- Mold can be in your house even if you cannot locate it with the naked eye.
- Mold enjoys moist, dark areas with ample food I.E Sheet rock, wallpaper etc.
- Food can already contain Mold and Mold toxins in them before you'll ever see it grow.
- Anti-Biotics are made from mold like Penicillium and many others.
- Ammonia, Oregano Oil, Neem Seed Oil, Borax, Baking Soda - all kill mold. Ammonia kills Toxins.
- Bleach, Peroxide cannot kill Class A molds. They eat that happily as food, some lower level molds can be killed by these agents if medical grade, but will not kill the toxins. Also takes repeated treatments on a hourly basis.
- First stage of Mycotoxin sickness will have no Physical symptoms.
- Mold can exist under layers of sheet rock, wallpaper and Bathtub Stalls.
- Mold Allergies are not Allergies - It is your body either fighting it off, or Becoming very sick from it.
- Steroids, Anti-Biotics, and Immune suppressing drugs make the body more vulnerable to Mold Toxins.
- Candida Albicans is a bad body yeast that is already in our digestive track.
- Mold enjoys existing in a low Ph level environment. Candida in a pH of 7.
- Candida Albicans produces toxins that are carcinogenic to humans.
- Mold and Yeast Toxins aka Mycotoxins can and will invade brain cavity.
- Not all molds are created equal. Some are more hazardous then others.
- Toxins will lower immune system functions - Even in healthy bodies. Then once this happens...
- ANYONE CAN GET SICK FROM MOLD.
- Doratomyces spp (no information on hazard classification)
- Fusarium spp (hazard class A)
- Stachybotrys chartarum (hazard class A)
- Trichoderma spp (hazard class B)
- Scopulariopsis spp (hazard class B)
- Aspergillus versicolor (hazard class A)
- Aureobasidium pullulans (hazard class B)
- Aspergillus repens (no information on hazard classification)
- Wallemia sebi (hazard class C)
- Chaetomium spp., particularly Chaetomium globosum
- Scopulariopsis spp.
- Aspergillus versicolor
- Aspergillus fumigatus
- Fusarium spp.
- Aspergillus flavus (hazard class A)
Aspergillus flavus: is a saprotrophic and pathogenic fungus with a cosmopolitan distribution. It is best known for its colonisation of cereal grains, legumes, and tree nuts. Post-harvest rot typically develops during harvest, storage, and/or transit. A. flavus infections can occur while hosts are still in the field (pre-harvest), but often show no symptoms (dormancy) until post-harvest storage and/or transport. In addition to causing pre-harvest and post-harvest infections, many strains produce significant quantities of toxic compounds known as mycotoxins, which when consumed are toxic to mammals. A. flavus is also an opportunistic human and animal pathogen, causing aspergillosis in immunocompromised individuals. Aspergillius Flavus: flavus colonies are commonly powdery masses of yellow-green spores on the upper surface and reddish-gold on the lower surface (underneath).
Many develop symptoms much like allergic reactions such as runny nose, itchy eyes, or swelling of the throat in the case of allergic aspergillosis. Rashes and open sores can develop as well without any symptoms prior to development. This however, is no allergic reaction. THIS MUST BE CLEAR. Allergist are completely ignorant of this and prescribe things like inhalers, anti-biotics and steroids which will not help people sick with this illness. Steroids weaken the immune system, and coupled with anti-biotics which kill off the good bacteria in the gut, hell runs havoc in our bodies. Inhalers also have steroids in them so it is a bad idea to take any of these things if you are sick from ANY TOXINS or MOLD.
The growth of the fungus Aspergillus in human tissue or within aircontaining spaces of the body, such as bronchus or pulmonary cavity, is termed aspergillosis (Bennett, 1979a). The physiological condition of the exposed individual thus appears to be of paramount importance. Patients exhibiting aspergillosis are generally immunocompromised, and thus susceptible to otherwise common and usually harmless microorganisms. Factors that may lead to immunosuppression include an underlying debilitating disease (e.g., chronic granulomatous diseases of childhood), chemotherapy, and the use of supraphysiological doses of adrenal corticosteroids (Bennett, 1980).
Pulmonary aspergillosis is the most common clinical manifestation of aspergillosis. The most common symptoms of pulmonary aspergillosis are a chronic productive cough and hemoptysis (coughing up blood). According to a standard medical textbook, "Aspergillus can colonize ectatic bronchi, cysts, or cavities in the lung. Colonization is usually a sequel of a chronic inflammatory process, such as tuberculosis, bronchiectasis, histoplasmosis, or sarcoidosis. A ball of hyphae may form within an aircontaining space, particularly in the upper lobes, and is termed an aspergilloma. The fungus rarely invades the wall of the cavity, cyst, or bronchus in such patients" (Bennett, 1979a). It is not clear what role Aspergillus plays in non-invasive lung disease. Plugs of hyphae may obstruct bronchi. Perhaps allergic or toxic reaction to Aspergillus antigens could cause bronchial constriction and damage (Bennett, 1980).
Both the severity of aspergillosis and the patient's prognosis are dependent on the physiologic status of the patient. Invasion of lung tissue in aspergillosis is almost entirely confined to immunosuppressive patients (Bennett, 1980). Roughly 90 percent of invasive pulmonary case patients will have two of these three conditions: severe immunosuppression (less than 500 granulocytes per cubic millimeter of peripheral blood), supraphysiological doses of adrenal corticosteroids, and a history of taking cytotoxic drugs such as azathioprine (Bennett,1980). In addition, the type of disease produced affects the patient's chances for recovery. For example, simple colonization is treatable, but if the simple colonization becomes chronic or invades neighboring tissues, the infection becomes more difficult to treat (McGinnis, 1980). Surgical excision has been used successfully to treat invasive aspergillosis of the paranasal sinus as well as non-invasive sinus colonization. Intravenous amphotericin B has resulted in arrest or cure of invasive aspergillosis when immunosuppression is not severe (Bennett, 1980). Pleural aspergillosis often responds well to surgical drainage alone (Bennett, 1979b).
Although Aspergillus fumigatus is the usual cause of aspergillosis (Bennett, 1979b), there have been several recent case reports of pulmonary aspergillosis caused by A. niger. For example, Kierownik (1990) described a 66-year-old man who was admitted to the hospital with pulmonary lesions and cavitation of his lung. Fungi were cultured and the sputum contained fungal forms typical for A. niger complicating a pulmonary abscess in the course of a pneumonia. KorzeniowskaKosela et al. (1990) also describe a pulmonary aspergilloma caused by A. niger. Medina et al. (1989) reported on cases of bilateral maxillary sinusitis and a right pansinusitis.
A. niger was implicated in a case described by Louthrenoo et al. (1990), in which an amputation of the right foot had to be performed on a malnourished 70 yearold man who presented with a painful black "gangrenous appearing" mass on the right foot. Tissue samples showed not only branching hyphae, but dark pigmented fungal fruiting heads with double sterigmata in which Aspergillus niger was identified.
Although Aspergillus niger is regarded as an opportunistic pathogen (Padhye, 1982; Walsh and Pizzo, 1988), an earlier report said that it can cause otomycosis in healthy, uncompromised persons who have no underlying disease (Austwick, 1965). Otomycosis is the name given to the growth of Aspergillus, often A. niger, on ceruman and desquamated debris in the external auditory canal. The condition is benign. Of 159 suspected cases of otomycosis in Nigeria, 36 were specifically confirmed on the basis of demonstrating microscopically fungal structures in epithelial debris plugs and a positive culture (Gugnani et al., 1989). Another 31 cases gave positive cultures but were negative microscopically, and thus were considered of doubtful fungal pathology. Again, A. niger was predominant.
Indoor Cladosporium sp. may be different than the species identified outdoors. It is commonly found on the surface of fiberglass duct liner in the interior of supply ducts. They infest HVAC systems with very little ease when not properly cleaned and maintained. A wide variety of plants are food sources for this fungus. It is found on dead plants, woody plants, food, straw, soil, paint and textiles. It can cause mycosis. Produces greater than 10 antigens. Antigens in commercial extracts are of variable quality and may degrade within weeks of preparation. Common cause of extrinsic asthma (immediate-type hypersensitivity: type I). Acute symptoms include edema and bronchiospasms, chronic cases may develop pulmonary emphysema.
As a health hazard, Chaetomium globosum produces very high quantities of mycotoxins, especially chaetoglobosins A and C when growing on gypsum board. It is a known agent of skin and nail infections in humans and is more rarely a cause of cerebral and systemic infections in immunocompromised individuals. Although Chaetomium globosum is reported to have type I & III allergens the spores are not easily aerosolized and hence exposure to airborne spores may be rather limited. However, exposure to cytotoxic mycotoxins and also fine hyphal fragments released from dried mycelia could be a major concern.Chaetomium spp. are among the fungi causing infections wholly referred to as phaeohyphomycosis. Fatal deep mycoses due to Chaetomium atrobrunneum have been reported in an immunocompromised host. Brain abscess, peritonitis, cutaneous lesions, and onychomycosis may also develop due to Chaetomium spp.
Chaetomium colonies are rapidly growing, cottony and white in color initially. Mature colonies become grey to olive in color. From the reverse, the color is tan to red or brown to black
Septate hyphae, perithecia, asci and ascospores are visualized. Perithecia are large, dark brown to black in color, fragile, globose to flask shaped and have filamentous, hair-like, brown to black appendages (setae) on their surface. Perithecia have ostioles (small rounded openings) and contain asci and ascospores inside. Asci are clavate to cylindrical in shape and rapidly dissolve to release their ascospores (4 to 8 in number). Ascospores are one-celled, olive brown in color, and lemon shaped. Chaetomium is one of the most common moulds in water-damaged buildings. Species of Chaetomium are strongly cellulolytic moulds commonly found in soil, on paper, straw, cloth, cotton and other cellulose-containing substrates. They have caused problems in libraries, archives, and the food industry. Because of their bio-deterioration ability, several strains are used in testing materials for mould growth resistance.
Spores (ascospores) of Chaetomium are produced within structures (asci) contained in a flask-shaped fruiting body known as perithecium. On spore maturity, the walls of the asci dissolve releasing mucilaginous spores within the perithecium. The spores ooze out of the perithecium (plural perithecia) and get trapped by coiled or dichotomously branched hairs that grow around the neck of the perithecium. Since the spores are cemented together by mucilage and also trapped by hairs, few become airborne until the mould has completely dried out or disturbed, say during renovations or mould remediation. It is therefore not uncommon to find low Chaetomium spore counts in pre-remediation samples and relatively higher counts in post-remediation samples.