If the goose that laid the golden egg had a real-life counterpart, it would be C. metallidurans. This hardy little bacterium consumes toxic metals and excretes tiny gold nuggets, but how and why it does so has never been fully understood. Now, German and Australian researchers have peered inside the microorganism and figured out that mechanism.
If you think humans are polluting the planet to a degree never before seen in history, well, “You’re suffering from a species-level delusion of grandeur,” insists science writer Annalee Newitz in her new book, Scatter, Adapt, and Remember. “We’re not even the first creatures to pollute the Earth so much that other creatures go extinct.” That foul distinction belongs to ancient cousins of ours: cyanobacteria.
About 2.5 billion years ago, the Earth was much different than it is today. Rotating at faster speeds, there were about 450 20-hour days in a year. Far from cool and invigorating, the planet’s atmosphere was superheated, and comprised mostly of methane and carbon, not oxygen and nitrogen, the primary constituents of today’s atmosphere. The surface was no more hospitable to modern life. Magma seeped and bubbled amidst immense, acidic oceans. 2.5 billion years ago, Earth was a hot mess.
But in this environment — one we would deem noxious — life persisted. Oxygen-despising anaerobic bacteria floated in the ocean deep, kept cozy by hot magma streams. They subsisted on simple amino acids and sugars. Earth was turbulent, but alive.
Then cyanobacteria ruined everything. As the first organisms to use photosynthesis, they drank in the oceans’ water and absorbed photons from sunlight, using the energy from those photons to separate water’s two hydrogen molecules from its lone oxygen molecule. Afterwards, the microbes consumed the hydrogen and spit out the oxygen as a waste product.
This recipe was so successful that after millions of years cyanobacteria, also known as blue-green algae, nearly blanketed the planet’s surface, continuously belching boatloads of oxygen in the process. All of the smokestacks from all of today’s factories and power plants couldn’t come close to their polluting prowess.
Eventually, Earth’s natural oxygen absorbers — like iron — became saturated with the gaseous element, and an “oxygen apocalypse” ensued. We recognize oxygen as a bringer of life, but it’s also a powerful degrader of organic compounds and quite toxic to anaerobes. With oxygen now suffusing throughout the atmosphere, pretty much all life except the cyanobacteria gradually became extinct. Excess oxygen also reacted with the atmosphere’s methane, turning it into a weaker greenhouse gas: carbon dioxide. With a diminished ability to retain heat, the planet entered an ice age that lasted upwards of 300 million years!
One thing that this fascinating, true story demonstrates is that one bacteria’s trash is another life form’s treasure. Over many millions of years, organisms evolved that could use the built-up oxygen, mixing it with sugars to create energy. Pollution problem solved.
Will we ever atone for the dirty sins of our blue-green cousins and give the Earth totally back to the anaerobes? Probably not. It will take a far more concerted pollution effort than the comparatively paltry one we are currently mustering.
Attribution: Ross Pomeroy, RealScience
Gut microbes may be another way to tackle obesity, new research suggests.
Could a transplant of gut bacteria be the key to tackling obesity?
Scientists found that by altering the levels of gastric bugs in mice, they were able to induce rapid and significant weight loss.
The change occurred after bacteria from obese mice that had undergone gastric bypass surgery were transplanted into ordinary animals.
Surgery had the effect of altering the make-up of the gut flora, introducing a different balance which promoted slimming.
When this new mix of microbes was transferred to non-obese mice, the weight loss benefits were transferred too.
The U.S. research shows that gastric bypasses do more than prevent food being digested. Much of their impact is due to altered ecology in the gut.
‘It may not be that we will have a magic pill that will work for everyone who’s slightly overweight,’ said study leader Dr Peter Turnbaugh, from Harvard University, Boston.
‘But if we can, at a minimum, provide some alternative to gastric bypass surgery that produces similar effects, it would be a major advance.’
Gastric bypasses work by rearranging the gut so that it accommodates less food.
The research showed that after surgery different kinds of microbe began to take over. In particular, the gut became dominated by verrucomicrobia and gammaproteobacteria. In contrast levels of the Firmicutes family of bugs fell.
It took less than a week for the rebalancing to occur, and the effect continued for months afterwards.
The new population of bugs appeared to drive weight loss, and continued to do so when transferred to a non-obese group of mice that had not undergone a gastric bypass.
‘Simply by colonizing mice with the altered microbial community, the mice were able to maintain a lower body fat and lose weight – about 20 per cent as much as they would if they underwent surgery,’ said Dr Turnbaugh.
He suspected an even more dramatic result would have been seen if the mice receiving the bugs had been fattened up beforehand.
How particular populations of microbes induce weight loss remains unclear.
The answer may be linked to waste products the bugs excrete, according to the research published in the journal Science Translational Medicine.
Along with the altered microbes, the scientists found changes in the concentration of certain short-chain fatty acids. Previous studies have suggested the molecules may trigger signals that cause the body to speed up metabolism, or store fewer calories as fat.
‘A major gap in our knowledge is the underlying mechanism linking microbes to weight loss,’ said Dr Turnbaugh. ‘There were certain microbes that we found at higher abundance after surgery, so we think those are good targets for beginning to understand what is taking place.’
Co-author Dr Lee Kaplan, from Massachusetts General Hospital in Boston, said: ‘We need to learn a good deal more about the mechanisms by which a microbial population changed by gastric bypass exert its effects, and then we need to learn if we can produce these effects – either the microbial changes or the associated metabolic changes – without surgery.
‘The ability to achieve even some of these effects without surgery would give us an entirely new way to treat the critical problem of obesity, one that could help patients unable or unwilling to have
Attribution: Anna Hodgekiss, Mail Online
Fears over wave of deadly superbugs invading U.S. hospitals that are resistant to antibiotics
Hospitals in the U.S. have been hit by a wave of ‘nightmare bacteria’ that have become increasingly resistant to even the strongest antibiotics.
Public health officials have warned that in a growing number of cases existing antibiotics do not work against the superbug, Carbapenem-Resistant Enterobacteriaceae (CRE).
Patients became infected with the bacteria in nearly 4% of U.S. hospitals and in almost 18% of specialist medical facilities in the first half of 2012, according to the Centers for Disease Control and Prevention (CDC).
Dr Tom Frieden, director of the CDC, said in a statement that the strongest antibiotics ‘don’t work and patients are left with potentially untreatable infections.’
He said scientists were ‘raising the alarm’ over the problem following increasing concern.
Increasing numbers of patients in U.S. hospitals have become infected with CRE, which kills up to half of patients who get bloodstream infections from them, according to a new CDC report.
Some of the more than 70 types of Enterobacteriaceae bacteria – including E-coli – have become gradually resistant over a long period of time, even to so-called, ‘last resort drugs’ called carbapenem.
During the last ten years, the percentage of Enterobacteriaceae that are resistant to these last-ditch antibiotics rose by 400 %. One type of CRE has increased by a factor of seven over the last decade, Fox News reports.
CRE infections usually affect patients being treated for serious conditions in hospitals, long-term acute-care facilities and nursing homes. Many of these people will use catheters or ventilators as part of their treatment – which are thought to be used by bacteria to enter deep into the patient’s body.
Only six states currently require that healthcare providers report cases of CRE. The CDC said the bugs spread from person to person, often on the hands of medical workers and that they are able to pass on their antibiotic resistance to other kinds of germs.
The bacteria were present in just one U.S. state in 2001, but have now spread to 42, Dr Frieden said at a news conference.
Seven people died, including a 16-year-old boy, in one serious outbreak of Klebsiella pneumoniae in 2011 at the National Institutes of Health Clinical Center in Bethesda, Maryland, the Sun reports.
The CDC is trying to raise awareness of the antibiotic resistant germs, urging health centres to control them effectively by taking proper precautions such as washing hands and grouping patients with CRE together.
Attribution: Sam Adams, Daily Mail
They used an enzyme isolated from the marine bacterium Bacillus licheniformis which they were originally researching for cleaning ships’ hulls.
Newcastle University scientists claim that the enzyme can ‘cut through’ plaque on teeth and clean hard-to-reach areas.
The Newcastle University team will tell the Society for Applied Microbiology Summer Conference that it could have a range of medical applications, including teeth cleaning.
Dr Nicholas Jakubovics of Newcastle University’s School of Dental Sciences believes better products offering more effective treatment can be made using the enzyme.
He said: ‘Plaque on your teeth is made up of bacteria which join together to colonise an area in a bid to push out any potential competitors.
‘Traditional toothpastes work by scrubbing off the plaque containing the bacteria – but that’s not always effective – which is why people who religiously clean their teeth can still develop cavities.
When threatened, bacteria shield themselves in a slimy protective barrier known as a biofilm.
It is made up of bacteria held together by a web of extracellular DNA which binds the bacteria to each other and to a solid surface – in this case in the plaque around the teeth and gums.
The biofilm protects the bacteria from attack by brushing, chemicals or even antibiotics.
But after studying Bacillus licheniformis, which is found on the surface of seaweed, Newcastle University scientists found that when the bacteria want to move on, they release an enzyme which breaks down the external DNA. That breaks up the biofilm and releases the bacteria from the web.
‘When I initially began researching how to break down these layers of bacteria, I was interested in how we could keep the hulls of ships clear but we soon realised that the mechanism we had discovered had much wider uses.
‘If we can contain it within a toothpaste we would be creating a product which could prevent tooth decay.
‘This is just one of the uses we are developing for the enzyme as it has huge potential such as in helping keep clean medical implants such as artificial hips and speech valves which also suffer from biofilm infection.’
The team will now look to collaborate with industry to carry out more tests and product development.
Attribution: Daily Mail