Lipoproteins released from treatment of "Treponema pallidum" infections are believed to induce the Jarisch-Herxheimer reaction. The Herxheimer reaction has shown an increase in inflammatory cytokines during the period of exacerbation, including tumor necrosis factor alpha, interleukin-6 and interleukin-8.

The Jarisch–Herxheimer reaction is traditionally associated with antimicrobial treatment of syphilis. The reaction is also seen in the other diseases caused by spirochetes: Lyme disease, relapsing fever, and leptospirosis. There have been case reports of the Jarisch-Herxheimer reaction accompanying treatment of other infections, including Q fever, bartonellosis, brucellosis, trichinellosis, and African trypanosomiasis.

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

Some of the drugs associated with serum sickness are:

- allopurinol

- barbiturates

- captopril

- cephalosporins

- griseofulvin

- penicillins

- phenytoin

- procainamide

- quinidine

- streptokinase

- sulfonamides

- rituximab

- ibuprofen

- infliximab

Although genetic factors govern susceptibility to atopic disease, increases in atopy have occurred within too short a time frame to be explained by a genetic change in the population, thus pointing to environmental or lifestyle changes. Several hypotheses have been identified to explain this increased rate; increased exposure to perennial allergens due to housing changes and increasing time spent indoors, and changes in cleanliness or hygiene that have resulted in the decreased activation of a common immune control mechanism, coupled with dietary changes, obesity and decline in physical exercise. The hygiene hypothesis maintains that high living standards and hygienic conditions exposes children to fewer infections. It is thought that reduced bacterial and viral infections early in life direct the maturing immune system away from T1 type responses, leading to unrestrained T2 responses that allow for an increase in allergy.

Changes in rates and types of infection alone however, have been unable to explain the observed increase in allergic disease, and recent evidence has focused attention on the importance of the gastrointestinal microbial environment. Evidence has shown that exposure to food and fecal-oral pathogens, such as hepatitis A, "Toxoplasma gondii", and "Helicobacter pylori" (which also tend to be more prevalent in developing countries), can reduce the overall risk of atopy by more than 60%, and an increased rate of parasitic infections has been associated with a decreased prevalence of asthma. It is speculated that these infections exert their effect by critically altering T1/T2 regulation. Important elements of newer hygiene hypotheses also include exposure to endotoxins, exposure to pets and growing up on a farm.

Risk factors for drug allergies can be attributed to the drug itself or the characteristics of the patient. Drug-specific risk factors include the dose, route of administration, duration of treatment, repetitive exposure to the drug, and concurrent illnesses. Host risk factors include age, sex, atopy, specific genetic polymorphisms, and inherent predisposition to react to multiple unrelated drugs (multiple drug allergy syndrome).

A drug allergy is more likely to develop with large doses and extended exposure.

The allergic diseases—hay fever and asthma—have increased in the Western world over the past 2–3 decades. Increases in allergic asthma and other atopic disorders in industrialized nations, it is estimated, began in the 1960s and 1970s, with further increases occurring during the 1980s and 1990s, although some suggest that a steady rise in sensitization has been occurring since the 1920s. The number of new cases per year of atopy in developing countries has, in general, remained much lower.

When a medication causes an allergic reaction, it is called an allergen. The following is a short list of the most common drug allergens:

- Antibiotics

- Penicillin

- Sulfa drugs

- Tetracycline

- Analgesics

- Codeine

- Non-steroidal anti-inflammatory drugs (NSAIDs)

- Antiseizure

- Phenytoin

- Carbamazepine

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.

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.

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.

Alpha-gal allergies develop after a person has been bitten by the lone star tick in the United States, the European castor bean tick, and the paralysis tick in Australia. Alpha-gal is not naturally present in apes and humans, but is in all other mammals. If a tick feeds on another mammal, the alpha-gal will remain in its alimentary tract. The tick will then inject the alpha-gal into a person's skin, which in turn will cause the immune system to release a flood of IgE antibodies to fight off the foreign carbohydrate. Researchers still do not know which specific component of tick saliva causes the reaction.

A 2012 preliminary study found unexpectedly high rates of alpha-gal allergies in the Western and North Central parts of the United States, which suggests that the allergy may be spread by unknown tick species. Examples of alpha-gal allergies were even present in Hawaii, where none of the ticks identified with the allergies live. Human factors were suggested but no specific examples were provided.

Alpha-gal is present in the anti-cancer drug cetuximab, as well as the IV fluid replacements Gelofusine and Haemaccel. Blood thinners derived from porcine intestine and replacement heart valves derived from porcine tissue may also contain alpha-gal.

There has been at least one instance of a man with an alpha-gal allergy going into anaphylaxis after receiving a heart valve transplant. Some researchers have suggested that the alpha-gal which is prevalent in pig's tissue and used for xenografts may contribute to organ rejection.

Venom from stinging or biting insects such as Hymenoptera (ants, bees, and wasps) or Triatominae (kissing bugs) may cause anaphylaxis in susceptible people. Previous systemic reactions, which are anything more than a local reaction around the site of the sting, are a risk factor for future anaphylaxis; however, half of fatalities have had no previous systemic reaction.

A little known and often misdiagnosed reaction to the rabies vaccine in dogs, this problem may develop near or over the vaccine administration site and around the vaccine material that was injected, or as a more widespread reaction. Symptoms include ulcers, scabs, darkening of the skin, lumps at the vaccine site, and scarring with loss of hair. In addition to the vaccination site, lesions most often develop on the ear flaps (pinnae), on the elbows and hocks, in the center of the footpads and on the face. Scarring may be permanent. Dogs do not usually seem ill, but may develop fever. Symptoms may show up within weeks of vaccination, or may take months to develop noticeably.

Dogs with active lesion development and / or widespread disease may be treated with pentoxyfylline, a drug that is useful in small vessel vasculitis, or tacrolimus, an ointment that will help suppress the inflammation in the affected areas.

Owners and veterinarians of dogs who have developed this type of reaction should review the vaccination protocol critically and try to reduce future vaccinations to the extent medically and legally possible. At the very least, vaccines from the same manufacturer should be avoided. It is also recommended that the location in which future vaccinations are administered should be changed to the rear leg, as far down on the leg as possible and should be given in the muscle rather than under the skin.

Some examples:

- Allergic asthma

- Allergic conjunctivitis

- Allergic rhinitis ("hay fever")

- Anaphylaxis

- Angioedema

- Urticaria (hives)

- Eosinophilia

- Penicillin allergy

- Cephalosporin allergy

- Food allergy

- Sweet itch

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.

People with atopic diseases such as asthma, eczema, or allergic rhinitis are at high risk of anaphylaxis from food, latex, and radiocontrast agents but not from injectable medications or stings. One study in children found that 60% had a history of previous atopic diseases, and of children who die from anaphylaxis, more than 90% have asthma. Those with mastocytosis or of a higher socioeconomic status are at increased risk. The longer the time since the last exposure to the agent in question, the lower the risk.

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.

In immunology, the Arthus reaction (, ) is a type of local type III hypersensitivity reaction. Type III hypersensitivity reactions are immune complex-mediated, and involve the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium, synovium), and glomeruli. This reaction is usually encountered in experimental settings following the injection of antigens.

The Arthus reaction involves the in situ formation of antigen/antibody complexes after the intradermal injection of an antigen. If the animal/patient was previously sensitized (has circulating antibody), an Arthus reaction occurs. Typical of most mechanisms of the type III hypersensitivity, Arthus manifests as local vasculitis due to deposition of IgG-based immune complexes in dermal blood vessels. Activation of complement primarily results in cleavage of soluble complement proteins forming C5a and C3a, which activate recruitment of PMNs and local mast cell degranulation (requiring the binding of the immune complex onto FcγRIII), resulting in an inflammatory response. Further aggregation of immune complex-related processes induce a local fibrinoid necrosis with ischemia-aggravating thrombosis in the tissue vessel walls. The end result is a localized area of redness and induration that typically lasts a day or so.

Arthus reactions have been infrequently reported after vaccinations containing diphtheria and tetanus toxoid. The CDC's description:

Arthus reactions (type III hypersensitivity reactions) are rarely reported after vaccination and can occur after tetanus toxoid–containing or diphtheria toxoid–containing vaccines. An Arthus reaction is a local vasculitis associated with deposition of immune complexes and activation of complement. Immune complexes form in the setting of high local concentration of vaccine antigens and high circulating antibody concentration. Arthus reactions are characterized by severe pain, swelling, induration, edema, hemorrhage, and occasionally by necrosis. These symptoms and signs usually occur 4–12 hours after vaccination. ACIP has recommended that persons who experienced an Arthus reaction after a dose of tetanus toxoid–containing vaccine should not receive Td more frequently than every 10 years, even for tetanus prophylaxis as part of wound management.

Allergies to a specific pollen are usually associated with OAS reactions to other certain foods. For instance, an allergy to ragweed is associated with OAS reactions to banana, watermelon, cantaloupe, honeydew, zucchini, and cucumber. This does not mean that all sufferers of an allergy to ragweed will experience adverse effects from all or even any of these foods. Reactions may be associated with one type of food, with new reactions to other foods developing later. However, reaction to one or more foods in any given category does not necessarily mean a person is allergic to all foods in that group.

The term morbilliform refers to a rash that looks like measles. The rash consists of macular lesions that are red and usually 2–10 mm in diameter but may be confluent in places.

Patients with measles will have the rash but there are other syndromes and infections that will display the same symptom such as patients with Kawasaki disease, meningococcal petechiae or Waterhouse-Friderichsen syndrome, Dengue, congenital syphilis, rubella, Echovirus 9, drug hypersensitivity reactions (in particular with certain classes of antiretroviral drugs, such as abacavir and nevirapine, and also the antiepileptic drug phenytoin), or other conditions may also have a morbilliform rash.

One cause of morbilliform rash is an allergic reaction to transfused blood/blood components. In such a case, the skin lesions would develop within a few hours (Approx. 4hours) of transfusion along with pruritus. The condition may even present with other symptoms, such as conjunctival oedema, oedema in the lips and tongue, and even localised angioedema. On rare occasions, the condition may even escalate to anaphylactic shock where pulmonary restrictions are seen. The associated cause for this is a reaction against an allergen that is seldom identified during testing. Transfusing products with anti-IgA antibodies to IgA-deficient patients has also been a suspected cause for such reactions. Management usually relates to the stoppage of transfusion for around 30minutes, until given antihistamines take effect. Transfusion may even be continued after, if no further progression is seen.

Anticonvulsant/sulfonamide hypersensitivity syndrome is a potentially serious hypersensitivity reaction that can be seen with drugs with an aromatic amine chemical structure, such as aromatic anticonvulsants (e.g. diphenylhydantoin, phenobarbital, phenytoin, carbamazepine, lamotrigine), sulfonamides, or other drugs with an aromatic amine (procainamide). Cross-reactivity should not occur between drugs with an aromatic amine and drugs without an aromatic amine (e.g., sulfonylureas, thiazide diuretics, furosemide, and acetazolamide); therefore, these drugs can be safely used in the future.

The hypersensitivity syndrome is characterized by a skin eruption that is initially morbilliform. The rash may also be a severe Stevens-Johnson syndrome or toxic epidermal necrolysis. Systemic manifestations occur at the time of skin manifestations and include eosinophilia, hepatitis, and interstitial nephritis. However, a subgroup of patients may become hypothyroid as part of an autoimmune thyroiditis up to 2 months after the initiation of symptoms.

This kind of adverse drug reaction is caused by the accumulation of toxic metabolites; it is not the result of an IgE-mediated reaction. The risk of first-degree relatives’ developing the same hypersensitivity reaction is higher than in the general population.

As this syndrome can present secondary to multiple anticonvulsants, the general term "anticonvulsant hypersensitivity syndrome" is favored over the original descriptive term "dilantin hypersensitivity syndrome."

Causes include infection with dermatophytosis, Mycobacterium, viruses, bacteria and parasites. Eczematous conditions including contact allergic dermatitis and stasis dermatitis as well as stitches and trauma have also been associated with id reactions. Radiation treatment of tinea capitis has been reported as triggering an id reaction.

Treatment usually involves adrenaline (epinephrine), antihistamines, and corticosteroids.

If the entire body is involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.