Mud fever is caused by an infection of the skin by bacteria, including "Dermatophilus congolensis", and often "Staphylococcus spp." Dermatophytes (fungal organisms such as "Malassezia" or "Trichophyton") can also contribute, as can chorioptic mange mites. Photosensitivity or irritant contact may contribute in certain cases. Rarely, vasculitis can cause continued inflammation.

Under normal circumstances the skin acts as a protective barrier, preventing microorganisms from entering the horse's system and doing any damage. However, the integrity of the epidermis can become compromised through the abrasion of soil grit, sand or stable bedding on cold, wet skin. The continual wetting of the skin causes a breakdown of the protective barrier of the epidermis, allowing the bacterium to enter and cause infection.

Shared boots, wraps, grooming supplies, and horse-handler's hands can all serve as fomites, carrying the causative organism(s) from one individual to another. For this reason, mud fever should be considered a contagious disease, and general hygiene steps should be taken to limit cross-contamination.

Horses and ponies standing for hours in muddy, wet paddocks and at gates are a common sight during the winter months and early spring. It is in these conditions that mud fever thrives. Generally, those horses and ponies with white socks are more prone to the condition, although Mud Fever will affect horses of all breeds, ages and colours.

As with any bacterial infection, mud fever can become a very serious condition very quickly. The legs can become swollen and sore and open sores can become quickly infected. Often, such is the level of damage to the skin that these open sores can become very difficult to heal and can result in proud flesh, permanent hair loss and in severe cases the need for skin grafts.

In draft horses, particularly Clydesdales, Shires, and Belgians, a similar-appearing, but more serious condition occurs called chronic progressive lymphedema. This condition appears to be genetically-linked, starting early in life and progressing, causing thickening, fibrosis, and predisposing to secondary infections. This disease can progress enough to require euthanasia.

Preventative action should be taken as soon as the paddocks start to become wet and muddy. Rotation of paddocks keeps horses from having to stand in wet, muddy ground. Electric fencing may also prevent horses from standing for long periods in the deep mud that collects in high traffic areas.

Rainscald (also known as "dermatophilosis", "rain rot" and "streptothricosis") is a common skin disease in horses that is caused by the bacterium "Dermatophilus congolensis". This is the same organism that causes Mud fever in horses. This disease is very common in cows, sheep and goats and is also found occasionally in cats, dogs, and humans. D. congolensis is a gram-positive bacterium that is thought to originate from the soil. It commonly causes disease in moist tropical areas, but can also be found in wet northern environments. Moisture and high temperatures facilitate the dispersal and penetration of zoospores into the skin, contributing to the spread of the disease.

Ticks, biting flies, and contact with other infected animals also causes the spread of rainscald. Once in the skin, the bacteria cause inflammation of the skin as well as the typical symptoms associated with rainscald.

There are two different manifestations of rainscald: the winter form, which is more severe due to the longer coat of the horse, and the summer form, which is less severe. Horses are usually affected on the back, head, and neck, where insects commonly bite, and the legs, which are commonly infected if the horse is kept in moist footing. Initially, the horse will display a matted coat and bumps which will then progress to crusty scabs and lesions. The animal may also be itchy and display signs of discomfort.

"Warm water immersion foot" is a skin condition of the feet that results after exposure to warm, wet conditions for 48 hours or more and is characterized by maceration ("pruning"), blanching, and wrinkling of the soles, padding of toes (especially the big toe) and padding of the sides of the feet.

Foot maceration occur whenever exposed for prolong periods to moist conditions. Large watery blisters appear which are painful when they open and begin to peel away from the foot itself. The heels, sides and bony prominences are left with large areas of extremely sensitive, red tissue, exposed and prone to infection. As the condition worsens, more blisters develop due to prolonged dampness which eventually covers the entire heel and/or other large, padded sections of the foot, especially the undersides as well as toes. Each layer in turn peels away resulting in deep, extremely tender, red ulcerations.

Healing occurs only when the feet are cleansed, dried and exposed to air for weeks. Scarring is permanent with dry, thin skin that appears red for up to a year or more. The padding of the feet returns but healing can be painful as the nerves repair with characteristics of diabetic neuropathy. Antibiotics and/or antifungal are sometimes prescribed.

Foot immersion is a common problem with homeless individuals wearing one pair of socks and shoes for extensive periods of time, especially wet shoes and sneakers from rain and snow. The condition is exacerbated by excessive dampness of the feet for prolonged periods of time. Fungus and bacterial infections prosper in the warm, dark, wet conditions and are characterized by a sickly odor that is distinct to foot immersion.

"Tropical immersion foot" (also known as "Paddy foot", and "Paddy-field foot") is a skin condition of the feet seen after continuous immersion of the feet in water or mud of temperature above 22 degrees Celsius (roughly 72 degrees Fahrenheit ) for two to ten days.

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.

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

Lipoproteins released from treatment of "Treponema pallidum" infections are believed to induce the Jarisch-Herxheimer reaction. The Herxheimer reaction has shown an increase in inflammatory cytokines during the period of exacerbation, including tumor necrosis factor alpha, interleukin-6 and interleukin-8.

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.

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.

A Jarisch–Herxheimer reaction () is a reaction to endotoxin-like products released by the death of harmful microorganisms within the body during antibiotic treatment. Efficacious antimicrobial therapy results in lysis (destruction) of bacterial cell membranes, and in the consequent release into the bloodstream of bacterial toxins, resulting in a systemic inflammatory response.

Jarisch–Herxheimer reactions are usually not life-threatening.

Carrión's disease, or Oroya fever, or Peruvian wart is a rare infectious disease found only in Peru, Ecuador, and Colombia. It is endemic in some areas of Peru, is caused by infection with the bacterium "Bartonella bacilliformis", and transmitted by sandflies of genus "Lutzomyia".

Cat scratch disease occurs worldwide. Cats are the main reservoir of "Bartonella henselae", and the bacterium is transmitted to cats by the cat flea "Ctenocephalides felis". Infection in cats is very common with a prevalence estimated between 40-60%, younger cats being more commonly infective. Cats usually become immune to the infection, while dogs may be very symptomatic. Humans may also acquire it through flea or tick bites from infected dogs, cats, coyotes, and foxes.

Trench fever, produced by "Bartonella quintana" infection, is transmitted by the human body louse "Pediculus humanus corporis". Humans are the only known reservoir. Thorough washing of clothing may help to interrupt the transmission of infection.

A possible role for ticks in transmission of "Bartonella" species remains to be elucidated; in November 2011, "Bartonella rochalimae", "B. quintana", and "B. elizabethae" DNA was first reported in "Rhipicephalus sanguineus" and "Dermacentor nitens" ticks in Peru.

Since its first description in the 1960s, only seven people worldwide have been reported to have survived PAM as of 2015, with three in the United States and one in Mexico; one of the US survivors had brain damage that is probably permanent. Less than 1% of people with naegleriasis survive.

Person-to-person transmission is exceedingly unusual; and patients with melioidosis should not be considered contagious. Lab workers should handle "B. pseudomallei" under BSL-3 isolation conditions, as laboratory-acquired melioidosis has been described.

In endemic areas, people (rice-paddy farmers in particular) are warned to avoid contact with soil, mud, and surface water where possible. Case clusters have been described following flooding and cyclones and probably relate to exposure. Other case clusters have related to contamination of drinking water supplies. Populations at risk include patients with diabetes mellitus, chronic renal failure, chronic lung disease, or an immune deficiency of any kind. The effectiveness of measures to reduce exposure to the causative organism have not been established. A vaccine is not yet available.

After exposure to "B. pseudomallei" (particularly following a laboratory accident) combined treatment with co-trimoxazole and doxycycline is recommended. Trovafloxacin and grepafloxacin have been shown to be effective in animal models.

The disease is rare and highly lethal: there have only been 300 cases as of 2008. Drug treatment research at Aga Khan University in Pakistan has shown that "in-vitro" drug susceptibility tests with some FDA approved drugs used for non-infectious diseases have proved to kill "Naegleria" "fowleri" with an amoebicidal rate greater than 95%. The same source has also proposed a device for drug delivery via the transcranial route to the brain.

The number of cases of infection could increase due to climate change, and was posited as the reason for 3 cases in Minnesota in 2010, 2012, and 2015. In 2016, an infection was contracted in Maryland, four miles south of the Pennsylvania border;

As of 2013, numbers of reported cases were expected to increase, simply because of better informed diagnoses being made both in ongoing cases and in autopsy findings.

A sizable industry has developed in Japan around services and products that help people deal with hay fever, including protective wear such as coats with smooth surfaces, masks, and glasses; medication and remedies; household goods such as air-conditioner filters and fine window screens; and even "hay fever relief vacations" to low-pollen areas such as Okinawa and Hokkaido. Some people in Japan use medical laser therapy to desensitize the parts of their nose that are sensitive to pollen.

Treatment of infections caused by "Bartonella" species include:

Some authorities recommend the use of azithromycin.

Filicollis anatis is an endoparasite in the Polymorphidae family of thorny-headed worms. Adults have been found to occur in waterbirds such as ducks, where they cause a condition known as filicollosis. Larval stages occur in invertebrate hosts such as crayfish.

A study in the Chernihiv region of Ukraine found that "F. anatis" infected ducks throughout their grazing period, but not in the winter; it also found that the parasite's eggs could remain viable throughout the winter when buried in mud under natural conditions.

Acanthocephalans such as "F. anatis" form capsules in their intermediate arthropod hosts to protect the developing larvae from the host immune system. "F. anatis" forms its capsules primarily by secreting material during the initial (acanthellar) stage after infecting the intermediate host.

Hay fever was relatively uncommon in Japan until the early 1960s. Shortly after World War II, reforestation policies resulted in large forests of cryptomeria and Japanese cypress trees, which were an important resource for the construction industry. As these trees matured, they started to produce large amounts of pollen. Peak production of pollen occurs in trees of 30 years and older. As the Japanese economy developed in the 1970s and 1980s, cheaper imported building materials decreased the demand for cryptomeria and Japanese cypress materials. This resulted in increasing forest density and aging trees, further contributing to pollen production and thus, hay fever. In 1970, about 50% of cryptomeria were more than 10 years old, and just 25% were more than 20 years old. By 2000, almost 85% of cryptomeria were over 20 years old, and more than 60% of trees were over 30 years old. This cryptomeria aging trend has continued since then, and though cryptomeria forest acreage has hardly increased since 1980, pollen production has continued to increase. Furthermore, urbanization of land in Japan led to increasing coverage of soft soil and grass land by concrete and asphalt. Pollen settling on such hard surfaces can easily be swept up again by winds to recirculate and contribute to hay fever. As a result, approximately 25 million people (about 20% of the population) currently suffer from this type of seasonal hay fever in Japan.

The U.S. Centers for Disease Control and Prevention (CDC) publishes a journal "Emerging Infectious Diseases" that identifies the following factors contributing to disease emergence:

- Microbial adaption; e.g. genetic drift and genetic shift in Influenza A

- Changing human susceptibility; e.g. mass immunocompromisation with HIV/AIDS

- Climate and weather; e.g. diseases with zoonotic vectors such as West Nile Disease (transmitted by mosquitoes) are moving further from the tropics as the climate warms

- Change in human demographics and trade; e.g. rapid travel enabled SARS to rapidly propagate around the globe

- Economic development; e.g. use of antibiotics to increase meat yield of farmed cows leads to antibiotic resistance

- Breakdown of public health; e.g. the current situation in Zimbabwe

- Poverty and social inequality; e.g. tuberculosis is primarily a problem in low-income areas

- War and famine

- Bioterrorism; e.g. 2001 Anthrax attacks

- Dam and irrigation system construction; e.g. malaria and other mosquito borne diseases

Metal fume fever is due to the inhalation of certain metals, either as fine dust or most commonly as fumes. Simple metal compounds such as oxides are equally capable of causing it. The effects of particularly toxic compounds, such as nickel carbonyl, are not considered merely metal fume fever.

Exposure usually arises through hot metalworking processes, such as smelting and casting of zinc alloys, welding of galvanized metals, brazing, or soldering. If the metal concerned is particularly high-risk, the residue from cold sanding processes may also cause fume fever, even if the dose is lower. It may also be caused by electroplated surfaces or metal-rich anti-corrosion paint, such as cadmium passivated steel or zinc chromate primer on aluminium aircraft parts. Exposure has also been reported in use of lead-free ammunition, by the harder steel core stripping excess metal from the jacket of the bullet and barrel of the rifle.

The most plausible metabolic source of the symptoms is a dose-dependent release of certain cytokines, an event which occurs by inhaling metal oxide fumes that injure the lung cells. This is not an allergic reaction, though allergic reactions to metal fumes can occur.

Methicillin-resistant Staphylococcus aureus (MRSA) evolved from Methicillin-susceptible Staphylococcus aureus (MSSA) otherwise known as common "S. aureus". Many people are natural carriers of "S. aureus", without being affected in any way. MSSA was treatable with the antibiotic methicillin until it acquired the gene for antibiotic resistance. Though genetic mapping of various strains of MRSA, scientists have found that MSSA acquired the mecA gene in the 1960s, which accounts for its pathogenicity, before this it had a predominantly commensal relationship with humans. It is theorized that when this "S. aureus" strain that had acquired the mecA gene was introduced into hospitals, it came into contact with other hospital bacteria that had already been exposed to high levels of antibiotics. When exposed to such high levels of antibiotics, the hospital bacteria suddenly found themselves in an environment that had a high level of selection for antibiotic resistance, and thus resistance to multiple antibiotics formed within these hospital populations. When "S. aureus" came into contact with these populations, the multiple genes that code for antibiotic resistance to different drugs were then acquired by MRSA, making it nearly impossible to control. It is thought that MSSA acquired the resistance gene through the horizontal gene transfer, a method in which genetic information can be passed within a generation, and spread rapidly through its own population as was illustrated in multiple studies. Horizontal gene transfer speeds the process of genetic transfer since there is no need to wait an entire generation time for gene to be passed on. Since most antibiotics do not work on MRSA, physicians have to turn to alternative methods based in Darwinian medicine. However prevention is the most preferred method of avoiding antibiotic resistance. By reducing unnecessary antibiotic use in human and animal populations, antibiotics resistance can be slowed.

Ticks should be removed promptly and carefully with tweezers and by applying gentle, steady traction. The tick's body should not be crushed when it is removed and the tweezers should be placed as close to the skin as possible to avoid leaving tick mouthparts in the skin; mouthparts left in the skin can allow secondary infections. Ticks should not be removed with bare hands. Hands should be protected by gloves and/or tissues and thoroughly washed with soap and water after the removal process.

A match or flame should not be used to remove a tick. This method, once thought safe, can cause the tick to regurgitate, expelling any disease it may be carrying into the bite wound.