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Hiring a Lab Technician

7 Feb

I’m a Fatboy Slim fan, and when I decided to write today’s post, “Praise You” started playing in my head.  Besides the fact that I need to update my music taste, it reminded me that I want to thank all my faithful followers out there for waiting around for me to post again.

It’s been ages (2 years to the day) since I’ve posted and I salute you both.

Many things have changed since I was blogging last… I’m now the proud SciMom to two little rugrats, and a tenure-track faculty member at Wazzu.  [I feel somehow obligated to assert the obvious fact here that all opinions given in this blog are my own and have absolutely nothing to do with my university.]

That’s right folks, 2 virtual petri dishes that crawl and drool and snot all over the place, AND all the responsibilities of a brand-new, wet-behind-the-ears ass prof (assistant professor, for those of you confused about the abbreviation); I’m just a glutton for punishment.

This has given me a new-found sense of juxtaposition: freedom, weighed down by grant-writing; imagination, mired in the realities of funding priorities; and an awesome new job, potentially debunked at tenure-review time.

I, therefore, chose to attempt to squeeze into my painstakingly time-managed work-day schedule some time for fun-writing (aka, blogging).  The shape and form and overall thrust of this blog will largely remain the same – Microbes do, in fact, still rule the world, and I will continue to extoll their virtues.  However, I hope to also cover science and science events more broadly and may even share the odd job posting. (a clear transition into…)

With my very first blog as a new tenure-track faculty, I will shamelessly let you all know that I need to hire a lab technician.  I need someone with experience in soil microbiology and molecular biology, cultivation-dependent and independent techniques.  The pay is not particularly great to start and I can’t cover relocation costs, but the boss is usually pretty cool and she’s super enthusiastic about what she does.   And you should know that Eastern Washington/northern Idaho is not the big city, but rather the outdoor-enthusiast’s playland.  So, for the full job description and details, contact her directly.

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Dogs, Dust, and the Hygiene Hypothesis

7 Feb

ResearchBlogging.org Since I’m still only getting about 3 or 4 hours of sleep at night, extracurricular reading for this blog has to be uber-interesting to maintain my attention long enough to keep me from falling asleep halfway through the abstract.  Not to say that anything microbial isn’t particularly interesting, but the bar has been set a little higher now that I’m a SciMom, and baby girl likes to eat… a lot.

So, in looking for something exceptionally interesting to blog about this week, I stumbled on the perfect storm for today’s paper, which piqued my interest for several reasons that may or may not be obvious you folks out in readerland.   First, I just had a baby a few months ago and find myself continuously thinking I need to do more research on this or that which will affect the baby’s health and wellbeing.  Second, I have “indoor pets”, namely several German Shepherds (see the shamelessly cute photo below) and two cats.  Third, I was diagnosed with allergy-induced asthma when I was about 9 years old and have struggled with it ever since (you may be wondering at this point, why on earth I would have so many indoor pets if I have allergic asthma… just call me a glutton for punishment, but I love my dogs).

The unifying theme of the paper, however, and overarching interest for me is, of course, due to the very cool and omnipresent impacts of microbial ecology.

Exactly how microbial ecology plays a role in a study on prenatal and early childhood exposure to indoor pets and how that affects immunoglobulin E may not be overtly obvious, so let me explain.

What does hygiene have to do with it?

First, you need a cursory understanding of something called the “hygiene hypothesis”.  It’s pretty huge in the health news these days so I wouldn’t be surprised if you’re at least vaguely familiar with the concept.  Essentially, it’s the idea expressed beautifully by Rob Dunn in Eating off the floor: How clean living is bad for you.  The basic idea is that the more of our little microscopic friends that we are exposed to early in life, the healthier we are overall due to stimulation of our immune systems in a way that allows natural development and response to true pathogens.  Early exposure to a range of microbes is thought to essentially “teach” our immune systems what is good, safe, or at least not a threat, versus those organisms that can really make us sick and should be eliminated.

The slightly longer than 5-second rule...

If we live in an environment where everything is sterile (at least as much as possible), our air is filtered, antimicrobials are everywhere, antibiotics are over-prescribed, and we aren’t exposed to microbes and parasites, then our immune systems may begin to overreact to anything and everything regardless of the potential harm it might cause us. This would explain the rise in autoimmune disorders and asthma, some even include eczema and hay fever.

As cool as all that is, it is only a hypothesis at the moment, which means we need (lots) more evidence (a.k.a. data) to be able to assert these ideas as a theory, much less a fact (of course we all know that in Science, reaching the status of “theory” is as good as it gets… only the media and snopes assert “facts”).  And it’s even a fairly vague hypothesis at that.  We’re not sure which types of microbes we need to be exposed to, how many, at what times, and precisely which aspects of our immune system will or won’t be affected.

The word for the day: Pets

There is currently a lot of work ongoing around the globe to get at some of these different aspects of the hygiene hypothesis and hopefully begin to provide us with the data we need to assert that, in fact, microbial exposure is a good thing for the development of the human immune system.  One such study came out in 2010  in the Journal of Allergy and Clinical Immunology which compared the microbial communities in dust of homes with and without pets.  They proved what all us pet-owners already know, that the dust of homes with pets supported a much more diverse microbial population than the homes without pets.

Dust mite

In this most recent paper, Suzanne Havstad and her colleagues took this idea one step further.  They set out set out to provide more details of the dynamic interplay between these pet-based dust microbial populations and the human immune system.  This particular puzzle piece involved testing immunoglobulin E (IgE) levels in the blood of young children in response to their exposure, or lack thereof, to indoor pets.

What is IgE, anyway?

Admittedly, the various components of human immune system (and vertebrate biology, for that matter) are well outside the scope of my own training and expertise.  I will therefore refer you to the following article on Immunoglobulin E and this medical article on pediatric asthma (you’ll find the bits on the hygiene hypothesis in under “Pathophysiology”).

In a  nutshell, IgE is part of our immune system which is triggered by allergens and parasites in your environment, including worms.  It causes inflammation that helps your body defend against intruders and keep you healthy.  However, it’s also thought to play a very significant role in pediatric asthma since blood IgE levels in asthma sufferers are typically much higher than non-asthmatics.  Essentially, some people’s immune systems overreact to things like dust, pollen, dander, etc, which leads to excessive production of IgE which in turn causes inflammation of tissues in lungs and bronchial tubes and asthma (not being able to breathe) is the result.

What Suzanne Havstad and her colleagues were able to conclusively prove was that children who were exposed to indoor pets in utero or in their early years had significantly lower IgE levels than those who weren’t exposed to pets.  The more diverse microbial community of the homes with pets must be interacting with the children’s immune systems and fostering the lower IgE levels, right?  It’s certainly possible and makes all the sense in the world to somebody like me.

However, just because [A (pets) = B (more diverse dust  microbial communities)] and [A (pets) = C (lower IgE levels)], doesn’t necessarily in this case mean that B =C as well.  There could be any number of other factors for children in the homes with indoor pets that may or may not have been measured, such as lifestyle, diet, exercise, and exposure to other allergens or toxins in their environment.  These other factors could also be influencing IgE levels.

However, what makes this study more compelling is that they also found an effect of the child’s mode of delivery:  vaginally versus Cesarean section.   The reason I say that this makes the study more compelling is because it’s been found that infants delivered vaginally have an entirely different microbiome (indigenous microbial community) than those delivered by C-section.  This lends some weight to the idea that microbial populations influence IgE levels.

What does it all mean?

This study seems to doubly lend support to the idea than early microbial exposure impacts human immune

A shamelessly cute German Shepherd puppy.

response, particularly via IgE levels.   Indoor pets can clearly increase the diversity and abundance of the microbial populations of your household dust (not a fact, that in and of itself, I really want to spend a lot of time thinking about) and exposure to that dust may actually be a good thing, in moderation (i.e. we probably shouldn’t spoon-feed the dust to anybody), for children’s developing immune systems.  Take home message: every kid needs a dog, or a cat, or both, or to at least get a little dirty every now and then… which means my little girl has got this covered!
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Havstad, S., Wegienka, G., Zoratti, E., Lynch, S., Boushey, H., Nicholas, C., Ownby, D., & Johnson, C. (2011). Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Journal of Allergy and Clinical Immunology, 128 (4), 880-8850000 DOI: 10.1016/j.jaci.2011.06.039

Back at Blog

17 Jan

Ok, it’s been 8 months, 34 weeks, 241 days, loads of morning sickness, and one brand new baby since my last post, but I’m back to work and back at blog.

I can’t make any promises about the frequency of my posts in the new year, but I will do my best to keep up on comments and make some meaningful contributions to the science bloggosphere in the months to come.

Today, I ease into things with a re-post from one of my favorite microbial blogs, Small Things Considered over at the American Society for Microbiology blog site.

Have a look and consider (again – hopefully) this important question: The vast quantities of information and sequence data we gain from molecular techniques, without appropriate application and mindful interpretation, what does it really mean and where does it really get us in the end?

That Scary Restroom Microbiota

by Elio Schaechter and Joshua Fierer

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ASM New Orleans: Here we come!

19 May

The American Society for Microbiology 

Some of you may already be aware of the rapidly approaching 111th General Meeting of the American Society of Microbiology (ASM) in New Orleans, May 21st through the 24th.  I’m pretty excited to say this will be my very first opportunity to attend the ASM meeting.  This may be a little surprising considering the fact that if you have any idea what this blog is all about, you know that Microbiology is what I do, it’s what I study, immerse myself in, and it’s what I love.

So why on earth haven’t I attended one of these meetings before?  It just so happens that my work (study, love, etc) also falls within the realm of soils, biogeochemistry, environment, and ecology, as well.  Accordingly, over the course of my professional life to date, I have only attended soils, environmental, and ecological professional meetings.  I have been advised by colleagues in the past that the ASM meetings are extremely large and primarily catered to medical/clinical and basic microbiology crowds and that I would actually glean the most useful knowledge (for my particular line of work) from the more applied meetings.

My Agenda at the ASM Meeting

This year I decided to find out for myself about the ASM General Meeting (and blog it thoroughly).  I’ve taken it as my personal mission to track down and report on as much environmental microbiology (and microbial ecology) at the meeting as I possibly can.  My cover will be as a lowly postdoc presenting a poster on my most recent work with fungi and Pb-contaminated soils.  Wish me luck!

In the meantime…

I’ve heard some talk about the new way of doing things at this year’s meeting and thought I’d look into it a little beforehand.

At the inaugural meeting of ASM  in 1899, at the time called the Society of American Bacteriologists, there were roughly 30 professionals in attendance (Miller, et al. 2010).  In recent years you can expect upwards of 10 to 15 thousand attendees in any given year with a very wide range of areas of expertise, a veritable smorgasbord of high-tech vendors, and people from all over the world, from students and undergraduates to postdocs and profs, even true, historical icons.  However, the clinical microbiology community still accounts for roughly 1/3 of the meeting’s attendance.  Obviously, there have been some big changes in the society and this year’s dynamic platform is an attempt to adjust the design and flow of the meeting to accommodate the new demographic, while still meeting the needs of the core.

This year a new mission statement for the meeting was adopted by the Society: “The ASM General Meeting showcases the central role of microbes in the biosphere by communicating today’s cutting edge science in the diverse areas influenced by microbes.” (Miller, et al. 2010) Which actually sounds quite promising, if you ask me.

Apparently, one of the most dramatic changes to the general meeting involves the number and nature of session and includes a parallel meeting, specifically tailored to the needs of the clinical microbiology community entitled “Medical Microbiology Track.”  Not exactly my cup of tea, but to each his own.

Each morning there will be only 4 concurrent sessions focused on topics of broad interest, which is a reduction in the number of session since years past.  The goal is to “showcase” inspirational interdisciplinary science with minimal overlap and maximum appeal.

That all sounds well and good, (actually it sounds pretty fantastic and exciting to the incorrigible science dork), but we’ll have to see how it all plays out in the real world.

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ResearchBlogging.orgMiller JF, McFall-Ngai M, & Casadevall A (2010). A New Design for the ASM General Meeting. mBio, 1 (5) PMID: 21151775

Microbes Make it Snow

1 Feb

This post was chosen as an Editor's Selection for ResearchBlogging.orgThe recent snow and ice, and deeper snow, and even more ice, across much of the U.S. over the past few weeks have finally inspired me to put together my first post for the new year.  You’re probably wondering how on earth microbes have anything to do with the 3 feet of snow you had to dig your car out from under last week…  

…but hear me out.

Blowing in the wind

I have two “believe it or not” statements for today: First, believe it or not, microbes are ubiquitous in the Earth’s atmosphere (Bowers et al. 2009, and others).  “Ubiquitous” is a fantastic word that simply means “absolutely everywhere” and it’s especially true with microbes.  As a soil microbiologist, I immediately think of soils and sediments all over the globe and the wide array of fungi and bacteria that keep the planet green (and purple and red and brown), and it makes sense because there are so many things to eat in soils.  There’s a never-ending supply of nutrients from dead and decaying plants, worms, insects, other microbes, and even weathering rocks.  But I also know that out in the open ocean microbes are abundant and provide the foundation for the food chain, not to mention nutrient cycling and overall marine ecosystem health.  We’ve known these things for quite some time now (hence, my “microbe-centric” view of life). Our Microbial Planet Poster

What doesn’t always make sense to a terrestrial biologist is that microbes are also extremely abundant in the air around us, above and beyond our reach, floating in the breeze and being carried thousands of miles on trans-oceanic trade winds.   It’s true, though, and for years we assumed that these microbes must be in a sort of hibernation mode, because there’s nothing to eat, harsh conditions often including extreme dryness, cold temperatures and powerful UV radiation from the sun.  More recently, however,  we’ve begun to understand that only a portion of these airborne microbes are hibernating, while others remain active, usually bound in soil particles or cloud droplets (Sattler et al. 2001).  And as long as these little guys are metabolically active, they have the potential to make changes to their environment, even in the atmosphere.

Ice, Ice, Baby (sorry, I couldn’t help myself)

Which leads me to my second “believe it or not” statement for the day:  many of those atmospheric microbes have been found to nucleate ice (Bauer et al. 2003).  What I mean by “nucleate ice” is that they can serve as the starting point for ice crystals to begin to form.   What makes this really cool (pardon the pun) is that ice-nucleating microbes have been found to make specific proteins on the surface of their cells which catalyze the formation of ice crystals at relatively high temperatures.  This action not only allows the crystals to form outside the microbe, rather than inside where ice crystals would damage cellular membranes and kill the microbe, but the formation of these crystals also releases very small amounts of heat energy, keeping the microbe that much safer from freezing. 

Commercial snow-seeding material.

Commercially available snow-seeder.

You might have heard about these guys (indirectly) before if you’ve ever heard of “cloud seeding.”  There’s a commercially available freeze-dried preparation of ice-nucleating bacteria that many ski resorts will shoot up into the clouds to help encourage snowfall.  A slightly less well-known practice is the application of “ice-minus” bacteria to reduce crop loss due to frost.  In that case, growers have taken advantage of specific mutant bacteria which lack the genes for the ice-nucleating protein and spray these bacteria across the foliar surfaces so that ice won’t form as easily.  The idea here is that ice-nucleating bacteria are very commonly found on plant surfaces, and can lead to frost damage.  But those lacking the gene (called “ice-minus”) when applied to the plants, outcompete the natural bacteria, and reduce the formation of frost on plant surfaces.   

Atmospheric Microbes = Snow

How bacteria make up snowflakes.

Bacteria and snowflakes.

But these ice-nucleating bacteria exist all over the world, in the soil and in the air around us and may be affecting more than just the ski slopes and strawberries.  A very interesting study by a group of scientists out at the University of Colorado in Boulder recently looked specifically at ice-nucleating bacteria and how microbial abundances in the atmosphere may alter atmospheric conditions (Bowers, et al 2009).   In order to address this question, they took a number of air samples from the Storm Peak Laboratory at the top of Mt. Werner near Steamboat Springs, CO.  Their air samples contained over 640 different bacterial species (via genetic sequence), but their data indicated they did not even begin to sample the full diversity of the airborne microbial community.  Despite variable weather conditions during sampling, the total airborne microbial numbers remained stable and didn’t change throughout the sampling period.  However, with increasing relative humidity, there was a significant increase in ice-nucleating bacteria.  They found that the abundance of ice-nucleating bacteria was significantly greater in cloudy air samples, than in clear (or non-cloudy) air samples.  They even suggested that some bacteria may be able to respond to favorable (humid and cloudy) conditions and adjust their concentrations of ice-nucleating proteins, consequently increasing the ice-nucleation potential of these species.

Take-home message…

So, what does all this have to do with the massive downfall of snow and ice this season?  Well, as much as I love to blame global warming for more extreme weather events, we don’t have to connect a whole lot of dots to be able to believe that atmospheric microorganisms may be playing a role as well. 

The more people we have on the planet, the greater population densities become, and the more disturbance we cause to land surfaces, the more soil, dust, particulate matter, bacteria and fungi rise into the atmosphere and interact with our weather patterns.  Much the same way that cloud seeding works, it seems our activities down here are affecting the number of microbes and consequently cloud formation (bioprecipitation, if you will) up there.

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Bauer, H., Giebl, H., Hitzenberger, R., Kasper-Geibl, A., Reischl, G. Zibuschka, F., and H. Puxbaum. 2003.  Airborne bacteria as cloud condensation nuclei.  Journal of Geophysical Research, 108:4658.

ResearchBlogging.orgBowers, R., Lauber, C., Wiedinmyer, C., Hamady, M., Hallar, A., Fall, R., Knight, R., & Fierer, N. (2009). Characterization of Airborne Microbial Communities at a High-Elevation Site and Their Potential To Act as Atmospheric Ice Nuclei Applied and Environmental Microbiology, 75 (15): 5121-5130 DOI: 10.1128/AEM.00447-09

 

Griffin, D.W. 2004.  Terrestrial microorganisms at an altitude of 20,000 m in Earth’s atmosphere. Aerobiologia, 20:135-140.

Sattler, B., Puxbaum, H., and R. Psenner. 2001.  Bacterial growth in super-cooled cloud droplets.  Geophysical Research Letters, 28:239-242.

The Trouble With Triclosan

1 Dec

Just a few products you might find Triclosan in.

An article was released online Monday in Environmental Health Perspectives which surprised me. For the last five or six years I’ve been enthusiastically extolling the evils of triclosan in the environment, but the connection with human immune dysfunction really caught me by surprise, most likely because I’m a microbiologist (this is probably not news to all you toxicologists out there). As someone who suffers both indoor and outdoor allergies (including hayfever) as well as allergy-induced asthma, it’s no small thing for the authors to be able to say with such a level of confidence…

“… higher levels of triclosan were associated with greater odds of having been diagnosed with allergies or hayfever (p<0.01).”   Clayton, et al., 2010.

The mechanism of impact on the human immune system isn’t clear yet, but in reading the article I discovered that triclosan has been associated with not only endocrine disruption, but also central nervous system effects and thyroid problems for several years now.

This knowledge becomes particularly disturbing when you consider the fact that since it’s creation in the 1960’s, triclosan (also known by its more descriptive chemical name: 2,4,4’-trichloro-2’-hydroxydiphenyl ether) has been added to countless consumer products as an antimicrobial and preservative, including but certainly not limited to: hand soaps, laundry detergents, toothpastes, wound disinfection solutions, deodorants, facial tissues, plastic kitchen utensils, medical devices, and toys.

If a product’s label says “Antimicrobial” you can bet it contains triclosan or a triclosan derivative. Do a quick literature search and you’ll find we’re discovering new uses for it every month, incorporating it into plastics and personal care products of all kinds. Consequently, triclosan and its derivatives are now found in the urine and tissues of over 75% of all Americans, and in soils, sediments, and waterways all over the world.

Enter, environmental microbial populations.

What you might be thinking is that since triclosan is added to things for its antimicrobial properties, it must be wiping out hordes of bacteria and fungi, reducing their numbers worldwide… well, not exactly.

Some bacteria are naturally resistant to triclosan, like certain Pseudomonas species, while in others it actually causes mutagenesis (directed mutations) of their already existing resistance factors. What that means, is that bacteria have already developed a way to resist or survive a number of toxins, like heavy metals or salts, and when they are exposed to triclosan, their resistance factors actually adjust to treat triclosan in the same manner.

A great example would be common bacterial efflux pumps; these are mechanisms within the cellular membrane designed to “pump” a specific toxin right back out of the cell, where it can’t hurt the bacteria. When a bacterium is exposed to triclosan, these pumps go into over-drive and begin to pump out anything that remotely resembles an antimicrobial or antibiotic.

The tripartite efflux pump of Salmonella, which pumps out antibacterial drugs to foster multidrug resistance. Image: Cambridge Dept of Pathology.

There could hardly be a better use for the old adage, “What doesn’t kill us, make us stronger.”

 This type of triclosan-induced antimicrobial resistance has been proven in model species like E. coli, Salmonella enterica, Staphylococcus aureus, and Mycobacterium tuberculosis, but to date it’s been uncertain if these same effects are true of environmental species (common soil and water bacteria). Pycke, et al.(2010) set out to answer that question and their work was published in a recent article in Applied and Environmental Microbiology.

I guess the good news from their work would be that the species of environmental bacteria the authors tested (Rhodospirillum rubrum) was fairly sensitive to triclosan, and the concentrations needed to inhibit its growth and even kill this bacteria were similar to some of the most sensitive species that have been tested to date.

What this means to you: when you use an antibacterial soap to wash your hands, you’re probably killing off 90% of these types of bacteria on in your hands, i.e. they are very susceptible to high concentrations.

The not so good news is that under low-levels of triclosan exposure, the very same efflux mechanisms that I described above were able to confer resistance to these bacteria, and not just to triclosan, but also to a wide range of antibiotics including tetracycline, chloramphenicol, fluroquinolones, and others.

What this means to you: after you wash your hands with antibacterial soap, and that triclosan is diluted in water and washed out into your septic or local waste-water treatment plant, the environmental bacteria exposed to lower levels of triclosan are not killed, but essentially “turn on” their efflux pumps and become resistant to some of the most common antibiotics in use.

We used to think that a bacterium had to first be exposed to a specific antibiotic in order to become resistant to it (or at least one of his pals was exposed and passed on the genetic resistance); now we know that our own waste-streams, laden with chronic levels of the very antimicrobial products our culture clings to, are fostering even greater levels of antibiotic resistant bacteria in the environment.

To sum up

Two reasons not to buy or use products with antimicrobial chemicals like triclosan or triclosan derivatives:
1.) Increased incidence of hayfever, allergies, and immune dysfunction;
2.) Decimation of the human race by antibiotic resistant diseases. (ok, maybe that’s a little overblown, but you get the idea)

If the one doesn’t make you think twice, surely the other will.

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ResearchBlogging.org
Clayton, E., Todd, M., Dowd, J., & Aiello, A. (2010). The Impact of Bisphenol A and Triclosan on Immune Parameters in the US Population, NHANES 2003-2006 Environmental Health Perspectives DOI: 10.1289/ehp.1002883

Pycke, B., Crabbe, A., Verstraete, W., & Leys, N. (2010). Characterization of Triclosan-Resistant Mutants Reveals Multiple Antimicrobial Resistance Mechanisms in Rhodospirillum rubrum S1H Applied and Environmental Microbiology, 76 (10), 3116-3123 DOI: 10.1128/AEM.02757-09

Fungi that eat lead

19 Nov

This post was chosen as an Editor's Selection for ResearchBlogging.orgBioavailability = solubility (for the most part)

To discuss heavy metals (lead, nickel, mercury, cadmium, silver, copper, and so on) and how they can be detrimental to the environment or toxic to people, plants, or animals, we have to first posses a vague understanding of bioavailability and bioaccessibility.  These terms describe whether or not the substance in question can cross an organism’s cellular membrane, which allows the organism’s internal system access to the substance.

This might sound a little confusing at first, but if the toxin can’t get inside the organism, it can’t do damage (i.e. if the small child didn’t eat the paint flakes, he wouldn’t suffer from lead poisoning).  Whether or not a toxic heavy-metal can enter into the cells of a plant, microbe, and even a human, depends on the solubility of that metal, and the solubility of any given metal will change according to what it’s chemically bound with. For an entertaining visual demonstration of chemical bonding, I thought you might enjoy this video …

But seriously, bioavailability…

The child eating lead based paint is actually a good illustration of what I’m trying to convey here.  The lead typically found in lead based paint is lead carbonate or lead chromate, which means the lead is chemically bound with carbon and oxygen, or chromium and oxygen.  Humans cannot absorb that type of lead through our skin and therefore it isn’t toxic unless ingested, in which case our digestive processes dissolve the different lead-compounds and we absorb the lead into our systems.

However, lead nitrate is another story altogether.  In lead nitrate, the lead is bound with nitrogen and oxygen and is extremely toxic because it is highly soluble in water; we can absorb it through our skin fairly easily, so we don’t have to eat it for it to become bioaccessible.

Most of the time, bioaccessabilty and bioavailability, relate directly back to the solubility of a substance.  If it’s not soluble, it’s not bioavailable, and vice versa.  The more bioavailable a toxin is, the more dangerous it is, to us and the environment at large.

But what about the microbes…?

With all that in mind, I find it particularly interesting to know that various microorganisms found in the soils, sediments, and waters of contaminated sites (mines, smelters, spill sites, etc.) have been discovered over the last 50 years capable of converting insoluble metal compounds (such as lead carbonate) into more soluble forms.   These microbes are able to convert metals from relatively inert forms into readily available (often bioavailable) forms and have received much attention for their biotechnological applications, such as dissolving useful metals from metal ores (termed “bioleaching”).

In fact, in 1995, Geoffrey Gadd and his colleagues at the University of Dundee (Dundee, U.K.) developed a particularly useful method to screen soil fungi for their potential ability to solubilize heavy metals in the lab (Gadd et al, 1995).  They were able to incorporate any one of a variety of insoluble metal compounds into the agar of a Petri dish and measure the rate at which the fungus could dissolve the metals.  They tested the method using aluminum, cobalt, manganese and zinc and found many fungi from a common “garden soil” sample were able to dissolve insoluble zinc and cobalt just as quickly as they could grow and expand across the Petri dish.

A common fungus dissolves the highly insoluble lead carbonate as it grows across a Petri dish.

In my own experiments recently, I’ve tested this method and have a nice photo of a fairly common fungus (Aspergillus niger) literally dissolving lead carbonate, just like the lead carbonate found in lead-based paints. (photo at right)

This may initially seem like a bad thing… soil organisms turning relatively insoluble and inert metals into the more soluble, and consequently more bioavailable, forms.  But learning about the natural process and understanding how it all works actually affords science a new and developing tool in the ongoing struggle against contamination.  We can apply our knowledge to clean up efforts and remediation work on contaminated sites, and even biotechnology for lower-impact mining techniques.

Of course, we have a long way to go with the organisms I’m working on right now, but along the way they help us understand which contamination sites can cause the most dangerous types of human exposure and why.  It all comes back to how the toxins interact with the microbes in the soil!

So, back to the lab I go this afternoon to see how my other fungi are breaking down lead (or not) and converting metals from insoluble forms to the bioavailable forms (after I watch that chemical bonding video one more time for laughs!)

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ResearchBlogging.orgSayer, J., Raggett, S., & Gadd, G. (1995). Solubilization of insoluble metal compounds by soil fungi: development of a screening method for solubilizing ability and metal tolerance Mycological Research, 99 (8), 987-993 DOI: 10.1016/S0953-7562(09)80762-4