Mold Allergies


The term and concept of “allergy” were coined by a Viennese pediatrician named Clemens von Pirquet in 1906.[1] He observed that the symptoms of some of his patients might have been a response to outside allergens such as dust, pollen, or certain foods. For a long time, all hypersensitivities were thought to stem from the improper action of inflammatory immunoglobulin class IgE. However, it soon became clear that several different mechanisms utilizing different effector molecules were responsible for the myriad of disorders previously classified as “allergies”. A new four-class (now five) classification scheme was designed by P. G. H. Gell and R. R. A. Coombs. Allergy has since been kept as the name for Type I Hypersensitivity, characterized by classical IgE mediation of effects.

Signs and symptoms

Allergy is characterized by a local or systemic inflammatory response to allergens. Local symptoms are:

Nose: swelling of the nasal mucosa (allergic rhinitis)
The distinctive behavior known as a nasal salute, also known as allergy salute, is the habit of wiping of the nose in an upward direction due to itching.
Eyes: redness and itching of the conjunctiva (allergic conjunctivitis)
Airways: bronchoconstriction, wheezing, and dyspnoea, sometimes outright attacks of asthma
Ears: a feeling of fullness, possibly pain, and impaired hearing due to the lack of eustachian tube drainage.
Skin: various rashes, such as eczema, hives (urticaria) and contact dermatitis.
Head: while not as common, headaches are seen in some with environmental or chemical allergies.

Allergic Response

The systemic allergic response is also called anaphylaxis. Depending on the rate of severity, it can cause cutaneous reactions, bronchoconstriction, edema, hypotension, coma and even death. Hay fever is one example of an exceedingly common minor allergy — large percentages of the population suffer from hayfever symptoms in response to airborne pollen. Asthmatics are often allergic to dust mites. Apart from ambient allergens, allergic reactions can be due to medications.


There are several methods for the diagnosis and assessment of allergies.

Skin test: The typical and most simple method of diagnosis and monitoring of Type I Hypersensitivity is by skin testing, also known as prick testing due to the series of pricks made into the patient’s skin. Small amounts of suspected allergens and their extracts (pollen, grass, mite proteins, peanut extract, etc.) are introduced to sites on the skin marked with pen or dye (the ink/dye should be carefully selected, lest it causes an allergic response itself). The allergens are either injected intradermally or into small scratchings made into the patient’s skin, often with a lancet. Common areas for testing include the inside forearm and back. If the patient is allergic to the substance, then a visible inflammatory reaction will usually occur within 30 minutes. This response will range from slight reddening of the skin to full-blown hives in extremely sensitive patients. After performing the skin test and receiving results, the doctor may apply a steroid cream to the test area to reduce discomfort (such as itching and inflammation).

Problems with skin test

While the skin test is probably the most preferred means of testing because of its simplicity and economics, it is not without complications. Some people may display a delayed-type hypersensitivity (DTH) reaction which can occur as far as 6 hours after application of the allergen and last up to 24 hours. This can also cause serious long-lasting tissue damage to the affected area. These types of serious reactions are quite rare. Additionally, the application of previously unencountered allergens can sensitize certain individuals to the allergen, causing the inception of a new allergy in susceptible individuals. Skins tests also are not always able to pinpoint a patient’s specific allergies if the patient has an allergy but does not react to the skin test allergen.

Total IgE count

Another method used to qualify type I hypersensitivity is measuring the amount of serum IgE contained within the patient’s serum. This can be determined through the use of radiometric and colorimetric immunoassays. Even the levels the amount of IgE specific to certain allergens can be measured through the use of the radioallergosorbent test (RAST).


There are limited mainstream medical treatments for allergies. Probably the most important factor in rehabilitation is the removal of sources of allergens from the home environment and avoiding environments in which contact with allergens is likely.


Hyposensitization is a form of immunotherapy where the patient is gradually vaccinated against progressively larger doses of the allergen in question. This can either reduce the severity or eliminate hypersensitivity. It relies on the progressive skewing of IgG (“the blocking antibody”) production, as opposed to the excessive IgE production seen in hypersensitivity type I cases. Delivery can occur via allergy injection, or sublingual immunotherapy, allergy drops taken under the tongue. Though not commonly offered in the U.S., sublingual immunotherapy is gaining attention internationally.  The second form of immunotherapy involves the intravenous injection of monoclonal anti-IgE antibodies. These bind to free and B-cell IgE signaling such sources of destruction. They do not bind to IgE already bound to the Fc receptor on basophils and mast cells as this would stimulate the allergic inflammatory response. The first agent in this class is omalizumab. An experimental treatment form, potentiated enzyme desensitization, has been tried with some success but is not in widespread use. EPD uses dilutions of allergen and an enzyme, beta-glucuronidase, to which T-regulatory lymphocytes respond by favoring desensitization, or down-regulation, rather than sensitization. EPD is also under development for the treatment of autoimmune diseases.