Stachybotrys chartarum

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1. Classification

a. Higher order taxa

Eukaryota (Kingdom), Fungi (Domain), Ascomycota (Phylum), Sordariomycetes (Class), Hypocreales (Order), Stachybotryaceae (Family), Stachybotrys (Genus [1].

b. Species

Stachybotrys chartarum

2. Description and significance

Stachybotrys chartarum, more commonly known as black mold, is a fungus prevalent in various environments, ranging from damp indoor spaces to food sources that both humans and livestock ingest [2]. Although its morphology and taxonomy were initially described in the 1830s by August Carl Joseph Corda, subsequent studies throughout the 20th century have raised questions about its size, ratio of conidia and phialides, and delineation from other species [3]. S. chartarum produces mycotoxins associated with detrimental health effects in humans and animals. It is the proposed pathogen for localized incidences of pulmonary hemorrhage in infants and other severe pulmonary conditions [4]. Current research efforts are still trying to discern the scope of its biological capabilities regarding indoor air quality and human health effects [3].

3. Genome structure

The complete genome of S.chartarum strain 51-11 spans approximately 40Mb [5]. With 9 sequence runs performed by Illumina Sequencing, there were approximately 736 million bases total, with about 2,600 bases per read5. The GC content for the S.chartarum genome is 53% [6]. Furthermore, based on the genes essential for satratoxin and atranone production (satratoxin cluster, SC1-3, sat or atranone cluster, AC1, atr), S. chartarum can be categorized into three groups: the S-type possessing all sat- but no atr-genes, the A-type lacking the sat- but harboring all atr-genes, and the H-type having only certain sat- and all atr-genes [6]. Genotype H is believed to represent the most ancient form of this fungus, with genotype S emerging from a loss of AC1 and the simultaneous acquisition of SC2 [6]. The development from genotype H to genotype A is believed to be accompanied by the loss of SC1 and SC3 [6].

4. Cell structure

S.chartarum, a gram-negative fungus, possesses a rigid cell wall primarily composed of chitin [7, 8]. When cultivated in media, it exhibits a dark color, giving rise to its common name. This fungus forms raised, circular colonies and consists of nonmotile bodies known as thalli, composed of apically elongating walled filaments (hyphae), which constitute the primary growth form of S. chartarum [9]. This structure can also branch out and become intertwined to form complex structures (e.g. rhizomorphs) [9]. Additionally, S. chartarum contains cellular cross walls called septa [8]. In S. chartarum, sporulation is triggered when food becomes depleted, as well as during its reproduction cycle [9].

5. Metabolic processes

S. chartarum exists in two chemotypes that produce different mycotoxins. Chemotype A produces atranones, while chemotype S produces macrocyclic trichothecenes [10]. The mutually exclusive production of either satratoxins or atranones defines the chemotypes A and S [6]. Macrocyclic trichothecenes include satratoxins, which are suspected to cause harm to humans and other animals [10]. Mycotoxin production and sporulation in S. chartarum are intertwined processes suspected to be regulated by G-protein signaling pathways, which also control developmental processes and stress responses [10]. The presence of neighboring colonies in strains of S. chartarum also stimulates mycotoxin production and sporulation [10]. S. chartarum is a chemoorganotroph which means that it obtains energy from the oxidation of organic compounds [11]. Nitrogen is a crucial element for the metabolism of S. chartarum; as nitrogen availability increases, it manufactures a higher mycotoxin production [10]. Common home building materials such as gypsum board, wood board, plywood, and cellulose insulation are all susceptible to S. chartarum decomposition under moist conditions [12]. S. chartarum produces an extracellular enzyme, cellulase, to digest and break down these home-building materials, which primarily consist of cellulose [13].

6. Ecology

S. chartarum is found around the world, usually in areas high in cellulose [14]. It grows optimally in moist environments with a minimum water activity (aw) of at least 0.95 [15]. This poses a problem for flooded or damp homes, where S. chartarum can thrive. As moisture and aw decrease, so do the activity and growth of S. chartarum [15]. However, sporulation isn’t negatively affected when moisture decreases to an aw of 0.95. Thus, even when flooded homes are dried out, there is still a risk of spore contamination [15]. The optimal temperature for growth of this fungus is 30°C, although sporulation can still occur at temperatures reaching 15-20°C [15]. As the temperature deviates from 30°C, the total radial growth and rate of growth decreases [16]. Because of S. chartarum’s ability to decompose cellulose, buildings with cellulose insulation and wood supports are prime candidates for fungal growth [17]. S. chartarum generally does not compete well with other fungi and is rarely found outside [17]. However, this fungus has been found and isolated from soybean roots [18].

7. Pathology

S. chartarum affects the pulmonary health of humans. The mold releases spores and mycotoxins, toxic compounds to humans and some animals, including horses [19]. These toxins are found airborne in buildings with S. chartarum [20]. Pulmonary issues are attributed to the production of these toxins, where any growth of S. chartarum in buildings could cause illness in the residents [21]. Black mold causes nonspecific health-related problems, often called building-related illnesses or “sick building syndrome” [19]. Spore and toxin exposure activates an immune response that causes inflammation in the lungs [22, 23]. It can also cause arterial remodeling or airway obstruction [24, 25]. Symptoms may include those associated with interstitial lung disease (ILD), such as difficulty breathing or dry coughing [25]. The mold is also associated with skin and eye irritation [26].

S. chartarum poses a health hazard to animals as well. In 1945, an outbreak of "stachybotryotoxicosis" affected horses, other animals, and farm workers, causing excessive mucus discharge, mucous generation in the mouth, nose, and throat, lowered immunity, anemia, and death [20]. This resulted from ingesting farm feed infected by S. chartarum and its toxins [20]. Farm workers and animals showed disease symptoms when they inhaled farm dust and spores. Skin contact with infected vegetation also caused the skin to break and ooze [20].

There is speculation of an association between S. chartarum exposure and acute idiopathic pulmonary hemorrhage among infants [27]. This association was primarily due to an outbreak of cases in Cleveland, Ohio, from 1993 to 1998 in buildings that contained S. chartarum growth; however, the CDC could not determine a true association between disease outbreak and S. chartarum growth [27].

8. Cleaning Techniques

The presence of black mold or S. chartarum in damp homes and indoor environments requires treatment to prevent toxin exposure [28]. Cleaning techniques involving bleach and detergent have proven more effective in reducing toxins and spores compared to methods like steam cleaning and gamma irradiation [28]. The efficiency of antimicrobial cleaners has been tested, with Lysol All-Purpose Cleaner-Orange Breeze (full strength) ranking as the most effective, along with Borax and Orange Glo Multi-Purpose Degreaser being effective as well [29]. Antimicrobial paints can be applied to previously contaminated interior gypsum wallboards (drywall) to prevent regrowth after cleaning. A study found the most effective paints were Permawhite, M-1 Additive and Poterscept [30]. Chlorine dioxide gas has been utilized to treat indoor molds and eliminate their spores, but it was discovered that S. chartarum remained toxic even after exposure to this gas [31].

9. Current Research

One area of current research delves into the health effects and detection methods associated with S. chartarum. In a study involving mice repeatedly exposed to two different strains, IBT 9460 (strain A) and IBT 7711 (strain B), of S. chartarum, researchers observed consistent inhalation-induced inflammation and arterial remodeling in the lungs [24]. Notably, strain A triggered a faster response to S. chartarum exposure than strain B [24]. Furthermore, individuals exposed to S. chartarum for at least three months reported heightened respiratory, dermatological, ocular, and fatigue symptoms [26]. These findings highlight the adverse health effects of repeated S. chartarum exposure, impacting the respiratory, central nervous, mucous, and immune systems.

Another significant area of research centers on the toxicity of S. chartarum and its implications for individuals residing in contaminated buildings. Occupants of such buildings have reported health issues linked to their environment [21]. Additionally, S. chartarum is known to produce two primary types of mycotoxins: Satratoxins and Atranones. While atranones exhibit lower toxicity compared to satratoxins, both mycotoxin types pose substantial health risks [8].

Advances in research have facilitated the identification of specific biomarkers associated with S. chartarum exposure. Clinical biomarkers, such as antibodies against S. chartarum and antigenic components like Stachyhemolysin and Stachyrase-A, have been successfully identified [32]. These biomarkers offer valuable diagnostic tools for accurately assessing S. chartarum exposure.

S. chartarum's adaptability is a growing concern. Researchers have discovered its presence not only in traditional indoor environments but also in soil and other cellulose-rich substances, indicating its ability to thrive in various settings [18]. This versatility raises additional concerns about the potential for exposure in different environments.

10. References

It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.