Causes of Allergic bronchopulmonary aspergillosis
List of causes of Allergic bronchopulmonary aspergillosis
Following is a list of causes or underlying conditions
(see also Misdiagnosis of underlying causes of Allergic bronchopulmonary aspergillosis)
that could possibly cause Allergic bronchopulmonary aspergillosis includes:
More causes:
see full list of causes for Allergic bronchopulmonary aspergillosis
Causes of Allergic bronchopulmonary aspergillosis (Diseases Database):
The follow list shows some of the possible medical causes of Allergic bronchopulmonary aspergillosis
that are listed by the Diseases Database:
Source: Diseases Database
Allergic bronchopulmonary aspergillosis Causes: Book Excerpts
Allergic bronchopulmonary aspergillosis as a complication of other conditions:
Other conditions that might have
Allergic bronchopulmonary aspergillosis as a complication may,
potentially, be an underlying cause of Allergic bronchopulmonary aspergillosis.
Our database lists the following as having
Allergic bronchopulmonary aspergillosis as a complication of that condition:
Related information on causes of Allergic bronchopulmonary aspergillosis:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Allergic bronchopulmonary aspergillosis may be found in:
Causes of Allergic bronchopulmonary aspergillosis: Online Medical Books
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Review excerpts from medical books online, free, without registration,
for more information about the causes of Allergic bronchopulmonary aspergillosis.
Aspergillosis:
Causes
(Professional Guide to Diseases (Eighth Edition))
Aspergillus is found worldwide, commonly in decaying vegetation, such as fermenting compost piles and damp hay. It's transmitted by inhalation of fungal spores or, in aspergillosis endophthalmitis, by the invasion of spores through a wound or other tissue injury. It's a common laboratory contaminant.
Aspergillus produces clinical infection only in people who become especially vulnerable to it. Such vulnerability can result from excessive or prolonged use of antibiotics, glucocorticoids, or other immunosuppressive agents; from radiation; from such conditions as acquired immunodeficiency syndrome, Hodgkin's disease, leu-kemia, azotemia, alcoholism, sarcoidosis, bronchitis, or bronchiectasis; from organ transplants; and, in aspergilloma, from tuberculosis or another cavitary lung disease.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Allergic purpuras:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The most common identifiable cause of allergic purpura is probably an autoimmune reaction directed against vascular walls, triggered by a bacterial infection (particularly streptococcal infection). Typically, upper respiratory tract infection occurs 1 to 3 weeks before the onset of symptoms. Other possible causes include allergic reactions to some drugs and vaccines, to insect bites, and to some foods (such as wheat, eggs, milk, and chocolate).
Allergic purpura affects more males than females and is most prevalent in children ages 3 to 7. The prognosis is more favorable for children than adults.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
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
Aspergillosis:
Causes
(Handbook of Diseases)
Aspergillus is found worldwide, commonly in fermenting compost piles and damp hay. It’s transmitted by inhalation of fungal spores or, in aspergillosis endophthalmitis, by the invasion of spores through a wound or other tissue injury.
Aspergillus produces infection only in persons who become especially vulnerable to it. Such vulnerability can result from excessive or prolonged use of antibiotics, glucocorticoids, or other immunosuppressants; from radiation; from such conditions as acquired immunodeficiency syndrome, Hodgkin’s disease, leukemia, azotemia, alcoholism, sarcoidosis, bronchitis, or bronchiectasis; from organ transplants; and, in aspergilloma, from tuberculosis or another cavitary lung disease.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Allergic purpura:
Causes
(Handbook of Diseases)
The most common identifiable cause of allergic purpura is probably an autoimmune reaction directed against vascular walls, triggered by a bacterial infection (particularly streptococcal infection). Typically, an upper respiratory tract infection occurs 1 to 3 weeks before the onset of symptoms. Other possible causes include allergic reactions to some drugs and vaccines, allergic reactions to insect bites, and allergic reactions to some foods (such as wheat, eggs, milk, and chocolate).
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Coccidioido-mycosis:
Causes
(Handbook of Diseases)
Coccidioidomycosis is endemic to the southwestern United States, especially between the San Joaquin Valley in California and southwestern Texas. It’s also found in Mexico, Guatemala, Honduras, Venezuela, Colombia, Argentina, and Paraguay.
It may result from inhalation of C. immitis spores found in the soil in these areas or from inhalation of spores from dressings or plaster casts of infected persons. It’s most prevalent during warm, dry months.
Because of population distribution and an occupational link (it’s common in migrant farm laborers), coccidioidomycosis generally affects Filipino Americans, Mexican Americans, Native Americans, and Blacks. With primary infection, the incubation period is from 1 to 4 weeks.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Aspergillosis:
Aspergillosis - risk factors
(The 5-Minute Pediatric Consult)
- Other than those with otomycosis or allergic bronchopulmonary disease, most patients infected with Aspergillus are immunocompromised in some way. Patients at risk include those with malignancy, solid-organ transplantation, bone marrow transplantation, HIV, and congenital immunodeficiencies.
- Transplantation, solid-organ transplantation
Aspergillosis - pathophysiology
- The most common portal of entry for Aspergillus is the respiratory tract; however, damaged skin or operative wounds, the cornea, and the ear can also serve as sites of entry.
- The development of disease depends on the interaction between the organism (virulence) and the host, specifically host defense mechanisms.
- Aspergillus produces toxic metabolites such as elastase, cytotoxins, endotoxins, phospholipases, and various inhibitors of immune function.
- Aspergillus is an unusual pathogen in immunocompetent patients. The first line of defense in the lungs is the macrophages. Neutrophils are also a key part of the host defense against Aspergillus.
- Conditions that alter the normal immunologic mechanisms predispose to invasive aspergillosis; leukemia (neutropenia), corticosteroids (decreased neutrophil mobilization and macrophage killing), chronic granulomatous disease (decreased oxidative-mediated killing)
Aspergillosis - etiology
Aspergillus sp., most commonly Aspergillus fumigatus
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
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