Humans usually become infected after swimming in lakes or other bodies of slow-moving fresh water. Some laboratory evidence indicates snails shed cercariae most intensely in the morning and on sunny days, and exposure to water in these conditions may therefore increase risk. Duration of swimming is positively correlated with increased risk of infection in Europe and North America, and shallow inshore waters may harbour higher densities of cercariae than open waters offshore. Onshore winds are thought to cause cercariae to accumulate along shorelines. Studies of infested lakes and outbreaks in Europe and North America have found cases where infection risk appears to be evenly distributed around the margins of water bodies as well as instances where risk increases in endemic swimmer's itch "hotspots". Children may become infected more frequently and more intensely than adults but this probably reflects their tendency to swim for longer periods inshore, where cercariae also concentrate. Stimuli for cercarial penetration into host skin include unsaturated fatty acids, such as linoleic and linolenic acids. These substances occur naturally in human skin and are found in sun lotions and creams based on plant oils.

Various strategies targeting the mollusc and avian hosts of schistosomes, have been used by lakeside residents in recreational areas of North America to deal with outbreaks of swimmer's itch. In Michigan, for decades, authorities used copper sulfate as a molluscicide to reduce snail host populations and thereby the incidence of swimmer's itch. The results with this agent have been inconclusive, possibly because:

- Snails become tolerant

- Local water chemistry reduces the molluscicide's efficacy

- Local currents diffuse it

- Adjacent snail populations repopulate a treated area

More importantly, perhaps, copper sulfate is toxic to more than just molluscs, and the effects of its use on aquatic ecosystems are not well understood.

Another method targeting the snail host, mechanical disturbance of snail habitat, has been also tried in some areas of North America and Lake Annecy in France, with promising results. Some work in Michigan suggests that administering praziquantel to hatchling waterfowl can reduce local swimmer's itch rates in humans. Work on schistosomiasis showed that water-resistant topical applications of the common insect repellent DEET prevented schistosomes from penetrating the skin of mice. Public education of risk factors, a good alternative to the aforementioned interventionist strategies, can also reduce human exposure to cercariae.

The diagnosis of flea allergy dermatitis is complicated by the grooming habits of pets. Cats in particular are very efficient at grooming out fleas, often removing any evidence of infestation. Fleas begin biting within 5 minutes of finding a host, and there are no flea treatments that kill fleas before biting occurs.

Paederus dermatitis (also called linear dermatitis or dermatitis linearis) is skin irritation resulting from contact with the hemolymph of certain rove beetles, a group that includes the genus Paederus. Other local names given to Paederus dermatitis include spider-lick, whiplash dermatitis, and Nairobi fly dermatitis.

The active agent is commonly referred to as pederin, although depending on the beetle species it may be one of several similar molecules including pederone and pseudopederin.

"Blister beetle dermatitis," a term more properly used for the different dermatitis caused by cantharidin from blister beetles, is also sometimes used to describe paederus dermatitis caused by rove beetles.

Most of the mites which cause this affliction to humans are from the order Acari, hence the name Acariasis. The entire taxonomic classification to order would be:

- Kingdom: Animalia

- Phylum: Arthropoda

- Subphylum: Chelicerata

- Class: Arachnida

- Order: Acari (At the order level, there is still substantial argument among researchers as to how to categorize Acari. Some call it a subclass, others a superorder, "Acarina".)

Specific species involved include:

- Acariformes

- Trombidiformes

- "Trombicula" species (trombiculosis or chiggers)

- "Demodex" species (Demodicosis)

- "Pyemotes tritici"

- "Cheyletiella"

- Sarcoptiformes

- "Sarcoptes scabiei" (Scabies)

- Parasitiformes

- "Dermanyssus gallinae"

- "Liponyssoides sanguineus"

- "Ornithonyssus bacoti", "Ornithonyssus bursa", "Ornithonyssus sylviarum"

- Another candidate is "Androlaelaps casalis". However, based on this mite's life style as a predator on other mite species (such as the previously-mentioned "Dermanyssus gallinae"), it is highly unlikely to be a cause of acariasis.

Some of these reflect reports existing of human infestation by mites previously believed not to prey on humans.

The flea found most commonly on both dogs and cats with a flea infestation is the cat flea, "Ctenocephalides felis". Pets that develop FAD have an allergic response to flea saliva injected during flea feeding. The itch associated with just one flea bite persists long after that flea is gone and leads to significant self-trauma.

Once pederin is on the skin from the initial beetle contact, it may also be spread elsewhere on the skin. "Kissing" or "mirror-image" lesions where two skin areas come in contact (for example, the elbow flexure) are often seen. Washing the hands and skin with soap and water is strongly recommended, if contact with a rove beetle has occurred.

Initial skin contact with pederin shows no immediate result. Within 12–36 hours, however, a reddish rash (erythema) appears, which develops into blisters. Irritation, including crusting and scaling, may last from two to three weeks.

One study reported best results with a treatment regimen that combined topical steroids with oral antihistamines and antibiotics. The authors hypothesized that antibiotics were helpful because of the possible contamination of skin by pederin-producing bacteria.

There are several complications with the terminology:

Acariasis is a term for a rash, caused by mites, sometimes with a papillae (pruritic dermatitis), and usually accompanied by severe itching sensations. An example of such an infection is scabies.

The closely related term, mange, is commonly used with domestic animals (pets) and also livestock and wild mammals, whenever hair-loss is involved. "Sarcoptes" and "Demodex" species are involved in mange, but both of these genera are also involved in human skin diseases (by convention only, not called mange). "Sarcoptes" in humans is especially severe symptomatically, and causes the condition scabies noted above.

Another genus of mite which causing itching but rarely causes hair loss because it burrows only at the keratin level, is "Cheyletiella." Various species of this genus of mite also affect a wide variety of mammals, including humans.

Mite infestation sometimes implies an ectoparasitic, cutaneous condition such as dermatitis. However, it is possible for mites to invade the gastrointestinal and urinary tracts.

MeSH uses the term "Mite Infestations" as pertaining to Acariformes. However, mites not in this grouping can be associated with human disease. (See "Classification", below.)

The term Acari refers to ticks and mites together, which can cause ambiguity. (Mites are a paraphyletic grouping).

Mites can be associated with disease in at least three different ways: (1) cutaneous dermatitis, (2) production of allergin, and (3) as a vector for parasitic diseases. The language used to describe mite infestation often does not distinguish among these.

Although wetness alone has the effect of macerating the skin, softening the stratum corneum, and greatly increasing susceptibility to friction injury, urine has an additional impact on skin integrity because of its effect on skin pH. While studies show that ammonia alone is only a mild skin irritant, when urea breaks down in the presence of fecal urease it increases pH because ammonia is released, which in turn promotes the activity of fecal enzymes such as protease and lipase. These fecal enzymes increase the skin's hydration and permeability to bile salts which also act as skin irritants.

There is no detectable difference in rates of diaper rash in conventional disposable diaper wearers and reusable cloth diaper wearers. "Babies wearing superabsorbent disposable diapers with a central gelling material have fewer episodes of diaper dermatitis compared with their counterparts wearing cloth diapers. However, keep in mind that superabsorbent diapers contain dyes that were suspected to cause allergic contact dermatitis (ACD)." Whether wearing cloth or disposable diapers they should be changed frequently to prevent diaper rash, even if they don't feel wet. To reduce the incidence of diaper rash, disposable diapers have been engineered to pull moisture away from the baby's skin using synthetic non-biodegradable gel. Today, cloth diapers use newly available superabsorbent microfiber cloth placed in a pocket with a layer of light permeable material that contacts the skin. This design serves to pull moisture away from the skin in to the microfiber cloth. This technology is used in most major pocket cloth diapers brands today.

The interaction between fecal enzyme activity and IDD explains the observation that infant diet and diaper rash are linked because fecal enzymes are in turn affected by diet. Breast-fed babies, for example, have a lower incidence of diaper rash, possibly because their stools have higher pH and lower enzymatic activity. Diaper rash is also most likely to be diagnosed in infants 8–12 months old, perhaps in response to an increase in eating solid foods and dietary changes around that age that affect fecal composition. Any time an infant’s diet undergoes a significant change (i.e. from breast milk to formula or from milk to solids) there appears to be an increased likelihood of diaper rash.

The link between feces and IDD is also apparent in the observation that infants are more susceptible to developing diaper rash after treating with antibiotics, which affect the intestinal microflora. Also, there is an increased incidence of diaper rash in infants who have suffered from diarrhea in the previous 48 hours, which may be because fecal enzymes such as lipase and protease are more active in feces which have passed rapidly through the gastrointestinal tract.

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.

Atopy is a hereditary and chronic (lifelong) allergic skin disease. Signs usually begin between 6 months and 3 years of age, with some breeds of dog, such as the Golden Retriever showing signs at an earlier age. Dogs with atopic dermatitis are itchy, especially around the eyes, muzzle, ears and feet. In severe cases the irritation is generalised. If the allergens are seasonal, the signs of irritation are similarly seasonal. Many dogs with house dust mite allergy have perennial disease. Some of the allergens associated with atopy in dogs include pollens of trees, grasses and weeds, as well as molds and House dust mite. Ear and skin infections with the bacteria "Staphylococcus pseudintermedius" and the yeast "Malassezia pachydermatis" are common secondary to atopic dermatitis.

Food allergy can be associated with identical signs and some authorities consider food allergy to be a type of atopic dermatitis.

Diagnosis of atopic dermatitis is by elimination of other causes of irritation including fleas, scabies and other parasites such as Cheyletiella and lice. Food allergy can be identified through the use of elimination diet trials in which a novel or hydrolysed protein diet is used for a minimum of 6 weeks and allergies to aeroallergens can be identified using intradermal allergy testing and/or blood testing (allergen-specific IgE ELISA).

Treatment includes avoidance of the offending allergens if possible, but for most dogs this is not practical or effective. Other treatments modulate the adverse immune response to allergens and include antihistamines, steroids, ciclosporin and immunotherapy (a process in which allergens are injected to try to induce tolerance). In many cases shampoos, medicated wipes and ear cleaners are needed to try to prevent the return of infections.

New research into T-cell receptor peptides and their effects on dogs with severe, advanced atopic dermatitis are being investigated.

Garlic allergy or allergic contact dermatitis to garlic is a common inflammatory skin condition caused by contact with garlic oil or dust. It mostly affects people who cut and handle fresh garlic, such as chefs, and presents on the tips of the thumb, index and middle fingers of the non-dominant hand (which typically hold garlic bulbs during the cutting). The affected fingertips show an asymmetrical pattern of fissure as well as thickening and shedding of the outer skin layers, which may progress to second- or third-degree burn of injured skin.

Garlic dermatitis is similar to the tulip dermatitis and is induced by a combined mechanical and chemical action. Whereas the former mechanism acts via skin rubbing which progresses into damage, the major cause of the latter is the chemical diallyl disulfide (DADS), together with related compounds allyl propyl disulfide and allicin. These chemicals occur in oils of plants of the genus "Allium", including garlic, onion and leek.

Garlic allergy has been known since at least 1950. It is not limited to hand contact, but can also be induced, with different symptoms, by inhaling garlic dust or ingesting raw garlic, though the latter cases are relatively rare. DADS penetrates through most types of commercial gloves, and thus wearing gloves while handling garlic has proven inefficient against the allergy. Treatment includes avoiding any contact with garlic oil or vapours, as well as medication, such as administering acitretin (25 mg/day, orally) or applying psoralen and ultraviolet light to the affected skin area over a period of 12 weeks (PUVA therapy).

Urushiol-induced contact dermatitis is caused by contact with a plant or any other object containing urushiol oil. The oil adheres to almost anything with which it comes in contact, such as towels, blankets, clothing, and landscaping tools. Clothing or other materials that touch the plant and then, before being washed, touch the skin are common causes of exposure.

For people who have never been exposed or are not yet allergic to urushiol, it may take 10 to 21 days for a reaction to occur the first time. Once allergic to urushiol, however, most people break out 48 to 72 hours after contact with the oil. Typically, individuals have been exposed at least once, if not several times, before they develop a rash. The rash typically persists one to two weeks, but in some cases may last up to five weeks.

Urushiol is primarily found in the spaces between cells beneath the outer skin of the plant, so the effects are less severe if the plant tissue remains undamaged on contact. Once the oil and resin are thoroughly washed from the skin, the rash is not contagious. Urushiol does not always spread once it has bonded with the skin, and cannot be transferred once the urushiol has been washed away.

Although simple skin exposure is most common, ingestion of urushiol can lead to serious, systemic reactions. Burning plant material is commonly said to create urushiol-laden smoke that causes a systemic reaction, as well as a rash in the throat and eyes. Firefighters often get rashes and eye inflammation from smoke-related contact. A high-temperature bonfire may incinerate urushiol before it can cause harm, while a smoldering fire may vaporize the volatile oil and spread it as white smoke. However, some sources dispute the danger of burning urushiol-containing plant material.

A hot spot, or "acute moist dermatitis", is an acutely inflamed and infected area of skin irritation created and made worse by a dog licking and biting at itself. A hot spot can manifest and spread rapidly in a matter of hours as secondary Staphylococcus infection causes the top layers of the skin to break down and as pus becomes trapped in the hair. Hot spots can be treated with corticosteroid medications and oral as well as topical antibiotic application, as well as clipping hair from around the lesion. Underlying inciting causes include flea allergy dermatitis, ear disease or other allergic skin diseases. Dogs with thick undercoat are most subject to getting hot spots.

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.

A rarely cited double-blind study in 1982 reported that a course of oral urushiol usually hyposensitized subjects.

There is no good evidence that a mother's diet during pregnancy, the formula used, or breastfeeding changes the risk. There is tentative evidence that probiotics in infancy may reduce rates but it is insufficient to recommend its use.

People with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.

Irritant contact dermatitis (ICD) can be divided into forms caused by chemical irritants, and those caused by physical irritants. Common chemical irritants implicated include: solvents (alcohol, xylene, turpentine, esters, acetone, ketones, and others); metalworking fluids (neat oils, water-based metalworking fluids with surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); and alkalis (drain cleaners, strong soap with lye residues).

Physical irritant contact dermatitis may most commonly be caused by low humidity from air conditioning. Also, many plants directly irritate the skin.

According to the hygiene hypothesis, when children are brought up exposed to allergens in the environment at a young age, their immune system is more likely to tolerate them, while children brought up in a modern "sanitary" environment are less likely to be exposed to those allergens at a young age, and, when they are finally exposed, develop allergies. There is some support for this hypothesis with respect to AD. Those exposed to dogs while growing up have a lower risk of atopic dermatitis. There is also support from epidemiological studies for a protective role for helminths against AD. Likewise children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurised milk.

Defatting can be prevented by wearing appropriate protective clothing such as gloves, lab coats and aprons when working regularly with defatting agents. Prolonged skin contact or chronic defatting of the skin increases the possibility for developing irritant contact dermatitis and has the potential to worsen pre-existing skin conditions. Patients with chronic dermatitis are advised to use non-irritating soaps and dishwashing liquids sparingly and to choose those with a neutral pH and minimal defatting capability.

Most cases are well managed with topical treatments and ultraviolet light. About 2% of cases are not. In more than 60% of young children, the condition subsides by adolescence.

Irritant contact dermatitis is a form of contact dermatitis that can be divided into forms caused by chemical irritants and those caused by physical irritants.

The skin should be cleaned and kept dry, and topical antibiotics can be applied to the area. Systemic antibiotics are not needed.

Control relies on prompt detection, isolation and treatment of affected cattle. Footpaths should be kept as dry as possible and slurry build-up should be avoided. Regular footbaths should be organised, using formalin, copper sulphate or a thymol-based disinfectant. In 2013, a safer and alternative to chemicals for hoof baths called Thymox Technology was proven, through field testing, to kill the main bacteria causing digital dermatitis.

In a small percentage of cases, atopic dermatitis is caused by sensitization to foods. Also, exposure to allergens, either from food or the environment, can exacerbate existing atopic dermatitis. Exposure to dust mites, for example, is believed to contribute to one's risk of developing AD. A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for fast foods. Atopic dermatitis sometimes appears to be associated with celiac disease and non-celiac gluten sensitivity, and the improvement with a gluten-free diet indicates that gluten is a causative agent in these cases.