The majority of individuals who receive a sting from an insect experience local reactions. It is estimated that 5-10% of individuals will experience a generalized systemic reaction that can involve symptoms ranging from hives to wheezing and even anaphylaxis. In the United States approximately 40 people die each year from anaphylaxis due to stinging insect allergy. Potentially life-threatening reactions occur in 3% of adults and 0.4–0.8% of children.

Nickel allergy results in a skin response (rash) after the skin comes in direct and sustained contact with any item which releases a large amount of free nickel from its surface. The skin reaction can occur at the site of contact, or sometimes spread beyond to the rest of the body. Cutaneous exposure can cause localized erythematous, pruritic, vesicular, and scaly patches. Ingestion of nickel may cause a systemic reaction, that will affect a larger skin surface. Examples of systemic reactions can include hand dermatitis, baboon syndrome, or generalized eczematous reactions.

Within the workplace, individuals may be exposed to significant amounts of nickel, airborne from the combustion of fossil fuels, or from contact with tools that are nickel-plated. Historically, workplaces where prolonged contact with soluble nickel has been high, have shown high risks for allergic contact nickel dermatitis. For example, nickel dermatitis was common in the past among nickel platers. Due to improved industrial and personal hygiene practices, however, over the past several decades, reports of nickel sensitivity in workplaces, such as the electroplating industry, have been sparse. In the workplace, exposure reduction includes personal protection equipment and other risk management measures.

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.

Common allergens implicated include the following:

- Nickel (nickel sulfate hexahydrate) – has been recognized as a significant cause of allergy. This metal is frequently encountered in stainless steel cookware, jewelry and clasps or buttons on clothing. Current estimates gauge are that roughly 2.5 million US adults and 250,000 children suffer from nickel allergy, which costs an estimated $5.7 billion per year for treatment of symptoms. A significant portion of nickel allergy is preventable.

- Gold (gold sodium thiosulfate) – precious metal often found in jewelry and dental materials

- Balsam of Peru (Myroxylon pereirae) – used in food and drink for flavoring, in perfumes and toiletries for fragrance, and in medicine and pharmaceutical items for healing properties; derived from tree resin. It may also be a component of artificial vanilla and/or cinnamon flavorings.

- Chromium – used in the tanning of leather. Also a component of uncured cement/mortar, facial cosmetics and some bar soaps.

- Urushiol – oily coating from plants of Toxicodendron genus – poison ivy, poison oak, and poison sumac. Also found in mango plants and cashews.

- Sap from certain species of mangrove and agave

- Thiomersal – mercury compound used in local antiseptics and in vaccines

- Neomycin – topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap, and pet food. Found by itself, or in Neosporin or Triple Antibiotic

- Fragrance mix – group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes, and dental products

- Formaldehyde – preservative with multiple uses, "e.g.", in paper products, paints, medications, household cleaners, cosmetic products, and fabric finishes. Often released into products by the use of formaldehyde releasers such as imidazolidinyl urea, diazolidinyl urea, Quaternium-15, DMDM Hydantoin, and 2-bromo-2-nitropropane-1,3-diol.

- Cobalt chloride – metal found in medical products; hair dye; antiperspirant; metal-plated objects such as snaps, buttons or tools; and in cobalt blue pigment

- Bacitracin – topical antibiotic found by itself, or as Polysporin or Triple Antibiotic

- Quaternium-15 – preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).

- Colophony (Rosin) – rosin, sap or sawdust typically from spruce or fir trees

- Topical steroid – "see" steroid allergy

- Photographic developers, especially those containing metol

- Topical anesthetics – such as pramoxine or diphenhydramine, after prolonged use

- Isothiazolinones – preservatives used in many personal care, household, and commercial products.

- Mercaptobenzothiazole – in rubber products, notably shoes, gloves, and car tires.

- Soluble salts of platinum – "see" platinosis

The more poignant part of this disorder is the lack of desensitization for water and aqua intile injection as allergen even on repeated exposure. Avoidance of allergen as a general principle in any allergic disorder necessitates the evasion of water exposure. Topical application of antihistamines like 1% diphenhydramine before water exposure is reported to reduce the hives. Oil in water emulsion creams, petrolatum as barrier agents for water can be used prior to shower or bath with good control of symptoms. Therapeutic effectiveness of various classes of drugs differs from case to case.

Allergic diseases are strongly familial: identical twins are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins. Allergic parents are more likely to have allergic children, and those children's allergies are likely to be more severe than those in children of non-allergic parents. Some allergies, however, are not consistent along genealogies; parents who are allergic to peanuts may have children who are allergic to ragweed. It seems that the likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not.

The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk. Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years. The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.

Overall, boys have a higher risk of developing allergies than girls, although for some diseases, namely asthma in young adults, females are more likely to be affected. These differences between the sexes tend to decrease in adulthood.

Ethnicity may play a role in some allergies; however, racial factors have been difficult to separate from environmental influences and changes due to migration. It has been suggested that different genetic loci are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.

Chronic stress can aggravate allergic conditions. This has been attributed to a T helper 2 (TH2)-predominant response driven by suppression of interleukin 12 by both the autonomic nervous system and the hypothalamic–pituitary–adrenal axis. Stress management in highly susceptible individuals may improve symptoms.

In the United States, only about 4% of patients with photosensitive disorders are reported to have been diagnosed with solar urticaria. Internationally, the number is slightly larger at 5.3%. Solar urticaria may occur in all races but studies monitoring 135 African Americans and 110 Caucasians with photodermatoses found that 2.2% of the African Americans had SU and 8% of the Caucasians had the disease showing that Caucasians have a better chance of getting the disease. Globably 3.1 per 100,000 people are affected and females are more likely to be affected than males. The age ranges anywhere from 5–70 years old, but the average age is 35 and cases have been reported with children that are still in infancy. Solar urticaria accounts for less than one percent of the many documented urticaria cases. To put that into a better perspective, since its first documented case in Japan in 1916, over one hundred other instances of the disease have been reported.

Aquagenic urticaria, once known as a rare physical urticaria, is reclassified as separate subtype of urticaria. It was first reported by Walter B Shelley et al. in 1964. Pruritic hives on contact with water mostly presenting for the first time during puberty in females of reproductive age is seen in aquagenic urticaria. Males are less often affected. Even if majority cases are sporadic in nature, familial cases are also recorded. Water in all forms such as tap or sea water, swimming pool, sweat, tears, saliva can induce the lesions.

Solar urticaria is an immunoglobulin E-mediated hypersensitivity that can be introduced through primary or secondary factors, or induced by exogenous photosensitization. Primary SU is believed to be a type I hypersensitivity (a mild to severe reaction to an antigen including anaphylaxis) in which an antigen, or substance provoking an immune response, is "induced by UV or visible radiation." Secondary SU can occur when a person comes into contact with chemicals such as tar, pitch, and dyes. People who use drugs such as benoxaprofen or patients with erythropoietic protoporphyria may also contract this secondary form. These items that cause this photosensitivity are exogenous photosensitizers because they are outside of the body and cause it to have a greater sensitivity to light.

Also, there have been a few unorthodox (unusual) causes of solar urticaria. For those susceptible to visible light, white T-shirts may increase the chances of experiencing an outbreak. In one case, doctors found that the white T-shirt absorbed UVA radiation from the sun and transformed it into visible light which caused the reaction. Another patient was being treated with the antibiotic tetracycline for a separate dermatological disorder and broke out in hives when exposed to the sun, the first case to implicate tetracycline as a solar urticaria inducing agent.

It is not yet known what specific agent in the body brings about the allergic reaction to the radiation. When patients with SU were injected with an irradiated autologous serum, many developed urticaria within the area of injection. When people who did not have SU were injected, they did not demonstrate similar symptoms. This indicates that the reaction is only a characteristic of the patients with solar urticaria and that it is not phototoxic. It is possible that this photoallergen is located on the binding sites of IgE that are found on the surface of mast cells. The photoallergen is believed to begin its configuration through the absorption of radiation by a chromophore. The molecule, because of the radiation, is transformed resulting in the formation of a new photoallergen.

Insect sting allergy is the term commonly given to the allergic response of an animal in response to the bite or sting of an insect. Typically, insects which generate allergic responses are either stinging insects (wasps, bees, hornets and ants) or biting insects (mosquitoes, ticks). Stinging insects inject venom into their victims, whilst biting insects normally introduce anti-coagulants into their victims.

The great majority of insect allergic animals just have a simple allergic response – a reaction local to the sting site which appears as just a swelling arising from the release of histamine and other chemicals from the body tissues near to the sting site. The swelling, if allergic, can be helped by the provision of an anti-histamine ointment as well as an ice pack. This is the typical response for all biting insects and many people have this common reaction.

Mosquito allergy may result in a collection of symptoms called skeeter syndrome that occur after a bite. This syndrome may be mistaken for an infection such as cellulitis.

In anaphylactic patients the response is more aggressive leading to a systemic reaction where the response progresses from the sting site around the whole body. This is potentially something very serious and can lead to anaphylaxis, which is potentially life-threatening.

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.

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.

Some of the drugs associated with serum sickness are:

- allopurinol

- barbiturates

- captopril

- cephalosporins

- griseofulvin

- penicillins

- phenytoin

- procainamide

- quinidine

- streptokinase

- sulfonamides

- rituximab

- ibuprofen

- infliximab

Allergic inflammation is an important pathophysiological feature of several disabilities or medical conditions including allergic asthma, atopic dermatitis, allergic rhinitis and several ocular allergic diseases. Allergic reactions may generally be divided into two components; the early phase reaction, and the late phase reaction. While the contribution to the development of symptoms from each of the phases varies greatly between diseases, both are usually present and provide us a framework for understanding allergic disease.

The early phase of the allergic reaction typically occurs within minutes, or even seconds, following allergen exposure and is also commonly referred to as the immediate allergic reaction or as a Type I allergic reaction. The reaction is caused by the release of histamine and mast cell granule proteins by a process called degranulation, as well as the production of leukotrienes, prostaglandins and cytokines, by mast cells following the cross-linking of allergen specific IgE molecules bound to mast cell FcεRI receptors. These mediators affect nerve cells causing itching, smooth muscle cells causing contraction (leading to the airway narrowing seen in allergic asthma), goblet cells causing mucus production, and endothelial cells causing vasodilatation and edema.

The late phase of a Type 1 reaction (which develops 8–12 hours and is mediated by mast cells) should not be confused with delayed hypersensitivity Type IV allergic reaction (which takes 48–72 hours to develop and is mediated by T cells). The products of the early phase reaction include chemokines and molecules that act on endothelial cells and cause them to express Intercellular adhesion molecule (such as vascular cell adhesion molecule and selectins), which together result in the recruitment and activation of leukocytes from the blood into the site of the allergic reaction. Typically, the infiltrating cells observed in allergic reactions contain a high proportion of lymphocytes, and especially, of eosinophils. The recruited eosinophils will degranulate releasing a number of cytotoxic molecules (including Major Basic Protein and eosinophil peroxidase) as well as produce a number of cytokines such as IL-5. The recruited T-cells are typically of the Th2 variety and the cytokines they produce lead to further recruitment of mast cells and eosinophils, and in plasma cell isotype switching to IgE which will bind to the mast cell FcεRI receptors and prime the individual for further allergic responses.

Allergenic extracts, hormones and vaccines can also cause serum sickness.

The first step in treatment following a bee sting is removal of the stinger itself. The stinger should be removed as quickly as possible without regard to method: studies have shown the amount of venom delivered does not differ whether the sting is pinched or scraped off and even a delay of a few seconds leads to more venom being injected. Once the stinger is removed, pain and swelling should be reduced with a cold compress. A topical anesthetic containing benzocaine will kill pain quickly and menthol is an effective anti-itch treatment. Itching can also be relieved by antihistamine or by a steroid cream.

Many traditional remedies have been suggested for bee stings including damp pastes of tobacco, salt, baking soda, papain, toothpaste, clay, garlic, urine, onions, aspirin or even application of copper coins. As with jellyfish stings, ammonia and ammonia-containing liquids, such as window cleaner, are often suggested as a way to immediately cleanse the skin and remove excess venom, and sweat itself (which also contains small amounts of ammonia) may provide some small relief.

Bee venom is acidic, and these interventions are often recommended to neutralize the venom; however, neutralizing a sting is unlikely to be effective as the venom is injected under the skin and deep into the tissues, where a topically applied alkali is unable to reach, so neutralization is unlikely to occur. In any case, the amount of venom injected is typically very small (between 5 and 50 micrograms of fluid) and placing large amounts of alkali near the sting site is unlikely to produce a perfectly neutral pH to stop the pain. Many people do claim benefit from these home remedies but it is doubtful they have any real physical effect on how much a sting hurts or continues hurting. The effect is probably related to rubbing the area or the mind perceiving benefit. Furthermore, none of these interventions have been proven to be effective in scientific studies and a randomized trial of aspirin paste and topical ice packs showed that aspirin was not effective in reducing the duration of swelling or pain in bee and wasp stings, and significantly increased the duration of redness. The study concluded that ice alone is better treatment for bee and wasp stings than aspirin.

The sting may be painful for a few hours. Swelling and itching may persist for a week. The area should not be scratched as it will only increase the itching and swelling. If swelling persists for over a week or covers an area greater than , medical attention should be sought. Doctors often recommend a tetanus immunization. For about 2 percent of people, a hypersensitivity can develop after being stung, creating a more severe reaction when stung again later. This sensitisation may happen after a single sting, or after a series of stings where they reacted normally. A highly allergic person may suffer anaphylactic shock from certain proteins in the venom, which can be life-threatening and requires emergency treatment. People known to be highly allergic may carry around epinephrine (adrenaline) in the form of a self-injectable EpiPen for the treatment of an anaphylactic shock.

For patients who experience severe or life-threatening reactions to insect stings, allergy injections composed of increasing concentrations of naturally occurring venom may provide protections against future insect stings.

A bee sting is a sting from a bee (honey bee, bumblebee, sweat bee, etc.). The stings of most of these species can be quite painful, and are therefore keenly avoided by many people.

Bee stings differ from insect bites, and the venom or toxin of stinging insects is quite different. Therefore, the body's reaction to a bee sting may differ significantly from one species to another. In particular, bee stings are acidic, whereas wasp stings are alkali, so the body's reaction to a bee sting may be very different than to that of a wasp sting.

The most aggressive stinging insects are vespid wasps (including bald-faced hornets and other yellow jackets) and hornets (especially the Asian giant hornet). All of these insects aggressively defend their nests.

Although for most people a bee sting is painful but otherwise relatively harmless, in people with insect sting allergy, stings may trigger a dangerous anaphylactic reaction that is potentially deadly. Additionally, honey bee stings release pheromones that prompt other nearby bees to attack.

Pathogenically, it is a Type II Hypersensitivity reaction where circulating complement-fixing IgG antibodies bind to an antigen (a 180-kDa protein, BP-180) in the hemidesmosomes (attach basal cells of epidermis to the basal lamina and hence to dermis) of the dermoepidermal junction (DEJ) , leading to blister formation as loss of hemidesmosomes causes the epidermis to separate from dermis. The immune response is even more highly restricted to the NC16A domain. The primary site of autoimmunity seems not to be the skin, but the placenta, as antibodies bind not only to the basement membrane zone of the epidermis, but also to that of chorionic and amniotic epitheli. Aberrant expression of MHC class II molecules on the chorionic villi suggests an allogenic immune reaction to a placental matrix antigen, thought to be of paternal origin .Recently, both IgA22 and IgE24 antibodies to either BP180 or BP230 have also been detected in pemphigoid gestationis.

Bumblefoot is a common infection for domesticated poultry and waterfowl such as chickens, ducks and quail. Due to constant walking on hard, rough, or sharp surfaces, birds can develop small wounds on the bottom of their feet. These wounds are very susceptible to infection by opportunistic bacterial pathogens, chiefly "Staphylococcus aureus". Treatment often requires opening the wound to drain the pus, soaking it in epsom salts, and antibiotic treatment and local application of the antiseptic pyodine as local dressing.

Pregnant women with PG should be monitored for conditions that may affect the fetus, including, but not limited to, low or decreasing volume of amniotic fluid, preterm labor, and intrauterine growth retardation. Onset of PG in the first or second trimester and presence of blisters may lead to adverse pregnancy outcomes including decreased gestational age at delivery, preterm birth, and low birth weight children. Such pregnancies should be considered high risk and appropriate obstetric care should be provided. Systemic corticosteroid treatment, in contrast, does not substantially affect pregnancy outcomes, and its use for PG in pregnant women is justified. PG typically reoccurs in subsequent pregnancies. Passive transfer of the mother’s antibodies to the fetus causes some (about 10%) newborns to develop mild skin lesions, but these typically will resolve within weeks of parturition.

Vitamin K reactions occur after injection with vitamin K, and there are two patterns of presentation, (1) a reaction may occur several days to 2 weeks after inection with skin lesions that are pruritic, red patches and plaques that can deep-seated, involving the dermis and subcutaneous tissue, or (2) with subcutaneous sclerosis with or without fasciitis, that appears at the site of injection many months after treatment. The latter pseudosclerodermatous reaction has been termed Texier's disease and lasts several years.

Bumblefoot (ulcerative pododermatitis) is a bacterial infection and inflammatory reaction on the feet of birds, rodents, and rabbits. Ulcerative pododermatitis is referred to as "sore hocks" when it affects a rabbit and "bumblefoot" when it affects a bird. The terms "sore hocks" and "bumblefoot" are used interchangeably when describing ulcerative pododermatitis in rodents. The infection can usually be attributed to poor husbandry practices, therefore is much more likely to occur in captive animals than in those in the wild. It is caused by bacteria, namely strains of "Staphylococcus", "Pseudomonas" and "Escherichia coli" "(E. coli)", with "S. aureus" being the most common cause of the infection.

In addition to vaccine-specific factors, vets and owners should also consider pet-specific factors that have been shown to increase the risk of adverse reactions in both dogs and cats. Examples of such factors include:

- age,

- number of vaccinations per office visit,

- size,

- general health of the animal,

- breed,

- neutered status, and

- past vaccination history.