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What Doesn’t Kill Microbes, Makes Them Stronger

Here is the article I presented in class, check the media library for my lecture slides.

What Doesn’t Kill Microbes, Makes Them Stronger

by Martin Enserink on February 11, 2010 6:02 PM | Permanent Link | 12 Comments

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If you are taking antibiotics, your doctor will admonish you not to skip any pills and to continue the treatment even after you start to feel better. That’s because failure to kill the bugs making you sick can cause some of them to become resistant to the antibiotics. Now, a new study explains how nonlethal antibiotic concentrations can lead to resistance. The drugs trigger the release of so-called reactive oxygen species (ROS) inside bacteria, which in turn cause mutations in the bugs’ DNA–including some that happen to cause resistance.

Traditionally, the development of antibiotic resistance–a big and growing problem in medicine–has been seen as a passive phenomenon. Haphazard mutations occur in bacterial genomes, and bacteria randomly swap genetic elements. Every now and then, a mutation or a bit of newly acquired DNA enables the microbes to detoxify antibiotics, pump them out of the cells, or render them harmless in another way. When these microbes are exposed to antibiotics, natural selection will allow them to outcompete the ones that aren’t resistant.

But in the past 6 years, a different view has emerged, says microbiologist Jesús Blázquez of the Spanish National Research Council in Madrid. Researchers have discovered that mutation rates in bacteria sometimes go up in response to stress, in some cases promoting resistance. And studies by Blázquez and others have shown that the antibiotics themselves can cause this phenomenon, called hypermutability.

The new study, led by systems biologist James Collins of Harvard University explains how this is possible. A few years ago, Collins’s group discovered that antibiotics can trigger the production of ROS, also known as free radicals, which can cause mutations in DNA. At high levels, the group discovered at the time, these mutations helped kill the microbes. But what about nonlethal doses of antibiotics, the researchers wondered. Could they, through the release of ROS, trigger the very mutations that make bacteria resistant?

To find out, the group treated Escherichia coli bacteria with low levels of the antibiotics norfloxacin, ampicillin, and kanamycin. The drugs increased levels of ROS, the team reports today in Molecular Cell. Using a simple procedure to estimate the number of mutations occurring in a cell culture, the team found that higher ROS levels led to higher mutation rates in the bacterial genomes–up to an eightfold rise in the case of norfloxacin. Next, they showed that low-level treatments did indeed trigger resistance–in many cases, not just against the drug itself, but to a whole series of other antibiotics as well.

The probable explanation, says Collins, is that antibiotics create a “whole zoo of mutants” in a bacterial population–including some that happen to be resistant to one or more drugs. The findings could have a practical upshot, Collins says. For instance, if researchers could find molecules that prevent hypermutability, they could be combined with antibiotics to prevent or delay resistance.

The paper provides more evidence that antibiotics aren’t just selecting certain mutations, but causing them, says molecular geneticist Susan Rosenberg of Baylor College of Medicine in Houston, Texas. “And they have shown that the mechanism involved is the release of reactive oxygen species,” she says. The paper also reinforces just how versatile microbes are, Blázquez adds. “Again, it seems that bacteria use adversity as a stimulus to adapt to almost everything,” he says.

Scientists Identify Opium Poppy Codeine and Morphine Genes



Discovery raises possibility of manufacturing painkillers more cheaply using vats of microbes rather than fields of flowers

Ian Sample, Science Correspondent 

The Guardian, Monday 15 March 2010


Scientists have identified the two genes in opium poppies which are used to make codeine and morphine, two of the most important painkillers in a doctor’s armoury.

The discovery opens the door to alternative ways of making the drugs which do not involve giving over vast areas of farmland to growing the flowers. One hope is to transfer the genes into microbes, which could be grown in vats and provide huge quantities of the drugs at a fraction of the cost of farming and processing the plants.

Researchers said the findings could lead to the creation of strains of opium poppies that cannot make morphine, the opiate chemical turned into heroin and exported from Afghanistan and other countries for illicit use.

More than 2,500 hectares of British fields have been turned into opium poppy farms to meet NHS demands for morphine, a potent painkiller that was first isolated in 1806. The flower variety, Papaver somniferum, has been grown commercially in the UK since 2002 and differs from the common red flower, which does not contain morphine.

Pharmaceutical companies extract the drugs by processing seed pods stripped from the flowers, producing an annual national yield of codeine and morphine of 100 tonnes. Some 27m pills containing codeine are sold over the counter every year in a painkiller market worth £500m.

A team led by Peter Facchini at the University of Calgary, in Canada, identified the two genes used to make codeine and morphine from out of 23,000 in the opium poppy. The finding, reported in the journal Nature Chemical Biology, ends a 50-year quest.

“The evolution of these two genes in a single plant species has had such a huge impact on humanity over the past several thousand years,” said Facchini. “Our discovery allows this unique genetic power to be harnessed.”

Microbes are already used by the medical industry to mass produce synthetic insulin for diabetics and steroids for treating rheumatoid arthritis.

Last year, Tasmania’s attorney-general, Lara Giddings, raised concerns over the impact of opium poppy farms on wildlife. Farmers in the country, the world’s largest producer of legal opium, reported that wallabies had been hopping around in circles after eating the plants.

In 2008, the European Union’s drug agency warned that Britain faced a heroin crisis following a record harvest of poppies in Afghanistan, which accounts for 90% of the world’s illicit opium. By blocking one of the genes, scientists said they could create a strain of poppies that produce codeine but do not go on to convert this into morphine, the source of heroin.

This would “allow the direct recovery of codeine from the plant and prevent the formation of morphine, which would preclude the illicit synthesis of heroin,” the scientists write in the journal.


My thoughts and criticisms: 

This article was very informative and touched on many different issues that this discovery could effect. I liked that it did not merely report on the financial gains that artificial production of these drugs can have, but also the sociological and environmental as well. Also, these gains are relevant to a variety of people, not just those in the health and science professions. The article did not go into great detail about the actual discovery of the genes, but they quoted Facchini and gave a historical backdrop to the discovery which I thought was also beneficial. 

However, I did have some problems with the article. There was no mention on the potential effect on the farmers that legally grow opium. In places such as Tasmania, the worlds largest producer of legal opium, many farmers and other various workers could lose their jobs if morphine and codeine were suddenly only produced in labs. Also, the addition of the issue of illegal poppy growing in Afghanistan and the subsequent heroin problems in Great Britain was unnecessary. Firstly, the plan to somehow go to Afghanistan and plant poppies that do not yield opium is far fetched at best. Even if they did plant these poppies, this does not entail that all opium producing poppies would suddenly vanish. Here, it appears as if the writer is stretching too far to have an emotional impact on the reader; giving the impression that this discovery will eventually lead to a huge decrease in heroin production and use in their own backyard. This discovery will not be a ‘miracle cure’ to the problems of illegal drug trade and addiction. Also, it is not addressed whether this lower cost of producing these drugs will have a financial impact on the consumer, or just the pharmaceutical company that can now make even more money. As well,  if it is now easier to make opium and if it is cheaper will there be a greater influx of these drugs into our society? This could be a serious problem, and it was not addressed in the article. Perhaps most importantly is the sheer fact that this discovery has just been found, so it is still not altogether clear if it is possible to artificially create these drugs, therefore all of these effects could not materialize at all. 


Annelise Dowd



Whiter laundry and a surprising new treatment for kids’ eczema

Whiter laundry and a surprising new treatment for kids’ eczema

Treatment of Staphylococcus aureusColonization in Atopic Dermatitis Decreases Disease Severity

Science Centric | 27 April 2009 13:32 GMT

It’s best known for whitening a load of laundry. But now simple household bleach has a surprising new role: an effective treatment for kids’ chronic eczema.

Chronic, severe eczema can mar a childhood. The skin disorder starts with red, itchy, inflamed skin that often becomes crusty and raw from scratching. The eczema disturbs kids’ sleep, alters their appearance and affects their concentration in school. The itching is so bad kids may break the skin from scratching and get chronic skin infections that are difficult to treat, especially from methicillin-resistant Staphylococcus aureus (MRSA).

Researchers from the Northwestern University Feinberg School of Medicine have discovered powerful relief in the form of diluted beach baths. It’s a cheap, simple and safe treatment that drastically improves the rash as well as reduces flare-ups of eczema, which affects 17 percent of school-age children.

The study found giving paediatric patients with moderate or severe eczema (atopic dermatitis) diluted bleach baths decreased signs of infection and improved the severity and extent of the eczema on their bodies. That translates into less scratching, fewer infections and a higher quality of life for these children.

The typical treatment of oral and topical antibiotics increases the risk of bacterial resistance, something doctors try to avoid, especially in children. Bleach kills the bacteria but doesn’t have the same risk of creating bacterial resistance.

Patients on the bleach baths had a reduction in eczema severity that was five times greater than those treated with placebos over one to three months, said Amy S. Paller, M.D., the Walter J. Hamlin Professor and chair of dermatology, and professor of paediatrics, at the Feinberg School. Paller also is an attending physician at Children’s Memorial Hospital.

The study will be published in the journal Pediatrics 27 April.

‘We’ve long struggled with staphylococcal infections in patients with eczema,’ Paller said. She noted more than two-thirds of eczema patients have evidence of staphylococcus on their skin, the bacteria that most commonly causes infection and worsens the eczema. ‘This study shows that simple household bleach, which we think decreases the staphylococcus on the skin, can help these children.’

In the study, Paller and researchers treated 31 paediatric patients (6 months to 17 years old) who had eczema and a bacterial staph infection for 14 days with oral antibiotics. Half of the patients received bleach in their bath water (half a cup per full standard tub), while the other half received a look-alike placebo. Patients were also instructed to put a topical antibiotic ointment or placebo control into their nose (where the staphylococcus can also grow) for five sequential days of each month. All were instructed to bathe in the bleach twice a week, and soak for five to 10 minutes for three months.

Paller said bathing in the diluted bleach bath water was surprisingly odor-free because of the small amount of bleach added. ‘In our clinics, no one had the just-out-of-the-swimming pool smell,’ she said.

The research team saw such rapid improvement in the kids taking the real bleach baths that they terminated the study early because they wanted the children getting the placebo to get the same relief.

‘The eczema kept getting better and better with the bleach baths and these baths prevented it from flaring again, which is an ongoing problem for these kids,’ Paller said. ‘We presume the bleach has antibacterial properties and decreased the number of bacteria on the skin, which is one of the drivers of flares.’

Northwestern researchers launched the study to confirm their hunch about the potential of bleach baths, ‘since bleach has been used by hospitals in the past few years as a disinfectant to decrease MRSA,’ Paller said.

One interesting finding in the study was the eczema on the body, arms and legs improved dramatically with the bleach baths, but the face, which was not submerged in the bath, did not improve, further evidence of the positive effect of the bath.

As a result of the study, Paller suggests that kids who have eczema on their face close their eyes and mouths and dunk under the water to help improve the lesions. In her practice, patients have found that even daily bleach baths are well tolerated. The bleach baths may also be useful for individuals with frequent staphylococcus infection, whether related to eczema or not, and in adults with eczema and recurrent infections.

To help treat a rising number of severe cases of eczema, Northwestern’s Feinberg School has recently opened an Eczema Care and Education Centre.

The new centre offers patients one-on-one instruction for treating eczema, while a support group helps patients and their families cope with the emotional aspects of the disease.

‘This is a disorder that can drive people crazy,’ said Peter Lio, M.D., director of the Eczema Care and Education Centre and an assistant professor of dermatology and of paediatrics at the Feinberg School. ‘Eczema beats people down.’

Lio said he just worked with an 11-year-old girl who had missed a half-year of school because of her severe eczema. ‘As we were working with her and demonstrating how to treat her skin, she started weeping,’ he said. ‘Between the tears, she said ‘I’m crying because I know I’m going to get better.’ ‘

Scientists believe eczema may be triggered by urban pollutants and toxins and/or allergies, and certainly shows a genetic tendency. ‘We don’t have all the answers and are still learning about this disease,’ Lio said.

Read More at: from the original journal.

My Thoughts:

Overall, I thought it was a very well written article and has some beneficial information that may really help children with severe eczema.  I liked how it is a method that is attempting to treat bacterial-related diseases and disorders without using antibiotics to try to get rid of the harmful bacterial strains. I think that it is an accurate study and has a lot of research and trials that have gone into testing to see if the treatment is beneficial or not.

I think that the study needs to determine the optimal treatment and dosage of the bleach, however in the meantime I think that the bleach baths are worth trying for patients that have severe eczema.  Although it will probably never cure eczema for everyone, there will certainly be a number of patients who will benefit a lot.

I also think that there should be some additional studies done to assess the effectiveness and long-term safety of bleach baths with a greater number of patients.  If they find that it is a safe way to kill the bacteria, they they should find an easy and inexpensive way that anyone can go and get so they can do it at home themselves.  Finally, I think that they should measure quantitatively the reduction in bacterial numbers with this treatment.

UBC Scientist Purifying Mine Waste with Bacteria

Scientists in B.C. are looking to tiny creatures to help find a better way to clean up pollution from some of the province’s biggest mining operations.

The creatures are heavy-metal-eating microbes, and they’re being used to process the toxic byproducts produced over decades by the Teck Resources Limited zinc and lead mine in the city of Trail.

A wetlands system brimming with metal-hungry bacteria is one way to clean up dangerous substances without using harsh chemicals.

But the tiny life forms are not completely reliable.

“They don’t necessarily work properly,” admits Sue Baldwin, an associate professor of chemistry and biological engineering at UBC.

But after 10 years and a lot of biological tweaking, they are working properly at the Trail site, about 650 kilometres southwest of Calgary.

Some of the bacteria actually eat heavy metals while others help remove the arsenic and cadmium from the water.

Baldwin is trying to learn from the Teck example to help other mine sites try similar methods.

‘Like gardening’

“It’s very much like gardening,” said Baldwin. “It’s sometimes more like an art than a science.”

The science involves figuring out which microbes are doing what. It’s a difficult task because the bacteria are microscopic and there could be thousands of different kinds working together.

“Isolating each microbe, and sequencing its genome … would take forever,” said Baldwin. “We try to capture the ‘metagenome’ of the whole community.”

Metagenomics is a new area of biology that involves examining at the DNA of many organisms at once so scientists can build an overall picture of which genes are working, and which might be causing pollution of their own.

“In solving one environmental problem, we don’t want to create another one,” said Baldwin.

Baldwin said mining companies around B.C. and in other parts of the world are keeping an eye on her research, as the industry strives for greener ways to clean up after itself.

My thoughts:
I think that this is a good idea, and that it benefits society and cleans the environment. This also benefits the organisms living in environments polluted by mine waste. The problem with the article is that there were no studies showing whether or not this purification process works well. It was also stated in the article that the bacteria “don’t necessarily work properly” and that it took over 10 years of tweaking to get these microbes to start working correctly, so it seems a bit inconsistent.

Microbial answer to plastic pollution?

ScienceDaily (Mar. 31, 2010) — Fragments of plastic in the ocean are not just unsightly but potentially lethal to marine life. Coastal microbes may offer a smart solution to clean up plastic contamination, according to Jesse Harrison presenting his research at the Society for General Microbiology’s spring meeting in Edinburgh.

The researchers from the University of Sheffield and the Centre for Environment, Fisheries and Aquaculture Science have shown that the combination of marine microbes that can grow on plastic waste varies significantly from microbial groups that colonise surfaces in the wider environment. This raises the possibility that the plastic-associated marine microbes have different activities that could contribute to the breakdown of these plastics or the toxic chemicals associated with them.

Plastic waste is a long-term problem as its breakdown in the environment may require thousands of years. “Plastics form a daily part of our lives and are treated as disposable by consumers. As such plastics comprise the most abundant and rapidly growing component of man-made litter entering the oceans,” explained Jesse Harrison.

Over time the size of plastic fragments in the oceans decreases as a result of exposure to natural forces. Tiny fragments of 5 mm or less are called “microplastics” and are particularly dangerous as they can absorb toxic chemicals which are transported to marine animals when ingested.

While microbes are the most numerous organisms in the marine environment, this is the first DNA-based study to investigate how they interact with plastic fragments. The new study investigated the attachment of microbes to fragments of polyethylene — a plastic commonly used for shopping bags. The scientists found that the plastic was rapidly colonised by multiple species of bacteria that congregated together to form a ‘biofilm’ on its surface. Interestingly, the biofilm was only formed by certain types of marine bacteria.

The group, led by Dr. Mark Osborn at Sheffield, plans to investigate how the microbial interaction with microplastics varies across different habitats within the coastal seabed — research which they believe could have huge environmental benefits. “Microbes play a key role in the sustaining of all marine life and are the most likely of all organisms to break down toxic chemicals, or even the plastics themselves,” suggested Mr Harrison. “This kind of research is also helping us unravel the global environmental impacts of plastic pollution,” he said.

My comments:

I have a couple concerns about this article:

One is that it seems to overstate the imminence and assuredness of this ‘solution.’ In the opening paragraph, the author says the idea “may offer a smart solution to clean up plastic contamination.” But as you read on, it’s clear that they are nowhere near to having a workable solution. They are only in the very preliminary stages of identifying the bacteria that might breakdown plastics:

The researchers […] have shown that the combination of marine microbes that can grow on plastic waste varies significantly from microbial groups that colonise surfaces in the wider environment. This raises the possibility that the plastic-associated marine microbes have different activities that could contribute to the breakdown of these plastics or the toxic chemicals associated with them. (emphasis mine)

I would have appreciated them putting it into context with a timeline. What still needs to happen before this plan would be workable? How long might it take to get to there? Years? Decades? What is the best case scenario for how long it might take? What is the worst case? What do marine biologists expect to happen to the ecosystem in the meantime? (In other words, will it be ready in time to prevent mass extinction?)

I feel like we’re just starting get some traction on getting people to reduce plastic; I’d hate people to read a headline like “Microbes to be used for breaking up plastics” and think to themselves: “Cool, problem solved.”

Click here for the original article.

Microbial Threat Lists: Obstacles in the Quest of Biosecurity?

Arturo Casadevall and David A. Relman

Abstract | Anxiety about threats from the microbial world and about the deliberate misuse of microorganisms has led to efforts to define and control these dangers using lists and regulations. One list with tremendous legal implications and a potentially huge impact on research is the Select Agents and Toxins List, which was created by the US Government to limit the possession of and access to particular microorganisms and toxins. In this article, in addition to highlighting general problems with taxonomy-based, microorganism-centric lists, we discuss our view that such lists may have the paradoxical effect of increasing the societal vulnerability to biological attack and natural epidemics by interfering with the sharing of microbial samples and hindering research on vaccines and therapeutics.

Humankind has a delicate and intricate set of relationships with a microbial world of astonishing diversity. In recent times, these relationships have become increasingly strained, reflecting the emergence of new pathogens as agents of naturally occurring disease as well as the possibility that some microorganisms could be deliberately used to cause harm. Faced with this situation and the imperative of developing public-health countermeasures, it is a natural desire to begin to organize, categorize and prioritize these threats. A common feature of such efforts is the generation of a list, sometimes in rank-descending order on the basis of importance or some other metric. A list gives the appearance that one has bounded and specified an issue or problem and can suggest or define priorities. But lists are, by their nature, incomplete and, more impor- tantly, they can inappropriately limit creative or broad thinking as well as subtly mislead viewers into organizing their world view in

a narrow and biased manner. Today, research, resource investment

and public health strategies in microbiol- ogy and infectious diseases have been co-opted and commandeered to a degree that is unprecedented in history by a few lists, most notably by the Select Agents and Toxins List (SATL). The implications of this are potentially profound and not entirely beneficial. In this Science and Society article, we explore the ramifications of the SATL for microbiology and microbiologists. Our goal is to identify and discuss the positive and negative aspects of microbial threat lists and to provide recommendations for maximiz- ing the benefits and minimizing the detri- ments of such lists. Although we focus here on the SATL, the problems that we discuss are generic and pertain to all lists of biologi- cal agents and toxins that are created for the purposes of regulation and prioritization of resource allocation. Examples of other lists are the Australia Group List and the National Institute of Allergy and Infectious Diseases Category A, B, and C Priority Pathogens List.

The Select Agents and Toxins List

Beginning in the 1990s, laws and regula- tions to control the access to and the use of particular microorganisms and their products were formulated in the shadow of terrorist acts against the United States and other countries, with the goal of reduc- ing the risk to society of deliberate attacks with biological agents. These efforts were preceded by the Biological Weapons and Toxins Convention of 1972 that sought to achieve an international ban on the use of microorganisms and toxins in warfare. One result of those laws and regulations in the United States was the generation of a list of organisms that now carry the designa- tion ‘Select Agents and Toxins’ (for more information, see the National Select Agent Registry website). Other nations and inter- national organizations have carried out similar actions or have at least contemplated doing so. The current SATL is jointly admin- istered by the US Department of Health and Human Services and the US Department of Agriculture and contains approximately 80 microbial agents and toxins, defining them, de facto, by their taxonomic name.

The inclusion of a microorganism on the SATL imposes substantial regulatory restric- tions on the access to and possession and distribution of this organism1. For example, to work on microorganisms that are present on the SATL, institutions must register with the US Government, and individuals with access to these organisms must undergo background checks that can be highly intrusive and time consuming. A regula- tory framework is now in place that imposes strict protocols on how such microorganisms are accessed, transported, maintained and disposed of, with violations carrying consid- erable penalties. The inclusion of a micro- organism or toxin on the SATL is based on the consideration of several criteria, includ- ing its effect on human health, its contagion potential and the availability of vaccines and therapeutics. The SATL is reviewed regularly to include and exclude microorganisms and toxins on the basis of new developments.

Benefits and drawbacks

The laws and regulations that gave rise to the SATL were intended to provide a potential benefit to society by both restricting access to certain microorganisms and creating a legal infrastructure for the prosecution of individuals who are found to be in possession of these organisms without proper registra- tion. To fully appreciate the benefits and drawbacks of the SATL, it is important to note the distinction between biosafety and biosecurity. Biosafety is defined by the WHO as the containment principles, technologies and practices that are implemented to prevent unintentional exposure to pathogens and toxins or their accidental release2. By contrast, biosecurity is defined as the protec- tion, control and accountability for valuable biological materials (including information) in laboratories in order to prevent their unauthorized access, loss, theft, misuse, diversion or intentional release2. Although biosafety and biosecurity are related, and fre- quently confused by both the public and sci- entific community, these two terms differ in the crucial criterion of intent. In this regard, it is essential to note that the SATL is prima- rily an instrument of biosecurity. These laws bypass the thorny issue of intent by assum- ing that unregulated possession of these agents is in itself a threat to society regard- less of intended use, and they thus provide society with a powerful prosecutorial tool for law enforcement. It can be argued that the SATL-associated regulations also mitigate risk from biosafety concerns by imposing

a strict regulatory environment on labora- tories working with such microorganisms. However, in the United States, guidance for issues such as reducing the likelihood of accidents involving pathogenic micro- organisms and using the correct laboratory practices for handling microorganisms are derived from biosafety regulations3 that

do not have the regulatory authority of the SATL. Thus, the contribution of the SATL to public biosafety, if any, is modest and primarily limited to immediate laboratory personnel, as (with the exception of variola virus) many of the agents on the SATL, such as Bacillus anthracis, Coccidioides spp. and Francisella tularensis, are not contagious. For microorganisms that no longer circulate in the environment in a disease-causing form, such as variola virus, or that are difficult to obtain from natural sources, such as Ebola virus, the SATL makes an important poten- tial contribution to biosecurity by greatly restricting access to these agents.

For agents that can be recovered from the environment or endemic regions or that can be synthesized in the laboratory by individuals with microbiological knowledge, the possible contributions of the SATL to biosecurity are less obvious. The fact that the organisms in the US anthrax letters of 2001 presumably originated from a federal labora- tory facility4 has provided a powerful justi- fication for the oversight of laboratories that handle such agents. However, B. anthracis causes recurring outbreaks of veterinary anthrax in North America, where the organ- ism can be recovered from animal carcasses5. Similarly, Burkholderia pseudomallei, another bacterium on the SATL, can be readily recovered from the environment in endemic regions6. Hence, restricting access to such microorganisms through their inclusion on the SATL could reasonably be assumed to pose a hindrance to their acquisition for nefarious uses, but these regulations cannot be expected to stop determined individu- als from obtaining these organisms from environmental sources.

The security of society also requires a vigorous research enterprise, as knowledge is essential for defeating potential threats by the creation of diagnostics, vaccines and new therapies. In this regard, the SATL is a potential double-edged sword, and one can appreciate a paradoxical scenario in which the absence of these countermeasures increases the likelihood that an agent is included on the SATL, but such counter- measures may not be forthcoming if the reg- ulations interfere with the relevant medical research that is needed. The causative agent of soybean rust, Phakopsora pachyrhizi, was removed from the SATL for reasons that included the urgent need for timely research on effective means to manage this disease7; this effectively acknowledged the potential detrimental effect of the ‘Select Agent’ desig- nation on the research that is needed to con- trol such microorganisms. Furthermore, the cost to society of burdensome regulations could extend to work on health problems other than the intended diseases associated with the agents themselves. For example, some agents on the SATL, such as botulinum toxin, ricin and anthrax toxins, have thera- peutic uses in neurological disorders and cancer8. Regulations that inhibit research with certain microorganisms could reduce preparedness against future nefarious or natural outbreaks with that agent and could conceivably interfere with the development of therapies against other conditions that rely on products from such organisms.

Unfortunately, there are no good metrics with which to quantify work that is not car- ried out as a result of burdensome regulations, but it is reasonable to posit that as regulations proliferate so investigators who have a choice are more likely to work in less restricted areas of science. As choice in science is often a feature of academic and scientific success, the notion that some of our most capable sci- entists could opt to work in areas of research that have fewer burdensome regulations raises troubling issues for our future preparedness against biological weapons and certain emerging infectious diseases.

In short, the authors of this article, Dr. Casadevall and Dr. Relman, discus some of the implications of compiling and publishing lists of microorganisms and toxins which could potentially be used as biological weapons. On the one hand, they argue that by recognizing these toxins and microorganisms as potential threats to humanity, institutions  such as the US Department of Health and Human Services have the means to safeguard people’s safety due to their restrictive and punitive policies on accessing and handling those agents. On the other hand they state that, for scientists, the difficult access to such agents hinders the purposes of scientific research to improve diagnostics, vaccines, and treatments for human health conditions that might or might not be directly related to toxins and microorganisms listed as potential bio threats.

I think the article offers a valid criticism regarding the offset of this particular kind of preventive measure against terrorism. First, if agents are included in microbial threat lists based on their effect on human health, its contagion potential, and the availability of vaccines and therapeutics, how can one decrease the likeness that some microbes and toxins might become potential threats if studies aimed to develop vaccine and improve therapeutics are discouraged? As far as we can see, policy has not been tailored to the needs of the general public and the scientific community refraining scientists from doing their work. Second, restricting access to stored biological agents does not prevent the individuals from synthesizing the same organisms or obtaining them from environmental sources. Such is the case of B. anthracis, which according to the article, this microorganism causes recurring outbreaks of veterinary anthrax in North America.

Overall, measures taken towards biosecurity should not be limited to grouping agents and toxins in microbial threat lists. Effective countermeasures against these selected pathogens should also be prioritized by developing antimicrobial drugs and vaccines and finding methods to restore or promote health across the globe at affordable rates, paying special attention to those who are immunocompromised individuals.

Hannali J

Beware the Myth of Grass-Fed Beef

Cows raised at pasture are not immune to deadly E. coli bacteria.

By James E. McWilliams

Posted Friday, Jan. 22, 2010, at 7:24 AM ET

On Monday, Huntington Meat Packing Inc. recalled a whopping 864,000 pounds of beef thought to contain a particularly nasty strain of E. coli bacteria called O157:H7. Coming shortly after the recall of 248,000 pounds of beef by National Steak and Poultry on Christmas Eve—and dozens of other scares over contaminated beef and pork—this latest news reminds consumers yet again that the mass production of meat can be very dangerous indeed.

Consumers who still have an appetite for burgers and sirloins have been pushed toward alternative food sources. In particular, they’ve started to seek out more wholesome meat from animals raised in accordance with their natural inclinations and heritage. According to Patricia Whisnant, president of the American Grassfed Association, there’s been a dramatic rise in demand for cattle reared on a pasture diet instead of an industrial feed lot. Grass-fed beef should account for 10 percent of America’s beef consumption overall by 2016, she says—a more than threefold increase from 2006.

The comparative health benefits of grass-fed beef are well documented. Scores of studies indicate that it’s higher in omega 3s and lower in saturated fat. But when it comes to E. coli O157:H7, the advantages of grass-fed beef are not so clear. In fact, exploring the connection between grass-fed beef and these dangerous bacteria offers a disturbing lesson in how culinary wisdom becomes foodie dogma and how foodie dogma can turn into a recipe for disaster.

Could grass-fed beef ever be afflicted with the sort of E. coli O157:H7 outbreak that led to the December recall? Not according to the conventional wisdom among culinary tastemakers. This idea rose to the top of the journalistic food chain in the fall of 2006, when food activist Nina Planck wrote about the bacteria strain on the op-ed page of the New York Times. At that time, people were getting sick from bad organic spinach, but the contamination seemed to have originated with herds of conventionally raised cattle that lived upstream. Not every animal excretes this nasty type of E. coli, she argued. “It’s not found in the intestinal tracts of cattle raised on their natural diet of grass, hay, and other fibrous forage. No, O157 thrives in a new—that is, recent in the history of animal diets—biological niche: the unnaturally acidic stomachs of beef and dairy cattle fed on grain, the typical ration on most industrial farms.”

The Times speaks, the world listens. Planck’s appraisal of grain- vs. grass-fed beef was highlighted on the Web sites for the Organic Consumers Association, the Center for a Livable Future, Grist, and, among other enviro-foodie venues. A few months later, Hannah Wallace of Salon warned that “a cow’s corn diet can also make us sick” on account of the acidic environment it creates for bacteria. Even Michael Pollan, perhaps the most widely read food writer on the planet, explained in a New York Times Magazine piece, “The lethal strain of E. coli known as 0157:H7 … was unknown before 1982; it is believed to have evolved in the gut of feedlot cattle.” These animals, he added, “stand around in their manure all day long, eating a diet of grain that happens to turn a cow’s rumen into an ideal habitat for E. coli 0157:H7.”

For many consumers, the case was closed: To avoid E. coli O157:H7, just eat grass-fed beef.

Unfortunately, the scientific evidence tells a very different story. Planck’s assertion seems to be based on a 1998 report published in the journal Science. In this study, the authors fed three cows a variety of diets in order to ascertain how feed type influenced intestinal acidity in cows and, in turn, how intestinal acidity influenced the concentration of acid-resistant strains of E. coli. They hypothesized that these strains would be especially dangerous to humans, since they could survive the low-pH environment of the human stomach. It turned out that grain-fed cattle did indeed have a much more acidic stomach than those fed grass or hay. And sure enough, they had a million times more acid-resistant E. coli in their colons.

This was good news for grass-fed beef: Eliminate grain from a cow’s diet and you’ll keep its intestines from getting too acidic and spawning dangerous, acid-resistant bacteria. There was only one catch. The authors of the Science piece never specifically tested for E. coli O157:H7. Instead, they guessed that the pattern of O157:H7 growth and induction of acid-resistance would mirror that of E. coli strains that are always living in the colons of cattle. If this assertion were true, E. coli O157:H7 would reach dangerous levels only in gastrointestinal tracts of grain-fed cows.

But between 2000 and 2006, scientists began to take a closer look at the effect of diet on E. coli O157:H7 specifically. A different set of findings emerged to indicate that this particular strain did not, in fact, behave like other strains of E. coli found in cattle guts. Most importantly (in terms of consumer safety), scientists showed in a half-dozen studies that grass-fed cows do become colonized with E. coli O157:H7 at rates nearly the same as grain-fed cattle. An Australian study actually found a higher prevalence of O157:H7 in the feces of grass-fed rather than grain-fed cows. The effect postulated (and widely publicized) in the 1998 Science report—that grain-fed, acidic intestines induced the colonization of acid-resistant E. coli—did not apply to the very strain of bacteria that was triggering all the recalls.

What might explain this discrepancy? Scientists wondered whether there could be two subtypes of E. coli O157:H7 with varying degrees of acid-resistance. By that logic, the microbes from the grass-fed guts would be less resilient—and therefore less dangerous—than the ones that were growing up in the cows reared on grain. So they started running tests to find out.

In 2003, a research team from the University of Idaho reported no difference at all in the levels of acid resistance between E. coli O157:H7 from grass- and grain-fed cattle. (In both cases resistance was high.) Their conclusion stands in direct contrast to the broad claims about grain diets that have been made in the popular press since 2006. It must be that some other factor or factors were responsible for the development of E. coli O157:H7.

We don’t yet know what these might be. But four studies, published between 2003 and 2005, have developed an intriguing hypothesis. Maybe, some reasoned, E. coli O157:H7 behaves differently from other strains because it develops in a different part of the cow’s intricate digestive system. Sure enough, O157:H7 turned out to have a strong tendency to congregate in the recto-anal junction, whereas most other E. coli tend to gather primarily in the colon. Given that, we might presume that the production of E. coli O157:H7 depends more on its unique location than on what its cow host happens to be eating.

The point in dredging up these studies—ones the media never covered—is not to play gotcha with advocates of grass-fed beef. (As mentioned above, grass-fed beef may be healthier than conventional beef over all, and kinder to the animals.) Instead, it’s a warning that advocacy for a trendy food choice might result in a public health hazard. Such a fear is confirmed by consulting the cooking directions provided by many purveyors of grass-fed beef. The home page for one major producer explains that “cooking ‘real food’ is not the same as cooking concocted food. … Grass-fed meats are best when raw (steak tartar), rare, or medium rare.” Given that the FDA recommends cooking ground beef to 160 degrees to guarantee safety from E. coli, this eat-it-undercooked advice could be dangerous.

When it comes to the intricacies of our food system—and especially the meat industry—what’s true one day can be less true the next. A case in point involves the final FDA report (PDF) on the source of the 2006 E. coli O157:H7 outbreak that motivated Planck to write her seminal Times op-ed. Released in March 2007, it suggests that the spinach wasn’t contaminated by grain-fed, industrial cattle. Rather, the culprits were more likely to have been wild pigs or pastured (i.e., grass-fed) cattle—animals that were, of course, doing nothing more than eating what they were meant to eat.

Einstein researchers discover 2 new ways to kill TB

Findings could help tame extremely drug-resistant strains

Researchers at Albert Einstein College of Medicine of Yeshiva University have found two novel ways of killing the bacteria that cause tuberculosis (TB), a disease responsible for an estimated two million deaths each year. The findings, published in the March 21 online issue of Nature Chemical Biology, could lead to a potent TB therapy that would also prevent resistant TB strains from developing.

“This approach is totally different from the way any other anti-TB drug works,” says William R. Jacobs, Jr., Ph.D., the study’s senior author and professor of microbiology & immunology and of genetics at Einstein, as well as a Howard Hughes Medical Institute investigator. “In the past few years, extremely drug resistant strains of TB have arisen that can’t be eliminated by any drugs, so new strategies for attacking TB are urgently needed.”

Tuberculosis is caused by the bacterial species Mycobacterium tuberculosis. In searching for a new Achilles’ heel for M. tuberculosis, Dr. Jacobs and colleagues focused on an enzyme called GlgE. Previous research had suggested that GlgE might be essential for the growth of TB bacteria. GlgE would also be an excellent drug target because there are no enzymes similar to it in humans or in the bacteria of the human gut.

The GlgE research revealed a previously unknown enzymatic pathway by which TB bacteria convert the sugar trehalose (consisting of two glucose molecules) into longer sugar molecules known as alpha glucans – building blocks that are essential for maintaining bacterial structure and for making new microbes through cell division. GlgE was the third of four enzymes involved in this pathway leading to alpha glucans molecules.

Sure enough, when the researchers inhibited GlgE, the bacteria underwent “suicidal self-poisoning”: a sugar called maltose 1-phosphate accumulated to toxic levels that damaged bacterial DNA, causing the death of TB bacteria grown in Petri dishes as well as in infected mice.

“We were amazed when we knocked out GlgE that we saw this DNA damage response,” says Dr. Jacobs. “That’s usually a very effective way to kill bacteria, when you start damaging the DNA.”

The researchers discovered a second way of killing TB after observing a crucial connection between their novel alpha glucan pathway and a second pathway that also synthesizes alpha glucans.

When the researchers knocked out one of the other enzymes in their novel pathway, the pathway’s shutdown didn’t kill the bacteria; similarly, inactivating an enzyme called Rv3032 in the second alpha glucan pathway failed to kill the microbes. But inactivating both of those enzymes caused what the researchers term synthetic lethality: two inactivations that separately were nonlethal but together cause bacterial death.

“The bacteria that cause TB need to synthesize alpha glucans,” notes Dr. Jacobs. “And from the bacterial point of view, you can’t knock out both of these alpha glucan pathways simultaneously or you’re dead. So if we were to make drugs against GlgE and Rv3032, the combination would be extremely potent. And since TB bacteria need both of those alpha glucan pathways to live, it’s very unlikely that this combination therapy would leave behind surviving bacteria that could develop into resistant strains.”

Dr. Jacobs adds that findings from this study could also enhance treatment of diseases caused by other species of mycobacteria. Leprosy, for example, which still occurs in the U.S. and other countries, is caused by a mycobacterium related to TB. Treating leprosy now involves using several different drugs, some of which are also used to treat tuberculosis.

The group’s paper, “Self-Poisoning of Mycobacterium tuberculosis by targeting GlgE in an a-glucan pathway,” appears in the March 21 online edition of Nature Chemical Biology. In addition to Dr. Jacobs, other Einstein researchers involved in the study were Rainer Kalscheuer, Ph.D., Brian Weinrick, Ph.D., and Karolin E. Biermann, M.S. Other researchers include Karl Syson and Stephen Bornemann, John Innes Centre; Zhen Liu and James C. Sacchettini, Texas A&M University; and Usha Veeraraghavan and Gurdyal Besra; University of Birmingham in the United Kingdom.

Albert Einstein College of Medicine has filed a patent application on the discoveries described in the paper.

About Albert Einstein College of Medicine of Yeshiva University

Albert Einstein College of Medicine of Yeshiva University is one of the nation’s premier centers for research, medical education and clinical investigation. During the 2009-2010 academic year, Einstein is home to 722 M.D. students, 243 Ph.D. students, 128 students in the combined M.D./Ph.D. program, and approximately 350 postdoctoral research fellows. The College of Medicine has 2,775 full time faculty members located on the main campus and at its clinical affiliates. In 2009, Einstein received more than $155 million in support from the NIH. This includes the funding of major research centers at Einstein in diabetes, cancer, liver disease, and AIDS. Other areas where the College of Medicine is concentrating its efforts include developmental brain research, neuroscience, cardiac disease, and initiatives to reduce and eliminate ethnic and racial health disparities. Through its extensive affiliation network involving five medical centers in the Bronx, Manhattan and Long Island – which includes Montefiore Medical Center, The University Hospital and Academic Medical Center for Einstein – the College of Medicine runs one of the largest post-graduate medical training programs in the United States, offering approximately 150 residency programs to more than 2,500 physicians in training. For more information, please visit
Deirdre Branley | Source: EurekAlert!
Further information:

“Caring for Ourselves if like Caring for the Planet”

“Caring for ourselves is like caring for the planet”

By David Suzuki and Faisal Moola

Ecosystems come in all shapes and sizes, often without distinct boundaries. And what happens in one ecosystem affects other ecosystems.

We can even consider the human body as an ecosystem, or perhaps more correctly as a number of interrelated ecosystems. According to a recent article in the scientific journal Nature, “The human body is one of the most important ecological study sites of the coming decade.”

The article’s author, David A. Relman, chief of infectious diseases at Veterans Affairs Palo Alto Health Care System in California, writes: “Humans depend on the microbial communities that colonize them for a surprising suite of benefits. These include: extracting energy from food, educating the immune system and protection from pathogens. Yet, despite the recent attention to this indigenous microbiota, we are relatively ignorant of what our ‘extended self’ comprises or how it works.”

If we didn’t have microbes, which are mainly bacteria, living in and on us, we wouldn’t be able to digest our food or breathe properly, and we’d be more vulnerable to numerous types of disease and infection. Scientists estimate that our bodies contain 10 times as many bacteria as human cells, numbering around 100 trillion, and that the human gut alone contains 500 to 1,000 species of bacteria.

The microbes that help our body function properly are referred to as “normal flora” or “microbiota”. But, like all ecosystems, our body’s ecosystems can be disrupted. If we pollute our bodies, either intentionally or unintentionally, the normal flora can become overwhelmed to the point that they don’t function as well as they should. Sometimes this may result simply in a case of upset stomach or indigestion, but often, especially if the pollution is ongoing, it can result in serious disease and death.

What we expose our bodies and the microbes within them to can also have unintended consequences. Although antibiotics have offered a lot of benefits to human health, we’re now seeing that decades of their use, often as “growth promoters” in feed for chickens, hogs, and cows, is leading to new illnesses and infections as sometimes-harmful bacteria evolve to be resistant to antibiotics and to our own microbial defences.

The more we learn about the microbial communities in our own bodies, the more we see that a balance must be maintained, for our own sake and for the sake of our human communities. According to New York microbiology professor Martin J. Blaser, “evolution has selected for those microbial populations that maintain and increase the fitness of both individual hosts and the group as a whole.”

If we want our own bodies to be healthy, we must ensure that we have access to wholesome food, clean water, and good air. And we should avoid exposing ourselves to anything that would negatively affect the health of our own cells or the microbes that keep those cells healthy.

This is really no different than what happens in all ecosystems. If we put too much garbage and pollution in to the air, water, or ground, we upset the balance created by all the organisms and natural cycles in the environment. Our planet itself has a lot of similarities to the human body. Water circulates around and through the Earth in a complex hydrological cycle, regulating temperature and keeping plants and animals alive, just as blood circulates through our bodies. The natural organisms of the Earth’s ecosystems, like the microbes in our bodies, also offer numerous services that we rely on to survive and be healthy.

And for both the human body and the Earth, carbon is an essential element. Carbon is the second most abundant element in the human body, after oxygen, and it also cycles through the Earth, its inhabitants, and its atmosphere. Normally, carbon is absorbed from the atmosphere though photosynthesis and is put back through respiration and decay. But when we upset the balance by cutting down too many of the plants or trees that absorb the carbon and by burning fuels that put too much carbon back into the atmosphere, we put the Earth’s health, and thus the health of all of us, at risk.

We must learn to treat the Earth as we would treat ourselves. After all, we are part of nature, and if we don’t look after its health, we aren’t looking after our own health.

My Comments:

– I think this is a great article that examines another perspective to view approach the way we should view and treat our environment. The author talks about how it is important to recognize and understand that microbes play an important part in the environment as well as inside the human body. Therefore, the way we take care of our bodies is the same way we should be taking care of the environment.

– evident is also an intercorrelating relationship happens between the health of our bodies and the health of the environment: We need a healthy environment to be healthy ourselves

– overall this is a good perspective to look at; however, I think it would make for a stronger case if it were to give practical ways and tips to live out this paradigm

– also, this article is strictly addressed to people who live in economically stable environments. Many people in the third world countries don’t even have the bare necessities for survival…how can they be thinking about cleaning the environment when they struggle to survive?

Thanks for reading!

Emily Leung

Nestle Cookie Dough Is Recalled- published June 2009

Nestlé USA recalled its Toll House refrigerated cookie dough on Friday after health officials linked the dough to infections from the bacteria E. coli in as many as 66 people in 28 states.

The recall, by a company with a reputation for strong quality-control measures, once again demonstrates the difficulty of ensuring the safety of the nation’s food supply. The increasingly disparate nature of contaminated foods — recently including pistachios, peanut butter and chicken pot pies — has complicated the task of illness hunters and food inspectors because no one is sure anymore which foods may be risky.

“You can’t assume it’s the usual ground beef or fresh produce,” said Dr. David Acheson, associate commissioner for foods at the Food and Drug Administration.

E. coli O157, the strain linked to the Nestlé dough, is a particularly dangerous pathogen normally found in contaminated meat. It causes abdominal cramping, vomiting, and bloody diarrhea. Most adults recover within a week, but the disease can lead to serious kidney damage and death.

“We’re all having trouble figuring out how E. coli O157 gets in cookie dough,” said Dr. Timothy F. Jones, Tennessee’s state epidemiologist. “This wasn’t on anybody’s radar screen.”

Officials have been hunting since March for the cause of cases from across the country that shared the same genetic fingerprint. Because most victims were young and female, the investigation was unusual from the start. Twenty-five people have been hospitalized, including seven who suffered a severe complication called hemolytic uremic syndrome. No one has died.

Among the early food suspects were strawberries and fruit smoothies, but neither quite fit. On Wednesday, health investigators in Washington State proposed a link with Nestlé’s raw cookie dough, prompting officials in the rest of the country to re-interview victims. All six in Minnesota confirmed eating raw dough, said Carlota Medus, an epidemiologist in the state health department.

On Friday, the F.D.A. advised consumers to throw out any Nestlé refrigerated cookie dough they have. Although cooking may kill the bacteria, handling the raw dough could spread the contaminant to hands and cooking surfaces.

Nestlé is telling consumers to return cookie and brownie dough products to grocers for a full refund.

“We made the decision to proactively withdraw the product,” said Laurie MacDonald, a company spokeswoman, who noted that even in normal circumstances, cookie dough should never be eaten raw. She pointed to the product’s label, which states, “Bake before consuming.”

Bill Marler, a food-safety lawyer, scoffed at that statement.

“Those three words do not constitute an adequate warning,” Mr. Marler said, “and Nestlé should not be blaming their victims for doing what everyone in America does, and that is to eat and handle cookie dough before it’s cooked.”

No other Nestlé Toll House products are affected, including already baked Toll House cookies, Toll House morsels, chocolate baking bars, cocoa or Dreyer’s and Edy’s ice cream with cookie dough ingredients.

Legislators and advocates said the recall should be a spur to action in Congress on legislation to overhaul the food-safety system.

“This most recent E. coli outbreak serves as a reminder that Congress must pass the strongest food-safety legislation possible to protect our food supply,” said Representative Rosa DeLauro, Democrat of Connecticut.

Sarah Klein, a staff lawyer at the Center for Science in the Public interest, added, “If there was ever any doubt that we’ve reached a crisis, this should provide the proof.”

The House Energy and Commerce Committee approved a bipartisan measure on Wednesday that would give the food and drug agency more money and authority to inspect food facilities and to force contaminated ingredients off the market. Food manufacturers would have to write and carry out safety plans, paying an annual registration fee to help finance enforcement.

The House is expected to take up the measure this summer. Members of the Senate Health Committee have promised to take up companion legislation after a food-safety working group appointed by President Obama issues a report.

While legislation may improve food safety, the Nestlé case shows that food scares will continue, public health officials said. Nestlé is already known for its insistence on adhering to the kind of strict safety measures mandated in the proposed legislation. For example, Nestlé refused to buy from the Peanut Corporation of America, the source of a peanut butter scare last year, after it failed two Nestlé audits. Many other large food buyers were not so thorough.

“It doesn’t matter how much money or how many laws you put in place, the system will always have contamination problems,” said Dr. Acheson of the F.D.A.

The agency is continuing to investigate the source of the contamination.

“Was it a contaminated ingredient, and if so what?” Dr. Acheson asked. “Or was it a problem that occurred inside the facility during processing?”

Whatever the answer, the list of questions that health officials must ask those who suffer food poisoning continues to grow.

My thoughts…

– While most of us know that eating raw cookie dough is not good for us, we have all tried it and I would guess that the majority of us would never imagine that it would contain E.Coli. As Bill Marler says, the label “bake before consuming” doesn’t exactly constitute a proper warning.

 – The article explains how Nestle is known for adhering to strict safety measures, using the example that they “refused to buy from the Peanut Corporation of America, the source of a peanut butter scare last year, after it failed two Nestle audits.” However, a second article, published July of 2009, described how Nestle routinely refuses to share safety data with inspectors since, it is not required by law. However, during a salmonella outbreak at the Peanut Corporation of America in Georgia- the F.D.A was “forced to use its antiterrorism powers to get data.” So the fact that Nestle refused to buy from the corporation doesn’t necessarily say much about the company’s high standards, it simply means that they knew they were at risk of being caught.

 – Subsequently, approximately a year after these articles were published, Nestle had yet another incidence of cookie dough contamination with E. Coli, proving that they in fact do not strictly adhere to safety measures.