superbug

New research helps create new antibiotic that evades bacterial resistance.

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UIC research helps create new antibiotic that evades bacterial resistance
T. thermophilus HB27 strain expressing Cfr-like methylase.

Scientists at the University of Illinois Chicago and Harvard University have developed an antibiotic that could give medicine a new weapon to fight drug-resistant bacteria and the diseases they cause.

The antibiotic, cresomycin, described in Science, effectively suppresses pathogenic bacteria that have become resistant to many commonly prescribed antimicrobial drugs.

The promising novel antibiotic is the latest finding for a longtime research partnership between the group of Yury Polikanov, associate professor of biological sciences at UIC, and colleagues at Harvard. The UIC scientists provide critical insights into cellular mechanisms and structure that help the researchers at Harvard design and synthesize new drugs.

In developing the new antibiotic, the group focused on how many antibiotics interact with a common cellular target—the ribosome—and how drug-resistant bacteria modify their ribosomes to defend themselves.

More than half of all antibiotics inhibit growth of pathogenic bacteria by interfering with their protein biosynthesis—a complex process catalyzed by the ribosome, which is akin to “a 3D printer that makes all the proteins in a cell,” Polikanov said. Antibiotics bind to bacterial ribosomes and disrupt this protein-manufacturing process, causing bacterial invaders to die.

But many bacterial species evolved simple defenses against this attack. In one defense, they interfere with antibiotic activity by adding a single methyl group of one carbon and three hydrogen atoms to their ribosomes.

Scientists speculated that this defense was simply bacteria physically blocking the site where drugs bind to the ribosome, “like putting a push pin on a chair,” Polikanov said. But the researchers found a more complicated story, as they described in a paper published last month in Nature Chemical Biology.

By using a method called X-ray crystallography to visualize drug-resistant ribosomes with nearly atomic precision, they discovered two defensive tactics. The methyl group, they found, physically blocks the binding site, but it also changes the shape of the ribosome’s inner “guts,” further disrupting antibiotic activity.

Polikanov’s laboratory then used X-ray crystallography to investigate how certain drugs, including one published in Nature by the UIC/Harvard collaboration in 2021, circumvent this common form of bacterial resistance.

“By determining the actual structure of antibiotics interacting with two types of drug-resistant ribosomes, we saw what could not have been predicted by the available structural data or by computer modeling,” Polikanov said. “It’s always better to see it once than hear about it 1,000 times, and our structures were important for designing this promising new antibiotic and understanding how it manages to escape the most common types of resistance.”

Cresomycin, the new antibiotic, is synthetic. It’s preorganized to avoid the methyl-group interference and attach strongly to ribosomes, disrupting their function. This process involves locking the drug into a shape that is pre-optimized to bind to the ribosome, which helps it get around bacterial defenses.

“It simply binds to the ribosomes and acts as if it doesn’t care whether there was this methylation or not,” Polikanov said. “It overcomes several of the most common types of drug resistance easily.”

In animal experiments conducted at Harvard, the drug protected against infections with multidrug-resistant strains of common disease drivers including Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa. Based on these promising results, the next step is to assess the effectiveness and safety of cresomycin in humans.

But even at this early stage, the process demonstrates the critical role that structural biology plays in designing the next generation of antibiotics and other life-saving medicines, according to Polikanov.

“Without the structures, we would be blind in terms of how these drugs bind and act upon modified drug-resistant ribosomes,” Polikanov said. “The structures that we determined provided fundamental insight into the molecular mechanisms that allow these drugs to evade the resistance.”

New Antibiotic Slays Deadly Superbug in Early Trial

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News Picture: New Antibiotic Slays Deadly Superbug in Early TrialBy Robin Foster HealthDay Reporter

FRIDAY, Jan. 5, 2024

Researchers report that a new type of antibiotic has proved its mettle against a deadly superbug.

Acinetobacter baumannii, a bacteria that goes by the nickname CRAB when it becomes antibiotic-resistant, can trigger serious infections in the lungs, urinary tract and blood, according to the U.S. Centers for Disease Control and Prevention. Unfortunately, it’s resistant to a class of powerful broad-spectrum antibiotics called carbapenems.

Now, in a study published Jan. 3 in the journal Nature, researchers from Harvard University and the pharmaceutical company Hoffmann-La Roche discovered that a new type of antibiotic, zosurabalpin, can kill A. baumannii.

Zosurabalpin employs a unique method of action, researcher Dr. Kenneth Bradley, global head of infectious disease discovery with Roche Pharma Research and Early Development, told CNN.

“This is a novel approach, both in terms of the compound itself but as well as the mechanism by which it kills bacteria,” he explained. A. baumannii is a Gram-negative bacteria, meaning it is protected by both inner and outer membranes, making it difficult to attack.

In this study, the scientists first tried to identify and then fine-tune a molecule that could cross those double membranes and eliminate the bacteria.

After years of improving the potency and safety of a number of compounds, the researchers chose one modified molecule.

How does it work? Zosurabalpin prevents the movement of large molecules called lipopolysaccharides to the outer membrane of the bacteria, where they keep the protective membrane intact. This causes the molecules to accumulate inside the bacteria’s cell to the point where the cell becomes so toxic that it dies.

In the study, zosurabalpin worked against more than 100 CRAB samples. It also reduced the levels of bacteria in mice with CRAB-induced pneumonia and prevented the death of mice with sepsis triggered by the bacteria.

Zosurabalpin is now being tested in phase 1 clinical trials, to assess its safety in humans, the researchers told CNN.

Still, the public health threat of antimicrobial resistance remains a huge problem globally due to a lack of effective treatments, Dr. Michael Lobritz, worldwide leader of infectious diseases at Roche Pharma Research and Early Development, told CNN.

In the United States, there are more than 2.8 million antimicrobial-resistant infections each year. More than 35,000 people die as a result, according to the CDC’s 2019 Antibiotic Resistance Threats Report.

Even though zosurabalpin is years away from human use, it’s an extremely promising development, Dr. César de la Fuente, presidential assistant professor at the University of Pennsylvania, told CNN.

“I think from an academic perspective, it is exciting to see a new type of molecule that kills bacteria in a different way,” de la Fuente said. “We certainly need new out-of-the-box ways of thinking about antibiotic discovery, and I think this is a good example of that.”

The only drawback to the discovery is that the modified molecule will work only against the specific bacteria it is designed to kill, the researchers noted.

However, de la Fuente said this new method could turn out to be better than many broad-spectrum antibiotics.

“For decades, we’ve been obsessed with creating or discovering broad-spectrum antibiotics that kill everything,” he noted. “Why not try to come up with specific, more targeted antibiotics that only target the pathogen that is causing the infection and not all the other things that might be good for us?”

Tools for Detecting a “Superbug”: Updates on Candida auris Testing

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ABSTRACT

Candida auris is an emerging yeast species that has the unique characteristics of patient skin colonization and rapid transmission within health care facilities and the ability to rapidly develop antifungal resistance. When C. auris first started to appear in clinical microbiology laboratories, it could be identified only by using DNA sequencing. In the decade since its first identification outside of Japan, there have been many improvements in the detection of C. auris. These include the expansion of matrix-assisted laser desorption ionization–time of flight mass spectrometry (MALDI-TOF MS) databases to include C. auris, the development of both laboratory-developed tests and commercially available kits for its detection, and special CHROMagar for identification from laboratory specimens. Here we discuss the current tools and resources that are available for C. auris identification and detection.

SUMMARY

As more laboratories have focused on the identification of C. auris, the number of available tools for detection and identification has increased. However, not all laboratories can implement a laboratory-developed test, and many do not have access to MALDI-TOF MS or a Vitek 2 system. The number of alternative commercially available tests is still quite limited, which leaves definitive identification of C. auris as a send-out test in many facilities. An especially glaring deficiency is the lack of a point-of-care test for detection of C. auris colonization. This would be an important tool for the identification of colonized patients, which plays an important role in the implementation of infection control practices, especially in cities where C. auris has become endemic. Candida auris continues to spread across the United States and across the world, and it has become a notifiable disease in many U.S. states and municipalities. While we may only be able to slow the spread, more tools for its detection and identification will allow us to combat it at the point of individual patient care.

Superbug Risk Is Alarmingly High

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salmonella

Story at-a-glance

  • A European Union report found high levels of drug-resistant bacteria in humans, animals and food
  • Multidrug-resistant salmonella was noted as a particularly serious threat
  • Countries that have taken steps to reduce the use of antimicrobials in animals have lower levels of antimicrobial resistance and decreasing trends

The threat of antimicrobial resistance is increasing around the globe, including in the European Union (EU), where the European Centre for Disease Prevention and Control (ECDC) and the European Food Safety Authority (EFSA) released a new report on this urgent matter.1

Antimicrobial resistance refers to microorganisms — bacteria, fungi, viruses and parasites — that, after exposure to antimicrobial drugs (such as antibiotics, antifungals, antivirals, antimalarials, and anthelmintics), evolve and become impervious to them.2

The resulting “superbugs” pose a serious threat to public health. In the EU, 25,000 deaths occur every year due to infections caused by antimicrobial-resistant bacteria alone.3

EU Reports High Levels of Drug-Resistant Bacteria, Especially Salmonella

Data submitted by 28 EU member states in 2015 revealed antimicrobial resistance remains high in bacteria from humans, animals and food in the E.U., with multidrug-resistant salmonella noted as a particularly serious threat.

Nearly 30 percent of the salmonella isolates that can cause illness in humans displayed multidrug resistance, including to sulfonamides (more than 32 percent), tetracyclines (28 percent) and ampicillin (nearly 28 percent).4

One particularly common type of salmonella in humans, monophasic salmonella typhimurium, had “extremely high” multidrug-resistance rates of 81 percent, leading Mike Catchpole, chief scientist at ECDC, to state:5

“Prudent use of antibiotics in human and veterinary medicine is extremely important to address the challenge posed by antimicrobial resistance. We all have a responsibility to ensure that antibiotics keep working.”

Infection with salmonella is the second-most common foodborne infection in the EU, second only to infections caused by campylobacter. Among campylobacter isolates from humans, “very high to extremely high” resistance to the drug ciprofloxacin was reported — in some cases 80 percent to 100 percent.6

Reducing the Use of Antibiotics in Food Animals Is Associated With Lower Rates of Antimicrobial Resistance

Of note, the report found lower levels of antimicrobial resistance in Northern and Western Europe compared to the Southern and Eastern regions. The differences most likely are due to differences in antimicrobial use, particularly in agricultural cases.

Marta Hugas, head of EFSA’s biological hazards and contaminants unit, said in a press release:

” … [C]ountries where actions have been taken to reduce, replace and re-think the use of antimicrobials in animals show lower levels of antimicrobial resistance and decreasing trends.”7

In animals and meat, meanwhile, the presence of superbugs was also concerning. The report noted that bacteria resistant to carbapenems, which are antibiotics typically used as a last resort when all other antibiotics have failed, were detected for the first time in EU animals and food.8

Resistance to colistin, another last-resort antibiotic, was also revealed, as was resistance to salmonella, campylobacter and E. coli in animals and meat. University of Minnesota’s Center for Infectious Disease Research and Policy (CIDRAP) reported:9

“Among the salmonella isolates from pig meat, the highest levels of resistance were reported for ampicillin (44.7 percent), sulfamethoxazole (48.5 percent), and tetracyclines (49.1 percent).

… Among salmonella isolates from fattening pigs, moderate or high to extremely high resistance was reported for tetracyclines and sulfonamides, with slightly lower levels of ampicillin resistance.

In C [campylobacter] coli isolates from fattening pigs, overall resistance was very high for ciprofloxacin (62.1 percent), nalidixic acid (60.8 percent), and tetracycline (66.6 percent), and high for erythromycin (21.6 percent).

In E coli from fattening pigs, high levels of resistance were found to tetracyclines (54.7 percent), sulfamethoxazole (44.2 percent), ampicillin (39.3 percent), and trimethoprim (35.3 percent), with 38.1 percent of isolates displaying MDR [multidrug resistance]. Resistance levels in indicator E coli isolates from calves were also high … ”

Antibiotic Resistance is Now Found in Every Country

This problem is not unique to the EU; it is very much a global concern, as the World Health Organization (WHO) notes antibiotic resistance is present in every country.10

The Review on Antimicrobial Resistance (AMR), which was commissioned in July 2014 by the UK Prime Minister and which produced its final report in 2016, further explained that without action to curb the growing rates of antimicrobial resistance worldwide, we’re headed for an era where antibiotics stop working and “we’re cast back into the dark ages of medicine.”11

According to the AMR, antibiotic-resistant infections may lead to 50,000 deaths every year in the U.S. and EU, while:12

“The global burden of infections resistant to existing antimicrobial medicines is now growing at an alarming pace. Drug-resistant infections are already responsible for more than half a million deaths globally each year.

Early research commissioned by the Review suggests that if the world fails to act to control resistance, this toll will exceed 10 million each year by 2050 and have cost the world over 100 trillion USD in lost output.”

Why Is Antimicrobial Resistance on the Rise?

Antimicrobial resistance is a natural phenomenon, which occurs when a select few microbes survive treatment with antimicrobial drugs, often via genetic changes, and then grow and thrive.

“This leads to antibiotics becoming less effective over time and in many extreme cases, ultimately useless,” according to AMR. But the review notes that antimicrobial resistance is a growing threat today for two main reasons:13

  • The use of antimicrobials has increased, which means microbes are exposed to many such drugs, and in greater concentrations, which increases the likelihood of resistance developing
  • There are very few new drugs in development, especially in the case of antibiotics, to take the place of the drugs rendered ineffective by growing resistance

In conventional medicine, the lack of rapid diagnostic tests to identify disease-causing microbes is adding to the problem, as doctors may be forced to rely on broad-spectrum drugs that may not end up curing the disease (but at the same time expose the person to drugs that increase the risk of drug resistance).

The review also highlights the role of antibiotics used for animals, often for purposes of promoting growth, not treating disease, along with untreated waste products that allow drug resistance to be spread through the environment.14 Vytenis Andriukaitis, EU commissioner for health and food safety, said in a press release:15

“Antimicrobial resistance is an alarming threat putting human and animal health in danger. We have put substantial efforts to stop its rise, but this is not enough. We must be quicker, stronger and act on several fronts.”

Some Experts Say ‘Finishing the Entire Round’ of Antibiotics May Make Resistance Worse

If you’ve ever been prescribed antibiotics, you’ve likely heard the advice to finish the entire prescription, even if you feel better after just a couple of days. This is important, it’s said, because stopping early could allow some bacteria to survive, increasing the risk of antibiotic resistance.

In a report by STAT, it’s revealed, however, that a growing number of experts believe this rationale “doesn’t make any sense,” and taking antibiotics longer than necessary may actually be leading to increased drug resistance.16

The issue has become so pressing, and the number of critics of the old “finish the entire prescription” mantra so large, that it’s going to be examined at a March 2017 WHO meeting in Geneva, Switzerland.

The suggestion to continue antibiotic treatment after the resolution of symptoms was started when antibiotic resistance was not a concern, and is done to prevent relapses, not resistance, according to a report prepared by the WHO Expert Committee on the Selection and Use of Essential Medicines.17

They cite multiple studies that show shorter may be better when it comes to antibiotic treatment. According to one review published in JAMA Internal Medicine in September 2016:18

“Other than tuberculosis — which is caused by a very slowly replicative organism that spends much of its time in a nonreplicating state — for every bacterial infection for which trials have compared short-course with longer course antibiotic therapy, short-course therapy has been just as effective, and with reduced selective pressure driving resistance.

Use of shorter courses of antibiotic therapy is therefore greatly preferable to longer courses of therapy … Health care professionals should be encouraged to allow patients to stop antibiotic treatment as early as possible on resolution of symptoms of infection.

Ultimately, we should replace the old dogma of continuing therapy past resolution of symptoms with a new, evidence-based dogma of “shorter is better.”

In a sign that even the U.S. Centers for Disease Control and Prevention (CDC) may be open to this new dogma, at the end of the conventional advice to “not stop taking the antibiotics early,” they’ve added the caveat, “unless your healthcare professional tells you to do so.”19

Sanderson Refuses to Budge on Antibiotics

A number of poultry producers have already taken steps to cut down or eliminate antibiotics from their production. Tyson, Pilgrim’s Pride and Foster Farms have all announced they’re implementing procedures to reduce their use.

But this isn’t the case with Sanderson Farms, the third-largest poultry producer in the U.S. and also the only large producer that has refused to commit to limiting their use. In February 2017, a Sanderson Farms shareholder proposal that requested the company phase out the use of medically important antibiotics even failed to pass.20

The company has stated that using antibiotics preventively in food animals is not dangerous to human health and continues to use two antibiotics — gentamicin and virginiamycin — that are important for treating human infections.21

In May 2016, I urged you to pressure Sanderson Farms to come to its senses and join other major poultry producers in taking proactive steps to reduce its antibiotic use. Remarkably, the company decided to go public with its decision to continue using antibiotics instead, saying the antibiotic-free chicken trend is nothing but a marketing ploy devised to justify higher prices!

In reality, it’s known that when animals are given antibiotics, it promotes drug resistance in the microbes found in and on the animal, and those drug-resistant bacteria can then be spread to those who handle or eat the tainted meat.

Action Steps to Avert the Impending Crisis

The AMR included 10 steps to avert the crisis of antimicrobial resistance that is creeping over the globe. As you might suspect, one of them is to eliminate the unnecessary use of antibiotics in farming and ban agricultural use of antibiotics needed as a last-line of defense in human medicine.22

To encourage this process, the report suggests meats should be clearly labeled to help consumers make informed choices about whether they want to buy meats raised with antibiotics. Other action steps noted in the report include:

  • Improve sanitation: Developed countries need to focus on reducing hospital-acquired infections, while poor nations need to improve general living conditions with access to clean water and better sanitation and waste management. According to the report, economic development is critical, as improved sanitation alone could eliminate the need for 300 million courses of antibiotics given to treat diarrhea each year.
  • Implement a global surveillance network to better understand how and where antibiotics are being used, and how resistant microbes are spreading and affecting various drugs.
  • Eliminate unnecessary use of antibiotics in human medicine. In the U.S. only about one-quarter of all prescriptions for antibiotics are actually medically necessary and/or appropriate. The vast majority of people who get them have viral infections that do not respond to antibiotics. Part of the plan would be to improve diagnostic tests to identify bacterial infections and the most appropriate antibiotics to treat them.

As Drug-Resistance Spreads, What Can You Do?

High-quality colloidal silver may be a valuable addition to your medicine cabinet. The antimicrobial properties of silver have been known since 400 B.C., and silver was commonly used as an antimicrobial agent in wound management until the early 20th century. Its usage only diminished once antibiotics were introduced in the 1940s.

Low doses of silver can make antibiotics up to 1,000 times more effective and may even allow an antibiotic to successfully combat otherwise antibiotic-resistant bacteria.23 On a broader scale, the problem of antibiotic resistance really needs to be stemmed through public policy on a global level, but the more people who get involved on a personal level, the better. Such strategies include:

Using antibiotics only when absolutely necessary

Antibiotics are typically unnecessary for most ear infections, and they do NOT work on viruses. They only work on bacterial infections and, even then, they’re best reserved for more serious infections.

Taking an antibiotic unnecessarily will kill off your beneficial gut bacteria for no reason at all, which could actually make it more difficult for you to recover from your illness. If you do take a course of antibiotics, be sure to reseed your gut with healthy bacteria by eating fermented foods or taking a supplement.

As an all-around preventive measure, make sure your vitamin D level is optimized year-round, especially during pregnancy, along with vitamin K2. A number of other natural compounds can also help boost your immune system function to help rid you of an infection, including vitamin C, oil of oregano, garlic, Echinacea and tea tree oil.

Manuka honey can also be used for topical applications, as it’s effective against many bacteria, including some resistant varieties, such as MRSA.

Avoiding all antibacterial household products

This includes items such as antibacterial hand sanitizers and wipes, toothpaste, deodorants and detergents, as these too promote antibiotic resistance.

Properly washing your hands with warm water and plain soap, to prevent the spreading of bacteria

Be particularly mindful of washing your hands and kitchen surfaces after handling raw meats from CAFOs, as about half of all meat sold in grocery stores around the U.S. is likely to be contaminated with potentially dangerous bacteria.

Purchasing organic, antibiotic-free meats and other foods

Reducing the spread of antibiotic-resistant bacteria is a significant reason for making sure you’re only eating grass-fed, organically raised meats and animal products.

Besides growing and raising your own, which may not be an alternative for most people, buying your food from responsible, high-quality and sustainable sources is your best bet, and I strongly encourage you to support the small family farms in your area.

The superbug that doctors have been dreading just reached the U.S.

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The Post’s Lena Sun visited Walter Reed Army Institute of Research in Silver Spring, Md., where scientists there identified a strain of bacteria resistant to the last-resort antibiotic, colistin. The bacteria was found in a Pennsylvania woman. Microbiologist Patrick McGann explains how his team identified the gene that gives the bacteria this resistance
For the first time, researchers have found a person in the United States carrying bacteria resistant to antibiotics of last resort, an alarming development that the top U.S. public health official says could mean “the end of the road” for antibiotics.

The antibiotic-resistant strain was found last month in the urine of a 49-year-old Pennsylvania woman. Defense Department researchers determined that she carried a strain of E. coli resistant to the antibiotic colistin, according to a study published Thursday in Antimicrobial Agents and Chemotherapy, a publication of the American Society for Microbiology. The authors wrote that the discovery “heralds the emergence of a truly pan-drug resistant bacteria.”

Colistin is the antibiotic of last resort for particularly dangerous types of superbugs, including a family of bacteria known as CRE, which health officials have dubbed “nightmare bacteria.” In some instances, these superbugs kill up to 50 percent of patients who become infected. The Centers for Disease Control and Prevention has called CRE among the country’s most urgent public health threats.

Health officials said the case in Pennsylvania, by itself, is not cause for panic. The strain found in the woman is still treatable with other antibiotics. But researchers worry that its colistin-resistance gene, known as mcr-1, could spread to other bacteria that can already evade other antibiotics.

It’s the first time this colistin-resistant strain has been found in a person in the United States. In November, public health officials worldwide reacted with alarm when Chinese and British researchers reported finding the colistin-resistant strain in pigs and raw pork and in a small number of people in China. The deadly strain was later discovered in Europe and elsewhere.

“It basically shows us that the end of the road isn’t very far away for antibiotics — that we may be in a situation where we have patients in our intensive care units, or patients getting urinary-tract infections for which we do not have antibiotics,” CDC Director Tom Frieden said in an interview Thursday.

[1 in 3 antibiotics prescribed in U.S. are unnecessary]

“I’ve been there for TB patients. I’ve cared for patients for whom there are no drugs left. It is a feeling of such horror and helplessness,” Frieden added. “This is not where we need to be.”
Separately, researchers at the Agriculture Department and the Department of Health and Human Services reported that testing of hundreds of livestock and retail meats turned up the same colistin-resistant bacteria in a sample from a pig intestine in the United States. USDA said it is working to identify the farm the pig came from.

CDC officials are working with Pennsylvania health authorities to interview the patient and family to identify how she may have contracted the bacteria, including reviewing recent hospitalizations and other health-care exposures. The CDC hopes to screen the patient and her contacts to see if others might be carrying the organism. Local and state health departments also will be collecting cultures as part of the investigation.

[‘A nightmare superbug’: What is it? And what are the risks?]

The woman was treated in an outpatient military facility in Pennsylvania, according to a Defense Department blog post about the findings. Samples were sent to the Walter Reed National Military Medical Center for initial testing. Additional testing was done by a special Defense Department system that tracks multi-drug-resistant organisms.

Thursday’s study did not disclose further details about the Pennsylvania woman or the outcome of her case. The authors could not be reached for comment. A spokesman at the Pennsylvania Department of Health was not immediately available to comment on the case.

Pennsylvania Gov. Tom Wolfe (D) issued a statement saying his administration immediately began working with the CDC and the Defense Department to coordinate “an appropriate and collaborative” response.

[Feds ramp up efforts to deal with antibiotic resistance]

“We are taking the emergence of this resistance gene very seriously,” he said, adding that authorities will take all necessary actions to prevent it from becoming a widespread problem with “potentially serious consequences.”

Sen. Robert P. Casey Jr. (D-Pa.) said he is concerned about the reports. In a statement, Casey said he supported legislation for and participated in hearings about antibiotic-resistant bacteria, which he said “present an urgent public health problem that we must focus on intensively.” He said he planned to get a full briefing on the case in the coming days.

Colistin is widely used in Chinese livestock, and this probably led bacteria to evolve and gain a resistance to the drug. The gene probably leaped from livestock to human microbes through food, said Yohei Doi, an infectious-disease doctor at the University of Pittsburgh who has studied the problem.
“Food handlers may be at higher risk,” he said. In places like China, where live animal markets are often in close proximity to food stalls, it may be more likely for the bacteria to spread from animals to humans.

He and other experts in infectious diseases called for speedier action to curb the overuse of antibiotics in livestock worldwide.

“It’s hard to imagine worse for public health in the United States,” Lance Price, director of the Antibiotic Resistance Action Center and a George Washington University professor, said Thursday in a statement about the case. “We may soon be facing a world where CRE infections are untreatable.”

Scientists rang the alarm bells about the gene in November, but not enough attention was paid. “Now we find that this gene has made its way into pigs and people, and people in the U.S.,” Price said. “If our leaders were waiting to act until they could see the cliff’s edge — I hope this opens their eyes to the abyss that lies before us.”

Scientists and public health officials have long warned that if the resistant bacteria continue to spread, treatment options could be seriously limited. Routine operations could become deadly. Minor infections could become life-threatening crises. Pneumonia could be more and more difficult to treat.

Already, doctors had been forced to rely on colistin as a last-line defense against antibiotic-resistant bacteria. The drug is hardly ideal. It is more than half a century old and can seriously damage a patient’s kidneys. And yet, because doctors have run out of weapons to fight a growing number of infections that evade more-modern antibiotics, it has become a critical tool in fighting off some of the most tenacious infections.
Bacteria develop antibiotic resistance in two ways. Many acquire mutations in their own genomes that allow them to withstand antibiotics, although that ability can’t be shared with pathogens outside their own family.

[Scientists discover why pancreatic cancer resists chemotherapy drug]

Other bacteria rely on a shortcut: They get infected with something called a plasmid, a small piece of DNA, carrying a gene for antibiotic resistance. That makes resistance genes more dangerous because plasmids can make copies of themselves and transfer the genes they carry to other bugs within the same family as well as jump to other families of bacteria, which can then “catch” the resistance directly without having to develop it through evolution.

The colistin-resistant E. coli found in the Pennsylvania woman has this type of resistance gene.

Public health officials say they have been expecting this resistance gene to turn up in the United States.

“This is definitely alarming,” said David Hyun, a senior officer leading an antibiotic-resistance project at the Pew Charitable Trust. “The fact that we found it in the United States confirms our suspicions and adds urgency to actions we need to work on antibiotic stewardship and surveillance for this type of resistance.”

Late last year, as part of a broader budget deal, Congress agreed to give hundreds of millions of dollars to the federal agencies engaged in the battle against antibiotic-resistant bacteria.

The largest chunk of that money, more than $150 million, was slated to go to the CDC as part of an effort to build and strengthen capacity at state and local health departments to prevent and monitor superbug outbreaks.

Other funding went to the National Institutes of Health for research on combating antimicrobial resistance, as well as to an agency known as BARDA, which works on national preparedness for chemical and biological threats, including developing new therapies.

Breast Cancer Drug Beats Superbug .

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Researchers at University of California, San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences have found that the breast cancer drug tamoxifen gives white blood cells a boost, better enabling them to respond to, ensnare and kill bacteria in laboratory experiments.Tamoxifen treatment in mice also enhances clearance of th antibiotic-resistant bacterial pathogen MRSA and reduces mortality.

The study is published October 13 by Nature Communications.

“The threat of multidrug-resistant bacterial pathogens is growing, yet the pipeline of new antibiotics is drying up. We need to open the medicine cabinet and take a closer look at the potential infection-fighting properties of other drugs that we already know are safe for patients,” said senior author Victor Nizet, MD, professor of pediatrics and pharmacy. “Through this approach, we discovered that tamoxifen has pharmacological properties that could aid the immune system in cases where a patient is immunocompromised or where traditional antibiotics have otherwise failed.”

Tamoxifen targets the estrogen receptor, making it particularly effective against breast cancers that display the molecule abundantly. But some evidence suggests that tamoxifen has other cellular effects that contribute to its effectiveness, too. For example, tamoxifen influences the way cells produce fatty molecules, known as sphingolipids, independent of the estrogen receptor. Sphingolipids, and especially one in particular, ceramide, play a role in regulating the activities of white blood cells known as neutrophils.

“Tamoxifen’s effect on ceramides led us to wonder if, when it is administered in patients, the drug would also affect neutrophil behavior,” said first author Ross Corriden, PhD, project scientist in the UC San Diego School of Medicine Department of Pharmacology.

To test their theory, the researchers incubated human neutrophils with tamoxifen. Compared to untreated neutrophils, they found that tamoxifen-treated neutrophils were better at moving toward and phagocytosing, or engulfing, bacteria. Tamoxifen-treated neutrophils also produced approximately three-fold more neutrophil extracellular traps (NETs), a mesh of DNA, antimicrobial peptides, enzymes and other proteins that neutrophils spew out to ensnare and kill pathogens. Treating neutrophils with other molecules that target the estrogen receptor had no effect, suggesting that tamoxifen enhances NET production in a way unrelated to the estrogen receptor. Further studies linked the tamoxifen effect to its ability to influence neutrophil ceramide levels.

The team also tested Tamoxifen’s immune-boosting effect in a mouse model. One hour after treatment with tamoxifen or a control, the researchers infected mice with MRSA (methicillin-resistant Staphylococcus aureus), a “superbug” of great concern to human health. They treated the mice again with tamoxifen or the control one and eight hours after infection and monitored them for five days.

Tamoxifen significantly protected mice — none of the control mice survived longer than one day after infection, while about 35 percent of the tamoxifen-treated mice survived five days. Approximately five times fewer MRSA were collected from the peritoneal fluid of the tamoxifen-treated mice, as compared to control mice.

There are two caveats, the researchers said. First, while tamoxifen was effective against MRSA in this study, the outcome may vary with other pathogens. That’s because several bacterial species have evolved methods for evading NET capture. Second, in the absence of infection, too many NETs could be harmful. Some studies have linked excessive NET production to inflammatory disease, such as vasculitis and bronchial asthma.

“While known for its efficacy against breast cancer cells, many other cell types are also exposed to tamoxifen. The ‘off-target effects’ we identified in this study could have critical clinical implications given the large number of patients who take tamoxifen, often every day for years,” Nizet said.

Tamoxifen is taken daily by hundreds of thousands of patients worldwide for the treatment of estrogen receptor-positive breast cancer. The World Health Organization considers tamoxifen an “essential medicine,” due to its cost-effectiveness and safety profile. According to the breast cancer organization Susan G. Komen, generic tamoxifen cost patients about $100 per month in 2010.

Tamoxifen is not the only drug prescribed for other indications that just happen to also boost neutrophil activity. In 2010, Nizet and team reported that cholesterol-lowering statins also enhance NET formation. That study can be found here.

For Superbugs, Fight Fire With Fire: Non-Toxic C. Diff Bacteria Ward Off Antibiotic-Resistant Strain

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If you haven’t heard of Clostridium difficile, better known as C. difficile or C. Diff, you will soon. It’s one of the fastest growing superbugs, rivaling MRSA in both frequency and severity. Due to antibiotic resistance, a cure for C. difficile  has been elusive, but a recent study suggests that we’ve been looking in the wrong places and the only thing strong enough to fight off C. difficileis actually more C. difficile.

bacteria culture

According to a report published in the Journal of the American Medical Association, trials on 173 individuals with C. difficile infections showed that introducing a non-toxigenic C. difficile strain helped to dramatically cut the odds of repeat infections and is a promising start to finally getting an upper hand on this potentially fatal superbug.

In the study, conducted by researchers at Loyola University Health System in Illinois, patients with C. difficile infections were given spores of a non-toxin producing strain of C. difficile. Around 69 percent of the time the “friendlier” strain was able to occupy areas in the gut where the toxic C. difficile strain normally thrived. This inhibited the severe C. difficile from returning and only one in 50 of the patients experienced a recurrent C. difficile infection.

The research is still in its earliest stages, but the researchers are excited about the results. Although the patient remains infected with C. difficile, more importantly, the symptoms cease. The eventual goal of the research is to develop a treatment involving the digestion of “friendly” C. difficile spores to indefinitely prevent a patient once again falling ill from the infection.

“What we’re doing is establishing competition with the original, toxic strain,” Dr. Dale Gerding, one of the researchers involved in the study explained, as reported by the BBC. “I’m excited about this and looking forward to a phase-three [larger] trial. We think it’ll go a long way to reduce C. diff recurrence.”

C. difficile infections are almost exclusive to hospital settings, clinics, nursing homes and other health care facilities. The reason for this is that the bacteria take hold in individuals whose normal fauna of bacteria is disrupted due to antibiotic courses. Without the normal healthy bacteria standing in the way, the drug-resistant C. difficile can take hold and cause inflammation in the patient’s colon. According to the Centers for Disease Control and Prevention, C. difficile infections are widespread and each year it’s linked to about 29,000 deaths in the United States.

Symptoms of C. difficile infections include frequent diarrhea, fever, loss of appetite, nausea, and abdominal pain and tenderness. These infections are commonly treated with antibiotics, but due to the bacteria’s evolved resistance to treatment the infection returns in around 20 percent of cases. Currently fecal transplants are the most effective way to treat repeat C. difficile infections, but the recent study suggests an equally effective and far less invasive approach to the condition.

Drug-resistant superbug infections explode across U.S. hospitals: 500% increase foreshadows ‘new plague’ caused by modern medicine.

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Drug-resistant superbug infections have reached near-epidemic levels across U.S. hospitals, with an alarming 500% increase now documented in a study just published in the August issue of Infection Control and Hospital Epidemiology (the journal of the Society for Healthcare Epidemiology of America). (1)

superbug

Lead author of the study, Dr. Joshua Thaden, warned “This dangerous bacteria is finding its way into healthcare facilities nationwide… A CRE epidemic is fast approaching… Even this marked increase likely underestimates the true scope of the problem given variations in hospital surveillance practices.”

The study also found that an astonishing 94 percent of CRE infections were caused by healthcare activities or hospital procedures.

CRE superbugs explained

CRE (carbapenem-resistant Enterobacteriaceae) is an incredibly dangerous superbug causing nearly a fifty percent fatality rate once a patient is infected. The World Health Organization calls it “one of the three greatest threats to human health,” and all known antibiotics are useless in treating it.

CRE arose out of the systematic abuse of antibiotics by doctors, who inadvertently created the perfect breeding ground for deadly bacteria by using narrowly-targeted chemical medications that lack the kind of full-spectrum action found in nature (in herbs like garlic, for example). Because of their highly-targeted chemical approach, antibiotics encouraged bacteria to develop molecular defenses that resulted in widespread resistance to Big Pharma’s drugs. The situation is so bad today that the entire pharmaceutical industry has no drug, no chemicals and no experimental medicines which can kill CRE superbugs.

Even worse, there are virtually no new antibiotics drugs in the research pipelines, either. Drug companies have discovered that it’s far more profitable to sell “lifestyle management” drugs like statin drugs and blood pressure drugs than to sell antibiotics which treat acute infections. Antibiotics simply aren’t very profitable because relatively few people acquire such infections. Meanwhile, everyone can be convinced they might have high cholesterol and therefore need to take a statin drug for life.

Drug companies, in other words, have all but abandoned the industry of treating infections. Instead, they now primarily engage in the promotion of disease symptoms while selling drugs that attempt to alter measurable markers of those symptoms such as cholesterol numbers. Even though drug companies caused the superbug pandemic that’s now upon us, in other words, they have deliberately abandoned humanity in defending against those superbugs because it’s simply not profitable to do so.

The end of antibiotics has arrived: Humanity faces a new plague caused by modern medicine

The CDC has admitted that we are now living in a “post-antibiotics era.” As Infection Control Today states, “Antibiotic resistance is no longer a prediction for the future. It is happening right now in every region of the world and has the potential to affect anyone.” (2)

Dr. Arjun Srinivasan, associate director at the Centers for Disease Control and Prevention, went even further in a PBS interview, stating: (3)

We’ve reached the end of antibiotics, period… We’re here. We’re in the post-antibiotic era. There are patients for whom we have no therapy, and we are literally in a position of having a patient in a bed who has an infection, something that five years ago even we could have treated, but now we can’t.

Keep in mind that doctors refuse to use natural substances to treat infections, which is why they believe no defenses against superbugs exist. Their indoctrination into the world of pharmaceuticals is so deeply embedded in their minds, in other words, that they cannot even conceive of the idea that an herb, a food or something from Mother Nature might provide the answer to superbugs. See this Natural News article on natural antibiotics that kill superbugs. The list includes honey.

Hospitals are the perfect breeding grounds for superbugs

By their very design, hospitals are prefect breeding grounds for superbugs for six very important reasons:

1) They put all the infected people under one roof, creating a high density infectious environment.

2) They allow doctors and medical staff to quickly and easily carry and transmit infectious diseases to new patients. Previous studies have documented how superbugs easily ride on doctors’ ties, for example, or their mobile phones.

3) Medical staff still don’t wash their hands as frequently as they should. The intense time demands placed on them discourage careful hand washing, causing many to skip this crucial step between patient visits.

4) Hospitals almost universally refuse to use broad-spectrum antibacterial remedies which are not drugs. Natural substances like honey and garlic show extraordinary multi-faceted antibacterial properties, as do certain metals such as silver and copper. Yet because these substances are not developed by pharmaceutical companies which dominate the field of medical practice, they are simply ignored even though they could save many lives. (And a doctor who prescribes “honey” doesn’t sound as amazing and all-knowing as a doctor who prescribes “the latest, greatest laboratory breakthrough patented chemical medication.”)

5) Hospital practices suppress human immune function to the point of systemic failure. Rather than boosting immune function, conventional medical treatments such as antibiotics and chemotherapy cause immune system failure. Hospitals lack sunlight and hospital food lacks key immune-boosting minerals such as zinc and selenium. On top of that, most of the drugs prescribed to patients by hospitals deplete key nutrientsrequired for healthy immune function, leaving patients even more susceptible to superbug infections.

6) Hospital staff spread infectious diseases to their private homes. After acquiring an infection at work (at the hospital), staffers easily spread those infections to their own family members at home.

The antibiotics plague is upon us

We are right now living through the early stages of a global plague caused by modern medicine. The industry that created this plague is utterly defenseless against it, leaving humanity to fight for survival in a world that’s now far more dangerous than the one that existed before the invention of antibiotics.

Antibiotics have indeed saved millions of lives, and they forever have an important place in any medical practice. Yet their careless use — combined with medicine’s willful and foolish abandonment of natural antibiotics that work far better — has led humanity down the path of its own destruction.

Today, a simple scrape of your arm or leg might now be fatal. Infections that occur during routine medical procedures which would have once been considered minor issues are now deadly.

And the worst part is that the bacteria continue to evolve more elaborate defenses against drugs while increasing their transmissibility. Human hospitals (and entire cities) are, by design, ideal pandemic hubs that rapidly spread disease. Like it or not, humanity has created the perfect storm for a pandemic decimation of the global population.

What will Big Pharma do as this medical catastrophe unfolds? They’ll keep selling you more statin drugs, because that’s where the money’s made.

Sources for this article include:
(1) http://www.shea-online.org/View/ArticleId/29…

(2) http://www.infectioncontroltoday.com/news/20…

(3) http://www.pbs.org/wgbh/pages/frontline/heal…

Learn more: http://www.naturalnews.com/046041_CRE_superbugs_drug-resistant_infections_modern_plague.html#ixzz37qDas5zq

New single-dose antibiotic may help battle superbug MRSA.

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A single dose of a newly developed antibiotic may be just as effective as a longer course of standard antibiotics for the treatment of serious skin infections, including drug-resistant MRSA, which can be deadly.

The single dose of the new drug, called oritavancin, was found to cure MRSA, or methicillin-resistant Staphylococcus aureus, which typically requires a patient take antibiotics for up to 10 days and may involve a hospital stay.

“Oritavancin is unique in that because of its ability to stay in the body for long periods of time,” Dr. Ralph Corey, a professor of medicine and infectious diseases at Duke University School of Medicine and lead author on the paper, told CBS News. “You can be discharged from the ER to go back home and gradually cure the infection over the next seven to 10 days.”

For the study, just published in the New England Journal of Medicine, researchers conducted a randomized trial in which 475 patients were given oritavancin and 479 received an infusion of the older antibiotic vancomycin twice a day for 7 to 10 days.

Corey and his team found a single dose of oritavancin worked as well as vancomycin. The new drug reduced the size of skin lesions by 20 percent or more within the first 48 to 72 hours, and cured patients at the same rate as the standard antibiotic.

Antibiotics are a miracle of modern medicine, but many patients find it difficult to tolerate a typical course of the drugs, which can last anywhere between three days to two weeks. Patients can experience uncomfortable and debilitating side effects from the drugs, including gastrointestinal distress, yeast infections and allergic reaction. This often results in patients discontinuing their course of treatment, which has been shown to cause antibiotic resistance.

Corey’s study was funded by the Medicines Company, the drug company that owns the intravenous version of oritavancin. In February, the U.S. Food and Drug Administration accepted a filing of the new drug application.

The FDA has flagged the investigational drug as a “priority review,” which means the regulatory agency is required to consider the application within six months, rather than the usual 10 months or more. According to Medicine Company’s website, the FDA’s action date for oritavancin is August 6, 2014.

Warning over hospital superbug rise

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Klebsiella Pneumoniae
Nationwide research is being carried out into Klebsiella and its resistance to antibiotics

Sixteen people have died in Manchester in the past four years while infected with a highly resistant superbug, figures show.

Klebsiella pneumoniae carbapenemase (KPC) is causing increasing concern and a rising number of cases.

Some 1,241 patients were affected within the Central Manchester University Hospitals trust area from 2009 to 2013, the figures show.

Despite infection control, the numbers have increased year on year.

The figures, revealed in a Freedom of Information request by the BBC, found 62 patients so far have suffered blood poisoning – with 14 confirmed deaths within 30 days of infection – at Central Manchester University Hospitals NHS Foundation Trust.

Two further deaths have occurred in the current year, the hospital trust confirmed.

KPC, which causes urinary tract infections and pneumonia in sick patients, is resistant to carbapenems, the last major group of antibiotics to work against multidrug-resistant bacteria.

The trust said the chemical, an enzyme, that KPC uses to render antibiotics ineffective had now entered other bacteria, including E. coli and Enterobacter.

“This trust has and continues to make strenuous efforts to control and reduce this infection. We continue to work very closely with Public Health England at both a local and national level to develop solutions for the long-term management of patients,” it said.

The trust stated that all the patients who had died were seriously ill. Some had diabetes, kidney problems or transplant rejection; some were suffering from leukaemia or other forms of cancer.

Central Manchester Hospitals has already had to review guidelines on antibiotics and the treatment of patients who require bowel surgery or cancer treatment that may leave their immunity compromised.

‘Extremely unlucky’

Another Manchester hospital, the Christie, a specialist in cancer care, said nine patients had been colonised by KPC last year. but they had all been transferred to the cancer unit and there had been no cross-infection in the hospital.

A Freedom of Information request has also revealed two cases of KPC at New Cross Hospital in Wolverhampton, with one patient dying in the past two years.

Scientists say more research is needed into treating the KPC superbug

Microbiologist Dr Mike Cooper said that the patient who died was 96 and the form of KPC that had infected her was still susceptible to some drugs.

“There’s a huge element of luck in this. Either Manchester has been extremely unlucky or we have been extremely lucky not to have more cases,” he said.

Ten patients have also been infected at the University Hospital of North Staffordshire. Two had urinary tract infections, but neither patient died of blood poisoning.

Stoke’s microbiologist, Jeorge Orendi, said: “Unlike the situation in certain hospitals in Manchester and London, fortunately in our hospital and catchment area carbapenemase producers have remained rare to date.”

The KPC resistance mechanism first emerged in the US and spread to Israel. In Europe, it has taken hold in Greece and has reached epidemic proportions in Italy.

Gian Maria Rossolini, of the University of Siena, said that the first case was identified in Italy in 2008, but now 4% of all infections in Italy are resistant to carbapenems.

Aids epidemic

Dr Rossolini said deaths from blood infections were running at more than 40%, but for immune-compromised patients they could be as high as 80%.

Although KPC is still susceptible to an old and quite toxic antibiotic, colistin, in Florence this year more than 50% of KPC cases proved resistant to it.

“Although present in the UK, the problem seems to be still much more limited as compared to Italy and Greece,” he said.

Professor Laura Piddock, of Birmingham University, said: “It’s clear that what has gone on in Italy is our tomorrow. We have got to start preserving what we have got and use it wisely.

“If we are really serious about tackling this problem, we have to start viewing this in the same way as high-income countries viewed the Aids epidemic in the 90s.

Prof Peter Hawkey
Prof Peter Hawkey is mapping the spread of KPC across the country

“It’s going to take that sort of level of global policymaker decision-making to really tackle this issue properly.”

Research published in the Journal of Antibiotics found that colonisation with KPC is long-lasting, with 39% of patients still carrying KPC in their gut a year after being released from hospital.

In Birmingham, Prof Peter Hawkey is conducting nationwide research to identify the extent of KPC resistance and that of a more widespread, but slightly less virulent superbug, ESBL.

Patients in London, Southampton, Birmingham and Shropshire are being asked to send in faeces samples so the spread of the disease can be mapped.

Prof Hawkey said: “It makes sense whilst we are looking for these ESBL that we are also able to detect how many of these KPC organisms are in the community.

“I can conceive of techniques which may be able to make bacteria to kill these multidrug-resistant bacteria. It’s very much at an advanced research level at the moment, but in order to drive that, we need to know how big the problem is.”

Dr Rossolini said that the use of carbapenem antibiotics to control high levels of ESBL in the Midlands could actually help KPC take hold in the region.