Types of Mold

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A Few Points First on Mold:

  1. Mold can be in your house even if you cannot locate it with the naked eye.
  2. Mold enjoys moist, dark areas with ample food I.E Sheet rock, wallpaper etc.
  3. Food can already contain Mold and Mold toxins in them before you'll ever see it grow.
  4. Anti-Biotics are made from mold like Penicillium and many others.
  5. Ammonia, Oregano Oil, Neem Seed Oil, Borax, Baking Soda - all kill mold. Ammonia kills Toxins.
  6. 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.
  7. First stage of Mycotoxin sickness will have no Physical symptoms.
  8. Mold can exist under layers of sheet rock, wallpaper and Bathtub Stalls.
  9. Mold Allergies are not Allergies - It is your body either fighting it off, or Becoming very sick from it.
  10. Steroids, Anti-Biotics, and Immune suppressing drugs make the body more vulnerable to Mold Toxins.
  11. Candida Albicans is a bad body yeast that is already in our digestive track.
  12. Mold enjoys existing in a low Ph level environment. Candida in a pH of 7. 
  13. Candida Albicans produces toxins that are carcinogenic to humans.
  14. Mold and Yeast Toxins aka Mycotoxins can and will invade brain cavity.
  15. Not all molds are created equal. Some are more hazardous then others.
  16. Toxins will lower immune system functions - Even in healthy bodies. Then once this happens...
Molds commonly found in kitchens and bathrooms

- Cladosporium cladosporioides (hazard class B)
- Cladosporium sphaerospermum (hazard class C)
- Ulocladium botrytis (hazard class C)
- Chaetomium globosum (hazard class C)
- Aspergillus fumigatus (hazard class A)

Molds commonly found on/under wallpapers

- Cladosporium sphaerospermum
- Chaetomium spp., particularly Chaetomium globosum
- 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)

Molds commonly found on/under mattresses and carpets

- Penicillium spp., (Esp. Penicillium chrysogenum) (hazard class B)
- Penicillium aurantiogriseum (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.

Molds commonly found on window frames

- Aureobasidium pullulans
- Cladosporium sphaerospermum
- Ulocladium spp.

Molds commonly found in basement (cellars)

- Aspergillus versicolor
- Aspergillus fumigatus
- Fusarium spp.

Molds commonly found in flower pot soil

- Aspergillus fumigatus
- Aspergillus niger (hazard class A)
- Aspergillus flavus (hazard class A)


Below are some of the molds that contains these Mycotoxins with photos of what they look like on walls and inside homes. There is also a great website below that will show you the hundreds of other types of molds and how they effect human health.

Stachybotrys Spp:  Several strains of this fungus may produce a trichothecene mycotoxin- Satratoxin H - which is poisonous by inhalation. The toxins are present on the fungal spores. This is a slow growing fungus on media. It does not compete well with other rapidly growing fungi. The dark colored fungi grows on building material with a high cellulose content and a low nitrogen content. Areas with relative humidity above 55% and are subject to temperature fluctuations are ideal for toxin production. Individuals with chronic exposure to the toxin produced by this fungus reported cold and flu symptoms, sore throats, diarrhea, headaches, fatigue, dermatitis, intermittent local hair loss, and generalized malaise.

The toxins produced by this fungus will suppress the immune system affecting the lymphoid tissue and the bone marrow. Animals injected with the toxin from this fungus exhibited the following symptoms: necrosis and hemorrhage within the brain, thymus, spleen, intestine, lung, heart, lymph node, liver, and kidney. The mycotoxin is also reported to be a liver and kidney carcinogen. Affects by absorption of the toxin in the human lung are known as pneumomycosis. This organism is rarely found in outdoor samples. It is usually difficult to find in indoor air samples unless it is physically disturbed. The spores are in a gelatinous mass. Appropriate media for the growth of this organism will have a high cellulose content and a low nitrogen content. The spores will die readily after release. The dead spores are still allergenic and toxigenic.  This is a home that needs immediate evacuation, and people infected need to be put in a clean environment as soon as possible. These are the worst of all the molds.  Stachybotrys typically appears as a sooty black mold occasionally accompanied by a thick mass of white mycelia, the web structure that holds the mold. This mold thrives on water damaged cellulose rich materials in buildings such as sheet-rock paper, ceiling tiles, cellulose containing insulation backing and wall paper. Almost without exception, an extended saturation time and/or consistently high levels of humidity are required for this mold to proliferate.

Aspergillus Spp: is the one of the more deadly molds that produce Mycotoxins. It is brown or greenish in nature and spreads out in a blanket like pattern consuming the materials it's grown on top of. It could even be explained as having a sandy textured appearance. It can exist under your sheet rock and carpets hidden from view. In our airtight condos and houses with HVAC systems, we're pretty much living and working in perfect petri dishes for them to prosper.  This type of mold can cause a terrible sickness called  Aspergillosis. In order to get aspergillosis, you must breathe in fungal spores of Aspergillus, commonly Aspergillus fumigatus. These spores are found everywhere, and most people breath these spores into their bodies everyday. They are most commonly found in environments with soil or dust, or poor ventilated buildings and houses. Skin infections can be caused from contact with contaminated biomedical devices as well. Incubation times vary, but there are a few symptoms to watch for if the spores do colonize in your body.  
Aspergillus flavus:
is a saprotrophic and pathogenic[1] 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 Flavusflavus colonies are commonly powdery masses of yellow-green spores on the upper surface and reddish-gold on the lower surface (underneath).

Aspergillius Niger: Aspergillus niger is a fungus and one of the most common species of the genus Aspergillus. It causes a disease called black mold on certain fruits and vegetables such as grapes, onions, and peanuts, and is a common contaminant of food. It is ubiquitous in soil and is commonly reported from indoor environments, where its black colonies can be confused with those of Stachybotrys (species of which have also been called "black mold"). Some strains of A. niger produce potent mycotoxins called Ochratoxins A.  In addition to growth on carbon sources, many species of Aspergillus demonstrate oligotrophy where they are capable of growing in nutrient-depleted environments, or environments in which there is a complete lack of key nutrients. A. niger is a prime example of this; it can be found growing on damp walls, as a major component of mildew as this picture shows you.

        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. 

      People with invasive aspergillosis usually have nose stuffiness, headache, facial discomfort, cough (often with blood), fever, and chest pain, but in people with a normal immune system, the first three of these symptoms listed are most common. However, some people never get any symptoms at all.  It will quickly once set into the body I.E the lungs, will grow and prosper and take over the host body using all your nutrients trying to stay undetected, until its settled and Incorporated into your body as a whole. Then Shortly after the later stages, you will notice the sickness coming over your. I have a chapter on the Symptoms of Toxins which will help let you understand what is going on in your body.


Penicillium Spp:  A wide number of organisms have placed in this genera. Identification to species is difficult. Often found in aerosol samples. Commonly found in soil, food, cellulose, and grains. It is also found in paint and compost piles. It may cause hypersensitivity pneumonitis and allergic alveolitis in susceptible individuals. It is reported to be allergenic. It is commonly found in carpet, wallpaper, and in interior fiberglass duct insulation. Some species can produce mycotoxins.

Common cause of extrinsic asthma (immediate-type hypersensitivity: type I). Acute symptoms include edema and bronchiospasms, chronic cases may develop pulmonary emphysema. It can co-exists with other molds, It is known to co-exist with Cladesporium Sp, Aspergillius. I know from personal experience because it was what was in my building on the ceiling tiles found together growing. They were also located together growing on sheet rock once taken down to the bare wall.


Cladosporium Spp: is another terrible mold that is one of the most common anywhere.  It exists in nature on trees, plants, ground, and enjoys high levels of moisture just like most molds.  The outdoor numbers are reduced in the winter. The numbers are often high in the summer. Often found indoors in numbers less than outdoor numbers unless you exist in environment with high levels of humidity; it will prosper quickly. 

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.


Fusarium Spp: A common soil fungus and inhabitant on a wide array of plants, this fungi is often found in humidifiers and has been isolated from water-damaged carpets and a variety of other building materials. Human exposure may occur through ingestion of contaminated grains and possibly through the inhalation of spores. Fusarium spp. are frequently involved with eye, skin, and nail infections. More severely it can produce hemorrhagic syndrome (alimentary toxic aleukia) in humans which is characterized by nausea, vomiting, diarrhea, dermatitis, and extensive internal bleeding. Several species can produce the trichothecene toxins which target the circulatory, alimentary, skin, and nervous systems.

     Vomitoxin is one such tricothecene mycotoxin that has been associated with outbreaks of acute gastrointestinal illness in humans. Vomitoxin ends up creating terrible bats of vomiting in the infected patient or animal as the name suggests. Zearalenone is another mycotoxin produced by Fusarium. It is similar in structure to the female sex hormone estrogen and targets the reproductive organs.  Fusarium is one of the most drug-resistant fungi. Among the Fusarium spp., Fusarium solani in general tends to be most resistant of all. Fusarium strains yield quite high MICs for flucytosine, ketoconazole, miconazole, fluconazole, itraconazole, and posaconazole. The novel triazole, Syn-2869, has no activity against Fusarium. Fusarium spp. are intrinsically resistant to the novel glucan synthesis inhibitors, caspofungin, anidulafungin, and micafungin. Despite the lack of its activity alone, the combination of caspofungin with amphotericin B appears synergistic against some Fusarium isolates. The only antifungal drugs that yield relatively low MICs for Fusarium are amphotericin B, voriconazole, and natamycin. Compared to itraconazole, voriconazole yields notably lower MICs. Terbinafine may show good in vitro activity against some isolates. This is why I feel that natural ways of treatment and better diet, herbal rememdies and teas are a safer way to cleanse the body of such a toxin producing mold.

     Fusarium infections are difficult to treat and the invasive forms are often fatal. Amphotericin B alone or in combination with flucytosine or rifampin is the most commonly used anti fungal drug for treatment of systemic fusariosis. Lipid formulations of amphotericin B, such as liposomal amphotericin B and amphotericin B lipid complex are also used. However, most cases remain resistant and fail to respond to amphotericin B treatment. Granulocyte and GM-CSF transfusions concommitant to amphotericin B therapy may be life-saving in some immunosuppressed patients with disseminated fusariosis.


Chaetomium spp:  Some species of Chaetomium have been implicated in nosocomial infection of patients in hospital environment after bone marrow transplantation. Many species are also known to produce mycotoxins and are recognized human allergens. The most common species in water-damaged buildings is Chaetomium globosum. In many cases it occurs together with Stachybotrys chartarum and other hydrophilic moulds. It produces high quantities of biomass (up to 10 mg/cm2) on building materials. It has been isolated from wallpaper, drywall, baseboards, carpets and window frames. It is a major cause of biodeterioration of paper and other cellulose containing materials.

     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.

Macroscopic Features
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

Microscopic Features
     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.

Acremonium spp: are filamentous, cosmopolitan fungi commonly isolated from plant debris and soil. Acremonium (a.k.a. Cephalosporium) is a common type I & III allergen. Naturally found in soils, decaying organic matter, and plant debris, it is also an agricultural contaminant. This genus can be parasitic or saprophytic to plants and other living fungi, and some species cause vascular wilts in trees. Acremonium is the asexual state of Emericellopsis, Chaetomium, and Nectripsis. It has been known to produce a toxin from the trichothecene group and may also give off an unpleasant odor due to the production of volatile organic compounds (VOCs).
     This fungus is associated with occupant complaints such as nausea, vomiting and diarrhea. Acremonium has been isolated from cases of mycetoma, onychomycosis, mycotic keratitis, infection of the cornea, and infections of artificial implants. Morphological characteristics are the production of conidiophores and long, slender phialides; conidia are hyaline, 1-celled, and are collected in a slime drop. Colonies grow fast and are compact and moist, becoming overgrown with loose, cottony hyphae which are white, gray or rose in color. Indoor growth requires extremely wet conditions, and does not grow very well at 37°C. Culture - Potato dextrose agar or Malt extract agar, 20° - 25°C, 7 – 10 days.

      The sexual state of Acremonium is not well-defined. Thus, it is classified among the deuteromycetes group of fungi by some authorities. Others prefer to include it in Ascomycota phylum, due to its structural properties similar to those of this group. There are three main species of Acremonium implicated in infections: Acremonium falciforme, Acremonium kiliense, and Acremonium recifei. See the list of obsolete names and synonyms for older names of these species.  Acremonium is one of the causative agents of eumycotic white grain mycetoma. Rare cases of onychomycosis, keratitis, endophthalmitis, endocarditis, meningitis, peritonitis, and osteomyelitis due to Acremonium have also been reported.  This fungus is known to cause opportunistic infections in immunocompromised patients, such as bone marrow transplant recipients. Infections of artificial implants due to Acremonium spp. are occasionally observed.  Since Acremonium species are cosmopolitan in nature, they are also encountered as contaminants. Thus, their isolation in culture requires cautious evaluation. 

     The growth rate of Acremonium colonies is moderately rapid, maturing within 5 days. The diameter of the colony is 1-3 cm following incubation at 25°C for 7 days on potato glucose agar. The texture of the colony is compact, flat or folded, and occasionally raised in the center. It is glabrous, velvety, and membrane-like at the beginning. Powdery texture may also be observed. By aging, the surface of the colony may become cottony due to the overgrowth of loose hyphae. The color of the colony is white, pale grey or pale pink on the surface. The reverse side is either uncolored or a pink to rose colored pigment production is observed.  Acremonium spp. possess hyaline, septate hyphae which are typically very fine and narrow. Vegetative hyphae often form hyphal ropes. Unbranched, solitary, erect phialides are formed directly on the hyphal tips, the hyphal ropes, or both. The phialides are separated from hyphae by a septum and taper towards their apices. At the apices of the phialides are the hyaline conidia 2-3x4-8µm in size. They usually appear in clusters, in balls or rarely as fragile chains. The conidia are bound by a gelatinous material. They may be single or multicellular, fusiform with a slight curve or resemble a shallow crescent. These structural properties of conidia vary depending on the species. Acremonium falciforme usually produces crescentic, nonseptate conidia. Sometimes, 2- or 3-celled conidia may also be observed. Acremonium kiliense, on the other hand, has short straight conidia and the conidia of Acremonium recifei are usually crescentic and nonseptate.  The grains (500-2000µm in size) of Acremonium spp. are regular and oval to round in shape.


Alternaria Ssp: is another dark-colored mold. Exposure to Alternaria can provoke respiratory and asthmatic symptoms in susceptible persons. Alternaria will grow undetected under shower pans, bathtub linings, or anywhere dark and low on fresh air. Alternaria spores are large, club-shaped spores. These spores do not stay airborne as long as the smaller Aspergillus and Penicillium spores. In a damp basement of a new house, Alternaria can exist along and across foundation walls. Alternaria can grow as a result of a shower leak, leaky pipe, bad radiator, or in any wall as well with heavy moisture.

     Alternaria is a cosmopolitan dematiaceous (phaeoid) fungus commonly isolated from plants, soil, food, and indoor air environment. The production of melanin-like pigment is one of its major characteristics. Its teleomorphic genera are called Clathrospora and LeptosphaeriaThe genus Alternaria currently contains around 50 species. Among these, Alternaria alternata is the most common one isolated from human infections. Some authorities suggest that Alternaria alternata is a representative species complex rather than a single species and consists of several heterogenous species. While Alternaria chartarum, Alternaria dianthicola, Alternaria geophilia, Alternaria infectoria, Alternaria stemphyloides, and Alternaria teunissima are among the other Alternaria spp. isolated from infections, some Alternaria strains reported as causative agents remain unspecified.  Alternaria spp. have emerged as opportunistic pathogens particularly in patients with immunosuppression, such as the bone marrow transplant patients. They are one of the causative agents of phaeohyphomycosis.

   Cases of onychomycosis, sinusitis, ulcerated cutaneous infections, and keratitis, as well as visceral infections and osteomyelitis due to Alternaria have been reported. In immunocompetent patients, Alternaria colonizes the paranasal sinuses, leading to chronic hypertrophic sinusitis. In immunocompromised patients the colonization may end up with development of invasive disease. It is among the causative agents of otitis media in agricultural field workers.  Since Alternaria species are cosmopolitan and ubiquitous in nature, they are also common laboratory contaminants. Thus, their isolation in culture requires cautious evaluation. Alternaria spp. grow rapidly and the colony size reaches a diameter of 3 to 9 cm following incubation at 25°C for 7 days on potato glucose agar. The colony is flat, downy to woolly and is covered by grayish, short, aerial hyphae in time. The surface is grayish white at the beginning which later darkens and becomes greenish black or olive brown with a light border. The reverse side is typically brown to black due to pigment production.  Alternaria spp. have septate, brown hyphae.

     Conidiophores are also septate and brown in color, occasionally producing a zigzag appearance. They bear simple or branched large conidia (7-10 x 23-34 µm) which have both transverse and longitudinal septations. These conidia may be observed singly or in acropetal chains and may produce germ tubes. They are ovoid to obclavate, darkly pigmented, muriform, smooth or roughened. The end of the conidium nearest the conidiophore is round while it tapers towards the apex. This gives the typical beak or club-like appearance of the conidia.


       This is a wonderful site to see all the different kinds of molds that can invade your home, damage your health, and simply erode your immune system to cause other types of illness and sickness. I haven't reviewed their other services yet, So just use their descriptions which are wonderful and accurate.  I will update if they're a good Laboratory for testing mold soon.