Mold Testing-Household

[posey]

Well well. My Laptop has a short in it and the battery does not last 3 hours.

So, for whatever reason, I get some of the same emails on my PC as my Laptop Outlook but not all.

Anyway, I received an email from a person (will post her name if I get permission but she has M) about a test she did for Mold spores in her home. I remember one was Agent Green. I had a test kit I had bought awhile ago at Home Depot for $10., so I did the test.

I chose to do the one by the heat-A/C vents. I didn't tape it to the vent as directed tho, I just set it on the floor and turned on the a/c for 10 minutes. I didn't close all other vents either. You get a little bottle of stuff and a petri dish. Put stuff in dish, cover for an hour and it is now a gel. In 24 hours I had 2 green spots about the size of a dime. After 36 hours a slow growing mold began and it was white. By 48 hours it was spreading though out the whole petri dish and I saw there was some other stuff beginning. I sent it in for the lab analysis which costs $40. and am still waiting for results.

I now know what I have been breathing for quite some time and it explains why I can't breathe trough my nose.

I received an email on my PC from this person about water, which she had emailed me about before, fusarium and Agent Green. I think they are all in it.
It is long so I will have to break it up in posts. She is credible though or I wouldn't waste your time.

I will begin her last email in the next post. Check out Agent Green once.

posey

[posey]

8/20/10

Re: Tab water contamination of pathogens - pfeisteria, blue green algae, dinoflagellates, mutating fungi producing mycotoxins that are not killed by chlorine, nor reverse osmosis and are contaminating Pinellas County tap water supply, estuaries, lakes, rivers, Florida aquifer causing human illnesses

To all concerned scientists, environmentalists, politicians, and those suffering from the effects of Morgellons disease, chronic Lyme disease, mutating fungi bacterias and algae, and biotoxin exposure induced illnesses:

The chemical named Glyphosate found in Monsanto Roundup Weedkillers and insecticides mutates funguses, harmful bacterias, and algae into lethal pathogenics, and has been used by bio-weapons engineering labs in conjuction with Fusarium fungus to spray illegal crops plantations in South America.

The George Bush administration authorized the full force use and spraying on American territory of Agent Green as well, with the help of scientist Doctor David Sands (who helped create Agent Green, a mixture of Glyphosate and Fusarium Oxy) scientific report findings included below. Florida , Texas and California are the most sprayed states for the illegal crop and war on drugs, but the toxic spores has spread throughout our Nation. That is why Morgellons Disease and fungi mycotoxin / biotoxin diseases are more prevalent in these states, but it has now reached epidemic proportions throughout our Nation and other countries.

What has happened is that the spores of these bio-engineered and mutating biologicals carrying mycotoxins go airborn and travel great distances. The spores gravitate to moisture, homes air conditioning units, lakes, rivers, coastal areas, even county and city municipal water supply. Municipal water supplies are not specifically tested for toxic blue green algae, pfeisteria, cynobacteria, dinoflagellate biotoxins, mutated fungi. Chlorine does not kill the spores biotoxins of these organisms. Sea water reversed osmosis, even ozone applications of our drinking water in our county and municipal plants are not effectively eradicating these biotoxins and dinoflagellates, as the driking water travel through the conduits to the end users and contamination is happening. The actual source of re-contamination is yet to be researched and determined. I know that when I take a shower, I often afterwards get a crawling feeling on my hair that long ago I determined it could be a flagella. After reading Dr. Ritchie Shoemaker’s book, there is more evidence that these are possible dinoflagellates or blue green algae contaminating the county water supply. I have had to soak my hair with hydrogen peroxide to kill the organisms in the past 3 years. When I take a shower, the possibility of recontamination is there, as there are currently no actions in place to test the drinking water for the above specific pathogens, find the source of contamination, and have a systems in place to treat the water effectively for these mutating pathogens carrying biotoxins.

These lethal spores infect insects like mites, ticks, frogs, bats (many bats are dying in the US from a mutated white fungi on their nose carrying biotoxins) bees, trees, and humans causing illness. Many insects like the ambrosia beetle and ticks are also carrying these bio-weapon mutated funguses and if you get bit, you can contract it along with their insect larvae.

Many trees like orange trees, maples, oaks, are rotting and dying by the contamination of funguses that are mutating like green lichen, sooty mold, fusarium, aspergillus. The trees rot and die. These pathogenic mutations spores which carry chemical biotoxins are directly derived from exposures to Agent Green and the wide spread use of glyphosate in insecticides and weed killers.

In the past 6 years in Florida , property insurance companies have noticed an unusual increase in mold remediation claims. Many property insurance companies no longer insure for mold and mycotoxin contamination of homes. In my neighborhood, I have noticed that 50% of the foreclosed homes were not do to economic reasons, but people fleeing their homes do to mycotoxin / biotoxin toxicity and contamination causing them illness. I have verified this by observation and talking to people that actually fled their home, letting it foreclosed, do to their home environment was causing them illness and they did not know the cause nor how to decontaminate their home and treat their symptoms. Also many people keep this illness from others for obvious reasons.

I urge you to read a book by Doctor Ritchie Shoemaker called “Mold Warriors” about the kept silent US epidemics of biotoxin producing organisms like pfiesteria, blue green algae, cyanobacteria, ciguatera, mutated fungi, and co-infections from Lyme Disease.

I have informed Dr. Shoemaker about 2 pieces of his missing puzzle from my research on environmental toxicology producing human illnesses, and that is the use of Glyphosate chemicals and the authorized spraying of Agent Green in US territory by the Bush Administration and the scientist who helped create it, David Sands.

Miriam Fernandez, scientist from the Department of Agriculture in Saskatoon, Canada has been warning the United States Congress and The Department of Energy of how the toxic chemical glyphosate is mutating fungi and bacteria and is propagating these lethal pathogenics biotoxin carrying spores to our plants, animals, (our pets), and humans causing illness. So, do not believe when Monsanto bought out officials, etc try to cover this up by saying that Glyphosate is harmless, because it is NOT. IT is a BIOLOGICAL WARFARE CHEMICAL.

There are possible solutions to decontaminate the water and soil from these mutating pathogens and their bio-toxins. Research has point me to an environmental formula that can break the molecular structure of hydrocarbons like oil, and some pathogens into non-toxic micro nutrients that fish can eat or can be used as fertilizers. This ionized formula must be thoroughly tested for the application and development of drinking water treatment plants and sewage treatment using this renewable technology bringing both health to people and the environment. Read the environmental section of the following bio-energetic report:
Results of Twelve Months' Clinical Research :: Perfect Waters LLC

For all those contaminated with biotoxins from mutated fungi, borrelia burgdorferi, pfeisteria, blue green algae (cyanobacteria), etc. below is what I have done and currently doing to decontaminate my home environment, outside environment, and the protocol I am currently using to remove biotoxins from my body.

Outside environment - put clorox on tree trunk and branches contaminated with green lichen, white fusarium, sooty mold, which have now mutated and produce spores with biotoxins that can infect your home and other plants. If trees are fully contaminated and clorox was not succesful in removing the fungi...cut the tree down.

Home ambient air environment - buy a mold test kit from Home Depot. If toxic fungi like aspergillus, fusarium, penicillum, etc is found in your culture by the lab, then ozonate your home and that will kill all fungi, bacteria, insects, algae and their mycotoxins. I treated my home using a newly commercialized NASA technology using ozone which after a few hours, through a process of oxidation, he mmachine coverts the applied ozone back to oxygen so there will be no residue. PATI Air Technologies out of St. PetersburdFlorida, physicist Jeff Bleil 727-526-2990, did the ozone application in my home. VERY SUCCESSFUL.

Home tap water supply - I am in the process of contacting government, congressmen, water quality utility director, FEP agency, state environmental protection agency for them to test, and expedite effective action to eliminate the pathogens with mycotoxins in the drinking and water supply. YOU SHOULD ALL DO THE SAME AND CONTACT YOUR UTILTY WATER DEPARTMENT LAB DIRECTOR AND INFORM HIM TO TEST YOUR DRINKING WATER AND PUT A PLAN OF ACTION TO ELIMINATE CONTAMINANTS. I SUGGEST TESTING PERFECT SCIENCE WATER ENVIRONMENTAL FORMULAS TO TEST THE EFFECTIVENESS FOR ELIMINATING THESE PATHOGENS WITH THEIR MYCOTOXINS FROM THE WATER SUPPLY.

Internal body current protcol I am using - 1) Questran (CSM recommended by Dr. Ritchie Shoemaker out of Maryland) this is a cholesterol medication that binds cholesterol and biotoxins / mycotoxins in the intestine and expells them through the rectum. Is being very effective and is working. 2) TriVita Nopalea with Betalaine concentrated human cell detoxifying fprmula (it is very effecttive and gives you energy). 3) TriVita sublingual B-12 for energy and rebuilding healthy body cells. 4) 4-Life Rio Vida transfactor with cow cholustrum which teaches your immune system to fight pathogens and mycotoxins that cows in the fields have been exposed to and successfully fought (Effective in building your immune system, especially if you are one of those with defficient ggenes HLA DR). 5) Jerusalem Artichoke Flour with probiotics 6) I am also trying another very potent formula and I would let you All know later if it works and how I am doing with it.
To our restored good health, restored financial security & wellbeing.

[posey]

Re: READ Scientific Reports below

Did you know? Dr.Shoemaker received the Maryland Family Physician of 2000 award, and was a finalist for the National award.

This website provides information on chronic human illness caused by exposure to toxins produced by living organisms (biotoxins). Many biotoxins are neurotoxins in that they adversely affect neurologic function. Registered users will be able to complete questionnaires on exposure history, medical history and current symptoms. Users can also take a vision screening test that helps determine whether or not their health problems are likely to be caused by biotoxins. Deficits on the vision test, visual contrast sensitivity, have been associated with chronic illness caused by biotoxin exposure (1-. If the data suggest biotoxin-induced illness, users can obtain a treatment protocol that has been used to successfully treat many people. This paradigm for diagnosing and treating chronic, biotoxin-mediated illness is based on research by Ritchie C. Shoemaker, MD and on the clinical experiences of Dr. Shoemaker (1-.

Organisms that Produce Biotoxins
Many types of organisms produce substances that are toxic to humans. These include dinoflagellates found in estuaries and the ocean, cyanobacteria (blue-green algae) found in fresh water, fungi (mold) found in indoor air and outdoors, and some types of bacteria. Our initial research on acute and chronic, biotoxin-induced illness associated a complex of non-specific symptoms and deficits in visual contrast sensitivity with exposure to estuaries inhabited by the fish-killing dinoflagellate, Pfiesteria piscicida, and other toxic dinoflagellates in the toxic Pfiesteria complex (1-. Treatment for this illness, called Possible Estuary Associated Syndrome (PEAS) by the US Centers for Disease Control and Prevention (CDC; 9), according to our protocol was associated with recovery of vision and resolution of symptoms. Subsequent research indicated that this paradigm generalizes to chronic illness thought to be caused by toxins from a marine dinoflagellate, Ciguatera (Chronic Ciguatera Seafood Poisoning), cyanobacteria such as Cylindrospermopsis and Microcystis, various species of fungi such as Stachybotrys, Aspergillus, Penicillium, and Fusarium, and by spiders such as the Brown Recluse. Our research also suggested that toxins from tick-borne pathogens such as Borrelia burgdorferi (Lyme disease organism) and Babesia microti may cause chronic illness even after the spirochetes or intracellular protozoa (also called apicomplexans) have been killed by antibiotics. People who cannot naturally eliminate biotoxins develop chronic illness. The toxins can be eliminated, however, by using our treatment protocol, and good health can be restored.

Previous Diagnoses
Chronically ill patients successfully treated by Dr. Shoemaker and others using our treatment protocol had many previous diagnoses, including Depression, Chronic Fatigue Syndrome, Fibromyalgia, Irritable Bowel Syndrome, Multiple Sclerosis, Sick Building Syndrome, Bell's Palsy, learning disability, endometriosis, sensory-neural deafness, low vision, Chronic Soft Tissue Injury (usually from an automobile accident) and Post-Lyme Disease . The diagnosing physicians did not realize that their illness was caused by biotoxins. Some other diagnoses were thought to involve biotoxins, including Chronic Ciguatera Seafood Poison, Possible Estuary Associated Syndrome (PEAS) , spider bite and Mycotoxicosis, but there was no objective indicator like the vision test to assist in diagnosis, and no treatment like cholestyramine (CSM) to greatly enhance toxin elimination rates. We have also successfully treated people with the rare genetic disorder called Charcot-Marie-Tooth disease. This is a condition in which toxins are produced within the body, causing chronic illness.

How We Can Help You
Standard medical diagnostic tests are usually normal in patients who have these biotoxin-induced illnesses, which makes it difficult to diagnose and treat. We have a simple tool that assists in diagnosis by showing evidence of a neurological deficit. That screening tool is the visual contrast sensitivity test (VCS). A positive VCS test, in the presence of biotoxin exposure potential, and a symptom complex involving multiple systems, and in the absence of other historical, medical or treatment conditions that likely explain the symptoms, provide a basis for making a diagnosis of Probable Biotoxin-Mediated Illness. Users of this website can take a screening version of the VCS test and complete questionnaires on exposure potential, symptoms and medical history. When biotoxins are suspected, users can purchase a package that includes the treatment protocol and three additional vision tests that can be used to monitor recovery during treatment. Patients can request treatment by taking the protocol and the associated research articles to their local physician or to Dr. Shoemaker.

How the VCS Test Works
The visual system includes a complex neurological network that involves the retina, optic nerve, brain nuclei and the visual cortex. One of the main outputs of the visual system is pattern vision. The VCS tests is an indicator of ability to detect visual patterns. The test measures the least amount of contrast between light and dark bars (sinusoidal grating) that is needed for the viewer to detect the bars. VCS is measured at five different bar sizes (spatial frequencies) because perception of different bar sizes is mediated by different physiological components, and these components are differentially susceptible to effects from different toxic substances (10-17). The largest effects of biotoxins are at the mid-size bars (1-. To measure VCS, viewers are presented a series of bar patterns at each of the five bar sizes. Viewers respond by indicating that the bars are tilted to the left, tilted to the right, are straight up and down, or that they cannot see any bars. The pattern with the lowest contrast that is correctly identified is the measure of VCS for that bar size. Upon completing the VCS test, viewers receive a message indicating that biotoxins are (positive) or are not (negative) likely to be involved in their illness. The criteria for getting a "positive" VCS result is set high to avoid false positive results. This occasionally results in a false negative result; some cases of chronic-biotoxin induced illness may pass the VCS test a some times. VCS can be measured during treatment to monitor recovery.

To Learn Much More, Please Register (at NO COST)

Disclaimer
No guarantees for a cure for any disease are implicitly or explicitly given to anyone. No single vision test can fully describe function of the visual system or conclusively indicate the presence or absence of neurotoxins or neurotoxicity. Diagnoses cannot be made and medications cannot be prescribed without seeing a physician in person.


500 Market Street
Pocomoke City, MD 21851
info@chronicneurotoxins

Privacy Policy | © 2002-2009 ChronicNeurotoxins, Inc.

Prior to launching a new version of this website in June, 2002, the earlier version had been online for about a year and a half. Over 3,600 registered users had taken the preliminary and VCS tests. About half of the test results were positive for potential chronic, neurotoxin-induced illness. We do not know exactly how many of those used our treatment protocol with their local physician, or the outcome for all that did. We do know, however, that many used the protocol with success, and that many others were successfully treated by Dr. Shoemaker or another physician.

Welcome to ChronicNeurotoxins, Inc. Home Page

Did you know? Chronic headaches are yet another indicator of neurotoxin poisoning.

[posey]

Florida's New Public Health Menace

This outbreak is a striking example of an environmentally acquired illness arising from changes in chemical usage on land. The lakes around Orlando in Central Florida have a new, exotic invader, a toxin forming Cyanobacteria (commonly called blue-green algae) with a jaw-breaking name - Cylindrospermopsis - not found in Florida before 1995. Copper in the water normally kills this organism. In Australia, copper sulfate treatment of reservoirs has repeatedly caused algae cell death and release of endotoxin from the algae. Because normal water treatment (without activated charcoal filtering) doesn't remove cyanotoxins, they made many people sick and caused liver damage. In Brazil, water was pumped from a reservoir during a algal bloom into tanker trucks for transport to dialysis clinics. Of course, the water was treated with chlorine to kill any organisms that might be present. The treatment killed the algae, releasing their toxins into the water. Over a weekend, more than a 100 hemodialysis patients became severely ill with liver and nerve damage. The first sign of illness was often blindness. The poisoning resulted in the death of over 50 patients. The algae there were marginally resistant to copper, but simply killing the algae during a bloom is not the answer to safe drinking water.


In Florida, the algae is resistant to copper and also is resistant to a fungicide, benomyl (see chapter 4 and 5 in Desperation Medicine) that has been used widely in Florida. If you take a sample of water from a fresh water lake, even one from Florida a few years ago, you normally find over 300 species of algae. Statistically, none will be resistant to the lethal effects of copper. Anecdotally, all will grow, even if fungicides like benomyl are present. In Florida, the genetically altered Cylindro ignores any of the known algae poisons, including those noted above. Now drops of water from Lake Griffin, Lake Harris and Lake Apopka will likely have only Cylindro in it, having out competed other algae. In these lakes, and others that feed into the Oklawaha watershed that is the source of the St. John's River, Cylindro now comprises 95% of the total algal biomass. Cylindro is now found in over 80% of Florida's lakes, and is rapidly spreading throughout North America, probably on boats and the bodies of ill waterfowl.


Florida health and environmental agencies have been studying the explosive growth of Cylindro, but have not been able to develop a management plan as yet. Meanwhile, the algae have been linked to massive die-offs of migratory fish eating birds, especially pelicans, in newly flooded wetlands around the farms adjacent to Lake Apopka. Alligators are dying in record numbers in Lake Griffin, but not before behaving erratically and sluggishly, demonstrating neurotoxicity, much as fish poisoned by Pfiesteria behave.
Neurologic testing has shown clear evidence of the effects of a neurotoxin, but no one will officially confirm what many workers in the field believe: the algae toxins are killing the alligators. Even worse, the alligator eggs are not hatching despite being fertile.

The human illness acquired from exposure to toxins in Lake Griffin has all the typical neurotoxin symptoms. Patients are tired, with muscle aches, diarrhea, memory impairment and confusion. They cough, can't tolerate bright light and they hurt all over. Fortunately, the VCS test detects the toxin and therapy is beneficial. The problem of residential acquisition is that its difficult to avoid. What should a patient do if the evening breeze coming off a pea green lake onto his front porch carries a toxin in the mist that makes him sick over and over again?

Did you know? Pesticides are thought to change the balance between populations of organisms living in soil or water that at times actually favor disproportionate growth of existing, or the formation of "new", toxin forming organisms.



Pfiesteria - The Organism that Opened the Door to the World of Chronic, Biotoxin-Induced Illness

The chronic, neurotoxin-mediated human illness that results from acquisition of toxins made by the fish killing dinoflagellate Pfiesteria piscicida - and all its many relatives - was the first to be successfully diagnosed by VCS and successfully treated with toxin binding medications. This web site shows how the syndrome, termed Possible Estuary Associated Syndrome (PEAS) by the US CDC, and many others that are similar in mechanism of toxin action and similar in the diversity of systemic symptoms can be successfully treated with similar protocols.
Pfiesteria is present in estuaries from New Jersey to Texas (and recently discovered in Norway) where the downstream flow of rivers, loaded with agricultural chemicals, meets the incoming tide. Attack zones, sites where people repeatedly can get sick, are found in the loamy silt sediments of the deposition sides of slowly flushing rivers. Seemingly minor exposure to these attack zones, with or without the presence of dead fish or fish with lesions, can result in prolonged difficulty with short term memory, muscle aches, diarrhea, abdominal pain, shortness of breath and many more symptoms. Many patients incorrectly blame their PEAS illness on alternative diagnoses such as irritable bowel syndrome, environmental allergies, fibromyalgia, depression, age associated memory loss and other unproven entities.
PEAS became a major political issue in 1997 in the Chesapeake Bay (read Pfiesteria: Crossing Dark Water for the true story) when thousands of dead fish in many creeks and rivers were associated with illness in many humans. To read newspaper accounts though, the fear of Pfiesteria , which caused many people to stop eating seafood, was based on a few fish with lesions in a few creeks that might have made a few fishermen sick. To listen to the politicians and corporate environmental groups talk about the problem of nutrients causing Pfiesteria to bloom adds nausea to the list of symptoms of PEAS.
Nutrients, especially urea, have been shown to enhance Pfiesteria growth and toxin production. Cases of human illness occur only in areas where particular agricultural chemicals are present with the extra nutrients. Some fish kills and sick patients are found in estuaries with extremely low nutrient levels but high chemical levels. We don't know exactly why these small organisms turn to making toxin but we do know how to treat the commonly acquired illness that results from exposure to the toxin. A great concern (see "Why Johnny Can't Read, "chapter 11 in Desperation Medicine) is due to the effect of Pfiesteria toxins on the ability of children to learn.
The official CDC response to the problem of the human health threat from Pfiesteria has at times been inaccurate, misleading, unduly conservative and slow to keep pace with the science. If you have an unusual illness that appeared following exposure to an attack zone in an Eastern Seaboard estuary, especially from the Chesapeake Bay to West Palm Beach Florida, take the VCS test. Proper therapy shows improvement in vision and symptoms beginning in 36 hours.

[posey]

Did you know? Chemical toxins poison (but do not kill) fat-containing tissue in the body, including nerve, muscle, brain, sinus, upper airway, lung, and bile.



Ciguatera

Don't eat the barracuda, especially in August and September when levels may be the highest. What levels? Toxins, made by small dinoflagellates (Ciguatera) living under algae growing on a reef, accumulate in the fish that eat the algae. Ciguatoxins don't affect the fish. Those fish, when eaten by bigger fish and bigger fish again, concentrate the minute quantities of toxins to the point that the large predator fish including red snapper, grouper, jack and barracuda (among a group of 400 species across the world) often are an illness waiting to happen, disguised as a gourmet meal. This illness often, but not always, has an explosive onset with diarrhea and vomiting, and even more insidious is the chronic illness that set in for those unable to naturally eliminate the toxin.

More than 1,000,000 cases of Ciguatera Seafood Poisoning occur annually worldwide, especially in areas around Puerto Rico, Hawaii, Australia, Indonesia and Micronesia. Recent years have seen a large increase in South Florida. A map of the tropics is a map of Ciguatera. Just as in Pfiesteria cases, the illness has political and economic consequences. Ads promoting tourism in St. Thomas don't say, "come on a cruise, eat local fish, get sick and stay sick for years".

But it does happen and it is now happening more often, as tropical reefs around the world are attacked with silt, alien algae, pollution and chemical killers including pesticides, hydrocarbons and heavy metals (see chapter 3, Desperation Medicine).

If you are lucky enough to recover from Ciguatera after eating a poisoned fish, take the VCS test anyway. Like with Pfiesteria, a low level, chronic illness frequently occurs in which itching, fast heart rate, headache, nausea, fatigue and funny numbness may become a chronic problem. If you are unlucky and the illness sets in with its full force, don't expect the medical profession to be able to help you. Blood tests, MRI and EMG studies will be normal, as will the UGI series and GB sonogram. Even if diagnosed, prior to our protocol, there has been no effective treatment

If you develop a metallic taste or reversal of hot and cold sensation, your astute Family Practice physician may recognize the possibility of chronic ciguatera. Take the VCS test; it is the first step to return to normal health. Treatment may be prolonged, however, as Ciguatera frequently requires more time to reach cure than its cousin, Pfiesteria.

You might not have any dramatic symptoms with ciguatera at first, but feel bad after you drink alcohol, eat something sweet, or curiously, after eating fish (a sign of sensitization or an adverse reaction to even minute quantities of the toxins). Women may especially notice their symptoms before menses. Take the VCS test and begin our treatment protocol to start you on your way to recovery from an environmentally acquired, chronic, toxin-mediated illness.



Did you know? Millions of Americans likely have chronic discomfort and functional impairments they attribute to aging or other causes, not realizing these are due to biotoxins.



Use of pioglitazone to prevent intensification of persistent symptoms following cholestyramine treatment of patients with Post-Lyme Syndrome.

Ritchie Shoemaker, Dennis House
Center for Research on Biotoxin-Associated Illness (a not-for-profit Corporation)
500 Market Street, Suite 102, Pocomoke City, MD 21851

Introduction. Since the first description of Lyme disease there have been subsets of patients identified with persistent symptoms, refractory to antibiotics. A recent prospective study of 51 Post-Lyme Syndrome (PLS) patients demonstrating a mid-spatial frequency deficit in visual contrast sensitivity (VCS) showed significant reduction of symptoms with use of a cholestyramine (CSM) treatment protocol. The symptoms and VCS deficits in the PLS patients were similar to those demonstrated by patients with other chronic, neurotoxin-mediated illnesses reported previously. Early in the course of CSM treatment, 33% of the 51 PLS patients experienced a significant intensification of symptoms, a phenomenon not seen with different biotoxin exposures. Pretreatment in 12 subsequent PLS patients with pioglitazone, a PPAR agonist, was shown to prevent the intensification associated with CSM use and to reduce plasma levels of a pro-inflammatory cytokine, TNF alpha. A multisite, prospective clinical trial on pioglitazone and CSM use in PLS patients was conducted to confirm benefit of CSM therapy in PLS and determine if pretreatment with pioglitazone could prevent intensification. Methods. All patients referred to the study had long-standing symptoms following a known tick bite or exposure to areas where others had tick bites, and a clinical and/or laboratory diagnosis of Lyme Disease. Diagnostic parameters used by referring physicians included a history of erythema chronicum migrans (ECM) rash, ELISA assay, Borrelia burgdorferi Western blot, LUAT assay, PCR, CSF antibodies to B. burgdorferi and culture. Patients with a clinical diagnosis of PLS but without a positive serologic test were included at the discretion of the attending physician. 241 patients were included in the study at one of two centers, Pocomoke, MD or Chico, CA. All patients had past antibiotic treatment, but retained symptoms refractory to antibiotics. All patients were pretreated with pioglitazone (pio), 45mg daily for 10 days. On day 6 of pio, CSM treatment was initiated. An orally administered checklist monitored symptoms, and sequential VCS testing was performed. CSM was continued until the treatment endpoints of maximum symptom abatement and maximum improvement in VCS scores were noted. No antibiotics or other therapeutic interventions were administered during the study. Results. No patients had adverse effects from pio, including hypoglycemia or abnormal liver function tests. Only 5 of 241 (2%) patients experienced significant symptom intensification, not severe enough to stop treatment. 83.8% of patients had at least 50% reduction of symptoms following use of the CSM protocol, with complete resolution of symptoms in 23%. 3.4% of patients had no improvement. VCS deficits prior to treatment and resolution with treatment were better correlated with symptom abatement than other diagnostic markers. Conclusion. The results support the hypotheses that: 1) PLS may be a chronic, neurotoxin-mediated illness; 2) antibiotic treatment should be followed by adjuvant treatment with the pio and CSM protocol; 3) VCS is an effective diagnostic tool that can indicate neurotoxicity in PLS patients and; 4) TNF may participate in the intensification reaction. These results must be confirmed in a prospective double-blinded, placebo-controlled clinical trial, with frequent monitoring of TNF levels measured appropriately by validated laboratory protocols.



Use of atovaquone (Mepron) in patients coinfected with Borrelia burgdorferi and Babesia microti with symptoms refractory to antibiotics and cholestyramine.

Ritchie Shoemaker, Dennis House
Center for Research on Biotoxin-Associated Illness (a not-for-profit Corporation)
500 Market Street, Suite 102, Pocomoke City, MD 20851

Background

A recent two-site study of 341 patients with Lyme Disease and symptoms refractory to antibiotics (Post-Lyme Syndrome, PLS) showed benefit from a treatment protocol using pioglitazone to lower proinflammatory cytokine levels and cholestyramine (CSM) to bind and eliminate toxins. Statistical analyses showed a significant reduction in the number of symptoms and a significant improvement in visual contrast sensitivity (VCS) scores following treatment. These improvements paralleled those seen in patients with symptoms following exposure to other biotoxin-forming organisms, including dinoflagellate and fungal species. In the PLS studies, however, about 8% of patients did not respond to the toxin-binding protocol. Serologic measures indicated that these patients were disproportionately coinfected with Borrelia burgdorferi and Babesia microti. The coinfected patients had received 3 weeks of atovaquone, targeting b. microti, in combination with azithromycin, targeting b. burgdorferi, without binding therapy prior to the PLS study because recent studies reported success with this protocol. It was hypothesized that: 1) b. burgdorferi had been eliminated by azithromycin; and 2) 3 weeks of atovaquone therapy was insufficient to eliminate b. microti during coinfection with b. burgdorferi. The current study was designed to investigate the efficacy of atovaquone therapy on b. microti. infection during a 3 week period and, if indicated, during an additional 6 week period.

Methods

Twenty-five patients with serologic evidence of exposure to b. microti and b. burgdorferi and chronic symptoms despite 3 weeks of atovaquone and azithromycin therapy followed by toxin-binding therapy were enrolled in an FDA and IRB approved double-blinded, placebo-controlled, crossover clinical trial. Patients were randomly assigned either atovaquone or placebo for 3 weeks in combination with CSM, and then crossed over to the other arm of the trial for 3 weeks. Treatment with atovaquone and CSM, provided on an open label basis, for 6 additional weeks followed. Symptoms and VCS scores were recorded at initiation and at the end of weeks 3, 6, 9 and 12.

[posey]

Results

Twenty-one patients completed the trial, four dropped out; one for non-study related reasons, two because of CSM intolerance and one patient because of no improvement at 9 weeks. No patients showed notable symptom resolution or vision recovery at the end of week 6. After an additional 6 weeks of therapy, five patients had complete resolution of their longstanding symptoms and 16 had notable reduction in the number and/or severity of symptoms. The cohort showed a statistically significant reduction in symptom number and increase in VCS between initial and week 12 assessments. There were no adverse effects noted other than mild worsening of symptoms experienced by patients during the first few weeks of atovaquone therapy. Patients noticed clinical improvement near the end of the second 3-week course of atovaquone, and noted continued improvement during the third 3-week course of atovaquone and CSM therapy.

Discussion

The study results suggest that prolonged atovaquone therapy is required to eliminate b. microti. None of the patients had shown improvement after 3 weeks of atovaquone in combination with azithromycin therapy, after 3 weeks of binding therapy or after 3 weeks of atovaquone plus binding therapy. Six to 9 continuous weeks of azithromycin therapy are likely required for improvement in most cases. Studies of coinfected patients are needed to confirm and extend these results, particularly due to coinfection rates exceeding 10% in endemic areas. Additional issues to address include: 1) whether b. microti, like b. burgdorferi, also releases a toxin; 2) whether upregulation of anti-inflammatory cytokines triggered by b. burgdorferi toxins interfere with atovaquone's lethal mode of action on b. microti; 3) the role of pro-inflammatory cytokines in symptom induction and the course of coinfection; 4) possible extravascular sequestration of viable Babesia organisms; and 5) the role of the extrachromosomal 35 kb plastid DNA, homologous to DNA of Euglena, in maintaining viable Babesia organisms.

Sick Building Syndrome: Possible Association with Exposure to Mycotoxins from Indoor Air Fungi

HK Hudnell1, RS Shoemaker2
1US Environmental Protection Agency, Research Triangle Park, NC 27711 USA
2McCready Outpatient Services Center, Pocomoke City, MD 21851 USA

Introduction. Chronic human illness associated with residential or occupational buildings, commonly referred to as sick building syndrome (SBS), may be a multifactorial condition, involving in some cases volatile organic compounds, CO or CO2, pesticides, biologic agents, temperature and humidity, lighting, and neuropsychological status. Recent evidence indicated that the primary causative factor in a subset of SBS cases may be exposure to mycotoxins from indoor air fungi. A variety of fungal genera, including Stachybotrys, Aspergillus, Penicillium and Cladosporium, have been identified on interior cellulose materials following water intrusion. Many species have been shown to produce mycotoxins and release spores to air. Mycotoxin exposure has been associated with effects on the nervous, digestive, respiratory, cutaneous, urinary, reproductive, immune and other systems (1). Dr. Shoemaker's data from a series of cases are described to illustrate a new approach to diagnosis and treatment of mycotoxin-induced SBS. Methods. As in other biotoxin-induced chronic human illnesses for which techniques to identify toxins in tissues are unavailable, diagnosis was based on exposure potential, the presence of multiple system symptoms, and the absence of probable alternative causes of illness. Samples of fungi were observed growing in each building and analytically identified to assess exposure potential. Symptoms were systematically assessed in direct interview. A test of visual pattern detection ability, visual contrast sensitivity (VCS), was administered to each patient to assess its usefulness as an objective indicator of neurotoxicity in mycotoxicosis. Alternative explanation of illness were assessed with clinical and laboratory techniques, as well as with questions on medical history, potential for exposure to other toxins and life style. Cases were treated solely with an orally administered, non-absorbable polymer, cholestyramine (CSM), that binds salts from bile through anion exchange. CSM was previously used to successfully treat chronic illness induced by other biotoxins (2), presumably by preventing toxin recirculation through enterohepatic reabsorption, thereby enhancing toxin elimination rates. Results. One or more genera of toxin forming fungi was identified in each building. All cases reported neurologic symptoms and symptoms involving at least three other systems. All cases showed depressed VCS in the presence of normal visual acuity, indicative of a neurologic effect. No probable alternative causes of illness were identified. Following 2 weeks of CSM therapy in the absence of re-exposure, all cases showed normal VCS and at least a 90% resolution of symptoms. Relapse occurred only with re-exposure and resolved with re-treatment. Conclusions. Even in the absence of measures of airborne spore concentrations and mycotoxin levels in tissue, these results strongly support the hypothesis of mycotoxicosis in these SBS patients. Multiple system symptoms, the objective indication of a neurologic effect provided by VCS, relapse with re-exposure and successive recoveries following CSM therapy are consistent with this diagnosis. The CSM response in these chronically ill patients unresponsive to previous treatments has no known explanation other than enhancement of toxin elimination rates. This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.
References. 1. HM Ammann. Is indoor mold contamination a threat to health? http://www.doh.wa.gov/ehp/oehas/mold.html
2. RS Shoemaker & HK Hudnell. Possible estuary associated syndrome: symptoms, vision and treatment. Possible Estuary-Associated Syndrome: Symptoms, Vision, and Treatment

[posey]

Sick Building Syndrome: Possible Association with Exposure to Mycotoxins from Indoor Air Fungi

HK Hudnell1, RS Shoemaker2
1US Environmental Protection Agency, Research Triangle Park, NC 27711 USA
2McCready Outpatient Services Center, Pocomoke City, MD 21851 USA

Introduction. Chronic human illness associated with residential or occupational buildings, commonly referred to as sick building syndrome (SBS), may be a multifactorial condition, involving in some cases volatile organic compounds, CO or CO2, pesticides, biologic agents, temperature and humidity, lighting, and neuropsychological status. Recent evidence indicated that the primary causative factor in a subset of SBS cases may be exposure to mycotoxins from indoor air fungi. A variety of fungal genera, including Stachybotrys, Aspergillus, Penicillium and Cladosporium, have been identified on interior cellulose materials following water intrusion. Many species have been shown to produce mycotoxins and release spores to air. Mycotoxin exposure has been associated with effects on the nervous, digestive, respiratory, cutaneous, urinary, reproductive, immune and other systems (1). Dr. Shoemaker's data from a series of cases are described to illustrate a new approach to diagnosis and treatment of mycotoxin-induced SBS. Methods. As in other biotoxin-induced chronic human illnesses for which techniques to identify toxins in tissues are unavailable, diagnosis was based on exposure potential, the presence of multiple system symptoms, and the absence of probable alternative causes of illness. Samples of fungi were observed growing in each building and analytically identified to assess exposure potential. Symptoms were systematically assessed in direct interview. A test of visual pattern detection ability, visual contrast sensitivity (VCS), was administered to each patient to assess its usefulness as an objective indicator of neurotoxicity in mycotoxicosis. Alternative explanation of illness were assessed with clinical and laboratory techniques, as well as with questions on medical history, potential for exposure to other toxins and life style. Cases were treated solely with an orally administered, non-absorbable polymer, cholestyramine (CSM), that binds salts from bile through anion exchange. CSM was previously used to successfully treat chronic illness induced by other biotoxins (2), presumably by preventing toxin recirculation through enterohepatic reabsorption, thereby enhancing toxin elimination rates. Results. One or more genera of toxin forming fungi was identified in each building. All cases reported neurologic symptoms and symptoms involving at least three other systems. All cases showed depressed VCS in the presence of normal visual acuity, indicative of a neurologic effect. No probable alternative causes of illness were identified. Following 2 weeks of CSM therapy in the absence of re-exposure, all cases showed normal VCS and at least a 90% resolution of symptoms. Relapse occurred only with re-exposure and resolved with re-treatment. Conclusions. Even in the absence of measures of airborne spore concentrations and mycotoxin levels in tissue, these results strongly support the hypothesis of mycotoxicosis in these SBS patients. Multiple system symptoms, the objective indication of a neurologic effect provided by VCS, relapse with re-exposure and successive recoveries following CSM therapy are consistent with this diagnosis. The CSM response in these chronically ill patients unresponsive to previous treatments has no known explanation other than enhancement of toxin elimination rates. This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.
References. 1. HM Ammann. Is indoor mold contamination a threat to health? http://www.doh.wa.gov/ehp/oehas/mold.html
2. RS Shoemaker & HK Hudnell. Possible estuary associated syndrome: symptoms, vision and treatment. Possible Estuary-Associated Syndrome: Symptoms, Vision, and Treatment

Differential association of HLA DR genotypes with chronic, neurotoxin-mediated illnesses: Possible genetic basis for susceptibility?

Ritchie Shoemaker, Dennis House
Center for Research on Biotoxin-Associated Illness (a not-for-profit Corporation)
500 Market Street, Suite 102, Pocomoke City, MD 24851

ABSTRACT
The recently published paradigm of chronic biotoxin-induced illness involves multiple-system symptoms, a neurologic deficit as indicated by visual contrast sensitivity measurement, and symptom resolution concomitant with vision recovery following cholestyramine treatment to bind and eliminate toxins. Chronic illness can follow exposure to toxins from Ciguatera, Pfiesteria and other dinoflagellates (dinoflagellate-related illness, DRI), Aspergillis, Penicillium, Stachybotrys and other indoor air fungi (sick building syndrome, SBS), nasal resident coagulase negative Staphylococcus (CNS), and bacteria and protozoa associated with Post-Lyme Syndrome (PLS). Because some exposed individuals acquire only acute illness or are unaffected, we suspected that susceptibility to chronic illness was conferred by particular patterns of genetic polymorphisms, perhaps those coding for antigen presentation to immune T cells. Alleles at five loci on the class II human leukocyte antigen (HLA) genome were identified with commercial PCR analyses, 2 alleles for DRB1, DQ and DRB3, and 1 allele for DRB4 and DRB5, for 200 chronically ill patients with well established exposure potentials.

In each of the four patient classes, analyses identified unique and disproportionate patterns of HLA alleles within the patients' entire sets of alleles, relative to the entire patient population and to published frequencies in a large normal population. Statistically significant differences in allele fingerprints were: DRI - DRB1-4, DQ-8, DRB4-53; SBS - DRB1-7 or 17, DQ-2, DRB3-52A; CNS - DRB1-11, DQ-7, DRB3-52B; and PLS - DRB1-15, DQ-6, DRB5-51. The specific allele pattern was present in about 90% of patients in each class, and only about 5% of patients also showed an allele pattern associated with another patient class. The few patients with illness suspected to involve two types of exposure had allele patterns associated with risk from both types of exposure. In addition, several patients with histories of illness in more than one of the patient classes showed another allele pattern, DRB1-14, DQ-5 and DRB3-52B. Preliminary data indicated that the biotoxin exposure associated with each patient class and allele pattern may also be associated with a distinct pattern of elevation in proinflammatory cytokines.

These preliminary results suggest that distinct genetic patterns may be risk factors for chronic illness from exposure to particular classes of biotoxins. Susceptibility may involve cloaked or inappropriate presentation of antigens to T cells, and ensuing ineffective antibody production. A larger patient-population study that includes a prospective component is needed to confirm the possibility that particular HLA genotypes are risk factors for acquisition of chronic, neurotoxin-mediated illness, and to investigate the possible roles of proinflammatory cytokines in the toxic modes of action. Chronic inflammation is a known risk factor for development of a variety of diseases.

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Vibrotactile Threshold and Pin-Prick Sensitivity as Indicators of Subclinical Changes in Somatosensory Function: Effects of Environmental Exposure to Arsenic in Drinking Water

DA Otto1, HK Hudnell1, Y-H Li2, YJ Xia2
1US Environmental Protection Agency, Research Triangle Park, NC 27711 USA
2Institute of Endemic Disease, Huhhot, Inner Mongolia

Introduction. Peripheral neuropathy results from exposure to a variety of neurotoxic compounds. Clinical assessment of peripheral neuropathy is commonly based on electrophysio-logical measures of nerve conduction velocity (NCV). However, data on early, subclinical changes in neurologic function resulting from exposure to neurotoxicants are needed for human health risk assessment. Behavioral measures of vibrotactile thresholds (VTT) and pin-prick sensitivity (PPS) provide non-invasive methods for assessing somatosensory function that are suitable for use in field studies. VTT measures have previously identified subclinical effects from exposure to organic solvents, jet fuel, elemental mercury and organophosphate pesticides (1). The current study investigated the effects of environmental exposure to arsenic in drinking water on somatosensory function using VTT and PPS techniques. Methods. A population of farm families living in the Bamen region of Inner Mongolia chronically exposed to arsenic in well water were screened for potentially confounding factors. 309 residents (mean age 35.8 +/- 12.8 years) qualified for participation. Subjects were assigned to three exposure groups based on arsenic levels in individual wells as follows: low (<20 ug/L; N=97), medium (100-300 ug/L; N=109) and high (400-700 ug/L; N=103). VTT was measured on the dorsal surface of digit 2 and the ventral surface of digit 5 on each hand. PPS was assessed on both arms and both legs. Results. VTT was significantly elevated and PPS was significantly reduced in the high exposure group relative to both the medium and low exposure groups. The data suggested a larger exposure effect on PPS than VTT. Conclusion. These results indicate that subclinical effects of chronic arsenic exposure on somatosensory function are observable only at exposure levels well above those associated with increased risk for cancer. Differences between the VTT and PSS results suggest that small diameter unmyelinated axons with free nerve endings in superficial skin layers may be more susceptible to exposure than the larger diameter and myelinated axons with Pacinian corpuscle receptors located in deeper skin layers. This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.

(1) D Mergler. Behavioral Neurophysiology: Quantitative Measures of Sensory Toxicity. In: LW Chang & W Slikker (eds). Neurotoxicology: Approaches and Methods, New York, Academic Press, 1995, ch47 pp727-736.

Did you know? The retina of the eye can receive toxins through direct ocular absorption.



A New Diagnostic Tool And A New Drug Therapy Provide Major Weapons Against The Surging Epidemic of Post-Lyme Syndrome


Although most people don't realize it, the vector of one of the most debilitating diseases of the modern world can often be found crawling around in the hedges, shrubs and tall grasses of the typical American backyard.
Carried by several common species of tick, Lyme Disease - which leaves many of victims struggling with long-term chronic illness, Post-Lyme Disease (PLD) - is one of the fastest-growing infectious-disease epidemics both here and abroad, according to recent research.
How widespread is the current U.S. outbreak of this bacteria-triggered illness - which leaves many of its victims struggling for years with fatigue, headache, mental confusion, memory impairment, shortness of breath, sensitivity to bright light, abdominal pain, chronic muscle and joint pain and several other nasty complaints? (Symptoms can vary, but most PLD victims experience from four to six of the eight listed here.)
While some estimates put the total number of new cases each year at 300,000, the actual spread of Lyme is extremely difficult to measure. There is disagreement among the nation's physicians over the duration of the disease. According to some influential physicians, the bacterial infection can be cured in three weeks with heavy doses of antibiotics. Conventional wisdom dictates that if we drive out the Lyme bacteria (a spirochete named Borrelia burgdorferi) with germ-killing drugs, the painful symptoms of the disease will rapidly leave the patient.
But this assertion regarding the duration of PLD is now being challenged by thousands of Family Practice physicians around the country. Increasingly, the Family Practice docs are grappling with cases in which the major symptoms of Chronic Lyme persist for years, despite proper antibiotic treatment in patients.

Many physicians feel that diagnostic tests for Lyme are unreliable, due to differences between strains of the bacteria, and the potential for co-infections with Babesia or Ehrlichia. There are no chemical tests for the disease-causing toxin B. burgdorferi produces and release into human body, even as antibiotics are killing the bacteria. Without such tests, the medical debate over whether or not Lyme can be quickly cured has surged in recent years, provoking frequent battles in which physicians have attacked each other's credibility and integrity (and in a few cases, even their medical licenses).
All too often, suffering patients have been left in the middle, essentially ignored by doctors who contend that their long-term symptoms aren't the result of Chronic Lyme, but of "fibromyalgia," "depression," or "irritable bowel syndrome." These more familiar disorders allow the doctor to make a speedier diagnosis of an ailment for which there will be no "positive" lab test, either. In this way, patients can be quickly "helped out the door" - after the doc scribbles a prescription for an anti-depressant, or maybe an acid-blocker.
Already struggling with the debilitating symptoms of their tick-borne disease, Post-Lyme sufferers are patronized with insulting regularity by physicians who don't understand the biochemistry involved in chronic, neurotoxin-mediated illnesses, of which PLD is only one. As a result, these frustrated patients often wind up bouncing from physician to naturopath to herbalist to acupuncturist, among other "non-traditional healers." Along the way, they frequently spend tens of thousands of dollars on useless treatments.
But that situation is about to change, as more and more Family Practice physicians like Dr. Shoemaker find themselves treating Chronic Lyme in patients who tell them about their "years of brutal headaches and aching joints," while also describing themselves as "desperate to find a cure."
Why have so many medical researchers failed to understand the chronic aspect of Lyme disease?
In many cases, the problem has been that they simply don't understand the dynamics involved in the movement of organic neurotoxins throughout the human body.
Like the microorganisms that produce other toxin-linked diseases - such as the dinoflagellates Ciguatera and Pfiesteria, and the fungi that cause Sick Building Syndrome - Borrelia bacteria likely manufactures a nasty suite of neurotoxins which circulate in human fatty tissues, such as those found in nerve, muscle, brain, lung and bile, rather than in the bloodstream (as happens with more common illnesses such as pneumonia).
Because these bacterial poisons are moving through the body's fat storage system and bile, they cannot be reached by the "antibodies" that search out and destroy invading microorganisms in the bloodstream. Instead, they continue to travel throughout the tissues for years at a time, triggering such classic symptoms of Lyme Disease as fatigue, headaches, shortness of breath, joint aches and short-term memory impairment.
Frequently found today in the backyards or playgrounds of America's fast-spreading suburbs, the deer and Lone Star ticks that spread Lyme disease (named for the Connecticut town where it was discovered a few decades ago), take in the disease-causing Borrelia while ingesting the blood of deer or mice. When they later bite humans, the bacteria move from the mid-gut of the arachnid - now found commonly in all 50 states - into their human host. Within a matter of days, these spirochetes begin producing the brain-damaging neurotoxin(s) that cause the blurred vision and the muscle fatigue so commonly seen in cases of Chronic Lyme.
While treating hundreds of Chronic Lyme patients in my Maryland-based Family Practice in recent years, I was fortunate to come upon an already existing but little noticed physiologic test of neurologic function in the visual system- the "Visual Contrast Sensitivity" test, or VCS - that can tell a physician in five minutes whether or not the patient is suffering from the harmful effects of neurotoxins on the brain's ability to distinguish contrast between black, white and gray. The deficit in the visual pathways mirrors the adverse effect the neurotoxins are causing throughout the body.
The good news for Lyme patients everywhere is that VCS now gives the physician a reproducibly reliable, inexpensive and non-invasive test (it takes only five minutes) that makes a virtually foolproof diagnosis of Chronic Lyme readily available.

[posey]

Once the VCS test pinpoints the diagnosis, PLD can be effectively treated with a toxin-binding drug ("cholestyramine," or CSM) that filters the offending neurotoxins out of bile in the lower intestine. It was Dr. Shoemaker's good fortune to be able to demonstrate as much, while presenting the first scientific paper in the world's medical literature on "Treatment of Chronic Lyme Disease Using VCS and Toxin-Binding Therapy" in April, 2000, at a meeting of the American Society for Microbiology. That paper showed that VCS was a better test for confirming the presence of Lyme neurotoxins than any blood, urine or DNA test for the organism, itself.
Moreover, the VCS Test showed improvement with CSM treatment as symptoms abated.
A follow up study, first presented in the Biotoxin Symposium chaired by Dr. Hudnell's during the 8th International Symposium on Neurobehavioral Methods and Effects in Occupational and Environmental Health, Brescia, Italy, June, 2002, shows a 92-percent improvement rate in more than 200 patients with PLD. Their case histories prove conclusively that Chronic Lyme can be diagnosed effectively with VCS - and that it can be treated effectively with drug therapy, provided that it takes place under the rigorous supervision of a clinical physician expert in management of CSM therapy and drugs to downregulate proinflammatory cytokines.
Patients should never take this drug on their own, because it can trigger intensification of symptoms in the absence of pre-treatment by a physician to manage the cytokines.
As each summer's tick-and-Chronic-Lyme season begins in earnest, it's important to remember that you can catch this highly infectious and debilitating disease right in your own backyard. It's also important to understand that you can't prevent tick bites by "rolling up your pant legs" or applying a standard insect repellant, which has no effect on arachnids such as ticks. (The blunt fact is that the usual public health recommendations for preventing tick bites simply don't work.)
Remember, also, that more than 30 percent of Lyme patients don't get a rash, never even realize they'd been bitten by a tick - since many bites from these tiny parasites go unnoticed.
If you do get sick (and many people will, as the epidemic continues to spread), ask your physician about using the VCS Test as a diagnostic tool.

These days, the good news for Chronic Lyme sufferers is that the list of physicians who understand the links between long-term illness and neurotoxins is growing rapidly.

Why suffer needlessly from the painful symptoms of this debilitating disease? Instead, why not take the step of obtaining an inexpensive, five-minute diagnostic test? Then go get the toxin-binding therapy you need to resume a healthy and productive life.

[posey]

Did you know? Standard medical diagnostic tests are usually normal in patients who have these illnesses.



A PRIMER IN SICK BUILDING SYNDROME
LESSONS FROM THE SOMERSET COUNTY DISTRICT COURT

There are tremendous variations in the kinds of buildings that can become home to toxin-forming species of fungi. Any building that provides the proper mix of food and water can potentially be at-risk. When the building has air circulation that is closed, with little outside air input and windows that don't open, any intrusion of water can become the source of fungal blooms. The variations on how the building became sick (water intrusion through leaky roofs, windows or doors; wicking of water along a concrete slab or saturation of carpets; and pooling of surface water in basements come to mind) are relatively few. The Somerset County District Court Building in Princess Anne, Md., provides a great example of the most common problems seen in typical sick building syndrome (SBS) site investigations. This is a true story; it has been presented on TV, discussed in the newspaper and on radio.

It was the judge who called me, "Ritchie, I think I have a sick building here. The entrance foyer smells like a four day old wet sock, you can see the black mold on the ceiling tiles and all of us are sick." It seemed ironic; the debate about whether or not a building makes people sick usually ends up in court (or is settled before trial). This one already was in court! I agreed to do a site visit and test everyone who worked there using visual contrast sensitivity (VCS). Contrast testing is such an elegant diagnostic device--portable, non-invasive, reproducibly reliable, fast and low cost. A neurotoxin history, an essential part of the case definition of a SBS patient, is so easy to do once you learn how (it takes less time than asking a good cardiac history!), so I was ready to go.

The case definition of SBS isn't too complicated. You need to show exposure, a distinctive grouping of symptoms, presence of biomarkers, especially VCS, have no confounding exposures, respond to cholestyramine (CSM), proven to be effective when prescribed properly, as in our time-tested protocol, show relapse with re-exposure off medication, and again respond to CSM treatment. Seeing the biomarkers, blood tests, neurotoxicologic tests and physiologic measures of blood flow in the neural rim of the optic nerve, change in step with improvement or worsening of symptoms are important features that add to confirmation of the neurotoxic basis of SBS.

"Don't forget your CSM, Ritch," I could almost hear my wife say. No problem there. Over the past 4 years, I have sampled molds and tested patients in so many buildings that have subsequently made me sick that I don't forget to take my mycotoxin (fungal toxin) binding medication before exposure. I can just about tell within 20 minutes after entry into a building when mycotoxins are present. There is nothing else that gives me that distinctive hot taste on the sides of my tongue, queasy stomach, headache and sensitivity to the fluorescent lights found in nearly all office buildings. After being in the buildings with the worst mold contamination, I end up being extra-sensitive to smells, too. Visitors to my office after I have been testing in such a building often ask why a fan by my desk blows upward next to the computer. Get those fumes away from me! Fortunately, CSM, taken as a preventive measure, blocks the group of symptoms that define the acquisition phase of illness caused by toxin-forming fungal species. Maybe this time I won't again be forced to have the papers on my desk weighted down while my sensitivity to many chemicals is again being treated successfully.

So armed with my standardized light source, symptoms lists, VCS equipment and score sheets, I'm off to the architectural jewel of the judicial system in rural Somerset County, Md., about 15 miles from home. The single-level, colonial style building is only about 5 years old. Built on a concrete slab and surrounded by a paved parking lot, with marginal drainage at best, it has several suspect angles in the roof, and moisture-retaining carpet covering all the concrete. If the roof doesn't leak, just the run-off from the pavement could provide the moisture necessary to provide favorable habitat for growth of any number of genera of fungi. The drywall and composition ceiling tiles provide a welcome source of nutrients for fungi too. With the water (possibly) entering through the roof or from the outside, the mold could grow freely, hidden from view on the out-of-sight side of the cellulose construction materials. To be a fungus finder, one has to look where the sun doesn't shine!

The building was built to satisfy all codes (we might use a derivation of the "Nuremberg Trial" argument here that the real culprit in the explosion of the number of sick buildings, like this one, is a lack of understanding of fungal adaptation by those who write the building codes - does that mean those who knew the codes were inadequate have an ethical obligation to surpass them, thereby increasing building costs? Quality construction at the start, including putting the "V" in the HVAC, can save suffering and lots of money spent on remediation in the long run). It really isn't anyone's fault that the sewer pipes backed up shortly after the building opened. The indoor "flood" from the malfunctioning exhaust side of the plumbing might have started the fungus ball rolling. We will never know if that first water intrusion created the sanctuary that later nourished impressive numbers of Stachybotrys, Aspergillus and Penicillium. We can't dump all the blame on the plumbers because the front entry way lets in water whenever the wind comes from the West, as it usually does, except for the occasional Nor'easter that buffets this small Chesapeake Bay town. And the framing carpenters who are responsible for moisture seals around the doorway are off the hook too, because the concrete slab, poured as a foundation to save money, was like a fungal roller rink due to water draining off the impervious surface of the parking lot. Why didn't someone recognize that concrete slabs are portals of entry, especially in low-lying, high water-table areas? Sure, when the roof leaked, everyone noticed it. Just imagine the scene when an indoor trial was postponed because of rain!

Most sick buildings don't have this many sources of water intrusion. It usually is easy to isolate one source of water entry, like a roof with inadequate flashing or a basement with inadequate ventilation. Being able to pinpoint a single source of negligence gives attorneys an open invitation to get to work. Lawyers often pick out a responsible party, usually one with deep insurance pockets, as a target of negligence suits. Yet all the litigation, settled claims, abandoned buildings (how about the burned buildings!), and expensive retrofits won't do what our treatment protocols do: restore health of affected patients. We hope that we can identify and treat the patients before irreversible adverse downstream health effects caused by the pro-inflammatory cytokines, released in response to mycotoxin exposure in susceptible patients, either damage critical immunomodulatory hormone pathways in the hypothalamus or alter the normal defense mechanisms in mucus membranes, or (even worse) both. Once the exposure has gone on too long or with too much intensity, we have to do much more clinically to help SBS victims regain energy, cognitive function and quality of life. Don't think for a minute that ongoing mycotoxin exposure is benign. When I hear someone (especially someone with political power) say that a little mold isn't harmful, I wonder if they realize how dangerous their misinformation can become.

Letting adults work in a poisoned environment is bad enough, but just imagine if the sick building is a school. How will we know if our recognition of the effects of chronic exposure to mycotoxins is too late? Low scores on standardized tests? An increase in learning disorders? A rise in Ritalin prescriptions? An increase in absenteeism? Low SAT scores years later? The answers to these questions will only arrive when VCS testing becomes a mandatory part of the yearly school health evaluation, just like a hearing test and a visual acuity. And that will happen only when groups like the PTA demand action and no longer put up with empty statements, like "mold isn't harmful."
Remediation is costly, but so is impaired ability to learn.

So who was negligent in the construction of the courthouse? Who do the victims sue? Which water intrusion allowed the mold to grow? Who should pay for clean up and remediation? If everyone can blame someone else, who lets the bill stop on his or her desk? Why were so many fungi found? Which fungus made the judge sick?

When patients ask me why we rarely see "monocultures" of fungi in sick buildings, the answer is simple. A sick building simply lets fungi survive, reproduce and release mycotoxins and other compounds into the air the inhabitants breathe. With many organisms able to grow, and given food, water, cover and a chance to reproduce (the building amply provided for all of those), it is a fact of biology that multiple species will compete for small econiches well enough to survive. Every time the front door opened, for example, or when the judge came in on Saturdays to do some paper work, wearing his gardening shoes, a new opportunistic invader could have been introduced.