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Causes of Insect sting allergies

Contents
  1. Insect sting allergies: Introduction
  2. Excerpts from book chapters
  3. Related cause information

Insect sting allergies Causes: Book Excerpts

Related information on causes of Insect sting allergies:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Insect sting allergies may be found in:

Causes of Insect sting allergies: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Insect sting allergies.

Urticaria: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Idiopathic urticaria without angioedema
    –Most common diagnosis in patients with hives
    –Often related to food or drug allergies, bites, or stings
    –25% of patients with one episode will progress to chronic urticaria
  • Chronic urticaria
    –Idiopathic in 50% of cases
    –Chronic idiopathic urticaria spontaneously resolves within 2 years in 80% of patients
    –Criterion for chronic urticaria is duration of more than 6 weeks
  • Occult infection (e.g., sinusitis, oral infection, cholecystitis, vaginitis, prostatitis, hepatitis, HIV, tinea manus or pedis)
  • Malignancy
  • Thyroid disease
  • Drugs (e.g., radiocontrast media, penicillin, salicylates, benzoates, azo dyes)
    –May result in life-threatening episodes of urticaria and acute angioedema that can lead to anaphylaxis
  • Urticaria secondary to physical stimuli [e.g., exercise (cholinergic), vibratory pressure, sun exposure (solar urticaria), cold exposure]
    –Dermographism occurs in 5% of the population; manifests as a physical urticaria that arises in the distribution line of a scratch or rubbed skin area
  • Hereditary or acquired deficiency of complement factor C1
    –Generally appears as episodic angioedema in the absence of urticaria
    –Only in the absence of urticaria should hereditary or acquired complement deficiency be considered
  • Angioedema-urticaria-eosinophilia syndrome
    –Associated with elevated serum IgE, fever, and fluid retention during an acute attack
  • Urticarial vasculitis
    –Presents as urticaria that lasts longer than 12–24 hours
    –Associated with autoimmune disease (e.g., systemic lupus erythematosus)
  • Cutaneous mastocytosis/urticaria pigmentosa

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Urticaria: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Urticaria
    –Epidemiology: Lifetime incidence 20%; most cases resolve within 48 hours; chronic >6 weeks
    –Pathophysiology: Hypersensitivity reaction: allergens (IgE-mediated, prior sensitization), complement, and other cytokines activate mast cells and basophils to release histamine (also kinins, prostaglandins, serotonin) with plasma extravasation; wheals/hives: dermis edema
    –Triggers: Most cases are idiopathic
    –IgE-mediated: Insects (bees, wasps, scorpions, spiders, jellyfish), foods (eggs, shellfish, tree nuts, peanuts, tomatoes), drugs (penicillins, cephalosporins, NSAIDs, barbiturates, amphetamines, insulin, blood products), pollen, danders, food additives
    –Non-IgE-mediated: Infections (strep, EBV; hepatitis A, B, and C; adenovirus, enterovirus; fleas, mites), drugs (opiates, acetylsalicylic acid, local anesthetics), physical (exercise, cold/heat, UV light, water, pressure), contrast dyes, latex
  • Chronic urticaria: Associated with collagen vascular diseases (SLE, cryoglobulinemia), inflammatory bowel disease, malignancy, thyroiditis, hyperthyroidism, Behçet disease, vasculitis
  • Angioedema: 50% of urticaria cases; subcutaneous and mucous membrane edema
  • Anaphylaxis (IgE-mediated)
    –Most potent foods: Peanuts, fish
    –Mortality: 100–500 deaths/year in U.S.
    –Associated shock has a poor prognosis
    • Hereditary angioedema
      –High mortality
      –Most cases are autosomal dominant
      –C1 esterase inhibitor deficiency
      –Recurrent episodes of edema (face, upper airway, extremities)
      –Triggers: Trauma, surgery
      –Unresponsive to epinephrine, antihistamines
  • Others: Erythema multiforme, mastocytosis, guttate psoriasis, flushing, cellulitis

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Urticaria [Hives]: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Anaphylaxis

Anaphylaxis — an acute reaction — is marked by the rapid eruption of diffuse urticaria and angioedema, with wheals ranging from pinpoint to palm-size or larger. Lesions are usually pruritic and stinging; paresthesia commonly precedes their eruption. Other acute findings include profound anxiety; weakness; diaphoresis; sneezing; shortness of breath; profuse rhinorrhea; nasal congestion; dysphagia; and warm, moist skin.

Hereditary angioedema

With hereditary angioedema — an autosomal dominant disorder — cutaneous involvement is manifested by nonpitting, nonpruritic edema of an extremity or the face. Respiratory mucosal involvement can produce life-threatening acute laryngeal edema.

Lyme disease

Although not diagnostic of Lyme disease — a tick-borne disease — urticaria may result from the characteristic skin lesion (erythema chronicum migrans). Later effects include constant malaise and fatigue, intermittent headache, fever, chills, lymphadenopathy, neurologic and cardiac abnormalities, and arthritis.

Other causes

Drugs

Drugs that can produce urticaria include aspirin, codeine, dextrans, immune serums, insulin, morphine, penicillin, quinine, sulfonamides, and vaccines.

Radiographic contrast medium

Radiographic contrast medium, especially when administered I.V., commonly produces urticaria.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Urticaria and angioedema: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Urticaria and angioedema are common allergic reactions that may occur in 20% of the general population. The causes of these reactions include allergy to drugs, foods, insect bites and stings and, occasionally, inhalant allergens (animal dander and cosmetics) that provoke an immunoglobulin (Ig) E-mediated response to protein allergens. However, certain drugs may cause urticaria without an IgE response. When urticaria and angioedema are part of an anaphylactic reaction, they almost always persist long after the systemic response has subsided. This occurs because circulation to the skin is the last to be restored after an allergic reaction, which results in slow histamine reabsorption at the reaction site.

Nonallergic urticaria and angioedema are also related to histamine release. External physical stimuli, such as cold (usually in young adults), heat, water, or sunlight, may also provoke urticaria and angioedema. Dermographism urticaria, which develops after stroking or scratching of the skin, occurs in as much as 20% of the population. Such urticaria develops with varying pressure, usually under tight clothing, and is aggravated by scratching.

Several different mechanisms and underlying disorders may provoke urticaria and angioedema. These include IgE-induced release of mediators from cutaneous mast cells; binding of IgG or IgM to antigen, resulting in complement activation; and such disorders as localized or secondary infections (such as respiratory infection), neoplastic diseases (such as Hodgkin’s disease), connective tissue diseases (such as systemic lupus erythematosus), collagen vascular diseases, and psychogenic diseases.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Urticaria [Hives]: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Anaphylaxis

This life-threatening reaction is marked by the rapid eruption of diffuse urticaria and angioedema, with wheals ranging from pinpoint to palm-size or larger. Lesions are usually pruritic and stinging and preceded by paresthesia. Other acute findings include profound anxiety, weakness, diaphoresis, sneezing, shortness of breath, profuse rhinorrhea, nasal congestion, dysphagia, and warm, moist skin.

Lyme disease

Urticaria may result from the characteristic skin lesion (erythema chronicum migrans) produced by this tick-borne disease. Later effects include constant malaise and fatigue, intermittent headache, fever, chills, lymphadenopathy, neurologic and cardiac abnormalities, and arthritis.

Other causes

Drugs

Many drugs can produce urticaria. Among the most common are aspirin, atropine, codeine, dextrans, immune serums, insulin, morphine, penicillin, quinine, sulfonamides, and vaccines. In addition, radiographic contrast media commonly produce urticaria, especially when administered I.V.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Urticaria/Angioedema: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Ingestants

❑ Drugs

❑ Inhalants

❑ Hymenoptera venom

❑ Latex sensitivity

❑ Dermatographism

❑ Pressure urticaria

❑ Cholinergic urticaria

❑ Cold urticaria

❑ Solar urticaria

❑ Infection

❑ Urticarial vasculitis

❑ Hereditary angioedema

❑ Mastocytosis

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

anaphylaxis: Causes
(Handbook of Diseases)

The causes of anaphylactic reaction are ingestion of or other systemic exposure to a sensitizing drug or other substance.

Sensitizing substances

Sensitizing substances include serums (usually horse serum), vaccines, allergen extracts, enzymes (such as l-asparaginase), hormones, penicillin and other antibiotics, sulfonamides, local anesthetics, salicylates, polysaccharides, diagnostic chemicals (sulfobromophthalein, sodium dehydrocholate, and radiographic contrast media), foods (legumes, nuts, berries, seafood, and egg albumin) and sulfite-containing food additives, and insect venom (honeybees, wasps, hornets, yellow jackets, fire ants, mosquitoes, and certain spiders).

A common cause of anaphylaxis is penicillin, which induces anaphylaxis in 1 to 4 of every 10,000 patients treated with it. Penicillin is most likely to induce anaphylaxis after parenteral administration or prolonged therapy and in atopic patients who are allergic to other drugs or foods.

Pathophysiology

An anaphylactic reaction requires previous sensitization or exposure to the specific antigen, resulting in the production of specific immunoglobulin (Ig) E  antibodies by plasma cells. This antibody production takes place in the lymph nodes and is enhanced by helper T cells. IgE antibodies then bind to membrane receptors on mast cells (found throughout connective tissue, often near small blood vessels) and basophils.

On reexposure, the antigen binds to adjacent IgE antibodies or cross-linked IgE receptors, activating a series of cellular reactions that trigger degranulation — the release of powerful preformed chemical mediators (such as histamine, prostaglandins, and platelet activating factor) from mast cell stores. IgG or IgM enters into the reaction and activates the release of complement fractions.

This acute phase of the response occurs within minutes of exposure. Because of the systemic nature of the exposure, activation of mast cells is widespread, and the massive release of these powerful mediators near blood vessels leads to vascular collapse by stimulating contraction of certain groups of smooth muscles and by increasing vascular permeability. In turn, increased vascular permeability leads to decreased peripheral resistance and plasma leakage from the circulation to extravascular tissues (which lowers blood volume, causing hypotension, hypovolemic shock, and cardiac dysfunction).

In the later phase of this response (8 to 12 hours later), other mediators are synthesized and released, including chemokines, leukotrienes, and cytokines. These agents mediate the inflammatory response by recruiting eosinophils and lymphocytes. This delayed response may be less dramatic than the acute phase of anaphylaxis, but with a diffuse inflammatory response, further smooth-muscle contraction and edema can occur and progress to grave systemic symptoms.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Urticaria and angioedema: Causes
(Handbook of Diseases)

Urticaria and angioedema are common allergic reactions. Causes include allergy to drugs, foods, insect stings and, occasionally, inhalants, such as animal dander and cosmetics, that provoke an immunoglobulin (Ig) E-mediated response to protein allergens. However, certain drugs may cause urticaria without an IgE response.

When urticaria and angioedema are part of an anaphylactic reaction, they almost always persist long after the systemic response has subsided. This occurs because circulation to the skin is inhibited after an allergic reaction, which results in slow histamine reabsorption at the reaction site. Nonallergic urticaria and angioedema are probably also related to histamine release.

External physical stimuli, such as cold (usually in young adults), heat, water, or sunlight, may provoke urticaria and angioedema. Dermographism urticaria develops with varying pressure, usually under tight clothing, and is aggravated by scratching.  

Several different mechanisms and underlying disorders may provoke urticaria and angioedema. These include IgE-induced release of mediators from cutaneous mast cells; binding of IgG or IgM, resulting in complement activation; localized or secondary infections such as respiratory infection; neoplastic diseases such as Hodgkin’s disease; connective tissue diseases such as systemic lupus erythematosus; collagen vascular diseases; and psychogenic diseases.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Urticaria: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Anaphylaxis

An acute reaction, anaphylaxis is marked by the rapid eruption of diffuse urticaria and angioedema, with wheals ranging from pinpoint to palm-size or larger. Lesions are usually pruritic and stinging; paresthesia commonly precedes their eruption. Other acute findings include profound anxiety, weakness, diaphoresis, sneezing, shortness of breath, profuse rhinorrhea, nasal congestion, dysphagia, and warm, moist skin.

Hereditary angioedema

An autosomal dominant disorder, cutaneous involvement is manifested by nonpitting, nonpruritic edema of an extremity or the face. Respiratory mucosal involvement can produce life-threatening acute laryngeal edema.

Lyme disease

Although not diagnostic of this tick-borne disease, urticaria may result from the characteristic skin lesion (erythema chronicum migrans). Later effects include constant malaise and fatigue, intermittent headache, fever, chills, lymphadenopathy, neurologic and cardiac abnormalities, and arthritis.

Other causes

Drugs

Many drugs can cause urticaria; the most common include aspirin, atropine, codeine, dextran, immune serums, insulin, morphine, penicillin, quinine, sulfonamides, and vaccines. In addition, radiographic contrast medium commonly produces urticaria, especially when administered intravenously.

» READ BOOK EXCERPT ONLINE »

Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Urticaria: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Anaphylaxis

Anaphylaxis is marked by the rapid eruption of diffuse urticaria and angioedema, with wheals ranging from pinpoint to palm-size or larger. Lesions are usually pruritic and stinging; paresthesia commonly precedes their eruption. Other acute findings include profound anxiety; weakness; diaphoresis; sneezing; shortness of breath; profuse rhinorrhea; nasal congestion; dysphagia; and warm, moist skin.

Hereditary angioedema

Hereditary angioedema is an autosomal dominant disorder in which cutaneous involvement is manifested by nonpitting, nonpruritic edema of an extremity or the face. Respiratory mucosal involvement can produce life-threatening acute laryngeal edema.

Lyme disease

Although not diagnostic of this tick-borne disease, urticaria may result from the characteristic skin lesion (erythema chronicum migrans). Later effects of Lyme disease include constant malaise and fatigue, intermittent headache, fever, chills, lymphadenopathy, neurologic and cardiac abnormalities, and arthritis.

Other causes

Drugs

Many drugs can produce urticaria. Among the most common are aspirin, atropine, codeine, dextrans, immune serums, insulin, morphine, penicillin, quinine, sulfonamides, and vaccines. In addition, radiographic contrast medium commonly produces urticaria, especially when administered I.V.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Urticaria [Hives]: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Anaphylaxis.Anaphylaxis—an acute allergic reaction—is marked by the rapid eruption of diffuse urticaria and angioedema, with wheals ranging from pinpoint to palm-size or larger. Lesions are usually pruritic and stinging; paresthesia commonly precedes their eruption. Other acute findings include profound anxiety, weakness, diaphoresis, sneezing, shortness of breath, profuse rhinorrhea, nasal congestion, dysphagia, and warm, moist skin.

Hereditary angioedema.With hereditary angioedema, cutaneous involvement is manifested by nonpitting, nonpruritic edema of an extremity or the face. Respiratory mucosal involvement can produce life-threatening acute laryngeal edema.

Lyme disease.Although not diagnostic of Lyme disease, urticaria may result from the characteristic skin lesion (erythema chronicum migrans). Later effects include constant malaise and fatigue, intermittent headache, fever, chills, lymphadenopathy, neurologic and cardiac abnormalities, and arthritis.

Other causes

Drugs.Drugs that can produce urticaria include aspirin, codeine, dextrans, immune serums, insulin, morphine, penicillin, quinine, sulfonamides, and vaccines.

Radiographic contrast medium.Radiographic contrast medium, especially when administered I.V., commonly produces urticaria.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Mammalian Bites: Mammalian Bites - pathophysiology
(The 5-Minute Pediatric Consult)

Animal bites:

  • Crush-and-tear injuries can result from dog maulings, sometimes involving bone.
  • Cat bites are generally puncture-type wounds, penetrating deeper and carrying a higher risk of infection.
  • Human bites generally only violate skin, although penetration into joint and tendon sheath spaces can occur (especially bites overlying the metacarpal-phalangeal areas).
  • Reports of rates of infectious complications have yielded varying results. Early studies report that infection occurs in 3–18% of dog bites, 28–80% of cat bites, and 15–20% of human bites. Studies that are more recent have suggested an incidence of infection after dog and cat bites to be closer to 2–3%.
  • Bacteriologic analysis of infected animal and human wounds demonstrate polymicrobial cause, most commonly mixed aerobic and anaerobic species. Pasteurella species are the most frequent isolates from both dog bites (Pasteurella canis) and cat bites (Pasteurella multocida and Pasteurella septica).
  • Common anaerobes include Fusobacterium, bacterioids, Porphyromonas, and Prevotella.
  • For infected human bites, bacterial isolates include Streptococcus anginosus, Staphylococcus aureus, Eikenella corrodens, and Fusobacterium and Prevotella species.

Mammalian Bites - etiology

  • Animal bites:
    • Dogs
    • Cats
    • Rodents
    • Wild animals
  • Human bites

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008

Snake and Insect Bites: Snake and Insect Bites - pathophysiology
(The 5-Minute Pediatric Consult)

  • Snake bites:
    • Although there are ~120 snake species in the US, only 15% envenomate substances are capable of causing fatal reactions.
    • Snake venom consists of numerous enzymes and polypeptides that are neurotoxic, cytotoxic, and hemotoxic.
    • Pit viper venom produces significant local inflammation, injury to the vascular endothelium, and may lead to coagulopathy, thrombocytopenia, and shock.
    • The venom of the coral snake is primarily neurotoxic and may produce neuromuscular paralysis and respiratory depression.
  • Spider bites:
    • Most of 20,000 species of predominantly venomous spiders in the US lack fangs capable of penetrating human skin or toxin strong enough to produce more than a mild reaction. The black widow and brown recluse spiders can cause significant harm, however.
    • The black widow venom, α-atrotoxin, is a neurotoxin that stimulates myoneural junctions and nerve terminals by increasing synaptic release of acetylcholine and by initiating a massive influx of calcium causing severe skeletal muscle pain and cramping, and autonomic disturbances such as hypertension and sweating.
    • The brown recluse venom, mainly sphingomyelinase D, acts on RBC membranes, platelets, endothelial cells, and other cells, resulting in tissue infarction and necrosis. It causes the destruction of tissues at the site of the envenomation and triggers coagulopathy. Systemic symptoms are more likely to occur in children, presumably due to a smaller ratio of body weight to venom volume. Hemolysis, hemoglobinuria, disseminated intravascular coagulation, shock, seizures, and death rarely may occur.
  • Insect stings:
    • The fire ant bites with its jaws, and then swings its head around to inflict multiple stings. The venom has a direct toxic effect on mast cell membranes, causing an immediate wheal-and-flare reaction at the bite site.
    • The venoms of the bee, hornet, yellow jacket, and wasp contain antigens that trigger an IgE antibody response, resulting in allergic reactions that vary in severity from mild local effects to profound anaphylactic reactions.

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008


 » Next page: Symptoms of Insect sting allergies

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