shopify analytics ecommerce



Stachybotrys is one of several species of mold capable of producing mycotoxins under certain environmental conditions and is often found in water-damaged buildings. Stachybotrys may produce several different mycotoxins including a class known as trichothecenes. The trichothecenes are potent inhibitors of DNA, RNA and protein synthesis.

Stachybotrys chartarum made headlines in the early 1990s when cases of infant pulmonary hemosiderosis occurred associated with S. chartarum in Cleveland homes (Montana et al, 1997; Etzel al 1998). The results of the study was criticized by the U.S. Centers for Disease Control (CDC 1994, 1996). Dearborn et al (2002) published their follow up on the pulmonary hemorrhage in Cleveland. They answered and rebutted the CDC criticisms and pointed out that the water-damaged homes with multiple mold genera were the primary risk factor for the bleeding. 

Out of the 30 cases reviewed in 2001, only 10 of the 30 cases may have had side-stream tobacco smoke as a risk factor. 

In spite of the 2002 review, the CDC has not revised its criticism. I assume this is the government inaction. The inaction has occurred in spite of the fact that other case studies have been published (Flappan et 1999; Novotny and Dixit 2000; Tripi et al 2000; Athayde and Shore 1993).

It is important to note that the Cleveland cases were associated with water damage and multiple species of fungi. Research on the various fungal species, including Stachybotrys chartarum, found that multiple environmental factors present in water-damaged homes were probably responsible for the pulmonary bleeding in these events. These factors will be briefly reviewed herein.

Stachylysin, Siderophore and Other Hemolytic Proteins of Fungi and Bacteria

The homes where the pulmonary bleeding occurred were water damaged. Water intrusion lead to the growth of multiple species of fungi as well as Gram positive and negative bacteria (Thrasher and Crawley 1999; Shoemaker et al, 2010). 

Both fungi and bacteria contain hemolytic proteins as well as siderophores. 

The hemolysins cause lyse red blood cells while the siderophores sequester iron from host tissues and blood for utilization of microbial growth (Neilands 2010; Budzikiewicz 2020).  

Stachybotrys chartarum, isolated from the Cleveland homes, produces a hemolytic protein (Stachylysin) as well as a siderophore (Vesper et al 1999, 2000; 2002). Stachylysin has also been detected in the pooled sera of S. chartarum exposed building occupants (Van Emon et al 2003). Therefore, if the spore count is low, one must ask where the serum born stachylysin came from. 

In addition, Brasel et al, 2005a, b demonstrated the presence of macrocyclic trichothecenes in indoor air on particulates smaller than spores from S. chartarum. 

Moreover, macrocyclic trichothecenes were reported in the sera of symptomatic individuals exposed to S. chartarum in a water-damaged building (Brasel et al 2004) . 

The point is: 

What else in water-damaged buildings (WDB) is present that caused the pulmonary hemorrhage in the Cleveland infants? 

Part of the answer to that question lies in the information on water damage and biocontaminants provided on this web site. The other part comes from research on other fungi isolated from the Cleveland homes.

Fungal species were identified in the homes of infants with pulmonary hemorrhage (PH) vs control homes by quantitative polymerase change reaction and tested to determine hemolysis of sheep red blood cells (Vesper et al, 2004). 

The most interesting aspect of their findings was that fungi from the PH homes produced hemolysins far more readily than fungi from the control homes. The fungi that produces hemolysins are as follows: 

1. Aspergillus flavipes, flavus, fumigatus, niger, niveus, ochraceus, parasiticus, sclerotiorum, sydowii, terreus, unguis and versicolor; 

2. Penicillium canescens, chrysogenum, citrinum, decumbens, griseofulvum, islandicum oxalicum and variable; 

3. Others: Memnoniella echinata, Scopulariopsis brevicaulis, Stachybotrys chartarum, Trichoderma longibrachiatum, Ulocladium atrum and botrytis. 

Those with the most intense production were A. flavus, fumigatus niger and ochraceus, and S. chartarum, which are readily found in WDB. Thus, you name the poison.

S. chartarum Chemotypes

The following is a brief review of the toxins of S. chartarum. To obtain considerable information on toxins produced by this fungus and their adverse effects in animal models, please read the paper by Pestka et al, 2008

Two chemotypes of S. chartarum have been identified as genetically distinct subtypes. They produce secondary metabolites (Mycotoxins) as well as spirocyclic drimanes. Each of these will be briefly discussed.

Macrocyclic Trichothecenes

Trichothecenes belong to three structural groups: Types A, B and D. All trichothecenes have common C-9 to 10 double bound and C-12 and C-13 epoxide group.

Type A (T-2 toxins) has isovaleryl, hydrogen or hydroxyl moieties on the C-8 carbon position of the ring.

Type B (Vomitoxin) has a carbonyl group at the C-8 position.

Type D (Satratoxins, roridins). The macrocyclic compounds have a cyclic diester or triester ring linking C-4 to C-15 carbons.

The macrocyclic trichothecenes have been extensively studied both in vitro and in vivo, with mice and rats being the in vivo models. The in vivo mouse studies have revealed multiple toxic properties that have been reviewed by Pestka et al, 2008. The highlights of these experiments will be briefly listed here. You are referred to the Pestka paper for greater detail.

1. S. chartarum spores, when suspended in saline, release trichothecenes within minutes. A similar rapid release occurs in rat lungs.

2. Instillation of spores leads to detectable satratoxin in macrophage lysosomes, nuclear membrane of heterochromatin and rough endoplasmic reticulum. Similar findings occur in Type II alveolar cells.

3. Trichothecenes interfere with ribosome function and inhibit protein synthesis.

4. Trichothecenes activate p38, June N-terminal Kinase (JNK), extracellular signal-regulated kinase (ERK) and mitogen -activated protein kinases (MAPKs) via mechanism called “ribotoxic stress.” MAPK activation mediates both proinflammatory cytokine regulation and apoptosis.

5. Macrocyclic trichothecenes and other factors have the capacity to damage DNA.

6. Macrocyclic trichothecenes can form adducts to macromolecules, (e.g., serum albumin) modifying their structure and function and permitting body storage. Ten toxin molecules bind to one albumin molecule.

7. Instillation of spores as well as macrocyclic trichothecenes into the lungs of rodents causes inflammation and bleeding and production of pro-inflammatory cytokines. No observable adverse effect level (NOAEL) is 30 spores per gram body weight (Flemming et al, 2004).

8. Installation of satratoxin and roridin into the olfactory area of mice leads to damage and inflammation of the olfactory nerve, tract and lobe.


These mycotoxins are related to the dollabellane diterpenes and are designated Atranones A through G. The atranones evoke a rapid inflammatory response that is sustained for approximately 24 hours. They induce the appearance of macrophages, eosinophils and the cytokines MIP-2, TNF-α, and IL-6 .

Spirocyclic Drimanes

Up to 40 different spirocyclic drimanes are produced by S. chartarum. They have a wide spectrum of biological activity including inhibition of proteolytic enzymes, disruption of the complement system, inhibition of TNF--α release, endothelial receptor antagonism, stimulation of plasminogen, fibrinolysis, thrombolysis and cytotoxic and neurotoxic effects. Their role in the pathophysiologic effects of Stachybotrys needs further elucidation.


Other biologically active products include Stachylysin, proteinases, MVOCs, 1-3-beta-glucans and the interaction of other environmental cofactors including endotoxins, various Actinomycetes and environmental tobacco smoke.
Stachybotrys chartarum colonies

Stachybotrys chartarum colonies

Stachybotrys heavy growth

Stachybotrys heavy growth

Stachybotrys chartarum spores

Stachybotrys chartarum spores


Athayde J, Shore ET. 1991. Invasive pulmonary aspergillosis presenting as massive hemoptysis in a nonimmunoocompromised host. Chest 103:960-1.

Brasel TL, Campbell AW, Demers RE, Ferguson BS, Fink J, Vojdani A, Wilson SC, Straus DC. 2004. Detection of trichothecene mycotoxins in sera from individuals exposed to Stachybotrys chartarum in indoor environments. Arch Environ Health 59:417-23. 

Brasel TL, Martin JM, Carriker CG, Wilson SC Straus DC. 2005a. Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins in indoor environment. Appl Environ Microbiol 71:7376-88. 

Brasel TL, Douglas DR, Wilson SC, Straus DC. 2005b. Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins on particulates smaller than conidia. 71:114-22. 

Budzikiewicz . 2010. Microbial siderophores. Fortschr Chem Org Naturst 92:1-75.

CDC. 1994. Acute pulmonary hemorrhage/hemosiderosis among infants - Cleveland, January 1993-November 1994. MMWR 43:881-83.

CDC. 1996. Update. Pulmonary hemorrhage/hemosiderosis among infants-Cleveland, Ohio, 1993-1996. MMWR 46:33-5.

Etzel RA, Montana E, Sorenson WG, Kullman GJ, Allan TM, Dearborn, DG, 1998. Acute Pulmonary Hemorrhage in Infants Associated With Exposure to Stachybotrys atra and Other Fungi. Arch Pediatr Adolesc Med. 1998;152:757-762.

Flappan SM, Portnoy J, Jones P, Barnes C. 1999. Infant pulmonary hemorrhage in a suburban home with water damage and mold (Stachybotrys atra). Environ Health Perspec 107:927-30.

Flemming J, Hudson B, Rand TG. 2004. Comparison of inflammatory and cytotoxic lung responses in mice after intra tracheal exposure to spores of two different Stachybotrys chartarum strains. Toxicol Sci 78:267-75.

Montana E, Etzel RA, Allan TM, Horgan TE, Dearborn DG. 1997. Environmental risk factors associated with pediatric hemorrhage and hemosiderosis in a Cleveland Community. Pediatrics 99.

Neilands JB. 2010. Siderophores of bacteria and fungi. Microbiol Sci 1:9-14.

Novotny WE, Dixit A. 2000. Pulmonary hemorrhage in an infant following two weeks of fungal exposure. Paediatr Anesth 10:92-4.

Shoemaker RA., Mark L, McMahon S, Thrasher JD, Grimes C. 2010. Policyholders of America: Research Committee report on the diagnosis and treatment of chronic inflammatory response syndrome caused by exposure to the interior environment of water-damaged buildings. 

Share by: