Townsend Letter Article on Possible Mechanisms of Fungus Hypersensitivity
An Arthus reaction. (Image credit: Garland Publishing.)
October 13, 2016
The established alternative medicine journal Townsend Letter published an article on possible mechanisms of fungus hypersensitivities in its April 2016 edition.
The article is called “Fungus Allergy and Hypersensitivity in Mold-Related Illness.” It was written by Alan B. McDaniel, M.D.
Dr. McDaniel summarizes the issues involved:
Fungi (molds, yeasts, etc.) cause immunological inflammation three ways. They can stimulate IgE-mediated immediate hypersensitivity. They also provoke non-IgE late and delayed-type hypersensitivity. Some of them, such as Stachybotrys, will release toxins that directly activate the complement cascade.
Nearly every physician knows about the first of these, though tests usually show that IgE is rather insignificant. The latter is becoming more widely recognized and stimulates discussion of ingenious testing and treatment options. The second – non-IgE immune hypersensitivity – is the most commonly encountered but the least often recognized. Our challenge is learning how to distinguish between these problems.
He described some previous research as follows:
The dispute over defining allergy became so acrimonious that there could be no reconciliation even after 1963, when Gell and Coombs showed that there are at least 4 major types of acquired immune responses. Their four “classical” pathways are:
* type 1 reactions, caused by IgE (hay fever); they occur within minutes and give us protection against parasites;
* type 2 reactions, caused when immunoglobulin types G (IgG) or M (IgM) attach themselves to a foreign protein and provoke the complement cascade; these develop over hours to a day and protect against bacteria and viruses;
* type 3 reactions (Arthus reactions), occurring when IgG binds to a dissolved foreign substance and precipitates as an irritating, inflammatory complex; they occur in hours to a day and offer protection against toxins;
* type 4 reactions, caused by sensitized T-cells; these reactions peak at 48–72 hours (e.g., Tb skin-tests) and protect against bacteria.
Dr. McDaniel then commented:
Delayed type hypersensitivity to fungi was identified and described long ago. However, in keeping with the IgE-orthodoxy, delayed type reactions on skin tests were attributed to “pathogenic fungi” and the immediate type (IgE)-sensitivity was associated with non-pathogenic, or allergenic, fungi. In this author’s experience of recording late and delayed reactions after intradermal tests, the distinction is questionable. It is plausible that Arthus reactions are not “meaningless” – and that the type of sensitivity is what renders the fungus pathogenic, rather than the implied converse.
Dr. Alan McDaniel, M.D.
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