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December 2005

Volume 3 | Issue 12

Hello hello,

I hope you're enjoying the holiday season and will have a great year in 2006. I also hope that you'll find the attached articles both interesting and helpful. The first is about our immune system and allergic response. The second is about the fungi Memnoniella, and was written by one of our analysts, Priyuni Patel.

With best wishes,
Dave Gallup
Chairman


The Immune Response and Allergies
By: Dave Gallup

Introduction
Janet Gallup, EMLab's founder, worked for decades, often without a biosafety hood, with her nose a few inches from open Petri dishes covered with fungal growth. To this day, she shows no observable symptoms to either these past exposures, or to any current exposure. Others, like myself, Janet Gallup's son, have asthma attacks when exposed to some molds, but not others. Some people, for budget reasons, move into a low cost apartment that has mold growth on a wall and say that it doesn't bother them. Two years later, they have difficulty breathing in that same apartment. Our immune system is at work in all of these scenarios and a little understanding, while possibly dangerous, I find both interesting and helpful. It also may relate to a new remediation worker who says "Molds don't bother me, I don't need all of this protective gear."

Our immune system is very complex and a lot is not understood. Consequently, it would be naive to propose that it can be covered to any level of depth in such a short article. However, I do think that useful information can be communicated provided that we realize it is superficial in nature.

The innate immune system
How our immune system works can be broken into two big buckets. The innate immune system and the acquired immune system. The innate system is present at birth, is non-specific, and does not learn, have memory, or improve with repeated exposure to foreign or threatening bodies. This system would include things like physical barriers such as our skin or mucous membranes, antibacterial substances in secretions, the low pH of our stomachs, coughing, and vomiting. It also includes some specialized cells, such as Mast cells, who are capable of eliminating micro-organisms.

The acquired immune system
The other "big bucket" is the acquired immune system. This system is adaptive and specific. Our immune system learns to recognize and respond to previously unseen molecules or foreign bodies. This is the system that vaccines make use of to teach our bodies to respond quickly and strongly against agents like Chicken Pox.

Sensitization
The first step in an acquired immune response is called "sensitization." Really, it is just the immune system teaching itself what this foreign body looks like and preparing itself to react quickly and strongly to it if it sees it again in the future. Since allergies are an acquired response, note the implications of the preceding sentence. It implies that nobody is born allergic to a substance. They must first be exposed, and then, if they are genetically disposed, they may have reactions to subsequent exposures. How much a person must be exposed to, and the lag time between this initial exposure and future allergic responses with subsequent exposures is not well understood and, in some cases, controversial. It does, however, help explain why a person moving to a new region of the country, moving into a moldy apartment, or just starting out as a remediator, may not observe an allergic response initially, but may observe symptoms later, sometimes much later (years).

The process of sensitization, as you may imagine, is quite involved. There are many specific cells involved and a variety of information transfers. Essentially, when certain cells in the immune system, macrophages and B cells, see a foreign body, such as a bacteria or a spore, they gobble it up and break down the proteins (antigens) into short sections of proteins (called peptides). They then "show" these peptides on their surfaces. If another cell of the immune system, a T-cell, notices that both the macrophage and the B-cell are showing the same peptide, then the T-cell tells the
B-cell to both begin reproducing itself and to begin making antibodies. Production of these antibodies marks the completion of "sensitization" and may take a few weeks to show up in the blood stream after the initial exposure.

Re-exposure
These antibodies, and there are a variety of them, stay in the body for a long time and the body is now tuned to recognize that specific foreign body. If we are later exposed to that same specific foreign body, then the immune system responds by producing new antibodies in higher quantities and more quickly than with the first exposure. Some of these antibodies enable white blood cells to recognize and attack the invading bacteria or foreign body. One of these antibodies is called IgE and causes what we commonly call an "allergic" response. Some people will develop IgE to proteins in fungal spores, various pollens, dust mites, and other irritants. Some people will not. The exact reason for this difference is not well understood and is some combination of genetics and the environment. In any case, an IgE response often leads to typical symptoms of asthma, allergic skin disease, or other allergies. IgE was discovered around 1967 and most skin tests look for IgE antibodies. IgE is thought to have evolved as a defense against parasites since most allergic reactions take place in major sites of parasitic invasion such as the skin and respiratory tract. Additionally, the allergic reactions of tear production (watery eyes), mucus secretion (runny noses), sneezing, itching, etc. are also a means of expelling allergic proteins from the body.

Conclusion
An allergic response is the most common health effect related to fungal exposures that most IAQ investigators will encounter. The development of an allergic response depends upon the genetic make up of the individual exposed as well as their environment. The development of an allergic response may take years and is hard to predict. Some meaningful percentage of the population, often quoted as between 5 and 10%, are capable of developing an allergic response to fungi. Given these facts, it makes sense to keep environments free of indoor sources of fungal exposure and for individuals who routinely are exposed to high quantities to wear some form of protection so they do not start down the path towards an "IgE mediated response."

References
http://www.micro.msb.le.ac.uk/mbchb/1b.html http://www.cellsalive.com/antibody.htm http://www.worldallergy.org/professional/allergic_diseases_center/ige/ige_pf.html


Fungus of the month: Memnoniella
By: Priyuni Patel

The genus Memnoniella has worldwide distribution. It has been isolated from soil in tropical countries, cellulosic material like paper, wallpaper, cotton, textile, dead plant material. This fungus lacks a known sexual state and has consequently been placed in the Fungi Imperfecti. It is generally classified as a demateaceous (dark-walled) fungus.

There are very few species in this genus. Memnoniella is very well known in that it utilizes cellulose as major carbon source. It can be easily grown on commercially available cornmeal agar, Cellulose agar, and malt extract agar. The most commonly encountered species in indoor environments is M. echinata. This species has been isolated from air as well as surfaces. Similar to Stachybotrys species, Memnoniella species are also slow growing on artificial media and natural substrates. Because of this slow growth, faster growing fungi such as Penicillium, Aspergillus, Trichoderma, or Rhizopus can easily overgrow this fungus.

Identification of Memnoniella can be done easily in culture. Colonies are black, velvety or powdery, and can reach up to 4 cm in diameter in 3 weeks. The reverse side of colonies are yellowish brown to grayish. The sporulating structures are up to 220 μm long, unbranched, straight, solitary or in groups, the basal cell slightly inflated and hyaline or grayish at first, sometimes more or less smooth throughout, Spores (conidia) are simple, spherical or subspherical, attached to one another by common septum (cross wall) in long persistent chains, at first hyaline and smooth-walled. At maturity, colonies become black in color resembling Stachybotrys colonies. It is important to note that the most striking taxonomic character is the production of conidia (spores) in chains (see Fig. 1).

Figure 1: Microscopic photo of Memnoniella echinata.

The latter morphological character distinctly separates this genus from Stachybotrys in which the spores are produced in a gelatinous mass and not in chains (see Fig. 2) like Memnoniella.

Figure 2: Microscopic photo of Stachybotrys chartarum.

It is noteworthy that a few recent DNA studies suggested that the two genera might closely be related to one another; however, the molecular evidence does not strongly support such a close relationship and the two genera continue to remain separated.

M. echinata is occasionally recovered from indoor air. Since the spores of this fungus are dry, they can easily become airborne. If they are recovered on spore trap samples, the spores are often in distinct chains and are readily identified. Individual spores; however, are difficult to identify alone and may be confused with spores produced by Aspergillus niger, spores of which would typically be grouped as Penicillium/ Aspergillus type spores.

In direct microscopic examination, Memnoniella is usually identified easily. Generally, identification of this fungus on tape-lifts and bulk samples are much easier than on swab samples. The fungal structures, including the chains of spores, are easily broken a part during swab sampling, making it difficult to identify this fungus.



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