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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
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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).
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Figure
1: Microscopic photo of Memnoniella echinata.
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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.
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Figure
2: Microscopic photo of Stachybotrys chartarum.
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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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