Few treatments are fully efficacious once lesions have appeared. The only effective form of treatment is preventitive - i.e. prevent further insect bites - so these techniques will also be discussed here. Treatments generally fall into one of the following categories:

1) Insecticides and Repellents: These may be applied to the horse or its environment. The most commonly used and effective are permethrins. and benzyl benzoate Citronella has been used, with variable effect. Some sources advocate draining of any stagnant water or pools, to reduce the local breeding potential of the insects. Midge numbers are often larger near water sources, for example ponds, bogs, and slow moving water. Moving the horse away from these areas may help to prevent further problems.

2) Barrier Techniques: Rugs etc., that prevent flies and midges settling on the animal's skin to bite. These include "Boett Rugs" and fly masks. In addition, thin screens may be placed over stable doors and windows to exclude biting insects. Stabling the horse at times of day when the midges are most prevalent is also quite effective.

3) Immunotherapy: A wide variety immunotherapy and desensitisation protocols have been trialled in attempts to reduce or modify the immune response, with considerable success rates. So far, there appear to a significant benefit in more than 80% of equine cases. This particular BioEos product is now available through The National Sweet Itch Centre in the UK and ProVet in the EU. The underlying immune modulation is now proven to shift the immune system from a Th2 to a Th1 mode. BioEos is a research and development company with worldwide patents derived from many years of research at University College London and the many applications are being developed for use in both human, agricultural and aquaculture treatments. Current clinical trials for the treatment of pancreatic cancers (Immodulon Therapeutics) and the treatment of other chronic immune deficiency disorders (ActinoPharma) are putting this research into practical effect.

4) Nutritional supplements: Various supplements may be effective in individuals, including fatty acid supplemantation and linseed oil. However, although owners perceived an improvement, this was not bourne out by objective statistical analysis.

5) Symptomatic Control: Control of symptoms to some degree can be achieved with antihistamines (especially hydroxyzine, and with corticosteroids, although the potential side effects (e.g. laminitis, immune suppression) make this a less preferred option. In addition, antibiotics may be required to manage any secondary infection.

6) Alternative Medicines: A wide variety of herbal, homeopathic and other alternative remedies have been suggested. Among the natural remedies suggested are sulfur, wild geranium (as the base for a shampoo), Lavender oil, Aloe vera (to reduce the itching).

Overall, the wide variety of treatments proposed leads to the conclusion that no one method is universally effective.

Washing the infected area with an antiseptic solution is part of the treatment for mud fever. However, washing a horse's legs repeatedly can remove the natural oils in the skin and may allow the condition to become established. The legs should be dried thoroughly after washing with antibacterial shampoo using paper towels,

Also known as Queensland Itch, Seasonal Recurrent Dermatitis (SSRD) , Summer Itch or more technically, "Culicoides" Hypersensitivity.

Sweet Itch is a medical condition in equines caused by an allergic response to the bites of "Culicoides" midges. It may be found in any horses and ponies, especially in the warmer regions. It may also occur, too, in other equines. It is also found in Canada, Australia, the US and many other parts of the world.

One of the most important factors in successfully treating scratches is moving the horse to a clean and dry environment.

- Use paddock and pasture rotation and fences to keep horses from standing in wet and muddy ground for long periods of time.

- Keep the horse stall in the barn clean and dry.

- Avoid using leg wraps, tack items or devices that could increase moisture retention.

It is estimated that 2—3 percent of hospitalised patients are affected by a drug eruption, and that serious drug eruptions occur in around 1 in 1000 patients.

Drug eruptions are diagnosed mainly from the medical history and clinical examination. However, they can mimic a wide range of other conditions, thus delaying diagnosis (for example, in drug-induced lupus erythematosus, or the acne-like rash caused by erlotinib). A skin biopsy, blood tests or immunological tests can also be useful.

Drug reactions have characteristic timing. The typical amount of time it takes for a rash to appear after exposure to a drug can help categorize the type of reaction. For example, Acute generalized exanthematous pustulosis usually occurs within 4 days of starting the culprit drug. Drug Reaction with Eosinophilia and Systemic Symptoms usually occurs between 15 and 40 days after exposure. Toxic epidermal necrolysis and Stevens-Johnson syndrome typically occur 7–21 days after exposure. Anaphylaxis occurs within minutes. Simple exanthematous eruptions occur between 4 and 14 days after exposure.

TEN and SJS are severe cutaneous drug reactions that involve the skin and mucous membranes. To accurately diagnose this condition, a detailed drug history is crucial. Often, several drugs may be causative and allergy testing may be helpful. Sulfa drugs are well-known to induce TEN or SJS in certain people. For example, HIV patients have an increased incidence of SJS or TEN compared to the general population and have been found to express low levels of the drug metabolizing enzyme responsible for detoxifying sulfa drugs. Genetics plays an important role in predisposing certain populations to TEN and SJS. As such, there are some FDA recommended genetic screening tests available for certain drugs and ethnic populations to prevent the occurrence of a drug eruption. The most well known example is carbamezepine (an anti-convulsant used to treat seizures) hypersensitivity associated with the presence of HLA-B*5801 genetic allele in Asian populations.

DIHS is a delayed onset drug eruption, often occurring a few weeks to 3 months after initiation of a drug. Interestingly, worsening of systemic symptoms occurs 3-4 days after cessation of the offending drug. There are genetic risk alleles that are predictive of the development of DIHS for particular drugs and ethnic populations. The most important of which is abacavir (an anti-viral used in the treatment of HIV) hypersensitivity associated with the presence of the HLA-B*5701 allele in European and African population in the United States and Australians.

AGEP is often caused by antimicrobial, anti-fungal or antimalarial drugs. Diagnosis is often carried out by patch testing. This testing should be performed within one month after resolution of the rash and patch test results are interpreted at different time points: 48 hours, 72hours and even later at 96 hours and 120 hours in order to improve the sensitivity.

There have been numerous accounts of patients with "trichophyton" fungal infections and associated asthma, which further substantiates the likelihood of respiratory disease transmission to the healthcare provider being exposed to the microbe-laden nail dust In 1975, a dermatophyte fungal infection was described in a patient with severe tinea. The resulting treatment for mycosis improved the patient’s asthmatic condition. The antifungal treatment of many other "trichophyton" foot infections has alleviated symptoms of hypersensitivity, asthma, and rhinitis.

Treatment may include corticoids, astringents, and keratolytics. Dermatoses tend to be recurrent unless the use or contact can be avoided. Discontinuation of the instrument is curative in almost all cases, but usually impractical.

In medicine, animal allergy is hypersensitivity to certain substances produced by animals, such as the proteins in animal hair and saliva. It is a common type of allergy.

There are no laboratory or skin testing methods for testing salicylate sensitivity. Provocative challenge is one method of obtaining reliable diagnosis. Provocative challenge is intended to induce a controlled reaction as a means of confirming diagnosis. During provocative challenge, the person is given incrementally higher doses of salicylates, usually aspirin, under medical supervision, until either symptoms appear or the likelihood of symptoms appearing is ruled out.

In adults, the prevalence of IgE sensitization to allergens from house dust mite and cat, but not grass, seem to decrease over time as people age. However, the biological reasons for these changes are not fully understood.

Chronic exposure to human nail dust is a serious occupational hazard that can be minimized by not producing such dust. Best practice is to avoid electrical debridement or burring of mycotic nails unless the treatment is necessary. When the procedure is necessary, it is possible to reduce exposure by using nail dust extractors, local exhaust, good housekeeping techniques, personal protective equipment such as gloves, glasses or goggles, face shields, and an appropriately fitted disposable respirators to protect against the hazards of nail dust and flying debris.

Symptoms of an allergic reaction to animals may include itchy skin, nasal congestion, itchy nose, sneezing, chronic sore throat or itchy throat, swollen, red, itchy, and watery eyes, coughing, asthma, or rash on the face or chest.

Corticosteroids: For years, there was no treatment for atopic eczema. Atopy was believed to be allergic in origin due to the patients’ extremely high serum IgE levels, but standard therapies at the time did not help. Oral prednisone was sometimes prescribed for severe cases. Wet wraps (covering the patients with gauze) were sometimes used in hospitals to control itching. However, the discovery of corticosteroids in the 1950s, and their subsequent incorporation in topical creams and ointments, provided a significant advancement in the treatment of atopic eczema and other conditions. Thus, the use of topical steroids avoided many of the undesirable side-effects of systemic administration of corticosteroids. Topical steroids control the itching and the rash that accompany atopic eczema. Side-effects of topical steroid use are plentiful, and the patient is advised to use topical steroids in moderation and only as needed.

Immune modulators: Pimecrolimus and tacrolimus creams and ointments became available in the 1980s and are sometimes prescribed for atopic eczema. They act by interfering with T cells but have been linked to the development of cancer.

Avoiding dry skin: Dry skin is a common feature of patients with atopic eczema (see also eczema for information) and can exacerbate atopic eczema.

Avoiding allergens and irritants: See eczema for information.

Cutaneous disorders in musicians include frictional injury ("fiddler's neck"), hyperhidrosis, acne mechanica and vascular compromise. Other agents of irritant and allergic contact dermatitis may be rosewood, Makassar ebony, cocobolo wood, African blackwood, nickel, reed, propolis (bee glue), chromium and paraphenylenediamine. Patch testing can be performed for identification of the cause.

Because it is a rare disease, diagnosis is often complicated and takes a long time. Early in the disease patients may have erosions in the mouth or blisters on the skin. These blisters can be itchy or painful. Theoretically, the blisters should demonstrate a positive Nikolsky's sign, in which the skin sloughs off from slight rubbing, but this is not always reliable. The gold standard for diagnosis is a punch biopsy from the area around the lesion that is examined by direct immunofluorescent staining, in which cells are acantholytic, that is, lacking the normal intercellular connections that hold them together. These can also be seen on a Tzanck smear. These cells are basically rounded, nucleated keratinocytes formed due to antibody mediated damage to cell adhesion protein desmoglein.

Pemphigus vulgaris is easily confused with impetigo and candidiasis. IgG4 is considered pathogenic. The diagnosis can be confirmed by testing for the infections that cause these other conditions, and by a lack of response to antibiotic treatment.

Zirconium granulomas are a skin condition characterized by a papular eruption involving the axillae, and are sometimes considered an allergic reaction to deodorant containing zirconium lactate. They are the result of a delayed granulomatous hypersensitivity reaction, and can also occur from exposure to aluminum zirconium complexes. Commonly, zirconium containing products are used to relieve toxicodendron irritation. The lesions are similar to those from sarcoidosis, and commonly manifest four to six weeks after contact. They appear as erythrematous, firm, raised, shiny papules. Corticosteroids are used to ease the inflammation, but curative treatment is currently unavailable.

Diagnosis is based on history given by patient, including recent medications.

There is no standard treatment for PLC. Treatments may include ultraviolet phototherapy, topical steroids, sun exposure, oral antibiotics, corticosteroid creams and ointments to treat rash and itching.

One study identified the enzyme bromelain as an effective therapeutic option for PLC.

Examination of blood samples will allow identification of microfilariae of "M. perstans", and "M. ozzardi" based. This diagnosis can be made on the basis of the morphology of the nuclei distribution in the tails of the microfilariae. The blood sample can be a thick smear, stained with Giemsa or hematoxylin and eosin. For increased sensitivity, concentration techniques can be used. These include centrifugation of the blood sample lyzed in 2% formalin (Knott's technique), or filtration through a Nucleopore membrane.

Examination of skin snips will identify microfilariae of "Onchocerca volvulus" and "M. streptocerca". Skin snips can be obtained using a corneal-scleral punch, or more simply a scalpel and needle. It is important that the sample be allowed to incubate for 30 minutes to 2 hours in saline or culture medium and then examined. This allows for the microfilariae that would have been in the tissue to migrate to the liquid phase of the specimen. Additionally, to differentiate the skin-dwelling filariae "M. streptocerca" and "Onchocerca volvulus", a nested polymerase chain reaction (PCR) assay was developed using small amounts of parasite material present in skin biopsies.

An important salicylate drug is aspirin, which has a long history. Aspirin intolerance was widely known by 1975, when the understanding began to emerge that it is a pharmacological reaction, not an allergy.

A drug allergy is an allergy to a drug, most commonly a medication, and is a form of adverse drug reaction. Medical attention should be sought immediately if an allergic reaction is suspected.

An allergic reaction will not occur on the first exposure to a substance. The first exposure allows the body to create antibodies and memory lymphocyte cells for the antigen. However, drugs often contain many different substances, including dyes, which could cause allergic reactions. This can cause an allergic reaction on the first administration of a drug. For example, a person who developed an allergy to a red dye will be allergic to any new drug which contains that red dye.

A drug allergy is different from an intolerance. A drug intolerance, which is often a milder, non-immune-mediated reaction, does not depend on prior exposure. Most people who believe they are allergic to aspirin are actually suffering from a drug intolerance.

Drug allergies are attributed to "drug hypersensitivity," otherwise known as objectively reproducible symptoms or signs initiated by exposure to a drug at a dose normally tolerated by non-hypersensitive persons. Drug hypersensitivity reactions are the mediators of a drug allergy.

There are two mechanisms for a drug allergy to occur: IgE or non-IgE mediated. In IgE-mediated reactions, also known as Immunoglobulin E mediated reactions, drug allergens bind to IgE antibodies, which are attached to mast cells and basophils, resulting in IgE cross-linking, cell activation and release of preformed and newly formed mediators.

Research into using genetically modified T-cells to treat pemphigus vulgaris in mice was reported in 2016. Rituximab indiscriminately attacks all B cells, which reduces the body's ability to control infections. In the experimental treatment, human T cells are genetically engineered to recognize only those B cells that produce antibodies to desmoglein 3.

With discontinuation of offending agent, symptoms usually disappear within 4–5 days.

Corticosteroids, antihistamines, and analgesics are the main line of treatment. The choice depends on the severity of the reaction.

Use of plasmapheresis has also been described.