Trench foot can be prevented by keeping the feet clean, warm, and dry. It was also discovered in World War I that a key preventive measure was regular foot inspections; soldiers would be paired and each made responsible for the feet of the other, and they would generally apply whale oil to prevent trench foot. If left to their own devices, soldiers might neglect to take off their own boots and socks to dry their feet each day, but if it were the responsibility of another, this became less likely. Later on in the war, instances of trench foot began to decrease, probably as a result of the introduction of the aforementioned measures; of wooden duckboards to cover the muddy, wet, cold ground of the trenches; and of the increased practice of troop rotation, which kept soldiers from prolonged time at the front.

Unlike frostbite, trench foot does not require freezing temperatures; it can occur in temperatures up to 16° Celsius (about 60° Fahrenheit) and within as little as 13 hours. Exposure to these environmental conditions causes deterioration and destruction of the capillaries and leads to morbidity of the surrounding flesh. Excessive sweating (hyperhidrosis) has long been regarded as a contributory cause; unsanitary, cold, and wet conditions can also cause trench foot.

"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.

"Trench foot " is a medical condition caused by prolonged exposure of the feet to damp, unsanitary, and cold conditions. The use of the word "trench" in the name of this condition is a reference to trench warfare, mainly associated with World War I. Affected feet may become numb, affected by erythrosis (turning red) or cyanosis (turning blue) as a result of poor vascular supply, and feet may begin to have a decaying odour due to the possibility of the early stages of necrosis setting in. As the condition worsens, feet may also begin to swell. Advanced trench foot often involves blisters and open sores, which lead to fungal infections; this is sometimes called tropical ulcer (jungle rot).

If left untreated, trench foot usually results in gangrene, which can cause the need for amputation. If trench foot is treated properly, complete recovery is normal, though it is marked by severe short-term pain when feeling returns. As with other cold-related injuries, trench foot leaves sufferers more susceptible to it in the future.

Besides being exposed to any of the modes of transmission presented above, there are additional risk factors that increase one's chance of contracting athlete's foot. Persons who have had athlete's foot before are more likely to become infected than those who have not. Adults are more likely to catch athlete's foot than children. Men have a higher chance of getting athlete's foot than women. People with diabetes or weakened immune systems are more susceptible to the disease. HIV/AIDS hampers the immune system and increases the risk of acquiring athlete's foot. Hyperhidrosis (abnormally increased sweating) increases the risk of infection and makes treatment more difficult.

According to the National Health Service, "Athlete’s foot is very contagious and can be spread through direct and indirect contact." The disease may spread to others directly when they touch the infection. People can contract the disease indirectly by coming into contact with contaminated items (clothes, towels, etc.) or surfaces (such as bathroom, shower, or locker room floors). The fungi that cause athlete's foot can easily spread to one's environment. Fungi rub off of fingers and bare feet, but also travel on the dead skin cells that continually fall off the body. Athlete's foot fungi and infested skin particles and flakes may spread to socks, shoes, clothes, to other people, pets (via petting), bed sheets, bathtubs, showers, sinks, counters, towels, rugs, floors, and carpets.

When the fungus has spread to pets, it can subsequently spread to the hands and fingers of people who pet them. If a pet frequently gnaws upon itself, it might not be fleas it is reacting to, it may be the insatiable itch of tinea.

One way to contract athlete's foot is to get a fungal infection somewhere else on the body first. The fungi causing athlete's foot may spread from other areas of the body to the feet, usually by touching or scratching the affected area, thereby getting the fungus on the fingers, and then touching or scratching the feet. While the fungus remains the same, the name of the condition changes based on where on the body the infection is located. For example, the infection is known as tinea corporis ("ringworm") when the torso or limbs are affected or tinea cruris (jock itch or dhobi itch) when the groin is affected. Clothes (or shoes), body heat, and sweat can keep the skin warm and moist, just the environment the fungus needs to thrive.

Stem cell therapy may represent a treatment for promoting healing of diabetic foot ulcers. Diabetic foot ulcers develop their own, distinctive microbiota. Investigations into characterizing and identifying the phyla, genera and species of nonpathogenic bacteria or other microorganisms populating these ulcers may help identify one group of microbiota that promotes healing.

Steps to prevent diabetic foot ulcers include frequent review by a foot specialist, good foot hygiene, diabetic socks and shoes, as well as avoiding injury.

- Foot-care education combined with increased surveillance can reduce the incidence of serious foot lesions.

Atherosclerotic restriction to the arterial supply in peripheral artery occlusive disease may result in painful arterial ulcers of the ankle and foot, or give rise of gangrene of the toes and foot. Immobility of a person may result in prolonged pressure applied to the heels causing pressure sores.

Impaired venous drainage from the foot in varicose veins may sequentially result in brown haemosiderin discolouration to the ankle and foot, varicose stasis dermatitis and finally venous ulcers.

Other disorders of the foot include osteoarthritis of the joints, peripheral neuropathy and plantar warts.

Foot rot, or infectious pododermatitis, is a hoof infection commonly found in sheep, goats, and cattle. As the name suggests, it rots away the foot of the animal, more specifically the area between the two toes of the affected animal. It is extremely painful and contagious. It can be treated with a series of medications, but if not treated, the whole herd can become infected. The cause of the infection in cattle is two species of anaerobic bacteria, "Fusobacterium necrophorum" and "Bacteroides melaninogenicus". Both bacteria are common to the environment in which cattle live, and "Fusobacterium" is present in the rumen and fecal matter of the cattle. In sheep, "F. necrophorum" first invades the interdigital skin following damage to the skin, and causes interdigital lesions and slight inflammation. The second stage of the disease is marked by the invasion of the foot by the foot rot bacterium "Dichelobacter nodosus", a Gram-negative anaerobe. Usually, an injury to the skin between the hooves allows the bacteria to infect the animal. Another cause of foot rot may be high temperatures or humidity, causing the skin between the hooves to crack and let the bacteria infect the foot. This is one of the reasons foot rot is such a major problem in the summer. Foot rot is easily identifiable by its appearance and foul odor. Treatment is usually with an antibiotic medication, and preventing injury to the feet is the best way to prevent foot rot.

The disease is different in cattle and sheep and cross-infection is not thought to occur.

The first sign of a foot-rot infection is when the skin between the claws of the hoof begins to swell (cellulitis). Swelling usually appears 24 hours after infection. The skin between the toes may be very red and tender and the toes may separate because of all the swelling. This is very painful to the animal and can cause lameness. The animal may also have a raised body temperature. A crack can develop along the infected part and is yellow in color. The foot will have a foul odor. Tendons and joints in the area can become infected, which is much harder to treat. A condition known as "super foot rot" is seen in some animals. Super foot rot infection occurs much faster and is usually much more severe. Most normal foot rot treatments will not cure this foot rot and a veterinarian should be contacted immediately.

Vaccines have been developed, but their efficacy is questionable and the immunity they provide is of short duration.

The most common cause of foot pain is wearing ill fitting shoes. Women often wear tight shoes that are narrow and constrictive, and thus are most prone to foot problems. Tight shoes often cause overcrowding of toes and result in a variety of structural defects. The next most common cause of foot disease is overuse or traumatic injuries.

Prevention of diabetic foot may include optimising metabolic control (regulating glucose levels); identification and screening of people at high risk for diabetic foot ulceration; and patient education in order to promote foot self-examination and foot care knowledge. Patients would be taught routinely to inspect their feet for hyperkeratosis, fungal infection, skin lesions and foot deformities. Control of footwear is also important as repeated trauma from tight shoes can be a triggering factor. There is however only limited evidence that patient education has a long-term impact as a preventative measure.

"Of all methods proposed to prevent diabetic foot ulcers, only foot temperature-guided avoidance therapy was found beneficial in RCTs" according to a meta-analysis.

Training of the feet, utilizing foot gymnastics and going barefoot on varying terrain, can facilitate the formation of arches during childhood, with a developed arch occurring for most by the age of four to six years. Ligament laxity is also among the factors known to be associated with flat feet. One medical study in India with a large sample size of children who had grown up wearing shoes and others going barefoot found that the longitudinal arches of the bare-footers were generally strongest and highest as a group, and that flat feet were less common in children who had grown up wearing sandals or slippers than among those who had worn closed-toe shoes. Focusing on the influence of footwear on the prevalence of pes planus, the cross-sectional study performed on children noted that wearing shoes throughout early childhood can be detrimental to the development of a normal or a high medial longitudinal arch. The vulnerability for flat foot among shoe-wearing children increases if the child has an associated ligament laxity condition. The results of the study suggest that children be encouraged to play barefooted on various surfaces of terrain and that slippers and sandals are less harmful compared to closed-toe shoes. It appeared that closed-toe shoes greatly inhibited the development of the arch of the foot more so than slippers or sandals. This conclusion may be a result of the notion that intrinsic muscle activity of the arch is required to prevent slippers and sandals from falling off the child’s foot.

A diabetic foot is a foot that exhibits any pathology that results directly from diabetes mellitus or any long-term (or "chronic") complication of diabetes mellitus. Presence of several characteristic diabetic foot pathologies such as infection, diabetic foot ulcer and neuropathic osteoarthropathy is called diabetic foot syndrome.

Due to the peripheral nerve dysfunction associated with diabetes (diabetic neuropathy), patients have a reduced ability to feel pain. This means that minor injuries may remain undiscovered for a long while. People with diabetes are also at risk of developing a diabetic foot ulcer. Research estimates that the lifetime incidence of foot ulcers within the diabetic community is around 15% and may become as high as 25%.

In diabetes, peripheral nerve dysfunction can be combined with peripheral artery disease (PAD) causing poor blood circulation to the extremities (diabetic angiopathy). Around half of patients with a diabetic foot ulcer have co-existing PAD.

Where wounds take a long time to heal, infection may set in and lower limb amputation may be necessary. Foot infection is the most common cause of non-traumatic amputation in people with diabetes.

Flat feet can also develop as an adult ("adult acquired flatfoot") due to injury, illness, unusual or prolonged stress to the foot, faulty biomechanics, or as part of the normal aging process. This is most common in women over 40 years of age. Known risk factors include obesity, hypertension and diabetes. Flat feet can also occur in pregnant women as a result of temporary changes, due to increased elastin (elasticity) during pregnancy. However, if developed by adulthood, flat feet generally remain flat permanently.

If a youth or adult appears flatfooted while standing in a full weight bearing position, but an arch appears when the person plantarflexes, or pulls the toes back with the rest of the foot flat on the floor, this condition is called flexible flatfoot. This is not a true collapsed arch, as the medial longitudinal arch is still present and the windlass mechanism still operates; this presentation is actually due to excessive pronation of the foot (rolling inwards), although the term 'flat foot' is still applicable as it is a somewhat generic term. Muscular training of the feet is helpful and will often result in increased arch height regardless of age.

There are few good estimates of prevalence for pes cavus in the general community. While pes cavus has been reported in between 2 and 29% of the adult population, there are several limitations of the prevalence data reported in these studies. Population-based studies suggest the prevalence of the cavus foot is approximately 10%.

Yoga foot drop is a kind of drop foot, a gait abnormality. It is caused by a prolonged sitting on heels, a common yoga position of vajrasana. The name was suggested by Joseph Chusid, MD, in 1971, who reported a case of foot drop in a student who complained about increasing difficulty to walk, run, or climb stairs. The cause was thought to be injury to the common peroneal nerve, which is compressed and thereby deprived of blood flow while kneeling.

Yoga foot drop is a potential adverse effect of yoga, allegedly unmentioned by yoga teachers and books.

Juvenile plantar dermatosis (also known as "Atopic winter feet," "Dermatitis plantaris sicca," "Forefoot dermatitis," "Moon-boot foot syndrome," and "Sweaty sock dermatitis") is a condition usually seen in children between the ages of 3 and 14, and involves the cracking and peeling of weight bearing areas of the soles of the feet. One of the earliest descriptions was made by British dermatologist Darrell Wilkinson.

Scaly foot, or knemidocoptiasis is a bird ailment that is common among caged birds and also affects many other bird species. It is caused by mites in the genus "Knemidocoptes" which burrow into the bird's flesh. The tunnels made by the mites within the skin cause dermatitis and scaly lesions. Scaly face is caused by the same mite responsible for scaly foot and other related mites cause depluming. The condition is transmitted from one bird to another by direct prolonged contact.

Scaly foot, otherwise known as knemidocoptiasis, is caused by burrowing mites in the genus "Knemidocoptes". The condition can be compared with sarcoptic mange in mammals, but does not seem to cause the same level of itching. The birds chiefly affected are galliformes (chickens and turkeys), passerines (finches, canaries, sparrows, robins, wrens), and psittacine birds (parrots, macaws, parakeets, budgerigars). The condition sometimes additionally affects piciformes (woodpeckers, toucans) and anseriformes ducks, geese, swans), raptors and other birds. The two species of mite most often implicated are "K. jamaicensis" and "K. intermedius". Other related species of mite affect feather follicles and cause depluming. The mites are mostly transmitted by prolonged direct contact, particularly from parent bird to unfledged nestling.

Outcomes vary depending on the location of the disease, the degree of damage to the joint, and whether surgical repair was necessary. Average healing times vary from 55–97 days depending on location. Up to 1–2 years may be required for complete healing.

Morton's Toe is a minority variant of foot shape. Its recorded prevalence varies in different populations, with estimates from 2.95% to 22%.

The cause of PPE is unknown. Existing hypotheses are based on the fact that only the hands and feet are involved and posit the role of temperature differences, vascular anatomy, differences in the types of cells (rapidly dividing epidermal cells and eccrine glands).

In the case of PPE caused by PLD, the following mechanism has been demonstrated: sweat deposits and spreads the drug on the skin surface; then the drug penetrates into the stratum corneum like an external agent; palms and soles have high density of sweat glands, and their stratum corneum is approximately 10 times thicker than the rest of the body, and becomes an efficient long-term reservoir for the penetrating PLD, which was deposited on the skin before.

Acral erythema is a common adverse reaction to cytotoxic chemotherapy drugs, particularly cabozantinib, cytarabine, doxorubicin, and fluorouracil and its prodrug capecitabine.

Targeted cancer therapies, especially the tyrosine kinase inhibitors sorafenib and sunitinib, have also been associated with a high incidence of acral erythema. However, acral erythema due to tyrosine kinase inhibitors seems to differ somewhat from acral erythema due to classic chemotherapy drugs.