Many human diseases can be transmitted to other primates, due to their extensive biological similarities. As a result, centers that hold, treat, or involve close proximity to primates and some other kinds of animals (for example zoos, researchers, and animal hospitals), often take steps to ensure animals are not exposed to human diseases they can catch. In some cases animals are routinely immunized with the same vaccines given to humans.

- Leishmaniasis - Both zoonotic and anthroponotic.

- Influenza, Measles, pneumonia and various other pathogens - Many primates.

- Tuberculosis - Both zoonotic and anthroponotic, with birds, cows, elephants, meerkats, mongooses, monkeys, and pigs known to have been affected.

An anthroponotic disease, or anthroponosis, is an infectious disease in which a disease causing agent carried by humans is transferred to other animals. It may cause the same disease or a different disease in other animals. Since humans do not generally inflict bite wounds on other animals, the method of transmissions is always a "soft" contact such as skin to skin transmission. An example is chytridiomycosis which can be spread by humans with the fungus on their skin handling frogs with bare hands.

The reverse situation, a disease transmitted from animals to humans, is known as zoonotic.

It can also be defined as a human-to-human infection with no animal vector.

In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.

Tyzzer’s disease is an acute epizootic bacterial disease found in rodents, rabbits, dogs, cats, birds, pandas, deer, foals, cattle, and other mammals including gerbils. It is caused by the spore-forming bacterium "Clostridium piliforme", formerly known as "Bacillus piliformis". It is an infectious disease characterized by necrotic lesions on the liver, is usually fatal, and is present worldwide. Animals with the disease become infected through oral ingestion of the bacterial spores and usually die within a matter of days. Animals most commonly affected include young, stressed animals in laboratory environments, such as immature rodents and rabbits. Most commonly affected wild animals include muskrats "(Ondatra zibethicus)" and occasionally cottontail rabbits "(Lepus sylvaticus)". Even today, much remains unknown about Tyzzer’s disease, including how and why it occurs.

There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting

contaminated premises.

No serious long-term effects are known for this disease, but preliminary evidence suggests, if such symptoms do occur, they are less severe than those associated with Lyme disease.

Swine vesicular disease (SVD) is an acute, contagious viral disease of swine caused by the swine vesicular disease virus, an enterovirus. It is characterized by fever and vesicles with subsequent ulcers in the mouth and on the snout, feet, and teats. The pathogen is relatively resistant to heat, and can persist for a long time in salted, dried, and smoked meat products. Swine vesicular disease does not cause economically-important disease, but is important due to its similarity to foot-and-mouth disease.

Infections are treated with antibiotics, particularly doxycycline, and the acute symptoms appear to respond to these drugs.

Pacheco's disease is an acute and often lethal infectious disease in psittacine birds. The disease is caused by a group of herpesviruses, "Psittacid herpesvirus 1" (PsHV-1), which consists of four genotypes. Birds which do not succumb to Pacheco's disease after infection with the virus become asymptomatic carriers that act as reservoirs of the infection. These persistently infected birds, often Macaws, Amazon parrots and some species of conures, shed the virus in feces and in respiratory and oral secretions. Outbreaks can occur when stress causes healthy birds who carry the virus to shed it. Birds generally become infected after ingesting the virus in contaminated material, and show signs of the disease within several weeks.

The main sign of Pacheco's disease is sudden death, sometimes preceded by a short, severe illness. If a bird survives Pacheco's disease following infection with PsHV-1 genotypes 1, 2 or 3, it may later develop internal papilloma disease in the gastrointestinal tract.

Susceptible parrot species include the African gray parrot, and cockatoo. Native Australian birds, such as the eclectus parrot, Bourke's parrot, and budgerigar are susceptible to Pacheco's disease, although the disease itself has not been found in Australia.

The reservoirs of the disease are carrier chickens which could be health but harboring the disease or chronically sick chickens. The disease affects all ages of chickens. The disease can persist in the flock for 2-3 weeks and signs of the disease are seen between 1–3 days post infection. Transmission of the disease is through direct interaction, airborne droplets and drinking contaminated water. Chicken having infection and those carriers contribute highly to the disease transmission

Infectious coryza is a serious bacterial disease of chickens which affects respiratory system and it is manifested by inflammation of the area below the eye, nasal discharge and sneezing...The disease is found all over the world causing high economic losses. Economic loss is due to stumping off and reduction of egg production in case of laying chickens. The disease was discovered early 1930s by considering clinical signs

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.

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.

Pacheco's disease is an eponymously named disease; it is named after the Brazilian veterinarian, Genesio Pacheco, who first came across the disease in 1929, in an outbreak affecting the turquoise-fronted amazon parrot, "Amazona aestiva". Initially, Pacheco's disease was thought to be a manifestation of avian psittacosis. The causative agent of the disease, a herpesvirus, was not identified until 1975.

Pogosta disease is a viral disease, established to be identical with other diseases, Karelian fever and Ockelbo disease. The names are derived from the words Pogosta, Karelia and Ockelbo, respectively.

The symptoms of the disease include usually rash, as well as mild fever and other flu-like symptoms; in most cases the symptoms last less than 5 days. However, in some cases, the patients develop a painful arthritis. There are no known chemical agents available to treat the disease.

It has long been suspected that the disease is caused by a Sindbis-like virus, a positive-stranded RNA virus belonging to the Alphavirus genus and family Togaviridae. In 2002 a strain of Sindbis was isolated from patients during an outbreak of the Pogosta disease in Finland, confirming the hypothesis.

This disease is mainly found in the Eastern parts of Finland; a typical Pogosta disease patient is a middle-aged person who has been infected through a mosquito bite while picking berries in the autumn. The prevalence of the disease is about 100 diagnosed cases every year, with larger outbreaks occurring in 7-year intervals.

Vaccination is the only known method to prevent the development of tumors when chickens are infected with the virus. However, administration of vaccines does not prevent transmission of the virus, i.e., the vaccine is not sterilizing. However, it does reduce the amount of virus shed in the dander, hence reduces horizontal spread of the disease. Marek's disease does not spread vertically. The vaccine was introduced in 1970 and the scientist credited with its development is Dr. Ben Roy Burmester and Dr. Frank J Siccardi. Before that, Marek's disease caused substantial revenue loss in the poultry industries of the United States and the United Kingdom. The vaccine can be administered to one-day-old chicks through subcutaneous inoculation or by "in ovo" vaccination when the eggs are transferred from the incubator to the hatcher. "In ovo" vaccination is the preferred method, as it does not require handling of the chicks and can be done rapidly by automated methods. Immunity develops within two weeks.

The vaccine originally contained the antigenically similar turkey herpesvirus, which is serotype 3 of MDV. However, because vaccination does not prevent infection with the virus, the Marek's disease virus has evolved increased virulence and resistance to this vaccine. As a result, current vaccines use a combination of vaccines consisting of HVT and gallid herpesvirus type 3 or an attenuated MDV strain, CVI988-Rispens (ATCvet code: ).

Marek's disease is a highly contagious viral neoplastic disease in chickens. It is named after József Marek, a Hungarian veterinarian. Marek's disease is caused by an alphaherpesvirus known as 'Marek's disease virus' (MDV) or "Gallid alphaherpesvirus 2" (GaHV-2). The disease is characterized by the presence of T cell lymphoma as well as infiltration of nerves and organs by lymphocytes. Viruses "related" to MDV appear to be benign and can be used as vaccine strains to prevent Marek's disease. For example, the related Herpesvirus of Turkeys (HVT), causes no apparent disease in turkeys and continues to be used as a vaccine strain for prevention of Marek's disease (see below). Birds infected with GaHV-2 can be carriers and shedders of the virus for life. Newborn chicks are protected by maternal antibodies for a few weeks. After infection, microscopic lesions are present after one to two weeks, and gross lesions are present after three to four weeks. The virus is spread in dander from feather follicles and transmitted by inhalation.

The disease is regarded as extremely rare, with an incidence (new number of cases per year) of one case per million people. The patients are predominantly male (86% in a survey of American patients), although in some countries the rate of women receiving a diagnosis of Whipple's disease has increased in recent years. It occurs predominantly in those of Caucasian ethnicity, suggesting a genetic predisposition in that population.

"T. whipplei" appears to be an environmental organism that is commonly present in the gasterointestinal tract but remains asymptomatic. Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic. The possible immunological defect may be specific for "T. whipplei", since the disease is not associated with a substantially increased risk of other infections.

The disease is usually diagnosed in middle age (median 49 years). Studies from Germany have shown that age at diagnosis has been rising since the 1960s.

Persons with component deficiencies in the final common complement pathway (C3,C5-C9) are more susceptible to "N. meningitidis" infection than complement-satisfactory persons, and it was estimated that the risk of infection is 7000 times higher in such individuals. In addition, complement component-deficient populations frequently experience frequent meningococcal disease since their immune response to natural infection may be less complete than that of complement non-deficient persons.

Inherited properdin deficiency also is related, with an increased risk of contracting meningococcal disease. Persons with functional or anatomic asplenia may not efficiently clear encapsulated "Neisseria meningitidis" from the bloodstream Persons with other conditions associated with immunosuppression also may be at increased risk of developing meningococcal disease.

Chronic Lyme disease is a generally unrecognised diagnosis that encompasses "a broad array of illnesses or symptom complexes for which there is no reproducible or convincing scientific evidence of any relationship to "B. burgdorferi" infection." There is no clinical evidence that "chronic" Lyme disease is caused by a persistent infection. It is distinct from post-treatment Lyme disease syndrome, a set of lingering symptoms which may persist after successful treatment of infection with Lyme spirochetes. The symptoms of "chronic Lyme" are generic and non-specific "symptoms of life".

A number of alternative treatments are promoted for "chronic Lyme disease", of which possibly the most controversial and harmful is long-term antibiotic therapy, particularly intravenous antibiotics. Most medical authorities advise against long-term antibiotic treatment for Lyme disease, though they agree that some patients do experience lingering symptoms. Following disciplinary proceedings by State medical licensing boards in the United States, a subculture of "Lyme literate" physicians has successfully lobbied for specific legal protections, exempting them from the standard of care and Infectious Diseases Society of America treatment guidelines. This "troubling" political interference in medical care has been criticised as an example of "legislative alchemy", the process whereby pseudomedicine is legislated into practice.

White band disease (Acroporid white syndrome) is a coral disease that affects acroporid corals and is distinguishable by the white band of dead coral tissue that it forms. The disease completely destroys the coral tissue of Caribbean acroporid corals, specifically elkhorn coral ("Acropora palmata") and staghorn coral ("A. cervicornis"). The disease exhibits a pronounced division between the remaining coral tissue and the exposed coral skeleton. These symptoms are similar to white plague, except that white band disease is only found on acroporid corals, and white plague has not been found on any acroporid corals. It is part of a class of similar disease known as "white syndromes", many of which may be linked to species of "Vibrio" bacteria. While the pathogen for this disease has not been identified, "Vibrio carchariae" may be one of its factors. The degradation of coral tissue usually begins at the base of the coral, working its way up to the branch tips, but it can begin in the middle of a branch.

Cherry X disease also known as Cherry Buckskin disease is caused by a plant pathogenic phytoplasma. Phytoplasma's are obligate parasites of plants and insects. They are specialized bacteria, characterized by their lack of a cell wall, often transmitted through insects, and are responsible for large losses in crops, fruit trees, and ornamentals. The phytoplasma causing Cherry X disease has a fairly limited host range mostly of stone fruit trees. Hosts of the pathogen include sweet/sour cherries, choke cherry, peaches, nectarines, almonds, clover, and dandelion. Most commonly the pathogen is introduced into economical fruit orchards from wild choke cherry and herbaceous weed hosts. The pathogen is vectored by mountain and cherry leafhoppers. The mountain leafhopper vectors the pathogen from wild hosts to cherry orchards but does not feed on the other hosts. The cherry leafhopper which feeds on the infected cherry trees then becomes the next vector that transmits from cherry orchards to peach, nectarine, and other economic crops. Control of Cherry X disease is limited to controlling the spread, vectors, and weed hosts of the pathogen. Once the pathogen has infected a tree it is fatal and removal is necessary to stop it from becoming a reservoir for vectors.

Because the risk of meningococcal disease is increased among USA's military recruits, all military recruits routinely receive primary immunization against the disease.

Some herbaceous hosts naturally have the Cherry X Disease. Once the spreads to the cherry hosts, with the help of the mountain leafhoppers, the cherry leafhoppers can spread the disease around to other woody hosts. Here are some approaches at management with each host type:

Treatment is with penicillin, ampicillin, tetracycline, or co-trimoxazole for one to two years. Any treatment lasting less than a year has an approximate relapse rate of 40%. Recent expert opinion is that Whipple's disease should be treated with doxycycline with hydroxychloroquine for 12 to 18 months. Sulfonamides (sulfadiazine or sulfamethoxazole) may be added for treatment of neurological symptoms.