Urushiol causes an eczematous contact dermatitis characterized by redness, swelling, papules, vesicles, blisters, and streaking. People vary greatly in their sensitivity to urushiol. In approximately 15% to 30% of people, urushiol does not trigger an immune system response, while at least 25% of people have a very strong immune response resulting in severe symptoms. Since the skin reaction is an allergic one, people may develop progressively stronger reactions after repeated exposures, or have no immune response on their first exposure but show sensitivity on subsequent exposures.

Approximately 80% to 90% of adults will get a rash if they are exposed to 50 micrograms of purified urushiol. Some people are so sensitive that it only takes a trace of urushiol (two micrograms, or less than one ten-millionth of an ounce) on the skin to initiate an allergic reaction.

The rash takes one to two weeks to run its course and may cause scars, depending on the severity of the exposure. Severe cases involve small (1–2 mm), clear, fluid-filled blisters on the skin. Pus-filled vesicles containing a whitish fluid may indicate an infection. Most poison ivy rashes, without infections, will resolve within 14 days without treatment. Excessive scratching may result in infection, commonly by staphylococcal and streptococcal species; these may require antibiotics.

Nickel allergy (also referred to as Ni-ACD) is a form of allergic contact dermatitis (ACD) caused by exposure to the chemical element nickel.

Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis and Rhus dermatitis) is the medical name given to allergic rashes produced by the oil urushiol, which is contained in various plants, most notably those of the "Toxicodendron" genus: the Chinese lacquer tree, poison ivy, poison oak, and poison sumac. The name is derived from the Japanese word for the sap of the Chinese lacquer tree, "urushi". Other plants in the sumac family (including mango, pistachio, the Burmese lacquer tree, the India marking nut tree, and the shell of the cashew) also contain urushiol, as do unrelated plants such as "Ginkgo biloba."

As is the case with all contact dermatitis, urushiol-induced rashes are a Type IV hypersensitivity reaction, also known as delayed-type hypersensitivity. Symptoms include itching, inflammation, oozing, and, in severe cases, a burning sensation.

The American Academy of Dermatology estimates that there are up to 50 million cases of urushiol-induced dermatitis annually in the United States alone, accounting for 10% of all lost-time injuries in the United States Forest Service. Poison oak is a significant problem in the rural Western and Southern United States, while poison ivy is most rampant in the Eastern United States. Dermatitis from poison sumac is less common.

The symptoms of allergic contact dermatitis are very similar to the ones caused by irritant contact dermatitis, which makes the first even harder to diagnose. The first sign of allergic contact dermatitis is the presence of the rash or skin lesion at the site of exposure. Depending on the type of allergen causing it, the rash can ooze, drain or crust and it can become raw, scaled or thickened. Also, it is possible that the skin lesion does not take the form of a rash but it may include papules, blisters, vesicles or even a simple red area. The main difference between the rash caused by allergic contact dermatitis and the one caused by irritant contact dermatitis is that the latter tends to be confined to the area where the trigger touched the skin, whereas in allergic contact dermatitis the rash is more likely to be more widespread on the skin. Another characteristic of the allergic contact dermatitis rash is that it usually appears after a day or two after exposure to the allergen, unlike irritant contact dermatitis that appears immediately after the contact with the trigger.

Other symptoms may include itching, skin redness or inflammation, localized swelling and the area may become more tender or warmer. If left untreated, the skin may darken and become leathery and cracked. Pain can also be present.

The symptoms of allergic contact may persist for as long as one month before resolving completely. Once an individual has developed a skin reaction to a certain substance it is most likely that they will have it for the rest of their life, and the symptoms will reappear when in contact with the allergen.

Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance. Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue is present in the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis).

Contact dermatitis results in large, burning, and itchy rashes. These can take anywhere from several days to weeks to heal. This differentiates it from contact urticaria (hives), in which a rash appears within minutes of exposure and then fades away within minutes to hours. Even after days, contact dermatitis fades only if the skin no longer comes in contact with the allergen or irritant. Chronic contact dermatitis can develop when the removal of the offending agent no longer provides expected relief.

Irritant dermatitis is usually confined to the area where the trigger actually touched the skin, whereas allergic dermatitis may be more widespread on the skin. Symptoms of both forms include the following:

- Red rash. This is the usual reaction. The rash appears immediately in irritant contact dermatitis; in allergic contact dermatitis, the rash sometimes does not appear until 24–72 hours after exposure to the allergen.

- Blisters or wheals. Blisters, wheals (welts), and urticaria (hives) often form in a pattern where skin was directly exposed to the allergen or irritant.

- Itchy, burning skin. Irritant contact dermatitis tends to be more painful than itchy, while allergic contact dermatitis often itches.

While either form of contact dermatitis can affect any part of the body, irritant contact dermatitis often affects the hands, which have been exposed by resting in or dipping into a container (sink, pail, tub, swimming pools with high chlorine) containing the irritant.

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.

People with AD often have dry and scaly skin that spans the entire body, except perhaps the diaper area, and intensely itchy red, splotchy, raised lesions to form in the bends of the arms or legs, face, and neck.

AD commonly occurs on the eyelids where signs such as Dennie-Morgan infraorbital fold, infra-auricular fissure, periorbital pigmentation can be seen. Post-inflammatory hyperpigmentation on the neck gives the classic 'dirty neck' appearance. Lichenification, excoriation and erosion or crusting on the trunk may indicate secondary infection. Flexural distribution with ill-defined edges with or without hyperlinearily on the wrist, finger knuckles, ankle, feet and hand are also commonly seen.

Dermatitis symptoms vary with all different forms of the condition. They range from skin rashes to bumpy rashes or including blisters. Although every type of dermatitis has different symptoms, there are certain signs that are common for all of them, including redness of the skin, swelling, itching and skin lesions with sometimes oozing and scarring. Also, the area of the skin on which the symptoms appear tends to be different with every type of dermatitis, whether on the neck, wrist, forearm, thigh or ankle. Although the location may vary, the primary symptom of this condition is itchy skin. More rarely, it may appear on the genital area, such as the vulva or scrotum. Symptoms of this type of dermatitis may be very intense and may come and go. Irritant contact dermatitis is usually more painful than itchy.

Although the symptoms of atopic dermatitis vary from person to person, the most common symptoms are dry, itchy, red skin. Typical affected skin areas include the folds of the arms, the back of the knees, wrists, face and hands. Perioral dermatitis refers to a red bumpy rash around the mouth.

Dermatitis herpetiformis symptoms include itching, stinging and a burning sensation. Papules and vesicles are commonly present. The small red bumps experienced in this type of dermatitis are usually about 1 cm in size, red in color and may be found symmetrically grouped or distributed on the upper or lower back, buttocks, elbows, knees, neck, shoulders, and scalp. Less frequently, the rash may appear inside the mouth or near the hairline.

The symptoms of seborrheic dermatitis, on the other hand, tend to appear gradually, from dry or greasy scaling of the scalp (dandruff) to scaling of facial areas, sometimes with itching, but without hair loss. In newborns, the condition causes a thick and yellowish scalp rash, often accompanied by a diaper rash. In severe cases, symptoms may appear along the hairline, behind the ears, on the eyebrows, on the bridge of the nose, around the nose, on the chest, and on the upper back.

Type IV allergy, also known as allergic contact dermatitis, involves a delayed skin rash that is similar to poison ivy with blistering and oozing of the skin ("see urushiol-induced contact dermatitis"). It can be diagnosed through a positive skin patch test, although a negative test does not rule out a latex allergy.

Severe irritation takes place if a latex catheter is inserted in the urinary tract of a person allergic to latex. That is especially severe in case of a radical prostatectomy due to the open wound there and the exposure lasting e.g. two weeks. Intense pain may indicate such situation.

Allergic contact dermatitis (ACD) is a form of contact dermatitis that is the manifestation of an allergic response caused by contact with a substance; the other type being irritant contact dermatitis (ICD).

Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in humans. By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which these reactions occur are complex, with many levels of fine control. Their immunology centres on the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.

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).

Contact dermatitis is a type of inflammation of the skin.

It results from either exposure to allergens (allergic contact dermatitis) or irritants (irritant contact dermatitis). Phototoxic dermatitis occurs when the allergen or irritant is activated by sunlight. Diagnosis of allergic contact dermatitis can often be supported by patch testing.

Natural rubber latex can also cause irritant contact dermatitis, a less severe form of reaction that does not involve the immune system. Contact dermatitis causes dry, itchy, irritated areas on the skin, most often on the hands. Latex-glove induced dermatitis increases the chance of hospital-acquired infections, including blood-borne infections, being transmitted.

The cause of AD is not known, although there is some evidence of genetic, environmental, and immunologic factors.

Discoid eczema (nummular eczema, exudative eczema, microbial eczema) is characterized by round spots of oozing or dry rash, with clear boundaries, often on lower legs. It is usually worse in winter. Cause is unknown, and the condition tends to come and go. (ICD-10 L30.0)

Flea allergy dermatitis, FAD, is an eczematous itchy skin disease of dogs and cats. For both of these domestic species, flea allergy dermatitis is the most common cause of skin disease. Affected animals develop allergic reactions to chemicals in flea saliva. Symptoms of this reaction include erythema (redness), papules (bumps), pustules (pus-filled bumps), and crusts (scabs). If severe, hair loss will occur in the affected area. Dogs with flea allergy dermatitis often show hair loss and eczematous skin rash on the lower back, upper tail, neck, and down the back of the legs. Cats with flea allergy dermatitis may develop a variety of skin problems, including feline eosinophilic granuloma, miliary dermatitis, or self-inflicted alopecia from excessive grooming.

Josef Jadassohn described the first case of metal contact dermatitis in 1895, to a mercurial-based therapeutic cream, and confirmed the cause by epi-cutaneous patch testing. Systemic contact dermatitis (SCD) is defined as a dermatitis occurring in an epi-cutaneously contact-sensitized person when exposed to haptens systemically such as orally, per rectum, intravesically, transcutaneously, intrauterinely, intravenously, or by inhalation.

Systemic nickel allergy syndrome (SNAS) pathophysiology is extremely complex and not well understood. The clinical course is determined by an immunological interplay between two diverse types of T cells (Th1 and Th2 responses). SCD is often considered a subset of SNAS, but with only skin manifestations. SNAS presents with an array of symptoms ranging from respiratory to generalized skin rash to gastrointestinal symptoms Interestingly, a meta review evaluating SNAS found that 1% of patients sensitized to nickel reacted to the nickel content of a 'normal' diet, and with increasing doses of nickel more individuals reacted SNAS is a multilayered immunologic response demonstrating variance between individuals and doses of nickel exposure.

Dermatitis herpetiformis is characterized by intensely itchy, chronic papulovesicular eruptions, usually distributed symmetrically on extensor surfaces (buttocks, back of neck, scalp, elbows, knees, back, hairline, groin, or face). The blisters vary in size from very small up to 1 cm across.

The condition is extremely itchy, and the desire to scratch can be overwhelming. This sometimes causes the sufferer to scratch the blisters off before they are examined by a physician. Intense itching or burning sensations are sometimes felt before the blisters appear in a particular area.

Untreated, the severity of DH can vary significantly over time, in response to the amount of gluten ingested.

Dermatitis herpetiformis symptoms typically first appear in the early years of adulthood between 20 and 30 years of age.

Although the first signs and symptoms of dermatitis herpetiformis are intense itching and burning, the first visible signs are the small papules or vesicles that usually look like red bumps or blisters. The rash rarely occurs on other mucous membranes, excepting the mouth or lips. The symptoms range in severity from mild to serious, but they are likely to disappear if gluten ingestion is avoided and appropriate treatment is administered.

Dermatitis herpetiformis symptoms are chronic, and they tend to come and go, mostly in short periods of time. Sometimes, these symptoms may be accompanied by symptoms of coeliac disease, commonly including abdominal pain, bloating or loose stool, and fatigue.

The rash caused by dermatitis herpetiformis forms and disappears in three stages. In the first stage, the patient may notice a slight discoloration of the skin at the site where the lesions appear. In the next stage, the skin lesions transform into obvious vesicles and papules that are likely to occur in groups. Healing of the lesions is the last stage of the development of the symptoms, usually characterized by a change in the skin color. This can result in areas of the skin turning darker or lighter than the color of the skin on the rest of the body. Because of the intense itching, patients usually scratch, which can lead to the formation of crusts.

Chemical irritant contact dermatitis is either acute or chronic, which is usually associated with strong and weak irritants respectively. The following definition is provided by Mathias and Maibach (1978): The mechanism of action varies. Detergents, surfactants, extremes of pH, and organic solvents all directly affecting the barrier properties of the epidermis. These effects include removing fat emulsion, defatting of dermal lipids, inflicting cellular damage on the epithelium, and increasing the transepidermal water loss by damaging the horny layer water-binding mechanisms and damaging the DNA, which causes the layer to thin. Concentrated irritants have an acute effect, but this is not as common as the accumulative, chronic effect of irritants whose deleterious effects build up with subsequent doses (ESCD 2006).

Chemical irritants are often strong alkalis as found in drain cleaners and soap with lye residues. Many other chemical compounds can also cause contact dermatitiis.

Shiitake mushroom dermatitis (also known as "flagellate mushroom dermatitis", "mushroom worker's disease", and "shiitake-induced toxicoderma") is an intensely pruritic dermatitis characterized by disseminated 1mm erythematous micropapules seen in a linear grouped arrangement secondary to Koebnerization due to patient scratching. It is caused by the ingestion of shiitake mushrooms and was first described in 1977 by Nakamura. Although it is rarely seen outside of China and Japan due to a lower incidence of shiitake consumption outside these regions, there is a well-established association between flagellate dermatitis and shiitake mushroom (Lentinula edodes) ingestion. Bleomycin ingestion may also cause similar findings. On physical exam, one key difference between the two is that post-inflammatory hyperpigmentation changes are usually seen with bleomycin-induced flagellate dermatitis and are not typically present with shiitake mushroom induced flagellate dermatitis. The median time of onset from ingestion of shiitake mushrooms is typically 24 hours, ranging from 12 hours to 5 days. Most patients completely recover by 3 weeks, with or without treatment. Although the pathogenesis of shiitake induced flagellate dermatitis is not clear, the theory most argued for is a toxic reaction to lentinan, a polysaccharide isolated from shiitake mushrooms. However, Type I and Type IV allergic hypersensitivities have also been supported by the 24-hour median time of onset, clearance in 3–21 days, severe pruritus, benefit of steroids and antihistamines, and lack of grouped outbreaks in people exposed to shared meals containing shiitake mushrooms. Most cases reported shortly after its discovery were due to consumption of raw shiitake mushrooms, but several cases have since been reported after consumption of fully cooked mushrooms.

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.

Eyelid dermatitis is commonly related to atopic dermatitis or allergic contact dermatitis. Volatile substances, tosylamide, epoxy hardeners, insect sprays, and lemon peel oil may be implicated, with many cases of eyelid contact dermatitis being caused by substances transferred by the hands to the eyelids.

A stinging and burning sensation with rash is often felt and noticed, but itching is less common. Often the rash is steroid responsive, initially improving with application of topical steroid. The redness caused by perioral dermatitis has been associated with variable level of depression.

Initially, there may be small pinpoint papule either side of the nostrils. Multiple small (1-2mm) papules and pustules then occur around the mouth, nose and sometimes cheeks. The area of skin directly adjacent to the lips, also called the vermillion border, is spared and looks normal. There may be some mild background redness and occasional scale. These areas of skin are felt to be drier and therefore there is a tendency to moisturise them more frequently. Hence, they do not tolerate drying agents well and the rash can be worsened by them.

Perioral dermatitis is also known by other names including rosacea-like dermatoses, periorofacial dermatitis and periorificial dermatitis.

Unlike rosacea which involves mainly the nose and cheeks, there is no telangiectasia in perioral dermatitis. Rosacea also has a tendency to be present in older people. Acne can be distinguished by the presence of comedones and by its wider distribution on the face and chest. There are no comedones in personal dermatitis.

Other skin diseases which may resemble perioral dermatitis include:

- Rosacea

- Acne vulgaris

- Seborrheic dermatitis

- Allergic contact dermatitis

- Irritant contact dermatitis

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.

Skin disease may result from deficiency or overactivity of immune responses. In cases where there is insufficient immune responses the disease is usually described by the secondary disease that results. Examples include increased susceptibility to demodectic mange and recurrent skin infections, such as Malassezia infection or bacterial infections. Increased, but harmful immune responses, can be divided into hypersensitivity disorders such as atopic dermatitis, and autoimmune disorders (autoimmunity), such as pemphigus and discoid lupus erythematosus.