A 1999 Mayo Clinic Study cites molds as the cause of most of the chronic sinus infections that inflict 37 million Americans each year. Recent studies also link molds to the soaring asthma rate. Molds have been an under recognized health problem, but that is changing. Health-care professionals now know that molds can cause allergies, trigger asthma attacks and increase susceptibility to colds and flu. Anyone with a genetic predisposition can become allergic if exposed repeatedly to high enough levels. Last year Dr. David Sherris at the Mayo Clinic performed a study of 210 patients with chronic sinus infections and found that most had allergic fungal sinusitis. The prevailing medical opinion has been that mold accounted for 6 to 7 percent of all chronic sinusitis. The Mayo Clinic study found that it was 93 percent – the exact reverse. Newsweek, 12/4/00
There are over 100,000 known living species of fungus, some of which are beneficial to mankind. Mycologists estimate that there may be as many as 200,000 more unidentified species of fungus. Yeasts, molds, mildews, rusts, and mushrooms are types of fungus.
Mold nor spores cause illness, other than allergy and/or infections. It is the mycotoxins released when the molds’ food source (moisture) is severed.
To help comprehend how small mycotoxins are, one common housefly could carry about 7.35 billion attached to its external body hairs. Consequently, IF 50,000 constitute a theoretically lethal dose, a housefly could carry a lethal dose for over 100,000 individuals.
Outdoor spores are not a usual cause of toxicity, (except for allergies and infection), but when growing inside, molds produce toxins, which are in much higher concentration and can cause illness.
Indoor mold spores indicate mold growth, which indicates mycotoxin production. Currently, we can measure spores, identify spores, but it is difficult to measure mycotoxins. Stachybotrys produces at least 170 known mycotoxins, and probably more that have not been identified.
The trick with mold is to control the moisture and excessive food sources. If there are no structural defects that allow moisture in, then get a cheap hygrometer/thermometer ($25) and monitor it. Don’t let the humidity climb above 60% for two days or more. Pay attention to basements. Humidity sinks to the basement in the summer. If you have a little more money, get a humidistat or a dehumidifier installed on your “balanced” HVAC system.
Introduction to Mold
Molds, a subset of the fungi, are ubiquitous on our planet. Fungi are found in every ecological niche, and are necessary for the recycling of organic building blocks that allow plants and animals to live. Included in the group “fungi” are yeasts, molds and mildews, as well as large mushrooms, puffballs and bracket fungi that grow on dead trees. Fungi need external organic food sources and water to be able to grow. Molds can grow on cloth, carpets, leather, wood, sheet rock, insulation (and on human foods) when moist conditions exist (Gravesen et al., 1999). Because molds grow in moist or wet indoor environments, it is possible for people to become exposed to molds and their products, either by direct contact on surfaces, or through the air, if mold spores, fragments, or mold products are aerosolized. Many molds reproduce by making spores, which, if they land on a moist food source, can germinate and begin producing a branching network of cells called hyphae. Molds have varying requirements for moisture, food, temperature and other environmental conditions for growth. Indoor spaces that are wet, and have organic materials that mold can use as a food source, can and do support mold growth. Mold spores or fragments that become airborne can expose people indoors through inhalation or skin contact.
Mold spores are fungal reproductive cells of about the same size as pollen grains. They can occur in various colors and shapes, such as round, spheroid, banana-shaped, or tadpole-shaped. They can occur in enormous quantities, and at all times of the year. Mold spores can be found and generated at serious levels indoors, as well as out.
Fungi can invade healthy individuals and can cause a variety of effects. The most common response is allergies (runny nose, sneezing, sinus congestion, and skin rashes). Allergies result from inhaling mold spores. When environmental conditions become conducive, many molds develop fungal hyphae, small appendages containing spores. These spores are analogous to plant seeds and can be spread by the billions when air currents pass over the hyphae. Even dead fungi are capable of causing allergic symptoms.
Mold spores can be airborne, and get indoors through doors, windows or cracks and crevices, or be carried in from the outdoors on shoes and clothing. Building materials that were left outside before use can harbor viable (living) mold spores for many years. Indoor environments are never entirely free of molds. As a general rule of thumb, in a “healthy” building the concentration of spores and the mix of mold species tend to be similar to outdoor environment levels.
If buildings are air-conditioned, or windows and doors are kept closed in summer, the concentration of spores within should even be lower than outside levels. High moisture (above 70.0% relative humidity) in a building will invariably lead to mold, mildew, or other microbial growth. This growth requires four things: a nutrient source (found in most building materials), proper temperature (usually found indoors), mold spores (ubiquitous in ambient air), and water.
Some molds also produce toxins (poisons) which are thought to be useful in killing competing molds in their vicinity. These toxins can also have deleterious effects on humans when ingested, inhaled or in contact with the skin. The fungi that produce toxins are known as toxigenic fungi. Many fungi produce secondary toxic metabolites which can produce adverse health effects (mycotoxicoses) in animals and human. These metabolite are collectively known as mycotoxins. The latest World Health Organization (WHO) publication on mycotoxins, available in 1990, indicated that there are more than 200 mycotoxins produced by a variety of common fungi. Historically, mycotoxins are a problem to farmers and food industries and in Eastern European and third world countries. However, many toxigenic fungi, such as Stachybotry chartarum (also known as Stachybotrys atra) and species of Aspergillus and Penicillium, have been found to infest buildings with known indoor air and building-related problems. Many indoor air quality related problems have been traced to the growth of fungus in buildings. Almost without exception, these buildings have usually had chronic water or moisture problems.
Molds can have an impact on human health, depending on the nature of the species involved, the metabolic products being produced by these species, the amount and duration of individual’s exposure to mold parts or products, and the specific susceptibility of those exposed. Health effects generally fall into four categories.
Allergy, Infection, Irritation, Toxicity
Toxicity Molds can produce other secondary metabolites such as antibiotics and mycotoxins. Antibiotics are isolated from mold (and some bacterial) cultures and some of their bacteriotoxic or bacteriostatic properties are exploited medicinally to combat infections.
Mycotoxins are also products of secondary metabolism of molds. They are not essential to maintaining the life of the mold cell in a primary way (at least in a friendly world), such as obtaining energy or synthesizing structural components, informational molecules or enzymes. They are products whose function seems to be to give molds a competitive advantage over other mold species and bacteria. Mycotoxins are nearly all cytotoxic, disrupting various cellular structures such as membranes, and interfering with vital cellular processes such as protein, RNA and DNA synthesis. Of course they are also toxic to the cells of higher plants and animals, including humans. Mycotoxins vary in specificity and potency for their target cells, cell structures or cell processes by species and strain of the mold that produces them. Higher organisms are not specifically targeted by mycotoxins, but seem to be caught in the crossfire of the biochemical warfare among mold species and molds and bacteria vying for the same ecological niche.
Mycotoxin Effects – The class of small fungal secondary metabolites which has been given the name “mycotoxins” is definitely known to include many compounds which are highly toxic to vertebrates (such as humans). Most of the well characterized toxic effects are from animal feeding situations, either natural mycotoxicosis outbreaks caused by contaminated animal feed, or laboratory experiments based on feeding (or connected artificial experimental situations such as parenteral injection of purified toxins into experimental animals). Ingestion of mycotoxin-contaminated foods by humans results in similar symptoms. Toxic effects have also been found in laboratory experiments in which animals are exposed to mycotoxins via the respiratory tract. In cases involving humans and airborne exposure, the most suggestive of a direct mycotoxin effect are those in which heavily mold-exposed workers develop severe symptoms reminiscent of animal mycotoxicoses or contaminated-food mycotoxicoses.
As another example, classic stachybotryotoxicosis, described mostly from agricultural workers who handled or disturbed large quantities of material (usually hay or straw) contaminated by Stachybotrys chartarum, was characterized by “cough, rhinitis, burning sensation in the mouth, (throat) and nasal passages, and cutaneous irritation at (points) of toxin contact” (2). Nosebleeds were also common, and tracheal bleeding was occasionally reported. Whether such mycotoxin effects explain the symptoms seen in common building exposures has been disputed. It has been pointed out that, although the mycotoxins are often associated with disseminating fungal conidia, the quantities present may not be sufficient to explain the effects observed (3), at least not in terms of classic toxicosis. A number of mycotoxins or conidia of mycotoxigenic fungi, however, have also been shown to have effects such as activation of pulmonary alveolar macrophages (PAMs), DNA fragmentation in PAMs, inhibition of the oxidative burst killing mechanism in PAMs, and slowing of respiratory ciliary beat (e.g., 4). Such interactions with immune mechanisms may explain some symptoms not explained by toxicosis. Careful study of occupants of contaminated buildings suggests an association between inhalation of toxigenic fungi and nonspecific respiratory symptoms (5)
Moldy Odors are released from actively growing fungi may also pose a health risk. Not all molds produce mycotoxins, but numerous species do (including some found indoors in contaminated buildings). Toxigenic molds vary in their mycotoxin production depending on the substrate on which they grow (Jarvis, 1990). The spores, with which the toxins are primarily associated, are cast off in blooms that vary with the mold’s diurnal, seasonal and life cycle stage (Burge, 1990; Yang, 1995). The presence of competitive organisms may play a role, as some molds grown in monoculture in the laboratory lose their toxic potency (Jarvis, 1995). Until relatively recently, mold poisons were regarded with concern primarily as contaminants in foods. More recently concern has arisen over exposure to multiple mycotoxins from a mixture of mold spores growing in wet indoor environments. Health effects from exposures to such mixtures can differ from those related to single mycotoxins in controlled laboratory exposures. Indoor exposures to toxigenic molds resemble field exposures of animals more closely than they do controlled experimental laboratory exposures. Animals in controlled laboratory exposures are healthy, of the same age, raised under optimum conditions, and have only the challenge of known doses of a single toxic agent via a single exposure route. In contrast, animals in field exposures are of mixed ages, and states of health, may be living in less than optimum environmental and nutritional conditions, and are exposed to a mixture of toxic agents by multiple exposure routes. Exposures to individual toxins maybe much lower than those required to elicit an adverse reaction in a small controlled exposure group of ten animals per dose group. The effects from exposure may therefore not fit neatly into the description given for any single toxin, or the effects from a particular species, of mold.
Few toxicological experiments involving mycotoxins have been performed using inhalation, the most probable route for indoor exposures. Defenses of there respiratory system differ from those for ingestion (the route for most mycotoxin experiments). Experimental evidence suggests the respiratory route to produce more severe responses than the digestive route (Cresia et al.,1987). Effects from low level or chronic low level exposures, or ingestion exposures to mixtures of mycotoxins, have generally not been studied, and are unknown. Effects from high level, acute sub-acute and sub-chronic ingestion exposures to single mycotoxins have been studied for many of the mycotoxins isolated. Other mycotoxins have only information on cytotoxicity or in vitro effects.
Effects of multiple exposures to mixtures of mycotoxins in air, plus other toxic air pollutants present in all air breathed indoors, are not known. Effects of other biologically active molecules, having allergic or irritant effects, concomitantly acting with mycotoxins, are not known.
Measurement of mold spores and fragments varies, depending on instrumentation and methodology used. Comparison of results from different investigators is rarely, if ever, possible with current state of the art. While many mycotoxins can be measured in environmental samples, it is not yet possible to measure mycotoxins in human or animal tissues. For this reason exposure measurements rely on circumstantial evidence such as presence of contamination in the patient’s environment, detection of spores in air, combined with symptomology in keeping with known experiment allesions caused by mycotoxins, to establish an association with illness.
Response of individuals exposed indoors to complex aerosols varies depending on their age, gender, state of health, and genetic make-up, as well as degree of exposure. Microbial contamination in buildings can vary greatly, depending on location of growing organisms, and exposure pathways. Presence in a building alone does not constitute exposure.
Investigations of patients’ environments generally occur after patients have become ill, and do not necessarily reflect the exposure conditions that occurred during development of the illness. All cases of inhalation exposure to toxic agents suffer from this deficit. However exposures to chemicals not generated biologically can sometimes be re-created, unlike those with active microbial growth. Indoor environments are dynamic eco systems that change over time as moisture, temperature, food sources and the presence of other growing microorganisms change. Toxin production particularly changes with age of cultures, stage of sporulation, availability of nutrients, moisture, and the presence of competing organisms. After-the-fact measurements of environmental conditions will always reflect only an estimate of exposure conditions at the time of onset of illness. However, presence of toxigenic organisms, and their toxic products, are indicators of putative exposure, which together with knowledge of lesions and effects produced by toxins found, can establish association.
Field exposures of animals to molds (in contrast to controlled laboratory exposures) show effects on the immune system as the lowest observed adverse effect. Such immune effects are manifested in animals as increased susceptibility to infectious diseases. It is important to note that almost all mycotoxins have an immune suppressive effect, although the exact target within the immune system may differ. Many are also cytotoxic, so that they have route of entry effects that may be damaging to the gut, the skin or the lung. Such cytotoxicity may affect the physical defense mechanisms of there respiratory tract, decreasing the ability of the airways to clear particulate contaminants (including bacteria or viruses), or damage alveolarmacrophages, thus preventing clearance of contaminants from the deeper lung. The combined result of these activities is to increase the susceptibility of the exposed person to infectious disease, and to reduce his defense against other contaminants. They may also increase susceptibility to cancer (Jakabet al., 1994).
Because indoor samples are usually comprised of a mixture of molds and their spores, it has been suggested that a general test for cytotoxicity be applied to a total indoor sample to assess the potential for hazard as a rough assessment (Gareis, 1995).
Animal experiments in which rats and mice were exposed intranasally and intratracheally to toxic strains of S. chartarum, demonstrated acute pulmonary hemorrhage (Nikkulin et al. 1996). A number of case studies have been more recently published. One involving an infant with pulmonary hemorrhage in Kansas, reported significantly elevated spore counts of Aspergillus/Penicillium in the patient’s bedroom and in the attic of the home. Stachybotrys spores were also found in the air of the bedroom, and the source of the spores tested highly toxigenic. (Flappan et al., 1999). In another case study in Houston, Stachybotrys was isolated from bronchopulmonary lavage fluid of a child with pulmonary hemorrhage. (Elidemir et al., 1999), as well as recovered from his water damaged-home. The patient recovered upon removal and stayed well after return to a cleaned home. Another case study reported pulmonary hemorrhage in an infant during induction of general anesthesia. The infant was found to have been exposed to S. chartarum prior to the anesthetic procedure (Tripi et al., 2000). Still another case describes pulmonary hemorrhage in an infant whose home contained toxigenic species of Penicillium and Trichoderma (a mold producing trichothecene poisons similar to the ones produced by S. chartarum) as well as tobacco smoke (Novotny and Dixit, 2000) Toxicologically, S. chartarum can produce extremely potent trichothecene poisons, as evidenced by one-time lethal doses in mice (LD50) as low as 1.0 to 7.0 mg/kg, depending on the toxin and the exposure route. Depression of immune response, and hemorrhage in target organs are characteristic for animals exposed experimentally and in field exposures (Ueno, 1980; Jakab etal., 1994).
While there are insufficient studies to establish cause and effect relationships between Stachybotrys exposure indoors and illness, including acute pulmonary bleeding in infants, toxic endpoints and potency for this mold are well described. What is less clear, and has been difficult to establish, is whether exposures indoors are of sufficient magnitude to elicit illness resulting from toxic exposure.
What are these Mold Spores and Why are They so Dangerous?
Mold spores are tiny bacteria less than 4 microns in size — so small that as many as 250,000 spores can fit on a pin head and a person/farmer can inhale as many as 750,000 of these spores per minute! They are produced by microorganisms which grow in moist hay and stored grain silage where the moisture content is high (30%) and the area is poorly ventilated.
When farmers move or work with hay and silage materials in which mold spores have grown, the mold spores attach themselves to airborne dust particles. The farmer not only inhales dust particles which may not be extremely hazardous, but he also inhales mold spores which are a serious hazard. Heavy concentrations of mold spores appear as dry, white or grey powder or clouds.
The body has natural defense filtering systems (such as mucous lining, coughing and sneezing) against dusty air which helps remove some contaminants, BUT most contaminants overpower and pass through these defenses. Mold spores not only bypass defenses because of their number, but also because they are so small.
Very fine particles, like mold spores, move into, accumulate and settle into the lower lungs. There they produce toxins. Remember that the lungs transfer oxygen to the bloodstream, and most of the actual exchange of carbon dioxide and oxygen takes place in the lower lungs. Now the lungs become a roadway for toxic materials to travel through the bloodstream with the oxygen. The body’s reaction to the toxins permanently affects the lungs’ ability to transfer oxygen into the bloodstream. The lung tissue becomes permanently scared and each exposure to mold spores increases the damage.
The body’s last defense against these tiny invaders is to develop an allergy producing cold or pneumonia-like symptoms.
The Toxic Indoor Mold – Stachybotrys chartarum:
Berlin D. Nelson, Professor, Department of Plant Pathology, North Dakota State University, Fargo
Stachybotrys chartarum is a fungus that has become notorious as a mycotoxin producer that can cause animal and human mycotoxicosis. Indeed, over the past 15 years in North America, evidence has accumulated implicating this fungus as a serious problem in homes and buildings and one of the causes of the “sick building syndrome.” In 1993-1994, there was an unusual outbreak of pulmonary hemorrhage in infants in Cleveland, Ohio, where researchers found S. chartarum growing in the homes of the sick infants. This incident increased the awareness of home/building molds and brought this fungus to the immediate attention of the medical community. In recent years there has been a cascade of reports about toxic molds in the national media. The New York Times Magazine, August 12, 2001, ran a front page story on toxic mold. Newspaper articles such as “Fungus in ‘Sick’ Building” (New York Times, May 5, 1996) or “Mold in schools forces removal of Forks kids” (Fargo Forum, June 1997) are eye-catching news items. The nationally syndicated comic strip Rex Morgan ran a series on Stachybotrys, and television news shows have run entire programs on Stachybotrys contamination of homes. The fungus has resulted in multimillion dollar litigations and caused serious problems for homeowners and building managers who must deal with the human issues and remediation.
As a mycologist, I have been advising public officials and the general public on the issues concerning indoor molds. Our region experienced one of the greatest natural disasters of modern times when the Red River flooded in 1997. In Grand Forks, ND, alone, there were 9,000 flooded homes. There was an enormous need for information on the effects of the flood on human health in the Red River Valley. Because of the increasing awareness of molds in indoor air quality, a coordinated effort by city, state and federal officials to provide information on mold prevention was undertaken. In my observations following the flood and in subsequent years of dealing with indoor mold issues, I have been impressed with the common occurrence and extensive growth of S. chartarum in homes and buildings damaged by flood waters or other types of water incursions and the lack of knowledge by the general public and public and private institutions about this fungus. This review provides information on the fungus, its biologically active compounds, the history of the problem, the controversy about this fungus, and briefly comments on detection and remediation.
Stachybotrys chartarum (Ehrenb. ex Link) Hughes (synonyms= S. atra, S. alternans) was first described as S. atra by Corda in 1837 (5) from wallpaper collected in a home in Prague. It is a member of the Deuteromycetes, order Moniliales, family Dematiaceae, and is common on plant debris and in soil. The taxonomic treatment of the genus by Jong and Davis (38) is a good reference on identification while Hintikka (27) provides general information on biology. The fungus grows well on common mycological media such as potato dextrose, V-8 or cornmeal agar, and sporulates profusely forming dark masses of conidia. The fungus is relatively easy to identify because of the unique phialides of the genus and conidial morphology of the species. Conidiophores are determinate, macronematous, solitary or in groups, erect, irregularly branched or simple, septate, dark olivaceous, and often rough walled on the upper part. The phialides are large, 9-14 µm in length, in whorls, ellipsoid, olivaceous, and often with conspicuous collarettes. Conidia are ellipsoidal, unicellular, 7 to 12 by 4 to 6 µm, dark brown to black and often showing a ridged topography when mature. The ridged nature is readily apparent with scanning electron microscopy, but can also be observed with an oil immersion lens at 1000x. On lower power the spores appear verrucose. Young spores and some mature spores may be smooth. The phialides produce conidia singly and successively into a slime droplet that covers the phialides. Eventually the slime dries and the conidia are covered with the slime residue and remain on the conidiophore as a mass or ball of spores . The spores are therefore not readily disseminated in the air compared to other fungi such as Aspergillus. However, when the fungus and substrate dries and is disturbed by mechanical means or air movement, conidia can become bioaerosols. A genus similar to Stachybotrys, but with spores in chains is Memnoniella (38); it also has species that produces trichothecenes (35). Haugland et al. (21) have proposed relegation of Memnoniella to synonymy with Stachybotrys based on morphological characteristics and comparative sequence analysis of the nuclear ribosomal RNA operon.
S. chartarum growing on natural or man made substrates can often be identified by a person familiar with its growth pattern. However, there are some very dark dematiaceous Hyphomycetes which look similar, therefore microscopic examination of the fungus is needed to confirm identification. When the fungus is actively growing, the characteristic phialides and conidia are easy to observe, but when dry, the phialides collapse, are more difficult to observe, and emphasis must be placed on morphology of conidia. Although the traditional method of identification is based on morphology of the sporulating structures, PCR primers specific for S. chartarum are reported and may now be used in commercial microbiological laboratories to identify this fungus (7,20,58). A PCR product analysis using a fluorogenic probe has also been developed to quantify conidia of S. chartarum and can be used in the analysis of samples from mold contaminated indoor environments (22,52,58).
The fungus is strongly cellulolytic and will grow under conditions of low nitrogen. A simple way to grow the fungus is to streak some conidia onto wet Whatman filter paper in a petri dish and within a week spores are produced. If spores are placed on a small ridge made in the paper, the conidiophores will grow at an angle and allow a side view of conidial formation with a stereoscope. This is a convenient method to determine if spores are in chains to distinguish Stachybotrys from Memnoniella. Also, the filter paper method will allow isolation of S. chartarum away from many other fast-growing, but non cellulolytic fungi that would out-compete S. chartarum on rich media.
Mycotoxins and Other Biologically Active Metabolites
The mycotoxins and other biologically active compounds produced by S. chartarum are of concern to human health (23,32,33,57). Mycotoxin poisoning by this fungus is referred to as stachybotryotoxicosis.
S. chartarum produces a variety of macrocylic trichothecenes and related trichoverroids: roridin E and L-2; satratoxins F, G, and H; isosatratoxins F, G, and H; verrucarins B and J; and the trichoverroids, trichoverrols A and B and trichoverrins A and B. The satratoxins are generally produced in greater amounts than the other trichothecenes, but all compounds are produced in low quantities. They apparently occur in all parts of the fungus (53). The difficulty in obtaining, identifying, and purifying these toxins has slowed extensive studies on their biological activity. Hinkley and Jarvis (23) recently published analytical methods for the identification and quantification of bioactive compounds produced by this fungus. These methods were designed to quantitate individual compounds in culture extracts and detect low levels of trichothecenes in samples.
Macrocyclic trichothecenes are highly toxic compounds with a potent ability to inhibit protein synthesis (32). Numerous studies have demonstrated the toxicity of toxins from S. chartarum on animals and animal and human cells (42,45,49,51). Yang et al. (62) reported that satratoxin G was the most cytotoxic of eight trichothecenes tested on mammalian cells, even more toxic than the well known T-2 toxin associated with alimentary toxic aleukia. Other researchers have also reported the high toxicity of satratoxins compared to other trichothecenes (18). The LD50 in mice for satratoxins is ~1 mg/kg (32).
In addition, the fungus produces nine phenylspirodrimanes (spirolactones and spirolactams) and cyclosporin, which are potent immunosuppressive agents (33). Jarvis et al. (33) suggested that the combination of trichothecenes and these immunosuppressive agents may be responsible for the observed high toxicity of this fungus. New biologically active compounds are still being discovered in cultures of S. chartarum. Hinkley et al. (24,25) recently described the metabolites atranones A-G and two dolabellane diterpenes, but the complete biological activity of these compounds is unknown. Vesper and colleagues (57,59,60) reported some isolates produce Stachylysin, a hemolysin (compounds that lyse erythrocytes), and a hydroxamate siderophore. They suggest these compounds could be pathogenicity factors involved in pulmonary hemorrhage in infants exposed to S. chartarum.
There is considerable variation among isolates of S. chartarum in the production of mycotoxins and other metabolites (2,24,27,34,40). Indeed, Hinkley et al. (25) suggest there are two chemotypes of the fungus: the atranone and the macrocyclic trichothecene producers.
History of the Problem
In the Ukraine and other parts of eastern Europe during the 1930s, there were outbreaks of a new disease in horses and other animals that was characterized by symptoms such as irritation of the mouth, throat, and nose; shock; dermal necrosis; a decrease in leukocytes; hemorrhage; nervous disorder; and death (10,14,17,26,28). In 1938, Russian scientists determined the disease was associated with S. chartarum (then known as S. alternans) growing on the straw and grain fed to the animals. Intensive studies were then conducted resulting in the first demonstrated toxicity of S. chartarum in animals. Horses were actually fed cultures of the fungus. Contents from 30 petri plates containing the fungus were fed to horses and resulted in death, while even the contents of one plate resulted in sickness. Horses seem to be especially susceptible to these toxins; 1 mg of pure toxin is reported to cause death (14). Most outbreaks were associated with hay or feed that became infested during storage under wet conditions. The Russians coined the term stachybotryotoxicosis for this new disease. Since then, stachybotryotoxicosis has been reported on numerous farm animals from various parts of the world, especially in eastern Europe, but apparently has not been reported on animals in North America (26,55,61).
Hyperplastic dermatitis on a horse four days after feeding on straw infested with S. chartarum. Notice the scaly appearance of the upper lip area. Photograph reprinted from Sarkisov, A. Kh. 1954. Mikotoksikozi (Gribkovye otravleniia). Moscow. 216 pp. (click image for larger view).
Straw contaminated with S. chartarum (top) compared to clean straw. Persons handling this heavily contaminated straw could develop stachybotryotoxicosis.
In the late 1930s, stachybotryotoxicosis was reported in humans working on collective farms in Russia (10,14,17,29). People affected were those who handled hay or feed grain infested with S. chartarum or were exposed to the aerosols of dust and debris from the contaminated materials. Some of these individuals had burned the straw or even slept on straw-filled mattresses. The infested straw was often black from growth of the fungus.