Because this disease is highly durable in its equine host, it has proved very difficult to develop a vaccine for it. There are four main drugs on the market that are used to treat the clinical signs of dourine: Suramin, Diminazen, Cymerlarsan, and Quinapyramin. However, none of the listed drugs are a cure and even the individual animals that are treated will experience relapses. Although this disease is not fatal in all cases and spontaneous recovery can occur, the death rate is relatively high and listed at a mortality rate of over fifty percent.

This lack of a cure or vaccine is a definite problem in the equine industry, especially in developing countries where equines are highly valuable for both agriculture and transportation. Dourine is considered an endemic problem in developing countries, where over sixty percent of equines in the world are located. The protocol for this disease, as stated by OIE, currently stands at slaughter of seropositive animals. This is not an economically feasible option for many people who depend on horses for their livelihood. Therefore, it is crucial to continue research in this field and develop a viable vaccine.

"Trypanosoma equiperdum" is one of three known strains from the "Trypanosoma" family; along with "Trypanosoma evansi" and "Trypanosoma brucei". "Trypanosoma equiperdum" has been discovered to be most closely linked to "Trypanosoma evansi", so much so that even observation under microscope is not sufficient to differentiate between the two as their structure is very similar.

Dourine is a unique disease in the sense that it has no known vectors or fomites existing in the natural world, other than members of the equine family, including donkeys, mules, and horses. In a laboratory setting, "Trypanosoma equiperdum" has been manipulated to adapt to and proliferate in other species, such as dogs, rabbits, mice and rats, but this has never been observed to occur naturally and without scientific manipulation. Although this limits spread of the disease because it is restricted to the equine population alone, the organism has developed complex mechanisms over time to better equip itself for prolonged survival in the equine species. This parasite efficiently evades the host animal's immune system through the use of variable surface glycoproteins or VSGs. These VSGs allow the organism to constantly manipulate and change the surface structure of its proteins, which means it is constantly being presented to the immune system as a new foreign organism and this prevents the body from mounting a large enough immune response to eradicate the disease. In this sense, "Trypanosoma equiperdum" is a very efficient organism; it may infect less species than other diseases, but it infects and survives very efficiently within its specified hosts.

In an endemic herd, only a minority of the animals develops clinical signs; most animals either eliminate the infection or become asymptomatic carriers. The mortality rate is about 1%, but up to 50% of the animals in the herd can be asymptomatically infected, resulting in losses in production. Once the symptoms appear, paratuberculosis is progressive and affected animals eventually die. The percentage of asymptomatic carriers that develop overt disease is unknown.

MAP is capable of causing Johne's-like symptoms in humans, though difficulty in testing for MAP infection presents a diagnostic hurdle.

Clinical similarities are seen between Johne's disease in ruminants and inflammatory bowel disease in humans, and because of this, some researchers contend the organism is a cause of Crohn's disease. However, epidemiologic studies have provided variable results; in certain studies, the organism (or an immune response directed against it) has been much more frequently found in patients with Crohn's disease than asymptomatic people.

While obviously preventable by staying away from rodents, otherwise hands and face should be washed after contact and any scratches both cleaned and antiseptics applied. The effect of chemoprophylaxis following rodent bites or scratches on the disease is unknown. No vaccines are available for these diseases.

Improved conditions to minimize rodent contact with humans are the best preventive measures. Animal handlers, laboratory workers, and sanitation and sewer workers must take special precautions against exposure. Wild rodents, dead or alive, should not be touched and pets must not be allowed to ingest rodents.

Those living in the inner cities where overcrowding and poor sanitation cause rodent problems are at risk from the disease. Half of all cases reported are children under 12 living in these conditions.

Equine venereal diseases are sexually transmitted infections in horses. They include contagious equine metritis (CEM) (caused by "Taylorella equigenitalis") and equine coital exanthema (caused by equine herpesvirus 3).

Macrolides, tetracyclines and quinolones are active against "M. capricolum" subsp." capripneumoniae". Disease incidence is reduced by good hygiene and husbandry practices.

Movement restrictions and slaughtering infected animals are recommended for countries that are newly infected.

Contagious caprine pleuropneumonia (CCPP) is a cause of major economic losses to goat producers in Africa, Asia and the Middle East.

Disease is caused by members of the Mycoplasma genus - usually "Mycoplasma capricolum subsp. capricolum" but sometimes by "M. mycoides" subsp. "capri" or "M. mycoides" subsp. "mycoides". It is extremely contagious with very high morbidity and mortality rates, causing an interstitial fibrinous pleuropneumonia in infected goats. Infection is spread by close-contact aerosol, therefore overcrowding and confinement increases disease incidence. Stress factors such as malnutrition and long transport can also predispose animals to disease.

Goats are the only species affected, therefore the disease is not a zoonosis. There is no age breed or sex predilection, but clinical signs are often worse in younger animals.

When proper treatment is provided for patients with rat-bite fever, the prognosis is positive. Without treatment, the infection usually resolves on its own, although it may take up to a year to do so. A particular strain of rat-bite fever in the United States can progress and cause serious complications that can be potentially fatal. Before antibiotics were used, many cases resulted in death. If left untreated, streptobacillary rat-bite fever can result in infection in the lining of the heart, covering over the spinal cord and brain, or in the lungs. Any tissue or organ throughout the body may develop an abscess.

This disease affects the external genitalia, and is caused by equine herpesvirus 3. This disease remains with the horse for all its life. Equine coital exanthema is believed to only be transmitted during the acute phase of the disease through serous fluid from the blisters during sexual intercourse, and via breeding tools, handlers, etc.

Clinical signs include cute small lesions, no bigger than 2 mm in diameter around the vulva in mares, and on the sheath in stallions. The small bumps blister and then rupture, leaving raw, ulcerated, painful sores. While the majority of the symptoms are external, the presence of the virus can cause small and large plaque variants in tissues.

Cuterebriasis is a parasitic disease affecting rodents, lagomorphs (hares, rabbits, pikas), felines and canines. The etiologic agent is the larval development of bot flies within the "Cuterebra" or "Trypoderma" genera, which occurs obligatorily in rodents and lagomorphs, respectively. Felines and canines serve as accidental hosts, but research suggests only by "Trypoderma" spp. Entrance into the body by first instar larva occurs via mucous membranes of natural orifices or open wounds as opposed to direct dermic penetration.

"Rabbits, Hares & Lagomorphs"

Usually there do not appear to be any clinical signs. Subcutaneous cysts, warbles, may present upon larval deposition out of the body at maturation.

"Felines & Canines"

There are three forms in which Cuterebriasis may present:

- Myasis

- Cerebrospinal

- Respiratory

Myasis involves subcutaneous cyst formation due to 3rd larval instar maturation, occurring ~30 days post-entry into the body. Cysts are often found on the face, neck and trunk, but location varies with larval migration within the host. Serous discharge may be observed from these cysts, which are typically 3-5mm in diameter and include a central pore through which the larvae respire. This pore also serves as a means of exit for the larvae, which occurs anywhere between 3 and 8 weeks post-entry.

Cerebrospinal cuterebriasis results from larval migration to the brain. This is seen in cats, and is the proposed cause for feline ischemic encephalopathy and a suggestive causative agent of feline idiopathic vestibular disease. Symptoms of this type of presentation include lethargy, seizures, blindness, abnormal vocalization or gait, circling, and abnormal or no reflex responses. When affecting the central nervous system, cats are known to exhibit violent sneezing attacks that can onset weeks prior to manifestation of other clinical signs.

Respiratory disease results when larval migration occurs through the trachea, pharynx, diaphragm, or lungs. Cuterebriasis has been increasingly noted as a cause for dyspnea in felines.

Cryptococcosis is a defining opportunistic infection for AIDS, and is the second-most-common AIDS-defining illness in Africa. Other conditions that pose an increased risk include certain lymphomas (e.g., Hodgkin's lymphoma), sarcoidosis, liver cirrhosis, and patients on long-term corticosteroid therapy.

Distribution is worldwide in soil. The prevalence of cryptococcosis has been increasing over the past 20 years for many reasons, including the increase in incidence of AIDS and the expanded use of immunosuppressive drugs.

In humans, "C. neoformans" causes three types of infections:

- Wound or cutaneous cryptococcosis

- Pulmonary cryptococcosis

- Cryptococcal meningitis.

Cryptococcal meningitis (infection of the meninges, the tissue covering the brain) is believed to result from dissemination of the fungus from either an observed or unappreciated pulmonary infection. Often there is also silent dissemination throughout the brain when meningitis is present. "Cryptococcus gattii" causes infections in immunocompetent people (fully functioning immune system), but "C. neoformans v. grubii", and "v. neoformans" usually only cause clinically evident infections in persons with some form of defect in their immune systems (immunocompromised persons). People with defects in their cell-mediated immunity, for example, people with AIDS, are especially susceptible to disseminated cryptococcosis. Cryptococcosis is often fatal, even if treated. It is estimated that the three-month case-fatality rate is 9% in high-income regions, 55% in low/middle-income regions, and 70% in sub-Saharan Africa. As of 2009 there were globally approximately 958,000 annual cases and 625,000 deaths within three months after infection.

Although the most common presentation of cryptococcosis is of "C. neoformans" infection in an immunocompromised person (such as persons living with AIDS), the "C. gattii" is being increasingly recognised as a pathogen in what is presumed to be immunocompetent hosts, especially in Canada and Australia. This may be due to rare exposure and high pathogenicity, or to unrecognised isolated defects in immunity, specific for this organism.

Cryptococcosis, also known as cryptococcal disease, is a potentially fatal fungal disease. It is caused by one of two species; "Cryptococcus neoformans" and "Cryptococcus gattii". These were all previously thought to be subspecies of "C. neoformans" but have now been identified as distinct species.

Cryptococcosis is believed to be acquired by inhalation of the infectious propagule from the environment. Although the exact nature of the infectious propagule is unknown, the leading hypothesis is the basidiospore created through sexual or asexual reproduction.

Trombiculosis, trombiculiasis, or trombiculidiasis is a rash caused by trombiculid mites which is often referred to as a chigger bite.

Chiggers are commonly found on the tip of blades of grasses to catch a host, so keeping grass short, and removing brush and wood debris where potential mite hosts may live, can limit their impact on an area. Sunlight that penetrates the grass will make the lawn drier and make it less favorable for chigger survival.

Chiggers seem to affect warm covered areas of the body more than drier areas. Thus, the bites are often clustered behind the knees, or beneath tight undergarments such as socks, underwear, or brassieres. Areas higher in the body (chest, back, waist-band, and under-arms) are affected more easily in small children than in adults, since children are shorter and are more likely than adults to come in contact with low-lying vegetation and dry grass where chiggers thrive. An exceptional case has been described in the eye, producing conjunctivitis.

Application of repellent to the shoes, lower trousers and skin is also useful. Because they are found in grass, staying on trails, roads, or paths can prevent contact. Dusting sulfur is used commercially for mite control and can be used to control chiggers in yards. The dusting of shoes, socks and trouser legs with sulfur can be highly effective in repelling chiggers.

Another good strategy is to recognize the chigger habitat to avoid exposure in the first place. Chiggers in North America thrive late in summer, in dry tall grasses and other thick, unshaded vegetation. Insect repellents containing one of the following active ingredients are recommended: DEET, catnip oil extract (nepetalactone), citronella oil or eucalyptus oil extract. However, in 1993 issue a study reported on tests of two commercial repellents: DEET and citrus oil: "All chiggers exposed on the filter papers treated with DEET died and did not move off the treated papers. None of the chiggers that were placed on papers treated with citrus oil were killed." It was concluded that DEET was more effective than citrus oil.

Chiggers can also be treated using common household vinegar (5% acetic acid).

Beech bark disease is a disease that causes mortality and defects in beech trees in the eastern United States and Europe. In North America, the disease occurs after extensive bark invasion by the beech scale insect, "Cryptococcus fagisuga". Through a presently unknown mechanism, excessive feeding by this insect causes two different fungi ("Neonectria faginata" (previously "Nectria coccinea var. faginata") and "Neonectria ditissima" (previously "Nectria galligena")) to produce annual cankers on the bark of the tree. The continuous formation of lesions around the tree eventually girdles it, resulting in canopy death. In Europe, "N. coccinea" is the primary fungus causing the infection. Infection in European trees occurs in the same manner as it does in North American trees. Though the disease still appears in Europe, it is less serious today than it once was.

Buerger's is not immediately fatal. Amputation is common and major amputations (of limbs rather than fingers/toes) are almost twice as common in patients who continue to smoke. Prognosis markedly improves if a person quits smoking. Female patients tend to show much higher longevity rates than men. The only known way to slow the progression of the disease is to abstain from all tobacco products.

There are a few controls for beech bark disease. One important management strategy is prohibiting the movement of nursery stock or other materials that may harbor the beech scale insect. Insecticides, generally not applied under forest conditions, are primarily used on high-value ornamental trees. The use of other organisms as controls is also a possibility. The ladybird beetle is a beetle that preys on the beech scale insect. A fungus that parasitizes the "Neonectria" fungus could also be employed. The problem with using these organisms to control beech bark disease is that their impact on the disease has not been evaluated extensively. In a forest setting, controlling the beech bark disease is too costly. Timely salvage cutting can reduce economic losses of beech in a forest. In stands where beech bark disease is established, silvicultural best practice is to retain large overstory trees which show visual resistance (no scale, cankers or fungus), remove heavily infested/dying trees and then treat sprouts from infested trees with herbicides. The residual, resistant parent trees are future sources of resistant seed/sprouts. Resistance to beech bark disease in a stand may be 1%-5% of trees or more, with significant regional variation. A study of 35 sites in three Canadian provinces found resistance rates ranging from 2.2%-5.7%.

In 1985 the UAE established a national program to prevent transmission of acquired immune deficiency syndrome (AIDS) and to control its entry into the country. According to World Health Organization estimates, in 2002−3 fewer than 1,000 people in the UAE were living with human immunodeficiency virus (HIV)/AIDS.

Obesity is a growing health concern with health officials stating that obesity is one of the leading causes of preventable deaths in the United Arab Emirates. According to Forbes, United Arab Emirates ranks 1 on a 2007 list of fattest countries with a percentage of 68.3% of its citizens with an unhealthy weight.

The cause of the disease is thought to be autoimmune in nature and heavily linked to tobacco use in patients with Buerger's as primary disease.

About 5 to 10% of women are affected by aerobic vaginitis. Reports in pregnant women point to a prevalence of 8.3–10.8%.

When considering symptomatic women, the prevalence of AV can be as high as 23%.

The proximal causes of fiddler’s neck are friction and pressure, but both repetitive shearing stress and occlusion with consequent trapping of sweat give rise to progressive damage. This damage along with poor hygiene predisposes the area to local infection, and such infection can progress to scarring and other long-term effects. Hot weather is reported to exacerbate fiddler’s neck, as are tiredness, playing emotional music, and playing in smaller groups where individual stress is higher. Type I hypersensitivity reactions may also be involved, particularly to rosewood and ebony in the chinrest and tailpiece, as well as to varnish of the instrument body when chinrests are not used and to rosin deposits on the instrument and on chin cloths. Nickel or other metal allergies are common causes if the chin rest has a metal clip that comes into constant contact with the skin. Rosin exposure in particular may lead to abietic acid dermatitis.

Fiddler’s neck does not usually form unless the musician is practicing or playing for more than a few hours each day, and only seems to develop after a few years of serious playing. Thus, when not infected or otherwise problematic, fiddler’s neck may be known as a benign practice mark and may be worn proudly as an indication of long hours of practice. Blum & Ritter (1990) found that 62% of 523 professional violinists and violists in West Germany experienced fiddler’s neck, with the percentage among violists being higher (67%) than among violinists (59%). Viola players are believed to be more predisposed to developing fiddler’s neck than violinists because the viola is larger and heavier, but this has not been empirically confirmed.

The development of fiddler’s neck does not depend on preexisting skin problems, and Blum & Ritter find that only 23% of men and 14% of women in their study reported cutaneous disorders in other parts of the face (mainly acne and eczema) that were independent of playing the violin or viola. Fiddler’s neck may exacerbate existing acne, but acne may also be limited solely to the lesion and not appear elsewhere. Nonetheless, musicians with underlying dermatologic diseases like acne and eczema are more endangered by fiddler’s neck than others. Males may develop folliculitis or boils due to involvement of beard hair.