal,

- breed,

- neutered status, and

- past vaccination history.

In Asia and in parts of the Americas and Africa, dogs remain the principal host. Mandatory vaccination of animals is less effective in rural areas. Especially in developing countries, pets may not be privately kept and their destruction may be unacceptable. Oral vaccines can be safely distributed in baits, a practice that has successfully reduced rabies in rural areas of Canada, France, and the United States. In Montreal, Quebec, Canada, baits are successfully used on raccoons in the Mount-Royal Park area. Vaccination campaigns may be expensive, and cost-benefit analysis suggests baits may be a cost-effective method of control. In Ontario, a dramatic drop in rabies was recorded when an aerial bait-vaccination campaign was launched.

The number of recorded human deaths from rabies in the United States has dropped from 100 or more annually in the early 20th century to one or two per year due to widespread vaccination of domestic dogs and cats and the development of human vaccines and immunoglobulin treatments. Most deaths now result from bat bites, which may go unnoticed by the victim and hence untreated.

Prognosis is good with early, aggressive treatment (92% survival in one study).

In 2004, American teenager Jeanna Giese survived an infection of rabies unvaccinated. She was placed into an induced coma upon onset of symptoms and given ketamine, midazolam, ribavirin, and amantadine. Her doctors administered treatment based on the hypothesis that detrimental effects of rabies were caused by temporary dysfunctions in the brain and could be avoided by inducing a temporary partial halt in brain function that would protect the brain from damage while giving the immune system time to defeat the virus. After 31 days of isolation and 76 days of hospitalization, Giese was released from the hospital. She survived with all higher level brain functions intact, but an inability to walk and balance. On a 2013 podcast of NPR's "Radiolab", 9 years after her discharge from the hospital, Giese recounted: "I had to learn how to stand and then to walk, turn around, move my toes. I was really, after rabies, a newborn baby who couldn't do anything. I had to relearn that all ... mentally I knew how to do stuff but my body wouldn't cooperate with what I wanted it to do. It definitely took a toll on me psychologically. You know, I'm still recovering. I'm not completely back. Stuff like balance, and I can't run normally."

Giese's treatment regimen became known as the Milwaukee protocol, which has since undergone revision with the second version omitting the use of ribavirin. Two of 25 patients survived when treated under the first protocol. A further 10 patients have been treated under the revised protocol, with a further two survivors.

FVRCP vaccines have also come under scrutiny of late due to possible risks to long term health. A study at Colorado State University noted an association between vaccination with parenteral (injectable) FVRCP vaccinations and development of antibodies against feline kidney tissue. Antibody development is hypothesized to develop when the immune system reacts to protein contaminants from the cell line used to cultivate vaccinial viruses. The cell line in question, the Crandell-Rees Feline Kidney (CRFK) cell line, was derived from a cat kidney. It is currently unknown whether this antibody development can lead to renal disease, though a recent follow-up study demonstrated evidence of inflammation on re-biopsy samples from some of the study cats.

The cause of juvenile cellulitis is unknown. Cytologic examination of aspirates of affected lymph nodes, pustules, abscesses, and joint fluid rarely reveal bacteria, and culture results of intact lesion are always negative for bacterial growth, suggesting a nonbacterial etiology. As signs resolve following treatment with glucocorticoids, the cause is likely to be an immune disorder.

Juvenile cellulitis, also known as puppy strangles or juvenile pyoderma, is an uncommon disease of dogs. Symptoms include dermatitis, lethargy, depression and lameness. When puppies are first presented with what appears to be staphylococcal pyoderma, juvenile cellulitis, a relatively rare condition, may not be considered.

Strangling involves one or several mechanisms that interfere with the normal flow of oxygen into the brain:

- Compression of the carotid arteries or jugular veins—causing cerebral ischemia.

- Compression of the laryngopharynx, larynx, or trachea—causing asphyxia.

- Stimulation of the carotid sinus reflex—causing bradycardia, hypotension, or both.

Depending on the particular method of strangulation, one or several of these typically occur in combination; vascular obstruction is usually the main mechanism. Complete obstruction of blood flow to the brain is associated with irreversible neurological damage and death, but during strangulation there is still unimpeded blood flow in the vertebral arteries. Estimates have been made that significant occlusion of the carotid arteries and jugular veins occurs with a pressure of around , while the trachea demands six times more at approximately .

As in all cases of strangulation, the rapidity of death can be affected by the susceptibility to carotid sinus stimulation. Carotid sinus reflex death is sometimes considered a mechanism of death in cases of strangulation, but it remains highly disputed. The reported time from application to unconsciousness varies from 7–14 seconds if effectively applied to one minute in other cases, with death occurring minutes after unconsciousness.

Strangling is compression of the neck that may lead to unconsciousness or death by causing an increasingly hypoxic state in the brain. Fatal strangling typically occurs in cases of violence, accidents, and is one of two main ways that hanging may cause death (alongside breaking the victim's neck).

Strangling does not have to be fatal; limited or interrupted strangling is practised in erotic asphyxia, in the choking game, and is an important technique in many combat sports and self-defence systems.

Strangling can be divided into three general types according to the mechanism used:

- Hanging—Suspension from a cord wound around the neck

- Ligature strangulation—Strangulation without suspension using some form of cord-like object called a garrote

- Manual strangulation—Strangulation using the fingers or other extremity

Aortic stenosis in the Rottweiler appears to be true subvalvular aortic stenosis (SAS), similar to that in the Newfoundland dog, as opposed to the valvular form (seen more in boxer dogs) or the supravalvular form sometimes seen in people.

Canine subvalvular aortic stenosis (SAS) is an abnormal, congenital heart murmur caused by subaortic stenosis (SAS). There is a high incidence of this condition among Rottweiler dogs.

There is very good evidence that it is heritable, passed on from generation to generation genetically. This genetic trait is what is called polygenic, so that the inheritance is complex. An animal might have the genes for SAS, yet have no actual sign of SAS. Also, an animal might have signs of subaortic stenosis, and yet offspring with signs of SAS may not be seen for a couple of generations. Any animal that has subaortic stenosis should not be bred, because they can definitely pass the defect on to future offspring. There is some controversy as to whether the parents of an animal with SAS should be bred again.

Heart murmurs are graded on a scale of 1 to 6, with one being very mild and six being very serious, with some animals dying before they reach this high stage due to a sudden leap in the grade or through long-term slowing down. Murmurs can exist due to a large number of heart problems (infection, trauma, anemia, etc.; some are innocent, with no cardiac pathology. Tests such as chest X-rays, echocardiography, and electrocardiography can be performed to evaluate the severity of the situation

The condition is usually detected during puppy visits to the veterinarian by hearing a heart murmur during physical examination. A heart murmur is the abnormal sound of blood rushing through one of the heart valves. Instead of just the heartbeat, a whistle of blood flow through a narrowed opening is heard. The puppy will most likely appear normal in all other respects. There is a possibility that the murmur may come and go, or it may develop slowly; this can be determined by frequent checks of a puppy's heart during its first few months. The chance for long-term survival of SAS is low.

Puppies and dogs diagnosed with subaortic stenosis can suffer from heart failure and sudden death. If a dog with SAS develops heart failure, medications can be prescribed to alleviate the clinical signs (sudden/strong lethargicism, continuous heavy panting, rise in temperature etc.)

The OFA has established a Congenital Heart Registry whose guidelines were established by veterinary cardiologists. A dog which auscultates normally at 12 months of age is considered to be free of congenital heart disease; upon confirmation of this, the OFA will issue a certificate.

Puppy pregnancy syndrome is a psychosomatic illness in humans brought on by mass hysteria.

The syndrome is thought to be localized to villages in several states of India, including West Bengal, Assam, Bihar, Jharkhand, Orissa, and Chhattisgarh, and has been reported by tens of thousands of individuals. It is far more prevalent in areas with little access to education.

People suffering from this condition believe that shortly after being bitten by a dog, puppies are conceived within their abdomen. This is said to be especially likely if the dog is sexually excited at the time of the attack. Victims are said to bark like dogs, and have reported being able to see the puppies inside them when looking at water, or hear them growling in their abdomen. It is believed that the victims will eventually die – especially men, who will give birth to their puppies through the penis.

Witch doctors offer oral cures, which they claim will dissolve the puppies, allowing them to pass through the digestive system and be excreted "without the knowledge of the patient".

Doctors in India have tried to educate the public about the dangers of believing in this condition. Most sufferers are referred to psychiatric services, but in rare instances patients fail to take anti-rabies medication in time, thinking that they have puppy pregnancy syndrome and thus the witch doctor's medicine will cure them. This is further compounded by witch doctors stating that their medicine will fail if sufferers seek conventional treatment.

Some psychiatrists believe that the syndrome meets the criteria for a culture-bound disorder.

Osteoarthritis, a common symptom associated with Canine Hip Dysplasia in German Shepherds ultimately results in pain and inflammation. The causes are from bone degradation in which the bone is less rigid, cartilage dissipates and structure of joints becomes weak.

Diet can have a major impact for German Shepherds that are exposed to Canine Hip Dysplasia. Incorporating Omega-3 fatty acids such as Docosahexaenoic acid(DHA) and Eicosapentaenoic acid(EPA) into the diet can result in improved symptoms of the disease. Omega 3 fatty acids can help decrease inflammation that occurs from osteoarthritis, as well as improvement in locomotion of dogs who have the disease. EPA and DHA can be supplemented into the diet through fish oils and in return is beneficial for reducing joint inflammation.

Glucosamine and Chondroitin sulfate are Nutraceuticals that can also be added into the diet to help treat osteoarthritis and its quality of life reducing effects. Both nutraceuticals help with improvement of cartilage, joint health and repairing of tissues. This inclusion will allow for a stronger support and reduced negative effects of osteoarthritis. Another nutrient that can help improve the structural support of the body in German Shepherds is Vitamin C. Vitamin C contributes to the building blocks of collagen that can help to strengthen the joints.

Hip dysplasia may be caused by a femur that does not fit correctly into the pelvic socket, or poorly developed muscles in the pelvic area. Large and giant breeds are most susceptible to hip dysplasia (possibly due to the body mass index (BMI) of the individual animal, though, many other breeds can suffer from it. The Orthopedic Foundation for Animals maintains a list of top 100 breeds affected.

To reduce pain, the animal will typically reduce its movement of that hip. This may be visible as "bunny hopping", where both legs move together, or less dynamic movement (running, jumping), or stiffness. Since the hip cannot move fully, the body compensates by adapting its use of the spine, often causing spinal, stifle (a dog's knee joint), or soft tissue problems to arise.

The causes of hip dysplasia are considered heritable, but new research conclusively suggests that environment also plays a role. To what degree the causality is genetic and what portion environmental is a topic of current debate. Neutering a dog, especially before the dog has reached an age of full developmental maturity, has been proven to almost double the chance he or she will develop hip dysplasia versus intact dogs or dogs that were neutered after reaching adulthood Other environmental influences include overweight condition, injury at a young age, overexertion on the hip joint at a young age, ligament tear at a young age, repetitive motion on forming joint (i.e. jogging with puppy under the age of 1 year). As current studies progress, greater information may help provide procedures to effectively reduce the occurrence of this condition.

The problem almost always appears by the time the dog is 18 months old. The defect can be anywhere from mild to severely crippling, and can eventually cause severe osteoarthritis.

It is most common in medium-large pure bred dogs, such as Newfoundlands, German Shepherd Dogs, retrievers (such as Labradors, Tollers, or Goldens), rottweilers and Mastiff, but also occurs in some smaller breeds such as spaniels and pugs.

Some systemic diseases can become symptomatic as a skin disorder. These include many endocrine (hormonal) abnormalities, such as hypothyroidism, Cushing's Syndrome (hyperadrenalcorticism), and tumors of the ovaries or testicles.

It is known to occur in Scotch Collies (smooth and rough collies), Shetland Sheepdogs, Australian Shepherds, Border Collies, Lancashire Heelers, and Nova Scotia Duck Tolling Retrievers. Frequency is high in Collies and Shetland Sheepdogs, and low in Border Collies and NSDTRs. In the United States, incidence in the genotype of collies has been estimated to be as high as 95 percent, with a phenotypic incidence of 80 to 85 percent.