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Stachybotrys is a filamentous fungus occasionally isolated as a contaminant from nature and indoor environments. The geographic distribution of Stachybotrys is wide. It has been isolated from contaminated grains, tobacco, insulator foams, indoor air, and water-damaged buildings. Stachybotrys produces trichothecene mycotoxins known as satratoxins. These toxins may lead to pathological changes in animal and human tissues [787, 1415].
The genus Stachybotrys has a single well-known species, Stachybotrys chartarum.
See the summary of synonyms for the Stachybotrys sp.
Similar to various genera of filamentous fungi, Stachybotrys produces trichothecene mycotoxins, the satratoxins. Trichothecenes are potent inhibitors of DNA, RNA, and protein synthesis. They modulate inflammatory reactions and alter alveolar surfactant phospholipid concentrations. These toxins may be acquired by ingestion of food products contaminated with the fungus or experimentally, via direct inhalation of the spores [100, 340, 1116, 1648, 1804, 1805, 2034, 2183, 2266, 2269]. In addition to its mycotoxins, Stachybotrys produces an hemolysin, stachylysin, which lyses sheep erythrocytes. The existence of the mycotoxin, as well as the stachylysin, has been demonstrated in some strains [2183, 2319, 2320, 2321].
The pathogenicity of Stachybotrys was first observed in cattle and horses in Russia in 1920. Stomatitis, rhinitis, conjunctivitis, pancytopenia and neurological disorders developed in animals following ingestion of hay contaminated with Stachybotrys. The syndrome was called stachybotrytoxicosis [787, 1046, 1415, 2183]. This outbreak was the first to draw attention to Stachybotrys and its toxins. Later in the 1970s, it was claimed that Yellow Rain attacks in Southeast Asia were associated with the use of aerosolized trichothecenes as an agent of biologic warfare. However, this claim remained scientifically unproven [2069].
Following these, animal studies have been undertaken to demonstrate the pathogenic effects of the trichothecenes. In one of these investigations, intranasal administration of trichothecenes to mice was studied. Severe intra-alveolar, bronchiolar, and interstitial inflammation were observed following the intranasal exposure [1648]. However, simulation of intranasal exposure by exposing the mice to extensive surface growth of toxigenic Stachybotrys and high air flow did not produce these toxic effects, suggesting that the development of toxicosis in nature following inhalation is unlikely [2435]. This finding also suggested that mycotoxins of Stachybotrys can be produced or get airborne only under certain environmental settings [2183].
Stachybotrys has interested health care workers for two reasons. The first is its possible role in development of sick building syndrome. Stachybotrys is one of the contaminants inhabiting buildings with major problems in mechanical system design, construction, and operational strategies, leading to excess indoor moisture. However, Stachybotrys is only one of the fungal genera isolated in these buildings and in fact it is less common and in lesser amounts compared to other mould genera. Aspergillus, Penicillium, Alternaria, and Cladosporium spp. are more frequently isolated under these settings. Also, the definition and diagnosis of sick building syndrome is unclear and even more importantly, sick building syndrome may result from several chemical and physical factors as well as biological factors, including moulds. These ideas suggest the possibility that Stachybotrys may play a role in development of sick building syndrome, but most probably together with other factors [471, 2254].
In a nested case-referent study of adult-onset asthma, domestic exposures to moulds, environmental tobacco smoke, and the presence of a wood stove were found to be associated with adult-onset, building-related asthma [2238]. On the other hand, in three buildings with moisture-damaged interior surfaces where Stachybotrys chartarum, Aspergillus versicolor, and Penicillium spp. were isolated and satratoxins were detected, cases with symptoms consistent with potential asthma and interstitial lung disease were identified [1051]. The presence of IgE specific to Aspergillus spp., Cladosporium, and Stachybotrys chartarum in serum was found to be related to the sick building syndrome in another study [1290].
The second reason why Stachybotrys drew attention was its possible role in development of acute idiopathic pulmonary hemorrhage and hemosiderosis in infants. In the years 1993 to 1998, several infant cases of acute idiopathic pulmonary hemorrhage and hemosiderosis were reported. Stachybotrys was cultivated in their water-damaged houses. The initial cases consisted of 37 infants living in a limited geographic area in Cleveland, Ohio. Later, reports on additional cases followed [81, 101, 544, 694, 745, 1561]. Also, Stachybotrys was isolated from bronchoalveolar lavage fluid of a child with pulmonary hemorrhage [660]. Why did the infants, but not the adults, get the disease? Most authors speculated that the rapidly growing lungs of the infants were probably more vulnerable to the pathogenic effects of Stachybotrys toxins. These toxins presumably produced capillary fragility and eventually precipitated pulmonary hemorrhage in the rapidly growing lungs [544, 2253].
However, despite all that was reported about the association between acute idiopathic pulmonary hemorrhage and Stachybotrys, later analysis showed that the presented data were misleading. No statistically-significant association between acute idiopathic pulmonary hemosiderosis and Stachybotrys could be found [97, 102]. In summary, what we know today is limited and speculative and thus the health risks of environmental exposure to Stachybotrys are unclear. The actual role of Stachybotrys alone in development of human disease is yet poorly defined. We don't know whether it is similar or unlike the other mycotoxin-producing filamentous fungi with respect to its pathogenic potential. Other mycotoxin-producing moulds which are found to achieve higher indoor concentrations than Stachybotrys, should be evaluated with respect to their potential to produce acute idiopathic pulmonary hemorrhage and other pathologies.
For more detailed information and for sanitation and preservation measures against indoor Stachybotrys contamination, please see our general discussion of environmental infestations and our specific discussions of both sick building syndrome and diseases due to environmental moulds.
Stachybotrys produces cottony, rapidly growing colonies which mature in about 4 days. From both front and reverse, the color of the colony is white initially and turns to black by aging [1295].
Septate hyphae, conidiophores, phialides, and conidia are observed. The hyphae and the conidiophores appear hyaline initially and become darkly pigmented with age. The conidiophores which may be simple or branched, bear phialides at their apices. These phialides are hyaline or pigmented, cylindrical in shape, and have swollen upper portions. They form clusters of 3 to 10. The conidia (4.5 x 9 µm) are oval, hyaline or pigmented, 1-celled, and in clusters [1295].
No special precautions other than general laboratory precautions are required.
No data are available.
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References
81. Anonymous. 1994. Acute pulmonary hemorrhage/hemosiderosis among infants--Cleveland, January 1993-November 1994. MMWR Morb Mortal Wkly Rep. 43:881-3.
97. Anonymous. 1999. Report of the CDC Working Group on Pulmonary Hemorrhage/Hemosiderosis. Published online at http://www.cdc.gov/od/ads/pulhem_inf.htm.
100. Anonymous. 1998. Toxic effects of indoor molds. American Academy of Pediatrics. Committee on Environmental Health. Pediatrics. 101:712-4.
101. Anonymous. 1997. Update: pulmonary hemorrhage/hemosiderosis among infants--Cleveland, Ohio, 1993-1996. MMWR Morb Mortal Wkly Rep. 46:33-5.
102. Anonymous. 2000. Update: pulmonary hemorrhage/hemosiderosis among infants--Cleveland, Ohio, 1993-1996. MMWR Morb Mortal Wkly Rep. 49:180-4.
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