Canada’s federal government is launching an initiative to combat antibiotic resistant bacteria. This is a very sensible thing to do, given how bacterial evolution is creating resistant strains at a higher rate than the one at which we are inventing new antibiotics. MRSA and its relatives could well signal a return to a world in which morbidity and mortality from bacterial illness start shifting back towards the levels prevalent before antibiotics were widely available.
We largely have ourselves to blame for the existence of these bugs. Every time a doctor prescribes unnecessary antibiotics in order to get a patient out of their office, we give them another chance to get stronger. The same goes for when a patient stops taking an antibiotic prescription when they feel better, rather than when it runs out, potentially leaving a few of the most resistant bugs behind to infect others. The same is true for all the ‘antibacterial’ soaps and cleaning products out there. Putting triclosan in soap is pretty poor prioritization. Outside the body, it makes the most sense to kill bugs with things they cannot evolve resistance to: like alcohol or bleach. Using the precious chemicals that kill them but not us to clean countertops is just bad thinking. Finally, there is the antibiotic-factory farming connection discussed extensively here before.
The federal plan involves a number of prudent steps, many of them specifically targeted to MRSA and Clostridium difficile. These include more active patient screening, better sanitization of hospital rooms, use of prophylactics like gloves and masks, and the isolation of patients with resistant strains. Given that there were 13,458 MRSA infections in Ontario hospitals in 2006, it seems that such an initiative is overdue. It would be exceedingly tragic if we comprehensively undermined one of the greatest discoveries in the history of medicine through carelessness and neglect.
Defenceless against influenza
National Post Published: Monday, February 04, 2008
The World Health Organization announced mystifying news last week: The garden-variety influenza virus H1N1 that periodically besets the world, and is doing so this winter, seems to be developing a startling new resistance to Tamiflu (oseltamivir), the first and most important of antiviral drugs for influenza.
That such a thing should happen is curious. No one bothers much with Tamiflu as a primary weapon of attack against the regular flu– at least not outside Japan, where aggressive marketing by a subsidiary of the global patent-holder, Hoffman-La Roche, has convinced the populace to more or less pop the stuff like candy. For flu programs in nursing homes and hospitals elsewhere, other antivirals come a lot cheaper and work just as well.
Epidemic community-associated methicillin-resistant Staphylococcus aureus: Recent clonal expansion and diversification
Emerging and re-emerging infectious diseases, especially those caused by drug-resistant bacteria, are a major problem worldwide. Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) appeared rapidly and unexpectedly in the United States, resulting in an epidemic caused primarily by isolates classified as USA300. The evolutionary and molecular underpinnings of this epidemic are poorly understood. Specifically, it is unclear whether there has been clonal emergence of USA300 isolates or evolutionary convergence toward a hypervirulent phenotype resulting in the independent appearance of similar organisms. To definitively resolve this issue and understand the phylogeny of USA300 isolates, we used comparative whole-genome sequencing to analyze 10 USA300 patient isolates from eight states in diverse geographic regions of the United States and multiple types of human infection. Eight of 10 isolates analyzed had very few single nucleotide polymorphisms (SNPs) and thus were closely related, indicating recent diversification rather than convergence. Unexpectedly, 2 of the clonal isolates had significantly reduced mortality in a mouse sepsis model compared with the reference isolate (P = 0.0002), providing strong support to the idea that minimal genetic change in the bacterial genome can have profound effects on virulence. Taken together, our results demonstrate that there has been recent clonal expansion and diversification of a subset of isolates classified as USA300. The findings add an evolutionary dimension to the epidemiology and emergence of USA300 and suggest a similar mechanism for the pandemic occurrence and spread of penicillin-resistant S. aureus (known as phage-type 80/81 S. aureus) in the 1950s.
Tracking global E.coli ‘crucial’
A system must be set up to monitor the global spread of a drug-resistant form of E.coli which can cause fatal blood poisoning, Canadian scientists urge.
Meat wagon: pork superbug!
The Pink-Bubble-Gum- Flavored Dilemma
Why doctors give out antibiotics you don’t need.
By Zachary Meisel
Posted Wednesday, May 21, 2008, at 3:21 PM ET
The profligate prescription of antibiotics—for children and adults with upper respiratory infections, sinus infections, and even middle-ear infections—is a problem because most of these illnesses are caused by viruses, not bacteria, which are what conventional antibiotics attack. Of more concern is the direct connection between antibiotic use and the emergence of drug-resistant “superbugs”: As the medicine eliminates germs that are sensitive to it, drug-resistant mutant strains prosper. The result is a major public-health problem. Antibiotic-resistant infections such as methicillin-resistant Staphylococcus aureus may cause more deaths in the United States than AIDS does.
In the doctor’s office or the ER, it’s hard to tell the difference between bacterial and viral infections, and so doctors are tempted to prescribe antibiotics whenever they’re unsure. That’s especially true when doctors think that patients expect to take the medicine home, according to a recent study. Investigators interviewed patients with respiratory infections who went to the ER in 10 hospitals affiliated with medical schools, asking whether the patients expected to receive antibiotics and about whether they were satisfied with the care they received when they were discharged. The researchers also asked physicians why they prescribed antibiotics. The main conclusion was that doctors were significantly more likely to prescribe if they believed that patients expected them to—but did a lousy job predicting which patients those actually were. And the patients most satisfied with their care were the ones who left the ER with a better understanding of their condition, antibiotics or no antibiotics. The take-home message for doctors like me: Spend an extra five minutes talking to your patients about their medical problems, and you can send them away happy and without unnecessary medicine.
In the presence of drugs, pathogens have evolved sophisticated mechanisms to inactivate these compounds (e.g. by pumping out compounds, mutating residues required for the compound to bind, etc.), and they do so at a rate that far exceeds the pace of new development of drugs. Examples include drug resistant strains of Staphylococcus aureus, Klebsiella pneumonia, and Pseudomonas aeruginosa, and Mycobacterium tuberculosis (TB) among bacterium and HIV-1 among viruses. Indeed, no new antibiotics have been developed against TB in thirty years. Efforts to develop new antibiotics by the pharmaceutical industry by large-scale screens of chemical libraries which inhibit bacterial growth have largely failed, and new tetracycline and sulfanilamide analogs will likely engender resistance and will quickly be rendered useless.
Vancomycin-resistant Staphylococcus aureus
The new generation of resistant infections is almost impossible to treat
By Mark Frauenfelder
I’ve read a lot of stories about antibiotic-resistant infections, but this New Yorker piece by Jerome Groopman called “Superbugs” stands out.
Frederick Ausubel, a bacterial geneticist at the Massachusetts General Hospital, in Boston, is searching for drugs to combat bacterial virulence, using tiny animals like worms, which have intestinal cells that are similar to those in humans, and which are susceptible to lethal microbial infection. The worm that Ausubel is studying, Caenorhabditis elegans, is one and a half millimetres in length. “You are probably going to have to screen millions of compounds and you can’t screen millions of infected mice,” Ausubel said. “So our approach was to find an alternative host that could be infected with human pathogens which was small enough and cheap enough to be used in drug screens. What’s remarkable is that many common human pathogens, including Staphylococcus and Pseudomonas, will cause intestinal infection and kill the worms. So now you can look for a compound that cures it, that prevents the pathogen from killing the host.”
Surgeons not following steps to reduce infections
Updated Mon. Nov. 17 2008 8:15 AM ET
The Canadian Press
TORONTO — Alberta surgeons aren’t always following guidelines aimed at minimizing the risk patients will develop an infection as a result of their surgery, a new survey reveals.
Experts concerned about dangers of antibacterial products
Canadian Medical Association calls on the federal government to ban all antibacterial household products because of fears they cause bacterial resistance
JENNIFER YANG
From Friday’s Globe and Mail Last updated on Friday, Aug. 21, 2009 10:17AM EDT
A growing body of research is showing that antibacterial products can cause bacterial resistance, thus decreasing the effectiveness of antibiotics. The most common ingredient in antibacterial products is a chemical compound called triclosan, which was invented more than 35 years ago and used by doctors during surgical scrubs.
But as the chemical creeps into more and more household products, it’s also causing bacteria to become more resistant – not just to triclosan, but also other antibiotics such as isoniazid, a drug used to treat and prevent tuberculosis.
Researchers are also finding that the majority of women are now showing traces of triclosan in their breast milk, Dr. Khatter says. “We don’t know what the potential impacts of that are,” he says. “Breast milk is kind of the canary in the coal mine. It’s the easiest way we can measure if something’s building up in people.”
MRSA ‘superbug’ found in ocean, public beaches
By Steve Sternberg, USA TODAY
SAN FRANCISCO — Public beaches may be one source of the surging prevalence of the superbug known as multidrug-resistant Staphylococcus aureus, researchers here said Saturday.
A study by researchers at the University of Washington has for the first time identified methicillin-resistant Staph aureus (MRSA) in marine water and beach sand from seven public beaches on the Puget Sound.
The researchers identified Staph bacteria on nine of 10 public beaches that they tested. Seven of 13 Staph aureus samples, found on five beaches, were multidrug resistant, says lead investigator Marilyn Roberts.
“Our results suggest that public beaches may be a reservoir for possible transmission of MRSA,” she told the Interscience Conference on Antimicrobial Agents and Chemotherapy here, the leading international conference on new and resurgent diseases.
Antibiotic resistance clue found
US scientists have uncovered a defence mechanism in bacteria that allows them to fend off the threat of antibiotics.
It is hoped the findings could help researchers boost the effectiveness of existing treatments.
The study published in Science found that nitric oxide produced by the bacteria eliminates some key effects of a wide range of antibiotics.
One UK expert said inhibiting nitric oxide synthesis could be an important advance for tackling tricky infections.
Antibiotic resistance, for example with MRSA, is a growing problem and experts have long warned of the need to develop new treatments.
Art That Illustrates the Danger of Antibacterial Everything
What you’re looking at is the art of bacterial adaptation. It’s beautiful. It should also make you a little uncomfortable, and a little hopeful. Part of a collaboration between Professor Eshel Ben-Jacob, of Tel-Aviv University, and Professor Herbert Levine of UCSDs National Science Foundation Frontier Center for Theoretical Biological Physics, these pictures are a visual representation of the way bacteria evolve to overcome life-threatening obstacles—like, say, hand gel. The art is also about the way bacteria fight back, which involves a form of communication. The researchers hope to use that skill against the bacteria to create a new generation of antibacterial weaponry.
Stop Whining About Antibiotic Abuse
We can win our battle against bacteria. Here’s how.
By Brian Palmer
Posted Wednesday, Dec. 2, 2009, at 12:17 PM ET
It’s more than a little embarrassing to be decisively losing a battle of wits to unicellular organisms. At least the bacteria are smart enough to develop new strategies every now and then. We plodding humans have been fighting antibiotic resistance the same way for decades: by restricting access to antibiotics and developing new drugs to kill off problem bugs. It hasn’t worked, and it’s never going to. Until we make a tactical shift, resistance is going to become more common and more dangerous. But these seemingly indomitable microbes have a soft underbelly. To recognize it, you have to understand how bugs develop drug resistance in the first place.
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When one cell “solves” a drug, it can package up the genetic recipe and transfer it to other bacteria. An entire colony of bacteria can develop antibiotic resistance with a single lucky mutation. And your body, which graciously hosts about 2 quadrillion bacterial cells—20 times your total number of human cells—is one enormous genetic swap meet. Most of your resident bacteria are either helpful or harmless. But some of them have been in our guts long enough to have seen our full menu of antibiotics. So even the so-called “normal flora” can archive antibiotic resistance and either go rogue themselves or spread it to more virulent invaders.
Klebsiella pneumoniae is one such bacterium. It has resided in the human gastrointestinal tract for as long as we have been able to identify microbes. Each time someone is treated for strep throat, syphilis, Lyme disease, or any other bacterial illness, it learns a little more about our medical arsenal. In 1996, doctors identified a strain of Klebsiella that produced an enzyme called KPC, which has the ability to destroy virtually all modern antibiotics.
The mutant Klebsiella is harmless in the G.I. tract, but if it escapes to another part of the body—because of poor hygiene or any number of other minor slip-ups—it can turn a routine urinary-tract infection into a life-and-death struggle. To make matters worse, Klebsiella has transferred the genetic recipe for KPC to other—sometimes more dangerous—pathogens. Doctors are now seeing strains of E. coli and Pseudomonas that can produce KPC. To combat the bugs, doctors can either throw a cocktail of antibiotics at the infection or dig up classes of antibiotics that were abandoned decades ago because of their intolerable toxicity.
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Because almost all antibiotic resistance relies on genetic transfer, this technique might be the solution we’ve been seeking since the very first colony of bacteria solved penicillin in 1944. In the best-case scenario, coupling antibiotics with anti-genetic transfer agents could eliminate the need to ration antibiotics.
MRSA superbug strain ‘tracked’ via genome
Researchers have developed a technique for precisely tracking the spread of the superbug MRSA in hospitals.
The team from the Wellcome Trust Sanger Institute in Cambridge looked at the genomes of MRSA strains from across the globe and at one hospital in Thailand.
They were able to spot small changes that allowed them to track the strain back to an individual patient.
They say this adds to the understanding of how MRSA can spread so rapidly and should lead to better treatments.
New Wave of Antibiotic-Resistant Bacteria
“New strains of ‘Gram-negative’ bacteria have become resistant to all safe antibiotics. Though methicillin-resistant Staphylococcus aureus (MRSA) is the best-known antibiotic-resistant germ, the new class of resistant bacteria could be more dangerous still. ‘The bacteria, classified as Gram-negative because of their reaction to the so-called Gram stain test, can cause severe pneumonia and infections of the urinary tract, bloodstream, and other parts of the body. Their cell structure makes them more difficult to attack with antibiotics than Gram-positive organisms like MRSA.’ The only antibiotics — colistin and polymyxin B — that still have efficacy against Gram-negative bacteria produce dangerous side effects: kidney damage and nerve damage. Patients who are infected with Gram-negative bacteria must make the unsavory choice between life with kidney damage or death with intact kidneys. Recently, some new strains of Gram-negative bacteria have shown resistance against even colistin and polymyxin B. Infection with these new strains typically means death for the patient.”
Resistance to antibiotics
The spread of superbugs
What can be done about the rising risk of antibiotic resistance?
ON DECEMBER 11th 1945, at the end of his Nobel lecture, Alexander Fleming sounded a warning. Fleming’s chance observation of the antibiotic effects of a mould called Penicillium on one of his bacterial cultures had inspired his co-laureates, Howard Florey and Ernst Chain, two researchers based in Oxford, to extract the mould’s active principal and turn it into the miracle cure now known as penicillin. But Fleming could already see the future of antibiotic misuse. “There is the danger”, he said, “that the ignorant man may easily underdose himself and by exposing his microbes to non-lethal quantities of the drug make them resistant.”
Penicillin and the other antibiotics that its discovery prompted stand alongside vaccination as the greatest inventions of medical science. Yet Fleming’s warning has always haunted them. Antibiotic resistance has now become a costly and dangerous problem. Some people fear there may be worse to come: that a strain of resistant bacterium might start an epidemic for which no treatment was available. Yet despite Fleming’s warning and despite a fair understanding of the causes of resistance and how they could be dealt with, dealing with them has proved elusive. Convenience, laziness, perverse financial incentives and sheer bad luck have conspired to nullify almost every attempt to stop the emergence of resistance.
There are good reasons to hope that the extreme threat of a resistant epidemic will never come to pass—not least that 65 years of routine antibiotic use have failed to prompt one. Even so, the lesser problems of resistance continue to gnaw away at medicine, hurting people and diverting resources from more productive uses, often in the countries that can least afford it.
Antibiotic resistance: It’s more than just staph
by Maggie Koerth-Baker
Here’s something that really is killing kids: A new strain of scarlet fever that’s about twice as resistant to antibiotics as previous antibiotic-resistant strains. This is heart-wrenching. My thoughts are with the families in Hong Kong suffering through this outbreak.
Deadly superbug outbreak hits problem-plagued network of Ontario hospitals
KAREN HOWLETT
Last updated Monday, Jul. 04, 2011 1:24PM EDT
A deadly outbreak of a highly contagious superbug has claimed the lives of 15 patients in Southern Ontario, raising questions about whether enough is being done to prevent and control the spread of hospital-acquired infections.
Niagara Health System, a sprawling network of seven hospitals serving 434,000 people in a dozen communities, has declared an outbreak of Clostridium difficile, commonly known as C. difficile, at three of its sites.
N to the Rescue
Jake Yeston
In the war against infectious disease, bacteria are in the process of scoring a frightening tactical victory. Vancomycin is often used as the antibiotic to treat strains that have evolved resistance to other drugs, but it too is falling prey to resistant strains. A simple swap of oxygen for protonated nitrogen (more specifically, lactate for alanine) by the bacteria at vancomycin’s binding site is remarkably effective at disarming the drug’s mechanism of action. Xie et al. fight back by introducing a compensatory swap of their own—NH for O at the complementary site on the vancomycin framework. This modification leads not only to high-affinity binding with a model of the resistant target, it also conserves impressive binding affinity with a model of the native target (just a factor of 2 shy of vancomycin itself). In other words, the NH-substituted drug derivative appears to have the capacity to bind either to the lactate site or to the alanine site, which the authors rationalize by a flexible protonation equilibrium that would render the drug’s nitrogen center an effective H-bond donor or acceptor. The authors furthermore observe promising results with the modified drug against vancomycin-resistant bacteria in culture.
J. Am. Chem. Soc. 133, 10.1021/ja207142h (2011).
http://www.sciencemag.org/content/333/6047/twil.full
“Klebsiella pneumoniae is a common cause of pneumonia, urinary tract, and bloodstream infections in hospital patients. The superbug form is resistant even to a class of medicines called carbapenems, the most powerful known antibiotics, which are usually reserved by doctors as a last line of defense. The ECDC said several EU member states were now reporting that between 15 and up to 50 percent of K. pneumoniae from bloodstream infections were resistant to carbapenems. To a large extent, antibiotic resistance is driven by the misuse and overuse of antibiotics, which encourages bacteria to develop new ways of overcoming them. Experts say primary care doctors are partly to blame for prescribing antibiotics for patients who demand them unnecessarily, and hospitals are also guilty of overuse.”
HEALTH officials are paid to feel apprehensive. For some years they have feared that tuberculosis (TB), an ancient scourge tamed by modern drugs, might evolve into a new, indestructible state. New strains of mycobacterium tuberculosis have already emerged, some resistant to isoniazid and rifampicin, two of the best known treatments, and some resistant to additional injected drugs. The advent of completely resistant TB seemed inevitable. Now it may have arrived.
On January 17th doctors in Mumbai declared that a dozen patients at Hinduja National Hospital had contracted TB that responded to no treatment. Three had already died. If the claim is proven true, it would usher a new era for an old foe.
M. tuberculosis does its dirty work mainly in the lungs, where it destroys tissue. A cough, sneeze or even idle chatter can propel the bacterium into the air, then into the lungs of another person. In the 20th century antibiotics helped to quash TB in much of the rich world. But the bacterium has mutated. This has often been blamed on patients who do not take a full course of medication, giving the bacterium the chance to adapt.