Guest guest Posted August 11, 2007 Report Share Posted August 11, 2007 http://www.aehf.com/articles/2003Symp.htm SPEECH TITLE: " Pathology of Trichothecene Mycotoxins in Man " Abstract Information & Notes A. Croft, D.V.M., Ph.D. Date of talk: Thursday, June 19, 2003, 2:00pm Environmental Diagnostic Group Inc. Phone: 715/757-3756 521 Hilltop Dr. Fax: 715/757-9302 Madison, WI 53711 E- mail: doccroft@... Veterinary School Attended: University of Minnesota Medical School Attended: University of Wisconsin, Madison, Wisconsin Major and date of Graduation: Ph.D. in Medical Pathology from the University of Wisconsin, Madison, Wisconsin. Current Job Description: Study Human diseases within the environment from outbreak of human disease as a Medical Pathologist. Other Information: Was on Faculty of the University of Wisconsin as Medical Pathologist, was accepted by the National Institute of Health as a Medical Pathologist, qualified to research human diseases. Obtain over $900,000 of highly competitive research grants from the national Institute of Health while at the University of Wisconsin. Disclosure Statement: None SPEECH TITLE: " Pathology of Trichothecene Mycotoxins in Man " The speaker has provided the information below. 1.) Goals and objectives: To demonstrate the pathologic changes in the primary target organs after inhalation verses ingestion exposure to Trichothecene Mycotoxins in man. 2.) Outline of talk/abstract: A. History of Mycotoxicosis, B. Detection of " Sick Buildings " ingestion verses inhalation exposure. Signs and Symptoms expressed by over 6,000 patients exposed to Trichothecene Mycotoxins, attempting to establish diagnosis. C. The pathologic changes associated with inhalation exposure to trichothecene mycotoxins. D. The primary organs involved with inhalation Mycotoxicosis. 3.) Conclusion of what is to be learned: The primary target organs of this disease and how this mycotoxin affects every cell in the body. 4.) References: a. Croft, W.A., Jarvis, B.B., and Yatawara, C.S.,: Airborne Outbreak of Trichothecene Toxicosis, In: Atmospheric Environ, 20(3), 549-552 (1986). b. Croft, W.A., Jastromski, B.M., Croft, A.L., and s, H.A., " Clinical Confirmation of Trichothecene Mycotoxicosis In Patient Urine, " In: Journal of Environmental Biology 23(3), 301-320 (2002). The Pathology of Trichothecene Mycotoxicosis In Humans 1. The Fingerprint of the Agent Causing the Disease is Displayed Within the Cells or Tissue of The Body. 2. Degeneration and Necrosis of The Entire Central Nervous System, Cardiovascular, lung, Digestive Tract, Spleen, Liver, Kidney, Pancreas, Immune, Skin, Reproductive, Eye, Urinary Bladder and Prostate. 3. The Signs and Symptoms Described For Trichothecene Mycotoxicosis Match the Pathology Observed. 4. Every Cell in The Body is Affected or Susceptible to Trichothecene Mycotoxins When Exposed. 5. The Exposed Cells Are Not Allowed to Grow and Make Cellular Products in The Rough Endoplasm Reticulum Represents of First Mechanism of Action on The Cells. 6. The Burning or Denaturation of Tissue From the Epoxide Molecule is Another Mechanism of Action on The Cells of The Body Causing Intense Scarring of Organs. (Like Phenol) 7. The Rapidly Turnover Organs Systems Are Affected The Most Severe, G.I. Tract, Immune System and Reproductive, (like radiation damage) 8. The Central Nervous System is Severely Affected and is A Primary Target Organ. The Neurons in the Cerebral Hemispheres, White and Grey Matter, Brain Stem and even the Ependymal Cells. The Purkinje Cells of The Cerebellum Are Severely Affected That Affect Motion and Balance. The Dorsal and Ventral Motor Neurons Are Destroyed Causing Amyotrophic Lateral Sclerosis. Peroxidation of Peripheral Nerves is Also Observed. The Central Nervous System is The Organ Most Affected as Reported By People Exposed to Toxic Mold. 9. Lack of Cellular Production, Epoxide- Peroxidation of Lipid Membranes, Loss of Vessels, Loss of Oxygen From Severe Lung Scarring, and Loss of Proper Nutrients Due Loss of Functional Absorption of Intestine Affect the Brain and All Organs of The Body. 10. The Trichothecene Mycotoxins are Cumulative in Their Health Effects on Organ Systems. 11. Trichothecene Mycotoxins are " Hit and Run " Poisons and are not Stored in The Body. 12. Inhalation of Trichothecene Mycotoxins Are More Poisonous As Observed by The Intense Scarring of The Alveolar Tissue Than Consumption Due To The Neutralization of Mycotoxin by Bacteria. 13. Depression of the Immune System Allows for Increase Infections by Bacteria, Viral, Fungal and Cancer to Form. 14. Yeasts are allowed to Colonize the Intestine Tract Because They Are Resistant to Trichothecene Mycotoxins. 15. Yeast Can Cause Diabetes Mellitus, Gout and Prevent Proper Liver Function to Detoxify Xenobiotics. 16. Trichothecene Mycotoxins are Released Within the Urine and Feces as Evidenced by The Pathology Observed Within Those Tissues. 17. Children Exposed to Trichothecene Mycotoxins are 100 to 1000 X more susceptible because stems are killed not allowing for additional growth within the individual. 18. There is No Safe Level of Exposure to Trichothecene Mycotoxins. 19. The third Mechanism For Trichothecene Mycotoxicosis is To Develop Anaphylaxis to Mold Allergens When Mycotoxin Leaves The Body. Dr. Croft, (Medical Pathologist) Stages of Mycotoxicosis: For Inhalation of Mycotoxin The three Stages (1-3) ranging from lower to higher severity of poisoning were modified according to exposure via the air as opposed to ingestion already established (Forgacs et al., 1962; Joffe, 1971). A separate Stage of convalescence occurs when a patient is completely removed from the contaminated premises and the source of mycotoxin or mold spores. Stage 1: The primary changes are in the brain, respiratory and immune systems, mucus membranes and gastrointestinal tract. Signs and symptoms may include burning sensation in the mouth, tongue, throat, palate, esophagus, and stomach, which is a result of the action of the toxin on the mucous membranes and skin in the exposed areas. Moist areas of the body armpits, under breasts, belt line and groin are more sensitive or first affected. Patients may report burning within the eyes, ears and nose. Patients also reported that their tongues felt swollen and stiff. Mucosa of the oral cavity may be hyperemic. Mild gingivitis, stomatitis, glositis, and esophagitis developed. Inflammation, in addition to gastric and (small and large) intestinal mucosal, resulted in vomiting, diarrhea and abdominal pain. Excessive salivation, headache, dizziness, weakness, fatigue and tachycardia were also present. There may be fever and sweating. The respiratory system develops burning sensations and congestion. Severe exposure to mycotoxin within the lungs may lead to congestion, edema and failure, due to caustic action. Body temperature remains normal and controllable by the patient. The poisoning appears and disappears relatively quickly in this Stage with the exception of, lungs and central nervous system. Initially (Stage 1), the patient's symptoms are very uncomfortable or painful. As the poisoning continues and the patient progress toward Stage 2, he or she becomes accustomed to the presence of the mycotoxin and a quiescent period follows due to lack of nerve sensation. Depending on exposure levels, the first Stage may last from 3 - 9 days. In scoring the 50 signs and symptoms listed in Tables-1 and 2, an average score range of 20-45 represents Stage 1. Stage 2 : This Stage is often called the latent Stage or incubation period because the patient feels apprehensive, but is capable of normal activity in the beginning of this Stage. Every organ of the body is affected by degeneration and necrosis with continued exposure. The primary target organs for an individual become evident over time, due to biological variation. These are disturbances in the central and autonomic nervous systems resulting in headaches, mental depression, loss of short-term memory, loss of problem- solving ability, various neuropsychiatric manifestations, meningism, severe malaise and fatigue, narcolepsy, loss of temperature control, hyperesthesia or numbness of body areas, and cerebellar dysfunction including hypotonia, attitude and gait, dysmetria, asthenia, vertigo, disturbances of speech, and loss of balance (Best, 1961). Spinal cord degeneration may also be observed in gait and reflex abnormalities, such as the ability to drive vehicles, ride bicycles or pass sobriety tests (inability to tolerate ethyl alcohol). Attention deficient disorder may be observed in children. Various systems may include: Eyes: visual disturbances, floating objects, light sensitive, lack of tears, burning and itching. Ears: burning, itching, and loss of hearing. Immune and hematopoietic: progressive loss of white and red cells including a decrease of platelets and hemoglobin, and high susceptibility to bacterial, mycotic and viral infections, debilitating chemical and allergies. Gastrointestinal: metallic taste in mouth, tooth loss, gum problems, stomatitis, sores in gums and throat, nausea, vomiting, diarrhea or constipation, excessive flatulence, abdominal distention, hepatitis, pancreatitis, and diabetes mellitus. Respiratory : burning and bleeding from nasal membranes, respiratory difficulty, asthma, extreme susceptibility to cold, flu and pneumonia. Skin: thinning of hair on head, burning on face, rashes, irritation, and edema. Renal: proteinuria, possible hematuria. Reproductive: irregular ovarian cycles, increased menstrual flow, fibroid growths in uterus, cystic development in mammary glands, and tumors of mammary and prostate glands. Musculoskeletal : somatitis, muscle weakness, spasms, cramps, joint pain, enlargement of joints in hand, and clubbing of fingers. Cardiovascular: chest pain, palpitations, ruptures of atrial walls, myocardial infection and aneurysm of arteries. The skin and mucous membranes may be icteric, pupils dilated, the pulse soft and labile, and blood pressure may decrease or increase. The body temperature does not exceed 38 degree C and the patient may be afebrile, or chilled. Visible hemorrhagic spots may appear on the skin. Thoughts of suicide may be prominent in the person's mind at this time or anytime in Stage 2. Human bonding is very important for survival. Degeneration and hemorrhages of the vessels marks the transition from the second to the third Stage of the disease and may not be consistently observed. The degeneration of the vital organs including serious respiratory insufficiency or asthma and CNS degeneration will take the patient into Stage three along with development of necrotic angina. If exposure continues, depending on exposure levels, Stage 2 may continue from weeks to months or even years until the symptoms of the third Stage develop. Evaluating the 50 signs and symptoms (Table-1 and 2) by assigning a score (0-least intense to 5-most intense or severe) to each symptom, we have determined that an average score range of 45-180 represents Stage 2. Stage 3: Severe degeneration of the vital organs. The transition from the second to the third Stage is sudden. In this Stage, the patient's resistance is already low, and violent severe symptoms are present, especially under the influence of stress, or associated with physical exertion and fatigue. The first visible sign of this Stage may be lung, brain or heart failure (heart attack), with or without the appearance of petechial hemorrhage on the skin of the trunk, the axillary and inguinal areas, the lateral surfaces of the arms and thighs, the face and head, and in serious Cases, the chest. The petechial hemorrhages vary from a few millimeters to a few centimeters in diameter. There is increased capillary fragility and any slight trauma may cause the hemorrhages to increase in size. Aneurysms of the brain or aorta may be observed by angiography. Hemorrhages may also be found on the mucous membranes of the mouth and tongue, and on the soft palate and tonsils. There may be severe interstitial thickening or scarring of the lungs, or respiratory failure. Nasal, gastric and intestinal hemorrhages and hemorrhagic diathesis may occur. Necrotic angina begins in the form of catarrhal symptoms and necrotic changes soon appear in the mouth, throat, and esophagus with difficulty and pain on swallowing. Severe degeneration of the skin on the face, eyelids, and loss of lashes is also often present. Necrotic lesions may extend to the uvula, gums, buccal mucosa, larynx, vocal cords, lungs, stomach, and intestines and other internal organs such as the liver and kidneys and are usually contaminated with a variety of avirulent bacteria. Bacteria infection causes an unpleasant odor from the mouth due to the enzymatic activity of bacteria on proteins. Areas of necrosis may also appear on the lips and on the skin of the fingers, nose, jaws, and eyes. Regional lymph nodes are frequently enlarged. Esophageal lesions may occur and involvement of the epiglottis may cause laryngeal edema and aphonia (loss of voice). Death may occur by strangulation. Patients may suffer an acute parenchymatous hepatitis accompanied by jaundice. Bronchopneumonia, pulmonary hemorrhages, and lung abscesses are frequent complications. Tumors may develop of various organs, including skin, urinary bladder, brain, mammary gland, bone, immune, liver, prostate, possibly resulting in death. The most common cause of death is brain failure due to both direct effects of the mycotoxin on the central nervous system and indirect effects due to respiratory failure or lack of oxygen to the brain caused by the severe caustic inflammation (fibrinous exudation) reaction with the lung tissue, rendering it non-functional. Again, using the scoring system represented in Tables-1 and 2, an average score of greater or equal 180 represents Stage 3. Stage of Convalescence: The course and duration of this Stage 3 depends on the intensity of the poisoning and complete removal of the patient from the premises or source of mycotoxin. Therefore, the duration of the recovery period is variable. There is considerable cellular necrosis and scarring to all major organs of the body in which cells will not regenerate, including the brain, spinal cord, eyes, lung, heart, liver, pancreas, kidney, adrenal, and blood vessels. If the disease is diagnosed during the first Stage, hospitalization is usually unnecessary, but allergies and asthma should be monitored closely. If the disease is diagnosed during the second Stage and even at the transition from the second to third Stages, early hospitalization may preserve the patient's life. If however, the disease is only detected during the third Stage, death cannot be prevented in most Cases. 1. Croft, W. A., Jastromski, B. M., Croft, A. L., and s, H. A., " Clinical Confirmation of Trichothecene Mycotoxicosis in Patients Urine " , In: Journal of Environmental Biology 23(3), 301-320 (2002) 2. .Forgacs, J., and W. T. Carll : Mycotoxicoses. In : Advances in Veterinary Science. Academic Press, New York and London, pp 273-372 (1962). Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 16, 2007 Report Share Posted August 16, 2007 , thank you for posting this. There are a number of things he just mentions in passing that I think are really important to understanding why stachy is so damaging. People should take the phrases described in Dr. Croft's paper that they don't understand and take them to a medical encycopedia web site so they can understand the meanings of them. One good site is at http://www.medterms.com/script/main/hp.asp Also, people should be aware of PubMed at http://www.ncbi.nlm.nih.gov/sites/entrez At the PubMed web site you can easily search for any medical term, for example: http://www.ncbi.nlm.nih.gov/sites/entrez?term=trichothecene & sourceid=mozilla-sea\ rch & db=PubMed & orig_db=PubMed & dispmax=20 & dopt=DocSum On 8/12/07, tigerpaw2c <tigerpaw2c@...> wrote: > http://www.aehf.com/articles/2003Symp.htm > > SPEECH TITLE: " Pathology of Trichothecene Mycotoxins in Man " > > Abstract Information & Notes > > A. Croft, D.V.M., Ph.D. > Date of talk: Thursday, June 19, 2003, 2:00pm > > Environmental Diagnostic Group Inc. > Phone: 715/757-3756 > > 521 Hilltop > Dr. > Fax: 715/757-9302 > > Madison, WI > 53711 E- > mail: doccroft@... > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 17, 2007 Report Share Posted August 17, 2007 Barb, You know that its extremely difficult to catch stachy when it is sporulating, don't you? So not finding stachy spores in spore trap air samples or not finding stachy spores on bulk samples does not mean that you don't have stacy, it means that its not sporulating. Research done by Dr. Straus and others has shown that many buildings that have had water issues have high levels of macrocyclic trichothecenes in 'particles smaller than conidia' - Those particles stay toxic for a long time if they are not addressed. I am surprised you have not simply stripped all the sheetrock off of your walls piece by piece and cleaned them out. That is often what needs to be done. See http://aem.asm.org/cgi/content/abstract/71/1/114 or for a reprint PDF http://aem.asm.org/cgi/reprint/71/1/114.pdf >Stachy has never been found in my house but I had significant amount of tricothecenes in my urine per tested by Dr Croft. I never thought about that. I don't think that given the persistance of stachy toxins that its surprising at all. >Professional testing done once and rest culture plates. I KNOW culture plates do not catch stachy but I figure if I find where house mold is coming from, and clean it up, I will have caught the stachy also plus alot of bacteria as well. >I could spend every penny I have trying to find a particular type of mold Why? Why not just get the whole place cleaned out as best as you can and then keep it dry? >so just looking at the big picture. If some place has had enough wetness to have stachy, figure other molds must be there also. Wouldn't that be true, or does stachy TAKE OVER an area and kill other molds and is there all by itself??? --- In , LiveSimply <quackadillian@...> wrote: > > , thank you for posting this. There are a number of things he > just mentions in passing that I think are really important to > understanding why stachy is so damaging. > > ---original posting---- http://www.aehf.com/articles/2003Symp.htm SPEECH TITLE: " Pathology of Trichothecene Mycotoxins in Man " Abstract Information & Notes A. Croft, D.V.M., Ph.D. Date of talk: Thursday, June 19, 2003, 2:00pm Environmental Diagnostic Group Inc. Phone: 715/757-3756 521 Hilltop Dr. Fax: 715/757-9302 Madison, WI 53711 E- mail: doccroft@... > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 17, 2007 Report Share Posted August 17, 2007 Barb, The stachy in my home did not show on initial air-sample testing, and actually, it was 'accidently' found during remediation for the other molds that did. It was inside the wall cavity surrounding the tub/shower (and shared with my bedroom). The ceramic tile shower appeared to be in good condition, all grout intact and caulking well maintained. They said the grout 'failed' due to age - it was allowing the water to seep through, even though there were no visible cracks. A very small, old-looking water stain on the basement ceiling was sanded by the remediation crew and it crumbled and gave way to reveal the problem in the wall above. The stachy was inside two adjoining walls around the tub, and spreading through the subfloor under the tub and on the other side under the hardwood bedroom floor. There was no indication in the bathroom or bedroom that this was happening (except how awfully sick I was). The only sign was the small dry watermark type stain below on the basement ceiling - which wasn't even black; probably about as big around as the diameter of a drinking glass. Clearance testing after all contaminated materials were removed was then positive for stachy - because it had been disturbed. And, apparently then the spores were still in the air. The only logical explanation for how sick I was is that the toxins, but not the spores, were present before and during that initial test. I think with current, common testing methods, stachy can be a stealth mold. Sue > LiveSimply <quackadillian@...> wrote: > > Barb, > > You know that its extremely difficult to catch stachy when it is sporulating, > don't you? > > So not finding stachy spores in spore trap air samples or not finding > stachy spores on bulk samples does not mean that you don't have stacy, > it means that its not sporulating. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 18, 2007 Report Share Posted August 18, 2007 stachy dies back when it dries and isn't really noticeable. the only tome you might see it is when it's wet and growing. and it really likes the dark, I never saw any black mold for years only noticed my house dust was getting black toward the end of liveing there when it was getting accumalated pretty heavy in the first floor walls. the dry mold dust was what was makeing me more sick more constant as it accumalated in the house. my experience with it is that it's when it's dry and airborne is when it gets in your system. I always had relief when it was rainy. the spores and toxins accumalate inside,settle and get stirred up by windy days and air currents from heating systems. in a cictoria built home with steep roof and open inside walls to basement most accumalation was roof edges(sofit area) and because tin drip on roof ledges was not done right this added to leaks thar ran inside walls down to basement and mold dust settled to the basement and areas inside walls which resulted in higher exposures when dry windy days stirred it up and blew into liveing areas and in winter from dry mold dust getting blown up from basement. to me haveing stachy from roof leaks where it dies between rains means lots of myco's being put out everytime it grows and starts drying. weather it was the 100+ years of dust in this home or the extra help of bat poo and pee(from them getting in where flashing was missing on the roof) or the horse hair plaster that help it grow, I dont know. what I do know is that the second home which had a constant moisture/hummidity problem, aspergillus/penicillium,chaetomium,alternaria where the over takeing molds. stachy was found there on tape test so it was there but the moisture in this home may have kept it weighed down and slimed more. but what ever blew out of the duct work made me throw up constantly amoung other things and vomitoxin comes to mind. however mold testing there was not done while I was still liveing there and ac was on but with moisture problems in this home it might be very hard to get good testing if asp/pen is going to overgrow on test samples.? and I cant afford more testing right now. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 18, 2007 Report Share Posted August 18, 2007 Jeanine, where did you do tape tests that found stachy...on door ledges or in cold air returns...? > > stachy dies back when it dries and isn't really noticeable. > the only tome you might see it is when it's wet and growing. and it > really Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 19, 2007 Report Share Posted August 19, 2007 Thanks Carl, I have little dought that there were several molds not detected in my second house and with moisture problems and humidity documented even in the fall when air tests were done and humidity was twice as hugh as outside, no dought of voc's and bacteria there. a correction on my post that ac was NOT on at time of testing and I was no longer liveing there. went in once that summer and it was like a sauna in there. ever see a house so infested that it created it's own moisture problem? to much to get into with this place but basidly fraud,fraud and more fraud. a half assed remediation took place in order to make it appear liveable after setting 30+ years broke down, mold infested. the list is a long one for lies on disclosure statement. a example: it advertized a new drilled well with plentiful water supply which ended up being a 60+ year old bang well, contaminated,caseing completely rusted away and they put 5 ft. of new caseing in the top and a new well cap on it. NRD put camera's down in it. surface water running in,ect. had to fill it as it's been caveing in around it. a case of ex realestate agent and her husband that knew exactly what was at stake, bought cheap, rigged up to sale by another real estate broker,lifelong friends. they even went and got a lawyer together and had him send me a letter saying I was hurrassing them and to have no further contact. this was after they had no problem haveing house tested for rayon but when rayon testing co. said it needed tested for toxic molds I was than hurrassing them by asking for this to be done. and gee, at the time the real estate broker was begging me to let him work out the problems found so far which included the well and had been promiseing me a new drilled well and was so nice lol's that he even insisted on testing the water for contamination himself when after the first several weeks went by and the water in the " new " drilled well didn't clear up like promised. you know, those new drilled wells have to run awhile at first. thing was, his water test came back normal while the health dept. tests didn't. hehe, oops I forgot to tell him that the health dept. and NRD had been on the case of the contaminated " new drilled well " . and when I did tell him after he handed me his results that showed no contamination, he became quite nervous and than said we'd just go by the results of the health dept. as he probably did his wrong. thing is that no matter how wrong you do it you cant make contaminated water come back not contaminated. just a small example of goings on at the death house that tried to kill me.. Quote Link to comment Share on other sites More sharing options...
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