Tinea corporis is caused by a tiny fungus known as dermatophyte. These tiny organisms normally live on the superficial skin surface, and when the opportunity is right, they can induce a rash or infection.

The disease can also be acquired by person-to-person transfer usually via direct skin contact with an infected individual. Animal-to-human transmission is also common. Ringworm commonly occurs on pets (dogs, cats) and the fungus can be acquired while petting or grooming an animal. Ringworm can also be acquired from other animals such as horses, pigs, ferrets and cows. The fungus can also be spread by touching inanimate objects like personal care products, bed linen, combs, athletic gear, or hair brushes contaminated by an affected person.

Individuals at high risk of acquiring ringworm include those who:

- Live in crowded, humid conditions.

- Sweat excessively, as sweat can produce a humid wet environment where the pathogenic fungi can thrive. This is most common in the armpits, groin creases and skin folds of the abdomen.

- Participate in close contact sports like soccer, rugby, or wrestling.

- Wear tight, constrictive clothing with poor aeration.

- Have a weakened immune system (e.g., those infected with HIV or taking immunosuppressive drugs).

Because fungi prefer warm, moist environments, preventing ringworm involves keeping skin dry and avoiding contact with infectious material. Basic prevention measures include:

- Washing hands after handling animals, soil, and plants.

- Avoiding touching characteristic lesions on other people.

- Wearing loose-fitting clothing.

- Practicing good hygiene when participating in sports that involve physical contact with other people.

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.

Advice often given includes:

- Avoid sharing clothing, sports equipment, towels, or sheets.

- Wash clothes in hot water with fungicidal soap after suspected exposure to ringworm.

- Avoid walking barefoot; instead wear appropriate protective shoes in locker rooms and sandals at the beach.

- Avoid touching pets with bald spots, as they are often carriers of the fungus.

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.

no approved human vaccine exist against "Dermatophytosis". For horses, dogs and cats there is available an approved inactivated vaccine called "Insol Dermatophyton" (Boehringer Ingelheim) which provides time-limited protection against several trichophyton and microsporum fungal strains.

Tinea capitis caused by species of "Microsporum" and "Trichophyton" is a contagious disease that is endemic in many countries. Affecting primarily pre-pubertal children between 6 and 10 years, it is more common in males than females; rarely does the disease persist past age sixteen. Because spread is thought to occur through direct contact with afflicted individuals, large outbreaks have been known to occur in schools and other places where children are in close quarters; however, indirect spread through contamination with infected objects ("fomites") may also be a factor in the spread of infection. In the USA, tinea capitis is thought to occur in 3-8% of the pediatric population; up to one-third of households with contact with an infected person may harbor the disease without showing any symptoms.

The fungal species responsible for causing tinea capitis vary according to the geographical region, and may also change over time. For example, "Microsporum audouinii" was the predominant etiological agent in North America and Europe until the 1950s, but now "Trichophyton tonsurans" is more common in the USA, and becoming more common in Europe and the United Kingdom. This shift is thought to be due to the widespread use of griseofulvin, which is more effective against "M. audounii" than "T. tonsurans"; also, changes in immigration patterns and increases in international travel have likely spread "T. tonsurans" to new areas. Another fungal species that has increased in prevalence is "Trichophyton violaceum", especially in urban populations of the United Kingdom and Europe.

It may appear as thickened, scaly, and sometimes boggy swellings, or as expanding raised red rings (ringworm). Common symptoms are severe itching of the scalp, dandruff, and bald patches where the fungus has rooted itself in the skin. It often presents identically to dandruff or seborrheic dermatitis. The highest incidence in the United States of America is in American boys of school age.

There are three type of tinea capitis, microsporosis, trichophytosis, and favus; these are based on the causative microorganism, and the nature of the symptoms. In "microsporosis", the lesion is a small red papule around a hair shaft that later becomes scaly; eventually the hairs break off 1–3 mm above the scalp. This disease used to be caused primarily by "Microsporum audouinii", but in Europe, "M. canis" is more frequently the causative fungus. The source of this fungus is typically sick cats and kittens; it may be spread through person to person contact, or by sharing contaminated brushes and combs. In the United States, "Trichophytosis" is usually caused by "Trichophyton tonsurans", while "T. violaceum" is more common in Eastern Europe, Africa, and India. This fungus causes dry, non-inflammatory patches that tend to be angular in shape. When the hairs break off at the opening of the follicle, black dots remain. "Favus" is caused by "T. schoenleinii", and is endemic in South Africa and the Middle East. It is characterized by a number of yellowish, circular, cup-shaped crusts (scutula) grouped in patches like a piece of honeycomb, each about the size of a split pea, with a hair projecting in the center. These increase in size and become crusted over, so that the characteristic lesion can only be seen around the edge of the scab.

A dermatomycosis is a skin disease caused by a fungus. This excludes dermatophytosis.

Examples of dermatomycoses are tinea and cutaneous candidiasis.

With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.

The exact causes of dyshidrosis are unknown. In 2013, a randomized, double-blind, placebo-controlled cross-over study by the University Medical Center Groningen reported that dyshydrosis outbreaks on the hands increased significantly among those allergic to house dust mites, following inhalation of house dust mite allergen.

Food allergens may be involved in certain cases. Cases studies have implicated a wide range of foods including tuna, tomato, pineapple, chocolate, coffee, and spices among others. A number of studies have implicated balsam of Peru.

Id reaction and irritant contact dermatitis are possible causes.

Hangnails can become infected and cause paronychia, a type of skin infection that occurs around the nails. Treatments for paronychia vary with severity, but may include soaking in hot salty water, the use of oral antibiotic medication, or clinical lancing. Paronychia itself rarely results in further complications but can lead to abscess, permanent changes to the shape of the nail or the spread of infection.

About 1 in 2,000 people are affected in Sweden. Males and females appear to be affected equally.

A hangnail is a small, torn piece of skin, more specifically eponychium or paronychium, next to a fingernail or toenail.

Other rashes that occur in a widespread distribution can look like an id reaction. These include atopic dermatitis, contact dermatitis, dyshidrosis, photodermatitis, scabies and drug eruptions.

Hand eczema is a common condition: study data indicates a one-year prevalence of up to 10% in the general population. It is estimated that only 50–70% of people affected consult a doctor. The frequency of severe, chronic and recurrent forms of hand eczema is estimated at 5–7%. Approximately 2–4% of hand eczema patients also report that external (topical) therapy is insufficient.

Several factors adversely affect the long-term prognosis, including the development of the condition prior to the 20th birthday, the severity of initial manifestations, and eczema during childhood. Women, especially those under 30, are more frequently affected than men.

There are a number of different causes of skin inflammation of the hands, the interplay of which is also significant: environmental factors such as excessive water; contact with allergens or irritants; and genetic disposition. A single catalyst is seldom responsible for the development of hand eczema in patients.

The most important infectious skin diseases of cats is ringworm or dermatophytosis. Other cat skin infections include parasitic diseases like mange and lice infestation.

Other ectoparasites, including flea and tick infestations are not considered directly contagious but are acquired from an environment where other infested hosts have established the parasite's life cycle.

Another common skin infection is cat bite abscess. A mixture of bacteria introduced by a bite wound cause infections in pockets under the skin and affected cats often show manic depression and fever.

The cat must have a supply of niacin, as cats cannot convert tryptophan into niacin like dogs. However, diets high in corn and low in protein can result in skin lesions and scaly, dry, greasy skin, with hair loss. Another B vitamin, biotin, if deficient causes hair loss around the eyes and face. A lack of B vitamins can be corrected by supplementing with a vitamin B complex, and brewers yeast.

Gram-negative toe web infection is a cutaneous condition that often begins with dermatophytosis.

Gram-negative toe web infection is a relatively common infection. It is commonly found on people who are engaged in athletic activities while wearing closed-toe or tight fitting shoes. It grows in a moist environment. Gram-negative is mixed bacterial infection with the following organisms:

- Moraxella

- Alcaligenes

- Acinetobacter

- Pseudomonas

- Proteus

- Erwinia

This mixing of infection and organisms may also cause a mild secondary infection of tinea pedis.

While the condition has been seen in over 60 breeds of dog (including cross breeds), certain breeds have been found to be more susceptible than others to sebaceous adenitis:

- American Akita and Akita Inu

- Standard Poodle

- Vizsla

- English Springer Spaniel

- Chow Chow

- Samoyed

- Weimaraner

- Havanese

Breeds also mentioned in scientific literature as having some susceptibility include:

- German Shepherd

- Dachshund

- Old English Sheepdog

- Lhasa Apso

- Boxer

- Collie

- Toy Poodle

- Mixed-breeds

Sebaceous adenitis has no sex-predisposition. Sebaceous adenitis also occurs in cats, rabbits and horses.

The signs of sebaceous adenitis are caused by an inflammatory disease process which affects the sebaceous glands of the skin. The cause of the inflammatory disease is unknown. Different breeds of dogs may have different underlying causes of the disease.

Research is currently underway to find if there is a genetic predisposition for sebaceous adenitis; the exact mode of inheritance remains unknown.

In Standard Poodles, sebaceous adenitis is most likely an autosomal recessive inherited disease, with variable expression.

PPE invariably recurs with the resumption of chemotherapy. Long-term chemotherapy may also result in reversible palmoplantar keratoderma. Symptoms resolve 1–2 weeks after cessation of chemotherapy (Apisarnthanarax and Duvic 2003).

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.