Stages of Mycotoxicosis. The following is an article by Dr. William Croft

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Stages of Mycotoxicosis
Our official diagnosis is mycotoxicosis. The following is an article by Dr. William Croft (website http://www.edgi.org/).

Stages of Mycotoxicosis: For Inhalation of Mycotoxin

The three Stages (1-3) ranging from lower to higher severity of poisoning were modified according to exposure via the air as opposed to ingestion already established (Forgacs et al., 1962; Joffe, 1971). A separate Stage of convalescence occurs when a patient is completely removed from the contaminated premises and the source of mycotoxin or mold spores.

Stage 1: The primary changes are in the brain, respiratory and immune systems, mucus membranes and gastrointestinal tract. Signs and symptoms may include burning sensation in the mouth, tongue, throat, palate, esophagus, and stomach, which is a result of the action of the toxin on the mucous membranes and skin in the exposed areas. Moist areas of the body armpits, under breasts, belt line and groin are more sensitive or first affected. Patients may report burning within the eyes, ears and nose. Patients also reported that their tongues felt swollen and stiff. Mucosa of the oral cavity may be hyperemic. Mild gingivitis, stomatitis, glositis, and esophagitis developed. Inflammation, in addition to gastric and (small and large) intestinal mucosal, resulted in vomiting, diarrhea and abdominal pain. Excessive salivation, headache, dizziness, weakness, fatigue and tachycardia were also present.

There may be fever and sweating. The respiratory system develops burning sensations and congestion. Severe exposure to mycotoxin within the lungs may lead to congestion, edema and failure, due to caustic action. Body temperature remains normal and controllable by the patient. The poisoning appears and disappears relatively quickly in this Stage with the exception of, lungs and central nervous system. Initially (Stage 1), the patient’s symptoms are very uncomfortable or painful. As the poisoning continues and the patient progress toward Stage 2, he or she becomes accustomed to the presence of the mycotoxin and a quiescent period follows due to lack of nerve sensation. Depending on exposure levels, the first Stage may last from 3 - 9 days. In scoring the 50 signs and symptoms listed in Tables-1 and 2, an average score range of 20-45 represents Stage 1.

Stage 2: This Stage is often called the latent Stage or incubation period because the patient feels apprehensive, but is capable of normal activity in the beginning of this Stage. Every organ of the body is affected by degeneration and necrosis with continued exposure. The primary target organs for an individual become evident over time, due to biological variation. These are disturbances in the central and autonomic nervous systems resulting in headaches, mental depression, loss of short-term memory, loss of problem-solving ability, various neuropsychiatric manifestations, meningism, severe malaise and fatigue, narcolepsy, loss of temperature control, hyperesthesia or numbness of body areas, and cerebellar dysfunction including hypotonia, attitude and gait, dysmetria, asthenia, vertigo, disturbances of speech, and loss of balance (Best, 1961). Spinal cord degeneration may also be observed in gait and reflex abnormalities, such as the ability to drive vehicles, ride bicycles or pass sobriety tests (inability to tolerate ethyl alcohol). Attention deficient disorder may be observed in children. Various systems may include: Eyes: visual disturbances, floating objects, light sensitive, lack of tears, burning and itching. Ears: burning, itching, and loss of hearing. Immune and hematopoietic: progressive loss of white and red cells including a decrease of platelets and hemoglobin, and high susceptibility to bacterial, mycotic and viral infections, debilitating chemical and allergies. Gastrointestinal: metallic taste in mouth, tooth loss, gum problems, stomatitis, sores in gums and throat, nausea, vomiting, diarrhea or constipation, excessive flatulence, abdominal distention, hepatitis, pancreatitis, and diabetes mellitus. Respiratory : burning and bleeding from nasal membranes, respiratory difficulty, asthma, extreme susceptibility to cold, flu and pneumonia. Skin: thinning of hair on head, burning on face, rashes, irritation, and edema. Renal: proteinuria, possible hematuria. Reproductive: irregular ovarian cycles, increased menstrual flow, fibroid growths in uterus, cystic development in mammary glands, and tumors of mammary and prostate glands. Musculoskeletal : somatitis, muscle weakness, spasms, cramps, joint pain, enlargement of joints in hand, and clubbing of fingers. Cardiovascular: chest pain, palpitations, ruptures of atrial walls, myocardial infection and aneurysm of arteries.

The skin and mucous membranes may be icteric, pupils dilated, the pulse soft and labile, and blood pressure may decrease or increase. The body temperature does not exceed 38 degree C and the patient may be afebrile, or chilled. Visible hemorrhagic spots may appear on the skin. Thoughts of suicide may be prominent in the person’s mind at this time or anytime in Stage 2. Human bonding is very important for survival.

Degeneration and hemorrhages of the vessels marks the transition from the second to the third Stage of the disease and may not be consistently observed. The degeneration of the vital organs including serious respiratory insufficiency or asthma and CNS degeneration will take the patient into Stage three along with development of necrotic angina. If exposure continues, depending on exposure levels, Stage 2 may continue from weeks to months or even years until the symptoms of the third Stage develop. Evaluating the 50 signs and symptoms (Table-1 and 2) by assigning a score (0-least intense to 5-most intense or severe) to each symptom, we have determined that an average score range of 45-180 represents Stage 2.

Stage 3: Severe degeneration of the vital organs. The transition from the second to the third Stage is sudden. In this Stage, the patient’s resistance is already low, and violent severe symptoms are present, especially under the influence of stress, or associated with physical exertion and fatigue. The first visible sign of this Stage may be lung, brain or heart failure (heart attack), with or without the appearance of petechial hemorrhage on the skin of the trunk, the axillary and inguinal areas, the lateral surfaces of the arms and thighs, the face and head, and in serious Cases, the chest. The petechial hemorrhages vary from a few millimeters to a few centimeters in diameter. There is increased capillary fragility and any slight trauma may cause the hemorrhages to increase in size.

Aneurysms of the brain or aorta may be observed by angiography. Hemorrhages may also be found on the mucous membranes of the mouth and tongue, and on the soft palate and tonsils. There may be severe interstitial thickening or scarring of the lungs, or respiratory failure. Nasal, gastric and intestinal hemorrhages and hemorrhagic diathesis may occur. Necrotic angina begins in the form of catarrhal symptoms and necrotic changes soon appear in the mouth, throat, and esophagus with difficulty and pain on swallowing. Severe degeneration of the skin on the face, eyelids, and loss of lashes is also often present.

Necrotic lesions may extend to the uvula, gums, buccal mucosa, larynx, vocal cords, lungs, stomach, and intestines and other internal organs such as the liver and kidneys and are usually contaminated with a variety of avirulent bacteria. Bacteria infection causes an unpleasant odor from the mouth due to the enzymatic activity of bacteria on proteins. Areas of necrosis may also appear on the lips and on the skin of the fingers, nose, jaws, and eyes. Regional lymph nodes are frequently enlarged. Esophageal lesions may occur and involvement of the epiglottis may cause laryngeal edema and aphonia (loss of voice). Death may occur by strangulation.

Patients may suffer an acute parenchymatous hepatitis accompanied by jaundice. Bronchopneumonia, pulmonary hemorrhages, and lung abscesses are frequent complications. Tumors may develop of various organs, including skin, urinary bladder, brain, mammary gland, bone, immune, liver, prostate, possibly resulting in death. The most common cause of death is brain failure due to both direct effects of the mycotoxin on the central nervous system and indirect effects due to respiratory failure or lack of oxygen to the brain caused by the severe caustic inflammation (fibrinous exudation) reaction with the lung tissue, rendering it non-functional. Again, using the scoring system represented in Tables-1 and 2, an average score of greater or equal 180 represents Stage 3.

Stage of Convalescence: The course and duration of this Stage 3 depends on the intensity of the poisoning and complete removal of the patient from the premises or source of mycotoxin. Therefore, the duration of the recovery period is variable. There is considerable cellular necrosis and scarring to all major organs of the body in which cells will not regenerate, including the brain, spinal cord, eyes, lung, heart, liver, pancreas, kidney, adrenal, and blood vessels. If the disease is diagnosed during the first Stage, hospitalization is usually unnecessary, but allergies and asthma should be monitored closely. If the disease is diagnosed during the second Stage and even at the transition from the second to third Stages, early hospitalization may preserve the patient’s life. If however, the disease is only detected during the third Stage, death cannot be prevented in most Cases.

1. Croft, W. A., Jastromski, B. M., Croft, A. L., and Peters, H. A., “Clinical
Confirmation of Trichothecene Mycotoxicosis in Patients Urine”, In: Journal of
Environmental Biology 23(3), 301-320 (2002)

2. .Forgacs, J., and W. T. Carll : Mycotoxicoses. In : Advances in Veterinary
Science. Academic Press, New York and London, pp 273-372 (1962)

---------------NEWS FLASH----------
REPORT COMPLETE: October 12, 2009
DATE OF ANALYSIS:
Peter Helfrich
35 Clinton St., Apt #10
Plattsburgh, NY 12901

REPORT ID:1118
SAMPLES RECEIVED: 1
Dear Peter,

This is a final report from MouldWorks for the single bulk sample we received October 5th, 2009, taken from your home at 35 Clinton St., Apt. #10, Plattsburgh, NY. Here are your results.

1118-1 tape (Bathroom - Behind Shower)
Microscope:

Penicillium sp./Aspergillus sp.
Stachybotrys sp.

Cultured

Aspergillus sydowii
Aspergillus versicolor
Oedocephalum glomerulosum
Stachybotrys sp.
Trichoderma harzianum
Actinomycetes
Dry-spored Acremonium sp.

General Comments

Our analysis of the above set of samples found abundant evidence of a mold infestation in the bathroom sampled in this home. The sample contained viable spores, vegetative cells and/or reproductive structures from a variety of fungal species, including many molds which require moderately high to extremely high levels of available moisture before they can colonize an indoor site. The presence of these microorganisms can be directly attributed to elevated levels of available moisture locally. Specifically, Stachybotrys requires a water activity of at least 0.94 before it can germinate and colonize indoor sites. Water activity is a measure of the proportion of moisture available to organisms growing on a semi-solid substrate. Finding molds indoors that require such high levels of moisture is a strong indication that this site has experienced flooding, leaks or other water intrusion events. I gather from the chain of custody form that the shower stall had been leaking for some time and this is almost certainly the source of the moisture that supports these colonies. Without first addressing the moisture problems behind the mold growth, molds will undoubtedly continue to plague this site.

Due to the presence of several toxigenic mold species, I'd strongly recommend having a professional come in and clean up the infestation properly to avoid stirring up spores and risking further personal exposure. A professional mold remediator will have the equipment and expertise needed to remove the colony safely, under containment, ensuring that any spores released during the work are removed from the building. It is important that any remediation job is guaranteed with third-party air sampling for mold spores following completion. Without this step, you have no way of knowing whether the project succeeds in improving the indoor air quality

Health Effects

Some of the molds found in this sample have the potential to adversely affect your health. In the paragraphs below, I'll detail some of the risks thought to be associated with exposure to each of the concerning molds that were identified. Let's start by looking at the most concerning mold found in this sample, Stachybotrys.

The whole issue of stachybotryosis and trichothecene mycotoxins is reviewed in a recent book by Nicholas Money (Carpet Monsters and Killer Spores, Oxford University Press). He concludes that Stachybotrys should be taken very seriously indeed. Here is what the findings of the last 5 years suggest:

Stachybotrys toxins include a very potent trichothecene, Satratoxin G, which may seriously damage lungs and internal organs. It is probably the agent responsible for the burning sensation when active strains are inhaled (not advised). In a study published just a little over a year ago, researchers at Michigan State University established a link between Satratoxin G and the death of nerve cells in the part of the brain responsible for the sense of smell in mice. Researchers allowed mice to sniff a single dose of Satratoxin G equivalent to that which a person without respiratory protection would be exposed to in a room contaminated with Stachybotrys chartarum. They then tracked the damage to the neurons lining the nasal passages of the mice at time intervals after exposure. Every mouse exposed to Satratoxin G developed a significant loss of these nerve cells through a process known as apoptosis within a day of exposure. In apoptosis, a type of programmed cell death, cells essentially commit suicide, in this case in response to exposure to Satratoxin G. Additionally, each exposed mouse developed inflammation of the nasal lining and the olfactory bulb, the part of the brain that relays sensory information from the nose to other parts of the brain. Significantly, this inflammation and loss of nerve cells were also triggered by exposing the mice to smaller doses over five consecutive days indicating a cumulative effect.

Although it isn't yet known how Satratoxin G affects human noses, it is known that the nerve cells damaged in the mouse study are similar in both species. Studies in the past have focused on the role very small mold spores or pieces of spores might play in irritating the lungs. However, this study conclusively shows that the nasal passages may be damaged as well. The nose acts as a "scrubber" removing significant amounts of both very large (>5 microns) and very small (nanoparticle-sized) constituents of aerosols. More work needs to be carried out on the effect these particles have once deposited.

In addition there are several other categories of nasty substances made by the fungus, including several which are immune system depressants and may account for vulnerability of people who are chronically exposed to the toxin to respiratory illness - colds, etc. The fungus also makes stachylysin, which causes leakage of blood from the small capillaries and breakdown of the red blood cells.

There are two species of Stachybotrys commonly recovered from interior habitats, S. chartarum and S. chlorohalonata (formally described just a few years ago). These two species can be distinguished on a special culture medium, and I did this routinely in the past. However, after discovering several instances in which both species were present in the same sample, I thought it prudent to consider any Stachybotrys infestation as potentially hazardous. Only about half of S. chartarum strains make trichothecenes, but they may make the other kinds of toxins mentioned above. S. chlorohalonata does not make trichothecenes, but it does make other mycotoxins known to be mutagenic.

It has been claimed that the spores of Stachybotrys are too large to get far into the respiratory passages. However, it is now known that the trichothecenes in Stachybotrys chartarum are localized in the spores and that tiny fragments of the spores (sub-micron sized) can become airborne. These observations suggest in turn that aerosols containing mycotoxins can be generated in environments where Stachybotrys infestations occur even if no spores are seen in air samples. Indeed, pure mycotoxins have been filtered from the air in buildings where Stachybotrys infestations are severe. Given this information, it would be prudent to regard any Stachybotrys infestation as a potential danger and treat the site with respect.

The two Aspergillus species observed in the cultures prepared from your sample are also of some concern. These molds can produce huge numbers of dry spores which are easily lofted into the air and are slow to settle. Spores from any species of Aspergillus should therefore be presumed allergenic. In addition, each of the species identified in this sample may present additional health risks worth discussing:

Aspergillus versicolor produces the mycotoxin sterigmatocystin. This compound is a chemical cousin to aflatoxin, one of the most mutagenic substances known. Fortunately, sterigmatocystin is much less mutagenic than aflatoxin, but sources I consult advise caution when dealing with this mold. Beyond this, it is now known that A. versicolor also produces aerosols of sub-micron particulates that could easily penetrate deep into the respiratory tract; these tiny particles can be mycotoxin-laden, creating a dangerous situation. Very recent work has shown that mycotoxin production in these fungi occurs only at relative humidities in excess of 90% when growing on wallboard and other building materials. The author (Kristian Nielson) concludes that sites which have experienced alternate cycles of wetting and drying are at most risk for mycotoxin contamination. Sites such as this, in which Aspergillus versicolor is mixed in with Trichoderma, Actinomycetes or other wet wall microorganisms, are at maximum risk for contamination by sterigmatocystin. Having said all of that, I must mention that sterigmatocystin does not become really mutagenic until it has been acted on by enzymes in the liver, and it is an open question whether inhaled mycotoxins ever get to the liver.

Aspergillus sydowii is a frequent agent of invasive aspergillosis. The fungus is able to enter the body through the epithelial cells of the lung and disseminate through the blood resulting in acute pneumonia. Although this sounds quite frightening, this condition requires the patient to have a previously existing severe loss of immunocompetence for the fungus to gain hold. Cases in otherwise healthy patients haven't been reported.

Lastly, the Actinomycetes found in this sample are not molds at all, but filamentous bacteria. They produce huge numbers of really minute dry spores which are probably allergenic, since their small size would allow them to penetrate respiratory passages efficiently. Actinomycetes typically grow in wet sites and are part of the wet wall syndrome. These bacteria are typically ignored in mold reports - but they should not be. Workers in Finland have reported that some Actinomycete spores, unlike most toxic mold spores, may actually trigger inflammatory responses in the lungs.


All samples have been processed and analyzed using MouldWorks SOP 1, SOP 2 and SOP 7.

All samples were inspected prior to processing to ascertain their condition. Unless expressly stated in the report, all samples were in adequate condition for analysis.
Sincerely,



Matt Visser
Mycologist and Lab Manager

MouldWorks, LLC
3190 Lakeview Drive
Beulah, MI 49617
541-844-6236