The following is an excerpt from a paper published by Dr. Vincent Marinkovich, an immunologist from Redlands California who died in 2007 of pancreatic cancer.
I hope to include the entire work at a later date. (The introduction makes me think of the salmonella outbreak at the peanut plant.I read recently that there was a leak in the roof at the plant.) At any rate it is one of the best treatises I have seen on the issues surrounding mold exposure.
There is much about the health effects of fungi that is not understood. Exposure to high ambient fungal spore levels in a water damaged home or building is, more likely than not, a mixed bag. Not only are more than one fungal genus likely to be present but bacteria such as Legionella or Actinomycetes may be present in sufficient quantities to add complexity to the resulting symptoms (Fink, 1984). Endotoxins are frequently found in abundance when Gram negative bacteria abound as when sewage is the source of the water (Rylander, 2002). In addition, insects such as mosquito larvae or other mold-feeding insects (mites) may be contributing to the airborne organic particle burden. Even large rodent populations have been discovered in older, run-down, water damaged homes and buildings. All of these can contribute to the disease patterns seen in patients exposed to "fungi" in water-damaged structures.
Innate and Adaptive Immunity
Fungal exposure itself can produce a confounding array of symptoms as different elements of the body’s defense systems are triggered. Early in the course of exposure, the innate immune system can be activated as endotoxins or fungal elements enter the body tissues. This inflammation can proceed without any involvement of the adaptive immune system with its antibodies and activated T-cells (Kauffman, et al, 2000). However, after a few days or weeks of antigen presentation on an inflamed mucosa, the adaptive system is likely to become involved as antibodies and T-cells specifically reactive to fungal antigens are generated. This will add to the inflammation of the affected tissues. And, finally, fungal elements become directly involved if mycotoxins or other inflammatory triggers are formed that can cause toxic injury to specific organ systems. One need only be reminded of such fungal compounds as alcohol, lysergic acid (LSD), antibiotics, cyclosporin or mushroom toxins to appreciate the ability of such organic molecules to cause symptoms.
Physicians who treat patients with mold related problems are often challenged by the variations in the disease symptoms and the multi-organ involvement that are presumably the result of exposure to environments heavily contaminated with fungi. They may accept the likelihood that fungal exposure is the cause of their patient’s symptoms, but not understand the underlying pathophysiology. Still, an attempt is made to treat the patient, essentially by utilizing various programs that remove the patient from the fungi. Over time, they learn that the clinical patterns seen in such patients are consistent, the diagnosis can be accurately made and the response to therapy is very good.
There are other physicians who deny that fungi as encountered in homes or office-type workspaces are capable of causing illness. These physicians generally are not primary care givers and can dismiss the patient’s complaints because of their apparent complexity without a consequence. They are better designated as theorists who base their negativity on arguments that the lack of sufficient evidence-based proof of a causal relationship of fungal exposure to human disease proves that such a relationship is not possible. They dismiss all case reports (Marinkovich et al., 1975) (Fink et al., 1971), epidemiological studies (Dearborne, 2002) (Etzel et al., 1998) and clinical observations of experienced clinicians as worthless and such patients as malingerers or psychiatrically disturbed (Hardin et al., 2003). They seem to lack the vision to accept the challenge of the possibility that injury to multiple organ systems may result from exposure to large amounts of fungal derived materials (such as spores and/or mycotoxins) in a home or office environment. They are wrong and they can do a great deal of harm. First in denying the patient’s symptoms, and secondly by blocking disability requests from such patients injured by exposure to fungi in their workplaces. They are guilty of using poor scientific logic because it is close minded. Such thinking has no place in a medical setting where there are sick patients who need help.
III. Clinically relevant characteristics of fungi:
Fungi are nature’s recyclers. They are extremely abundant in nature, carrying the mandate to reduce all organic matter to its basic constituents. The organisms are armed with several features that allow them to satisfy this mandate. They are microscopic cells which are numerous in all climates where temperatures are above freezing; they exist in two forms, an active, growing form and a dormant, hardy, drought resistant and easily wind-borne form (the spore, also known by the scientific name of conidia). They are superbly versatile and can grow on virtually any wet surface. They secrete their digestive enzymes (Kurup, 2003), digest their environment and absorb their necessary foodstuffs from their immediate, digested environment. Among the products of digestion are toxins (known as mycotoxins because they are derived from fungi), which help them control the potential intrusion of competing organisms into their space. Each of these characteristics plays a role in the disease patterns seen in fungal illness.
The job of fungal spores is to broadcast the organism widely in the environment. They are tiny, lightweight and easily airborne. They are in all natural environments the most prevalent particles in the air at all times. Even at the height of a pollen season, the pollen particles are outnumbered ten to one by fungal spores. The human body is marvelously equipped to deal with such large numbers of potentially infectious particles in the air. The filtering capacity of the nasal mucosa easily removes the larger spores, greater than 10 microns in diameter, from the inspired air. Once trapped on the mucosa, the tiny hairs on mucosal surfaces (cilia) move the particles toward the throat where they are swallowed and destroyed by the acid in the stomach. Some of the smaller spores, less than 10 microns in diameter, may be inhaled into the lungs (Geiser et al., 2000). But even here the normal self-cleansing functions of the lung, which includes its own cilia and mucus production, are mobilized and particles are moved upward and swallowed. A small subset of the tiniest spores, less than three microns in diameter, may be inhaled and trapped in the alveoli and terminal bronchioles beyond the reach of the cilia. They are handled by the scavenger cells in the lungs, the alveolar macrophages.
This is extremely important to understanding the pathophysiology of fungal exposure because once the fungal elements have reached the alveoli they have entered the tissue space from which they can be absorbed into the blood stream.
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