Superbugs: fighting the flood of antimicrobial resistance

Posted on 14 Nov 2017 by Barbara Kiser

Posted on behalf of Andrew Jermy

Enterobacter cloacae, Enterococcus faecalis, Staphylococcus epidermidis and the Superbugs exhibition.

Petri dishes with cultured Enterobacter cloacae, Enterococcus faecalis, Staphylococcus epidermidis and Escherichia coli at the London Science Museum’s Superbugs exhibition.{credit}® The Board of Trustees of the Science Museum{/credit}

Antimicrobial resistance has spread to London this month. The source of the outbreak? The Science Museum: its new exhibition, Superbugs, explores this monumental issue and our responses to it.

As Superbugs graphically shows, the inflammatory tone of the many headlines predicting an impending antibiotic apocalypse is not baseless. The evolution and spread of resistance among serious (and increasingly commonplace) bacterial infections continues to blunt much of our antibiotic arsenal, and make routine operations significantly more risky. Such infections now claim almost 700,000 lives annually, a figure that could rise to more than 10 million by 2050.

Superbugs isn’t out simply to scare, however. Much like Nature Microbiology, the journal I edit, the Science Museum aims to join the ‘resistance against resistance’ by shining a light on the problem’s scale, and the range of potential solutions.

The monumental ‘wall’ and towers at the exhibition.{credit}{credit}® The Board of Trustees of the Science Museum{/credit}{/credit}

The physical design of the installation aptly reflects aspects of the crisis. A vast illuminated wall dominates; set into it is a series of displays. This monolith, emblazoned with the show’s title, speaks of antibiotics’ barrier function — how they act as a great dam holding back a flood of infections. Standing in front of this cracked levee are 12 small towers into which have been set Petri dishes. Each contains a different type of (inactive) microbe, including MRSA and Neisseria gonorrhoeae — like outposts of resistance that have breached the barricade and now mingle among the crowds. It’s a powerful scene.

I was drawn irresistibly to the inset display cases. Combining text with striking visuals and interactive content, these take the visitor through medical history, from the discovery and introduction of antibiotics in the first half of the twentieth century, to the rise of resistance in the years following the introduction of each new drug, to ongoing efforts to revitalize our dwindling drug cabinet. Peppered through are personal testimonies. We meet doctors explaining why antibiotics are overprescribed; a nurse reminding of the fundamental importance of their work on infection control; designers who create products that enable no-touch use, or incorporate anti-bacterial materials, to reduce the risk of transmission.

Interviews with nurses, medics and others waging war on antibiotic resistance feature in the exhibition.

A display on the people at the frontline of ‘resistance against resistance’.{credit}® The Board of Trustees of the Science Museum{/credit}

We hear a recording of bacteriologist and discoverer of penicillin Alexander Fleming, describing how microbes can become ‘educated’ to resist a drug. A culture of Penicillium mold grown from a stock of his original sample is shown nearby. A video describes the harrowing experience of Geoffrey Pattie, a cancer patient who during surgery contracted a strain of Klebsiella pneumoniae resistant to all current antibiotics. He spent five months in an isolation ward, and today lives with the life-altering effects of the infection, such as reduced mobility.

Nearly half of antibiotic use occurs in agriculture, to treat and prevent infection in livestock, but often also to promote growth. The drugs and bacterial resistance genes that they select for become widespread in terrestrial and marine environments, giving a large potential reservoir from which resistance can leap into clinically relevant pathogens. Inevitably, that is a serious problem for human health. The show reveals some of the technological fixes that are being investigated, including automated systems for monitoring livestock welfare to allow targeted interventions rather than treating an entire herd prophylactically. Also presented are possible alternative approaches to tackling infections, such as phages (viruses that kill bacteria) sourcing new antibiotic leads from oceans, soils and host-associated microbiomes in humans, komodo dragons and leafcutter ants.

The promise of such efforts is stirring. But finding a new antibiotic class that will make it to the clinic is “like searching for a needle in a field of haystacks”, cautions one researcher interviewed.

The bacteria leafcutter ants use to defend their nests against fungi and microbes excrete chemicals that are effective antibiotics.

The bacteria leafcutter ants use to defend their nests against fungi and microbes excrete chemicals that are effectively antibiotics.{credit}® The Board of Trustees of the Science Museum{/credit}

What isn’t covered in much depth is the parlous state of the antibiotic R&D pipeline. Many large pharmaceutical companies have closed their antibiotic development programmes in recent years. That includes Pfizer, the main sponsor of the exhibit — although the company did announce in 2016 that it planned to acquire AstraZeneca’s antibiotics division, and reinforced a strategic focus on tackling infectious diseases. The economics of antibiotic discovery and development is complicated: to bring a drug to market takes a massive investment in time and finances. Yet we will need these new drugs to be used ever more sparingly in future. So, under the current system, there is actually a disincentive for industry to put in the necessary investment – they would never break even, let alone see a return.

Superbugs is doubly timely. This week (13-19 November) is the World Health Organization’s World Antibiotics Awareness Week 2017, an opportunity to take stock of progress. Antibiotic resistance, until recent years a concern only of clinicians and microbiologists, is now globally recognised as a crisis through the work of key individuals, such as Britain’s chief medical officer Sally Davies, and reports from national and international bodies. In 2016 this culminated in the UN High-Level Meeting on Antimicrobial Resistance (see this Nature Microbiology editorial).The rise in academic research and conferences focused on antimicrobial resistance is a positive sign that new approaches can and will be found, despite the issues with the pharma marketplace and the ongoing hunger for antibiotics in agriculture and medicine.

But we remain a long way from winning what the Science Museum describes succinctly as the “fight for our lives”. Hopefully this polished, fact-packed exhibition will call many more to arms — from the lay visitor to the family doctor, local farmer and political representative.

Andrew Jermy is chief editor at Nature Microbiology. He tweets at @jermynation.

Superbugs: The Fight for Our Lives is free, and at the Science Museum until spring 2019.

For Nature’s full coverage of science in culture, visit www.nature.com/news/booksandarts.

Graphic window on a refugee scientist

Posted on 28 Sep 2017 by Barbara Kiser

3Q: Erik Nelson Rodriguez

{credit}Erik Nelson Rodriguez/NPR{/credit}

Graphic artist Erik Nelson Rodriguez is an innovative comics journalist. With reporter Darryl Holliday, he began creating nonfiction stories in graphic-novel form at university, covering issues such as gun violence. In 2016, US National Public Radio (NPR) invited Rodriguez to collaborate on an account of Syrian refugee Nedal Said: a trained microbiologist and teacher, Said fled the war in 2013 and is now a researcher in Leipzig. The result, The Scientist Who Escaped Aleppo, is part of NPR’s special series on refugee scientists: a testament to the ordeals endured, and the extraordinary potential offered, by the refugee community.

What did you learn from working on this project?

I did not know much about the refugee crisis other than data I had researched for news graphics — statistics on people moving through the Mediterranean into Europe. Just seeing the astounding numbers trying to get away from war zones and how many did not make it past the sea affected me. But it wasn’t until I worked with NPR on Nedal Said’s story that I felt the full weight. To look, under a microscope, at the ordeal an individual has to go through to obtain a better life was a heavy lesson. I was shocked by the number of hurdles Nedal faced, whether escaping from detention or sleeping in parks in the frozen rain — and by how long he was away from his family as he travelled to find a new life for them. I also learned that there are programmes to help refugees trained in science. One is the Philipp Schwartz Initiative, a collective effort by Germany’s foreign office and other institutions named in honour of a Jewish scientist who fled Germany in 1933. I was pleased to find countries creating these opportunities for refugees to integrate after their harrowing journeys — especially when refugees are so happy to give back to that society.

Syrian microbiologist and teacher Nedal Said pictured before he fled the war in 2013.{credit}Erik Nelson Rodriguez/NPR{/credit}

How did you convey Said’s story visually?

NPR provided a timeline of Said’s travels from Turkey to the Balkans to Germany. It gave details about each location, along with interviews describing first-hand experiences. This formed the basis for the storyboard. It was important to me to show Nedal in his work and family life. He was described as always helping others through his scientific knowledge and skills as an educator, so we wanted to display him in those situations. We made sure that his family was highlighted: he was potentially sacrificing his life for them. I researched Aleppo during different periods to see what kind of destruction took place, and created panels featuring tanks, rifles, bullet-ravaged buildings. We re-edited the piece later to help things flow in a vertical comic strip. Aesthetically, I aimed to translate the grittiness and bleakness of the written material. I tried to convey the fear and dread of Said through his facial expressions. I used dark, somewhat sketchy lines to match the story’s tone, but kept a cartoonish quality as a subtle undertone. Working with the editors and researchers was really rewarding.

Said’s ordeals as a refugee were legion.{credit}Erik Nelson Rodriguez/NPR{/credit}

How can this kind of storytelling help refugees?

Seeing one individual’s journey to escape war and possible death will, I believe, help the public understand that these are just other people in very different circumstances. Having these stories told in detail with audio and visual representations will hopefully shed more light on how refugees struggle to escape the dark reality of their cities’ destruction. In particular, I hope that the public will understand better that without resources, people escaping war-torn countries do not have the opportunity to develop research, knowledge or a decent life, even if they are well educated. Yet the scientific community could gain from the experience and education of people such as Said, as they can provide original ideas developed thousands of miles away, adding fresh perspectives or processes. I hope visual storytelling can highlight these and other invisible parts of the world to show the public on the other side what they cannot see.

Interview by Leonie Mueck, a former senior physics editor at Nature and now division editor at PLOS ONE. She volunteers for the Cambridge Refugee Resettlement Campaign. She tweets at @LeonieMueck. This interview has been edited for length and clarity.

The Scientist Who Escaped Aleppo — on which Rodriguez worked with editors and researchers Meredith Rizzo, Rebecca Davis, Joe Palca, Madeline Sofia and Andrea Kissack — can be seen here in full. You can find information on future projects by Rodriguez and Holliday on their website.

For Nature’s full coverage of science in culture, visit www.nature.com/news/booksandarts.

Mutation rates of Mycobacterium tuberculosis: From the archives (2013)

Posted on 07 Apr 2017 by Catherine Potenski

Mycobacterium tuberculosis- credit: NIH-NIAID (CC-BY)

Continuing with our month-long celebration of Nature Genetics 25^thanniversary, I have chosen to highlight a study by Sarah Fortune and colleagues estimating mutation rate differences between different lineages of Mycobacterium tuberculosis published in June 2013.

Multidrug resistance in M. tuberculosis is a global problem, and understanding the origins and dynamics of the emergence of resistance is an important scientific and public health endeavor.

Building on their previous work that used whole genome sequencing to estimate mutation rates of M. tuberculosis during latent infection, the authors then went on to study the rate at which different strains acquire drug resistance mutations. Using classical fluctuation tests and measuring rifampicin resistance in both clinical and laboratory isolates, they determined the mutation rates for strains from lineage 2 and lineage 4, observing an order of magnitude difference between them, with lineage 2 having the higher rate. These lineage 2 strains also acquired resistance to other antibiotics (ethambutol, isoniazid) at a higher rate than lineage 4 strains.

The authors then sought to relate the in vitro data to the in vivo infection environment. They analyzed whole-genome sequences from a lineage 4 outbreak and determined the base substitution rate; the in vivo data were in concordance with the in vitro per-day mutation rate.

Finally, the authors took these data and developed a simulation model of the evolution of drug resistance during infection in a human host. They simulate the emergence of multidrug resistance and show that in the model, individuals infected with lineage 2 strains had a substantially higher risk of acquiring multidrug resistance mutations.

Using a combination of in vitro, clinical and simulated data, Ford et al. contributed to our understanding of the emergence of multidrug resistance, highlighting the differences between strains and underscoring the importance of timely and sufficient treatment.

A CRISPR screen for HIV targets

Posted on 21 Dec 2016 by Catherine Potenski

A new study published online this week in Nature Genetics reports the discovery of novel host targets of HIV infection identified from a high-throughput CRISPR/Cas9-based screen. This screen was performed in CD4 + T-cells and was designed to find candidate genes required for successful HIV infection, but whose inactivation did not affect cell viability. In this way, potential drug targets for anti-HIV therapy could be discovered.

Park et al., Nature Genetics 2016

The authors found two known (CCR5 and CD4) and three novel (ALCAM, SLC35B2 and TPST2) cellular factors that, upon abrogation, prevented HIV infection but did not have any negative effects on the cell itself. These new genes are involved in sulfation and cell aggregation pathways and represent candidate targets for interventional HIV therapy.

We spoke with first author Ryan Park to get some background on this research:

Previous screens for host factors affecting HIV pathogenesis found a high number of hits, with low reproducibility across screens. With your CRISPR/Cas9 approach, were you expecting similar results? Did the low number of hits in your screen surprise you?

We designed our screen stringently, as the existing literature has not been clear on what genes would potentially serve as good targets for host-directed anti-HIV therapies. Our goal was thus to identify these host factors with high confidence while maintaining an unbiased approach. The very low number of hits was certainly surprising, though, as you note, the limited overlap among the previous screens raised the suspicion of a high false positive rate and/or low reproducibility.

You find three novel genes that are dispensable for cell viability but that are needed for successful HIV infection. Do you think that there could be natural polymorphisms in these genes in human populations that might mitigate susceptibility to HIV entry and transmission?

In the Exome Aggregation Consortium (ExAC) dataset recently published in Nature, there are individuals with truncations and/or homozygous mis-sense mutations in each of the three genes, as well as ITGAL (the loss of which we find is protective against HIV infection in primary CD4+ T cells). More work remains to be done to determine whether these individuals are relatively less susceptible to HIV infection.

Due to the high mutation rate of HIV and the emergence of resistance to drug therapies, potential targeting of host factors can be a useful strategy. Do you envision these findings being utilized to develop novel anti-HIV therapies?

Host-targeted HIV therapies are of great interest for multiple reasons. Firstly, as you note, the emergence of drug-resistant HIV strains remains a major issue, particularly in settings where adherence to a daily antiretroviral regimen is challenging. Drug-resistant strains are less likely to emerge in the face of incomplete adherence to host-targeted therapies. Secondly, the identification of host factors may also serve as a basis for gene therapies (in which gene editing is used to produce a population of HIV-resistant target cells) that could result in a permanent HIV cure. As noted above, more work remains to be done to determine whether inactivation of these genes protects against HIV infection at the organismal level without causing detrimental effects.

How might this screen be adapted to find host factors important at other stages of the HIV life cycle and do you have future plans to explore such work?

Our screen captured all but the latest stages of the HIV life cycle (particularly virion assembly, budding, and maturation); this is because HIV Tat, which drives the GFP reporter in our cell line model, is expressed prior to these steps. Development of an alternative reporter system that is activated by virion budding or maturation would allow identification of host factors involved only at these late stages. Because completion of the HIV life cycle is not required for host cell killing by HIV, cells lacking these late-acting host factors may still not be captured in a screen; more importantly, these late-acting host factors may therefore not be attractive therapeutic targets.

Can this screening method be employed to find host factors important for infection by other viruses? Do you speculate that there would be viruses for which a large number of non-essential host factors would be identified as important for infection?

The key elements of our approach, which include identification of a physiologically relevant cell line and the use of a high-complexity genome-wide sgRNA library, can be readily generalized to identify host factors that are critical to the propagation of any viral pathogen yet dispensable for cell viability. Our findings suggest that the number of non-essential host factors that are critical for HIV infection is quite limited, and that many candidate host factors identified by other screens or targeted studies may not be required for HIV infection or may compromise cell viability. Whether this is the case for other viruses is hard to know, but we have demonstrated that our approach can be quite powerful and specific in identifying the range of potential host targets with high confidence.

Bacterial methylomes and antibiotic potentiation

Posted on 21 Mar 2016 by Catherine Potenski

Cohen et al., Nature Genetics, 2016

Antibiotics emerged as miracle drugs and “silver bullets” in the early 20^th century, revolutionizing medicine and our ability to combat infectious disease while positively impacting health and lifespans on a large scale. This remarkable triumph held steady for many years, and consequently antibiotic research and development diminished as a priority due to the seeming defeat of bacterial infections. However, the selective pressure that came with antibiotic exposure led to the development of bacterial resistance to these compounds, motivating renewed interest in what is now an extremely important public health issue. Mechanisms of resistance are many and ever-evolving, and we know now that it is not a matter of IF bacteria will become resistant to a class of antibiotics, but when. The search for new and potentially exploitable bacterial vulnerabilities, then, becomes a constant enterprise in order for us to keep pace with the bacteria in the antibiotics/resistance arms race.

Cohen et al., Nature Genetics, 2016

A new study this week in Nature Genetics describes how manipulating the bacterial DNA methylome affects susceptibility to multiple classes of antibiotics. The authors observed that deleting the dam gene, encoding a DNA methyltransferase, from E. coli causes increased susceptibility to sub-lethal doses of the β-lactam antibiotic ampicillin. Dam specifically methylates GATC sites, and deletion of any of the other three DNA methyltransferases found in E. coli had no effect on the level of antibiotic susceptibility. Using SMRT sequencing, the authors saw that genome-wide GATC methylation patterns did not change after exposure to ampicillin, so they sought alternative explanations for the observed phenotype. Continue reading →

Red blood cell production relies on white blood cell help

Posted on 17 Mar 2013 by Kevin Jiang

Red blood cell production in the bone marrow is a precarious process. Too few RBCs and you can become anemic; too many and you could be suffering from polycythemia vera, a rare, so-called ‘myeloproliferative’ genetic disorder marked by an abnormally high RBC count. Now, researchers have identified a surprising player in the regulation of RBC production under these disease conditions. Reporting online today in Nature Medicine, two independent teams describe the pivotal role of macrophages—amoeba-like white blood cells responsible for digesting harmful foreign microbes and removing old or dying cells—for generating RBCs in both anemic and over-proliferative conditions.

In one study, geneticist Stefano Rivella and his colleagues at the Weill Cornell Medical College in New York administered a drug that selectively kills macrophages in a mouse model of polycythemia vera. In these mice, RBCs are generated at almost twice the normal amount, leading to viscous blood, enlarged organs and increased risk for strokes and heart disease. The drug, called clodronate, appeared to cure these symptoms, however, drastically lowering macrophage population and bringing RBC counts back to normal levels compared with a control group of animals treated with saline.

These findings were independently confirmed by Paul Frenette, a stem cell biologist at the Albert Einstein College of Medicine, also in New York. His team used a genetically modified mouse in which macrophages expressed a gene that made them vulnerable to a toxin and arrived at similar conclusions. “When we depleted macrophages in this disease, we actually corrected the disease,” Frenette says. “Maybe this could be a new therapy for this type of disease, which is unexpected.”

Continue reading →

From tumors to tapeworms: parasite’s genome points to new uses for cancer drugs

Posted on 13 Mar 2013 by Yevgeniy Grigoryev

On the map: Taenia solium {credit}Shutterstock{/credit}

Commonly used cancer drugs could be repurposed to help eliminate tapeworm infections, according to the first full genome analysis of the human gut pathogen.

A team led by Matthew Berriman, a geneticist who studies parasites at the Welcome Trust Sanger Institute in Hinxton, UK, sequenced the genomes of three human-infective tapeworm species as well as a fourth tapeworm that lives in the intestines of rats and mice. Their analysis, published online today of Nature found that among more than 1,000 gene products that are predicted to be druggable in the parasite responsible for echinococcosis—a disease that affects an estimated 2–3 million people worldwide—more than 200 already have existing therapies (many in the oncology space) that block them.

“By providing reference genomes for these tapeworms, the study lays the foundation for the identification of new potential drug targets to kill the worms,” says P’ng Loke, a microbiologist at the New York University Langone Medical Center who was not involved in the study.

The cancer link makes sense given the life cycle of the tapeworm, notes Berriman. People typically ingest the parasite as eggs or larvae that then migrate to the host’s intestines where they develop into adult tapeworms. “When larvae infiltrate tissues and organs and cause large proliferating growth, [it’s] like metastasizing cancer,” he says.

The potential for new pharmacological interventions doesn’t end there, though. The genome map also revealed that the tapeworm’s parasitic lifestyle has led to a number of gene losses and molecular simplifications that could provide a wormy Achilles’ heel. Thanks to evolution, for example, tapeworms have lost genes involved in oxidative stress response, making them reliant on just one enzyme for this kind of cell detoxification.

Fortunately, drug repurposing could prove successful here, too. The tapeworm enzyme involved in oxidative stress, called thioredoxin glutathione reductase, is the target of multiple drugs that have been shown to kill blood flukes and flatworms. “We have identified clear vulnerabilities in the pathways the parasites rely on,” Berriman says.

Michael Brockhurst

Posted on 25 Mar 2010 by Corie Lok

University of Liverpool, UK

An evolutionary biologist marvels at how species evolve to help each other out.

Mutualistic interactions between species underpin much of nature’s biodiversity. These associations range from prolonged and intimate, such as those between nitrogen-fixing bacteria and leguminous plants, to fleeting — visits of pollinating animals to flowers, for example. Despite the wide-ranging importance of mutualisms, there have been few experimental studies on their origins or evolution.

In a fascinating experiment, Kristina Hillesland and David Stahl at the University of Washington in Seattle watched a novel two-species interaction develop from teetering baby steps to a stable, robust mutualism over just 300 generations (K. L. Hillesland and D. A. Stahl Proc. Natl Acad. Sci. USA 107, 2124–2129; 2010).

Grown in the lab with lactate as the sole nutrient source, the bacterium Desulfovibrio vulgaris and the archaeon Methanococcus maripaludis, which never interact in nature, had to collaborate to survive. D. vulgaris fermented lactate to produce acetate, carbon dioxide and hydrogen — a reaction that sustains growth only if the hydrogen concentration is kept low. M. maripaludis fulfilled this requirement by consuming hydrogen to reduce carbon dioxide to methane.

Communities were initially poorly adapted to do this, and underwent drastic fluctuations in population size, with some even going extinct. In other communities, however, natural selection ensured that the two processes were optimized, thereby jointly increasing the fitness of both species. Co-evolved communities outperformed their evolutionary ancestors by growing 80% faster and producing 30% more biomass.

The work demonstrates the evolution of a stable multispecies mutualism, enhancing our understanding of how such interactions, so important for biodiversity, come about in nature.

Monica Gotta

Posted on 13 Jan 2010 by Corie Lok

University of Geneva Medical School, Switzerland

A cell biologist connects her research to bacterial brain invasion.

My main interest is in understanding how some cells organize their structure and components asymmetrically — a property called cell polarity. When I moved to my current job in a medical faculty I was asked to teach a course on infectious diseases. So I was very excited by the publication of a paper from Mathieu Coureuil at the University of Paris Descartes and his colleagues that brings together my passion and my teaching activity. The work shows that a bacterial pathogen can reach the brain by destroying cell polarity (Coureuil, M. et al. Science 325, 83–87; 2009).

Few bacteria are able to cross the blood–brain barrier, and it is not known whether those that can do so by moving through or between cells. The bacterium Neisseria meningitidis can cross this barrier. It adheres to cells lining the brain’s blood vessels using type IV pili — hairlike appendages that connect the bacterium to the interior of these endothelial cells.

Using human brain endothelial cells and N. meningitidis in culture, Coureuil et al. show that a complex of polarity proteins — Cdc42, PAR6, PKC and PAR3, which form tight junctions between endothelial cells — are recruited to the site of bacterial adhesion. This results in depletion of these proteins at the junctions and thus the formation of gaps between infected cells.

Although this study was performed in cultured cells owing to a lack of suitable animal models, it strongly suggests that N. meningitidis enters the brain by disrupting the junctions between cells — allowing the bacteria to squeeze in between them — and not by penetrating the cells themselves.

This elegant paper unveils a route that may also be used by other pathogens that cross the blood–brain barrier. It also underscores an important function of cell polarity: protecting our brain from infectious diseases.

Julian Davies

Posted on 12 Sep 2007 by Corie Lok

University of British Columbia, Vancouver, Canada

A microbiologist wonders where diversity comes from.

Recent estimates indicate that the total number of bacteria in the biosphere approaches or exceeds 10 to the power 31. A major goal of microbiology is to understand what creates their diversity and how it is maintained.

Having trained as an organic chemist, I came to appreciate microbial diversity through the extravagance of small molecules that microbes produce. This reflects a diversity in microbial metabolism, which one might expect to have evolved as a result of the (organic) richness of the organisms’ environments. But a couple of recent publications present findings that do not sit easily with this view.

Our first inkling of the huge diversity of the microbial world came from the use of ribosomal-RNA typing in the late 1980s. In the 1990s, this morphed into the expanding field of metagenomics, which is now providing catalogues of microbial communities from diverse terrestrial and marine environments.

One comparison of such catalogues showed that the seemingly bare and boring Arctic tundra exceeds fertile forest soils in phylogenetic content (J. D. Neufeld and W. W. Mohn Appl. Environ. Microbiol. 71, 5710–5718; 2005). A more recent study compared information from more than 100 different environments, finding that the microbial content of soils is generally less diverse than that of sediments and hypersaline environments (C. A. Lozupone and R. Knight Proc. Natl Acad. Sci. USA 104, 11436–11440; 2007).

I am looking forward to seeing what happens when the Human Microbiome Project gets under way. What variety of microbes is there to find living within us? What are they all doing? In what way will the population depend on diet? Given that we don’t yet seem to understand the relationship between diversity and ecology, I am making no predictions.

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