The mortality rate of the virus largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate, where complications such as pneumonia and encephalitis are more common. In older dogs that develop distemper encephalomyelitis, vestibular disease may present. Around 15% of canine inflammatory central nervous system diseases are a result of CDV.

The prevalence of canine distemper in the community has decreased dramatically due to the availability of vaccinations. However, the disease continues to spread among unvaccinated populations, such as those in animal shelters and pet stores. This provides a great threat to both the rural and urban communities throughout the United States, affecting both shelter and domestic canines. Despite the effectiveness of the vaccination, outbreaks of this disease continue to occur nationally. In April 2011, the Arizona Humane Society released a valley-wide pet health alert throughout Phoenix, Arizona.

Outbreaks of canine distemper continue to occur throughout the United States and elsewhere, and are caused by many factors. These factors include the overpopulation of dogs and the irresponsibility of pet owners. The overpopulation of dogs is a national problem that organizations such as the Humane Society and ASPCA face every day. This problem is even greater within areas such as Arizona, owing to the vast amount of rural land. An unaccountable number of strays that lack vaccinations reside in these areas and are therefore more susceptible to diseases such as canine distemper. These strays act as a host for the virus, spreading it throughout the surrounding area, including urban areas. Puppies and dogs that have not received their shots can then be infected if in a place where many dogs interact, such as a dog park.

Ehrlichiosis is a nationally notifiable disease in the United States. There have been cases reported in every month of the year, but most cases are reported during April–September. These months are also the peak months for tick activity in the United States.

From 2008-2012, the average yearly incidence of ehrlichiosis was 3.2 cases per million persons. This is more than twice the estimated incidence for the years 2000-2007. The incidence rate increases with age, with the ages of 60–69 years being the highest age-specific years. Children of less than 10 years and adults aged 70 years and older, have the highest case-fatality rates. There is a documented higher risk of death among persons who are immunosuppressed.

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.

Traditionally, canine transmission is directly from sandfly to dog. Cases in the United States have proven "L. infantum" transmission from dog to dog by direct contamination with blood and secretions, as well as transplacentally from an infected bitch to her pups. This mode of transmission seems to be unique to the "L. infantum" Mon1 strain found in the United States. Although "in utero" transmission is likely the predominant method of disease spread amount the "L. infantum" Mon1 strain, it is still a viable parasite (has not lost virulence factors associated with sandfly-uptake) which can be transmitted via sandfly bite. A Brazilian study of 63 puppies from 18 "L. donovani"-infected parents found no evidence of congential or transplacental infection.

The prognosis is good for dogs with acute ehrlichiosis. For dogs that have reached the chronic stage of the disease, the prognosis is guarded. When bone marrow suppression occurs and there are low levels of blood cells, the animal may not respond to treatment.

Numerous strains and subgenus strains of "Leishmania" exist; with sandfly genome projects still underway, strains are still being discovered.

In the Old World, leishmaniasis transmitted by sandflies of the genus "Phlebotomus" documented in dogs are:

- "L. donovani" in Sri Lanka

- "L. infantum" (began appearing dogs in the United States in 2000)

New World leishmaniasis strains are spread by "Lutzomyia"; however, research speculates the North American sandfly could be capable of spreading, but this is to date unconfirmed. Dogs are known resorvoirs of "L. infantum", and the spread of disease from dog to dog has been confirmed in the United States.

- Suspected causes of canine visceral leishmaniasis are geographic variants of the "Leishmania donovani" complex, including "L. infantum, L. chagasi" and "L. donovani".

The Mexicana ("L. mexicana, L. amazonensis, L. venezuelensis", and "L. pifanoi") and Viannia ("L. braziliensis, L. guyanensis, L. panamensis" and "L. peruviana") strains are not commonly found in dogs. Subgenus Viannia strains are found only in Central and South America, all of which cause leishmaniasis in humans.

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.

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.

Ehrlichiosis (; also known as canine rickettsiosis, canine hemorrhagic fever, canine typhus, tracker dog disease, and tropical canine pancytopenia is a tick-borne disease of dogs usually caused by the organism "Ehrlichia canis". "Ehrlichia canis" is the pathogen of animals. Humans can become infected by "E. canis" and other species after tick exposure. German Shepherd Dogs are thought to be susceptible to a particularly severe form of the disease, other breeds generally have milder clinical signs. Cats can also be infected.

The most common symptoms include headache, muscle aches, and fatigue. A rash may occur, but is uncommon. Ehrlichiosis can also blunt the immune system by suppressing production of TNF-alpha, which may lead to opportunistic infections such as candidiasis.

Most of the signs and symptoms of ehrlichiosis can likely be ascribed to the immune dysregulation that it causes. A "toxic shock-like" syndrome is seen in some severe cases of ehrlichiosis. Some cases can present with purpura and in one such case the organisms were present in such overwhelming numbers that in 1991 Dr. Aileen Marty of the AFIP was able to demonstrate the bacteria in human tissues using standard stains, and later proved that the organisms were indeed Ehrlichia using immunoperoxidase stains.

Experiments in mouse models further supports this hypothesis, as mice lacking TNF-alpha I/II receptors are resistant to liver injury caused by ehrlichia infection.

3% of human monocytic ehrlichiosis cases result in death; however, these deaths occur "most commonly in immunosuppressed individuals who develop respiratory distress syndrome, hepatitis, or opportunistic nosocomial infections."

Rabies can be contracted in horses if they interact with rabid animals in their pasture, usually being bitten on the muzzle or lower limbs. Signs include aggression, incoordination, head-pressing, circling, lameness, muscle tremors, convulsions, colic and fever. Horses that experience the paralytic form of rabies have difficulty swallowing, and drooping of the lower jaw due to paralysis of the throat and jaw muscles. Incubation of the virus may range from 2–9 weeks. Death often occurs within 4–5 days of infection of the virus. There are no effective treatments for rabies in horses. Veterinarians recommend an initial vaccination as a foal at three months of age, repeated at one year and given an annual booster.

Rabies is a viral zoonotic neuroinvasive disease which causes inflammation in the brain and is usually fatal. Rabies, caused by the rabies virus, primarily infects mammals. In the laboratory it has been found that birds can be infected, as well as cell cultures from birds, reptiles and insects. Animals with rabies suffer deterioration of the brain and tend to behave bizarrely and often aggressively, increasing the chances that they will bite another animal or a person and transmit the disease. Most cases of humans contracting the disease from infected animals are in developing nations. In 2010, an estimated 26,000 people died from rabies, down from 54,000 in 1990.

Rabies is a viral disease that exists in Haiti and throughout the world. It often causes fatal inflammation of the brain in humans and other mammals, such as dogs and mongooses in Haiti. The term "rabies" is derived from a Latin word that means "to rage"; rabid animals sometimes appear to be angry. Early symptoms can include fever and tingling at the site of exposure, followed by one or more of the following symptoms: violent movements, uncontrolled excitement, fear of water, an inability to move parts of the body, confusion, and loss of consciousness. Once symptoms appear, death is nearly always the outcome. The time period between contracting the disease and showing symptoms is usually one to three months; however, this time period can vary from less than a week to more than a year. The time between contraction and the onset of symptoms is dependent on the distance the virus must travel to reach the central nervous system.

Haiti is one of five remaining countries in the Americas where canine rabies is still a problem. It has the highest rate of human rabies deaths in the western hemisphere with an estimated two deaths each week. Only about seven deaths are reported to health authorities each year due to poor surveillance, limitations in diagnostic capacity, and lack of awareness and education about the disease among Haitians.

Globally, 59,000 people die from rabies each year. This is the equivalent of one person dying every nine minutes, with half of the people who die from rabies being under the age of 15. The Pan American Health Organization (PAHO) and the Pan American Center of foot-and-mouth disease (PANAFTOSA) led a mission to eliminate dog-mediated rabies in the American region by 2015. These organizations are cognizant of the regional control of rabies. The PAHO and PANAFTOSA visited Haiti in early December, 2013, and the objectives of the mission were to assess the status of Haiti’s rabies program as delivered by the Haitian Ministry of Agriculture, Natural Resources and Rural Development (MARNDR) and the Ministry of Health (MSPP). The mission was to seek opportunities for collaboration between Haiti, Brazil, and the Centers for Disease Control and Prevention (CDC) in Haiti.

Even in 2017, rabies in Haiti is still identified as a national problem, even with PEP proposed.

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.

A canine vector-borne disease (CVBD) is one of "a group of globally distributed and rapidly spreading illnesses that are caused by a range of pathogens transmitted by arthropods including ticks, fleas, mosquitoes and phlebotomine sandflies." CVBDs are important in the fields of veterinary medicine, animal welfare, and public health. Some CVBDs are of zoonotic concern.

Many CVBD infect humans as well as companion animals. Some CVBD are fatal; most can only be controlled, not cured. Therefore, infection should be avoided by preventing arthropod vectors from feeding on the blood of their preferred hosts. While it is well known that arthropods transmit bacteria and protozoa during blood feeds, viruses are also becoming recognized as another group of transmitted pathogens of both animals and humans.

Some "canine vector-borne pathogens of major zoonotic concern" are distributed worldwide, while others are localized by continent. Listed by vector, some such pathogens and their associated diseases are the following:

- Phlebotomine sandflies (Psychodidae): "Leishmania amazonensis", "L. colombiensis", and "L. infantum" cause visceral leishmaniasis (see also canine leishmaniasis). "L. braziliensis" causes mucocutaneous leishmaniasis. "L. tropica" causes cutaneous leishmaniasis. "L. peruviana" and "L. major" cause localized cutaneous leishmaniasis.

- Triatomine bugs (Reduviidae): "Trypanosoma cruzi" causes trypanosomiasis (Chagas disease).

- Ticks (Ixodidae): "Babesia canis" subspecies ("Babesia canis canis", "B. canis vogeli", "B. canis rossi", and "B. canis gibsoni" cause babesiosis. "Ehrlichia canis" and "E. chaffeensis" cause monocytic ehrlichiosis. "Anaplasma phagocytophilum" causes granulocytic anaplasmosis. "Borrelia burgdorferi" causes Lyme disease. "Rickettsia rickettsii" causes Rocky Mountain spotted fever. "Rickettsia conorii" causes Mediterranean spotted fever.

- Mosquitoes (Culicidae): "Dirofilaria immitis" and "D. repens" cause dirofilariasis.

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.

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.

Cat flu is the common name for a feline upper respiratory tract disease. While feline upper respiratory disease can be caused by several different pathogens, there are few symptoms that they have in common.

While Avian Flu can also infect cats, Cat flu is generally a misnomer, since it usually does not refer to an infection by an influenza virus. Instead, it is a syndrome, a term referring to the fact that patients display a number of symptoms that can be caused by one or more of the following infectious agents (pathogens):

1. Feline herpes virus causing feline viral rhinotracheitis (cat common cold, this is the disease that is closely similar to cat flu)

2. Feline calicivirus—(cat respiratory disease)

3. "Bordetella bronchiseptica"—(cat kennel cough)

4. "Chlamydophila felis"—(chlamydia)

In South Africa the term cat flu is also used to refer to Canine Parvo Virus. This is misleading, as transmission of the Canine Parvo Virus rarely involves cats.

Cutaneous leishmaniasis is endemic in all tropical and subtropical areas of the world. The distribution of this disease is very tightly linked to geography, and villages even 15 miles apart can have very different rates of cutaneous leishmaniasis.

Most species of "Leishmania" are capable of infecting humans and causing cutaneous leishmaniasis. In the New World, these organisms include "L. amazonensis", "L. braziliensis", "L. guyanensis", "L. lainsoni", "L. lindenbergi", "L. mexicana", "L. naiffi", "L. panamensis", "L. peruviana", "L. shawi", and "L. venezuelensis". Old World species that cause cutaneous leishmaniasis include "L. aethiopica", "L. infantum", "L. major", and "L. tropica". With the exception of "L. tropica" — which is commonly associated with human settlements and therefore considered to be an anthroponotic species — all of these organisms are zoonotic. As demographic changes occur in developing nations, some species that have traditionally been considered to be zoonotic (e.g., "L. panamensis") are becoming primarily human pathogens.

Dogs and rodents serve as the primary animal reservoir hosts in the sylvatic cycle, but people with chronic PKDL can also serve as important reservoir hosts for cutaneous leishmaniasis. The most common vectors for cutaneous leishmaniasis in the Old World are sandflies of the genus "Phlebotomus", while "Lutzomyia" and those within the family Psychodidae (especially the genus "Psychodopygus") are the most common vectors in the New World. There are more than 600 species of phlebotomine sandflies, and only 30 of these are known vectors. Cutaneous leishmaniasis has been seen in American and Canadian troops coming back from Afghanistan.

The Middle East, in 2016, seems to be experiencing an increase in the cutaneous leishmaniasis disease due to migrants fleeing the Islamic State of Iraq and the Levant. Reports of the increase in the disease have surfaced in Turkey, Lebanon, and elsewhere.

The huge increase in the spread of the disease is attributed to the refugee crises in the Middle East and North Africa over the past five years, particularly due to the displacement of millions of Syrian refugees. The outbreak among Syrian refugees was documented by the World Health Organisation (WHO) in 2012 and recognised as ongoing.

Affected dogs need to be isolated from other dogs and their bedding, and places they have occupied must be thoroughly cleaned. Other dogs in contact with a diagnosed case should be evaluated and treated. A number of parasitical treatments are useful in treating canine scabies. Sulfurated lime (a mixture of calcium polysulfides) rinses applied weekly or biweekly are effective (the concentrated form for use on plants as a fungicide must be diluted 1:16 or 1:32 for use on animal skin).

Selamectin is licensed for treatment in dogs by veterinary prescription in several countries; it is applied as a dose directly to the skin, once per month (the drug does not wash off). A related and older drug ivermectin is also effective and can be given by mouth for two to four weekly treatments or until two negative skin scrapings are achieved. Oral ivermectin is not safe to use on some collie-like herding dogs, however, due to possible homozygous MDR1 (P-glycoprotein) mutations that increase its toxicity by allowing it into the brain. Ivermectin injections are also effective and given in either weekly or every two weeks in one to four doses, although the same MDR1 dog restrictions apply.

Affected cats can be treated with fipronil and milbemycin oxime.

Topical 0.01% ivermectin in oil (Acarexx) has been reported to be effective in humans, and all mite infections in many types of animals (especially in ear mite infections where the animal cannot lick the treated area), and is so poorly absorbed that systemic toxicity is less likely in these sites. Nevertheless, topical ivermectin has not been well enough tested to be approved for this use in dogs, and is theoretically much more dangerous in zones where the animal can potentially lick the treated area. Selamectin applied to the skin (topically) has some of the same theoretical problems in collies and MDR1 dogs as ivermectin, but it has nevertheless been approved for use for all dogs provided that the animal can be observed for 8 hours after the first monthly treatment. Topical permethrin is also effective in both dogs and humans, but is toxic to cats.

Afoxolaner (oral treatment with a chewable tablet containing afoxolaner 2.27% w/w) has been shown to be efficient against both sarcoptic and demodectic mange in dogs.

Sarcoptic mange is transmissible to humans who come into prolonged contact with infested animals, and is distinguished from human scabies by its distribution on skin surfaces covered by clothing. For treatment of sarcoptic infection in humans, see scabies. For demodetic infection in humans, which is not as severe as it is in animals with thicker coats (such as dogs), see "Demodex folliculorum".

Sarcoptic mange, also known as canine scabies, is a highly contagious infestation of "Sarcoptes scabiei canis", a burrowing mite. The canine sarcoptic mite can also infest cats, pigs, horses, sheep, and various other species. The human analog of burrowing mite infection, due to a closely related species, is called scabies (the "seven year itch").

All these burrowing mites are in the family Sarcoptidae. They dig into and through the skin, causing intense itching from an allergic reaction to the mite, and crusting that can quickly become infected. Hair loss and crusting frequently appear first on elbows and ears. Skin damage can occur from the dog's intense scratching and biting. Secondary skin infection is also common. Dogs with chronic sarcoptic mange are often in poor condition, and in both animals and humans, immune suppression from starvation or any other disease causes this type of mange to develop into a highly crusted form in which the burden of mites is far higher than in healthy specimens.

A virus was initially thought to be the cause of DFTD, but no evidence of such a virus could be detected in the cancer cells. Calicivirus, 1080 poison, agricultural chemicals, and habitat fragmentation combined with a retrovirus were other proposed causes. Environmental toxins had also been suspected. In March 2006 a devil escaped from a park into an area infected with DFTD. She was recaptured with bite marks on her face, and returned to live with the other devils in the park. She wounded a male and by October both devils had DFTD, which was subsequently spread to two others (an incident that in retrospect would be understood in the context of the allograft theory of transmission, see following).

To understand the cause that was eventually found, it is important to understand that Tasmanian devil cells have 14 chromosomes; the oldest-known strain of the tumour cells, when these were studied, were shown to contain thirteen chromosomes, nine of which are recognizable and four of which are mutated “marker” chromosomes. More recently evolved strains have an additional mutant marker chromosome, for a total of fourteen chromosomes. Researchers identified the cancer as a neuroendocrine tumour, and found identical chromosomal rearrangements in all the cancer cells. The karyotype anomalies of DFTD cells are similar to those of cancer cells from canine transmissible venereal tumour (CTVT), a cancer of dogs that is transmitted by physical contact. Among the mutations present in the tumour genome is trisomy in chromosome 5p, as well as several single base mutations, and short insertions and deletions, e.g., deletions in the chromosomes 1, 2 and 3. Some of the mutated or deleted genes in DFTD are RET, FANCD2, MAST3 and BTNL9-like gene.

The theory that cancer cells themselves could be an infective agent (the Allograft Theory) was first offered in 2006 by Pearse, Swift, and colleagues, who analyzed DFTD cells from devils in several locations, determining that all DFTD cells sampled were genetically identical to each other, and genetically distinct from their hosts and from all other individual Tasmanian devils whose genetics had been studied; this allowed them to conclude that the cancer originated from a single individual and spread from it, rather than arising repeatedly, and independently. Twenty one different subtypes have been identified by analyzing the mitochondrial and nuclear genomes of 104 tumours from different Tasmanian devils. Researchers have also witnessed a previously-uninfected devil develop tumours from lesions caused by an infected devil’s bites, supporting the contention that the disease is spread by allograft, with transmission via biting, scratching, and aggressive sexual activity between individuals. News reports have reported speculation that the disease is spread by devils biting each other during the mating season. DFTD is rare in juveniles.

Since June 2005, three females have been found that are partially resistant to DFTD. Further research has shown that the infectious facial cancer may be able to spread because of low diversity in devil immune genes (MHC class I and II). The same genes are also found in the tumours, so the devil's immune system does not recognize the tumour cells as foreign.

As of this date, there are at least four strains of the cancer, which, with its monoclonal origin, supports the conclusion that it is evolving. Increased levels of tetraploidy have been shown to exist in the oldest strain of DFTD as of 2014, which correlates with the point at which devils became involved in a DFTD removal programme. Because ploidy slows the tumour growth rate, the DFTD removal programme has been suggested as a selective pressure favouring slower-growing tumours, and more generally that disease eradication programmes aimed at DFTD may encourage the evolution of DFTD. The existence of multiple strains may complicate attempts to develop a vaccine, and there are reports of concerns that the evolution of the cancer may allow it to spread to related species such as the quoll.

An international team of researchers reported in "Science" in January 2010 that DFTD likely originated in the Schwann cells of a single devil. Schwann cells are found in the peripheral nervous system, and produce myelin and other proteins essential for the functions of nerve cells in the peripheral nervous system. BBC reported that the researchers sampled 25 tumours and found that the tumours were genetically identical. Using deep sequencing technology, the study authors then profiled the tumours' transcriptome, the set of genes that are active in tumours; Time magazine reported that the transcriptomes closely matched those of Schwann cells, revealing high activity in many of the genes coding for myelin basic protein production. Several specific markers were identified by the team, including the MBP and PRX genes, which may enable veterinarians to more easily distinguish DFTD from other types of cancer, and may eventually help identify a genetic pathway that can be targeted to treat it.

Due to the decreased life expectancy of the devils with DFTD, affected individuals have begun breeding at younger ages in the wild, with reports that many only live to participate in one breeding cycle. Hence, Tasmanian devils appear to have changed breeding habits in response to the disease; females had previously begun to breed annually at age two, for about three more years, dying thereafter of a variety of causes. Populations are now characterised by onset of breeding at age one, dying of DFTD, on average, shortly thereafter. Social interactions have been seen to contribute to spread of DFTD in a local area.

In 2015, a variant form of the cancer was described which was tetraploid, not diploid like the main form of the cancer. The tetraploid form has been linked to lower mortality rates. The cell type origin of this strain of DFTD is unknown.