Mysterious honeybee deaths here too. Entry for August 30, 2007

This picture was taken by me recently in between the two towns mentioned in this article. There are what appear to be abandoned honeybee hive boxes in a field beside this spot. I was looking at them trying to figure out if I was right that there was no life in them there honeybee boxes because they looked abandoned.

Well, I had not planned this entry, but look what is in today’s paper. Now it is the bees right in the general vicinity of one of the areas I have been focused on since prior to 2003. So far, the avian influenza, over a million vanishing salmon, and now the bees, and then there is still the human and animal health trends. All right in my back yard metaphorically speaking while I keep getting told there is nothing wrong out here. Okay, is it just me, or is it lookin’ like I could be right and “they” could be lying, oops, I mean wrong.

I found an interesting little Science Teaser as it was called on one of our federal government agriculture related sights a few or four years back. It said that scientists were finding heat resistant fungus in blueberry soil. It is potentially possible to integrate this piece of information into some of the previous posts, including this one. Just thought I’d throw that in there.

Disappearing bees keep sweet industry guessing


Bees have disappeared from Jean-Marc Le Dorze’s hives.

By Kristine Thiessen
Mission Record

Aug 30 2007

Beekeeping is a high-risk business.

A spate of bad weather and a variety of mites can reduce Mission beekeeper Jean-Marc Le Dorze’s 2,000-plus hives by ten or 15 per cent each year.

Le Dorze is used to such losses, but for the first time in his 13 years running Golden Ear Apiaries, adult bees from a number of his hives just simply disappeared. Le Dorze is concerned, because he doesn’t know why. Not knowing “has never happened” to him before, he said.

Honeybees, those fuzzy, buzzing insects, could arguably be called the Fraser Valley’s unsung heroes.

“They’re the workhorse of American and Canadian bees on the pollination side,” said Le Dorze.

And for most consumers, it’s the pollination side that really matters. Honeybees are crucial to increasing berry crops like blueberries and cranberries.

“For blueberries, they can increase the crop by 50 per cent,” said Le Dorze. “They pollinate and then the fruit is larger, sweeter, and more uniform in size.”

To get a decent blueberry, each flower needs to be visited by a honeybee at least four times, explained John Gibeau, a vice president with the B.C. Honey Producer’s Association.

“There [are] about 7 million flowers per acre,” he said. “That’s about 28 million visits.”

In addition to the Fraser Valley’s berries, bees also pollinate pumpkins, zucchini, and “everything from alphalfa to seed oil production,” said Gibeau. “Honey production is probably about one-tenth of the value [compared to bees agricultural value].”

It’s not just Le Dorze’s critters that are dying off.

The Georgia Straight recently reported 23 per cent of B.C.’s colonies were wiped out last winter.

The unexplained disappearance of adult bees has been dubbed “colony collapse disorder,” or CCD.

“If you have a hive that’s collapsing and there’s not many bees . . . then that’s when they consider it CCD syndrome,” said Gibeau. “Bees will normally never abandon their brood.”

But while Le Dorze believes his bee disappearance is CCD, Gibeau chalks up this year’s bee losses in the Fraser Valley to the cool weather.

“The weather was just terrible this year for honeybees,” he said.

“They’re incapable of flying when the weather drops down to five or six degrees [Celcius]. Normally when it begins to cool, the bees come back home, where inside the hive is a nice and toasty 37 degrees.”

The Abbotsford beekeeper said it was the worst year he’s ever had in beekeeping.

Le Dorze agreed that the weather didn’t help.

“April was like this,” he said, gesturing at the cool and damp air one August morning.

However, while the weather played a role, Le Dorze speculates something inside the hives caused two to three per cent of his bees to disappear.

He pulled out trays of honeycomb and bees from the wooden crates that line the ground of his farm. Le Dorze pointed out the queen, the adults, the fuzzy young bees, and the antenna of a new bee emerging through a brown covering that caps the comb.

The brown coverings are the pupa, he explained. If the adults disappear from the hives and leave the brood, secondary pests will consume the pollen, the honey, and the wax.

This year, the pests didn’t enter the abandoned hives right away, and Le Dorze’s guess is that something in the hives discouraged them.

He’s anticipating an American study on CCD scheduled to come out in September, will link a pathogen to the collapse.Other guesses by scientists have ranged from viruses, to a group of pesticides, to a fungus, to new stresses like being trucked long distances.


A good Trichothecene Mycotoxin backgrounder Entry for August 30, 2007

My leg mid 2003
This is a picture of my leg (ankle) in mid 2003, when I lived at my known exposure sight. These are the sores I was getting. They were preceded by severe burning and tingling of the skin with no visible sign of any kind of a problem. This was followed within 2-3 days by bright red skin with increased burning, and the sores began to appear. I noted that the sores seemed to be located within hair follicles of the skin. At this time my hair was falling out in clumps, as it does for people undergoing chemotherapy treatment. I had a severe dry cough, dry mouth, tingling face and hands, very laboured breathing, and a knotting type pain in the area of the right liver lobe. I would wrap my feet in a quilt when I was sitting trying to watch television, listen to music, read, or do any idle activity as it felt like my feet and lower legs were being attacked by something, but I could see nothing there. At times, had visible signs of something going on not have been there, I may have been inclined to think I was going nuts. I noticed I was having involuntary tremoring, like Parkinson’s disease sufferers get. I was losing things. For reasons beyond my grasp, I was putting things where they did not belong, and could not find them. I was scared. I did not know what was happening to me, and no one in the government appointed relevant fields (public health officials, municipal inspectors, BCCDC), or the medical field was accommodating my pleas for answers. I was becoming convinced that I was going to die there.
These sores caused (or came with) an accumulation of clear fluid between the tissue layers that burned like lye.
I complained of blurry vision. Coordination problems, diarrhea, burning urine and stool, tooth pain, sharp chest pains, unexplained bruising with a strange trait,the bruises did not hurt, but these sores………oh my God!, did they burn!They also do something to the skin pigment. They were causing literal loss of pigment, where you would end up with a white scar where the sore was. Some of the sores actually ate away a bit of tissue and left little craters and purple or light brown scars, which are still there. As there were so many hazardous agents mixed together in my exposure, I was experiencing the effects of more than one thing happening to me. Can you imagine?! People still live there! I just stopped by there. Mistake. My feet are tingling like mad, and someone who has only been there a week has severe fatigue, runny nose, stuffed up, and burning tingling skin. This is more than 4 years after I left there. It is in the soil. You can smell it when you are standing in the yard. It is of coarse not only there, as it just does not work like that. It is however there in extremely high quantities. I could not stay inside the building as for one, it was very traumatising being there, and aside from that, I was having a severe reaction to the conditions there and could barely breathe.

This article has very good background summary on this topic.

Trichothecene Mycotoxins

Information on Trichothecene Mycotoxins

Trichothecene mycotoxins are produced by fungi (e.g., Fusaria, Trichoderma, Myrothecium, Stachybotrys); 60 are known. These were originally isolated as possible antifungal microbials or as antiplant agents. Analysis of trichothecene (and aflatoxin) exposures is complicated by their natural occurrence: Their presence alone does not prove a biological attack.

Iraq has admitted to possessing trichothecene mycotoxins and testing them in animals and has been accused of using them against Iran (UNSCOM, 1991, 1992, 1995; Zilinskas, 1997; Heyndrickx, 1984). The report of Iraqi possession of trichothecenes followed a considerable period of interest, attention, and controversy about their use in Southeast Asia (between 1974 and 1981, against Lao and Khmer populations by communist forces) and in Afghanistan (by Soviet forces) (Crocker, 1984; Haig, 1982; Schultz, 1982; Seagrave, 1981). Wannemacher and Wiener (1997), concluded that the Soviets and their clients have used trichothecenes, and the authors present a detailed review of the history of the subject and associated controversy. There may have been shortcomings in the epidemiological approaches (Hu et al., 1989). There were also many difficulties and inconsistencies in agent sampling, transport, and analysis.

These toxins, until discovered in Southeast Asian attack environments, had not been on the usual lists of potential toxin weapons (SIPRI, 1973). Analysts recognized that the toxins could produce the injuries encountered (Watson, Mirocha, and Hayes, 1984). Subsequent research identified properties of military significance, e.g., skin injury from nanogram amounts; eye injuries from micrograms; and serious central nervous system, respiratory, gastrointestinal, and hematological toxicity via multiple routes of exposure (Watson, Mirocha, and Hayes, 1984; Bunner et al., 1985; and Wannemacher and Wiener, 1997).


These mycotoxins have been poisoning people and animals for a long time. They grow well at low temperatures and frequently contaminate grain and other foodstuffs. They have been implicated in food-born illnesses on several continents (Ueno et al., 1984). A large disease outbreak in the Soviet Union during World War II, which involved thousands and had high mortality, was eventually traced to the consumption of grain contaminated by Fusaria molds, which had been left in the fields over the winter. The disease, alimentary toxic aleukia, resembled a severe radiation injury with nausea, vomiting, diarrhea, leukopenia, hemorrhagic diathesis, and sepsis.

These toxins are also hazardous via other routes. Domestic animals and farmers manifested skin and respiratory irritation and systemic malaise from exposure to contaminated dusts and hay. Human illnesses have arisen from trichothecene mycotoxin contamination of houses and ventilation systems, resulting in so-called “sick building” syndrome (Croft et al., 1986; Jarvis, 1985; Smoragiewicz et al., 1993). One family so exposed was affected with nonspecific symptoms whose cause was not identified for months (Myrothecium and Stachybotrys were identified). For a time, several trichothecene mycotoxins were tested as anticancer agents in clinical trials (Thigpen et al., 1981; Bukowski et al., 1982; Yap et al., 1979; Diggs et al., 1978; Murphy et al., 1978; Goodwin et al., 1981). Some laboratory accidents have added to experience with human exposure (Wannemacher and Wiener, 1997). In addition, there is considerable information on the effects of trichothecene mycotoxins on economically important animals (Ueno et al., 1984).

Reports of communist attacks on Lao tribal people, and later on the Khmer, began in 1974 with aircraft and helicopter delivery of colored smokes, dusts, and droplets. People near these attacks had signs and symptoms that did not resemble known chemical warfare agents. Later similar attacks were reported in Cambodia and Afghanistan. Symptoms included vomiting, dizziness, seizures, hematemesis, respiratory distress, hypotension, and blisters. Survivors were ill for a long time with rashes, joint pains, fatigue, and memory problems (Haig, 1982; Schultz, 1982; Crossland and Townsend, 1984).

Investigative teams in refugee camps were puzzled, identifying a t
oxic epidermolysis without other expected findings from known chemical agents (House, 1979), but intelligence analysts recognized the similarities to trichothecene intoxication. Later, clinical examinations, autopsies, laboratory tests, and tissue samples showed trichothecene mycotoxins (and a propylene-glycol carrier) together with tissue damage compatible with trichothecene effects (Crocker, 1984; Watson, Mirocha, and Hayes, 1984; Rosen and Rosen, 1982; Stahl et al., 1985).

Chinese analysts attributed a higher toxicity to trichothecene mycotoxins than to nerve agents. They alleged that, between 1975 and 1982, 6,000 Laotians; 1,000 Cambodians; and 3,000 Afghans had died from attacks with what came to be known as “yellow rain” (Fang, 1983).

During the Iran-Iraq War, especially in the fighting around Majoon Island, colored smokes and powders were used against Iranian forces, perhaps reflecting combinations of agents. Although controversial in the scientific community, Heyndrickx (1984) found trichothecene mycotoxins in Iranian casualties who appeared to have sustained mustard injuries. Although other laboratories did not confirm these findings from the same material, Professor Heyndrickx argued that biological tissues had degraded the toxin over time.[7]

It is not known if, during the Gulf War, any of the Iraqi chemical and biological facilities hit by Allied fire contained trichothecenes. Trichothecenes are very resistant to environmental degradation and resist heat below 500��F; hence, the production of effects after long-distance transport following explosive release is possible but unlikely because the chemical would be very diffuse by that time (U.S. Army, 1990; Wannemacher and Wiener, 1997; Trusal, 1985). However, no events described during the war closely correspond to known acute effects of trichothecene syndromes. Lethal effects require substantial doses (milligrams), but eye and skin irritation can occur at much lower levels (U.S. Army, 1990; Wannemacher and Wiener, 1997; Coulombe, 1993), raising the remote possibility that low-level exposures might have been misinterpreted as being due to some other cause.


Production using contemporary fermentation methods similar to those of brewing and antibiotic production is easy and inexpensive, and conventional bioreactors can readily produce tons of these agents (Wannemacher and Wiener, 1997). AD Little (1986, Ch. 4) described the conditions defining production. The large-scale production of Fusaria and trichothecenes for civil purposes in the former Soviet Union indicates the ease of large-scale production for other purposes (Buck et al., 1983). Formulations of T-2–one of the most potent trichothecenes–might also include polyethylene glycol, sodium lauryl sulfate, or dimethylsulfoxide (DMSO). These materials facilitate dispersal and handling of the toxin, possibly enhancing toxicity. Trichothecenes do not degrade to nontoxicity when exposed in the natural environment (for weeks at least) and are stable when stored. They can be delivered by mortars, artillery, free rockets, aerial bombs, and surface or aerial sprayers (Wannemacher and Wiener, 1997). Iraq possessed all the systems previously used to deliver trichothecenes.

T-2 is a skin-damaging agent of great potency (Bunner et al., 1985)–several hundred times more potent than mustards or lewisite (Wannemacher and Wiener, 1997). It is able to injure the eye in microgram amounts, which again indicates that it is more potent than mustards.

Toxicity by inhalation is comparable to mustards. NAS (1983) estimated that LC50 exposures of aerosols of 1 mg/m3 or surface contamination or LD50 of 1 g/m2 could readily be attained.

Trichothecenes readily result in vomiting, rather promptly at low concentrations, which might compromise the ability of exposed troops to use protective respirators. Other symptoms, including mild incapacitation, follow. Operationally, the persistence of trichothecenes makes them a threat even to military forces with protective equipment; Soviet troops in Afghanistan avoided operating in areas where these toxins were used (Fang, 1983). There are some indications that trichothecenes may have been used in combination with other agents in Southeast Asia and Afghanistan (Fang, 1983; Schultz, 1982).

Chemical and Physical Properties

The trichothecenes are classed as sesquiterpenes (Ueno, 1983). The members of this family of toxins vary depending on their side groups and include T-2, HT-2, nivalenol, deoxynivalenol, anguidine, diacetyoxyscirpenol (DAS), and crotocin.[8] When the toxins are extracted from fungal cultures, a yellow greasy residue remains. Had the various reported Asian attacks involved a crude extract containing some of that residue, the result might have been the yellow rain reported. The toxins are stable in air and light for weeks and can withstand heat; a temperature of 500��F is required to destroy T-2 (Trusal, 1985; Wannemacher and Wiener, 1997).

These toxins can be inactivated with 3- to 5-percent hypochlorite solutions (Wannemacher and Wiener, 1997). The toxins are relatively insoluble in water but are soluble in acetone, chloroform, DMSO, glycols, ethanol, and other organic solvents. They have a peppery odor and negligible vapor pressure. Detection

No military field detection systems currently deployed can detect trichothecenes, although laboratory techniques (e.g., antibody-ELISA, gas chromatography or mass spectroscopy, and thin-layer chromatography coupled to fluorimetry) have been used. Biological detection systems using animals are neither specific nor easy (Fontelo et al., 1983; Mirocha et al., 1984; Thompson and Wannemacher, 1984; Rosen and Rosen, 1982; NAS, 1983). Wannemacher and Wiener (1997), reviewing confirmatory procedures, indicated that mass spectroscopy is the procedure of choice, requiring little specimen “cleanup” and enabling detection of one part per billion (ppb) of toxin. More-complex systems being evolved may detect 0.1 ppb.

Toxicology and Toxicokinetics

Mechanisms of Action. The many mechanisms by which trichothecenes produce toxicity are varied, and their relative importance in producing illness is not fully understood (Coulombe, 1993). They include the following:

inhibition of protein synthesis, thought to be the most important effect (Ueno, 1983; Ueno et al., 1984; Tutelyan and Kravchenko, 1981)

inhibition of DNA synthesis (Thompson and Wannemacher, 1984), which might contribute to their radiomimetic properties

impairment of ribosome function (NAS, 1983; Coulombe, 1993; Tutelyan and Kravchenko, 1981)

inhibition of mitochondrial protein synthesis (Pace et al., 1985)

induction of reparable single strand breaks in DNA

immunosuppression, allowing secondary and opportunistic bacterial infections and possibly delayed hypersensitivity (Ueno, 1983; Yarom et al., 1984; Jagadeesan et al., 1982).

Trichothecenes react readily with thiol groups and, at low concentrations, inhibit thiol enzymes (e.g., creatine kinase, lactate dehydrogenase) (Tutelyan and Kravchenko, 1981; Ueno et al., 1984). They can be incorporated into lipid or protein elements of cell membranes. Tissue culture studies show alteration of membrane function (Coulombe, 1993; Pfeifer and Irons, 1985). Sulfhydryl effects in cell membranes are important in cell-to-cell interactions in the immune system. T-2 toxin induces cell membrane injury with hemolysis, apparently via a free-radical mechanism (Segal et al., 1983; Coulombe, 1993). Metabolism may be more important in detoxification than in producing toxicity.

Unlike the aflatoxins that require metabolic activation, the trichothecenes are directly toxic without activation, as their prompt effects on the gastrointestinal mucosa with epithelial cell necrosis suggest (Busby an
d Wogan, 1979).

T-2 and other trichothecene toxins are deacetylated in the liver.

Metabolites are also toxic but less so than T-2 (Ueno et al., 1984). Carboxyesterases (-SH serine esterases) in liver microsomes hydrolyze T-2 to the less potent HT-2. These enzymes may be clinically important. Inhibition of this enzyme by paraoxon (an organophosphate pesticide) in subclinical doses increases the toxicity of T-2 in mice (Johnsen et al., 1986). Other potent inhibitors of this enzyme are tri-o-cresyl phosphate (TOCP, an organophosphate), eserine (a carbamate), and diisopropyl fluorophosphate (DFP, a weak organophosphate nerve agent) (OSRD, 1946). These all inhibit hydrolysis of T-2 (Johnsen et al., 1986). This raises the strong possibility that similar compounds, such as PB; low levels of nerve agent; or other carbamate or organophosphate insecticides might enhance the toxicity of T-2 or other trichothecenes at low levels.

Exposure-Effect Relationships

T-2 toxin and other trichothecenes are absorbed slowly (12 to 24 hours) via the intact skin but rapidly through abraded skin. DMSO or similar penetrants can increase the rate of absorption, but even then the systemic toxicity appears slowly (Bunner et al., 1985; Schiefer, 1984; Kemppainen et al., 1986a, 1986b; Solberg et al., 1990).

The rapid appearance of symptoms after respiratory exposure in humans, along with the results of animal inhalation studies, indicates rapid absorption and high retention of aerosolized T-2 toxin, with the respiratory tree retaining small amounts (Creasia et al., 1987).[9] Tritium-labeled agent and immunoperoxidase studies have also been used to follow the distribution and disposition of T-2 toxin (Pace et al., 1985, Lee et al., 1984). Intramuscularly injected agent is distributed to liver, kidney, lung, and other tissues within 30 minutes. The plasma concentration has a biphasic course, with half-lives of 1.8 and 50 hours for the two phases. T-2 toxin and metabolites concentrate in bile with evidence of enterohepatic circulation. The liver and kidney are the main organs for detoxification. Oral intoxication showed T-2 toxin in the gastrointestinal tract and kidneys, but not in the liver, reflecting rapid hepatic metabolism. The brain showed a rapid uptake to levels higher than plasma but below many other tissues, with a rapid fall to levels similar to plasma in six hours. One would expect trichothecenes to enter the brain readily, since they are lipophilic (Wang, Wilson, and Fitzpatrick, 1992).

It has been shown, for example, that the effects of sustained low doses can accumulate to the clinical picture associated with alimentary toxic aleukia (Mayer 1953a, 1953 b; Lutsky et al., 1978). Or they can yield the more diffuse problems that Croft et al.(1986) and Jarvis (1985) reported: a case of ongoing illness for several years in a family of five, with recurring respiratory illness, flu syndromes, sore throats, diarrhea, cough, headaches, fatigue, and episodes of alopecia. One man had leg pains. Eventually, trichothecenes were identified in air ducts and ceiling material in the family’s house. Material extracted from these areas was toxic to rats and mice. Croft cited other reports by Forgacs (1972) of toxin exposures producing similar symptoms with central nervous system andneuropsychiatric manifestations.[10]

Respiratory is high and comparable to parenteral injections. Oral and dermal lethal toxicities are lower but produce similar systemic effects (Creasia et al., Dose Effect).


Skin Exposures

5-50 ng in liquid Min. erythema dose (guinea pig, rat) Ueno/Wannemacher et al. (1983)

209 ng/cm2 in liquid Min. erythema dose (monkey) Wannemacher/Bunner et al. (1983)

1 ��g/cm2 Irritation (guinea pig, rabbit) Fairhurst et al. (1987)

2 ��g Vesication, skin injury Bunner (1983)

0.25 mg/kg Severe illness, diarrhea (monkey) Bunner et al. (1983)

1.5 mg/kg in DMSO LD50 (rat; mean time to death, 19 hr.) Wannemacher (1983)

4.2 mg/kg in methanol LD50 (guin pigs; time to death 190 hr.) Wannemacher et al. (1983)


1 ��g Detectable corneal injury USAMRIID (1983)

2 ��g Severe corneal injury, conjunctivitis Bunner (1983)


0.24 mg/kg (abs) Mouse LD50 Creasia et al. (1987)

0.05 mg/kg (abs) Rat LD50 Bunner et al. (1985)

0.6-2.0 mg/kg (abs) Guinea pig LD50 Wieser (1997, p. 661)

5,479 mg-min/m3 Guinea pig LD50 AD Little (1986)

200-1,800 mg-min/m3 Estimated LCT50 U.S. Army (1990)

Systemic Toxicity

500 ��g/kg Estimated human LD50 U.S. Army (1990)

470 ��g/kg intram. Rat LD50 Bunner et al. (1985)

1.17 mg/kg Rat LD50 Bunner et al. (1985)

650 ��g/kgintram. Monkey LD20 Cosgriff et al. (1986)

790 ��g/kg intraven. Monkey LD50 AD Little (1986)

850 ��g/kgintram. Rat LD50 Chan and Gentry (1984)

111 mg/kgintram. Rabbit LD50 Chan and Gentry (1984)

Oral Toxicity

0.1-0.2 mg/kg Swine, emesis Busby and Wogan (79)

0.1-1.0 mg/kg Swine, diarrhea Ueno (1983a)

2.29 mg/kg Rat LD50 Bunner et al. (1985)

3.06 mg/kg Guinea pig LD50 AD Little (1986)

1.0 mg/kgb Male monkey LD100 Rukimi, Prasad, and Rao (1980)

1 5 mg/kg Estimated human LD50 U.S. Army (1990)

aNo primate data were located. bPer day for 15 days 1987; Bonomi et al., 1995; Wannemacher et al., 1993; Schiefer and Hancock, 1984).[11]

For less-than-lethal dosages and for all routes of administration, sequelae of leukopenia, thrombocytopenia, bleeding tendency, weakness, diarrhea, dyspnea, recurrent infections, vomiting, anorexia, and weight loss are expected. Other sequelae of acute exposures include prolonged rashes, joint pains and fatigue (Schultz, 1982), fever, chills, hypotension, confusion, somnolence, seizures, memory loss, hallucinations, and burning erythema (Belt et al., 1979; Murphy et al., 1978; Yap, et al., 1979; Diggs et al., 1978; Bukowski et al., 1982; Thigpen et al., 1981; Crossland and Townsend, 1984).

Pathology and Pathophysiology

The clinical manifestations of trichothecene intoxication are derived from several sources. They are summarized here prior to more detailed treatment of individual organ systems.

Known effects from evidence other than the yellow rain attacks are nausea, vomiting, seizures, central nervous system dysfunction, chills, fever, hypothermia, hypotension, epithelial necrosis, myelosuppression, and gastroenteritis with hematemesis and melena (bloody vomiting and stools). In the yellow rain attacks, the Hmong victims were probably exposed by several routes, including dermal, respiratory, and oral (the last from swallowing larger particles trapped in upper airways and returned to the oropharynx by ciliary action (Wannemacher and Wiener, 1997). Vomiting was induced and lasted several days. There was a feeling of intense heat, itching and burning of the skin, dizziness, tachycardia, chest pain, headache, and decreased vision. Within hours, victims reported intense eye pain, red eyes, bleeding gums, and hematemesis. Trembling was common, and some patients had seizures. Severe itching ensued with the formation of small hard blisters, some of which were hemorrhagic, occasionally progressing to large bullae. Abdominal pain and bloody diarrhea continued (Watson, Mirocha, and Hayes, 1984).

Khmer yellow rain ca
sualties had similar acute symptoms (Crossland and Townsend, 1984) with the following longer-term effects: intermittent weakness, anorexia, reduced memory and ability to concentrate, intermittent diarrhea, impotence, increased fatigue, cough and dyspnea, increased susceptibility to infection, and suspected increases in fetal abnormalities and spontaneous abortions (Haig, 1982; Schultz, 1982; Watson, Mirocha, and Hayes, 1984; Stahl et al., 1985; Crossland and Townsend, 1984). It must be noted that the Hmong cases with memory loss that Crossland described were not evaluated for the presence of toxins. These persons had undergone a harrowing experience, having been attacked, seen kinfolk die, fled, and become refugees. Severe apathy, confusion, and depression are common in survivors of natural or man-made disasters.

A limited autopsy was performed on a Kampuchean man injured in a toxic attack in February 1982, who died a month later having initially showed signs of recovery, then developing fever, jaundice, heoptysis, and anariax coma. Malaria was ruled out. The heart tissues showed interstitial myocardial hemorrhage and acute myocarditis, while the lungs showed only pulmonary edema. There was diffuse hepatitis with micronodular cirrhosis, as well as acute renal tubular necrosis. Tissues showed T-2 toxin in amounts ranging from 6.8 to 80 ppb, but there is little information with which to interpret the findings. The pathologist considered them to be compatible with mycotoxin poisoning (Stahl, Green, and Farnum, 1985).

Four stages were identified in the early Soviet Fusaria consumption incidents (a chronic oral exposure) (Mayer 1953a, 1953b):

Stage One begins within a few hours and lasts three to nine days. It consists of mild inflammation of the mouth and gastrointestinal tract, gastroenteritis, nausea, vomiting and diarrhea.

Stage Two is a quiet period of two weeks or more with few symptoms even while contaminated grain was still being ingested. There were laboratory abnormalities in some patients, but most appeared well.

Stage Three reveals the results of bone marrow aplasia with hemorrhagic diathesis, oral mucosal necrosis, and multiple infections.

Stage Four is a period of convalescence requiring several months after ingestion stopped.

Grain elevator workers are in a complex environment with dusts, plant products, and trichothecenes. They frequently experience coughing, breathlessness, wheezing, fever, and dermatitis (Kemppainen et al., 1986b); similar problems occur in “sick” buildings (Hendy and Cole, 1993; Jarvis, 1985).


Rats, mice, and guinea pigs die rapidly from large respiratory exposures (1 to 12 hours) but show little sign of pulmonary injury, unlike direct effects on gastrointestinal mucosa (Creasia et al., 1987; Wannemacher and Wiener, 1997; Bunner et al., 1985). At low levels of respiratory exposure, coughing and upper respiratory irritation occur. Higher exposures produce pulmonary edema, collapse, hypoxia, and death within a few hours, or more indolent symptoms with later pulmonary hemorrhage, hypotension and shock, edema, or infections (Rukmini, Prasad, and Rao, 1980; Lutsky et al., 1978; Bunner, 1983; Bunner et al. 1985). Fifty Hmong survivors reported the following: smell of gunpowder or pepper (14 percent), rhinorrhea (28 percent), nasal itching (14 percent), sore throat (40 percent), aphonia (26 percent), cough (60 percent), dyspnea (52 percent), severe chest pain (52 percent), and hemoptysis (18 percent). Systemic signs (vomiting, tachycardia, hypotension, etc.) follow. Oral or intravenous exposures result in pulmonary edema, hemorrhage, consolidation, and secondary pulmonary infection.

Toxicity by the respiratory route may be influenced by the material used to suspend the toxin (Creasia et al., 1987). Fibrinous exudate may be seen, and pulmonary fibrosis was a late complication in some of the trichothecene cancer trials (Goodwin et al., 1981). In contrast to inhaled ricin, where effects are confined to the lungs, respiratory exposure produces much less pulmonary change and pronounced systemic toxicity.


Conjunctivitis begins several hours after exposure, although the mechanism of the immediate visual disturbances is unclear. Corneal changes begin at 12 hours, with the peak effect in 24 to 48 hours. Blurred vision continues, with recovery from mild injuries in three to seven days. Hmong yellow rain victims reported eye pain and burning (68 percent), blurred vision (58 percent), and tearing (47 percent). Eyelid edema and scleral inflammation are associated with more-intense exposures. Corneal thinning can follow toxin exposure, with irregularities lasting up to six months (Bunner, 1983).


The skin responds to nanogram amounts of toxin with edema and inflammation. T-2 administered with DMSO to animals produced almost no local reaction (Bunner et al., 1985), but the systemic effects were substantial, although delayed, and cutaneous LD50s were elevated, compared to application without DMSO.

Dermal application can produce the same effects as oral administration: bone marrow, thymus, and lymphatic changes and gastrointestinal effects (Schiefer, 1984; Wannemacher et al., 1983).

Despite decontamination, a burning sensation developed from 4 to 24 hours in the contact area, followed by numbness. In cancer trials, erythema, burning stomatitis, and alopecia were common (Schiefer and Hancock, 1984; Murphy et al., 1978; Bukowski et al., 1982; Diggs et al., 1978; Belt et al., 1979; Yap et al., 1979; Thigpen et al., 1981; Goodwin et al., 1981). Hmong survivors reported persistent burning sensations, with tingling, itching, and pain lasting several hours. Some numbness lasted two days to several months in some victims. Scattered erythema was noted after a few hours, but only 23 percent reported blisters. In some cases, large hemorrhagic bullae occurred, with underlying necrosis. Necrotic areas sloughed easily when corpses were moved (Wannemacher and Wiener, 1997). Sequelae include secondary infections, hyperpigmentation, and recurrent rashes.


T-2 and other trichothecenes readily injure the rapidly dividing cells of the gastrointestinal tract. Tissue responses include edema, cytolysis, and sloughing, with loss of gastric epithelium and villus tips (Lee et al., 1984; Rukmini, Prasad, and Rao, 1980). The trichothecene DAS given intravenously showed marked gastrointestinal tract necrosis (Coppock et al., 1985) and pancreatic damage resulting in hyperglycemia. Some jaundice was seen in yellow rain victims. The liver is involved in detoxification, but liver failure is rare (Lutsky et al., 1978). Liver enzymes and amylase rise initially but return to normal in three to seven days (Bunner et al., 1985). As a later consequence, the bowel may become less resistant to bacterial penetration, which can increase susceptibility to infection (Lutsky et al., 1978).

Nervous System

The central nervous system effects are striking. Animals and humans exposed via the respiratory route show early central nervous system signs and symptoms. Symptoms reported from cutaneous exposures–burning pain followed by numbness–suggest that these toxins may directly affect the peripheral nerves.

The early and sustained vomiting suggests direct central nervous system effects involving chemotactic and vomiting centers. Hallucinations are a distinctive feature of trichothecene intoxications. Headaches, drowsiness, anxiety, confusion, and seizures occur, but their mechanisms have not been studied (Yap et al., 1979; Thigpen et al., 1981; Bukowski et al., 1982).

There are
few autopsy reports. DAS-poisoned swine showed cerebral hemorrhages (Coppock et al., 1985), while other animal studies showed meningeal bleeding and scattered petechial hemorrhages (Ueno et al., 1984). Experimental studies show alterations in levels of hydroxyindoleacetic acid and seratonin in the brain, with regional norepinephrine increases. Trichothecenes make the blood-brain barrier permeable to mannitol, although not dextran (Wang, Wilson, and Fitzpatrick, 1992). Intracerebral administration of T-2 decreased learning in mice, and intraperitoneal administration disturbed both learning ability and memory (Umeuchi et al., 1996).

The descriptions of chemotherapy patients (Thigpen et al., 1981; Yap et al., 1979), home exposures (Croft et al., 1986), and yellow rain cases (Watson, Mirocha, and Hayes, 1984; Crossland and Townsend, 1984) convey a picture of neurotoxicity, with somnolence, confusion, tremors, depression, weakness, malaise, and memory problems (some of which resemble findings in some Gulf veterans). In the cases just cited, however, symptoms appeared promptly, and there were other conspicuous indications of exposure.

Cardiovascular, Lymphatic, Hematologic

Among yellow rain victims reported chest pain, sometimes crushing, along with weakness. Animals poisoned with T-2 develop tachycardia and later bradycardia. Hypotension occurs early and may persist for several days, sometimes proceeding to shock. Hypotension and orthostatic hypotension were common in chemotherapy patients (7 to 40 percent) (Yap et al., 1979; Thigpen et al., 1981; Murphy et al., 1978; Bukowski et al., 1982). Mucous membranes are bright red, reflecting vasodilation. Commonly, hemorrhagic foci are found throughout the myocardium (Ueno et al., 1984; Stahl et al., 1985), and the electrocardiogram may show a prolonged P-R interval and prolongation of the QRS and QT intervals, reflecting conduction system abnormalities and increased risk of arrhythmias.

Beginning with the alimentary toxic aleukia diagnoses, bone marrow and lymphatic system injury has been a consistent finding (Mayer 1953a, 1953b; Ueno et al., 1984). Cell culture studies show stem cells to be sensitive to T-2 toxin. Mycotoxins produce profound alterations in hemostasis, as noted in yellow-rain cases and documented by primate studies (Cosgriff et al., 1986). Prothrombin and activated partial thromboplastin times are increased early in intoxication from decreased coagulation factors. Lethal hemorrhage risk is greater because T-2 inhibits platelet aggregation (Yarom et al., 1984).


There are clinical signs of muscle involvement. The among complained of weakness, fatigability, tremors, and cramps. Animals show flaccid weakness after T-2 poisoning. The early elevation of serum creatine kinase could reflect muscle or cardiac injury, or both. Isoenzyme studies have not been reported (Bunner, 1983).

Impaired immunity and infection resistance is another effect of these toxins. The ability of leukocytes to kill bacteria is impaired (Yarom et al., 1984); immunoglobulin levels are depressed; and cell-mediated immunity is suppressed (Jagadeesan et al., 1982; Schiefer, 1984; Ueno et al., 1984).

Renal output decreases after T-2 intoxication, and the toxin is found in substantial amounts in the kidney. Observed tubular necrosis could be related to hypotension and liver disorders

The endocrine effects of T-2 and other trichothecenes are not prominent. Adrenal cortical necrosis from T-2 exposure has been reported in rats (Thurman et al., 1986). Decreased spermatozoa production has been seen in several species.


The literature on trichothecene interactions is limited. Combining aflatoxins and trichothecenes may increase toxicity (Schultz, 1982; U.S. Army, 1990). No reports emerged of studies examining combined inhalation exposures. There were indications of synergism in feeding studies of chickens (Huff et al., 1988). (However, a study of DAS and aflatoxin in lambs did not show any enhanced toxicity from combined oral exposures of these toxins (Harvey et al., 1995). There is a strong possibility that the severity of trichothecenes could be potentiated by exposure even to low levels of organophosphate pesticides, carbamate pesticides or pretreatments, or low levels of nerve agent, through inhibition of carboxyesterases involved in detoxification (Johnson and Read, 1987). Drugs inducing the increase of detoxifying enzymes, such as epoxide hydrolase or cytochrome P450, may favorably interact to decrease toxin severity. Such drugs as phenobarbital, metoclopramide, metochlopramide carbamazepine, metyrapone, and clofibrate have shown beneficial effects in animal models (Fricke, 1993; Wannemacher and Wiener, 1997).

What to Look for in the Gulf Context

Because of the high sensitivity of the skin and eyes to trichothecenes, injuries to these organs should be looked for in unit medical records. Conjunctivitis, erythema, burning skin, and blurred vision were followed by nausea, vomiting, and diarrhea might increase suspicion of trichothecene exposure.[12]

Summary and Recommendations

The trichothecenes are credible biological warfare toxins for some purposes. However, there is no proof or even a strong indication of their use against U.S. forces in the Gulf. With more concentrated exposure, hematological changes, seizures and other serious sequelae might have been expected.

Current information arises from clinically recognized exposures or laboratory research. Trichothecenes have multiple toxic effects with potential long-term consequences, such as central nervous system injury, immune suppression, and prolonged disability. The sequelae noted in the Hmong, e.g., long-term memory problems; the animal memory studies; and the story of the household exposure may resemble some features of the illnesses in Gulf War veterans, but the expected hematological alterations have not been reported among Gulf War patients. Furthermore, the Hmong effects resulted from substantial exposures with major short-term consequences. Little is known about the behavioral effects of sustained low-level exposures. The extreme sensitivity of the skin and eyes to T-2 and other trichothecenes makes it unlikely that delayed systemic illnesses in Gulf veterans represent a late effect of exposure to toxin “fallout.” One would have expected an “epidemic” of painful dermatitis and conjunctivitis, as well as a number of other symptoms, which would have drawn attention to the exposure.

As in other cases, the AFIP should be consulted. The tests for trichothecenes are not routine, but have been used enough to be considered more than experimental. The AFIP might be consulted about the possibility of detecting trichothecene metabolites in tissue specimens obtained from the Gulf and immediately after. If used protective mask filters from the war period become available, it might be possible to analyze them for the presence of trichothecenes, which are very stable molecules. Had trichothecenes been used, it is possible that their toxicity might have been increased by interactions with nerve agents or PB, although this has not been studied explicitly.

To see actual article go here:

Pathology of Trichothecene Mycotoxins on and/or in Man Entry for August 28, 2007

The above photo is taken from my own pathology report. In the report the caption below the photo reads:

In Sub-Dermis please note fat cells with some evidence of increased staining indicating Fibrinous Inflamation of the fat cell membranes as observed in these lipomas. This is a large artery that demonstrates severe fibrinous inflamation of lumenal surface leading to almost occlusion of the vessel. This is consistently observed with Trichothecene Mycotoxin Exposure and places this patient into high Stage 2 and early Stage 3 of Trichothecene Mycotoxicosis. 150X

My pathology workup and report was done by the man in the following article (William A. Croft, D.V.M., PhD.), as was this photo. This article explains the stages of progression of the health effects of such exposure, and I hope it will be read by many as this stuff is far more widespread in the environment than any of us might like to believe. I am a living example of it’s harmful deadly effect. For some it brings about a very rapid death, and for others it is slow and extremely painful. I had produced a list of my own symptoms before meeting Dr. Croft. It was an almost identical list. It took a long time to find a medical professional that saw a recognizable pattern to my strange (complex as it is termed) set of symptoms. A lot of time was wasted. Time is a killer with this type of undiagnosed condition. Although this is only one of a battery of microbiological insults found ravaging my system, this one is key. It is of the most harmful and would prevent solutions to the other invaders from being of any usefulness, which I will discuss in separate entries here.So here is the article from the man who recognized my complex symptoms pattern when no one else did:

Abstract Information & Notes

William 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:

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 Peters, 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 suscep
tible 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. William 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 Peters, H. A., ���Clinical

Confirmation of Trichothecene Mycotoxicosis in Patients Urine���, In: Journal of

Environmental Biology 23(3), 301-320 (2002)

2. .Forgacs, J., and W. T. Carll : Mycotoxicoses. In : Advances in Veterinary

Science. Academic Press, New York and London, pp 273-372 (1962).

Toxic Black Mold & Air Quality Experts

Global Warming and Inland Water August 20, 2007

This picture is of a large creek out here that I remember being able to see the bottom of. Like so many of the water bodies here and elsewhere this is no longer the case. What is happening to our inland waters?

I went on a little tour of some of the spots I have been watching for the past 4+ years. I was not surprised at what I saw. I had predicted that what is now happening in our waterways was coming. I said it was just a matter of time. Now here it is. I used to find the strange multicoloured waterborne microbial masses in small (meaning narrow and relatively shallow) waterways where the water either moved very slowly to not at all, or where water flow had become impeded by a buildup of branches or other obstacles. In 2004, I predicted that this visible mass of microbial soup would eventually start accumulating in visible quantities in larger bodies of water. I suspected it was already there but would take longer in the larger water bodies to accumulate enough mass to become visible.

Well, here we are. Unfortunately, I was right. It is now showing up in large waterways such as creeks and next will be our lakes and rivers, and of coarse our watersheds. It first builds visible mass along the banks, and if the water does not keep the accumulation moving it will become visible throughout the waterbodies. While at a location a good two miles from here that looks exactly like this one, two ladies walking a dog and myself got talking. They never saw this before. I explained that it was only in the ditches last year. Now it is filling up the creeks. They asked if it could make the birds sick. I said very possibly. I know why they asked me that. The Avian Influenza hot zone is adjacent to the waterway where I met these ladies, and the one in the above photo snakes right through it. No one was ever completely satisfied with the explanation(s) given around the officially named Avian Influenza event. Perhaps it was, perhaps it was not, and then again, perhaps it was, plus more. There remains some discontentment in relation to the explanation(s) pertaining to that event to this day. No one feels the “whole story” was ever revealed in regard to this occurrence. I have to agree with the skeptics on this one, literally based on events within my own journey here that had relevance to the so named Avian Influenza event.

Someone came up with a novel way to prevent photographing the ditches I used to monitor. They no longer cut the grass in the ditches making it impossible without some intentional clearing effort to see clearly what is there, and virtually impossible to get a useful pic of same.

This won’t work with the large creeks though.

In the area where I find the most profound accumulation of this stuff there are several key factors. There is the geography. This is all land near a world famous fish bearing river, and high inland water table. There are quite a few creeks in the area.

The use of the land is in my opinion not practical or wise. There is a military base, a lot of farms, including factory farms and massive greenhouse operations, our dump, and the sewage treatment plant which also grows trees in this area fertilized with treated sewage.

There is a small island on the river, right across from the sewage treatment plant outflow which is a bird sanctuary. There was a lot of sawmill operations along this stretch of the river as well.

All this within a roughly 5 mile radius.

In the past recent years some of the sawmill or timber operations in this vicinity have moved their operations back from the river’s shore, which is of specific interest to me.

This after the Avian influenza outbreak in this area, followed by the disappearance of over a million fish also in this vicinity.

Our missing fish have never been officially accounted for to the best of my knowledge, and the salmon stocks have never recovered.

I have to include Global Warming here, as I have been watching and observing the recent hot weather’s effect on the waterborne microbial soup.

What I have seen is a huge surge in it’s cumulative visible mass during the hot spell. There are two possible contributors to this event that I am familiar with. It’s growth appears to be aided by heat, like yeast rises in the oven. It even reaches a stage of bubbling up and off gassing. The other contributor that I realize to be relevant is that with no rain falling the water has not been moving much if at all, thus aiding the accumulating masses without separation of the individual microbial entities. I noted that there is a nearly total absence of ground dwelling insects in areas where this is occurring in the water. This would be a serious concern as well, as the insects aerate (oxygenate) the soil.

I noted that myself and my dog have been battling respiratory difficulties accompanied by chest, lung, and sinus infection.

In discussion with others, the health trends out here are consistent in that whatever symptoms you have, others as well as animals are having them at the same time. On mass; back pain, leg pain, respiratory and sinus infections, headaches, excessive fatigue or full body weakness, nausea, burning tingling skin.

In talking with people around town, I also stumbled upon a pattern with the animals that is of interest here. The animals are searching for rain water. They do not want to drink the tap water. Nor do they want to drink water coming from people’s private wells. This is significant. There is a problem with the water out here if the animals do not want to drink it. One person I know tells me they have had to resort to buying bottled water for their pig, as the pig will not drink the well water or municipal tap water. My own dog seeks rain water accumulation. In lieu of this, I have two water bowls for him to choose from. One has municipal tap water. The other has municipal tap water with activated charcoal in it. He will only drink the one with the activated charcoal in it, and in so doing began to show some visible signs of improvement in his condition. So my question, and concern is: “Why is no problem being detected with this water when tested? Are “they” missing something, or………………..?” I say “or…………….”

Did you know?…

Algae induced by raw sewage is a health threat.

Toxic Algae produces neurotoxins which can do serious harm and cause extremely painful conditions. As well, with toxic algae exposure to yourself comes the risk of exposure to pfiesteria organisms also researchable under the term dinoflagellates. Incredibly nasty looking little invaders.

Then there is the fungus. Under normal climactic temperatures, nature destroys excess fungi in the environment once a year via freezing conditions. Freezing weather causes a natural once yearly die off of fungi, helping keep the quantity of fungi in the environment under control. With Global Warming this will cease to occur, and the quantities of potentially mycotoxin and neurotoxin producing fungi will be able to accumulate to reach health threatening levels present in the ambient, recreational, and agricultural environment, and you will get sick like me.

Do you know that heat resistant fungus has been detected in blueberry soil? Our bodies use heat as one of their primary defenders against invaders in our system. Get too much heat resistant fungus in your system, and you will have a problem as it will be able to survive at your body temperature. Heat resistant fungus is resistant to most chemical insults, therefore rendering most pharmaceutical interventions useless. This is a very real problem that already has a foothold in this polluted world. Global Warming will not bother it either, until we run out of water. Fungus needs moisture to grow. Not a problem here, as it doesn’t care if the water is clean or dirty. It will mutate (adjust or alter itself) to survive what ever conditions exist, as long as
it has moisture and some nutrients. When you think about it, fungus is in a position to outlive us as it will not be killed by the contamination that is causing Global Warming, but we surely will if we keep it up. We already have populations on mass that are in poor health as a result of our planetary conditions.