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Mold Testing

IMPORTANT: Mold spreads fast and can be very harmful, so call The Fix it Guys at 719.499.0218.

Mold air spore testing is insensitive, expensive and misses more mold toxins than it finds. Mold air spore testing provides misleading assurance that indoor toxic mold is not a problem and rapidly becomes prohibitively expensive, In reality, inhalation of gaseous mold neurotoxins is the primary route of toxic mold exposure. Mold toxins have been measured in symptomatic patient’s urine, when air mold spore testing appeared normal. Frequently wall cavities contain hidden mold colonies which outgas mold neurotoxins thru pores in suspended acoustic ceilings, slots in electrical outlets, etc. Over 300 different mold neurotoxins have been identified.

A sensitive cost effective mold testing protocol could include the following progression:

FUNCTIONAL ACUITY CONTRAST SENSITIVITY TEST, FACT, FOR EXPOSED INDIVIDUALS

Functional Acuity Contrast Sensitivity Test, FACT, also known as Visual Contrast Sensitivity Test, VCST, is available for $15.00, at www.chronicneurotoxins.com Test results are provided immediately and the test is 98 percent specific for neurotoxicity. Lyme Disease, mercury, lead, pesticides, and aromatic solvents, such as toluene, xylene and benzene can also cause a positive test result. People suffering symptoms from suspected indoor mold exposure should consider alternative housing arrangements and a trial of over the counter toxin binders, such as those available at Citrisafe certified, http://www.citrisafecertified.com

URINE MYCOTOXIN TESTING

Sensitive urine mycotoxin testing is available for about $700, without a prescription. Urine mycotoxin toxin testing can be a bargain, compared to the cost and insensitivity of testing buildings. It can be difficult to find a Physician willing to prescribe this painless test, although many health insurance programs will pay for it. The urine mycotoxin test can be ordered from Direct Lab, at https://directlabs.com/OrderTests/tabid/55/language/en-US/Default.aspx

C4A BLOOD TESTING

The single most sensitive serum (blood) test which can indicate Chronic Inflammatory Response Syndrome (CIRS) is alternative Complement 4, C4a. Published peer reviewed research reveals C4a is often highly elevated, compared to C3a, in individuals who are genetically hypersentive to indoor toxic mold exposure. The C4a blood test is available, without a prescription, from www.econolabs.com.

Most additional medical testing for mold toxicity requires a prescription from a Physician. The Citrisafe certified website contains a list of practitioners familiar with mold neurotoxicity testing and treatment.

ALEXETER RAPID ASP/PEN AND STACHYBOTRYS MOLD IDENTIFICATION KITS

ALEXETER ASP/PEN RAPID TEST KIT

The Alexeter Asp/Pen rapid test kit contains two collection swabs and two rapid test kits which can identify the presence of Aspergillus or Penicillium molds in 15 minutes. www.Alexeter.com Although many people associate Penicillium mold with moldy foods, Penicillium molds are major toxin formers, producing tremorgenic molds, including Roquefortine and Penitrim A. Aspergillus molds can produce potentially fatal Aflatoxin and Ochratoxin neurotoxins. IF THE ALEXETER ASP/PEN RAPID TEST REVEALS ONE OF THESE MOLDS, ADDITIONAL PRECAUTIONS SHOULD BE TAKEN, ESPECIALLY IF EXPOSED INDIVIDUALS SUFFER SYMPTOMS AND FAILED THE FACT/VCST VISION TEST AND/OR THE URINE MYCOTOXIN TEST.

ALEXETER RAPID STACHYBOTRYS MOLD RAPID IDENTIFICATION KIT

The Alexeter Stachybotrys rapid test kit can identify the presence of the extremely toxic black mold Stachybotrys molds in 15 minutes. www.Alexeter.com Stachybotrys can produce Trichothecene mold toxins, which Chinese scientists consider more toxic than nerve gas. T2 Trichothecene mold neurotoxins have been outlawed in biological warfare and apparently were used by Saddam Hussein, to kill almost 100,000 Kurds. Trichothecene toxins an cause symptoms in everyone, not just approximately 25 percent of the population who genetically clear mold toxins 468 percent slower. One milligram of Stachybotrys mold can kill an 800 pound horse and thousands of horses were killed by Stachybotrys contaminated hay in Ukraine.

Stachybotrys mold is very difficult to destroy and can continue outgassing extremely toxic trichothecene mold toxins, after it is dry and dead. Bleach and ozonation are inadequate to remediate Stachybotrys. Stachybotrys remediation should not be done without a full face respirator and hazmat suit - THIS IS NOT USUALLY A DO-IT-YOURSELF JOB

THESE INEXPENSIVE DEXTROSE AGAR TEST PLATES OFTEN GROW OUT MOLD WHEN OTHER TEST PLATES FROM HARDWARE AND BUILDING SUPPLY STORES FAIL TO. STERILE COTTON “Q” TIPS CAN BE PURCHASED AT MOST PHARMACIES, ALONG WITH SMALL BOTTLES OF STERILE SALINE SPRAY. DUST AND OTHER DRY SURFACES CAN BE SAMPLED WITH THE STERILE Q TIPS, AFTER THE TIP IS SPRAYED WITH STERILE SALINE SPRAY. THE SWAB SAMPLE SHOULD BE LIGHTLY STREAKED ACROSS THE SURFACE OF THE CIRCULAR CULTURE DISH IN A ZIGZAG PATTERN. WALLS, FURNITURE, CARPET, WASHING MACHINES, DUST, DRYWALL, INSULATION AND OTHER MATERIALS CAN BE SAMPLED, WITH THIS METHOD. PET FUR CAN BE SAMPLED WITH INSTRUCTIONS ON THE WWW.CITRISAFECERTIFIED.COM WEBSITE. THE SAME TECHNIQUE CAN BE USED TO SAMPLE FUR FROM DEER, ELK, ANTELOPE, BEAR, FOX AND OTHER ANIMAL TROPHIES, WHICH OFTEN CONTAIN MOLD SPORES

MOLD OFTEN BEGINS GROWING WITHIN 48 HOURS ON THESE MOLD CULTURE DISHES, BUT VISIBLE GROWTH MAY NOT BE PRESENT FOR 8 DAYS. IF VISIBLE GROWTH OCCURS, THESE PLATES CAN BE SHIPPED TO THE IMMUNOLYTICS LAB, FOR MOLD GENUS ANALYSIS FOR A COST OF $30 TO $45, DEPENDING ON HOW MANY SAMPLES ARE SENT. IMMUNOLYTICS WILL EMAIL ANALYSIS RESULTS.

ERMI DNA PCR TESTING OF 36 MOLD SPECIES, INCLUDING SOME MAJOR TOXIN FORMERS

THE ENVIRONMENTAL RELATIVE MOLDINESS INDEX, ERMI TEST COSTS ABOUT $150 AND IS A BARGAIN, COMPARED TO MOLD CULTURE TESTS, WHICH USUALLY ONLY IDENTIFY MOLD TO THE GENUS, NOT SPECIES LEVEL. SPECIES IDENTIFICATION IS IMPORTANT, SINCE DIFFERENT SPECIES OF ASPERGILLUS, PENCILLIUM, CHAETOMIUM AND OTHER TOXIC MOLD PRODUCE DIFFERENT NEUROTOXINS. DIFFERENT MOLDS CAN ALSO REQUIRE DIFFERENT TREATMENTS TO DESTROY THE MOLD. FOR EXAMPLE, DAVID STRAUSS, PHD, PUBLISHED A STUDY AT UNIVERSITY OF TEXAS, WHERE TESTING FOUND EXTREMELY TOXIC TRICHOTHECENE NEUROTOXINS THREE AND A HALF YEARS, AFTER STACHYBOTRYS CHARTARUM CONTAMINATED DRYWALL WAS TREATED WITH CHLORINE BLEACH. HE ALSO FOUND NEUROTOXINS THREE AND A HALF YEARS AFTER CHAETOMIUM CONTAMINATED CARPET WAS WASHED WITH DETERGENT.

ERMI DNA PCR TESTING OF 36 MOLD SPECIES, INCLUDING SOME MAJOR TOXIN FORMERS

THE ENVIRONMENTAL RELATIVE MOLDINESS INDEX, ERMI TEST COSTS ABOUT $150 AND IS A BARGAIN, COMPARED TO MOLD CULTURE TESTS, WHICH USUALLY ONLY IDENTIFY MOLD TO THE GENUS, NOT SPECIES LEVEL. SPECIES IDENTIFICATION IS IMPORTANT, SINCE DIFFERENT SPECIES OF ASPERGILLUS, PENCILLIUM, CHAETOMIUM AND OTHER TOXIC MOLD PRODUCE DIFFERENT NEUROTOXINS. DIFFERENT MOLDS CAN ALSO REQUIRE DIFFERENT TREATMENTS TO DESTROY THE MOLD. FOR EXAMPLE, DAVID STRAUSS, PHD, PUBLISHED A STUDY AT UNIVERSITY OF TEXAS, WHERE TESTING FOUND EXTREMELY TOXIC TRICHOTHECENE NEUROTOXINS THREE AND A HALF YEARS, AFTER STACHYBOTRYS CHARTARUM CONTAMINATED DRYWALL WAS TREATED WITH CHLORINE BLEACH. HE ALSO FOUND NEUROTOXINS THREE AND A HALF YEARS AFTER CHAETOMIUM CONTAMINATED CARPET WAS WASHED WITH DETERGENT.

THE ERMI DNA ANALYSISIS IS HIGHLY ACCURATE AND INCLUDES MANY OF THE MAJOR MOLD NEUROTOXIN FORMERS. ONE OF THE BEST DISCUSSIONS OF THE DEVELOPMENT, SENSITIVITY, METHODOLOGY AND INTERPRETATION OF THE ERMI TEST IS AVAILABLE AT HTTP://WWW.SURVIVINGMOLD.COM/DOCS/DIAGNOSIS/ERMI/ARTICLES/ERMI_V26_P32_FILTRATIONNEWS_2007.PDF

THE ENVIRONMENTAL RELATIVE MOLDINESS INDEX, ERMI, TEST IS AVAILABLE FROM ALEXETER TECHNOLOGIES, WWW.ALEXETER.COM AND NUMEROUS OTHER SOURCES. EMSL OFFERS THE ERMI TEST FOR $150, AT HTTP://WWW.EMSL.COM/PRODUCTCATALOGDETAILS.ASPX?NAME=MOLD-TEST-KIT-WITH-ERMI-5-DAY-TAT&PRODUCTID=MTK-ERMI-5D

TESTING DUST FOR TRICHOTHECENE BLACK MOLD TOXINS

HIGHLY SENSITIVE TESTING OF DUST IN HEATING, VENTILATION AND AIR CONDITIONING DUCTS IS AVAILABLE NOW AT HTTPS://WWW.INDOORAIRTEST.COM/DISPLAYPRODUCT.ASP?ID=34 THE TEST COSTS $93.00.

SO WHAT IF SPORE TRAPS CAN'T TELL SPECIES' DIFFERENCES?

SINCE MANY WATER-INTRUSION MOLDS LOOK THE SAME IN A MICROSCOPE, A SPORE TRAP ANALYSIS CAN'T PROVIDE SPECIES DIFFERENTIATION. THUS, A COMPARISON OF INDOOR AND OUTDOOR SAMPLES WON'T PROVIDE INFORMATION ON THE REAL DIFFERENCES BETWEEN SAMPLES, ONLY TOTAL COUNTS OF SPORES THAT APPEAR SIMILAR. THEREFORE, IF A GIVEN INDOOR SAMPLE HAS THE SAME TOTAL COUNTS AS A OUTDOOR SAMPLE BUT THE SPECIES ARE DIFFERENT, THE INSPECTION WOULD LIKELY MISS A MOISTURE-RELATED MOLD PROBLEM. THIS IS BECAUSE A SPORE TRAPS ASSUMES THAT THE SPECIES VARIATIONS ARE THE SAME FROM A GIVEN SET OF INDOOR AND OUTDOOR SAMPLES. REMEMBER: A SPORE TRAP COUNT WILL NOT IDENTIFY DIFFERENT SPECIES OF ASPERGILLUS OR PENICILLIUM IN A SET OF INDOOR AND OUTDOOR SAMPLES

DON'T SPORE TRAPS COLLECT SPORES IN THE SIZE RANGE OF MOST WATER-INTRUSION MOLDS?

NO. THE SPORE TRAP IS AN IMPACTION COLLECTOR. THE COLLECTION EFFICIENCY OF A SPORE TRAP IS DEPENDING UPON BOTH THE AIR FLOW RATE AND THE PHYSICS OF IMPACTION. IN SHORT, SPORE TRAPS DO NOT CAPTURE FUNGAL SPORES BELOW 3 TO 4 MICRONS IN DIAMETER. THIS MEANS THAT MOST SPECIES OF MOLDS OF ASPERGILLUS AND PENICILLIUM ARE COLLECTED AT VERY LOW RATES IN STANDARD SPORE TRAPS COMPARED TO LARGER MOLDS. THIS PHENOMENON IS A WIDELY-KNOWN BUT LITTLE-DISCUSSED FACT IN THE LABORATORY COMMUNITY.

SO HOW CAN WE OPTIMIZE COLLECTION?

TO COLLECT VIRTUALLY ALL MOLD SPORES, THE COLLECTION METHOD MUST COLLECT SPORES OF ALL SIZES. IDEALLY, A FILTER TYPE COLLECTOR WHERE AIR IS COLLECTED AND SAMPLED THROUGH A POROUS MEDIUM SHOULD BE USED. THE SPORELOCK™ SYSTEM MAKES THIS OPTION PRACTICAL. IN A SPORELOCK CARTRIDGE, THE AIR SAMPLE IS PULLED THROUGH A MEMBRANE FILTER WITH 0.8 MICRON NOMINAL PORE SIZE. THUS, UNLIKE FOR SPORE TRAPS, ALMOST ALL INTACT SPORES COLLECTED THROUGH THE FILTER WILL BE CAPTURED.

BUT CAN I ORDER A STANDARD DIRECT EXAMINATION SPORE COUNT FROM A SPORELOCK™?

ABSOLUTELY. THE FILTER FROM A SPORELOCK CAN BE REMOVED IN THE LABORATORY AND STUDIED BY DIRECT EXAMINATION, JUST LIKE A SPORE TRAP. IN FACT, FOR MOST LABS, COUNTING A SPORELOCK FILTER IS EVEN EASIER THAN COUNTING A SPORE TRAP!

SO IF SPORELOCK™ SOLVES THE "SMALL SPORE SIZE" ISSUE, WHY WOULD I NEED TO PERFORM THE MORE EXPENSIVE MSQPCR ANALYSIS?

REMEMBER THAT A SPORE COUNT IS NOT THE SAME AS A SPORE SPECIES IDENTIFICATION. WHETHER WE COUNT SPORES IN A STANDARD SPORE TRAP OR A SPORELOCK, WE STILL CANNOT DETERMINE THE SPECIES AS IN A MSQPCR.

OK, BUT WHY SHOULD I QUANTIFY AND DETERMINE THE SPECIES FOR 36 DIFFERENT MOLDS: THE EPA RELATIVE MOLDINESS INDEX AND GROUP 1 VERSUS GROUP 2 MOLDS

EXTENSIVE RESEARCH CONDUCTED BY THE U.S. EPA HAS ESTABLISHED THE EPA RELATIVE MOLDINESS INDEX, OTHERWISE KNOWN BY THE ACRONYM ERMI. THE ERMI SCORE NARROWS DOWN THE TOTAL NUMBER OF CRITICAL MOLD SPECIES TO 36 INDOOR-INDICATOR MOLD SPECIES. THE 36 SPECIES ARE SUBDIVIDED INTO TWO VERY DIFFERENT GROUPS OF MOLD (FUNGAL) SPECIES, REFERRED TO AS GROUP 1 AND GROUP 2 MOLDS. THE GROUP 2 MOLDS ARE FOUND TO BE COMMON IN MOST HOMES AND IN LOW CONCENTRATIONS. OCCUPANTS LIVING AND WORKING IN INDOOR ENVIRONMENTS THAT CONTAIN PREDOMINANTLY GROUP 2 MOLDS WERE HEALTHY AND SUFFERED FEW RESPIRATORY RELATED ILLNESSES, NOR DID THE BUILDING STRUCTURES SUFFER LEAKS AND WATER INTRUSION. HOWEVER, GROUP 1 MOLDS WERE MUCH LESS BENIGN, AND OCCUPANTS OF THESE HOMES AND ENVIRONMENTS SUFFERED SIGNIFICANT RESPIRATORY AND ASTHMA RELATED ILLNESSES. MOREOVER, GROUP 1 MOLDS WERE SIGNIFICANTLY CORRELATED TO WATER INTRUSION DUE TO POOR CONSTRUCTION OR LEAKING PIPES. FURTHERMORE, EPA SCIENTISTS AND OTHER REPUTABLE SCIENTIFIC INVESTIGATORS HAVE AMASSED A BODY OF PUBLISHED SCIENTIFIC RESEARCH THAT CONVEYS A MAJOR PARADIGM SHIFT IN THE WAY MOLD SAMPLES ARE BOTH COLLECTED AND ANALYZED.

IS DUST SAMPLING REALLY SUPERIOR TO AIR SAMPLING?

YES, IN SOME WAYS. EPA RESEARCHERS HAVE FOUND THAT MOLDS COLLECTED BY AIR SAMPLING ARE A POOR INDICATOR OF THE LEVEL OF CONTAMINATION FOR THE WORST HOUSEHOLD MOLDS (THE GROUP 1 OR WATER INTRUSION/ASTHMA MOLDS). SO THEY LOOKED ELSEWHERE, AND FOUND THAT EVERY INDOOR ENVIRONMENT HARBORS A STABLE MOLD RESERVOIR; THAT RESERVOIR WAS DUST. MOREOVER, THE DUST HELD AN HISTORICAL ACCOUNT OF INDOOR MOLD. CONVERSELY, AIR SAMPLES COLLECTED BY SPORE TRAPS, ALTHOUGH WIDELY USED, SHOW WEAK CORRELATION WITH UNHEALTHY ENVIRONMENTS. HENCE, INDOOR DUST HAS A HISTORICAL MOLDY TALE TO TELL, WHICH IS READ FROM THE MOLD DNA. SOMETIMES THAT TALE IS THE SORROWFUL ACCOUNT OF LEAKY ROOFS, WINDOWS OR PIPES (THE DNA IDENTIFIES MANY GROUP 1 MOLD SPECIES), OTHER TIMES IT IS A STORY OF A HAPPY DRY HOME (COMMON GROUP 2 MOLD SPECIES). ALL BUILDINGS HAVE DUST AND BY ANALYZING THE DNA IN THAT DUST FOR MOLD, ALL SKELETONS COME OUT OF THE CLOSET. AND THOSE SKELETONS, WHETHER GOOD OR BAD, ARE REFLECTED IN THE EPA'S ERMI INDEX. EMPHASIS ADDED

READ MORE DETAILS FROM DR. ED SOBEK OF ASSURED BIOTECHNOLOGY CORPORATION.

READ A TECHNICAL BRIEF ON THE DISADVANTAGES OF SPORE TRAP ANALYSIS.

Page Content courtesy of The Flood Crew

Indoor Mold Symptoms

The National Institute of Occupational Health and Safety has estimated 50 percent of buildings in the United States have been affected by water damage. Sick Building Syndrome can be caused by indoor mold, bacteria and bioaerosols produced when water damage is not dried, within 24 to 48 hours.

Dr. Ritchie Shoemaker, author of Surviving Mold and Mold Warriors has pioneered much of the original scientific research describing how indoor mold growth causes potentially disabling symptoms in approximately 25 percent of the population. Genetically, about 25 percent of the population clears mold toxins about 460 times slower than the other three quarters of the population. This group also has excessive autoimmune response and inflammation, when exposed to indoor mold toxins. The excessive inflammatory autoimmune response experienced by about one in four people exposed to Water Damaged Buildings is often called Sick Building Syndrome, SBS. Physicians and researchers studying or treating Sick Building Syndrome patients, have discovered a specific immune reaction, which they call Chronic Inflammatory Response Syndrome, CIRS, in Sick Building Syndrome sufferers.

Most of the symptoms caused by Sick Building Syndrome are caused by inhaled toxins, not skin contact.

CIRS-WDB is acquired primarily from inhalation of microbial products that are contaminants found in the complex mixture of the interior environment of WDB. We are aware that serious health problems, including fatalities, arising from ingesting kilograms of microbial-contaminated foods in developing countries are documented. Dermal contact and ingestion of settled WDB contaminants might theoretically contribute to the exposure burden of CIRS-WDB, but in reality, the quantities necessary to be harmful are unlikely to apply to daily life of patients in an indoor environment.

http://www.survivingmold.com/legal-resources/publications/poa-position-statement-paper

http://www.survivingmold.com/legal-resources/publications/poa-position-statement-paper

Symptoms reported by patients exposed to indoor mold included fatigue, weak, ache, cramp, unusual pain, ice pick pain, light sensitivity, headache, red eyes, visual blurring, tearing, sinus, cough, shortness of breath, abdominal pain, diarrhea, joint pain, morning stiffness, memory problems, impaired focus or concentration, word recall impairments, decreased assimulation, confusion, skin sensitivity, disorientation, mood swings, appetite changes, sweats, impaired temperature regulation, thirst, increased urination, static shocks, numbness, tingling, vertigo and metallic taste. These symptoms are from a study presented by Ritchie Shoemaker, MD in a paper presented at the International Mycology Congress, at Edinburgh, Scotland, on 8/1/10.No patient had all of these symptoms. Dr. Shoemaker stated in Public Health Alert, August, 2011 that indoor mold exposure can imitate all of the symptoms of Lyme Disease. He further observed Lyme Disease patients with mold toxicity will not recover, with antibiotic therapy, without dealing with mold toxicity. http://www.survivingmold.com/news-events/special-focus/publichealthalertorg

An article reprinted below reveals investigators have found trichothecene mold toxins, in ALS, Parkinson's and Lupus patients. Treatment with antifungal medications and toxin binders, improved health in some of these patients.

Citrisafe Certified lists the following symptoms and diseases which indoor mold can cause including Polycystic Ovary Syndrome, PCOS; Psoriasis; Meniere's; hearing loss; Restless Leg Syndrome; Irritible Bowel Disease; Gastric Esophageal Reflux Disorder; GERD; Fibromyalgia; and Chronic Fatigue Syndrome.

Like Syphilis and Lyme Disease, mold toxins can cause many symptoms and diseases.

INDOOR MOLD TOXINS ASSOCIATED WITH 93 PERCENT OF CHRONIC SINUSITIS

After reduction of indoor mold spore counts and use of antimicrobial nasal sprays, 94 percent of chronic sinusitiis patients had normal sinus endoscopic exams.

Arch Environ Health. 2003 Jul;58(7):433-41.

Chronic Sinusitis: Defective T-Cells Responding to Superantigens, Treated by Reduction of Fungi in the Nose and Air DONALD P. DENNIS Atlanta Center for ENT and Facial Plastic Surgery Atlanta, Georgia and Department of Otolaryngology—Head and Neck Surgery Northside Hospital Atlanta, Georgia and Department of Otolaryngology—Head and Neck Surgery Piedmont Hospital Atlanta, Georgia

ABSTRACT. In this study, the author used endoscopic sinus photography to study the effects of reduction of fungi in the nose, and in environmental air, on the sinus mucosa of 639 patients diagnosed with chronic rhinosinusitis. Sinus mucosal photographs were taken before and after reduction of fungal load in the nose and air, to determine if there was an optimum environmental air fungal load associated with sinus mucosal recovery to normal appearance. Systemic symptoms associated with fungal exposure, which resolved when fungus was removed from the patient and the environmental air and reappeared with recurrent environmental fungal exposure, are also discussed and are termed systemic fungal symptoms. Interventions consisted of nasal fungal load reduction with normal saline nasal irrigations and antimicrobial nasal sprays, and environmental air fungal load reduction with high-efficiency particulate air (HEPA) filtration in combination with ionizers or evaporation of a solution of botanical extract. Main outcome measures were obtained with environmental air 1-hr gravity-plate fungal colony counts, laser air particle counts, and endoscopic sinus photography. Blood levels of immunoglobulins IgG and IgE for 7 common molds were also determined. After intervention, 94% of patients who used antimicrobial nasal sprays and who reduced their environmental fungal air count to 0–4 colonies per 1-hr agar gravity-plate exposure (n = 365) exhibited normal sinus mucosa by endoscopic exam. Environmental air fungal counts that exceeded 4 colonies resulted in sinus mucosal abnormalities ranging from edema, to pus and/or nasal polyps at higher counts. Neutralization of allergy, and/or surgery, were used as appropriate following implementation of environmental measures. EMPHASIS ADDED

CHRONIC RHINOSINUSITIS (CRS) affects approximately 37 million Americans, or 1 in 6 (16.3%). It is more common than arthritis (12.47%), orthopedic im-pairment (12.14%), or hypertension (11.44%). CRS costs patients and insurance companies over $2.4 bil-lion per year for medication, hospitalization, and surgery. In excess of 200,000 sinus surgeries are performed every year in the U.S. Many patients remain refractory to surgery and antibiotic therapy, despite the more than 46.9 million prescription and nonprescription medications ordered annually.1 Antibiotics are not effective in treating CRS because they target bacterial super-growth and not the underlying fungal problem. In the most recent decade, the rate of CRS occurrence has been in- creasing steadily,1 but the pathogenesis of chronic sinusitis has not yet been determined. The standard school of thought is that fungus allergy is involved in fewer than 10% of cases,1 likely because fungi are visi- ble endoscopically in the nose in less than 10% of cases studied. However, fungi are present microscopically in 93% of cases examined by culture.2 By definition, all CRS patients also have secondary bacterial infections. It is likely that the immune reaction to microscopic fungi causes mucosal pitting and mucous stasis, both of which lead to the development of secondary bacterial infections.2 EMPHASIS ADDED

In 1999, researchers at the Mayo Clinic demonstrated a causal connection between fungi and CRS. They found that 93% of all CRS cases also met the diagnostic criteria for allergic fungal sinusitis (AFS). It was postulated that an immune reaction to fungi in the mucosa is likely responsible for AFS and most CRS.2 This fact was confirmed by Braun et al.3 in 2003. In addition, immunoglobulin (Ig)E-mediated hypersensitivity was not present in the majority of cases studied, regardless of whether nasal polyps were present. Because 93% of CRS cases were found to meet the diagnostic criteria for AFS, it is likely that AFS and CRS represent varying degrees of allergic response to the same fungal antigens, with AFS representing more ex- tensive production of polyps and allergic mucin. Therefore, AFS and CRS will be used synonymously in this ar- ticle. The Mayo Clinic’s diagnostic criteria for AFS are a) CRS; (b) presence of allergic mucin (clusters of eo- sinophils and their byproducts, such as Charcot-Leyden crystals and major basic protein); and (c) presence of fungal organisms in the mucin, confirmed by histology or culture, or both.2 In the present study, radioaller- gosorbent (RAST) delayed mold reaction testing re-vealed elevated fungus-specific IgG levels to 2 or more of 7 common fungi in all patients.

In CRS patients, the nasal mucous contains eosino-phils, Charcot-Leyden crystals, IgG fungal antibodies, no helper T-lymphocytes, and no antigen-processing cells (APCs).2 Peripheral blood and nasal mucosa of CRS patients contain fungal-specific elevated IgG and fungal antigens. These antigens activate helper T-lym- phocytes in the blood, producing cytokines (interleukin[IL]-5 and IL-13) that recruit eosinophils; lymphocytes from normal controls do not recruit eosinophils in response to fungal antigens.4 This fact is key to our hy- pothesis because it means that helper T-cells in CRS patients are bypassing APCs, and are therefore likely to have defective receptor sites.

IL-13 causes immunoglobulin isotype switching (e.g.,to IgE and IgG1) and IgG production by immature B lymphocytes. IL-5 promotes eosinophil activation and activates B cells for terminal differentiation into Ig-se- creting cells.4 Thus, both eosinophils and IgG are ready to migrate through the mucous membrane and attack the mold in the nasal mucous—a classic Type II hyper-sensitivity reaction (Fig. 1). Waxman et al.5 proposed a Gell-Coombs Type III hypersensitivity reaction6 in Aspergillus sinusitis and chronic bronchopulmonary disease. In AFS, the sinus mucosa contains small lymphocytes, plasma cells, and eosinophils—a condition similar to that seen in asthmatic bronchial mucosa.7 Systemic immune-complex–mediated disease (Type III hypersensitivity reaction) affects tissues of the kidneys, joints, skin, heart, and serosal surfaces. The reason for this specific organ/tissue predilection is unknown. More work is needed to determine if a Type III hypersensitivity reaction to fungus is responsible for the arthritis and other systemic fungal symptoms seen clinically. The only real difference between Type II and Type III reactions, then, is in the location of the antigen. Type II reactions are against antigens located on cell surfaces or on extracellular matrix components, whereas Type III re- actions occur against soluble or circulating antigens.

Systemic lupus erythematosis and most types of glomerulonephritis are the result of Type III immune in- jury.8 Therefore, in all types of allergic hypersensitivity reactions, when the antigen (fungus) is removed the re- action stops. This fact forms the basis for our CRS treatment goal: to remove fungal antigen from both the nose and the environmental air, in order to stop the fungal immune reaction and allow the sinus mucosa to recover. Researchers have hypothesized that the immunopathology affecting more than 16% of the population is the result of a genetic defect in 1 or more of 9 genes (genes 2, 3, 5.1, 6.7, 8, 12, 13.1, 13.2, 17) on the out- side of the beta chain variable region of the T-cell receptor site (TCR Vβ genes)9–11 (Fig. 2). Normally, the antigen (fungus) must first be processed by an APC into smaller fragments, and these fragments must be trans- ported to the human leukocyte antigen (HLA) class II molecule on the surface of the APC, in order for the TCR site to recognize the antigen linked with the HLA II molecule and bind to it,6 causing the T-cell to release IL-5 and IL-13. Because the helper T-lymphocytes of CRS patients produce IL-5 and IL-13 when presented with fungal antigens, without APCs,4 the fungus is likely bypassing the APC HLA II molecule (the antigen-spe- cific area) and binding directly to the outside of the TCR Vβ site via defective gene(s) on the TCR Vβ chain. This genetic defect allows a microbe or toxin superantigen to bind to HLA class II histocompatibility molecules on APCs and TCR sites simultaneously, bypassing APC-induced activation of T-cells.9,10,12,13 The result is pro found activation of up to 30% of the body’s total T-cells,in contrast with the normal T-cell response of 0.01%.14 The subsequent superantigen-induced T-cell activation can cause systemic toxicity and is the likely mechanism for fungal-induced sinusitis and systemic disease.9

Superantigens are thought to be associated with systemic disease (e.g., human retrovirus in breast can- cer,9,15 Type I diabetes, and multiple sclerosis16). Super-antigens have also been linked causally to psoriasis17–19 and rheumatoid arthritis.20,21 Some fungi are thought to function as superantigens4,9 Our clinical observations have supported such an association because both the CRS and systemic fungal symptoms (e.g., arthritis, memory loss, 6th nerve palsy, dizziness, hearing loss, seizures, fatigue, vision problems, severe headaches, gastroesophageal reflux disease, gastrointestinal disturbances, asthma, IgG subclass deficiency, and fibromyalgia) have resolved with the use of antimicrobial nose sprays and environmental fungal removal protocol, and return when the protocols are discontinued or when fungal levels in air rise. This retrospective observational study and literature review were conducted to formulate an hypothesis for the cause of CRS and systemic symptoms associated with fungal exposure.

EMPHASIS ADDED

Treatment protocols. Both the patients themselves and the air in their home, office, and/or car environments (wherever fungal load was found to be elevated) were treated to reduce fungal load. Treatment of patients consisted of (a) normal saline nasal irrigations twice daily to remove fungi mechanically and (b) 2 antimicrobial nasal sprays (containing 2 structurally different antibiotics, an antifungal, and a steroid), administered as 3 sprays, 4 times daily for 4–10 wk, depending on the time required to clear the sinus mucosa, as verified by endoscopic exam. Our nasal spray protocol is summarized in Table 1.

Environmental remediation consisted of reducing air fungal load by following an environmental treatment protocol that included finding and repairing moisture intrusion and implementing portable high-efficiency particulate air (HEPA) filtration or inline central heating, ventilaton, and air conditioning system (HVAC) filtration (94% efficient at 0.35-µm particle size), in combination with either ionizers or the disbursement of botanical extract by evaporation. The odorless botanical extract was dispersed by the patient or environmental consultant by placing 2–4 foil-covered containers,with wicks perforating the foil, on top of a portable HEPA air filtration unit that exited clean air from the top of the machine. These setups were placed in each room used by the patient. In some cases, Room VI 2500 ionizers were used in combination with portable HEPA air filters, instead of the botanical extract. (Botanical extract and an ionizer could not be used in the same room because the ionizer destroys the activity of the extract.) With the patients’ permission, sources of moisture intrusion were identified and controlled. Cars were treated by spraying botanical extract into the HVAC system from the outside suction vent at the windshield on both sides, and on the inside of the car. (Portable HEPA filters, botanical extract containers, and ionizers were supplied by National Allergy Supply, Inc. [Atlanta, Georgia] and PharmaSource Int’l, Inc. [Denver, Colorado]; central inline air filters and moisture intrusion correction were supplied by Mead Indoor EnviroTech,Inc. [Atlanta, Georgia].)

All environmental treatment devices were evaluated for effectiveness by an independent mycology laborato- ry prior to use in the study. Before each device was tested, a gravity-exposure Sabouraud dextrose agar (SDA) plate (PharmaSource Int’l, Inc. [Denver, Colorado]) was exposed for 1 hr inside a test room documented to contain fungal colonies too numerous to count (TNTC). All devices reduced the test room’s fungal colony count from TNTC to 0–2 colonies by day 6.

Monitoring.

Prior to treatment of the patient and environment, endoscopic sinus photography was performed, and nose and air fungal cultures were taken.

Bacterial cultures were taken when visible pus was present. A Calgi swab on SDA was used for nose culture, and a 1-hr gravity SDA plate exposure for the environment. Plates containing nose swab samples were incubated in a dark area at room temperature for 3 days. If growth was observed, the plate was sent to a mycology laboratory (Quest Diagnostics Mycology Laboratory [Atlanta, Georgia]) for counting and identification.

Air samples were taken by exposing open plates in the areas where the patient spent most time, as well as in areas of likely contamination (e.g., bedroom, kitchen, den, office, car, basement, crawlspace, attic) for 1 hr with the central HVAC fan in the “on” position. The plates were placed at least 0.91 m (3 ft) from any wall. After exposure, the plates were enclosed in foil and sent to a mycology laboratory (Mold Lab Int’l [Knoxville, Tennessee]) for evaluation.

After treatment of the patient and air to reduce fungal load—in accordance with the aforementioned protocols—1-hr SDA plate exposures were repeated for the environmental air, and a 2nd set of endoscopic sinus photographs were taken for each patient. Comparisons were then made between the environmental fungal colony counts and the endoscopic sinus photographs. If nasal and environmental air fungal cultures did not correspond, a different source of sinus infection was suspected.

Laser air particle counts were performed by Mead Indoor EnviroTech (Atlanta, Georgia) before and after treatment of environmental air. A ParticleScan Pro laser airborne particle counter (IQAir, Inc. [Santa Fe Springs, California]) set at 0.3 µm per 1 ft3 (0.03 m3) was used to count particles. The resulting values were expressed as number of particles per 0.1 ft3 for convention. The RAST assay was used to detect serum IgG (delayed mold reac- tion) and IgE fungus-specific antibody levels for 7 common fungal antigens: Alternaria alternata/tenuis, Aspergillus fumigatus, Candida albicans, Cephalosporium acre, Cladosporium herbarum, Helminthosporium halodes, and Penicillium notatum/chrysogenum. Antibodies for the same 7 antigens were tested by Esoterix Lab- oratory Services, Inc. (Austin, Texas) with enzymatic immune assay.

Literature review. A review of current literature was conducted to aid in formulating an hypothesis for the pathogenesis of both AFS and systemic fungal symptoms.

Results

A total of 639 patients with persistent CRS were studied. After treatment of the patients and their environ- ments to reduce fungal load, 343 of the patients, who had abnormal sinus mucosa before treatment, showed normal mucosa without infection. Nasal mucosa failed to normalize in 22 patients. Of these, 3 were found to have lymphoma (1 T-cell and 2 B-cell) and 19 had persistent positive nasal fungal cultures (likely resulting from uncontrolled exposure to environmental fungi). In 219 cases, patients were unable to reduce the mold counts in their environments below 5 colonies and had various degrees of mucosal disease remaining. Fifty-five patients were lost to follow-up. All patients had elevated fungus-specific serum IgG levels to 2 or more of the 7 common fungi tested.

Particle and fungal counts.

Laser air particle counts higher than 50,000 particles per 0.1 ft3 (0.003 m3) at 0.3-µm particle size were associated with sinus mucosa abnormalities ranging from edema, to polyps and/or pus.

However, counts below 50,000 were associated with sinus mucosal health only if mold counts were below 5 colonies per 1-hr gravity-plate colony count. Approximately 90% of patients cultured both mold and bacteria. The bacteria types seen were typical and have been described by many researchers. It is generally agreed that chronic antibiotic treatment does not stop CRS.

Literature review.

Review of the current literature supported our hypothesis that the pathogenesis of CRS, AFS, and systemic fungal symptoms is a genetic defect at the TCR Vβ site, requiring antigen (fungus) presence. When more than 4 fungus colonies (per 1-hr gravity-plate exposure) are present in these patients’ environ- mental air, chronic sinusitis and/or multiple systemic symptoms can present clinically.

Systemic fungal symptoms.

The most common systemic symptoms seen to occur with fungal exposure, to resolve with fungal removal, and to recur with repeated fungal exposure are listed below. When these symptoms occur and recur in this manner, it is logical to hypothesize that fungi are the causative agents. The symptoms vary widely among patients and are general. No symptom is listed unless it began with fungal exposure, was concurrent with positive nasal and environmental fungal cultures, and resolved with fungal removal. The following systemic fungal symptoms were observed in our study subjects:

  • Headache in the frontal sinus, radiating to the temples.
  • Dizziness—both imbalance and vertigo with spinning—and impaired depth perception (e.g., patient misses stair step going down). .
  • Hearing loss—both high- and low-frequency, both temporary and permanent. .
  • Tremors, with severe leg pain and thigh weakness. In-ability to walk. Non-neurological muscle weakness, . fibromyalgia, lip and hand paresthesias, seizures (rare). .
  • Pain in some or all joints. .
  • Cognitive disorder and memory loss (e.g., cannot do serial 7’s [mental subtraction: 100 – 7 = 93, 93 – 7 = 86, etc.], cannot remember instructions, and cannot tell directions to common places). .
  • Other symptoms, including loss of smell and taste,chronic sinus infections, bloating diarrhea, esophageal reflux (specific to hypopharyngeal, esophageal, and gastric candidiasis), severe fatigue. .
  • Immune suppression IgG subclass deficiency. .

See Figure 1 for the likely mechanism of the Type III hy- persensitivity reaction.

When patients were treated with the combination of medical therapy (Table 2) and environmental remedia- tion described herein, symptoms of sinus congestion, headache, pressure, and pain, as well as the other systemic symptoms reported, generally tended to resolve within 2–8 wk after 1-hr gravity-plate fungal counts fell below 5 colonies.

Discussion

On the basis of 16 yr of clinical experience with 639 patients—using the treatment protocol described herein and monitoring with both endoscopic photography and sinus CT scans—it can be stated that “As long as fungi remain, so will the irritation and the sinusitis.” Experience has also shown that 1-hr gravity SDA agar plate exposure is a simple, reliable, and predictable method of assessing environmental fugal levels to determine human health risk. The following scale correlates with the results we obtained by comparing endoscopic sinus photos at various mold colony counts with laser air particle counts (Fig. 3 and 4): (a) a count of 0–4 total fun- gal colonies per room is within a normal range for sinus health, (b) a count of 5–8 colonies per room is cause for concern—illness is probable in patients with the IgG immune reaction to fungi herein described, and (c) a count of 9+ colonies per room is hazardous—illness is very likely among the CRS patient population. Laser air particle counts below 50,000 per 0.003 m3 (0.1 ft3), at 0.3 µm particle size, were associated with sinus mucosal health. However, environmental air particle counts in this range, with fungal colony counts greater than 4, were associated with sinus mucosal abnormalities. In other words, high fungal counts will overpower an otherwise clean air particle count and cause illness.

Key points in treatment.

Removal of the antigen (fungi) from the patient and the air halts the reaction (i.e., CRS and systemic fungal symptoms). Nasal irrigation with normal saline is essential for reducing nasal antigen load and antigen-induced inflammation. Because more than 90% of patients cultured both fungi and bacteria, combined antifungal and antibiotic nasal sprays are key to long-term control of CRS. Appropriate use of oral antibiotics, antifungals (fluconazole, delayed-release grapefruit seed extract capsules, terbina- fine, itraconazole, voriconazole) and antihistamine/decongestants is also recommended. Clinical experience has shown that immunotherapy for IgE- and IgG-specific molds is beneficial, with neutralization as needed.

Mixed respiratory vaccine for chronic Staphylococcus aureus is helpful if staph is consistently cultured. Ap- proximately 10% of patients studied had severe nasalpolyposis and cultured staph. IgE to both staphylococ- cal enterotoxin B and dermatiaceous fungi are almost always found together in situ in hypertrophic sinus disease nasal polyps.22 Endoscopic sinus surgery is essential for patients who fail medical therapy. However, absent removal of fungus from the nose and air, bacterial sinusitis remains, regardless of immunotherapy, vaccine, or surgical intervention.

The 93% of CRS patients in the Mayo study2 who had positive fungal nasal cultures also exhibited secondary bacterial infections, likely as a result of the mucosal pitting and mucus pooling that occurs when an eosinophilbinds to fungi in the nasal mucosa, ruptures, and releases major basic protein into the mucosa. This may explain our observation that antibiotic nose sprays are more effective when combined with an antifungal spray. When fungi were successfully removed from the nose and air, 94% of patients showed endoscopic sinus mucosal improvement to a normal appearance (i.e., no mucosal edema, polyps, or purulence), as depicted in Figures 3 and 4.

Trichothecene Mold Toxin Found in ALS, Parkinson's and Lupus

Antifungal Medications and Toxin Binders Reduced Symptoms

Trichothecene mold toxins were found in ALS, Parkinson’s and Lupus patients. Trichothecene mycotoxins are produced by molds including Fusarium, Trichoderma, Trichothecium and the infamous Stachybotrys chartarum black mold. Urine mold toxin testing for trichothecene, aflatoxin and ochratoxin is available with a Physician’s order. Dr. Rick Sponaugle, Medical Director of Florida Detox reports about ninety seven percent of the urine mycotoxin texts he has ordered, were positive for at least one mycotoxin.

Treatment with antifungal medications and toxin binders, including activated charcoal, and prescription Cholestyramine produced improvements in some patients suffering from ALS, Parkinson’s and Lupus.

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(WO/2008/021970) TREATMENT OF MOTOR NEURON DISEASE, INCLUDING CERTAIN NEUROLOGICAL DISORDERS, MOTOR NEUROPATHIES AND CHRONIC INFLAMMATORY DISEASES

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WO 2008021970 20080221

TREATMENT OF MOTOR NEURON DISEASE, INCLUDING CERTAIN NEUROLOGICAL DISORDERS, MOTOR NEUROPATHIES AND CHRONIC

INFLAMMATORY DISEASES

Cross-Reference to Related Applications

[0001] This application claims priority to US Provisional Application No. 60/836,382, filed August 9, 2006 and US Provisional Application No. 60/917,526, filed May 11, 2007, the disclosures of which are incorporated herein by reference in their entirety.

Background of the Invention

[0002] The present invention relates to new methods of treating motor neuron diseases, such as ALS.

[0003] Amyotrophic Lateral Sclerosis (ALS, sometimes called Lou Gehrig’s disease, Maladie de Charcot or motor neurone disease) is a progressive, almost invariably fatal neurological disease. ALS is a progressive illness with combined degeneration of the lower and upper motor neurons. It was first described by J. M. Charcot in 1874. According to a review by Rowland, L. P. et al. that appeared in the N. E. J. Med. (2001) 344(22): 1688-1700, ALS has two meanings. In the first it is a collection of adult-onset diseases with progressive degeneration of motor neurons. In the second sense, ALS refers to a specific form of motor neuron disease with both upper and lower motor neuron signs. [0004] “Amyotrophic” refers to the muscle atrophy, weakness and fasciculations found in the lower motor neuron deficits. “Lateral sclerosis” refers to the hardening of the lateral columns of the spinal cord due to degeneration and gliosis of the corticospinal columns. The upper motor neuron findings result in overactive tendon reflexes, Hoffman’s sign, clonus and Babinski signs.

[0005] If only the lower motor neurons are involved it is the variant progressive spinal muscular atrophy. If the upper motor neurons are more involved then it is called primary lateral sclerosis. But at autopsy both lower and upper motor neurons show involvement.

[0006] Other motor neuron disorders that could mimic symptoms of ALS include, but are not limited to, myasthenia gravis and cervical spondylotic myelopathy. A particularly difficult differential is multifocal motor neuropathy with positive GMl ganglioside antibodies, which responds to IV gammaglobulin. Treatment of the foregoing disorders is also contemplated by the invention. EMPHASIS ADDED

[0007] Thus the invention contemplates the treatment of motor neuron disease, including certain neurological disorders, motor neuropathic disorders, chronic inflammatory diseases, autoimmune disorders and . These conditions (in addition to those already described above) include, but are not limited to, Parkinson’s Disease, Guillain-Barre Syndrome, Porphyria, Systemic Lupus Erythematosus and Multiple Sclerosis. In addition, the present invention includes the therapeutic treatment of neurologic diseases resembling Amyotrophic Lateral Sclerosis or Parkinsonism, Autoimmune Disorders similar to Systemic Lupus Erythematosis, and Hypercoagulable disorders such as Lupus Anticoagulant disorder or Anti Phospholipid Syndrome causing chronic thrombosis, pulmonary emboli, strokes, and heart attacks.

Summary of the Invention

[0008] The invention is directed to the treatment of patients in need of treatment, generally, those who either have been diagnosed as suffering from or are presenting or exhibiting symptoms of a motor neuron disease or certain neurological disorders, motor neuropathies and chronic inflammatory diseases. In an embodiment of the invention, those certain neurological disorders, include chronic idiopathic neurological diseases. It has been surprisingly discovered that such patients can be treated by the administration of one or more active ingredients that are effective against, or otherwise antagonize the effects of, mycotoxin-producing organisms. Not wishing to be bound by theory, the inventor believes that a patient responding to the invention is suffering from a pathogenic

condition that is brought about by chronic poisoning due to extended exposure to one or more mycotoxins produced by one or more pathogens, including a fungus. In a preferred embodiment of the invention, a patient present symptoms of disease is treated with an effective amount of one or more anti- fungal agents.

Detailed Description of the Invention

[0009] The following aspects could also be involved in patients with ALS and other motor neuron diseases leading to slow relentless muscle paralysis or porphyria: The patient is immunocompromised due to one or more factors, such as diabetes mellitus, radiation or environmental exposures to toxins. However, sometimes a patient is not immunocompromised and becomes exposed to a fungus alone. Signs of immunosuppression could be depressed immunoglobulin production, lymphopenia and T- cell depletion. This suppressed lymphocytic immune system is predisposed to “opportunistic” infections by fungi. In any event, the patient is infected or colonized by one or more types of opportunistic fungi. Normally these fungi would cause minimal illness and be walled off in a granuloma and calcified. However, due to the immunosuppression the fungi are able to survive in the lymphatic or nervous system – chronically or indefinitely, releasing a steady low level of mycotoxins, including but not limited to trichothecenes, which progressively poison the patient over years. [0010] The selective motor paralysis could be due to the selective damage to mitochondria with ATP depletion. Of the known mycotoxins, the trichothecenes are especially potent and cause selective damage to mitochondria in motor neurons and skeletal muscle with ATP depletion and progressive muscular weakness and paralysis. Fungal or mycotic infections are often ignored as a cause of human disease given their ubiquity. Labs will report fungal infections without further speciation assuming it is insignificant. Physicians will write off a fungal infection as “colonization” without recommending further treatment for the diagnosed patient. Prior to the method of the invention it was widely believed that fungi are usually benign and simply “colonize” without causing pathology.

[0011] It is believed by the inventor that many motor neuron disease are forms of mycotoxicosis caused by mycotoxins released from opportunistic fungi colonizing the orifices of the human body. For discussion of mycotoxicosis, please see, J. W. Bennett & M. Klich, Clinical Microbiology Reviews (July 2003) 16(3):497-516. In the past these opportunistic fungi were ignored due to their low invasive capacity. One theory of the present invention is that these fungi with lower pathogenicity can cause human illness due to their release of potent toxins, if the fungus can survive or colonize especially the upper air ways. [0012] The known mycotoxins include: a. Aflatoxins (molecular weight ca. 300) from Aspergillus species b. Citrinin (molecular weight ca. 250) from Penicillium and Aspergillus species c. Ergot alkaloids (molecular weight ca. 600) from Claviceps d. Fumonisins (molecular weight ca. 600) from Fusarium species e. Ochratoxins (molecular weight ca. 400) from Aspergillus and Penicillum species f. Patulin (molecular weight ca. 200) from Penicillium species g. Trichothecenes (molecular weight ca. 400) from Fusarium, Myrothecium, Phomopsis, Stachybotrys, Trichoderma, Trichothecium and other species h. Zearalenone (molecular weight ca. 300) from Fusarium species i. Other mycotoxins such as yellow rice toxins

[0013] One embodiment of the present invention relates to treatment of fungi that cause opportunistic infection. Such fungi include members of the genus Fusarium. Species of the Fusarium genus that are possible targets for the treatment methods of the present invention include Fusarium aquaeductuum, Fusarium aquaeductuum var. media, Fusarium chlamydosporum, Fusarium coeruleum, Fusarium dimerum, Fusarium graminearum, Fusarium incarnatum, Fusarium moniliforme, Fusarium napiforme, Fusarium oxysporum, Fusarium proliferatum, Fusarium sacchari, Fusarium semitectum, Fusarium solani, Fusarium sporotrichoides, Fusarium sub glutinans, Fusarium tabacinum, and Fusarium verticillioides.

[0014] The present invention also relates to treatment of a patient diagnosed with or exhibiting symptoms of a motor neuron disease, neurological disorder, motor neuropathy, or chronic inflammatory disease by treating the patient for an opportunistic fungal infection. Examples of treatments for opportunistic fungal infections include administration of anti-fungal agents as well as blood filtration to remove toxins generated by fungi. Examples of blood filtration include an albumin column, a hepatic assist device (HAD), charcoal filtration, chromatography or a hepatic assist device. Guidance on treatment of toxicity and poison can be found in Brenner & Rector’s The Kidney, 7th edition, 2004. Sections of note in The Kidney that could be useful in the present invention include Chapter 62, Extracorporeal Treatment of Poisoning, and the sections entitled Urinary Alkanlinization and Acidification, Principles Governing Drug Removal by Extracorporeal Techniques, Dialysis Related Factors, Extracorporeal Techniques for Drug Removal, Hemoperfusion, Hemodialysis-Hemoperfusion, Table 62-6 Available Hemoperfusion Devices, Hemofiltration, and Continuous Renal Replacement Therapy. [0015] In the broader sense, the aforementioned mechanism could explain many chronic, idiopathic illnesses such as multiple sclerosis, Parkinsonism, Guillain-Barre Syndrome.

The common relationship between these diseases is that many infections can survive in humans for years and cause pathology by releasing potent toxins without obvious growth and direct physical damage. Due to the balance of apparent survival of the infection in a hostile environment within the human body, the organism causes indirect toxicity by releasing blood-borne poisons.

[0016] Major groups of toxins which may be implicated in this discovery include, but are not limited to, those described further, below.

[0017] Aflatoxins produced by Aspergillus species, they are largely associated with commodities produced in the tropics and sub-tropics, such as groundnuts, other edible nuts, figs, spices and maize. Alflatoxin Bl is the most toxic. [0018] Ochratoxin A is produced by Penicillium verrucosum, which is generally associated with temperate climates, and Aspergillus species which grows in warm humid conditions. Aspergillus ochraceus is found as a contaminant of a wide range of commodities including cereals and their products, fruit and a wide range of beverages and spices. Aspergillus carbonarius is the other main species associated in warm humid conditions found mainly on vine fruit and dried vine products particularly in the Mediterranean basin.

[0019] Patulin is associated with a range of fungal species and is found in moldy fruits, vegetables, cereals and other foods. It is destroyed by fermentation and so is not found in alcoholic drinks.

[0020] Fusarium toxins are produced by several species of the genus Fusarium, which infect the grain of developing cereals such as wheat and maize. They include a range of mycotoxins including the fumonisins, the trichothecenes, including deoxynivalenol, and zearalenone, the last two of which are very stable and can survive cooking. Diagnoses

[0021] In diagnosing this type of patient, the following history should be considered. The patient might have been exposed to a sufficiently high amount of environmental toxins or have a history of exposures. The patient could have evidence of immunodeficiency or multiple opportunistic infections that have longevity. Measurable toxins released by those infections that gradually increase in synchrony with the progression of the paralysis will be found in the patient. In particular, in the available patients, there is a steadily increasing anion-gap metabolic acidosis, as well as rising red cell protoporphyrins. EMPHASIS ADDED

Antifungal Treatment

[0022] In one embodiment of the present invention, ALS patients are treated with one or more anti-fungal agents. Treatment with antifungal agents should help aid the anion-gap metabolic acidosis and red cell protoporphyrins return toward normal levels and, in parallel, reduce the clinical findings especially the motor paralysis. Alternatively, oral binding agents (i.e. bile acid sequestrate) like cholestyramine, to bind up mycotoxin, are administered. The patients may also be subjected to hemodialysis with resins selected to remove mycotoxins. One or more of the preceding treatment regimens can also be combined. Preferably, the mycotoxins levels of the patient are tracked using available methods, using e.g., blood or urine samples of the patient. Optionally, one can measure ATP levels in muscles and spinal cord using, e.g., NMR/MRI – P31 scans. [0023] Antifungal agents can be administered to the patient in need thereof for a time period sufficient for the mycotoxins levels in a patient to be reduced or to completely disappear or otherwise become undetectable. Typically patients show a response over one to two months. Samples from a patient, e.g., body fluid, such as blood or urine, can be obtained and tested for a reduction in the levels of mycotoxin. Preferred antifungal agents include voraconazole (VFEND) and other antifungal agents that show activity against Fusarium infection. Other antifungal agents that are contemplated for administration include fluconazole, amphotericin B, terbinafme, flucytosine, itraconazole, ketoconazole posaconazole, ravuconazole, pimaricin, clotrimazole, econazole, ketoconazole, miconazole, oxiconazole, sulconazole, terconazole, tioconazole, amorolfme, butenafine HCl, naftif?ne, terbinafme, ciclopirox, olamine, haloprogin, tolnaftate, undecylenate, nikkomycin Z caspofungin, micafungin, anidulafungin, amphotericin B,lipid complex (ABLC), amphotericin B colloidal dispersion (ABCD,) liposomal amphotericin B (L- AMB), liposomal nystatin, griseofulvin, amorolfme, butenafine, nystatin and combinations thereof. The package insert sheets of the previously listed antifungal sheets, as well as the product reference sheets of all antifungal agents approved by the FDA, are hereby incorporated by reference. In one aspect of the invention, the antifungal agent is a prescription antifungal agent that is approved by the FDA. It is emphasized, however, that the invention is not limited to antifungal agents that are approved for marketing by the FDA. Any agent that exhibits antifungal activity is suitable for use in the invention. By antifungal activity is meant actually killing the fungus, disabling it, or acting to remove it or the mycotixins it produces from a patient by the action of binding, chelating and the like, separating or filtering the fungus or mycotoxins from a patient. Particularly useful antifungal agents are those that are capable of treating members of the genus Fursarium, which can cause opportunistic infections and produces the toxin trichothecenes. [0024] Dosages are given in the levels typically prescribed in the art. For example, antifungal regimens are commonly prescribed in line with regimens known in the art. For voraconazole, tablets are generally given orally, twice at day at a dosage of 300 mg/day. A dosage range of administration of 20 mg to 400 mg, preferably 100 mg to 400 mg, given orally administered, once, twice or three times daily is also contemplated. Alternatively, invra venous dosages of VFEND can be given, such as 3 to 6 mg/kg every 12 hours. For Amphotericin, dosages should be tailored, as is known in the art, in accordance with patient tolerance. For example, 0.1- 0.8 mg/kg/day, up to 2.5 g total doses, are possible.

Blood Filtration Treatment

[0025] Treatment with a charcoal column, also known as charcoal hemoperfusion or active charcoal hemoperfusion, can aid patients as well. Charcoal columns can be used under conditions that are standard in the art for treating those suffering from toxic ingestion, such as by eating poisonous mushrooms, for example amatoxin poisoning, or drug intoxication. For example charcoal hemoperfusion can be carried out with a cartridge of activated charcoal. Such charcoal can be coated with a membrane, such as cellulose, to reduce the undesirable deposition of blood components. An example of such commercially available cartridges are Adsorba® 150C (150 grams of activate charcoal) and Adsorba® 300C (300 grams of activate charcoal). Regimens for charcoal hemoperfusion can be based upon regimens already established for treatment of toxic ingestion. For example at a blood flow rate of 100-400 ml/min, preferably 250ml/min, treatment via French femoral catheters can be carried out for two to six hours a day, for two to five consecutive days. Other types of columns, such as resin columns and cartridges, and albumin columns and cartridges, are expected to have beneficial therapeutic effects. Hemoperfusion using affinity columns directed at the mycotoxins and charcoal cartridges or albumin cartridges can rapidly reduce the mycotoxin levels and result in remarkable improvement in the clinical findings. The capacity to dialyze these toxins preferably occurs with molecules at or below 550 molecular weight and the majority of mycotoxins are accessible to this technique.

[0026] Additionally, hepatic assistant devices (HADs) and extracorporeal liver support devices, which perform hemodialysis, can be used with the method of treatment of the present invention. Examples of HADs included plasmapheresis devices, albumin dialysis devices, and molecular absorption recirculation systems. HADs can be used to supplement ongoing treatment with antifungal agents or independently to treat patients without antifungal agents. In addition, for those patients who do not show results with antifungal agent administration, sometimes therapeutic results can be achieved with HADs or charcoal haemoperfusion.

Long Term Fiber and Charcoal Treatment

[0027] In addition, the administration of fiber and activated powdered charcoal can be beneficial. The patient is given increased doses of fiber, such a Metamucil. The goal is to increase intake to up to 30 gm/day as the patient tolerates, and add the activated charcoal 1-2 times a month for 5 years or more. This approach slowly removes poisons with minimal short term toxicity. Long term, the combination of high fiber and activated charcoal, can deplete multiple nutrients causing vitamin and mineral deficiencies. It is important over the long term to replete vitamins and minerals while monitoring for osteoporosis and vitamin deficiencies.

[0028] For the fiber, initially about 3 and 6 gm servings are mixed in room temperature water and then consumed. The dose is slowly increased over months to about 6 gm twice a day, then about 12 gm twice a day, then about 18 gm in the morning and about 12 gms at night. The patient should eventually have a regular bowel movement with every meal. Therefore, the preferred dosage range is from about 3 to 50 grams of fiber. [0029] For activated charcoal, patient is administered activated powdered charcoal, preferably added to the fiber, preferably about once or twice a month. In order to prevent vitamin and mineral depletion, patient should take double or triple doses of daily essential vitamins and minerals, such as B-Complex, Vitamins A, D, E, Omega Fatty Acids, Coenzyme Q, Folic Acid(3000-5000 meg/day), Pyridoxine 100 mg a day, and Magnesium

Chloride or Oxide(400-800 mg/day). Also need increase amounts of calcium or dairy products. Patients can be periodically checked for osteoporosis by methods known in the art such as Dex Scans. Known methods can be used to monitor the patients for vitamin and mineral deficiency. [0030] For charcoal, approximately 1 tablespoon can be administered.

Other Diseases

[0031] In general patients suffering from other diseases, besides ALS, that are chronic idiopathic or chronic idiopathic neurologic disorders such as multiple sclerosis, parkinsonism, Guillain Barre and porphyria can benefit from the antifungal treatment of the invention.

Detection of Mycotoxins

[0032] Measurement of blood for mycotoxins using mass spectroscopy can confirm the diagnosis of mycotoxicosis. In particular, new procedures can quantify these mycotoxins bound to serum proteins such as human albumin called Albumin Adducts, See Iwona Yikes, et al, Environ Health Perspectives 114(8): 1221-1226, Aug. 2006, Mycotoxin Adducts…

[0033] All references cited in this specification are incorporated by reference herein in their entirety.

Example 1

[0034] A 42 year old female was diagnosed with ALS. Patient had developed gradual onset of fasciculations, then weakness, then paralysis and became ventilator dependent. Only residual function was right distal phalanx of thumb and eyes. Exposure was at animal shelter, where patient was exposed to moldy dog food. Patient had markedly elevated protoporphyrins, positive anion gap metabolic acidosis and urine organic acids elevated with pattern consistent with mitochondrial damage. Trichothecene level in urinewas 13/18 and ELISA revealing the following antibodies in blood: aflatoxin, stachytoxin, trichothecene,T-2, mycophenolic acid, HSP70, ocratoxin, Stachyhemolysin, alternariol, chaetogloboside, vomitoxin. EMPHASIS ADDED

[0035] Patient was placed on a regimen of the antifungal voriconazole (VFEND) and hemoperfusion with activated charcoal. Voriconazole was administered orally, twice a day, at 200 mg per dosage. This treatment resulted in protoporphyrins returning to normal, resolution of anion gap, movement of left hand at wrist. Due to patient’s insurance provider denying payment for treatment by antifungals, voriconazole and charcoal regimen was stopped, and patient returned to previous state in about two weeks, including elevated protoporphyrin levels, positive anion gap, and loss of movement of left hand. EMPHASIS ADDED

Example 2

[0036] A 52 year old male was diagnosed with ALS. Patient was on ventilator with paralysis from neck down. Patient could move his chin only. Patient operates computer with head movement using dot on chin. The trichothecene level in patient’s urine was 10/18 and ELISA of blood showed stachytoxin, alternariol, aomitoxin, chaetoglobosins, trichothecene, mycophenolic acid, ochratoxin, and aspergillus. EMPHASIS ADDED

[0037] Patient was placed on a regimen according to the invention of voriconazole and cholestyramine. Voriconazole was administered orally, twice a day, at 300 mg per dosage. The administration of cholestyramine is optional. Patient displayed reduction in protoporphyrins, reduction anion gap metabolic acidosis, and elevated Kreb cycle metabolites. Antifungal therapy led to consistent improvement in the results of patient’s lab tests with a reduction in his metabolic acidosis and red cell protoporphyrins. Patient began to move hands for the first time in years. EMPHASIS ADDED

Example 3

[0038] A 44 year old female was diagnosed with ALS. Fasciculations began with leg cramps and due to respiratory failure was placed on a ventilator. Patient had slurred speech, dysarthria, near complete paralysis except movement of hands partially. Elevated protoporphyrins but minimal to no acidosis. Trichothecene level was 9/18 and ELISA showed positives for alternariol, vomitoxin, T-2, chaetogloboside, stachytoxin, trichothecene, mycophenolic acid, aflatoxin, aspergillus hemolysis. [0039] Treatment similar to that described above provides positive results. Voriconazole was administered orally, twice a day, at 300 mg per dosage. EMPHASIS ADDED

Example 4

[0040] A 65 year old female with progressive neurologic disorder was diagnosed at first as Guillain-Barre and then as ALS. She is still ambulatory though cachectic and homebound with diffuse weakness. Trichothecene level in urine was 8/18. Patient was treated with itraconazole (SPORONOX) but apparently unsuccessful for reasons that are unknown. EMPHASIS ADDED

Example 5

[0041] A 69 year old male with progressive neurologic disorder was diagnosed with Parkinson’s disease or ALS. Patient had muscle weakness and difficulty walking. Trichothecene level in 24 hr urine was 8/18 and ELISA of blood showed aspergillus, aflatoxin, ochratoxin, mycophenolic acid, trichothecene, stachyhemolysis, stachytoxin, cladosporium, chaetoglobosin, T-2, vomitoxin and alternariol. Apparently, patient was exposed to pathogens from a contaminated basement. EMPHASIS ADDED

[0042] Patient showed marked improvement in only two months of antifungal treatment, almost back to baseline. Interestingly, if the antifungal agents are stopped, there is a rapid return of the original symptoms. Exposure is unknown. Voriconazole was administered orally, twice a day, at 300 mg per dosage. EMPHASIS ADDED

Example 6

[0043] A 41 year old male was diagnosed with ALS. Patient experienced gradual onset of weakness and was diagnosed with ALS after he could not turn light switches on and off. Patient has dysarthria with slurred speech and is still ambulatory. Trichothecene level was 11/18. Exposure is unknown. EMPHASIS ADDED

[0044] Patient was placed on a regimen of the anti fungal voriconazole (VFEND) and charcoal, as described above. Voriconazole was administered orally, twice a day, at 300 mg per dosage. Positive improvement in symptoms is observed eventually. EMPHASIS ADDED

Example 7

[0045] A 41 year old female was diagnosed with systemic lupus erythematosis. Patient complained of mental confusion and weakness, and also had polyarthritis and chronic fatigue. Patient had been unsuccessfully treated with hydroxychloroquine sulfate (PLAQUENIL). The trichothecene level was 6/18. Patient had been likely exposed to fungus from building ventilation system; co-workers had also become ill. [0046] Patient was treated with Amphotericin B , Vfend and cholestyramine. Voriconazole was administered orally, twice a day, at 300 mg per dosage. Patient’s ANA test for first time in years reverted to normal and all of her symptoms and signs resolved within a few months. However, stopping treatment had gradual recurrence of symptoms but not to previous severity. EMPHASIS ADDED

Example 8

[0047] A 35 year old male was diagnosed with porphyria. Symptoms were chronic abdominal pain, personality disorder, and severe headaches. He was homebound unable to work due to symptoms. He was also hypercoagulable with recurring deep venous thrombosis. Trichothecene was 9-10/18. Patient’s wife (Example 7) was exposed to fungus from building ventilation system. EMPHASIS ADDED

[0048] After about 3-6 months of treatment using voriconazole, amphotericin B, and cholestyramine he had almost complete resolution of his symptoms. Voriconazole was administered orally, twice a day, at 300 mg per dosage. Patient went back to work after over 10 years of the illness. EMPHASIS ADDED

Example 9

[0049] Similarly, patients diagnosed with multiple sclerosis, Parkinson’s Disease, Guillain-Barre Syndrome and lupus are shown to improve using the methods of the invention.

[0050] Preferred embodiments have been described above to illustrate certain aspects of the invention. The invention should not be construed, however, as being limited to the specific embodiments described, as a reader of ordinary skill will appreciate that the invention is broad and generic in concept.

Example 10

[0051] Four patients (3 ventilator-dependent) with a diagnosis of Motor Neuron Disease/ Amyotrophic Lateral Sclerosis were found to have colonization of their upper airways by toxogenic fungi. Cultures of the tracheostomy, lung, sinuses & nasal passages grew out fungi known to produce mycotoxins including Dematiaceous moulds, Fusarium, Alternarium, Cladosporium, Phoma, Aspergillus and Penicillium. Blood work in all 4 patients showed Protoporphyrinemia without evidence of Iron Deficiency, as well as an Anion-Gap Metabolic Acidosis. Twenty four hour urines for Organic Acids were positive for Citric Acid Cycle Metabolites. Muscle biopsies were consistent with Denervation pattern. EMPHASIS ADDED

[0052] Prolonged treatment over a month with anti-fungal agents including Voraconazole, Posaconazole and Caspofungin resulted in partial to complete correction of the protoporphyrinemia and the anion-gap metabolic acidosis. Discontinuing the antifungal agents resulted in a rise in the protoporphyrin levels and anion-gap metabolic acidosis to the pre-treatment levels over a period of 2-4 weeks. Hemoperfusion with Charcoal Cartridges with continued anti-fungal therapy resulted in significant improvement in their motor function. Based on these findings, I would conclude that Colonization of the Upper Airways by Opportunistic Fungi can release significant levels Mycotoxins that exacerbate the clinical findings in patients with Amyotrophic Lateral Sclerosis. Reduction of the fungal colonization with anti-fungal agents and hemoperfusion with charcoal cartridgies can result in clinical improvement including a reduction in paralysis.

[0053] For a reference disclosing certain fungi known to produce mycotoxins, the reader is referred to J. W. Bennett & M. Klich, Mycotoxins, Clinical Microbiology Reviews (July 2003) 16(3):497-516, which also contains chemical structural information for certain mycotoxins. Indeed, certain mycotoxins, particularly macrocyclic trichothecenes, are known to produce adducts with human serum albumin (“HSA”). See, for example, Iwona Yikes et al. Environmental Health Perspectives (August 2006) 114(8): 1221-1226, which also contains a disclosure of a protocol for isolation of such mycotoxin-HSA adducts and their subsequent analysis and identification by selected techniques, including mass spectrometry. Hence, if desired, one can utilize mass spectrometry to confirm the presence of mycotoxins in biological samples (e.g., blood, tissue, or urine samples) taken from subjects suffering from disease conditions implicated by the present invention. For a disclosure on extracorporeal treatment of poisoning, please see, for example, I. J. Chang et al. in Brenner & Rector’s The Kidney, 7th Ed (2004), pg. 2733-2741, Chapter 62. The disclosures of all of the foregoing publications is incorporated in their entirety by reference herein. Other treatment regimens may also become apparent to one of ordinary skill once familiar with the aspects of the present invention.

Mycopathologia. 2010 Dec;170(6):377-90. Epub 2010 Jun 13.

Building-associated neurological damage modeled in human cells: a mechanism of neurotoxic effects by exposure to mycotoxins in the indoor environment.

Karunasena E, Larrañaga MD, Simoni JS, Douglas DR, Straus DC.

SOURCE

Department of Animal & Food Sciences, Texas Tech University, Lubbock, TX 79409, USA. enusha.karunasena@ttuhsc.edu

ABSTRACT

Damage to human neurological system cells resulting from exposure to mycotoxins confirms a previously controversial public health threat for occupants of water-damaged buildings. Leading scientific organizations disagree about the ability of inhaled mycotoxins in the indoor environment to cause adverse human health effects. Damage to the neurological system can result from exposure to trichothecene mycotoxins in the indoor environment. This study demonstrates that neurological system cell damage can occur from satratoxin H exposure to neurological cells at exposure levels that can be found in water-damaged buildings contaminated with fungal growth. The constant activation of inflammatory and apoptotic pathways at low levels of exposure in human brain capillary endothelial cells, astrocytes, and neural progenitor cells may amplify devastation to neurological tissues and lead to neurological system cell damage from indirect events triggered by the presence of trichothecenes.

Trichothecene mold toxin destroys kidney cells and lung fibroblasts

Toxicology. 2007 Oct 30;240(1-2):48-59. Epub 2007 Aug 1.

Cytotoxicity, metabolism and cellular uptake of the mycotoxin deoxynivalenol in human proximal tubule cells and lung fibroblasts in primary culture.

Königs M, Lenczyk M, Schwerdt G, Holzinger H, Gekle M, Humpf HU.

Institut für Lebensmittelchemie, Westfälische Wilhelms-Universität Münster, Corrensstrasse 45, 48149 Münster, Germany.

ABSTRACT

At the level of the whole animal, the toxic effects of the mycotoxin deoxynivalenol (DON) range from causing diarrhoea, vomiting, gastro-intestinal inflammation to necrosis of several tissues. It also affects the immune system and leads to kidney lesions. Although DON has been tested in different human and animal cell lines for its cytotoxicity, these tests might be limited due to the disadvantages of cell lines (e.g. immortalization, tumour derivation, longtime cultivation) and do not necessarily reflect the response of normal cells. In order to overcome this problem and to be closer to the human situation, we studied the effect of DON in human kidney epithelial cells (renal proximal tubule epithelial cells, RPTEC) and human lung fibroblasts (normal human lung fibroblast, NHLF) in primary culture. Cell viability, apoptotic and necrotic cell death, collagens I, III and IV as well as fibronectin secretion were determined. It could be demonstrated that DON has a distinct cytotoxic effect on human primary cells. A reduction in viability can be observed in both cell types, with fibroblasts reacting more sensitive. Furthermore, DON caused mainly necrotic cell death in kidney cells whereas mainly apoptotic cell death in fibroblasts. DON had no effect on collagen secretion in RPTEC cells. Collagen secretion was partially decreased in NHLF. In both cells, fibronectin secretion was reduced after 5 days of exposure. We also studied the metabolism and the cellular uptake of DON using LC-MS/MS. DON was neither metabolized by proximal tubule cells nor by fibroblasts. DON is incorporated into the cells whereas the intracellular amount of DON in kidney cells is higher than in fibroblasts. No accumulation of DON occurred in the cells. EMPHASIS ADDED

PMID: 1782597

Study Reveals How T-2 Mold Toxin Destroys Joint Cartilage

Trichothecene mold toxins, produced by Fusarium, Stachybotrys, Tricoderma and other molds, are a hidden cause of arthritis, memory loss, headache, fatigue, anxiety, panic attacks and insomnia.

Selenium can reduce cartilage destruction caused by Trichothecene mold toxin. Trichothecene is produced by Stachbotrys chartarum, "the infamous indoor “black mold,” Fusarium and Tricoderma molds, which can poison people, living or working in water damaged buildings.

Matrix Metalloproteinases transport mold and Lyme neurotoxins from the bloodstream, into tissues, including joint cartilage. Florida Detox and Wellness Institute uses Resveratrol from Polygonum cuspidatum, to arrest transport of neurotoxins into tissues, by metalloproteinases.

Real Time Labatories, LLC, www.RealTimeLab.com , offers urine testing of tricothecene, aflatoxin and ochratoxin.

Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect*

Si-yuan Li,1 Jun-ling Cao,†‡1 Zhong-li Shi,1 Jing-hong Chen,1 Zeng-tie Zhang,1 Clare E. Hughes,2 and Bruce Caterson†‡2

1Institute of Endemic Diseases, College of Medicine, Xi’an Jiaotong University; Key Laboratory of Environment and Genes Related to Diseases (Xi’an Jiaotong University), Ministry of Education; Key Laboratory of Microelement and Endemic Disease(Xi’an Jiaotong University), Ministry of Health; Xi’an 710061, China

2Laboratory of Connective Tissue Biology, School of Biosciences, Cardiff University, Cardiff CF10 3US, UK

‡Corresponding Author

†E-mail:caojl@mail.xjtu.edu.cn

, caterson@cardiff.ac.uk

Received June 20, 2007; Accepted November 7, 2007.

This article has been cited by other articles in PMC.

  • Other Sections?
  • Abstract
  • INTRODUCTION
  • MATERIALS AND METHODS
  • RESULTS
  • DISCUSSION
  • References

Abstract

Objective: To identify the relationship between T-2 toxin and Kashin-Beck disease (KBD), the effects of T-2 toxin on aggrecan metabolism in human chondrocytes and cartilage were investigated in vitro. Methods: Chondrocytes were isolated from human articular cartilage and cultured in vitro. Hyaluronic acid (HA), soluble CD44 (sCD44), IL-1? and TNF-? levels in supernatants were measured by enzyme-linked immunosorbent assay (ELISA). CD44 content in chondrocyte membrane was determined by flow cytometry (FCM). CD44, hyaluronic acid synthetase-2 (HAS-2) and aggrecanases mRNA levels in chondrocytes were determined using reverse transcription polymerase chain reaction (RT-PCR). Immunocytochemical method was used to investigate expressions of BC-13, 3-B-3(?) and 2-B-6 epitopes in the cartilage reconstructed in vitro. Results: T-2 toxin inhibited CD44, HAS-2, and aggrecan mRNA expressions, but promoted aggrecanase-2 mRNA expression. Meanwhile, CD44 expression was found to be the lowest in the chondrocytes cultured with T-2 toxin and the highest in control plus selenium group. In addition, ELISA results indicated that there were higher sCD44, IL-1? and TNF-? levels in T-2 toxin group. Similarly, higher HA levels were also observed in T-2 toxin group using radioimmunoprecipitation assay (RIPA). Furthermore, using monoclonal antibodies BC-13, 3-B-3 and 2-B-6, strong positive immunostaining was found in the reconstructed cartilage cultured with T-2 toxin, whereas no positive staining or very weak staining was observed in the cartilage cultured without T-2 toxin. Selenium could partly inhibit the effects of T-2 toxin above. Conclusion: T-2 toxin could inhibit aggrecan synthesis, promote aggrecanases and pro-inflammatory cytokines production, and consequently induce aggrecan degradation in chondrocytes. These will perturb metabolism balance between aggrecan synthesis and degradation in cartilage, inducing aggrecan loss in the end, which may be the initiation of the cartilage degradation.

The neurological significance of abnormal natural killer cell activity in chronic toxigenic mold exposures.

Anyanwu E, Campbell AW, Jones J, Ehiri JE, Akpan AI.

SOURCE

Neurosciences Research, Cahers Inc., Conroe, TX, USA. ebereanyanwu@msn.com

ABSTRACT

Toxigenic mold activities produce metabolites that are either broad-spectrum antibiotics or mycotoxins that are cytotoxic. Indoor environmental exposure to these toxigenic molds leads to adverse health conditions with the main outcome measure of frequent neuroimmunologic and behavioral consequences. One of the immune system disorders found in patients presenting with toxigenic mold exposure is an abnormal natural killer cell activity. This paper presents an overview of the neurological significance of abnormal natural killer cell (NKC) activity in chronic toxigenic mold exposure. A comprehensive review of the literature was carried out to evaluate and assess the conditions under which the immune system could be dysfunctionally interfered with leading to abnormal NKC activity and the involvement of mycotoxins in these processes. The functions, mechanism, the factors that influence NKC activities, and the roles of mycotoxins in NKCs were cited wherever necessary. The major presentations are headache, general debilitating pains, nose bleeding, fevers with body temperatures up to 40 degrees C (104 degrees F), cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, vertigo/dizziness, and in some cases, seizures. Although sleep is commonly considered a restorative process that is important for the proper functioning of the immune system, it could be disturbed by mycotoxins. Most likely, mycotoxins exert some rigorous effects on the circadian rhythmic processes resulting in sleep deprivation to which an acute and transient increase in NKC activity is observed. Depression, psychological stress, tissue injuries, malignancies, carcinogenesis, chronic fatigue syndrome, and experimental allergic encephalomyelitis could be induced at very low physiological concentrations by mycotoxin-induced NKC activity. In the light of this review, it is concluded that chronic exposures to toxigenic mold could lead to abnormal NKC activity with a wide range of neurological consequences, some of which were headache, general debilitating pains, fever, cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, and seizures.

PMID: 14625399 [PubMed

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Mold Toxicity

RECENT RESEARCH REVEALS 24 PERCENT OF POPULATION CLEARS MOLD TOXINS FROM THEIR BODY 468 TIMES SLOWER THAN THE REMAINING 76 PERCENT OF THE POPULATION. THIS EXPLAINS WHY THREE OUT OF FOUR UNRELATED WORKERS IN A MOLD TOXIC WORKPLACE MAY NOT BE SEVERELY AFFECTED BY INDOOR MOLD. IF YOU ARE EXPERIENCING SEVERE HEALTH SYMPTOMS, AFTER INDOOR WATER LEAKS OR IN A BUILDING WITH MOLDY, MUSTY ODORS, YOU ARE NOT CRAZY. SEE THE MOLD TESTING PAGE FOR RECOMMENDED TESTING. A FEW OF THE SCIENTIFIC STUDIES VALIDATING HEALTH EFFECTS OF INDOOR TOXIC MOLD ARE DISCUSSED BELOW.

STUDY REVEALS SATRATOXIN NEUROTOXIN CONCENTRATIONS FOUND IN MOLDY BUILDINGS CAUSED NEUROLOGICAL DAMAGE

(The infamous toxic black mold, Stachybotrys chartarum, produces Satratoxin neurotoxins, which caused neurological damage, at concentrations found in mold contaminated buildings)

Mycopathologia. 2010 Dec;170(6):377-90. Epub 2010 Jun 13.

Building-associated neurological damage modeled in human cells: a mechanism of neurotoxic effects by exposure to mycotoxins in the indoor environment.

Karunasena E, Larrañaga MD, Simoni JS, Douglas DR, Straus DC.

SOURCE

Department of Animal & Food Sciences, Texas Tech University, Lubbock, TX 79409, USA. enusha.karunasena@ttuhsc.edu

ABSTRACT

Damage to human neurological system cells resulting from exposure to mycotoxins confirms a previously controversial public health threat for occupants of water-damaged buildings. Leading scientific organizations disagree about the ability of inhaled mycotoxins in the indoor environment to cause adverse human health effects. Damage to the neurological system can result from exposure to trichothecene mycotoxins in the indoor environment. This study demonstrates that neurological system cell damage can occur from satratoxin H exposure to neurological cells at exposure levels that can be found in water-damaged buildings contaminated with fungal growth. The constant activation of inflammatory and apoptotic pathways at low levels of exposure in human brain capillary endothelial cells, astrocytes, and neural progenitor cells may amplify devastation to neurological tissues and lead to neurological system cell damage from indirect events triggered by the presence of trichothecenes. EMPHASIS ADDED

PMID:

20549560

Toxicol Ind Health. 2009 Oct-Nov;25(9-10):583-615. Epub 2009 Sep 30.

This 2009 study found aflatoxin mold toxins are transported to the brain temporal lobe. It also found gliotoxins in blood and lung secretions of Aspergillosis patients, with cancer. The gliotoxins were produced by A. fumigatus, A. terreus, A. niger and A. flavus. Aflatoxin B1 is one of the most carcinogenic substances known to man. Although the "toxic black mold" Stachybotrys chartarum has received more press, Aspergillus molds are more common in water damaged buildings and are also highly toxic. If Aspergillus mold is identified, 24 percent of the population with genetically decreased ability to clear mold neurotoxins are at high risk, in the building, till mold is destroyed and the building is decontaminated.

The biocontaminants and complexity of damp indoor spaces: more than what meets the eyes.

Thrasher JD, Crawley S.

SOURCE

National Toxic Encephalopathy Foundation, Las Vegas, Nevada, USA. toxicologist1@msn.com

ABSTRACT

Nine types of biocontaminants in damp indoor environments from microbial growth are discussed: (1) indicator molds; (2) Gram negative and positive bacteria; (3) microbial particulates; (4) mycotoxins; (5) volatile organic compounds, both microbial (MVOCs) and non-microbial (VOCs); (6) proteins; (7) galactomannans; (8) 1-3-beta-D-glucans (glucans) and (9) lipopolysaccharides (LPS--endotoxins). When mold species exceed those outdoors contamination is deduced. Gram negative bacterial endotoxins, LPS in indoor environments, synergize with mycotoxins. The gram positive Bacillus species, Actinomycetes (Streptomyces, Nocardia and Mycobacterium), produce exotoxins. The Actinomycetes are associated with hypersensitivity pneumonitis, lung and invasive infections. Mycobacterial mycobacterium infections not from M. tuberculosis are increasing in immunocompetent individuals. In animal models, LPS enhance the toxicity of roridin A, satratoxins G and aflatoxin B1 to damage the olfactory epithelium, tract and bulbs (roridin A, satratoxin G) and liver (aflatoxin B1). Aflatoxin B1 and probably trichothecenes are transported along the olfactory tract to the temporal lobe. Co-cultured Streptomyces californicus and Stachybotrys chartarum produce a cytotoxin similar to doxorubicin and actinomycin D (chemotherapeutic agents). Trichothecenes, aflatoxins, gliotoxin and other mycotoxins are found in dust, bulk samples, air and ventilation systems of infested buildings. Macrocyclic trichothecenes are present in airborne particles microm. Trichothecenes and stachylysin are present in the sera of individuals exposed to S. chartarum in contaminated indoor environments. Haemolysins are produced by S. chartarum, Memnoniella echinata and several species of Aspergillus and Penicillium. Galactomannans, glucans and LPS are upper and lower respiratory tract irritants. Gliotoxin, an immunosuppressive mycotoxin, was identified in the lung secretions and sera of cancer patients with aspergillosis produced by A. fumigatus, A. terreus, A. niger and A. flavus. EMPHASIS ADDED

PMID:

19793773

In an interview, Dr. Trasher explains that even opening a door in a mold contaminated building can increase exposure to airborne mold toxins and that many bacterial toxins also occur in water damaged buildings.

Let us keep in mind that air sampling does not detect hidden mold growth. Mold growth is hidden in places we do not see: attic, wall cavities, crawlspace, back side of carpeting and wall board. The attic wall cavities and crawl spaces are in communication with the interior of the home/building. Pressure shocks dislodge mold spores from these areas into the interior of the home. The pressure shocks include wind and opening and closing of doors.

1. WHAT IS A TOXICOLOGIST?

Good question. Most lay people do not understand what a toxicologist is. Basically, he/she studies the adverse (sometimes it can be beneficial) effects of organic and inorganic chemicals (heavy metals) on animals and humans. The studies undertaken involve pathology and the biochemical effects of the toxins. For example, it is established that mycotoxins produced by several species of molds can have several toxic effects. These include inhibition of protein synthesis, adduction to proteins and DNA producing adverse effects on the function of these biological molecules, inducement of cell death (apoptosis), toxicity to the immune system and brain, and synergism (the ability of one chemical to increase the toxicity of two chemicals combined). In this latter category it has been demonstrated that mycotoxins have synergism, mycotoxins and endotoxins (lipopolysaccharides) have synergism, and toxins produced by certain bacteria (Streptomyces and Nocardia) have synergism with mycotoxins.

2. NOT ALL TOXICOLOGISTS UNDERSTAND MOLD THE WAY YOU DO. HOW DID YOU COME TO HAVE THIS AREA OF EXPERTISE?

I do not know about other toxicologists, but I pride myself on reading and understanding all of the peer reviewed literature I can locate regarding a given toxic compound. In the case of indoor air there is a multitude of potential toxins. The indoor biocontaminants that occur in relation to water intrusion and microbial growth are an excellent example of this. The media, attorneys, and the medical profession have zeroed in on only two aspects of this environment: Molds and their mycotoxins. In reality the indoor environment is a complex mixture of biological contaminants. These include molds and their by-products, such as mycotoxins and hemolysins; bacteria and their by-products (gram negative and positive bacteria); microbial volatile organic compounds; exotoxins and endotoxins produced by bacteria; particulates, ranging from nanoparticles up to mold spore size, glucans and galactomannans.

Dr. Brasel and Dr. Gorny have demonstrated that the particles less than 2 microns also contain a significant quantity of bacterial and mold toxins. These small particles are inhaled deeply into alveolar spaces of the lungs and readily release their toxins into the blood. Thus, Dr. Brasel demonstrated trichothecenes in the sera of exposed subjects, while Van Emon demonstrated Stachylysin (hemolytic protein) in a different group of exposed humans. Also, nanoparticles (part of this fraction of particulates) readily enter the bloodstream from the alveolar spaces. Finally, Dr. Calderon-Garciduenas has demonstrated that particles attached to the olfactory neurons in the nasal cavity travel up the olfactory tract and enter the brain of humans, causing brain damage.

I have reviewed the literature on these various aspects and I have written a paper titled: "The Biocontaminants and Complexity of Damp Indoor Spaces: More than Meets the Eyes." This paper is scheduled to be published in Toxicology and Industrial Health in the September/October issue along with approximately 16 other papers on the adverse effects of exposure of humans to damp indoor spaces.

Study Found Volatile Mycotoxins in 62 Percent of Samples From Moldy Buildings

JEM Spotlight: Fungi, mycotoxins and microbial volatile organic compounds in mouldy interiors from water-damaged buildings.

Polizzi V, Delmulle B, Adams A, Moretti A, Susca A, Picco AM, Rosseel Y, Kindt R, Van Bocxlaer J, De Kimpe N, Van Peteghem C, De Saeger S.

Ghent University, Faculty of Pharmaceutical Sciences, Laboratory of Food Analysis, Harelbekestraat 72, B-9000 Ghent, Belgium.

Comment in:

J Environ Monit. 2009 Oct;11(10):1847-8.

Concerns have been raised about exposure to mycotoxin producing fungi and the microbial volatile organic compounds (MVOCs) they produce in indoor environments. Therefore, the presence of fungi and mycotoxins was investigated in 99 samples (air, dust, wallpaper, mycelium or silicone) collected in the mouldy interiors of seven water-damaged buildings. In addition, volatile organic compounds (VOCs) were sampled. The mycotoxins were analysed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) (20 target mycotoxins) and quadrupole time-of-flight mass spectrometry (LC-Q-TOF-MS). Morphological and molecular identifications of fungi were performed. Of the 99 samples analysed, the presence of one or more mycotoxins was shown in 62 samples by means of LC-MS/MS analysis. The mycotoxins found were mainly roquefortine C, chaetoglobosin A and sterigmatocystin but also roridin E, ochratoxin A, aflatoxin B(1) and aflatoxin B(2) were detected. Q-TOF-MS analysis elucidated the possible occurrence of another 42 different fungal metabolites. In general, the fungi identified matched well with the mycotoxins detected. The most common fungal species found were Penicillium chrysogenum, Aspergillus versicolor (group), Chaetomium spp. and Cladosporium spp. In addition, one hundred and seventeen (M)VOCs were identified, especially linear alkanes (C(9)-C(17)), aldehydes, aromatic compounds and monoterpenes.

Strauss DC, Wilson SC. Correspondence re Respirable trichothecene mycotoxins can be demonstrated in the air of Stachybotrys chartarum–contaminated buildings

  • Journal of Allergy and Clinical Immunology
  • This correspondence is in response to the American Academy of Allergy, Asthma and Immunology

position paper recently published in the Journal and entitled “The medical effects of mold exposure.”

The authors imply that the most important way that trichothecene mycotoxins could get into the human body is via the inhalation of Stachybotrys chartarum (SC) conidia. We have recently shown that the number of SC conidia in the air in a SC-infested building is not a good predictor for the amount of macrocyclic trichothecene mycotoxins (MTMs) in the air. This is because the MTMs can exist in the air on fungal fragments free of conidia, so the number of SC conidia found in the air should play only a small role in determining airborne MTM levels. This becomes very important because it has recently been shown that there are 514 times more SC fungal fragments released by this organism than there are SC conidia released. The authors also imply that the idea that the presence of mycotoxins in a building should give rise to an array of nonspecific complaints is “not consistent with what is known to occur when a toxic dose is achieved.” This simply is not the case.

Indeed, in a report examining the introduction of this type of mycotoxin (a trichothecene) into human beings, the opposite was observed. We know what kinds of symptoms are observed when a simple trichothecene (a preparation of diacetoxyscirpenol, also known as anguidine) is injected into humans. They are (among others) nausea, vomiting, low blood pressure, drowsiness, ataxia, and mental confusion. These symptoms are consistent with those reported by individuals in SC-infested buildings. The authors also state, “…however, potential levels of mycotoxins in nonagricultural air samples are too low to be measured practically with this technology.” That may be true regarding the discussed technology; however, we have measured MTMs in the air of nonagricultural buildings.

Finally, the authors stated, “Testing for airborne mycotoxins in nonagricultural environments cannot be used to diagnose mold exposure.” This is not the case. We have successfully preformed airborne testing for MTMs in nonagricultural settings.[6] In fact, we have used an ELISA to measure MTMs in the serum of individuals from SC-infested buildings. In conclusion, we feel that the following statements are true. SC has been shown to grow in buildings where people are having health problems. SC definitely produces MTMs in these situations. These MTMs definitely get into the air in these buildings, where they can be inhaled. They definitely are following, then, is the final question that remains to be answered: do the MTMs get into inhaled by people in these buildings.

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Plumbers + Roofers

Plumbers, Roofers, Heating, Ventilation and Air Conditioning (HVAC) specialists are crucial front line warriors in the fight against indoor toxic mold. Water intrusion must be controlled, to stop indoor toxic mold. Finding an unexpected plumbing or roof leak or dealing with a flooded building can be very stressful, especially if you are severely mold susceptible or can not afford to spend thousands of dollars repairing water damage.

The Fix it Guys work with skilled building trade professionals, including plumbers, roofers. If you have plumbing or roof leaks, please ask us for a referral.

Plumbers

IMPORTANT During a deep freeze, in Colorado, all available plumbers might become busy on emergency water pipe burst calls. DO NOT PROCRASTINATE CALLING A PLUMBER, IF YOU HAVE FROZEN OR BURST WATER PIPES, IN SUBZERO WEATHER. Call a plumber, before they are all busy on emergency calls.

Before the plumber arrives, the following steps can save you lots of money

Finding Plumbing Leaks in Wall Cavities

Plumbing leaks behind walls in bathrooms and kitchens can be especially difficult to find without destroying considerable drywall or wood paneling. When wet carpet, water seepage or mold growth is noticed in or near bathrooms, it is difficult to find the water leak source. Sinks and toilets usually have water supply shutoff valves, which can be turned clockwise to stop additional water flow. Unfortunately, many recently built homes do not have maintenance access windows, for bathtubs and shower plumbing valves and fixtures

Opening a hole in the paneling behind the shower or bathtub hot and cold water valves is usually required, to find and stop suspected bathroom wall cavity leaks. Sometimes a wooden baseboard molding is present and can be pried or unscrewed, from the wall, next to the floor. Removing the baseboard allows more accurate location of seepage or leaks, with less demolition than drilling or cutting holes in drywall or wood paneling

Usually a hole will need to be opened in the wall behind showers or bathtubs, to fix leaking hot or cold water pipes. If you place your ear against the wall, you can frequently hear running water, if hot or cold water valves or manifolds are leaking in the bathroom wall cavity. Inexpensive stethoscopes, often available from drug stores, Walmart, etc., can be used to more accurately find hidden water leaks in bathroom wall cavities.

When it is determined that a plumbing fixture is leaking in a wall cavity, a hole will need to be cut, to stop the plumbing leak and replace defective parts. An inexpensive drywall saw is easier to use than straight edge utility knifes, but the utility razor knife can usually cut thru typical gypsum drywall, behind showers. The wall cut should be made at about the same height as the hot and cold water valves. A cut about six inches by nine inches, will often allow enough room for repairs to be made

“Rescue tape,” often sold at auto part stores, Walgreen’s or Walmart, can often be wrapped tightly around a leaking hot or cold water pipe, to stop a plumbing leak, until a more proper plumbing repair can be made by a plumber, using proper parts and tools. Rescue tape is also very handy for emergency auto radiator hose repair.

After plumbing repairs are finished, you will want an easily accessible opening behind your shower or bathtub water controls. Many hardware and building supply stores sell inexpensive metal and wooden louver panels, for about $10 to $50. These inexpensive louver panels can be screwed down against the wall cut to cover it, when repair door behind every shower wall cavity. Remember, indoor toxic mold can begin growing 24 to 48 hours, after an indoor water leak.

If musty odors or mold are already present, call The Fix it Guys, for nontoxic, nondestructive fogging and deodorization to eliminate your mold problem.

Roof Repair

Roof Ice Dams cause many roof leaks and indoor mold problems. Many roofs have inadequate sealing or flashing at dormers, or ridge intersections. Inadequate roof pitch or insulation also contribute to roof leaks.

Duct Cleaning

Severely contaminated Water Damaged Buildings sometimes require duct cleaning

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Goldmorr Mold Treatment

Mark Stieber of The Fix it Guys, is a Certified Goldmorr Master Technician.

This unique system has had over eight years of complete success. The Goldmorr system is guaranteed to remove all types of mold, including toxic black molds, safely, quickly and less expensively than traditional methods. In most cases, home and business owners do not need to relocate while remediation takes place. Drywall and furnishings do not usually need to be removed. Most of the time we are in and out, in one day.

Goldmorr treatments have been verified by the EMSL lab to destroy 99.9999 percent of toxic Aspergillus and Stachybotrys mold.

Stachybotrys chartarum and Aspergillus niger Test - EMSL Analytical Inc.

"In conclusion, the test product, GM 2000, provided by 21st Global Pty, LTD was able to effectively disinfect (kill) both Aspergillus niger and Stachybotrys chartarum after 24hour exposure at room temperature. Specifically, GM 2000 was able to reduce Aspergillus niger by >99.99998% and Stachybotrys chartarum by >99.99996% "

Aspergillus niger - Log reduction of 6.96 and Stachybotrys chartarum - Log reduction of 6.39

Strachybotrys Chartarum and Aspergillusniger

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Sick Building Syndrome

Sick Building Syndrome May Be Caused by Bacteria, Mycotoxins, Volatile Organic Compounds and Fine Particles, In Addition to Mold Spores

Sick Building Syndrome May Affect Over 25 Percent of Population

Symptoms Reported By 48 Patients Exposed to Indoor Mold

The spectrum of signs and symptoms in descending order of frequency included:

Muscle and/or joint pain, 71%; Fatigue/weakness, 70%; Neurocognitive dysfunction , 67%; Sinusitis, 65%; Headache, 65%; Gastrointestinal problems, 58%; Shortness of breath, 54%; Anxiety/depression/irritability, 54%; Vision problems, 42%; Chest tightness, 42%; Insomnia, 40%; Dizziness, 38%; Numbness and tingling, 35%; Laryngitis/hoarseness, 35%; Nausea, 33%; Rashes, 27%; Tremors, 25%; Heart palpitations, 21%; Bronchitis/pneumonia, 21%; Nose bleeds, 13%; Nasal Septal Perforation, 2%

Explosion of Mold Cases in Homes, Workplaces and in Occupational Medical Practices,Allan D. Lieberman, M.D.

Symptoms observed more frequently in indoor mold exposed residents of St. Bernard Parish, in 2006, after the Katrina hurricane, included fatigue, weakness, ache, cramp, unusual pain, “ice pick” pain, headache, light hypersensitivity, red eyes, blurred vision, tearing, sinus problems, cough, shortness of breath, abdominal pain, diarrhea, joint pain, morning sickness, memory impairment, concentration impairment, confusion, word recall difficulty, decreased information assimilation, disorientation, skin sensitivity, increased thirst, increased urination, static shocks, mood swings, appetite changes, night sweats, body temperature regulation problems, numbness, tingling, vertigo, metallic taste and tremors.

Shoemaker, R C, Surviving Mold, Life in the Era of Dangerous Buildings, Appendix C, Otter Bay Books, 2010

Sick Building Syndrome Case Definition achieves 100 percent accuracy for adults,

Shoemaker, R C, (2010) Surviving Mold, p 752

  • (1) Potential for exposure (2) multiple symptoms from multiple systems (3) absence of confounding exposures, Lyme Disease, etc. Plus 3 of 6 of following
    • (1) Visual contrast sensitivity test deficit
    • (2) genetically susceptible HLA DR subtype
    • (3) elevated MMP9
    • (4) dysregulation of simultaneously measured ACTH/cortisol
    • (5) dysregulation of ADH/osmolality
    • (6) reduced MSH

“The best test for a sick building is a sick patient” Ritchie Shoemaker, MD

for more information, see http://www.survivingmold.com/

Non prescription alternative test for mold toxicity

Real Time Lab Urine DNA mycotoxin test

Available from http://+www.directlab.com, without prescription

(Mold toxins could originate from foods)

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