A good counterexample is E. coli, a species of bacteria that lives harmlessly in every person’s gut by the billions. A typical E. coli contains about 4,000 genes (we have about 20,000). Feeding on sugar, the microbe grows till it is ready to split in two. It makes two copies of its genome, almost always managing to produce perfect copies of the original. The single microbe splits in two, and each new E. coli receives one of the identical genomes. These two bacteria are, in other words, clones.
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A colony of genetically identical E. coli is, in fact, a mob of individuals. Under identical conditions, they will behave in different ways. They have fingerprints of their own.
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E. coli appears to follow a universal rule. Other microbes exploit noise, as do flies, worms and humans. Some of the light-sensitive cells in our eyes are tuned to green light, and others to red. The choice is a matter of chance. One protein may randomly switch on the green gene or the red gene, but not both.

In our noses, nerve cells can choose among hundreds of different kinds of odor receptors. Each cell picks only one, and evidence suggests that the choice is controlled by the unpredictable bursts of proteins within each neuron. It’s far more economical to let noise make the decision than to make proteins that can control hundreds of individual odor receptor genes.

Identical genes can also behave differently in our cells because some of our DNA is capped by carbon and hydrogen atoms called methyl groups. Methyl groups can control whether genes make proteins or remain silent. In humans (as well as in other organisms like E. coli), methyl groups sometimes fall off of DNA or become attached to new spots. Pure chance may be responsible for changing some methyl groups; nutrients and toxins may change others.

Scientists from Arizona State University report that minerals from clay promise could provide inexpensive, highly-effective antimicrobials to fight methicillin-resistant Staphylococcus aureus (MRSA) infections that are moving out of health care settings and into the community.
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Unlike conventional antibiotics routinely administered by injection or pills, the so-called “healing clays” could be applied as rub-on creams or ointments to keep MRSA infections from spreading
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In their latest study, funded by the National Institutes of Health, Williams, Haydel and their colleagues collected more than 20 different clay samples from around the world to investigate their antibacterial activities… The researchers identified at least two clays from the United States that kill or significantly reduce the growth of these bacteria

The scientists wanted to make sure they had a good control—a group of bacteria that didn’t grow at all—so they bathed some of the bacteria in antibiotics. But there was a problem: The bacteria didn’t just survive in the antibiotics, they consumed them. The researchers then gathered soil from 11 sites with varying degrees of exposure to human-made antibiotics (from manure-filled cornfields to an immaculate forest) and found that every site contained bacteria, including relatives of Shigella and the notorious E. coli that could survive solely on antibiotics. And these weren’t just piddling doses—the bacteria could tolerate levels of antibiotics that were up to 100 times higher than would be given to a patient, and 50 times higher than what would qualify a bacterium as resistant.

Microbiologists of the 1950’s did not appreciate the stunning extent to which bacteria swap genes… In 1959 Japanese hospitals experience outbreaks of multidrug-resistant bacterial dysentery. The shigella bacteria, which caused the outbreaks, were shrugging off four different classes of previously effective antibiotics: sulfonamides, streptomycins, chloramphenicols, and tetracyclines… In fact, the Japanese researches found it quite easy to transfer multidrug resistance from E. coli to shingella and back again simply by mixing resistant and susceptible strains together in a test tube.

today, some scientists think Coley had it right: Germs can teach our bodies how to fight back against tumors. Dr. John Timmerman, a cancer immunotherapy expert at UCLA’s Jonsson Cancer Center, says this revolution has produced “the most exciting sets of compounds in cancer immunolog
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The studies also imply that our cleaner, infection-free lifestyles may be contributing to the rise in certain cancers over the last 50 years, scientists say, because they make the immune system weaker or less mature. Germs cause disease but may also fortify the body, a notion summed up in a 2006 report by a team of Canadian researchers as “whatever does not kill me makes me stronger.”
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Other groups have been experimenting with injections of other types of heat-killed bacteria, including Myobacterium vaccae, a tuberculosis relative. In two studies in January’s European Journal of Cancer, researchers report that these bacteria may help fight certain lung and renal cancers.

Consumer advocates have been campaigning for years to curb the use of antibiotics in agriculture, citing studies that show that 70 percent of all U.S. antibiotics are administered in low doses - not to treat disease, but to promote the growth of pigs, sheep, chicken and cattle.
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But as early as 1963, British researchers tied the emergence of drug-resistant strains of salmonella in humans to antibiotics fed to cattle.

Dr. Jeff Brooks has been director of the UCSF lab for 29 years, and has watched with a mixture of fascination and dread how bacteria once tamed by antibiotics evolve rapidly into forms that practically no drug can treat.
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“We are on the verge of losing control of the situation, particularly in the hospitals,” said Dr. Chip Chambers, chief of infectious disease at San Francisco General Hospital. The reasons for increasing drug resistance are well known:
- Overuse of antibiotics, which speeds the natural evolution of bacteria, promoting new mutant strains resistant to those drugs.
- Careless prescribing of antibiotics that aren’t effective for the malady in question, such as a viral infection.
- Patient demand for antibiotics when they aren’t needed.
- Heavy use of antibiotics in poultry and livestock feed, which can breed resistance to similar drugs for people.
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Terry Hazen, senior scientist at Lawrence Berkeley National Laboratory and director of its ecology program, is not at all surprised by the tenacity of our bacterial foes. “We are talking about 3.5 billion years of evolution,” he said. “They are the dominant life on Earth.”

Bacteria have invaded virtually every ecological niche on the planet. Human explorers of extreme environments such as deep wells and mines are still finding new bacterial species. “As you go deeper into the subsurface, thousands and thousands of feet, you find bacteria that have been isolated for millions of years - and you find multiple antibiotic resistance,” Hazen said.

In his view, when bacteria develop resistance to modern antibiotics, they are merely rolling out old tricks they mastered eons ago in their struggle to live in harsh environments in competition with similarly resilient species.

“We have developed the first inhibitor of a key small molecule from Mycobacterium tuberculosis and Mycobacterium leprae (which causes leprosy) utilized to subvert human host’s defenses and damage and invade human host’s cells during infection,” explains study senior author Dr. Luis Quadri, Associate Professor of Microbiology and Immunology at Weill Cornell.
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“We are moving beyond antimicrobials such as antibiotics, which kill the bacterium directly, to anti-infectives, that may have no effect against the pathogen in the test tube but which do compromise its ability to infect and spread in the host,” he explains. “We believe that the expansion of the drug armamentarium to include such anti-infective drugs could help the fight against multi-drug resistant infection that has become such a challenge today.”
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“I believe that drugs targeting virulence factors are just one component of the paradigm shift in the antimicrobial drug discovery for the 21st century—one that will offer patients more options in the fight against truly global killers,” he says.

A new UC Davis study shows that a common antibacterial chemical added to bath soaps can alter hormonal activity in rats and in human cells in the laboratory — and does so by a previously unreported mechanism.

The findings come as an increasing number of studies — of both lab animals and humans — are revealing that some synthetic chemicals in household products can cause health problems by interfering with normal hormone action. Called endocrine disruptors, or endocrine disrupting substances (EDS), such chemicals have been linked in animal studies to a variety of problems, including cancer, reproductive failure and developmental anomalies.

The researchers found two key effects: In human cells in the laboratory, triclocarban increased gene expression that is normally regulated by testosterone. And when male rats were fed triclocarban, testosterone-dependent organs such as the prostate gland grew abnormally large. Also, the authors said their discovery that triclocarban increased hormone effects was new. All previous studies of endocrine disruptors had found that they generally act by blocking or decreasing hormone effects.

In their disclosure statement, the authors report that six of them have taken steps to patent their findings through the University of California.

All the bacteria living inside you would fill a half-gallon jug; there are 10 times more bacterial cells in your body than human cells
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The infestation begins at birth: Babies ingest mouthfuls of bacteria during birthing and pick up plenty more from their mother’s skin and milk—during breast-feeding, the mammary glands become colonized with bacteria. “Our interaction with our mother is the biggest burst of microbes that we get,”
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there are estimated to be more than 500 species living at any one time in an adult intestine, the majority belong to two phyla, the Firmicutes (which include Streptococcus, Clostridium and Staphylococcus), and the Bacteroidetes (which include Flavobacterium).
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probiotics - dietary supplements containing potentially beneficial microbes - have been shown to boost immunity. Not only do gut bacteria “help protect against other disease-causing bacteria that might come from your food and water,” Huffnagle says, “they truly represent another arm of the immune system.”
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But the bacterial body has made another contribution to our humanity - genes. Soon after the Human Genome Project published its preliminary results in 2001, a group of scientists announced that a handful of human genes - the consensus today is around 40 - appear to be bacterial in origin.

Once routinely treated with cheap antibiotics, TB is poised to make a terrifying comeback. More and more, doctors in developing nations are finding patients infected with strains of TB invulnerable to all but a handful of extremely expensive, exotic drugs. Worldwide, TB already infects one in every three people and sickens one in ten. Without new methods to stop the spread of drug-resistant strains, the cost of treating this ancient human pathogen could bankrupt even the most prosperous economies.
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TB could, in theory, develop resistance to this new class of drugs, too. But Alber thinks he can skew the odds to favor humans. Identifying a drug capable of knocking out several TB enzymes at once could make it next to impossible for the bacterium to evolve resistance on multiple fronts.

Though TB is a daunting foe, Alber remains confident about the prospects of beating the disease. “As a bacterium, it should be easier to treat than HIV or malaria. Those kinds of diseases-caused by viruses and protozoans-we generally don’t know how to cure,” Alber says. “From a scientific perspective, TB is a simpler problem.”

A team of Princeton scientists has discovered a key mechanism in how bacteria communicate with each other, a pivotal breakthrough that could lead to treatments for cholera and other bacterial diseases.

The mechanism is a chemical that cholera bacteria use for transmitting messages to each other, known as CAI-1, and has been isolated in the lab of molecular biologist Bonnie Bassler. Her team has shown that the chemical also can be used to disrupt the communication that exists among the bacteria, potentially halting the disease’s progress. The discovery could lead to an entirely new class of antibiotics.
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Higgins isolated the CAI-1 chemical, which occurs naturally in cholera. Then, Megan Pomianek, a graduate student in the laboratory of Martin Semmelhack, a professor of chemistry at Princeton, determined how to make the molecule in the laboratory. Higgins used this chemical essentially to control cholera’s behavior in lab tests.

The team found that when CAI-1 is absent, cholera bacteria act as pathogens. But when the bacteria detect enough of this chemical, they stop making biofilms and releasing toxins, perceiving that it is time to leave the body instead. “Our findings demonstrate that if you supply CAI-1 to cholera, you can flip their switches to stop the attack,” Higgins said.

Chemist Helen Blackwell of the University of Wisconsin-Madison praised the study, calling it a breakthrough for quorum sensing research, and possibly for medical science.

While only 14 percent of serious MRSA infections are the community associated kind, they have drawn attention in recent months with a spate of reports in schools, including the death of a 17-year-old Virginia high school student. Both hospital-associated and community-associated MRSA contained genes for the peptides. But their production was much higher in the CA-MRSA, the researchers said.
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The compounds first cause inflammation, drawing the immune cells to the site of the infection, and then destroy those cells. The research was conducted in mice and with human blood in laboratory tests. Within five minutes of exposure to the peptides from CA-MRSA, human neutrophils showed flattening and signs of damage to their membrane, researchers said. After 60 minutes, many cells had disintegrated completely.

“This elegant work helps reveal the complex strategy that S. aureus has developed to evade our normal immune defenses,” Dr. Anthony S. Fauci, NIAID director, said in a statement. “Understanding what makes the infections caused by these new strains so severe and developing new drugs to treat them are urgent public health priorities.”

Relman is a leader in rethinking our relationship to bacteria, which for most of the last century was dominated by the paradigm of Total Warfare. “It’s awful the way we treat our microbes,” he says, not intending a joke; “people still think the only good microbe is a dead one.” We try to kill them off with antibiotics and hand sanitizers. But bacteria never surrender; if there were one salmonella left in the world, doubling every 30 minutes, it would take less than a week to give everyone alive diarrhea. In the early years of antibiotics, doctors dreamed of eliminating infectious disease. Instead, a new paper in The Journal of the American Medical Association reports on the prevalence of Methicillinresistant Staphylococcus aureus (MRSA), which was responsible for almost 19,000 deaths in the United States in 2005—about twice as many as previously thought, and more than AIDS. Elizabeth Bancroft, a leading epidemiologist, called this finding “astounding.”

As antibiotics lose their effectiveness, researchers are returning to an idea that dates back to Pasteur, that the body’s natural microbial flora aren’t just an incidental fact of our biology, but crucial components of our health, intimate companions on an evolutionary journey that began millions of years ago.

Bacteria that cause cholera and bubonic plague turn from harmless to deadly with the flip of a genetic switch. Jam the switch and you might prevent infection, said Vladimir Svetlov, a microbiology research associate at Ohio State University and one of a group of scientists who defined the structure of a protein that appears to be the key. The discovery is one of many this year to identify structures and chemicals crucial to disease. All of this work could lead to new medicines.

At the same time, germs we once fought off with antibiotics are fighting back, forcing governments and health organizations worldwide to spend billions of dollars to find new remedies.
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Redinbo is part of a team that recently discovered that two osteoporosis drugs block a key site on E. coli bacteria, preventing it from passing antibiotic resistance genes to other E. coli.

By their nature, bacteria exchange pieces of their DNA with neighboring bacteria, leading to new forms that are virulent or resistant — or both. “This is not minor evolution,” said Irina Artsimovitch, associate professor of microbiology at Ohio State. “This is a huge genome exchange.”

Methods. The PubMed database was searched for English-language articles, using relevant keyword combinations for articles published between 1980 and 2006. Twenty-seven studies were eventually identified as being relevant to the review.

Results. Soaps containing triclosan within the range of concentrations commonly used in the community setting (0.1%ndash0.45% wt/vol) were no more effective than plain soap at preventing infectious illness symptoms and reducing bacterial levels on the hands. Several laboratory studies demonstrated evidence of triclosan-adapted cross-resistance to antibiotics among different species of bacteria.

Conclusions. The lack of an additional health benefit associated with the use of triclosan-containing consumer soaps over regular soap, coupled with laboratory data demonstrating a potential risk of selecting for drug resistance, warrants further evaluation by governmental regulators regarding antibacterial product claims and advertising. Further studies of this issue are encouraged.