Bio-Terror Scapegoats: Africa, Agriculture (Food & Animals), Airports & Air Travel, Al Qaeda, Bio Labs, Bio-Terrorism Is Easy, Bio-Terrorists (Bio-Hackers), Black Market, Bugs & Insects, Censorship / Lack Thereof, Domestic Terrorists, Exotic Animals (Zoonosis), Government Ineptitude, Mail-Order DNA, Mexico, Missile Shield Failure, Mutation, Natural Disaster, No Clinical Trials (Vaccines), and The Monkeys.
Source: Sunshine Project
Abstract: Investigations by the Sunshine Project show that genetic engineering has been used in the past decade to tinker with the genes of biological weapon agents. Researchers in the USA, UK, Russia, Germany and other countries introduced genes into hazardous bacteria that are likely to enhance the biowarfare possibilities of these microbes. Strains have been designed that can withstand antibiotics, are undetectable by traditional equipment, can overcome vaccines, or that cause unusual symptoms, thereby hampering diagnosis. In general, gene transfer can be used to build more effective biological weapons, it could be used to broaden the military biological warfare spectrum, making it more difficult to fight and control bioweapons.
"Military research seems to be out of control", says Jan van Aken, genetic engineering expert of the Sunshine Project. "Many research projects have a clear offensive potential. To just stick the label 'defense' on it is not enough. We urgently have to draw clear lines and prohibit genetic engineering with biological weapon agents."
At the same time, it is very unclear that efforts to strengthen the Biological Weapons Convention will succeed in the round of negotiations currently underway in Geneva. In light of the increasing biowarfare threat, the international community decided in 1994 to negotiate a Protocol to strengthen the Biological and Toxin Weapons Convention (BTWC). (1)
Considering that the
biowarfare threat is dramatically increasing due to the speedy development of
genetic engineering, a Bioweapons Convention that it not updated to reflect new
technological realitites will not create global security. "In light of
recent advancements in genetic engineering, updating and reinforcement of
international law that outlaws bioweapons is urgently needed." says
Edward Hammond of the Sunshine Project's Seattle office. A strong Protocol will
be a first step, that enhances tranparency, making it more difficult for
countries to conceal a bioweapons program, for example, in the guise of
Genetic Engineering: A New Class Of Biological Weapons
It sounds like science fiction, but it is a deadly reality: lethal microbes, with no cure, invisible to detection systems, and able to overcome vaccines. In 'defensive' programs, researchers in the USA, UK, Russia and Germany have genetically engineered biological weapons agents, building new deadly strains. And this is probably only the tip of the iceberg.
Genetic engineering can be used to broaden the classical bioweapons arsenal. Through genetic engineering, bacteria can not only be made resistant to antibiotics or vaccines, they can also be made even more toxic, harder to detect, or more stable in the environment. By using genetic methods that are standard procedures in thousands of labs worldwide, bioweapons can be made more virulent, easier to handle, and harder to fight. In short, more effective.
Military experts are perfectly aware of the danger of genetically engineered bioweapons, as their traditional defense measures - e.g.detection methods or vaccines - are easily sidestepped by the artificial microbes. The speedy development of genetic engineering is one driving force to strenghten the Bioweapons Convention and establish a verification system.
Example 1: Bacteria Causing Unusual Symptoms
Researchers from Obolensk near Moscow inserted a gene into Francisella tularensis, the causative agent of tularemia and a well known biological weapon agent. The gene made the bacteria produce beta-endorphin, an endogenous human drug, which caused changes in the behaviour of mice when infected with the transgenic bacteria. (2) According to the published results, the endorphin gene was not introduced into a fully virulent strain, but only into a vaccine strain.
If inserted into virulent F. tularensis, the victims would not show the usual symptoms of tularemia, but instead unusual symptoms that would obscure the diagnosis and delay therapy. Development of symptom-altered BW-agents has been identified as one possible application of genetic engineering for BW purposes by the US Department of Defense. (3)
Transferring A Lethal Factor To Harmless Human Gut Bacteria
Genetic engineering could make previously harmless bacteria lethal biological weapons by introducing deadly genes from a highly pathogenic organism. This was done by US researchers as early as 1986. They isolated the gene for the lethal factor of Bacillus anthracis, the causative agent of anthrax, and introduced into Escherichia coli, a normally harmless gut bacteria. The US team reported that the lethal factor protein was active in E. coli and displayed the same deadly effects as it did when in its native B. anthracis. (4)
Antibiotic Resistant Anthrax And Tularemia
Antibiotic resistance is often used as a marker gene in genetic engineering experiments. However, the very same genes could render biological weapons more dangerous by making agents less treatable. Any experiment with biological weapons agents using antibiotic resistance genes has a strong offensive potential, even if in the contect of âdefensiveÔ research. Despite this obvious problem, there is a long list of questionable experiments:
German military researchers at the Santitaetsakademie der Bundeswehr in Munich, the main BW research facility of the German army, cultured genetically engineered Francisella tularensis subsp. holarctica bacteria (5), a close relative of the causative agent of tularaemia. An antibiotic resistance marker gene (tetracyclin) was been inserted into these bacteria.
Recently, researchers from Porton Down in the UK used genes conferring resistance to antibiotics for genetic studies in fully virulent strains of anthrax. (6) In the late 1980s, a researcher at the University of Massaschussetts in Amherst also introduced antibiotic resistance genes into anthrax, making it less treatable with antibiotics. (7)
There are even more cases: Researchers from the Institut Pasteur in Paris (8) and from a Russian laboratory in Obolensk (near Moscow) (9) introduced antibiotic resistance genes into anthrax bacteria.
All these studies are allegedly "basic research", where antibiotic resistance is used as a marker gene. But it is obvious that the very same genetically engineered bacteria can be used to design more effective bioweapons compared to the natural anthrax strains.
In December 1997, the same Russian research group from Obolensk published a paper in a British scientific journal on another effort to genetically engineer anthrax. (10) By putting new genes into fully pathogenic strains of anthrax, the scientists altered anthraxÔs immunopathogenic properties, making existing anthrax vaccines ineffective against the new genetically-engineered types.
In most cases, detection of bioweapons relies on molecular recognition of the microbe using antibodies similar to the human immune system. Altering the immunogenicity not only overcomes vaccinations; but also the detection systems.
Western military experts were alarmed by this work. The chief of the bacteriology division at the US Army Medical Research Institute of Infectious Diseases (USAMRIID) in Fort Detrick, Md, Col. Arthur Friedlander, commented: "This is the first indication we're aware of in which genes are being put into a fully virulent strain. They genetically engineered a strain that's resistant to their own vaccine, and one has to question why that was done". (11)The Russian researchers also constructed a new vaccine against the new strain. This is of particular importance, as it could enable an army to use such a bioweapon by vaccinating their soldiers against a specific strain, while the enemy remains vulnerable. The case is an example of the frightening potential of genetic engineering applied to biological weapons research (Sunshine Project, 2000).
Title: Losing The Race With Bugs: Bacteria Beats New Drugs
Date: April 25, 2002
Abstract: Cheetahs eat gazelles. The fastest cheetahs catch more gazelles and breed more; and over generations, cheetahs get faster. But gazelles evolve, too. Faster gazelles live longer and breed more; over generations, they get faster, too.
The same evolutionary dynamics apply to humans and bacteria. We develop antibiotics that kill bacteria. They evolve resistance. We develop better drugs. They evolve resistance to the new drugs.
Cheetahs and gazelles evolve at the same pace. From about 1945 to the early 1980s, humans developed new drugs faster than bacteria evolved. But bacteria now are changing faster than our drugs.
The bugs are winning the race. The more antibiotics we use, the quicker they evolve resistant strains.
A common bacterium called pneumococcus, which causes ear and sinus infections as well as more serious illness, first showed resistance to penicillin in the 1960s. Into the early 1990s, only 5% of cases were resistant, according to the Centers for Disease Control and Prevention. By the end of the 1990s, penicillin couldn't touch nearly 40% of cases in some parts of the U.S.
Tuberculosis will kill more this year than last because a drug-resistant strain has evolved. "Strains of five bacterial species capable of causing life-threatening illnesses already evade every antibiotic in the clinician's armamentarium," says Stuart Levy, a Tufts University microbiologist.
The science is clear. The medical establishment is alarmed. The bioterrorism threat intensifies concern. The issue is: what to do?
Think of antibiotic effectiveness as a natural resource, like fish, that we're depleting rapidly, suggests economist Ramanan Laxminarayan of Resources for the Future, a think tank in Washington, D.C. "Everyone harvests this resource, caring only about himself and ignoring the potential harm to others," he says.
Each commercial fisherman profits by catching more fish, no matter how depleted the ocean stocks. Each parent will press a pediatrician for a drug if there's any chance it will cure a child. Yet if every parent and pediatrician does the same, they will speed the evolution of drug-resistant microbes. And what drug company will enlist its marketers to prod doctors to prescribe its antibiotics less?
Until now, the main remedy has been preaching, the equivalent of pleas to commuters to carpool. Government, doctors' groups and insurers are trying to persuade patients and doctors to avoid antibiotics where they won't work, in treating viral infections, for instance.
In northern California, Kaiser Permanente, the big HMO, has reduced antibiotic use by 30% during the past two years by showing doctors how their prescription patterns differ from peers and using posters to educate patients. The CDC, among other things, offers doctors "viral prescription pads" with treatment tips so patients whose ailments can't be helped by antibiotics don't go away empty-handed. It sees signs that this public-relations campaign is succeeding.
Such education is essential, but it won't suffice. So in quiet conversations, scientists and economists are beginning to think about stronger medicine.
One option is discouraging unnecessary drug use by charging consumers more for the most-overused antibiotics or for newer, heavily promoted drugs that ought to be held in reserve. Increasing drug prices -- even if only for people whose insurance policies cover most of the cost -- sounds jarring. But Mr. Laxminarayan draws the parallel to the campaign against smoking, which, he notes, "was accomplished through both cigarette-tax increases and information campaigns" after public pressure overwhelmed opposition from smokers and tobacco companies.
This approach assumes that resistance is simply caused by overuse. It isn't. Higher prices or an antibiotic tax won't solve the problem of incomplete treatment -- not finishing a prescribed dose or, in poor places, not having enough medicine to kill bacteria -- which also gives the bugs an edge.
The bugs also get an edge when doctors all tend to use the same drugs. Despite the famously decentralized U.S. health-care system, the five most commonly used antibiotics account for 80% of all antibiotic prescriptions.
To save money, insurers, hospitals and HMOs often limit the menu of drugs available, reasonably seeking to use the most cost-effective medicine. But using different drugs for the same ailment in different people or at different times, much as farmers rotate crops, may be prudent. This requires more coordination than is possible in the decentralized U.S. system, although some hospitals, prodded by the CDC, are moving in this direction.
Another solution would be to pull ahead of the microbes. A new pneumococcus vaccine will help. But we also need new potent families of antibiotics. We haven't found one in decades, and big pharmaceuticals firms are devoting R&D money to more-lucrative drugs that treat chronic conditions such as cancer or impotence.
So there is talk, and not just from drug companies, of new ways to stimulate research into new antibiotics. One possibility is tinkering with patent rules to make them broader, both to lure research money and to give drug companies more incentive to market drugs with an eye to the evolutionary dangers.
Devising the right remedies and selling
them won't be easy. It never is when near-term interests, whether those of
patients or of drug companies, diverge from the long-term interests of
humankind (UCLA, 2002).
Title: A Weapon Weakened: Antibiotics
Date: February 24, 2003
Source: LA Times
Abstract: Since hitting the market in 1987, Cipro has been the penicillin of its time, good for knocking out a wide variety of infections. But an increasing percentage of bacteria have grown resistant to this powerful antibiotic, narrowing treatment options and reminding us that microbes find ways to overcome every assault.
Researchers writing in the Feb. 18 issue of the Journal of the American Medical Assn. found that in hospital intensive care units, fewer bacteria responsible for respiratory and urinary tract infections are responding to Cipro. An analysis of bacteria samples from hospitals in 43 states plus the District of Columbia found that the percentage of bacteria like Pseudomonas and E. coli that are susceptible to Cipro fell from 89% in 1990-93 to 76% in 2000.
"The biggest fear is we are losing the battle, that nature can stay ahead of us with mutations," said Dr. Keith Beck, an infectious disease specialist at Harbor-UCLA Medical Center in Torrance.
For now, the arsenal isn't empty. Doctors treating vulnerable hospitalized patients can attack infections with so-called gram-negative bacteria like Pseudomonas using existing antibiotics, such as some penicillins and cephalosporins, and aminoglycosides like gentamicin and amikacin. Often, they'll use a combination of these drugs. Instead of overusing fluoroquinolones like Cipro and Levaquin for pneumonia, physicians can still rely on macrolides like erythromycin and clarithromycin (Biaxin) and cephalosporins, which do not create as much gram-negative resistance problems. Although all bacteria have inner-cell membranes, gram-negative bacteria are tough targets because they have an outer membrane that keeps some antibiotics from entering the cell; gram-positive bacteria have a single membrane.
But there's a misperception among consumers that there will always be a new antibiotic around the corner.
"It's not true anymore," said Dr. Stuart B. Levy, director of the Center for Adaptation Genetics and Drug Resistance at Tufts University in Boston. The antibiotic pipeline has slowed in recent years, even as the time it takes for a new drug to lose its effectiveness grows ever-shorter.
For gram-positive bugs, such as streptococcus and staphylococcus, there are powerful new drugs like Zyvox and Synercid and one still in trials called Daptomycin. But for the gram-negatives, there are fewer options. Some promising approaches are coming from small biotechnology companies. Levy started his own to develop new forms of tetracycline that get around the resistance problem. He's also working on molecules that interfere with a bacterium's ability to cause infection.
Although bacteria become resistant through mutations or by picking up resistant genes from other bugs, some of the problem is preventable.
About 75% of all antibiotics prescribed in the United States are given for upper respiratory illnesses: colds, sore throats, bronchitis, sinus and ear infections. Yet, at least half of those prescriptions aren't needed because the infections are caused by viruses, not bacteria. Every time patients take them unnecessarily or improperly -- for example, by not finishing a full course -- the strongest bugs survive the antibiotic hit and flourish.
Levy, founder of the international Alliance for the Prudent Use of Antibiotics, says consumers have come to think antibiotics kill everything: "They believe they're cure-alls; they believe they deserve to have them." And they have ready access through compliant doctors and online pharmacies. He cited the example of Americans stockpiling Cipro after it was prescribed to those potentially exposed to anthrax.
To curb inappropriate use, some hospitals have had success restricting antibiotic prescriptions.
Levy warns that by
overusing antibiotics, "we are sowing the seeds of our own destruction. You
can't imagine these fabulous drugs are creating in their wake the biggest
problem we've ever faced" (LA Times, 2003).
Title: CDC To Mix Avian, Human Flu Viruses In Pandemic Study
Date: January 24, 2004
Abstract: One of the worst fears of infectious disease experts is that the H5N1 avian influenza virus now circulating in parts of Asia will combine with a human-adapted flu virus to create a deadly new flu virus that could spread around the world.
That could happen, scientists predict, if someone who is already infected with an ordinary flu virus contracts the avian virus at the same time. The avian virus has already caused at least 48 confirmed human illness cases in Asia, of which 35 have been fatal. The virus has shown little ability to spread from person to person, but the fear is that a hybrid could combine the killing power of the avian virus with the transmissibility of human flu viruses.
Now, rather than waiting to see if nature spawns such a hybrid, US scientists are planning to try to breed one themselves—in the name of preparedness.
The Centers for Disease Control and Prevention (CDC) will soon launch experiments designed to combine the H5N1 virus and human flu viruses and then see how the resulting hybrids affect animals. The goal is to assess the chances that such a "reassortant" virus will emerge and how dangerous it might be.
CDC officials confirmed the plans for the research as described recently in media reports, particularly in a Canadian Press (CP) story.
Two ways to make hybrids
The plans call for trying two methods to create hybrid viruses, CDC spokesman David Daigle told CIDRAP News via e-mail. One is to infect cells in a laboratory tissue culture with H5N1 and human flu viruses at the same time and then watch to see if they mix. For the human virus, investigators will use A (H3N2), the strain that has caused most human flu cases in recent years, according to the CP report.
The other method is reverse genetics—assembling a new virus with sets of genes from the H5N1 and H3N2 viruses. Reverse genetics has already been used to create H5N1 candidate vaccines in several laboratories, according to Daigle. The National Institutes of Health (NIH) said recently it would soon launch a clinical trial of one of those vaccines.
Of the two methods, the co-infection approach was described as slower and more laborious, though closer to what happens in nature.
Any viable viruses that emerge from these processes will be seeded into animals that are considered good models for testing how flu viruses behave in humans, according to Daigle. The aim will be to observe whether the animals get sick and whether infected animals can infect others.
The World Health Organization (WHO) has been "pleading" for laboratories to do this research, because it could provide some evidence to back up the agency's warnings about the risk of a flu pandemic, according to the CP report.
Klaus Stohr, head of the WHO's global influenza program, was quoted as saying that if none of the hybrids caused disease, the agency might be inclined to dial down its level of concern. But if the experiments produce highly transmissible and pathogenic viruses, the agency will be more worried, he said.
Because of the obvious risks in creating viruses with the potential to spark a pandemic, the work will be done in a biosafety level 3 (BSL-3) laboratory at the CDC in Atlanta, Daigle told CIDRAP News.
"We recognize that there is concern by some over this type of work. This concern may be heightened by reports of recent lab exposures in other lab facilities," he said. "But CDC has an incredible record in lab safety and is taking very strict precautions."
Daigle said the US Department of Agriculture requires that highly pathogenic avian influenza (HPAI) viruses be treated as "Select Agents" and that research on them must be done in BSL-3 labs with "enhancements." These include "special provisions to protect both laboratory workers and the environment."
BSL-3 is the second highest level of laboratory biosecurity. It is used for work with pathogens that may cause serious or potentially lethal disease if inhaled, such as tuberculosis or St. Louis encephalitis, according to the CDC.
CDC experiments with HPAI viruses have to pass reviews by the agency's Institutional Biosafety Committee and Animal Care and Use Committee, Daigle said. The facilities involved are inspected by the USDA and the CDC's Office of Safety and Health, and staff members who work with Select Agents require special clearance.
It's been done before
The upcoming experiments will not break entirely new ground for the CDC, the CP story revealed. The agency already has made hybrid viruses with H5N1 samples isolated from patients in Hong Kong in 1997, when the virus first caused human disease.
The results of that research have not yet been published, and the CDC has said little about them. In the CP report, Dr. Nancy Cox, head of the CDC's influenza branch, commented only, "Some gene combinations could be produced and others could not."
Daigle added little to that. He said, "The reassortment work with the 1997 isolate was intermittently interrupted with SARS [severe acute respiratory syndrome] and then the 2004 H5N1 outbreak. We are currently concentrating our efforts on understanding the pathogenicity of the 2004 strains (non-reassortants) in mammalian models."He said the CDC hopes to prepare a report on that research "in the near future" (CIDRAP, 2004).
Title: Super-Bacteria Eat Antibiotics For Breakfast
Date: April 3, 2004
Abstract: Antibiotics are meant to kill bacteria, so it might be disheartening to learn that some bacteria can literally eat antibiotics for breakfast. In fact, some species can thrive quite happily on nothing but antibiotics, even at high concentrations.
The rise of drug-resistant bacteria poses a significant threat to public health and many dangerous bugs seem to be developing resistance at an alarming rate. The headline-grabbing MRSA may be getting piggybacks from livestock to humans, while several strains of tuberculosis are virtually untreatable by standard drugs.
But a startling new study reveals just how widespread antibiotic resistance really is. Gautam Dantas from Harvard Medical School managed to culture antibiotic-eating bacteria from every one of 11 soil samples, taken from farmland and urban areas across the US. All eleven were positively loaded with a diverse group of bacteria that were extremely resistant to a wide range of antibiotics at high concentrations.
In their natural environment, these soil bacteria are frequently exposed to a massive array of antibiotics from plants and other microbes, and have evolved ways of detecting and evading them. These resistant strains act as a living reservoir of innovative genetic means of resisting antibiotics, known as the ‘antibiotic resistome‘.
Dantas searched for resistant bacteria by culturing colonies that could grow in solutions where antibiotics were their only source of carbon. He tested 18 different antibiotics that are used to kill a variety of different bacterial species. Some of these were natural, others man-made; some were old, others new. But every single one managed to support at least one strain of bacteria. Six of them, including commonly used drugs like penicillin, vancomycin, ciprofloxacin and carbenicillin, even managed to feed bacteria from all 11 soils.
The degree of resistance in the soil bacteria was nothing short of
extraordinary. Dantas cultured a representative set of 75 resistant
strains and found that on average, they resisted 17 of the 18
antibiotics at low concentrations of 20 milligrams per litre (full bars
in image below). But even at higher concentrations of 1 gram per litre
(filled bars in image below), each strain managed to stand firm against
an average of 14 out of 18 drugs.
When Dantas studied some of these strains more closely, he found that they nullified the drugs using similar techniques to the drug-resistant versions of disease-causing bacteria. Some shunted the antibiotics out of their cells with molecular pumps, others used enzymes to cut up the drugs, and yet others reprogrammed their own genetic code to deprive antibiotics of their targets.
Reservoir of Resistance
The real danger is that the soil-living species could provide new defences that more dangerous ones can draw on to shrug off our best drugs. Bacteria are capable of passing genetic material between one another as easily as two humans might swap business cards, making it trivial for the soil super-bugs to pass their crucial genes on to more dangerous species. To see how easily this could happen, have a look at this earlier post about how the food poisoning bug Salmonella has passed a resistance gene on to the Black Death bacterium.
In principle, bacteria should be more able to successfully take up resistance genes from other closely related species. It’s worrying then that Dantas’s antibiotic-eaters belonged to such diverse groups. By establishing a family tree of the different strains, he found that they were members of at least 11 different bacterial groups, although over half of them came from just two orders – the Burkholderiales and the Pseudomonadales. These include a wide variety of species that are known to infect hospital patients with weakened immune systems.
They are known for their large genome sizes (well, large for bacteria anyway) and some groups have suggested that these sizeable genomes allow them to metabolise a wide range of chemicals, antibiotics included. This unusual diet will come as no surprise to many a microbiologist. Bacteria can colonise some of the most extreme environments on the planet and can survive on the most unlikely to food sources, from crude oil to toxic waste. Now, it seems that they can also survive solely on chemicals that are meant to kill them (Discovery, 2008).
Title: Bird Flu Virus Has Mutated Into Form That's Deadly To Humans
Date: March 6, 2008
Source: Natural News
Abstract: The avian flu has undergone a critical mutation making it easier for the virus to infect humans, according to a study conducted by researchers at the University of Wisconsin at Madison and published in the journal PLoS Pathogens.
"We have identified a specific change that could make bird flu grow in the upper respiratory tract of humans," lead researcher Yoshihiro Kawaoka said.
The H5N1 strain of influenza, also known as "bird flu," has decimated wild and domestic bird populations across the world since it emerged between 1999 and 2002. This highly virulent variety of the flu has been identified as a public health concern because in the past, varieties of influenza have mutated and crossed the species barrier to humans.
Since 2003, 329 humans have been confirmed infected with H5N1, with 201 fatalities. The vast majority of these worked closely with infected birds, such as in the poultry industry.
One of the primary things that keeps bird flu from infecting humans is that the virus has evolved to reproduce most effectively in the bodies of birds, which have an average body temperature of 106 degrees Fahrenheit. Humans, in contrast, have an average body temperature of 98.6 degrees, with temperatures in the nose and throat even lower (91.4 degrees). This vast temperature difference makes it very difficult for the bird flu virus to survive and grow in the human body.
In the current study, researchers found that a strain of H5N1 has developed a mutation that allows it to thrive in these lower temperatures.
"The viruses that are circulating in Africa and Europe are the ones closest to becoming a human virus," Kawaoka said. But he pointed out that one mutation is not sufficient to turn H5N1 into a major threat to humans.
"Clearly there are more mutations that are needed. We don't know how many mutations are needed for them to become pandemic strains."
"We are rolling the dice with modern poultry farming practices," warned consumer health advocate Mike Adams, author of the book How to Beat the Bird Flu. "By raising chickens in enclosed spaces, treating them with antibiotics, and denying them access to fresh air, clean water and natural sunlight, we are creating optimal conditions for the breeding of highly infectious diseases that can quickly mutate into human pandemics," Adams said. "Given current poultry farming practices, it is only a matter of time before a highly virulent strain crosses the species barrier" (Natural News, 2008).
Title: The Secret Of Drug-Resistant Bubonic Plague
Date: October 23, 2008
Abstract: The plague, or the Black Death, is caused by a microbe called Yersinia pestis. In the 14th century, this microscopic enemy killed off a third of Europe’s population. While many people consign the plague to centuries past, this attitude is a complacent one. Outbreaks have happened in Asia and Africa over the last decade and the plague is now recognised as a re-emerging disease. In 1996, two drug-resistant strains of plague were isolated from Madagascar. One of these, was completely resistant to all the drugs that are used to control outbreaks.
Anyone interested in bacteria can attest to their ability to evolve resistance to drugs. In the case of drug-resistant plague, the secret to its powers is a plasmid – a small free-floating ring of DNA, that carries drug resistance genes. Bacteria can trade plasmids across individuals, transferring genes between each other in ways that humans can only achieve with technology. The worry is that common and less harmful bacteria could transfer drug-resistance plasmids over to Yersinia, resulting in new resistant strains.
Timothy Welch and colleagues from the United States Department of Agriculture showed that this concern is well-founded. They found that the plague plasmid is virtually identical in parts to plasmids from an increasingly common strain of Salmonella that is also resistant to multiple drugs. They even found related plasmids were in other drug-resistant bacteria isolated from meat samples across the USA during quality control checks.A word of caution – this doesn’t mean that people risk contracting plague from eating meat. Even though the plasmids are strikingly similar, the bacteria involved are very different. But it does mean that the plague bacterium could potentially gain drug resistance from other common resistant bacteria, if they should both find themselves in the same human or flea host.
Despite this scary scenario, Welch’s study also provides us with a silver lining. We are aware of the threat and we know how to monitor for it, by searching for the plasmid. Monitoring is especially important because the plague has all the qualities you would look for in a potential biological weapon – a high fatality rate, no vaccine and possible air-borne transmission. If the worst happens, we will want to be prepared (Discovery, 2008).
Title: Drugs That Work Against Each Other Could Fight Resistant Bacteria
Date: December 13, 2008
Abstract: When normal bacteria are exposed to a drug, those that become resistant gain a huge and obvious advantage. Bacteria are notoriously quick to seize upon such evolutionary advantages and resistant strains rapidly outgrow the normal ones. Drug-resistant bacteria pose an enormous potential threat to public health and their numbers are increasing. MRSA for example, has become a bit of a media darling in Britain’s scare-mongering tabloids. More worryingly, researchers have recently discovered a strain of tuberculosis resistant to all the drugs used to treat the disease.
New antibiotics are difficult to develop and bacteria are quick to evolve, so there is a very real danger of losing the medical arms race against these ‘super-bugs’. Even combinations of drugs won’t do the trick, as resistant strains would still flourish at the expense of non-resistant ones. Antibiotic combos could even speed up the rise of super-bugs by providing a larger incentive for evolving resistance.
Clearly, fighting the rapidly evolving nature of bacteria is a dead end. So Remy Chait, Allison Craney and Roy Kishoni from Harvard Medical School used a different strategy – they changed the battle-ground so that non-resistant bacteria have the advantage. And they have done so using the seemingly daft strategy of using combinations of drugs that work poorly together, and even those that block each other’s effects.
The trio looked at two strains of the common bacteria Escherichia coli – one that was normal, and another that was resistant to doxycycline. Doxycycline is widely used to fight off a variety of bacterial invaders, but resistant E.coli use a specialised molecular pump to remove the drug. It can withstand 100 times more doxycycline than its normal counterparts.
First, the team hit the two strains with doxycycline and erythromycin, a combination of drugs that work particularly well together and enhance each other’s effects. The resistant strain was certainly more vulnerable to this double-whammy, but as expected, it always outperformed the normal bugs. With that advantage and enough time, it would inevitably evolve resistance to both drugs.
But Chait managed to remove this evolutionary impetus by combining
doxycycline with a third drug, ciprofloxacin, a combination that would
normally be useless. Doxycycline actually blocks the effects of
ciprofloxacin, and the two drugs together are weaker than either alone.
Predictably, the resistant bug did what it had evolved to do – it pumped
out doxycycline. But in doing so, it also unwittingly removed the block
on ciprofloxacin, restoring this second drug to its full killing power.
The normal strain encountered no such problem. By leaving the drugs alone, it never faced the full effects of either, and out-competed their more heavily-pummelled resistant cousins.
Chait cautions that it’s too early to transfer his findings across to hospital beds. The experiment used non-lethal antibiotic concentrations in a very controlled environment. But they have certainly pointed other researchers down a new and interesting path.
Combinations of drugs that block each other have previously been
dismissed by doctors because they would require higher doses. But
Chait’s study suggests that they could be the key to controlling
bacterial drug resistance. We clearly can’t stop bacteria from evolving,
but we can certainly steer the course of that evolution in our favour (Discovery, 2008).
Title: New Flu Strain Is A Genetic Mix
Date: April 24, 2009
Abstract: A deadly swine flu never seen before has broken out in Mexico, killing at least 16 people and raising fears of a possible pandemic. World Health Organization officials said the flu has killed about 60 Mexicans.
Here are some facts about the virus and flu viruses in general:
1. The World Health Organization has confirmed at least some of the cases are a never-before-seen strain of influenza A virus, carrying the designation H1N1.Title: Swine Flu Smoking Gun? CDC Was Combining Flu Viruses In 2004 Source: Natural News
2. Although it's called swine flu, this new strain is not infecting pigs and has never been seen in pigs. The threat is person to person transmission.
3. It is genetically different from the fully human H1N1 seasonal influenza virus that has been circulating globally for the past few years. The new flu virus contains DNA typical to avian, swine and human viruses, including elements from European and Asian swine viruses.
4. The World Health Organization is concerned but says it is too soon to change the threat level warning for a pandemic-- a global epidemic of a new and dangerous flu.
5. When a new strain of flu starts infecting people, and when it acquires the ability to pass from person to person, it can spark a pandemic. The last pandemic was in 1968 and killed about a million people.
6. Seven people in the United States have been diagnosed with the new strain. All have recovered, but the U.S. Centers for Disease Control and Prevention expects more cases.
7. Flu viruses mutate constantly, which is why the flu vaccine is changed every year, and they can swap DNA in a process called reassortment. Most animals can get flu, but viruses rarely pass from one species to another.
8. From December 2005 through February 2009, 12 cases of human infection with swine influenza were confirmed. All but one person had contact with pigs. There was no evidence of human-to-human transmission in those cases.
9. Symptoms of swine flu in people are similar to those of seasonal influenza -- sudden onset of fever, coughing, muscle aches and extreme tiredness. Swine flu appears to cause more diarrhea and vomiting than normal flu.
10. Seasonal flu kills between 250,000 and 500,000 people globally in an average year.
11. In 1976 a new strain of swine flu started infecting people and worried U.S. health officials started widespread vaccination. More than 40 million people were vaccinated. But several cases of Guillain-Barre syndrome, a severe and sometime fatal condition that can be linked to some vaccines, caused the U.S. government to stop the program. The incident led to widespread distrust of vaccines in general (Reuters, 2009).
Abstract: Last week, when what is now called a "swine flu" was first reported to be infecting and killing some people in Mexico, health officials noted it was a strain of flu never before seen. In fact, it is technically incorrect to call this simply a "swine" flu. Analyses showed it's a mixture of swine, human and avian viruses, according to the Centers for Disease Control (CDC). Moreover, it is genetically different from the fully human H1N1 seasonal influenza virus that has been circulating globally for the past few years. Bottom line: the new flu virus contains DNA from avian, swine viruses (including elements from European and Asian viruses) and human viruses.
So did this curious mixture just develop naturally, out of the blue? Is it the result of inhumane farming practices, as the Humane Society of the United States (http://www.hsus.org/) has suggested, that exposes immune-compromised pigs to all sorts of animal and human feces?
Well, maybe. But let's go back and look at the facts to see if any other scenario could be possible.
First of all, there's the troublesome detail that the virus has elements that come from multiple continents. Then there's the fact that true swine flu is only rarely transmissible to humans -- this flu is spreading human-to-human, most likely because it contains DNA from human flu.
Could someone have deliberately mixed these viruses together? Is that possible? Absolutely.
Was this virus mixing being done artificially in the lab, or had it already been done? Yes.
Who was blending potentially swine, human and/or avian viruses in labs? Were those horrible generic boogie men known to Americans far and wide as "terrorists" doing it? There's no proof of bioterrorism at work here yet. However, there is evidence the United States government has been working on concocting new flu virus blends.
So could the hysteria-provoking, new swine flu have escaped from a lab? Or was it deliberately released as some kind of test? When these kinds of questions are asked, the knee-jerk reaction of the mainstream media (MSM) is to giggle and talk about "conspiracy theories" and to joke about wearing tinfoil hats.
But here's the potential smoking gun, the facts that suggest a potential source of the pandemic could be CDC labs. And at the very least, this possibility deserves thoughtful examination and research.
The University of Minnesota Center for Infectious Disease Research and Policy (CIDRAP) is hardly a place most Americans have heard about and, apparently, the Center's web site has news the MSM isn't familiar with, either. But information they published years ago has now taken on an urgent importance. CIDRAP, along with the Canadian newspaper Canadian Press (CP), revealed back in 2004 that the CDC was launching experiments designed to mix the H5N1 (avian) virus and human flu viruses. The goal was to find out how likely it was such a "reassortant" virus would emerge and just how dangerous it might be. Of course, it's logical to wonder if they also worked with the addition of a swine flu virus, too.
Here's some background from the five-year-old report by the University of Minnesota research center: "One of the worst fears of infectious disease experts is that the H5N1 avian influenza virus now circulating in parts of Asia will combine with a human-adapted flu virus to create a deadly new flu virus that could spread around the world. That could happen, scientists predict, if someone who is already infected with an ordinary flu virus contracts the avian virus at the same time. The avian virus has already caused at least 48 confirmed human illness cases in Asia, of which 35 have been fatal. The virus has shown little ability to spread from person to person, but the fear is that a hybrid could combine the killing power of the avian virus with the transmissibility of human flu viruses. Now, rather than waiting to see if nature spawns such a hybrid, US scientists are planning to try to breed one themselves -- in the name of preparedness."
And CDC officials actually confirmed the government had plans for the research. The CIDRAP News folks did a great job covering this important issue, which was apparently mostly ignored by the MSM back in 2004, and CIDRAP News wrote to the CDC for information. This e-mail produced an answer from CDC spokesman David Daigle who admitted the CDC was working on the project in two ways. "One is to infect cells in a laboratory tissue culture with H5N1 and human flu viruses at the same time and then watch to see if they mix. For the human virus, investigators will use A (H3N2), the strain that has caused most human flu cases in recent years," the CIDRAP story stated. This co-infection approach was described as slow and labor-intensive. However, it was a way to produce a new virus that appeared to be closer to what develops in nature.
There was another, faster way CDC scientists could create the mix, too. Called reverse genetics, it involves piecing together a new virus with genes from the H5N1 and H3N2 viruses. Reverse genetics had already been used successfully to create H5N1 candidate vaccines in several laboratories, the CDC's Daigle wrote. "Any viable viruses that emerge from these processes will be seeded into animals that are considered good models for testing how flu viruses behave in humans... The aim will be to observe whether the animals get sick and whether infected animals can infect others," he revealed in his e-mail.
What's more, the CP reported the CDC had already made hybrid viruses with H5N1 samples isolated from patients in Hong Kong in 1997, when there was the first outbreak of that virus, dubbed the "Hong Kong flu". It is not clear if the results of that research were ever published. Back in 2004, Dr. Nancy Cox, then head of the CDC's influenza branch, would tell the CP only: "Some gene combinations could be produced and others could not."
The CP's report noted that the World Health Organization (WHO) had been "pleading" for laboratories to do this blending-of-viruses research. The reason? If successful, these flu mixes would back up WHO's warnings about the possibility of a flu pandemic. In fact, Klaus Stohr, head of the WHO's global flu program at the time, told the CP that if the experiments were successful in producing highly transmissible and pathogenic viruses, the agency would be even more worried -- but if labs couldn't create these mixed flu viruses, then the agency might have to ratchet down its level of concern.
The 2004 CIDRAP News report addressed the obvious risks of manufacturing viruses in labs that, if released, could potentially spark a pandemic. However, the CDC's Daigle assured the Minnesota research group the virus melding would be done in a biosafety level 3 (BSL-3) laboratory. "We recognize that there is concern by some over this type of work. This concern may be heightened by reports of recent lab exposures in other lab facilities," he told CIDRAP. "But CDC has an incredible record in lab safety and is taking very strict precautions."
Five years later, we must ask more questions. Were those safety measures enough? Was the CDC creating or testing any of these virus mixes in or near Mexico? What other potentially deadly virus combinations has the US government created? Don't US citizens, as taxpayers who funded these experiments, have a right to know? And for all the residents of planet earth faced with a potentially deadly global epidemic, isn't it time for the truth? (Natural News, 2009).
Title: Anthrax Bacteria Get Help From Viruses And WormsTo Survive
Date: August 12, 2009
Abstract: When the bacteria that cause anthrax (Bacillus anthracis) aren’t ravaging livestock or being used in acts of bioterrorism, they spend their lives as dormant spores. In these inert but hardy forms, the bacteria can weather tough environmental conditions while lying in wait for their next host. This is the standard explanation for what B.anthracis does between infections, and it’s too simple by far. It turns out that the bacterium has a far more interesting secret life involving two unusual partners – viruses and earthworms.
A dying animal can release up to a billion bacterial cells in every single millilitre of blood. This torrent of microbes provides a feast of riches for bacteriophages – viruses that infect bacteria. Raymond Schuch and Vincent Fischetti from the Rockefeller University have found that the anthrax bacterium depends on becoming infected by phages. They began by isolating several strains of phages that specifically infect B.anthracis. The viruses hailed from a range of sources, including the soil, plant roots and worm guts. <
When these phages find bacterial targets, they inject their own DNA, which insinuates itself into the genome of the host. This process is called lysogeny and it is essential for the bacterium’s survival. The added viral DNA encodes proteins called sigma factors that change how bacterial genes are switched on. In doing so, they change the behaviour of the bacteria, giving them new abilities that boost their survival and allow them to colonise an intermediate host – the earthworm.
With their newly incorporated viral DNA, some bacteria formed spores while others were actually prevented from doing so, depending on the phage. Regardless, all the anthrax bacteria grew at almost twice the rate. The phage DNA brought out the social side of the bacteria, inducing them to cluster in groups. It also made them more likely to secreted more complex sugar molecules that form the building blocks of biofilms – the bacterial equivalent of towns and cities. Amid this matrix of sugars, the cells find shelter and protection.
Small wonder then that the infected bacteria are much better are surviving for long durations. Their advantage was so great in comparison to virus-free strains that Schuch and Fischetti suggest that phage infections may actually be necessary if anthrax bacteria are to survive in soil. Indeed, duo identified three bacterial genes that are activated by the phages and that are necessary for eking out a living in soil. When they inactivated these genes, the bacteria survived in these environments for the briefest of times.
The bacteria don’t have to survive in isolation either. Schuch and Fischetti speculate that their biofilms act as a staging ground from which to find a new host. Again, their viral hitchhikers come into play, giving them the ability to set up long-term colonies in the guts of earthworms. That’s hardly an easy environment, for it’s extremely low in oxygen and most bacteria are digested or excreted. Any permanent hangers-on must be able to stick tightly to the walls of the gut. The genetic manipulations of the virus could activate some latent ability of the bacteria to do just that.
The idea of worms as alternative hosts for anthrax bacteria, in between their decimations of livestock, was first put forward by Louis Pasteur in the 19th century, after he noticed that the soil near anthrax carcasses were rife with earthworms. Ignored for over a century, Pasteur’s idea has finally been confirmed.
The viruses within the bacteria aren’t totally dormant. Within a small proportion of cells, they multiply as viruses typically do, bursting out of their host and shedding thousands of infectious daughter virses into the environment. This process may kill a few of the anthrax bacteria, but it provides a route for the survivors to trade genetic material between each other.
As phage DNA hops in and out of bacterial genomes, they could take snippets of local DNA with them, transferring them from host to host and increasing the genetic diversity of the population. Don’t underestimate how extreme these changes can be: in a previous study, Jonathan Kiel showed that a phage taken from a related species, Bacillus cereus, managed to change a strain of anthrax bacteria so greatly that it was no longer genetically recognisable as the original strain, or even as the right species!
The picture painted by this new study is a far cry from the somewhat dull idea of anthrax bacteria lying dormant in the soil. Instead, it seems that the bacteria lead a secret life, and a most dynamic one, involving hidden potential unleashed by bacterial invaders-turned-partners (Discovery, 2009).
Title: Norway Says Found H1N1 Mutation In Flu Victims
Date: November 20, 2009
Abstract: Norwegian health authorities said on Friday they have discovered a potentially significant mutation in the H1N1 influenza strain that could be responsible for causing the severest symptoms among those infected.
"The mutation could be affecting the virus' ability to go deeper into the respiratory system, thus causing more serious illness," the Norwegian Institute of Public Health said in a statement.
There was no reason to believe the mutation had any implication for the effectiveness of flu vaccines or antiviral drugs made by groups such as Roche (ROG.VX), GlaxoSmithKline (GSK.L), Novartis (NOVN.VX) and AstraZeneca (AZN.L), the authorities said.
The World Health Organisation said that the mutation did not appear to be widespread in Norway and the virus in its mutated form remained sensitive to antivirals and pandemic vaccines.
A similar mutation had been detected in H1N1 viruses circulating in several other countries, including China and the United States, in severe as well as in some mild cases, it said.
"Although further investigation is under way, no evidence currently suggests that these mutations are leading to an unusual increase in the number of H1N1 infections or a greater number of severe or fatal cases," the WHO said in a statement.
H1N1, a mixture of swine, bird and human viruses, has killed at least 6,770 people globally, according to its latest update.
In Norway the mutation was found in the bodies of two people killed by the virus and of one person made seriously ill. The two infected by the mutated virus who died were among the first fatalities from the H1N1 pandemic in Norway, the institute said.
It was unclear whether the mutated virus was transmitted among humans, the health authorities said.
"Based on what we know so far, it doesn't seem like the mutated virus is circulating in the population, but rather that spontaneous changes have happened in the three patients," director Geir Stene Larsen at the public health institute said in the statement.
Norway has seen relatively more fatalities in the flu pandemic compared to the size of the population versus other European countries, with 23 confirmed deaths.
Public health authorities have said this could be due to the country being hit early in the pandemic's northern hemisphere winter wave, before a mass vaccination programme got underway.
"Nevertheless, it is important to study if there's still something about the Norwegian fatalities that separate us from other countries, and that make us learn something that strengthens our treatment of the seriously ill," director Bjorn-Inge Larsen at the Norwegian Directorate of Health said.
Dr. Anne Schuchat of the U.S. Centers for Disease Control and Prevention said, "This mutation has been seen sporadically."
She said it is sometimes seen in patients who have mild influenza symptoms.
"I think it is just too soon to say what this might mean long term," Schuchat told reporters in a telephone briefing. (Reporting by Richard Solem; Additional reporting by Stephanie Nebehay in Geneva and Maggie Fox in Washington; Editing by Matthew Jones and Louise Ireland) (Reuters, 2009).
Title: Fighting Bacteria With Bacteria – Common Nose Germ Provides New Weapon Against Superbugs
Date: May 19, 2010
Abstract: Our bodies are under siege, constantly fighting back assaults from disease-causing bacteria. But we are also home to many harmless bacterial species that are share our bodies to no ill effects. Now, it seems that these ‘commensals’ could be our hidden allies against their harmful cousins. In one such ally, a group of scientists has just discovered a potential new weapon against Staphylococcus aureus.
S.aureus is incredibly common, colonising the noses of a third of people in the USA, UK, Japan and other countries. Often, these colonies do nothing untoward, but if a full-blown infection sets in, the result can include life-threatening diseases like pneumonia, meningitis, toxic shock syndrome, endocarditis and sepsis. With the rise of MRSA and other staph strains that shrug off our most common antibiotics, the threat posed by this common nose bug has never been greater.
But S.aureus doesn’t have our noses to itself. It has to jostle for space with a close relative called Staphylococcus epidermidis. It’s the most common commensal in our noses and, indeed, the most common contaminating bacterium in laboratory equipment. S.epidermidis is harmless, except in people whose immune systems have been compromised. But more interestingly, it has the ability to stunt the growth of its more infamous cousin. Now, Tadayuki Iwase from Jikei University has isolated the protein it uses to do so.
Iwase swapped the noses of 88 volunteers and found that virtually all of them were colonised by S.epidermidis. However, S.aureus had only set up shop in just under a third. On the whole, the two bacteria seem to be able to co-exist in harmony, but Iwase found that some strains of S.epidermidis are anathemas to S.aureus.
Specifically, they caused problems for S.aureus’s ability to set up biofilms, the bacterial equivalent of cities. Thousands of bacteria swarm within these communities, embedded in a slimy matrix of DNA, proteins and sugars. Within biofilms, bacteria are harder to kill, making them an important public health challenge. But according to Iwase, some strains of S.epidermidis not only prevent S.aureus from creating biofilms, they also destroy existing ones. People who were colonised by these defensive strains were around 70% less likely to be colonised by S.aureus.
To work out the weapon that was keeping the rival bacteria are bay, Iwase let cultures of S.epidermidis cut a swath through S.aureus biofilms and analysed their secretions when the destruction had reached its peak. He managed to isolate a single protein called Esp or ‘S.epidermidis serine protease’ in full. The protein was absent from strains that couldn’t wipe out S.aureus biofilms and present in strains that could. If Iwase gave the latter bacteria them a chemical that negates the Esp protein, or if he removed the esp gene from them entirely, they lost their competitive edge against S.aureus.
Esp even works in tandem with our own defensive proteins, including one called hBD2 (human beta-defensin 2) that’s secreted by our skin cells. Alone, hBD2 can kill bacteria but it’s a bit of a wimp about it, while Esp (for obvious reasons) has no bacteria-killing ability of its own. But together, their powers are far greater, and they effectively kill S.aureus, even when it was under the protection of biofilms. (The idea that the two proteins have co-evolved with one another is an intriguing question for another time.)
As a final test, Iwase introduced the competitive strains of S.epidermidis into the noses of volunteers who were already colonised by S.aureus. Sure enough, these transplanted bacteria eliminated their evolutionary cousins. Even a purified dose of Esp alone did the trick.
These experiments are very exciting. Humans are fighting a pitched (possibly losing) battle against staph and MRSA in particular, and our antibiotic arsenal is falling short. What better source of new weapons than other bacteria that have been fighting the same fight for millennia? Obviously, there’s a lot of work to do to turn Esp into a viable treatment, but this study is a promising first step.
Even better, it seems that, for some unclear reason, S.aureus can’t evolve resistance to Esp. With its biofilms under attack, you would expect S.aureus to quickly adapt, but after a year of culturing the two species together, Iwase couldn’t find any evidence that of resistance (Discovery, 2010).
Title: Charitable Bacteria Protect Vulnerable Sisters From Antibiotics
Date: September 1, 2010
Abstract: Humans are capable of great charity, taking hits to their bank accounts and bodies to benefit their peers. But such acts of altruism aren’t limited to us; they can be found in the simple colonies of bacteria too.
Bacteria are famed for their ability to adapt to our toughest antibiotics. But resistance doesn’t spring up evenly across an entire colony. A new study suggests that a small cadre of hero bacteria are responsible for saving their peers. By shouldering the burden of resistance at a personal cost, these charitable cells ensure that the entire colony survives.
Henry Lee from the Howard Hughes Medical Centre assaulted a vat of Escherichia coli with increasingly strong waves of the drug norfloxacin, always using just enough to seriously impede their growth without killing them outright. As expected, the group became more resistant over time. By the end of the experiment, they were shrugging off doses of antibiotics that would have previously killed them.
But Lee found that not all the bacteria were equal. Most still remained vulnerable to the drug, and the group’s overall defences were bolstered by a small group of highly resistant individuals. The leaders of the resistance had all developed a mutation in a gene called all had particularly high levels of a protein called tryptophanase. Tryptophanase breaks down the amino acid tryptophan and produces indole, a chemical that acts like a call to arms. It rallies the colony into action.
When bacteria detect indole, they start mass-producing molecular pumps that evict any drugs that have breached their walls. With these molecules, the beleaguered bacteria can pump out norfloxacin faster than it can kill them.
Indole also tells bacteria to start toughening up. In response, the cells tune down certain genes that norfloxacin would normally use to kill them and tune up genes that protect their insides from damage. By producing indole, the most resistant bacteria were prompting changes in their weaker neighbours that greatly increased the amount of norfloxacin they could withstand.
When Lee peered into the genes of the most resistant cells, he found that their own resistance was the result of several personal adaptations that averted death by norfloxacin. They had altered genes that would normally be targeted by the drug, removing its targets. They had switched on genes that protect them from chemical damage or that mass-produce produce drug-pumps. None of these mutations affect the production of indole; they just gave the mightiest cells the chance they needed to produce this rallying chemical.
When Lee challenged his bacteria with another drug called gentamicin, he found exactly the same thing – a resistant elite promoting the survival of the group by releasing waves of indole. This seems to be a general tactic, rather than a drug-specific one.
Producing indole isn’t easy; it takes energy to manufacture. Why
should a small number of bacteria shoulder this burden to protect other
members of the colony? Lee thinks that relationships are the answer.
Having multiplied from common ancestors, the bacteria in the group are
all related to one another and carry virtually the same genes. In this
light, making a small sacrifice for the sake of genetically identical
others is a good move (Discovery, 2010).
Title: Tough Bacteria Use Domesticated Viruses To Resist Antibiotics
Date: January 5, 2011
Abstract: Even bacteria get sick. Tiny though they are, bacteria can be infected by even tinier viruses known as phages. Like tiny hypodermic needles, phages inject their genetic material into their bacterial hosts, turning them into factories for making more phages. The host usually dies in the aftermath. But some bacteria have turned these enemies into their allies. By adding the viruses’ DNA into their own genomes, they have become superbugs, able to tolerate harsh environments and shrug off antibiotics.
Once phages have injected their genes into a bacterium, they can make copies of themselves in two ways. The first is a brutish approach. The genes commandeer the host, using it to manufacture new viruses that eventually burst out of the cell – this is the lytic cycle. Alternatively, the phage DNA can infiltrate the bacterium’s genome, becoming part of it. When the bacterium divides in two, it copies the phage’s genes along well as its own. This is the lysogenic cycle, an altogether stealthier approach to making more phages.
Within the bacterial genome, the viral DNA is called a prophage. After being copied many times over in these new surroundings, it can pop out again to create a new phage. The prophage is little more than a genetic parasite. But sometimes, a prophage gets trapped by a crippling mutation. Unable to pop out, it becomes a genetic fossil, forever stuck within its host and destined only to preserve a trace of a past infection.
These captives are called cryptic prophages and they can make up a fifth of a bacterium’s DNA. Their existence is puzzling. Bacteria are known for having small, streamlined genomes, yet in they have foreign and potentially harmful viral DNA loitering among their genes. Why?
To find out, Xiaoxue Wang from Texas A&M University found all nine cryptic prophages from the common bacterium Escherichia coli and, with care and precision, snipped them all out. And to his surprise, the bacteria were the worse for it.
The prophages weren’t essential by any means. Without them, the bacteria survived quite reasonably, although they grew more slowly than normal strains. But they proved to be wimps when challenged with difficult conditions. They became up to 400 times more sensitive to antibiotics. They succumbed more readily to extremely salty or acidic conditions. And they were almost completely unable to form biofilms – fortified ‘cities’ where the microbes gather under the shelter of substances that they themselves secrete.
In many of these cases, Wang could weaken the bacteria by removing a single prophage, which suggests that many of the genes are active parts of the host. The cryptic prophages are no longer selfish parasites, nor are they truly passive fossils. Rather, they have been domesticated to serve their host.
There are other examples of phages bestowing important powers upon the bacteria they infect. E.coli is typically harmless but if it gets infected with the right phage, it can turn into a monster that causes dysentery. The phage inserts two genes into the bacterium’s genome, which allow it to produce poisons called Shiga toxins. Phages carry the CTX toxin that the bacterium Vibrio cholerae needs to cause cholera. Phages allow the bacteria that causes anthrax to find shelter in the guts of earthworms. Phages even allow bacteria to come to the aid of aphids. But in these cases, the phage genes need to pop out of their host. In the case of the cryptic prophages, even though the viral genes stay put, the bacterium still reaps the benefits.
Bacteria are great survivors, able to adapt to a wide variety of conditions, from oil-soaked oceans to arsenic-rich lakes to antibiotic-treated humans. Wang’s study suggest that phages could provide bacteria with new ways of coping with these environments, maybe even acting as vehicles for transporting genes from one species to another. He writes, “In effect, the cell uses the tools it obtained from its former enemy, phage, to cope with new environments.”
Now that we know about these alliances, we could use them to our
advantage. Wang suggests that we could find new ways of preventing
bacteria from resisting our antibiotics by blocking the proteins
produced by their domesticated viruses (Discovery, 2011).
Title: Fighting Evolution With Evolution – Using Viruses To Target Drug-Resistant Bacteria
Date: May 31, 2011
Abstract: We are losing the war against infectious bacteria. They are becoming increasingly resistant to our antibiotics, and we have few new drugs in the pipeline. Worse still, bacteria can transfer genes between each other with great ease, so if one of them evolves to resist an antibiotic, its neighbours can pick up the same ability. But Matti Jalasvuori from the University of Jyvaskyla doesn’t see this microscopic arms-dealing as a problem. He sees it as a target.
Usually, antibiotic-resistance genes are found on rings of DNA called plasmids, which sit outside a bacterium’s main genome. Bacteria can donate these plasmids to one another, via their version of sex. The plasmids are portable adaptations – by trading them, bacteria can rapidly respond to new threats. But they aren’t without their downsides. Plasmids can sometimes attract viruses.
Bacteriophages (or “phages” for short) are viruses that infect and kill bacteria, and some of them specialise on those that carry plasmids. These bacteria may be able to resist antibiotics, but against the phages, their resistance is futile.
Scientists have known about these plasmid-hunting phages for over four decades, but Jalasvuori has only now shown that they could prove useful to us. He found that the phages can dramatically reduce the level of antibiotic resistance in colonies of bacteria, by selectively assassinating the plasmid-carriers.
Jalasvuori worked with two common gut bacteria – Escherichia coli and Salmonella enterica – both of which carried plasmids with antibiotic-resistance genes. In the absence of phages, all of the bacteria resisted antibiotics. When Jalasvuori added a phage called PRD1, that proportion fell to just 5% within 10 days.
The bacteria adapted to the phage assault by jettisoning their plasmids, and with them, their antibiotic-resistance genes. These survivors were now resistant to phages, but the vast majority of them could once again be killed by antibiotics.
The method isn’t perfect. A small proportion of the bacteria resisted both phages and antibiotics. However, Jalasvuori found that they also formed smaller colonies and had lost the ability to swap genes between one another. Their invincibility came at a substantial cost – compared to normal cells, they were hobbled eunuchs.
Targeting plasmids is a clever strategy that uses the rapid evolution of bacteria against them. Rather than coming up with new weapons in an ever-escalating arms race, Jalasvuori made it too costly for bacteria to keep their defences. It’s like tackling gun crime by penalising gun ownership rather than developing better bullet-proof vests.
However, Jalasvuori is refreshingly cautious about his work. He says, “There are a number of important caveats to these promising preliminary results.” For a start, his bacteria evolved under the threat of phages, but not antibiotics. If they had been exposed to both, there would almost certainly have been more double-resistant strains, which could have ultimately found ways of getting over their weaknesses.
On top of that, not all plasmids are the same; some could potentially hide from threatening phages, and go on to harbour resistance genes. Finally, as Jalasvuori writes, “As with all test-tube studies, the relevance to natural environments is unclear.”
It’s debatable whether this would ever lead to a practical way of
dealing with drug-resistant microbes, but it’s certainly a lead. And
with a problem as worrying as antibiotic resistance, every lead is an
interesting one (Discovery, 2011).
Title: House Mice Picked Up Poison Resistance Gene By Having Sex With Related Species
Date: July 21, 2011
Abstract: Since 1948, people have been poisoning unwanted rats and mice with warfarin, a chemical that causes lethal internal bleeding. It’s still used, but to a lesser extent, for rodents have become increasingly resistant to warfarin ever since the 1960s. This is a common theme – humans create a fatal chemical – a pesticide or an antibiotic – and our targets evolve resistance. But this story has a twist. Ying Song from Rice University, Houston, has found that some house mice picked up the gene for warfarin resistance from a different species.
Warfarin works by acting against vitamin K. This vitamin activates a number of genes that create clots in blood, but it itself has to be activated by a protein called VKORC1. Warfarin stops VKORC1 from doing its job, thereby suppressing vitamin K. The clotting process fails, and bleeds continue to bleed.
Rodents can evolve to shrug off warfarin by tweaking their vkorc1 gene, which encodes the protein of the same name. In European house mice, scientists have found at least 10 different genetic changes (mutations) in vkorc1 that change how susceptible they are to warfarin. But only six of these changes were the house mouse’s own innovations. The other four came from a close relative – the Algerian mouse, which is found throughout northern Africa, Spain, Portugal, and southern France.
The two species separated from each other between 1.5 and 3 million years ago. They rarely meet, but when they do, they can breed with one another. The two species have identifiably different versions of vkorc1. But Song found that virtually all Spanish house mice carry a copy of vkorc1 that partially or totally matches the Algerian mouse version. Even in Germany, where the two species don’t mingle, a third of house mice carried copies of vkorc1 that descended from Algerian peers.
What does the Algerian version of the gene do? Song found out after getting a tip from a pest control officer who she works with. He told her that he was having trouble getting rid of house mice in a German bakery, even after trying a powerful second-generation rodenticide called bromadiolone, or “super-warfarin”.
The officer sent over some of these resistant mice and when Song looked at their genes, she found a surprise. Both copies of their vkorc1 genes were perfect matches for the version carried by Algerian mice, but the rest of their genes showed them to be house mice. This tiny out-of-place gene made all the difference – it made the house mice nigh-invulnerable to warfarin and its chemical relatives. Super-warfarin kills around 85% of normal house mice, but it only worked against 9% of the German ones with the Algerian gene.
By the time humans developed warfarin, Algerian mice already had a head-start in resisting it. These rodents live in open, scrubby habitats and they feed mostly on seeds. They don’t get a lot of food that’s rich in vitamin K, such as leafy green vegetables and Song thinks that their vkorc1 genes have adapted to help them cope with this vitamin deficiency – indeed, it’s one of the fastest-evolving genes in its entire genome.
It just so happens that the same adaptations also allow the mice to resist pesticides like warfarin that target vitamin K. It’s probably no coincidence that other rodents which specialise on grains – such as the golden hamster and Egyptian spiny mouse – also tend to tolerate warfarin-based chemicals.
The Algerian mice transferred their resistance to house mice by breeding with them, somewhere between 5 and 32 years ago. Hybrids between the two species would normally suffer from physical problems that limit their survival in the wild, and around half of them are sterile.
But these mice were buoyed by their warfarin-resistant copies of vkorc1. At a time when humans were using warfarin and related poisons, these hybrid mice had suddenly gained a valuable defence, one powerful enough to compensate for their other disadvantages. They survived and mated with other house mice, spreading the resistance gene to their own pups.
In this way, the mice are rather reminiscent of bacteria. Individual bacteria can develop genetic tweaks that render them invulnerable to antibiotics, but they can also pick up such mutations from one another. They do so via their equivalent of sex – a process called conjugation where genetic material passes across physical bridges, established across two bacteria. The house mice have done something similar, picking up a warfarin-resistant version of vkorc1 by having sex with Algerian mice.
Humans were probably responsible for these lucky liaisons. The two
species used to live in completely different parts of the world. They
would never have met, had humans not brought house mice with them as
they expanded into Western Europe. Once the two species showed up in the
same place, they started mating. Later, humans were again responsible
for giving the hybrids an edge over their pure-bred house mouse
relatives. Our attempts to kill them merely unveiled a strength that had
been hiding for centuries (Discovery, 2011).
Title: It’s Back: Bird Flu Returns, And This Time It’s Mutated
Date: August 30, 2011
Abstract: During the last couple of flu seasons, we were all worried about H1N1, a new and virulent strain of influenza, but this winter we may have to contend with a much deadlier foe: H5N1, or bird flu. Some Asian countries are reporting this week the first cases of a mutant strain of the virus spreading in poultry.
The U.N. Food and Agriculture Organization (FAO) reported on Monday that the H5N1 virus has mutated, something that public health officials had feared would happen and that could possibly make the virus more dangerous to people.
In its original form, H5N1 primarily infects wild birds and poultry, including geese, chickens, ducks and turkeys, but only rarely jumps into people. Still, the fact that some people have become infected with H5N1 by eating improperly prepared and contaminated poultry — the virus has killed 331 people and infected 565 since it first appeared in 2003 — led experts to warn that it was only a matter of time before it altered into a form that made it easier to spread to humans.
It’s not clear yet whether that has happened, but health authorities are concerned by the an new H5N1 variant spreading in poultry in both China and Vietnam; the new strain is resistant to current vaccines. In the years since H5N1 began spreading among bird and poultry flocks, millions of birds have been culled, and many countries have adopted vaccination programs to inoculate domestic fowl to prevent the spread of the virus. But six countries have continued to see H5N1 among their poultry population each year: Bangladesh, China, Egypt, India, Indonesia and Vietnam.
And after declining since a peak in cases in 2005-06, when some 4,000 cases were reported, the rate of H5N1 outbreaks among both animals and people has started to inch up this year. “When you look at 2011, there is a trend upward in cases,” says Juan Lubroth, FAO’s chief veterinary officer. “And in several countries that had experience with H5N1 already, they are seeing a new introduction of [the virus]. We want to alert the community that we are seeing an upswing of cases.”
Already, Cambodia, which shares a border with Vietnam, has reported eight cases of H5N1 infection this year, and all have been fatal. It’s not clear whether any of these involved the mutant strain, but experts say the more cases of infection among humans and birds there are, the more opportunities the virus has to recombine and mutate into a form that is more easily transmissible to people.
Containing the new H5N1 strain, known as H5N1 126.96.36.199, may be a challenge, since many of the infected fowl are wild species that migrate, and can easily spread the virus over thousands of miles. In the past two years, experts have tracked the original version of H5N1 to regions where it has never been reported before. It has also shown up again in places that had been virus-free for several years, including Israel, the Palestinian territories, Bulgaria, Romania, Nepal and Mongolia.
The same could happen with H5N1 188.8.131.52. “What has surprised us a bit is the geographical spread and also some concerns that the vaccine readily used in combating H5N1 is not as effective with this particular strain,” says Lubroth. “There is a concern there, so we wanted to alert the world community.”
But as alarming as the appearance of the mutant, vaccine-resistant strain is, some experts say that it’s not that surprising. Unlike the vaccines we use against human flu, influenza inoculations for poultry don’t change year to year, so it was just a matter of time before a resistant strain would emerge.
Most agriculture experts continue to use the same vaccine for 10 to 20 years with reasonable success in containing influenza in their flocks. “The reason the vaccine is now not working well is that the [Vietnamese] eventually pushed their luck too far,” says Ruben Donis, chief of the molecular virology and vaccines branch in the influenza division of the U.S. Centers for Disease Control and Prevention (CDC). “They have been using the same vaccine from 1996, so the virus in the vaccine is 15 years old.”
Lubroth says that Chinese health authorities are currently working on a new vaccine that could block the mutant influenza strain more effectively, and that FAO is discussing with Vietnamese authorities how best to proceed with their poultry vaccination in light of the appearance of the new virus. Continuing to inoculate poultry with an ineffective vaccine would only push the virus to mutate more rapidly toward a resistant and possibly more virulent strain.
Health authorities aren’t sure how the new strain will impact the upcoming human flu season, but they aren’t taking any chances. When the World Health Organization’s influenza experts met in February to decide which strains to include in the upcoming seasonal flu shot, they also selected certain virus strains to be stockpiled in case of an outbreak. One of those was a version of H5N1 of the same clade, or group, as the mutant strain now circulating among the birds in China and Vietnam. That means that the virus is ready to go for testing and development into a vaccine should it suddenly emerge as a problem among people.
And such preparedness is critical when it comes to the notoriously unpredictable flu. In an earlier statement on FAO’s website, Lubroth noted, “The general departure from the progressive decline [in H5N1 cases] observed in 2004-2008 could mean that there will be a flare up of H5N1 this fall and winter, with people unexpectedly finding the virus in their backyard. Preparedness and surveillance remain essential. This is no time for complacency. No one can let their guard down with H5N1” (TIME, 2011).
Title: Bacteria: Resisting Antibiotics Since At Least 30,000 BC
Date: August 31, 2011
Abstract: The rise of drug-resistant bacteria is one of the most important threats facing modern medicine. One by one, our arsenal of antibiotics is coming up short against microbes that can pump them out, slip under their notice, deactivate them, or even eat them. But these tricks aren’t new. Bacteria have been defeating antibiotics for millennia, long before Alexander Fleming noticed a piece of mould killing off bacteria in a Petri dish. And the best proof of that longstanding struggle has just emerged from the ice-fields of Alaska.
In 30,000-year-old samples of frozen soil, Vanessa D’Costa and Christine King from McMaster University have found a wide variety of antibiotic-resistant genes. They would have allowed ancient bacteria to shrug off many modern drugs such as tetracyclines, beta-lactams and vancomycin.
Vancomycin resistance is especially interesting. This drug has traditionally been used as weapon of last resort, a drug to use when all others have failed. When vancomycin-resistant bacteria first emerged in 1987, it was a surprising blow. Since then, resistant versions of more common bacteria, such as staph (VRSA) have reared their heads.
These superbugs neutralise vancomycin using a trio of genes known collectively as vanHAX. Together, they alter the protein that’s attacked by the drug, rendering it useless. D’Costa and King found that their ancient sequences include the entire vanHAX cluster. They even resurrected these ancient genes, created proteins from them, and showed that they have the same shape, and do the same thing, as their modern counterparts.
D’Costa and King write that their results disprove the idea that antibiotic resistance is a modern phenomenon. Instead, it’s been part of bacterial life long before the modern use of antibiotics. But I’m really not sure how many people would still hold to that view. First, many antibiotics come from natural sources. Penicillin, the first to be synthesised, famously comes from Fleming’s surreptitious mould. These natural antibiotics evolved to keep bacteria at bay between 40 million and 2 billion years ago, so it’s extremely likely that bacteria have been resisting them for just as long.
Second, we know that the environment is teeming with resistance genes. In her own earlier study, D’Costa found that soil bacteria are a massive reservoir for resistance genes – a “resistome “ – which infectious bacteria could draw upon. Meanwhile, Gautam Dantas found that our soils are so full of resistant bacteria that random sampling produced strains that not only resist antibiotics, but actually eat them. He also found that the bacteria in our guts are another reservoir of resistance.
Regardless, D’Costa and King’s point stands: they have certainly found the oldest known examples of resistance genes. There have been similar claims in the past, but all of them controversial. Bacteria are so omnipresent that any team claiming to have found ancient samples must bend over backwards to prove that these aren’t modern contaminants. And none of the previous groups did this well enough, which means that their claims have not been replicated.
To show that their samples are authentically ancient, D’Costa and King pulled out all the stops. They did all of their lab work in special clean rooms. They showed that their samples included DNA from other animals that lived at the right time, such as mammoths, but nothing from species that are common today, like elk, moose or spruce. They even sprayed their drilling equipment, and the surface of their unearthed ice cores, with glow-in-the-dark bacteria. This way, they could immediately tell if anything from the outside world had leached into the interior parts of the cores – the parts where they drew their samples from. Nothing had.So what does this mean for the problem of antibiotic resistance today? Is this an old problem that is being blown out of proportion? Can we let the wanton use of antibiotics in modern healthcare and agriculture off the hook? Hardly. These conditions still create intense evolutionary pressures that favour the rise of resistant bacteria. The fact that resistant genes are widespread and ancient does not change that. It simply means that in times of need, beleaguered bacteria have a vast and longstanding range of defences to draw from. For every new sword that we fashion, there is a millennia-old shield lying around, just waiting to be brandished again (Disocvery, 2011).
Title: FAO Warnings Follow Rise In Replikins Count For Both H5N1 And Swine Flu
Date: August 31, 2011
Abstract: The possible combination of influenza strains H1N1 (high infectivity) and H5N1 (high lethality) is a matter of global concern (1, 2). Bioradar UK Ltd announced today (3) first, that the Replikin Counts of the two virus strains have risen simultaneously, not seen previously. Additionally, the rise is to their highest levels in 50 years (H1N1, 16.7; H5N1, 23.3), and that clinical outbreaks of each strain are now occurring. These simultaneous conditions may increase the risk that the two virus strains might come into contact with each other more frequently, facilitating transfer of genomic material to form a hybrid (Replikins, 2011).
Title: Five Easy Mutations To Make Bird Flu A Lethal Pandemic
Date: September 16, 2011
Soure: New Scientist
Abstract: H5N1 bird flu can kill humans, but has not gone pandemic because it cannot spread easily among us. That might change: five mutations in just two genes have allowed the virus to spread between mammals in the lab. What's more, the virus is just as lethal despite the mutations.
"The virus is transmitted as efficiently as seasonal flu," says Ron Fouchier of the Erasmus Medical Centre in Rotterdam, the Netherlands, who reported the work at a scientific meeting on flu last week in Malta.
"This shows clearly that H5 can change in a way that allows transmission and still cause severe disease in humans. It's scary," says Peter Doherty, a 1996 Nobel prizewinner for work in viral immunology.
H5N1 evolved in poultry in east Asia and has spread across Eurasia since 2004. In that time 565 people are known to have caught it; 331 died. No strain that spreads readily among mammals has emerged in that time, despite millions of infected birds, and infections in people, cats and pigs. Efforts to create such a virus in the lab have failed, and some virologists think H5N1 simply cannot do it.
The work by Fouchier's team suggests otherwise. They first gave H5N1 three mutations known to adapt bird flu to mammals. This version of the virus killed ferrets, which react to flu viruses in a similar way to humans. The virus did not transmit between them, though.
Then the researchers gave the virus from the sick ferrets to more ferrets - a standard technique for making pathogens adapt to an animal. They repeated this 10 times, using stringent containment. The tenth round of ferrets shed an H5N1 strain that spread to ferrets in separate cages - and killed them.
The process yielded viruses with many new mutations, but two were in all of them. Those plus the three added deliberately "suggest that as few as five are required to make the virus airborne", says Fouchier. He will now test H5N1 made with only those five.
All the mutations have been seen separately in H5N1 from birds. "If they occur separately, they can occur together," says Fouchier. Malik Peiris of the University of Hong Kong, a flu virologist, says this means H5N1 transmissible between humans can evolve in birds, where it is circulating already, without needing to spend time in mammals such as pigs.
Peter Palese, a flu specialist at Mount Sinai Medical Center in New York City who has expressed doubts that H5N1 can adapt to mammals, is not convinced.
"Ferrets are not humans," he says. "H5N1 has been around for a long time" and failed to mutate into a form that can jump between people.
"That it has not adapted doesn't mean it cannot," replies Jeffery Taubenberger of the US National Institutes of Health in Bethesda, Maryland, who studies how a bird flu became the deadly pandemic of 1918 (New Scientist, 2011).Title: Making Viruses The Natural Way
Date: December 2, 2011
Abstract: When it comes to viruses, we humans like to pretend we know much more than we really do. It’s understandable. The influenza virus, for example, has only ten genes. It is just a shell that delivers genes and proteins into a host cell, where it hacks the biochemistry to manufacture more viruses. It seems like such an easy biological problem to solve.
Yet the flu and other viruses hide a complexity which virologists have only partly uncovered. The idea that someone could intentionally design a super-lethal virus from scatch–as plausible as it may seem–is, for now, a delusion.
If you’ve been following the news this past week, you may think I’ve just been proven wrong. Reports have surfaced about two teams of scientists producing flu viruses that could potentially kill millions if they escaped from the labs. The scientists have the viruses locked up tight for now, and government officials are debating whether they can publish their results. (New Scientist and Science have excellent reports.)
So is this evidence that scientists have become viral Frankensteins, who can engineer pathogens at will? Hardly.
The new research is part of a long-running struggle to understand how new flu strains arise. It’s clear that all flu viruses that infect humans ultimately evolved from viruses that infect birds. From time to time, people can pick up these viruses, which infect their airway. Depending on the strain, bird flu may be harmless or lethal to humans. But for the most part, it can’t get from one human to another. It’s too well adapted for life in birds.
On rare occasion, a bird flu does manage to adapt to humans. It may experience natural selection, it may pick up some genes from human flu viruses, or both. Scientists are still trying to figure out what it takes for a flu virus to make this transition. It’s an important question, not just as a matter of fundamental biology but as a matter of global health. When new bird flus jump to humans, we lack immune defenses against them, and they can thus cause worldwide pandemics.
Flu experts have had their eye on one strain of bird flu in particular for a while now: H5N1. It’s proven extraordinarily lethal, and yet, since it first came to light in 1997, it hasn’t managed to make the big leap and start spreading from person to person. If you get H5N1, you’re in big trouble. But not many people get it. Yet.
Does this mean that H5N1 just doesn’t have what it takes to become the next great pandemic? Or does it mean the virus simply hasn’t evolved the right recipe yet?
Scientists have tried to answer this question by tinkering with the virus. Instead of trying to make a virus that spreads among people, they infected ferrets, which turn out to have much the same experience with the flu as we humans do. In April, CDC scientists published the latest of these studies. They focused their attention on a protein called hemagglutinin, which flu viruses use to get into host cells. Based on earlier experiments, the CDC scientists reasoned that the right tweak to the structure of hemagglutinin in H5N1 could switch it from binding strongly to bird cells to mammal cells.
But their rational tweaks failed. They concluded that there was a lot more to becoming a human flu that we don’t yet understand.
The studies that have now hit the news have succeeded where other experiments have failed. The difference is that instead of trying rational tweaks, the scientists sat back and let evolution do the tweaking.
According to the news reports, the scientists used a tried-and-true method known as serial passage. You infect an animal. It gets sick. You wait for the virus to replicate inside its animal host–as new mutants arise and natural selection favors some mutants over others–and then take some viruses from the sick animal and infect a healthy one. You repeat this, moving the virus from host to host.
Interesting things can happen when you let viruses evolve under these conditions. Natural selection can produce viruses with many new mutations, which together let them reproduce faster in the lab than their ancestors. And those viruses, in some cases, can be a lot more dangerous than their ancestors.
Back in 2007, for example, a virologist named Kanta Subbarao and her colleagues transformed the SARS virus this way. SARS evolved from a bat virus, crossing over into humans in 2003. It killed over 900 people before it mysteriously disappeared. Subbarao wanted to find a way to study SARS in lab animals, such as mice. Mice normally don’t get sick from human SARS viruses, though, even though the virus can replicate at a low rate inside them. Even when mice are genetically engineered so that they can’t develop an immune system, SARS can’t harm them.
So Subbarao and her colleagues that instead of changing the mice, they’d change the virus. They inoculated mice with the SARS virus, gave it a chance to replicate inside them, and then isolated the new viruses to infect new mice.
Over the course of just 15 passages, it changed from a harmless virus into a fatal one. One sniff of SARS was now enough to kill a mouse.
As Martin Enserink reports in Science, the new experiments on bird flu were similarly effective. They turned H5N1 into a ferret flu in just 10 generations. By the time the scientists were done, they no longer had to ferry the flu from one ferret to the next. A healthy ferret just had to be placed near a sick one; the virus could travel through the air. When they examined the new strain, they discovered five mutations in two genes. All five mutations have been found in natural H5N1 viruses–just not all in one virus.
A mammal-ready flu virus was beyond human reason, in other words, but it was fairly easy for evolution to find, given the right condtions. That suggests that H5N1 may not have far to evolve to make us its host. Of course, a serial passage experiment is not identical to the flu’s natural world, where it circulates among millions of birds and sometimes encounters people. But it’s disturbingly close.
And if it’s so easy for mutations to turn H5N1 into a human flu, the experimental viruses have a lot to tell us
about what we may be facing in the future. There’s no point in
condemning the scientists for tampering with nature. They were watching
nature do what it does disturbingly well (Discovery, 2011).
Title: The Polio Genome
It’s now possible to go from data printed on a piece of paper or stored in a compute and, without the organism itself, re-construct a life form.
John LaMontagne, National Institute of Allergey and Infectious Diseases, 2002
A genome is the genetic material of an organism. In 1981, two different research groups, Vincent Racaniello and David Baltimore at Massachusetts Institute of Technology and Eckard Wimmer’s team at State University of New York, Stony Brook, published the poliovirus genome. They used an enzyme to switch the single strands of viral ribonucleic acid—RNA—to double strands of deoxyribonucleic acid—DNA—and then determined the sequence of adenine, thymine, guanine, and cytosine encoding the five molecules that are the substance of the virus’s existence.
Poliovirus lacks the ability to correct its mutations, so its genome evolves at one to two nucleotide substitutions per week. It is always changing.
In 2002, investigators at the State University of New York in Stony Brook used the published genetic sequence to synthesize a DNA version of poliovirus. Then they used an enzyme to convert the DNA to RNA and grew the virus in a cell-free extract. Animal tests showed that the synthesized poliovirus caused paralysis.
did not use any machine for sequencing the poliovirus genome. It was
all done by hand—my hands! I used what was known as the ‘Maxam-Gilbert’
method, in which four different chemical reactions are carried out on
the DNA. The products are then fractionated on thin polyacrylamide gels,
which were poured manually, run, and then carefully removed from the
plates, dried, and exposed to X-ray film. The sequencing ‘ladders’ were
then read by myself on a light box and entered manually into a computer.
But we didn’t have individual computers back then, so I used a terminal
hooked up to an MIT central computer.”
—Vincent Racaniello, 1981 (NMAH, 2012).
Title: Bird Flu Mutation Study Stopped In Fear Of Deadly Global Outbreak
Date: January 21, 2012
Source: Russia Today
Abstract: Under pressure to put their research on hold due to fear of a biological disaster, an international team of scientists have voluntarily suspended their study on an advanced, incredibly deadly mutation of the H5N1 bird flu.
In an effort to better understand the deadly bird flu virus, Ron Fouchier of Erasmus Medical College in the Netherlands, Adolfo Garcia-Sastre of Mount Sinai School of Medicine in New York and Yoshihiro Kawaoka of the University of Wisconsin, Madison have been slaving over their study of the avian influenza. In conducting their own research, the team of scientists was able to mutate the original H5N1 virus into a much more lethal form to see how the outbreak could increase in intensity if not controlled outside of the lab. As word came around late last year that their research had returned a variation able to induce an international outbreak, however, the scientific community urged them to abandon their study in fear that the mutated strain would escape the lab and cause a deadly, worldwide outbreak.
With the fear failing to subside weeks later, the team of scientists has temporarily halted their research.
In its natural form, the bird flu virus has led to nearly 600 known cases and 340 deaths since it was discovered in 2003. That year there were only four outbreaks, all in East Asia, although in the years since an outbreak has claimed lives as far west as Egypt. The scientists were studying what damage a mutated strain of the virus could bring, but the US National Science Advisory Board for Biosecurity cautioned them to refrain from publishing the results of their finding, fearful that it would influence budding bioterrorists to use the study to create their own strain and launch an epidemic.
Despite the Board’s urging, others in the science community were skeptical. "In the end, is the likelihood of misuse outweighed by the danger of beginning a Big Brother society?" Professor Wendy Barclay of Imperial College London asked the Daily Mail last month.
The researchers say in a letter published in the journals Nature and Science on Friday that they will take a two-month break from their efforts. Since news of their study caught wind, the US government, the World Health Organization and other international bodies have been evaluating a way to go about publishing the findings in periodicals eventually, taking into account their research but avoiding the publishing of a how-go guide for biological warfare.
“We realize that organizations and governments around the world need time to find the best solutions for opportunities and challenges that stem from the work,” the scientists write.
“We hope that by having
a calm and reasoned discussion of the facts, scientists and biosecurity
experts can reach a better understanding and find ways to enable the
research to go forward while minimizing risks,” adds Kawaoka (Russia Today, 2012).
Title: Big Pharma Creates Resistant “White Plague”
Through Mass Drugging
Date: March 21, 2012
Source: Natural Society
Abstract: Thanks to widespread and unnecessary usage of antibiotics throughout the modern world, a heavily drug-resistant form of tuberculosis is now striking fear into the hearts of scientists and doctors alike. Affecting both poor and rich, those affected with the disease are put into quarantine and injected with a large number of super drugs. If the disease were to spread and develop, tuberculosis experts are worried that medical professionals would be helpless to stop it — at least when it comes to more of big pharma’s drugs. Natural solutions do exist, and they don’t involve the very drugs that spawned the ‘white plague’ in the first place.
India is receiving the bulk of the blame for spurring on the drug-resistant killer, as the country is known for its massive overuse of antibiotics. In fact, India has the most cases of multi-drug resistant tuberculosis in the world, with more than 100,000 cases of the disease. While multi-drug resistant tuberculosis is still quite deadly, it is the ‘extensively drug-resistant’ and ’totally drug-resistant’ tuberculosis that worries many health organizations and officials.
‘Totally a Man
Make no mistake that this is not a ‘natural’ evolution of disease, but a result of excessive drug use made possible by big pharma and mainstream health officials. Even members of the World Health Organization’s ‘Stop TB Partnership’ are outraged over the man-made disease progression, with member Lucica Ditiu stating that the drug-resistant TB “is a totally man-made disease”. Dr. Zarir Udwadia, also a TB specialist from India, had similar statements, explaining that that resistant strains were ”an accident waiting to happen.”
Dr. Udwadia published a report in the journal Clinical Infectious Diseases last year documenting four cases of totally drug-resistant tuberculosis. Currently, he has about twelve cases of the resistant disease with no treatment options left, and three have already died. Each medicine the doctor used to combat the mutated bacteria failed, with the bacteria immune to 12 drugs total. Dr. Udwadia explains that to even get to the point of developing such a drug resistant strain, it requires severe misuse of antibiotic drugs:
“To get to this stage, you have to have amplified resistance over years, with loads of misuse of (antibiotic) drugs. And no other country throws around second-line drugs as freely as India has been doing.”
It is clear that the resistant strain is a real threat to public health, with many experts concerned about a potential pandemic. Unfortunately these very same individuals who blow the whistle over the new resistant ‘white plague’ being a man-made disease are turning to even more pharmaceuticals to ‘treat’ the condition. This is a serious web of drug use, with drugs creating problems that require even more drug usage. There’s simply no room for a cure within this drug paradigm, because even if they make a drug powerful enough to wipe out the resistant tuberculosis bacteria, it comes with an onslaught of symptoms that ‘require’ more drugs.
In one case of treatment, for example, Anna Watterson was given so many drug injections in an attempt to treat the resistant disease that she was heavily bruised, constantly nauseous, and unable to go out into the sun.
Instead of subjecting yourself to this ‘drug web’, you can utilize natural solutions that will also serve to enhance other biological aspects of your life as well. Vitamin D3, for example, can not only boost your overall immunity and resistance to tuberculosis, but it can also help fight the disease once you’ve been infected. Scientists have even found that vitamin D intake can significantly reduce tuberculosis associated mortality on a global scale. But what if you’re infected with the totally resistant mega bacteria?
Garlic has been found to outpace drugs in the treatment of resistant tuberculosis, putting pharmaceuticals to shame and of course boosting your overall health in the process. This has been proven by more than one piece of peer-viewed research, with scientists finding garlic to be one of many natural solutions that should be considered by all medical professionals. Amazingly, there are 43 other natural substances documented as powerful solutions to tuberculosis, virtually all of which most doctors ignore. In the abstract of the study from the University of Health Sciences in Pakistan, scientists state:
“Alternate medicine practices with plant extracts including garlic should be considered to decrease the burden of drug resistance and cost in the management of diseases. “
Big pharma’s drugs
spawned this new plague, so why take them to fight it? Empower your health
naturally through nutrient-dense foods, supplements, and pure water. In
particular, stock up on vitamin D and turmeric — they will be highly beneficial in the event of a pandemic or disease
outbreak (Natural Society, 2012).
Title: Drug-Defying Germs From India Speed
Date: May 7, 2012
Abstract: Lill-Karin Skaret, a 67-year-old grandmother from Namsos, Norway, was traveling to a lakeside vacation villa near India’s port city of Kochi in March 2010 when her car collided with a truck. She was rushed to the Amrita Institute of Medical Sciences, her right leg broken and her artificial hip so damaged that replacing it required 12 hours of surgery.
Three weeks later and
walking with the aid of crutches, Skaret was relieved to be home. Then her
doctor gave her upsetting news. Mutant germs that most antibiotics can’t kill
had entered her bladder, probably from a contaminated hospital catheter in
India. She risked a life-threatening infection if the bacteria invaded her
bloodstream -- a waiting game over which she had limited control, Bloomberg Markets
magazine reports in its June issue.
“I got a call from my doctor who told me they found this bug in me and I had to take precautions,” Skaret remembers. “I was very afraid.”
Skaret was lucky. Eventually, her body rid itself of the bacteria, and she escaped harm from a new type of superbug that scientists warn is spreading faster, further and in more alarming ways than any they’ve encountered. Researchers say the epicenter is India, where drugs created to fight disease have taken a perverse turn by making many ailments harder to treat.
India’s $12.4 billion pharmaceutical industry manufactures almost a third of the world’s antibiotics, and people use them so liberally that relatively benign and beneficial bacteria are becoming drug immune in a pool of resistance that thwarts even high-powered antibiotics, the so-called remedies of last resort.
Poor hygiene has spread resistant germs into India’s drains, sewers and drinking water, putting millions at risk of drug-defying infections. Antibiotic residues from drug manufacturing, livestock treatment and medical waste have entered water and sanitation systems, exacerbating the problem.
As the superbacteria take up residence in hospitals, they’re compromising patient care and tarnishing India’s image as a medical tourism destination.
“There isn’t anything you could take with you traveling that would be useful against these superbugs,” says Robert Moellering Jr., a professor of medical research at Harvard Medical School in Boston.
The germs -- and the gene that confers their heightened powers -- are jumping beyond India. More than 40 countries have discovered the genetically altered superbugs in blood, urine and other patient specimens. Canada, France, Italy, Kosovo and South Africa have found them in people with no travel links, suggesting the bugs have taken hold there.
Drug resistance of all sorts is bringing the planet closer to what the World Health Organizationcalls a post-antibiotic era.
“Things as common as strep throat or a child’s scratched knee could once again kill,” WHO Director-General Margaret Chan said at a March medical meeting in Copenhagen. “Hip replacements, organ transplants, cancer chemotherapy and care of preterm infants would become far more difficult or even too dangerous to undertake.”
Already, current varieties of resistant bacteria kill more than 25,000 people in Europe annually, the WHO said in March. The toll means at least 1.5 billion euros ($2 billion) in extra medical costs and productivity losses each year.
“If this latest bug becomes entrenched in our hospitals, there is really nothing we can turn to,” says Donald E. Low, head of Ontario’s public health lab in Toronto. “Its potential is to be probably greater than any other organism.”
The new superbugs are multiplying so successfully because of a gene dubbed NDM-1. That’s short for New Delhi metallo-beta- lactamase-1, a reference to the city where a Swedish man was hospitalized in 2007 with an infection that resisted standard antibiotic treatments.
The superbugs are proving to be not only wily but also highly sexed. The NDM-1 gene is carried on mobile loops of DNA called plasmids that transfer easily among and across many types of bacteria through a form of microbial mating. This means that unlike previous germ-altering genes, NDM-1 can infiltrate dozens of bacterial species. Intestine-dwelling E. coli, the most common bacterium that people encounter, soil-inhabiting microbes and water-loving cholera bugs can all be fortified by the gene.
What’s worse, germs empowered by NDM-1 can muster as many as nine other ways to destroy the world’s most potent antibiotics.
NDM-1 is changing common bugs that drugs once easily defeated into untreatable killers, saysTimothy Walsh, a professor of medical microbiology at Cardiff University in Wales. Or as in Skaret’s case, the gene is creating silent stowaways poised to attack if they find a weakness -- or that can pass harmlessly when the body’s conventional microbes win out.
Cancer patients whose chemotherapy inadvertently ulcerates their gastrointestinal tract are especially vulnerable, says Lindsay Grayson, director of infectious diseases and microbiology at Melbourne’s Austin Hospital.
“These bugs go straight into their bloodstream,” Grayson says. Newborns, transplant recipients and people with compromised immune systems are at higher risk, he says.
Six infants died in a small hospital in Bijnor in northern India from April 2009 to August 2010 after NDM-1-containing bacteria resisted all commonly used antibiotics.
India is susceptible because it has many sick people to begin with. The country accounts for more than a quarter of the world’s pneumonia cases. It has the most tuberculosis patients globally and Asia’s highest incidence of cholera.
Most of India’s 5,000-plus drugmakers produce low-cost generic antibiotics, letting users and doctors switch around to find ones that work. While that’s happening, the germs the antibiotics are targeting accumulate genes for evading each drug. That enables the bugs to survive and proliferate whenever they encounter an antibiotic they’ve already adapted to.
India’s inadequate sanitation increases the scope of antibacterial resistance. More than half of the nation’s 1.2 billion residents defecate in the open, and 23 percent of city dwellers have no toilets, according to a 2012 report by the WHO and Unicef.
Uncovered sewers and overflowing drains in even such modern cities as New Delhi spread resistant germs through feces, tainting food and water and covering surfaces in what Dartmouth Medical School researcher Elmer Pfefferkorn describes as a fecal veneer.
Germs with the NDM-1 gene existed in 51 of 171 open drains along the capital’s streets and in two of 50 samples of public tap water, Walsh found in 2010.
Abdul Ghafur, an infectious diseases doctor in Chennai, southern India’s largest city, sees patients every week who suffer from multidrug-resistant infections. He and others who used to successfully combat infections with such common antibiotics as amoxicillin now must use more-expensive ones that target a broader range of germs but typically cause greater side effects. Some infections don’t respond to any treatment, evading all antibiotics, he says.
That’s bad news because the more frequently the NDM-1 gene is inserted into different bacteria, the more likely it will enter virulent forms of E. coli, sparking outbreaks that may be impossible to subdue, says David Livermore, who heads antibiotic resistance monitoring at the U.K.’s Health Protection Agency in London.
The gene may even spread to the microbial cause of bubonic plague, the medieval scourge known as Black Death that still persists in pockets of the globe.
“It’s a matter of time and chance,” says Mark Toleman, a molecular geneticist at Cardiff University. Plasmids carrying the NDM-1 gene can easily be inserted into the genetic material ofYersinia pestis, the cause of plague, making the infection harder to treat, Toleman says.
“There is a tsunami that’s going to happen in the next year or two when antibiotic resistance explodes,” says Ghafur, 40, seated at a polished wooden table in a consulting room in Chennai as patients fill 20 metal chairs in the waiting area, forcing others into the corridor. “We need wartime measures to deal with this now.”
R.K. Srivastava, India’s former director general of health services, says the government is giving top priority to antimicrobial resistance, including increasing surveillance of hospitals’ antibiotics use.
At the same time, it’s trying to preserve the country’s health-tourism industry. Bristling that foreigners coined a name that singles out their capital to describe an emerging health nightmare, officials say the world is picking on India for troubles that impede all developing nations.
When Indian researchers joined international teams studying the NDM-1 gene, the government questioned the data and methods of the scientists, among them Chennai microbiologist Karthikeyan K. Kumarasamy.
“These bacteria were present globally,” says Nirmal K. Ganguly, a former director general of the Indian Council of Medical Research and one of 13 members of a government task force created in September 2010 to respond to the NDM-1 threat.
“When you are blamed, the only reaction is that you put your back to the wall and fight.”
S.S. Ahluwalia, a former deputy opposition leader in the upper house of India’s parliament and a member of the Bharatiya Janata Party, says Western rivals want to muscle in on the medical tourism industry. Josef Woodman, founder of the guidebook “Patients Beyond Borders,” values the industry globally at $54 billion a year.
“These reports are meant to destabilize India’s emergence as a health destination,” says Ahluwalia, whose term ended in April.
About 850,000 medical tourists traveled to India in 2010 for treatments from lifesaving cancer operations to cosmetic surgeries, generating $872 million in revenue, according to the Associated Chambers of Commerce and Industry of India, or Assocham. The number of foreign patients is predicted to almost quadruple by 2015, the trade body says.
Manish Kakkar, a doctor researching infectious diseases at the New Delhi-based Public Health Foundation of India and a task force member, says the government has its priorities wrong.
“We have been in a phase of denial,” he says. “Rather than responding to the situation scientifically, we’ve completely diverted attention, saying that it’s attacking our medical tourism.”
Kakkar and others worry about NDM-1 because unlike germs such as VRE, short for the vancomycin-resistant enterococci bug that can cause infection around a patient’s surgical incision, NDM-1 is spreading beyond hospitals.
Two travelers from the Netherlands picked up an NDM-1 bug in their bowels after visiting India in 2009 although they hadn’t received medical care there, says Maurine Leverstein-van Hall, a clinical microbiologist at the University Medical Center in the Dutch city of Utrecht.
“That’s what’s scary,” she says. “It’s not just surgery or being near a hospital. In some way, you get it through the food chain or through the water.”
For now, it’s impossible to tell how common NDM-1 infections are or how often the mutant germs kill because testing and surveillance are inadequate in developing countries, says Keith Klugman, the William H. Foege chair of global health at Emory University’s Rollins School of Public Health in Atlanta.
Cardiff’s Walsh estimates 100 million Indians carry germs that harbor the NDM-1 gene, based on an extrapolation of studies in New Delhi and from neighboring Pakistan.
“It’s not measured, and that’s the problem,” says Klugman, who pinpoints India as the epicenter.
India’s jammed cities, poor sanitation and abundant antibiotics produce an ideal incubator, Harvard’s Moellering says.
“You have almost no control over the prescription of antibiotics,” says Moellering, who has studied drug resistance for four decades. “You have horrible sanitation problems in many parts of the country. You have incredible poverty, and you have crowding. When you put those four things together, it’s the perfect breeding ground for multidrug-resistant bacteria.”
Antibiotics even pollute India’s rivers, streams and soil. The bacteria that thrive in these places do so because they’ve developed resistance to the drugs they encounter. People or animals who ingest the water or soil may become colonized by the resistant germs.
Until the government built a pipeline to a modern sewage plant in 2010, the Patancheru Enviro Tech Ltd. treatment facility on some days released the equivalent of 45,000 daily doses of ciprofloxacin into the Isakavagu stream outside Hyderabad in southern India, Swedish researchers reported in 2007. The plant treated wastewater from drug-making factories.
Residue from ciprofloxacin, a mainstay treatment for E. coli infections, was so prevalent in river sediment downstream that lead researcher Joakim Larsson of the University of Gothenburg jokes, “Had ciprofloxacin been a little bit more expensive, we could probably mine it from the ground.”
India’s antibiotics overload is forcing doctors to rely on ever-more-powerful drugs. Many now turn to a class called penicillin-based carbapenems to treat ailments as routine as urinary tract infections, says Grayson, who was editor-in-chief of medical text “Kucer’s The Use of Antibiotics” (Hodder Arnold/ASM Press, 2010).
NDM-1 has rendered even carbapenems useless, sometimes leaving no way to fight infections. Two drugs potentially capable of treating NDM-1 bacteria have toxic side effects in some patients that include an increased risk of death.
“It’s an example of why we need to have good surveillance and why we need to have good antibiotic stewardship,” says Thomas R. Frieden, director of the U.S. Centers for Disease Control and Prevention in Atlanta. “We are looking at the specter of untreatable illness.”
Drugmakers have been slow to respond with new medicines. Most abandoned antibiotic discovery during the past decade, says Karen Bush, a microbiologist at Indiana University in Bloomington. She led teams that developed five bacteria-fighting drugs beginning in the 1970s in laboratories that are now part of AstraZeneca Plc (AZN), Bristol-Myers Squibb Co. (BMY), Johnson & Johnson and Pfizer Inc. (PFE)
Companies instead pursued hypertension and high-cholesterol drugs that patients take for a lifetime rather than a few weeks, she says.
Kumarasamy, the Chennai microbiologist, says he thought he was doing his country a favor when he helped track down the cause of unexplained deaths inside India. Instead, he sparked an international uproar over NDM-1.
Beginning in June 2000, Kumarasamy, now 36, studied bacteria and went from hospital to hospital in Chennai to collect specimens. He says he witnessed a steady increase in difficult-to-treat infections. Patients were dying, and doctors couldn’t identify what type of resistant germs killed them, he says.
“No matter how skilled or intelligent the doctor is, they are helpless when it comes to these infections,” he says over lunch of rice and curry in a noisy Chennai food court. He didn’t keep a tally of the deaths.
Kumarasamy, who received a Bachelor of Science degree from Navarasam Arts & Science College in Tamil Nadu state in 1997, says he began isolating bacteria from the blood, sputum, pus and urine of patients and freezing the samples. He quit his lab job in 2007 to study resistant germs for a doctorate in microbiology at the University of Madras. He’s winding up his thesis on carbapenem-resistant bacteria.
Kumarasamy’s curiosity spiked in 2008 when he realized he was dealing with something totally new. He reached out to Walsh, whose Cardiff lab was at the forefront of international antibiotic resistance research.
Around that time, Walsh was studying the case of a diabetic stroke patient of Indian origin. The man had festering bedsores and had been transferred from New Delhi to his home in Swedenfor treatment. When bacteria cultured from his urine and feces evaded more than a dozen drugs, including last-resort carbapenems, Christian G. Giske, a clinical microbiologist at Stockholm’s Karolinska University Hospital, sent the samples to Walsh’s lab.
In a hotel room in the Swedish capital, Walsh and Giske named the gene that made the bacteria immune to virtually all these antibiotics New Delhi metallo-beta-lactamase-1.
Beta-lactams are a class of antibiotics that includes penicillins, cephalosporins and carbapenems. Beta-lactamase is an enzyme that destroys those drugs. Metallo-beta-lactamases are so named because they contain zinc and destroy carbapenems, the most powerful beta-lactams.
Kumarasamy, suspecting something similar in his own specimens, asked Walsh to share the DNA sequence of this new bacterial gene. Walsh did -- and Kumarasamy got a match.
Kumarasamy began visiting Chennai hospitals anew to look for drug-resistant specimens. He also got samples from researchers in India’s northern Haryana state.
When his collection was added to those Walsh and his colleagues were studying, the researchers discovered the same NDM-1 gene from four countries: India, Pakistan, Bangladesh and the U.K. For most of the British patients, the link was recent travel to India or neighboring Pakistan.
In Kumarasamy’s samples from inside India, many cases emerged in people who hadn’t recently been hospitalized. That suggested the bacteria were spreading in the community.
“He is India’s unsung hero,” Walsh says.
The University of Madras initially thought so, too. It feted Kumarasamy after he became the youngest scholar from the 155-year-old institution to have research appear in any publication of the British medical journal “The Lancet.” His August 2010 paper, in “The Lancet Infectious Diseases,” became that publication’s most-read article that year.
The mood soured a few days later. Officials at India’s Ministry of Health & Family Welfare balked at the gene’s name, which threatened medical tourism’s public image.
“There was a lot of stress and tension, and I could not sleep properly for two months,” says Kumarasamy, who says he developed gastric reflux and heartburn.
The next month, authorities at the ministry grilled the eight Indian contributors to the “Lancet” report, including lead author Kumarasamy, according to two co-authors who declined to be identified because their employers don’t permit them to speak to the media.
‘Batten Down the
Officials questioned their data and chastised them for sending specimens overseas without approval, saying the researchers had violated a 13-year-old regulation, according to two in the group.
The Indian Council of Medical Research says it requires researchers to submit detailed proposals to send any bacterial collections abroad. The process may take at least four months.
“The regulations were already in place,” says Sandhya Visweswariah, a professor at the Indian Institute of Science in Bangalore.
The researchers countered that the rules were nebulous and were rarely enforced.
“It is suppression of scientific freedom,” Walsh says of the government behavior. “They just try to batten down the hatches and make everything very, very difficult and pretend nothing has happened.”
After front-page stories on the superbug appeared in Indian newspapers, the government formed an antibiotic resistance task force. It recommended in April 2011 that antibiotic use be tracked in the country’s 100,000 hospitals to find excessive prescribing. The group advised making it harder to get antibiotics without a prescription by requiring pharmacists to keep records for two years to aid audits and inspections.
Current rules make a prescription mandatory, but regulations are rarely enforced and it’s easy to get potent antibiotics, even intravenous ones, without a doctor’s assent. The group advised enacting rules allowing drug inspectors to immediately cancel the license of pharmacists dispensing unprescribed antibiotics.
Task force member Ganguly says tracking antibiotic use will be difficult.
“How do you regulate 1.2 billion people with so much diversity?” he asks.
While Kumarasamy was documenting NDM-1 in Chennai hospitals, pediatrician Vipin Vashishtha was discovering how deadly the gene can be.
In June 2010, new father Sanjeev Thakran, 28, rushed his half-hour-old son in a car through monsoon-soaked streets to Vashishtha’s Mangla Children’s Hospital in Bijnor. His wife, Lalita, had delivered baby Tapas in a maternity hospital across town three weeks early, and the infant was laboring for air.
Nurses in green scrubs warmed the 4-pound (1.8-kilogram) newborn in a dome-covered crib and fed him milk and medicines through a nasal tube. About 2 feet away, a frail-looking baby was connected to a ventilator, Sanjeev Thakran says.
Vashishtha, seated on a leather swivel chair in his consulting room, recalls thinking that Tapas might need only a few days of intensive care. Instead, the baby spent weeks in and out of the unit. Blood sometimes trickled from his nose and shriveling umbilicus, according to medical records.
Even though he was being treated with a carbapenem, the most powerful class of antibiotic, bacteria raged inside his tiny lungs and bloodstream, eventually attacking membranes covering his brain and spinal cord.
Other infants in the eight-crib neonatal intensive care unit were suffering, too. Vashishtha, 48, had tried several antibiotics without success. When carbapenems didn’t work, he says, he felt helpless because he knew he was dealing with a potentially incurable scourge.
Tapas died 11 weeks after he was admitted. Lab results identified the culprit a month later: NDM-1. The gene was in bacteria known as Klebsiella pneumoniae. The germ exists in people’s gastrointestinal tract and can cause pneumonia and urinary-tract infections in hospital patients.
The lab also found two soil-borne species that normally cause trivial infections but that were suddenly becoming killers.
Tapas was one of 14 infants at the hospital who were infected with NDM-1-containing bacteria over the course of 17 months. Six of the babies died. Among the eight survivors, half developed meningitis, arthritis or water on the brain, Vashishtha wrote to an Indian medical journal in February 2011.
“It was the most horrific period,” Vashishtha says as he fixes his eyes on the playpen where he amuses children in his office. “I was losing neonates at regular intervals. I suspected we were dealing with something quite different, something quite new.”
Vashishtha says he has improved infection control, walling off part of the ICU for contagious, complicated cases.
He can’t, however, control what happens outside his hospital. Sewage from nearby homes flows in an open drain along one wall of the two-story building.
Bijnor, like other small cities in Uttar Pradesh, lacks a modern underground drainage system. During the rainy season, it’s impossible not to wade through sewage water, the doctor says.
So far, Vashishtha has prevented more NDM-1 deaths. He fumigates his wards every four weeks and applies fresh paint every three months. He keeps hand-sanitizing liquid in his office, along the corridors and next to every bed in intensive care. Nurses must wash their hands with running water and soap and scrub with an antimicrobial sanitizer before handling patients.
“The first and foremost step to avoiding hospital-acquired infection is to wash hands properly,” he says.
India’s major hospitals are marshaling tactics from common cleanliness to computerized databases to outsmart resistant bacteria and prevent more tragedies.
Artemis Health Institute, a private, 300-bed specialty hospital in Gurgaon, southwest of New Delhi, employs an infection-control officer who collects data every month on the hospital’s four most troublesome bacteria to review patterns of drug resistance. The officer, Namita Jaggi, also serves as national secretary of a Buenos Aires-based group that collates infection information worldwide.
About 3 miles (4.8 kilometers) away, cardiac surgeon Naresh Trehan’s medical complex,Medanta-The Medicity, requires patients transferring from other hospitals to be screened for resistant bacteria. This procedure, routine in some Nordic countries, isn’t standard in India.
Medanta has a strict hand-washing policy and a 40-member team to monitor infections, says Trehan, 65, who trained in cardiac surgery at New York University and worked at Bellevue Hospital in Manhattan before returning to India in 1988.
“We have a very senior person whose sole responsibility is to keep the whole hospital under infection surveillance 24/7,” he says.
Livermore at the U.K.’s Health Protection Agency says these efforts may not be enough in a country where 626 million people defecate in the open and that treats only 30 percent of the 10.1 billion gallons of sewage generated each day. Even the most modern hospitals can’t exist as islands of cleanliness, he says.
“How does the hospital -- however good its surgeons and physicians -- isolate itself when its patients, staff and food all come from outside, where they are exposed to this soup of resistance?” he asks.
‘Hope for the
Bush, the antibiotics researcher, has been investigating novel ways to fight bacteria since 1977. She says combinations of existing drugs, including an experimental compound from AstraZeneca in late-stage patient studies, may neutralize some carbapenem-destroying enzymes.
Should these mixtures pan out, they may help the superdrugs regain at least some of their potency, potentially extending their usefulness for a decade or more, she says.
A drug candidate from Basel, Switzerland-based Basilea Pharmaceutica AG (BSLN) in early-stage trials shows some promise against NDM-1, she says.
“What’s frustrating is to see that companies refused to address the issue until the last few years,” Bush says. “There are still some that are trying, and that’s the hope for the future.”
Drugs that could once again tackle the world’s most resistant germs would be a relief for people worldwide, Norway’s Skaret among them. She spent more than six months fearing a microbial time bomb until she learned that the NDM-1 supergerms had passed from her system.
Even though she escaped physical harm, Skaret says, NDM-1 made her feel isolated. She says therapists, concerned about their own exposure, refused to help her with rehabilitation to recover from the car accident. Neighbors who delivered food were careful not to get too close.
“When they heard about it, they were very cautious,” she says.
If Walsh’s projection is accurate, 100 million Indians may be carrying the NDM-1 gene unwittingly and doing little to contain its spread. The number of countries reporting NDM-1 will continue to grow as more bacteria pick up the gene and people transport it around the globe.
To prevent a worldwide catastrophe, microbiologists Kumarasamy and Walsh -- along with scores of scientists and doctors inside and outside India -- are sounding an alarm.
sophisticated medicine, poor sanitation and heavy antibiotic usage, and you
have a rocket fuel to drive the accumulation of resistance,” Livermore says.
“That surely is what India has created” (Bloomber,
Title: Antibiotics Abuse Has Turned Ordinary Throat Infections Into Deadly
Date: May 8, 2012
Abstract: It is no longer a secret that drug-resistant bacteria are rapidly emerging and spreading all around the world as a result of the continued overuse and abuse of antibiotic drugs in both conventional medicine and industrial agriculture. But now it appears that the genes responsible for spawning these so-called "superbugs" are also spreading, and turning otherwise mild conditions such as throat infections into deadly killers.
Known as NDM-1, or New Delhi metallo-beta-lactamase-1, these genes basically hitch a ride on mobile DNA loops known as plasmids, and latch themselves onto various bacteria whenever and wherever they find an opportunity. The end result of this parasite-like invasion into bacteria is that even largely innocuous microbes can become extremely virulent and fully able to outsmart even the strongest antibiotic drugs available.
"Things as common as strep throat or a child's scratched knee could once again kill," said Margaret Chan, Director-General of the World Health Organization (WHO) at a recent meeting in Copenhagen, Denmark, about the phenomenon. "Hip replacements, organ transplants, cancer chemotherapy and care of preterm infants would become far more difficult or even too dangerous to undertake."
According to a recent report by Bloomberg, the spread of NDM-1 and antibiotic-resistant superbugs has become so extreme that even beneficial bacterial, also commonly referred to as "probiotics" or "gut microflora," are being affected as well. And as long as antibiotics continue to be abused in the careless way that they now are globally, the situation will only worsen over time until eventually even the most minor infections and injuries become fatal.
"If this latest bug becomes entrenched in our hospitals, there is really nothing we can turn to," said Donald E. Low, head of the public health lab in Toronto, Ontario. "Its potential is to be probably greater than any other organism."
Besides raising awareness about the issue and pushing for a complete moratorium on antibiotic drug use, there is little that can be done on a large scale to effectively stop the spread of antibiotic-resistant superbugs. But there are some simple steps you can personally take to help you and your family avoid superbug infection.
1. If you eat meat, purchase only pasture-raised, antibiotic- and hormone-free varieties. Conventional meat from animals raised in confined feedlots is often loaded with antibiotics, chemicals and other toxins that can exacerbate the superbug problems. By consuming only grass-fed, organic meats, you and your family will avoid repeated exposure to meat-based antibiotics and any superbugs that might be living in it.
2. Avoid taking antibiotic drugs, and instead try colloidal silver, garlic, coconut oil and other natural antibiotics. Instead of taking prescribed antibiotics for every minor ailment, which is contributing greatly to the spread of superbugs in society today, try boosting you and your family's immune systems with bacteria-resistant superfoods. You can also promote healthy bacterial growth that naturally fights off the deadly kind by drinking kombucha tea and eating kefir, yogurt, and other probiotic foods.
3. Educate your friends and neighbors about drug-resistant superbugs, and the dangers of antibiotic overuse. Many people are simply unaware of how antibiotic drug abuse is contributing to the rise of deadly superbugs. By sharing this information with your friends and neighbors, and teaching them about how to boost their immune systems naturally with herbs, superfoods, clean water, organic produce, and probiotics, you can help to bring about real change on a societal scale (NaturalNews, 2012).
Title: Mutant Bird Flu Would Be Airborne, Scientists Say
Date: June 21, 2012
Abstract: Here's what it takes to make a deadly virus transmissible through the air: as few as five genetic mutations, according to a new study.
This research, published in the journal Science, is the second of two controversial studies to finally be released that examines how the H5N1 bird flu virus can be genetically altered and transmitted in mammals. Publication of both studies had been delayed many months due to fears that the research could be misused and become a bio-security threat.
Although these particular engineered forms of H5N1 have not been found in nature, the virus has potential to mutate enough such that it could become airborne.
H5N1 influenza can be deadly to people, but in its natural forms it does not easily transfer between people through respiratory droplets, as far as scientists know. The World Health Organization has recorded 355 humans deaths from it out of 602 cases, although some research has questioned this high mortality rate.
The journals Science and Nature had agreed to postpone the publication of the two studies related to the genetically altered virus.
In January, the National Science Advisory Board for Biosecurity recommended that this research be published without "methods or details" that terrorists might be able to use for biological weapons. The board also said the data could assist in preparing for a possible future outbreak, however.
Then in February, the World Health Organization convened a meeting, at which the recommendation was to publish the studies - just not yet. In April, the National Institutes of Health chimed in, also recommending publication.
The first study to be published on the topic was in the journal Nature, and was led by the University of Wisconsin-Madison researcher Yoshihiro Kawaoka. It was released in May.
The other research group, which authored the new study in Science, was led by Ron Fouchier at the Erasmus Medical Center in Rotterdam, Netherlands.
Both Kawaoka and Fouchier's groups created a mutated version of H5N1 that made it easier to transmit from mammal to mammal. They used ferrets because these animals are a good approximation for how viruses behave in humans.
Fouchier's study examines what mutations would be necessary to get the virus airborne. He and colleagues found five mutations consistent in a form of the H5N1 flu virus that could spread among ferrets through the air.
None of the ferrets died after developing the flu, the researchers said.
In a separate analysis, researchers looked at the likelihood that an airborne avian flu virus would evolve on its own from the H5N1 currently found in nature.
This study, also published in Science this week, looked at nearly 4,000 strains of influenza virus and frequently found two of the five mutations that appear to be involved in airborne transmission. These two mutations have been found in viruses from both birds and humans, although not in naturally-occurring H5N1 strains.
Derek Smith of the University of Cambridge, who co-authored that study, said at a press briefing that it's possible that only three mutations are necessary for the virus to evolve.
Smith's group also did mathematical modeling to look at whether the other mutations could evolve when the bird flu jumps to a human or other mammal.
"We find that it is possible for such a virus to evolve three mutations within a single host," Smith said during the press call.
If it takes four for five mutations to become airborne, that would be more difficult - but it's unclear just how likely it would be, Smith said.
While the Nature study looked at how a bird flu virus could become airborne through mutations and re-assortment with other viruses, the latest research in Science suggests mutations alone could do the trick.
Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, told reporters that the benefits from the Science study, in terms stimulating ideas and pursuing ways to understand the transmissibility, adaptability and pathogenesis of the virus, outweigh the risks that someone will use the data for nefarious purposes.
"Does that mean that there's no risk? No, of course not. I can't
tell you at all
that there's no risk. But the benefits in my mind outweigh the risks," he said.
Making the research available generally will hopefully spark input on this topic from researchers in a wide variety of fields, he said.
It is technologically possible to create vaccine based on the genetic code of a flu virus strain including this one, researchers said. Several companies are already making H5N1 vaccines.
Research is ongoing to accelerate the amount of vaccine doses available by using adjuvants, which are agents that modify the effects of vaccines, Fauci said. There is also work ongoing into using computational sequencing to anticipate every possible influenza strain that could emerge, such that a databank could be established to prepare for the outbreak of any one of them, he said.
"Right now we're
in a much, much better position than we were when we had vaccine available
after the peak of the 2009 H1N1 two years ago," Fauci said (CNN, 2012).
Title: NIH Superbug Outbreak Highlights Lack Of New Antibiotics
Date: August 24, 2012
Source: Washington Post
Abstract: As doctors battled a deadly, drug-resistant superbug at the National Institutes of Health’s Clinical Center last year, they turned to an antibiotic of last resort.
But colistin, as it’s called, is not a fancy new creation of modern
biotechnology. It was discovered in a beaker of fermenting bacteria in Japan —
That doctors have resorted to such an old, dangerous drug — colistin causes kidney damage — highlights the lack of new antibiotics coming out of the pharmaceutical pipeline even in the face of a global epidemic of hospital-acquired bugs that quickly grow resistant to the toughest drugs.
It’s a case of evolution outrunning capitalism.
Between 1945 and 1968, drug companies invented 13 new categories of antibiotics, said Allan Coukell, director of medical programs at the Pew Health Group.
Between 1968 and today, just two new categories of antibiotics have arrived.
In 2011, the Food and Drug Administration approved one new antibiotic, which fights one of the many bacteria, Clostridium difficile, causing deadly hospital-borne infections.
“What kept us out of trouble for the last 60 years is that every time drug resistance caught up to us, the pharmaceutical companies would go back to the drawing board and develop the next generation of drugs to keep us ahead of the game,” said Brad Spellberg, an infectious diseases physician in Los Angeles who heads a microbial resistance task force for the Infectious Diseases Society of America. “That’s the part of the equation that’s changed. Drug companies are no longer trying to get one step ahead.”
Experts point to three reasons pharmaceutical companies have pulled back from antibiotics despite two decades of screaming alarms from the public health community: There is not much money in it; inventing new antibiotics is technically challenging; and, in light of drug safety concerns, the FDA has made it difficult for companies to get new antibiotics approved.
As a result, only four of the world’s 12 largest pharmaceutical companies are researching new antibiotics, said David Shlaes, a drug development veteran and consultant.
Last year, Pfizer, the world’s biggest drug company, closed its Connecticut antibiotics research center, laying off 1,200 workers. The company said it was moving the operation to Shanghai. But Shlaes said Pfizer is struggling to open the Chinese facility and has largely abandoned antibiotics.
While a new antibiotic may bring in a billion dollars over its lifetime, Shlaes said, a drug for heart disease may net $10 billion. Depression and erectile dysfunction drugs — typically taken daily for years, unlike antibiotics, which are used short-term — are also more profitable than antibiotics.
Congress recognized the problem earlier this year, inserting a provision in an FDA authorization bill to grant an additional five years of market exclusivity — meaning no competition from generics — for companies inventing new antibiotics.
“It’s a great first step,” said Spellberg, but he added that the provision “is not strong enough to turn things around.”
Shlaes said that concerns about antibiotic safety — driven by deaths linked to the drug Ketek that came to light in 2006 — have made the FDA reluctant to approve new antibiotics. “They’ve basically made it impossible for companies to develop and market antibiotics in the U.S.,” he said.
Ed Cox, head of the FDA’s office of microbial products, said the agency is “looking at new approaches” for speeding up the approval of new antibiotics, such as requiring smaller clinical studies and allowing research with patients such as those who have multiple infections. “We’re trying hard to address the challenges” faced by the drug industry in developing antibiotics, Cox said.
Such changes are “in the discussion and planning stage,” Cox added. “But this is a critical step so that folks in industry wanting to develop [antibiotics] can do so.”
Shlaes characterized the moves at FDA as “trying to paint themselves out of a corner.”
It’s an especially tight corner that hospital physicians find themselves in. Ten years ago, the Centers for Disease Control and Prevention reported that 1.7 million annual hospital-borne infections in the United States caused 99,000 deaths. The CDC is now updating those figures.
In a recent survey of infectious disease specialists, Spellberg said, 60 percent reported encountering infections resistant to every antibiotic.
“That’s the real crisis,” said Henry Masur, chief of NIH’s Critical Care
Medicine Department, who last year watched six patients die from the
bacterium Klebsiella pneumoniae when even colistin, that old
warhorse, stopped working. “The problem here is that we’re not developing
antibiotics fast enough to keep up with this” (Washington Post, 2012).
Title: Human And Soil Bacteria Swap Antibiotic-Resistance Genes
Date: August 30, 2012
Abstract: Soil bacteria and bacteria that cause human diseases have recently swapped at least seven antibiotic-resistance genes, researchers at Washington University School of Medicine in St. Louis report Aug. 31 inScience.
According to the scientists, more studies are needed to determine how widespread this sharing is and to what extent it makes disease-causing pathogens harder to control.
“It is commonplace for antibiotics to make their way into the environment,” says first author Kevin Forsberg, a graduate student. “Our results suggest that this may enhance drug resistance in soil bacteria in ways that could one day be shared with bacteria that cause human disease.”
Among the questions still to be answered: Did the genes pass from soil bacteria to human pathogens or vice versa? And are the genes just the tip of a vast reservoir of shared resistance? Or did some combination of luck and a new technique for studying genes across entire bacterial communities lead the scientists to discover the shared resistance genes?
Humans only mix their genes when they produce offspring, but bacteria regularly exchange genes throughout their lifecycles. This ability is an important contributor to the rapid pace of bacterial evolution. When a bacterial strain develops a new way to beat antibiotics, it can share the strategy not only with its descendants but also with other bacteria.
Earlier studies by other scientists have identified numerous resistance genes in strains of soil bacteria. However, unlike the seven genes described in this report, the earlier genes were dissimilar to their analogs in disease-causing bacteria, implying that they had crossed between the bacterial communities a long time ago.
Most of the antibiotics used to fight illness today originated from the soil. Bacteria use the antibiotics, in part, as weapons to compete with each other for resources and survival. Scientists have long acknowledged that gives environmental bacteria an evolutionary incentive to find ways to beat antibiotics.
“We wanted to try to get a broader sense of how often and extensively antibiotic-resistance genes are shared between environmental bacteria and pathogens,” says senior author Gautam Dantas, PhD, assistant professor of pathology and immunology.
The researchers isolated bacteria from soil samples taken at various U.S. locations. The bacteria’s DNA was broken into small chunks and randomly inserted into a strain of Escherichia coli that is vulnerable to antibiotics. Scientists treated the altered E. coli with multiple antibiotics.
“We knew that any E. coli that continued to grow after these treatments had picked up a gene from the soil bacteria that was helping it fight the antibiotics,” Forsberg says.
Scientists took the DNA from soil bacteria out of the surviving E. coli and prepared it for high-throughput sequencing. Dantas’ laboratory has developed techniques that make it possible to simultaneously sequence and analyze thousands of chunks of DNA from many diverse microorganisms. The DNA can be selected for a single function, such as antibiotic resistance.
When the scientists compared antibiotic-resistance genes found in the soil bacteria to disease-causing bacteria, they were surprised to find some genes were identical not only in the sections of the genes that code for proteins but also in nearby non-coding sections that help regulate the genes’ activities.
Since bacteria have such large population sizes and rapid reproduction times, their DNA normally accumulates mutations and other alterations much more quickly than the DNA of humans. The lack of changes in the resistance genes identified in the study suggests that the transfers of the genes must have occurred fairly recently, according to Dantas.
In some soil bacteria, the genes are present in clusters that make the bacteria resistant to multiple classes of antibiotics, including forms of penicillin, sulfonamide and tetracycline.“I suspect the soil is not a teeming reservoir of resistance genes,” Dantas says. “But if factory farms or medical clinics continue to release antibiotics into the environment, it may enrich that reservoir, potentially making resistance genes more accessible to infectious bacteria” (WUSTL, 2012).
Growing Concerns Over 'In The Air' Transmission Of Ebola
Date: November 16, 2012
Abstract: Canadian scientists have shown that the deadliest form of the ebola virus could be transmitted by air between species.
In experiments, they demonstrated that the virus was transmitted from pigs to monkeys without any direct contact between them.
The researchers say they believe that limited airborne transmission might be contributing to the spread of the disease in some parts of Africa.
They are concerned that pigs might be a natural host for the lethal infection.
What we suspect is happening is large droplets - they can stay in the air, but not long, they don't go far. But they can be absorbed in the airway” ~Dr Gary Kobinger Public Health Agency of Canada
Ebola viruses cause fatal haemorrhagic fevers in humans and many other species of non human primates.
Details of the research were published in the journal Scientific Reports.
According to the World Health Organization (WHO), the infection gets into humans through close contact with the blood, secretions, organs and other bodily fluids from a number of species including chimpanzees, gorillas and forest antelope.
The fruit bat has long been considered the natural reservoir of the infection. But a growing body of experimental evidence suggests that pigs, both wild and domestic, could be a hidden source of Ebola Zaire - the most deadly form of the virus.
Now, researchers from the Canadian Food Inspection Agency and the country's Public Health Agency have shown that pigs infected with this form of Ebola can pass the disease on to macaques without any direct contact between the species.
In their experiments, the pigs carrying the virus were housed in pens with the monkeys in close proximity but separated by a wire barrier. After eight days, some of the macaques were showing clinical signs typical of ebola and were euthanised.
One possibility is that the monkeys became infected by inhaling large aerosol droplets produced from the respiratory tracts of the pigs.
One of the scientists involved is Dr Gary Kobinger from the National Microbiology Laboratory at the Public Health Agency of Canada. He told BBC News this was the most likely route of the infection.
"What we suspect is happening is large droplets - they can stay in the air, but not long, they don't go far," he explained.
"But they can be absorbed in the airway and this is how the infection starts, and this is what we think, because we saw a lot of evidence in the lungs of the non-human primates that the virus got in that way."
The scientists say that their findings could explain why some pig farmers in the Philippines had antibodies in their system for the presence of a different version of the infection called Ebola Reston. The farmers had not been involved in slaughtering the pigs and had no known contact with contaminated tissues.
Dr Kobinger stresses that the transmission in the air is not similar to influenza or other infections. He points to the experience of most human outbreaks in Africa.
"The reality is that they are contained and they remain local, if it was really an airborne virus like influenza is it would spread all over the place, and that's not happening."
The authors believe that more work needs to be done to clarify the role of wild and domestic pigs in spreading the virus. There have been anecdotal accounts of pigs dying at the start of human outbreaks. Dr Kobinger believes that if pigs do play a part, it could help contain the virus.
"If they do play a role in human outbreaks it would be a very easy point to intervene" he said. "It would be easier to vaccinate pigs against Ebola than humans."
Other experts in the field were concerned about the idea that Ebola was susceptible to being transmitted by air even if the distance the virus could travel was limited. Dr Larry Zeitlin is the president of Mapp Biopharmaceuticals.
"It's an impressive study that not only raises questions about the reservoir of Ebola in the wild, but more importantly elevates concerns about ebola as a public health threat," he told BBC News. "The thought of airborne transmission is pretty frightening."
At present, an
outbreak of ebola in Uganda has killed at least two people near the capital
Kampala. Last month, Uganda declared itself Ebola-free after an earlier
outbreak of the disease killed at least sixteen people in the west of the
country (BBC, 2012).