Dark Secrets about Black Mold

by EH

Many of us likely start our day with a wonderful hot shower. Showering is a great time to relax and reflect on life.  Perhaps your eyes drift upwards to the ceiling while you contemplate what type of muffin you will eat this morning.  “What are those black spots on the ceiling”, you wonder…Don’t worry, if you ignore them they’ll probably just go away on their own. Days go by and you’ve forgotten all about the black specks that completely clash with the striped wallpaper in your bathroom.  Next thing you know, the black spots have formed a large hideous clump of blackness on your ceiling.  What’s worse is that the blackness is spreading to all parts of your bathroom! Oh well, that’s why you have roommates right?  They must have some sense of hygiene.  Besides you just cleaned the bathroom two weeks ago, so it’s not your problem this time. Next thing you know, you are experiencing a shortened attention span, confusion, hallucinations (no, not from the mushrooms you ate two days ago), impaired learning abilities and diarrhea.  Congratulations! You may have the toxic black mold Stachybotrys chartarum growing rampantly in your bathroom.  Good thing you passively approached that situation.

Figure 1.  Hyphae and Spores of S. chartarum.  The left picture
 shows a typical hyphae structure.  The right picture shows
 that the spores are ovoid in shape. (Andersen et al. 2003)

So now that you are too confused to reflect on your poor decisions, and luckily you won’t remember your mother scolding you for the disgusting mold present in your bathroom, lets learn about S. chartarum.  S. chartarum is a spore forming fungus that grows in high moisture environments usually on material high in cellulose content (4).  This mold is most commonly found after flooding and water damage, but your long showers have provided a perfect environment for this mold to grow in (I’d still just blame the landlord – that’s easier).  So why are you getting sick?  We eat molds all the time right – I mean cheese is delicious!  Unfortunately for us, S. chartarum produces many neurotoxins classified as trichothecene mycotoxins (3).  Trichothecene mycotoxins are potent inhibitors of protein synthesis in eukaryotic organisms.  What’s worse is that the spores of S. chartarum have been shown to contain theses toxins (3). S. chartarum typically grows in a sporulating form and forms hyphae which hold spores on the end (1).  These spores are small enough that they can become airborne and spread the mold to other places in your bathroom.   At the same time, you probably inhaled some with all the steam produced from the shower.

So now that you’ve inhaled these spores which contain trichothecene mycotoxins, let’s talk a little bit about the toxin.  The LD50 of trichothecene mycotoxins range from 0.5mg/kg – 300mg/kg in mice models (2).  This is good news, since it is unlikely you would receive a lethal dose.  Seriously, the air would be incredibly foggy with the concentration of spores necessary to kill you and if you choose to shower in that environment, you asked for it. Just because it won’t kill you, doesn’t mean it can’t make you sick.  Sickness from these mycotoxins are normally mild with general symptoms of nausea, headache and general malaise, but in severe cases neurological impairments can occur (2).  Now for the fun facts about trichothecene mycotoxins!  These toxins are incredibly hard to destroy. They can withstand freezing temperatures, UV light, and 500°F (3).  That’s some serious resilience! According to the CDC, the best way to deal with these toxins is by using bleach as a cleaning agent.  Not only is the toxin incredibly stable, but T-2 trichothecene mycotoxins are used in biological warfare.  What! Seriously?  Yes; according to Dr. William Deagle, the United States military reportedly conducts 90% of its current biological weapons research on these toxins. So now not only are you sick from this toxin, but you are on the short list of domestic terrorism for not cleaning your bathroom.  On a side note, if you do decide to clean your bathroom with bleach, don’t mix it with ammonia since that will produce mustard gas and then the FBI will really be onto you.

Figure 2.  S. chartarum  growth behind

a shower wall.

By now, you’re probably terrified of your bathroom and have vowed to never take a shower again.  Don’t worry, it’s not as dangerous as it sounds.  Most black mold found in your shower is NOT S. chartarum.  Usually it is either a species of Penicillin or Aspergillus.  But you should still clean this up, since Aspergillus creates aflatoxin mycotoxins which are one of the most powerful carcinogens (5).  Usually large S. chartarum growth is the result of a flood or a pipe breaking.  However this doesn’t mean it’s not lurking in the walls behind your shower. So, if you ever experience water damage, be sure to check for S. chartarum growth in the walls immediately to avoid horrible future consequences.  If you think you can move far north to avoid this fungus, think again.  S. chartarum is present worldwide so no matter where you live, it’s important to be conscious of potential water damage or damp areas.  The reason it is found worldwide is the ability of spores to withstand harsh climate types.  While it grows best in humid environments, the pathological effects were first characterized by the Russians when S. chartarum contaminated straw in 1938.  The workers became sick within two to three days of exposure.  To identify the effects of the disease, the workers rubbed some of the fungus onto their arms.  So if you are feeling brave, try to characterize it without seeing an expensive specialist!

So to summarize, S. chartarum is a fungus which grows best on cellulose in a humid environment.  This makes it a big problem after water damage as the humidity allows the organism to grow rapidly.  It is disseminated into nature through the production of spores which are highly resistant to selective environments. The spores contain trichothecene mycotoxins which can cause sickness when inhaled. The mycotoxins are extremely stable and can withstand extreme environments. This makes them difficult to remove without the help of bleach.  Exposure to the toxins can result in general discomfort, but high doses of it can cause neurological disorders. For these reasons, you should listen to your mother and maintain a clean shower.  Even if the mold is not S. chartarum, other molds such as Penicillin and Aspergillus can cause illness as well.  Cleaning mold will prevent large scale home remolding projects from having to occur.  And most importantly, you will feel better!

References

1.     Andersen, B., Nielsen, K., Thrane, U., Szaro, T., Taylor, J., Jarvis, B. (2003) Molecular and phenotypic descriptions of Stachybotrys chlorohalonata sp. Nov. and two chemotypes of Stachybotrys  found in water-damaged buildings.  Mycologia; 95(6): 1227-1238.

2.     Fung, F., & Richard, C. (2004)  Health Effects of Mycotoxins: A toxicological Overview.  Clinical Toxicology; 42(2): 217-234.

3.     Jarvis, B., Sorenson, W., Hintikka, E., Nikulin, M., Zhou, Y., Jiang, J., Wang, S., Hinkley, S., Etzel, R., Dearborn, D. (1998) Study of Toxin Production by Isolates of Stachybotrys chartarum and Memnoniella echinata Isolated during a Study of Pulmonary Hemosiderosis in Infants.  Applied Environmental Microbiology; 64(10): 3620-3625.

4.     Murtoniemi, T., Nevalainen, A., Hirvonen, M. (2003).  Effect of plasterboard composition of Stachybotrys  growth and biological activity of spores.  Applied Environmental Microbiology; 69(7): 3751-3757.

5.     Yu, J., Butchoko, R., Fernandes, M., Keller, N., Leonard, T., Adams, T. (1996) Conservation of structure and function of the aflatoxin regulatory gene aflR from Aspergillus nidulans and A. flavus.  Current Genetics; 29(6): 549-555.

Trichomonads Knockout Round

by HL

The enigmatic world in which we live seethes with danger. Silent killers lurk around every corner, assassins strike from the inside out and armies of natural born attackers wait to be released. This is the world of disease-causing microorganisms. Each organism competes to win the title of the fittest, most reproductively successful. Nothing will stop them in the race for survival. In this arena, the time has come for the final round among a group of parasitic flagellated protozoans, the Trichomonads. Nature has weeded out the weak, and only the top contenders remain, each displaying its most convincing and deadliest attributes. Trichomonas vaginalis, emerging from the depths of the urogenital tract in humans, will compete against T. gallinae, a seasoned fighter in the upper intestinal tract of its columbiform hosts.

While each organism occupies a distinct niche, they share crucial characteristics that aid them in the difficult life of parasitism, such as a similar build. In the class of flagellated protozoans, they possess not one but five flagella, four of which protruding from the cell and aiding in locomotion. Though they lack power-producing mitochondria, they harbor an interesting organelle, the hydrogenosome. This organelle not only has the capacity to produce essential energy for the cell, but it contains powerful antioxidant potential, without which this anaerobic microbe would succumb to the noxious effects of oxygen. These fighting machines are equipped with a barbed tail, or axostyle, ready to do serious damage to the host by latching onto tissues, causing irritation and inflammation¹. Neither can live freely and therefore is vulnerable to the dangerous environment of its host, stashing clandestine mechanisms to elude the immune system of those it infects.

Image of T. vaginalis 

Let’s focus in on T. vaginalis. This contender is no small fry, weighing in with a hefty genome comparable in size to the human genome.² Within its genome are 60,000 protein-encoding genes organized into six chromosomes, which enable it to adapt to diverse environments and be prepared for changes in pH, temperature, iron and zinc levels³. T. vaginalis is a strong predator, engulfing bacteria, vaginal epithelial cells and erythrocytes by phagocytosis. It is loaded with an array of attack mechanisms including toxic chemicals or cytotoxins that blow holes in erythrocyte membranes. T. vaginalis is a sneaky invader, penetrating the next victim in synchronization with the sexual activities of its human hosts, allowing it to invade the vaginal tract in women and the urogenital tract in men. The parasite breaks through a formidable wall of mucus to latch onto the epithelial cells of the vaginal lining⁶. Once attached, the invader morphs into an amoeba, increasing contact with the vaginal epithelial and creating its own minienvironment where it is capable of manipulating the pH and other factors till it can produce enough toxins to lyse the cell³.

The offensive strategies are average in comparison with its mechanisms of defense. These tactics are crucial when the host fights back. Nonetheless, T. vaginalis infects 250 million globally each year and Trichamoniasis is responsible for over half of the reported STI infections ⁵. Its success may be due to its unique mechanism to remain undetected by the powerful immune system of humans. T. vaginalis effectively resists lysis by thwarting the activity of complement proteins that guard the precious host, wait to attack a foreign invader and bring in more troops to help fight. In addition, it is armed with protein cleavers which degrade human immunoglobulin secreted by the host to rid the parasite⁷. It can also destroy a line of defense provided by the secretory leukocyte protease inhibitors residing in the mucus, rendering the inhibitors non-functional⁸.

Despite all this, there are more obstacles to overcome. The vagina of a female human host is an inhospitable place, highly acidic and constantly changing due to the raging hormonal influence producing a thick menstrual flow. The cells in the vagina are constantly sloughed off so T. vaginalis must maintain its iron grip on the host, lest it be wiped away by the current. Why does this microbe tolerate this bombardment from a menstrual female? Despite the unfavorable conditions, the vagina is an iron oasis compared to the zinc rich protstatic fluids encountered in the male which are toxic to the helpless protozoan. In the vagina, there is a reducing environment, which actually activates some pathogenic mechanisms of T. vaginalis.

Burrowing in the depth of the nucleus of T. vaginalis, a seething accomplice waits to ambush the unknowing host. This parasite itself is infected with up to four species of viruses, the Trichomonavirus, which exclusively infects the Trichomonas genus. Each virus wreaks its own havoc within the cell, changing the heterogeneity in the expression of certain cell surface proteins causing an aggregation of cell masses to form a syncytia, which then lyses and dies, releasing the virus⁴. Surprisingly the virus and protozoan live in harmony; the former provides the latter with phenotypic variation of surface immunogens on the molecule. Proteins such as P270 which are only expressed in T. vaginalis infected with the dsDNA virus are localized by the iron rich environment to the surface and confuse the host immune system⁹. Targeting T. vaginalis with antifungal medication alone is futile, as the virus is then released, triggering a cascade of host alarm signals that inflame the infected area. The response to the virus renders the patient more susceptible to devastating pregnancy complications (especially preterm birth), HIV infection and HPV-related cancer⁵.

With T. vaginalis battling for dominance against its human host, T. gallinae steps up in a different arena as a dangerous enemy to the avian community. This parasite infects mainly columbiform birds, such as the common carrier pigeon but occasionally can take down the most majestic birds of prey and delicate song birds. Its ability to jump avian host taxonomic groups can have dramatic effects in an instant. Disease emergence caused by T. gallinae in finches in Britain in 2005 is a prime example of the rapid die off of whole populations caused by this single-celled parasite^10.

In parasitic combat, T. gallinae is one of the oldest players, with infections in wildlife dating back to the 1500s. This doesn’t mean that T. gallinae is worn out; conversely, it suggests that over time T. gallinae has been honed into a perfect killing machine. It lies in the alimentary tract of birds, and arises to form lesions in the mouths of its hosts. These rice crispy-like inflammations impede the birds from eating and induce dramatic starvation that ultimately leads to the bird’s untimely death. The parasite has an arsenal of cytotoxic mechanisms, including cysteine peptidases and other molecules that damage the target cell plasma membrane, blowing holes in erythrocyte membranes with perforin-like activity.¹¹

Drawing done by Chris Glen of the

University of Queensland.

T. gallinae’s hit list contains a notable creature. The protozoan may be responsible for the devastating destruction and extinction of all dinosaurs. In a recent study done by Wolff et al, the skull of the best preserved fossil of a Tyrannosaurus rex, commonly known as Sue, was examined to determine the most likely cause of the gaping holes on its mandibles. Previously, actinomycosis, a bacterial bone infection, or bite wounds from other tyrannosaurids were suspected as the culprit. However, examination of 10 other prehistoric species with similar markings provided evidence that this avian transmittable protozoan was the cause of the lesions and ultimately starvation due to the severity of the infection. How would a previously unsusceptible beast be taken down by this minute microbe? The answer may lie in the carnivorous slaughter and devouring of infected prey, although this side of the story remains concealed in the distant history of the now inexistent creatures¹².

Despite these compelling tales of strife, struggle, and survival in the face of adversity, a winner must be named. Will it be the human parasite T. vaginalis, the leading cause of sexual transmitted infections, or T. gallinae, the avian parasite accused of starving dinosaurs to extinction? Both represent current threats to life on earth, but T. vaginalis delivers a heavy blow to the human population. For the sake of anthropological bias, T. vaginalis walks away with the crown.

Works Cited

1. Petrin D, Delgaty K, Bhatt R, Garber G. Clinical and microbiological aspects of Trichomonas vaginalis. Clin Microbiol Rev. 1998 Apr;11(2):300-17.

2. Carlton JM et al . Draft genome sequence of the sexually transmitted pathogen Trichomonas vaginalis. Science. 2007 Jan 12;315(5809):207-12.

3. Djana F. Harp, Indrajit Chowdhury. Trichomoniasis: evaluation to execution European Journal of  Obstetrics & Gynecology and Reproductive Biology, Volume 157, Issue 1, July 2011, Pages 3–9 http://dx.doi.org/10.1016/j.ejogrb.2011.02.024

4. Isolates of Trichomonas vaginalis concurrently Infected by strains of up to 4 Trichomonasvirus species (Totiviridae). J. Virol. May 2011 vol. 85 no. 9 4258-4270

5. Fichorova RN, Lee Y, Yamamoto HS, Takagi Y, Hayes GR, et al. (2012) Endobiont Viruses Sensed by the Human Host – Beyond Conventional Antiparasitic Therapy. PLoS ONE 7(11): e48418. doi:10.1371/journal.pone.0048418

6. Elisa E. Figueroa-Angulo, Francisco J. Rendón-Gandarilla, Jonathan Puente-Rivera, Jaeson S. Calla-Choque, Rosa E. Cárdenas-Guerra, Jaime Ortega-López, Laura I. Quintas-Granados, M. Elizbeth Alvarez-Sánchez, Rossana Arroyo, The effects of environmental factors on the virulence of Trichomonas vaginalis, Microbes and Infection, Available online 25 September 2012, ISSN 1286-4579, 10.1016/j.micinf.2012.09.004.(http://www.sciencedirect.com/science/article/pii/S1286457912002213)

7. D. Provenzano, J.F. Alderete Analysis of human immunoglobulin-degrading cysteine proteinases of Trichomonas vaginalis Infect. Immun., 63 (1995), pp. 3388–3395

8.  Lehker, Biology of Trichomonads. Current Opinion in Infectious Diseases Issue: Volume 13(1), February 2000, pp 37-45

9. J.F. Alderete Iron modulates phenotypic variation and phosphorylation of P270 in double-stranded RNA virus-infected Trichomonas vaginalis Infect. Immun., 67 (1999), pp. 4298–4302

10. Robinson RA, Lawson B, Toms MP, Peck KM, Kirkwood JK, et al. (2010) Emerging Infectious Disease Leads to Rapid Population Declines of Common British Birds. PLoS ONE 5(8): e12215. doi:10.1371/journal.pone.0012215

11. Amin A, Nöbauer K, Patzl M, Berger E, Hess M, et al. (2012) Cysteine Peptidases, Secreted by Trichomonas gallinae, Are Involved in the Cytopathogenic Effects on a Permanent Chicken Liver Cell Culture. PLoS ONE 7(5): e37417. doi:10.1371/journal.pone.0037417

12. Wolff EDS, Salisbury SW, Horner JR, Varricchio DJ (2009) Common Avian Infection Plagued the Tyrant Dinosaurs. PLoS ONE 4(9): e7288. doi:10.1371/journal.pone.0007288