The histomorphologic appearance of insect bites is usually characterized by a wedge-shaped superficial dermal perivascular infiltrate consisting of abundant lymphocytes and scattered eosinophils. This appearance is non-specific, i.e. it may be seen in a number of conditions including:

- Drug reactions,

- Urticarial reactions,

- Prevesicular early stage of bullous pemphigoid, and

- HIV related dermatoses.

Feeding bites have characteristic patterns and symptoms, a function of the feeding habits of the offending pest and the chemistry of its saliva.

The Mazzotti reaction, first described in 1948, is a symptom complex seen in patients after undergoing treatment of onchocerciasis with the medication diethylcarbamazine (DEC). Mazzotti reactions can be life-threatening, and are characterized by fever, urticaria, swollen and tender lymph nodes, tachycardia, hypotension, arthralgias, oedema, and abdominal pain that occur within seven days of treatment of microfilariasis. The Mazzotti reaction correlates with intensity of infection; however, there are probably multiple infection intensity-dependent mechanisms responsible for mediating this complex reaction.

The phenomenon is so common when DEC is used for the treatment of onchocerciasis that this drug is the basis of a skin patch test used to confirm that diagnosis. The drug patch is placed on the skin, and if the patient is infected with the microfilaria of "O. volvulus", localized pruritus and urticaria are seen at the application site.

A case of the Mazzotti reaction has been reported after presumptive treatment of schistosomiasis and strongyloidiasis with ivermectin, praziquantel and albendazole. The patient had complete resolution of symptoms after intravenous therapy with methylprednisolone.

This is an unusual form of epidemic epilepsy associated with onchocerciasis. This syndrome was first described in Tanzania by Louise Jilek-Aall, a Norwegian psychiatric doctor in Tanzanian practice, during the 1960s. It occurs most commonly in Uganda and South Sudan. It manifests itself in previously healthy 5–15-year-old children, is often triggered by eating or low temperatures and is accompanied by cognitive impairment. Seizures occur frequently and may be difficult to control. The electroencephalogram is abnormal but cerebrospinal fluid (CSF) and magnetic resonance imaging (MRI) are normal or show non-specific changes. If there are abnormalities on the MRI they are usually present in the hippocampus. Polymerase chain reaction testing of the CSF does not show the presence of the parasite.

Adult worms remain in subcutaneous nodules, limiting access to the host's immune system. Microfilariae, in contrast, are able to induce intense inflammatory responses, especially upon their death. "Wolbachia" species have been found to be endosymbionts of "O. volvulus" adults and microfilariae, and are thought to be the driving force behind most of "O. volvulus" morbidity. Dying microfilariae have been recently discovered to release "Wolbachia" surface protein that activates TLR2 and TLR4, triggering innate immune responses and producing the inflammation and its associated morbidity. The severity of illness is directly proportional to the number of infected microfilariae and the power of the resultant inflammatory response.

Skin involvement typically consists of intense itching, swelling, and inflammation. A grading system has been developed to categorize the degree of skin involvement:

- Acute papular onchodermatitis – scattered pruritic papules

- Chronic papular onchodermatitis – larger papules, resulting in hyperpigmentation

- Lichenified onchodermatitis – hyperpigmented papules and plaques, with edema, lymphadenopathy, pruritus and common secondary bacterial infections

- Skin atrophy – loss of elasticity, the skin resembles tissue paper, 'lizard skin' appearance

- Depigmentation – 'leopard skin' appearance, usually on anterior lower leg

- Glaucoma effect – eyes malfunction, begin to see shadows or nothing

Ocular involvement provides the common name associated with onchocerciasis, river blindness, and may involve any part of the eye from conjunctiva and cornea to uvea and posterior segment, including the retina and optic nerve. The microfilariae migrate to the surface of the cornea. Punctate keratitis occurs in the infected area. This clears up as the inflammation subsides. However, if the infection is chronic, sclerosing keratitis can occur, making the affected area become opaque. Over time, the entire cornea may become opaque, thus leading to blindness. Some evidence suggests the effect on the cornea is caused by an immune response to bacteria present in the worms.

The skin is itchy, with severe rashes permanently damaging patches of skin.

It resembles bacterial sepsis and can occur after initiation of antibacterials, such as mild silver protein, penicillin or tetracycline, for the treatment of louse-borne relapsing fever (80–90% of patients) and in tick-borne relapsing fever (30–40%). It usually manifests within a few hours of the first dose of antibiotic as fever, chills, rigor, hypotension, headache, tachycardia, hyperventilation, vasodilation with flushing, myalgia (muscle pain), exacerbation of skin lesions and anxiety. The intensity of the reaction indicates the severity of inflammation. Reaction commonly occurs within two hours of drug administration, but is usually self-limiting. It is observed in 50% of patients with primary syphilis and about 90% of patients with secondary syphilis.

A Jarisch–Herxheimer reaction () is a reaction to endotoxin-like products released by the death of harmful microorganisms within the body during antibiotic treatment. Efficacious antimicrobial therapy results in lysis (destruction) of bacterial cell membranes, and in the consequent release into the bloodstream of bacterial toxins, resulting in a systemic inflammatory response.

Jarisch–Herxheimer reactions are usually not life-threatening.

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.

Symptoms can take as long as 14 days after exposure to appear, and may include signs and symptoms commonly associated with hypersensitivity or infections.

- rashes

- itching

- joint pain (arthralgia), especially finger and toe joints

- fever, as high as 40 °C and usually appears before rash

- lymphadenopathy (swelling of lymph nodes), particularly near the site of injection, head and neck

- malaise

- hypotension (decreased blood pressure)

- splenomegaly (enlarged spleen)

- glomerulonephritis

- proteinuria

- hematuria

- shock

Serum sickness in humans is a reaction to proteins in antiserum derived from a non-human animal source, occurring 4–10 days after exposure. It is a type of hypersensitivity, specifically immune complex hypersensitivity (type III). The term serum sickness-like reaction (SSLR) is occasionally used to refer to similar illnesses that arise from the introduction of certain non-protein substances, such as penicillin. It was first characterized by Clemens von Pirquet and Béla Schick in 1906.

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.

When the body is exposed to the cold in individuals afflicted by the condition, hives appear and the skin in the affected area typically becomes itchy. Hives result from dilation of capillaries which allow fluid to flow out into the surrounding tissue which is the epidermis.They resolve when the body absorbs this fluid. The border of a hive is described as polycyclic, or made up of many circles, and changes as fluid leaks out and then is absorbed. Pressing on a hive causes the skin to blanch distinguishing it from a bruise or papule. Hives can last for a few minutes or a few days, and vary from person to person. Also, a burning sensation occurs. During a severe reaction, low blood pressure, which can be life-threatening, can occur. A serious reaction is most likely to occur if the hives occur with less than 3 minutes of exposure (during a cold test).

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.

Primary cold contact urticaria is a cutaneous condition characterized by s, and occurs in rainy, windy weather, and after swimming in cold water and after contact with cold objects, including ice cubes.

Generally, the areas affected are exposed skin not usually protected by clothing; however it can also occur in areas covered by clothing. Areas constantly subjected to the sun's rays may only be slightly affected if at all. People with extreme cases will also have reactions to light bulbs that emit a UV wavelength (any bulb that is not an LED). Parts of the body only thinly covered can also potentially be subjected to an outbreak.

Life with SU can be difficult. Patients are subject to constant itching and pain, as within minutes of the initial exposure to UV radiation a rash will appear. The urticarial reaction begins in the form of pruritus, later progressing to erythema and edema in the exposed areas of the skin. If vast areas of the body are affected, the loss of fluid into the skin could lead to light-headedness, headache, nausea, and vomiting. Extremely rarely, patients have been reported to experience an increase in heart rate that can cause a stroke or heart attack due to the body cavity swelling. Other rare side effects can be bronchospasm and glucose instability issues. Also, if a large area of the body is suddenly exposed the person may be subject to an anaphylactic reaction. Once free of exposure, the rash will usually fade away within several hours; rare and extreme cases can take a day or two to normalize depending on severity of the reaction.

Polymorphous light eruption (PMLE) is the easiest disease to mistake for solar urticaria because the locations of the lesions are similar (the V of the neck and the arms). However, patients with SU are more likely to develop lesions on the face. Also, a reaction with PMLE will take a greater amount of time to appear than with solar urticaria. Lupus erythematosus has been mistaken for SU; however, lesions from lupus erythematosus will take a longer amount of time to go away. Furthermore, when being tested for the two diseases, patients with SU have a reaction immediately while patients with lupus erythematosus will have a delayed reaction. Patients who have experienced solar urticarial symptoms from a young age could mistakenly be thought to have erythropoietic protoporphyria. However, the main symptom for this disease is pain and patients with have been found to have abnormal levels of protoporphyrin in their blood while these levels are normal in SU patients. Finally, cholinergic urticaria, or urticaria induced by heat, can occasionally appear to be solar urticaria because the heat from the sun will cause a person with the disease to have a reaction.

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.

Dermatographic urticaria manifests as an allergic-like reaction, in general a warm red wheal (welt) to appear on the skin. It can often be confused with an allergic reaction to the object causing the scratch, when in fact it is the act of being scratched that causes a wheal to appear. These wheals are a subset of [urticaria] (hives) that appear within minutes, in some cases accompanied by itching. The first outbreak of urticaria can lead to others on body parts not directly stimulated, scraped, or scratched. In a normal case, the swelling will decrease with no treatment within 15–30 minutes, but, in extreme cases, itchy red welts may last anywhere from a few hours to days.

Id reactions (also known as "disseminated eczema," and "generalized eczema") are types of acute dermatitis developing after days or weeks at skin locations distant from the initial inflammatory or infectious site. They can be localised or generalised. This is also known as an 'autoeczematous response' and there must be an identifiable initial inflammatory or infectious skin problem which leads to the generalised eczema. Often, intensely itchy, the red papules and pustules can also be associated with blisters and scales and are always remote from the primary lesion. It is most commonly a blistering rash with itchy vesicles on the sides of fingers and feet as a reaction to fungal infection on the feet, athlete's foot. Stasis dermatitis, Allergic contact dermatitis, Acute irritant contact eczema and Infective dermatitis have been documented as possible triggers, but the exact cause and mechanism is not fully understood. Several other types of id reactions exist including erythema nodosum, erythema multiforme, Sweet's syndrome and urticaria.

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.

Bullous drug reaction (also known as a "bullous drug eruption", "generalized bullous fixed drug eruption", and "multilocular bullous fixed drug eruption") most commonly refers to a drug reaction in the erythema multiforme group. These are uncommon reactions to medications, with an incidence of 0.4 to 1.2 per million person-years for toxic epidermal necrolysis and 1.2 to 6.0 per million person-years for Stevens–Johnson syndrome. The primary skin lesions are large erythemas (faintly discernible even after confluence), most often irregularly distributed and of a characteristic purplish-livid color, at times with flaccid blisters.

A number of studies have demonstrated adverse reactions in pets after administering vaccines to both dogs and cats. Concern about adverse effects has led to revised guidelines that alter the recommended frequency and methods/locations for both vaccination of dogs and feline vaccination.

Dermatographic urticaria (also known as dermographism, dermatographism or "skin writing") is a skin disorder and one of the most common types of urticaria affecting 2–5% of the population.

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.

Identifying a drug allergy can sometimes be the hardest part. Sometimes drug allergies are confused with nonallergic drug reactions because they both cause somewhat similar reactions. Symptoms of a drug allergy can include, but are not limited to, the following list.

- Hives

- Itching

- Rash

- Fever

- Facial swelling

- Shortness of breath due to the short-term constriction of lung airways or longer-term damage to lung tissue

- Anaphylaxis, a life-threatening drug reaction (produces most of these symptoms as well as low blood pressure)

- Cardiac symptoms such as chest pain, shortness of breath, fatigue, chest palpitations, light headedness, and syncope due to a rare drug-induced reaction, eosinophilic myocarditis