More Examples of the Crisis of Antibiotic Resistance by 1kiki

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More Examples of the Crisis of Antibiotic Resistance

POSTED BY: 1KIKI
UPDATED: Tuesday, March 8, 2016 14:16
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Monday, March 7, 2016 8:38 PM

Goodbye, kind world (George Monbiot) - In common with all those generations which have contemplated catastrophe, we appear to be incapable of understanding what confronts us.

More Examples of the Crisis of Antibiotic Resistance

Preemies' Gut Bacteria Reveal Vast Scope of Antibiotic Resistance

Preemies' Gut Bacteria Reveal Vast Scope of Antibiotic Resistance
Mon, 03/07/2016 - 3:00pm
WASHINGTON UNIVERSITY SCHOOL OF MEDICINE

A new study led by Washington University School of Medicine in St. Louis reveals extensive antibiotic resistance in the gut bacteria of premature infants. The researchers say these findings support the push to minimize routine use of antibiotics in these patients. CREDIT Pablo TsukayamaA new study led by Washington University School of Medicine in St. Louis reveals extensive antibiotic resistance in the gut bacteria of premature infants. The researchers say these findings support the push to minimize routine use of antibiotics in these patients. CREDIT Pablo Tsukayama
A new study of gut bacteria in premature infants reveals the vast scope of the problem of antibiotic resistance and gives new insight into the extreme vulnerability of these young patients, according to researchers at Washington University School of Medicine in St. Louis.

The study appears online March 7 in the journal Nature Microbiology.

The gut microbiome has emerged in recent years as a vital player in human health, affecting factors as diverse as nutritional status, bone development and immune function. The new study shows that the microbes colonizing the gastrointestinal tracts of babies born prematurely are not health-promoting or even benign organisms, but close relatives of bacteria known to cause hospital-acquired infections, including Escherichia coli (E. coli),Klebsiella and Enterobacter.

The researchers sequenced all of the DNA in the bacterial communities living in the preterm babies' guts. Using new techniques they developed, the investigators identified almost 800 genes in these bacterial communities that confer resistance to antibiotics. They noted that about 80 percent of these genes had not previously been associated with antibiotic resistance.

"Our study demonstrates that even well-studied bacteria -- the ones that we know cause disease or their close relatives -- have many genes associated with antibiotic resistance that have not been characterized before," said senior author Gautam Dantas, PhD, associate professor of pathology and immunology. "Premature babies do not always get bacterial infections that need treatment, but we have known for a long time that they are at higher risk for infection than babies born full term. Now, we know that preterm-infant guts are attracting exactly the wrong kinds of bacteria."

Because of this increased risk of infection, almost all preterm infants cared for in neonatal intensive care units (NICUs) receive antibiotics in the first two days of life, regardless of their health status. And a majority of those receive many more days of treatment.

"Extremely preterm infants often have multiple medical problems, with symptoms of prematurity overlapping with other conditions like infection," said co-author Barbara B. Warner, MD, a professor of pediatrics and neonatologist at St. Louis Children's Hospital. "The conventional wisdom has been antibiotics can't hurt and they might help. But our new study demonstrates that wide-scale use of antibiotics in this population does not come without cost."

The study included babies cared for in the NICU of St. Louis Children's Hospital, where the investigators collected 401 fecal samples from 84 preterm infants over the first three months of life. By sequencing all of the bacterial DNA in these fecal samples, the investigators identified resistance genes to 16 different antibiotics. The babies that received antibiotics only in the first few days of life served as a comparison group to the babies that received antibiotics early plus subsequent treatments later. On average, the babies that continued receiving antibiotics had a total of 21 days of treatment. All babies were born before 33 weeks' gestation.

In general, research from this and other groups suggests it is better to have a high diversity of bacterial species living in the gut. Compared with babies born full term, preterm infants were found to have 10-fold fewer species of bacteria colonizing the gut. And among the preterm babies, those receiving the most antibiotics showed the least species diversity. Giving breast milk was associated with increased bacterial diversity, as was each baby's increasing age, perhaps simply from having more time for exposure.

The specific antibiotics associated with the lowest species richness were drugs called meropenem, cefotaxime and ticarcillin-clavulanate. Dantas said the meropenem finding is particularly alarming, as it's part of the carbapenem class of drugs that are considered antibiotics of last resort. They are used to treat infections caused by bacteria closely related to the species most commonly found in these infants' GI tracts.

"Consider what is going on in terms of selection pressure," Dantas said. "As with any antibiotic, giving carbapenems encourages the selection of bacteria resistant to this drug. And if these microbes, which dominate these babies' guts, become resistant to carbapenems, the microbes go on the highest urgency threat list at the Centers for Disease Control and Prevention."

According to the CDC, carbapenem-resistant Enterobacteriaceae (CRE) are resistant to nearly all existing antibiotics and about half of patients in intensive care units who contract a bloodstream infection from CRE die from that infection. Enterobacteriaceae is a large family of bacteria that includes E. coli, Klebsiella and Enterobacter.

In the new study, the two antibiotics most commonly given to the preterm infants were found to be vancomycin and gentamicin, which both had divergent effects on species richness. The researchers were able to predict the direction of this effect with high accuracy, based on the sequences of bacteria present and the resistance genes they carried in samples taken before treatment.

The researchers also showed that treating with one antibiotic can dial up resistance to seemingly unrelated antibiotics. Dantas said this surprising finding makes sense because they found the majority of these microbes were resistant to multiple drugs, showing that resistance genes tend to cluster together in the same organisms.

"This data demonstrates the collateral damage these drugs can do," Dantas said. "If doctors give penicillin, it makes sense that you will see enrichment in the proportion of bacteria resistant to penicillin. But perhaps a vancomycin-resistant gene is nearby. A doctor may not even be giving vancomycin, but vancomycin resistance increases because the genes happen to be grouped together.

"This is a consequence of our history of antibiotic use," he added. "We've given these bacteria powerful reasons to collect all these resistance genes together."

Warner expressed hope that clinicians will use this information to make decisions about the best ways to treat these vulnerable patients.

"While antibiotics can certainly still be lifesaving, we are becoming more aware of the risks they pose," she said. "This study arms us with information that may help us push toward shorter antibiotic treatment courses and minimizing the use of broad-spectrum antibiotics."

Dantas expressed concern over the dwindling numbers of effective antibiotics and the fact that few new drugs are in development. He also suggested a shift in strategy for the design of new generations of antibiotics.

"If we can stop these bacteria from producing toxins, rather than kill them outright, we won't see the same selection pressure," he said. "We don't necessarily need to kill these bacteria, we just need to stop them from killing us."

CDC: Superbugs Cause 1 in 7 Infections Caught in Hospitals
Fri, 03/04/2016 - 9:45am
Mike Stobbe, AP Medical Writer

Supergerms cause 1 out of 7 infections caught in hospitals, health officials said Thursday.

The bugs include the staph infection MRSA (MUR'-suh) and five other bacteria resistant to many kinds of antibiotics, the Centers for Disease Control and Prevention reported.

That leaves hospitals with few - if any - medicines to fight dangerous infections in already-sick patients. "That's the scary thing," said Tim Landers, an Ohio State University expert on antibiotic-resistant infections.

Hospital-spread infections have long been a problem. The CDC estimates that on any given day, 1 in 25 patients have an infection that they picked up in the hospital. Officials have been pushing hospitals to do a better job keeping infections in check, with the government's Medicare program cutting payments to the worst hospitals.

The CDC looked at data from thousands of U.S. hospitals from 2008 through 2014, focusing on infections tied to certain surgical procedures and use of catheters.

It found superbugs caused 1 in 7 of the infections caught in general hospitals but 1 in 4 in specialized long-term hospitals.

The agency's director, Dr. Tom Frieden, called the long-term statistic especially "chilling." Those patients often have been under medical treatment for longer periods and have had more opportunity to be exposed to superbug infections, officials said.

Antibiotics became widely available in the 1940s, and today are used to kill or suppress the bacteria behind everything form strep throat to the plague. But as decades passed, some antibiotics stopped working. Experts say their overuse and misuse have helped make them less effective. Health officials have been raising alarms about it for years.

Fighting the problem requires more careful and judicious use of antibiotics, Frieden said.

"Doctors are the key to stamping out superbugs," Frieden said.

The report offered some good news: The rate of overall infection did continue to fall for certain surgical sites and catheters.

Source: Associated Press

Some Evidence of Reversibility

Animal Manure Increases Antibiotic-resistant Genes in Soil
Mon, 03/07/2016 - 9:43am

The use of animal manure increases the soil content of antibiotic-resistant genes. However, this is not an irreversible situation.

What does one of the world's longest-running field experiments - under Aarhus University in Denmark - have to do with the appearance of antibiotic resistance? The answer is that it forms the platform for illuminating the interaction between the use of animal manure and the appearance of genes for antibiotic resistance in soil.

New investigations show that when a certain type of antibiotic is phased in, the abundance of resistant genes in soil increases. When the antibiotic is phased out again, the abundance of resistant genes drops - and this happens relatively quickly. The scientists also found a correspondence in time between the first detection of antibiotic resistance in the health service and the detection of such genes for resistance in soil that had received applications of animal manure.

The analyses have been performed by British scientists using soil samples regularly collected since 1923 in the now 122-year-old fertiliser experiment at Askov Experimental Station at the Department of Agroecology, Aarhus University. The results of this partnership among Prof Bent Tolstrup Christensen (Aarhus University), Prof David W. Graham (project leader, Newcastle University in England) and Dr Charles Knapp (Strathclyde University in Scotland) have been described in an article in the prestigious scientific journal Nature Scientific Reports.

Resistance follows the rate of consumption

That bacteria can develop resistance to bacteria is not a new phenomenon. Genes that code for resistance to antibiotics existed even before we discovered and started using antibiotics. Multi-resistant genes have actually been found in 30,000-year-old DNA samples taken in permafrost areas. The problem is that a higher incidence of resistance to antibiotics is highly undesirable.

The experts studied the specific ß-lactam antibiotic resistant genes. Particularly this group of antibiotics is of considerable importance to human medicine. The resistant genes were chosen because their first appearance in the health system is well-documented.

- We found low levels of the resistant genes before 1960, both in manured soil and in soil treated with inorganic fertiliser, explains Prof Christensen from Department of Agroecology. He is project leader of the Askov Long-term Experiments and co-author of the article.

- Our analyses show a clear increase in the soil receiving animal manure. In the mid-1990s, the use of antibiotics as a growth promoter fell. This led to a corresponding rapid fall in the soil abundance of ß-lactam antibiotic resistant genes, says Christensen.

Throughout the period, the soil receiving inorganic fertiliser had very low levels of the resistant genes.

There is good news and there is bad news

Another important link is that the development of the abundance in soil of ß-lactam antibiotic resistant genes closely trail observations of their development in the health service. The timing of the first appearances of the resistant genes in the health service corresponds to the timing of their highest abundance in soil.

- Although the development in the abundance of resistant genes in soil mirrors what you see in the health service, research has not yet made a connection between the two. The results show, however, that the phasing out of antibiotics can swiftly lead to a reduction in the incidence of resistance - and that is good news, says Christensen.

The story does not end here. Analyses of the historical samples also showed another development that is more worrying. Since 1990 there has been a growing level of integrons in manured soil. Integrons promote the exchange of genetic material between bacteria and can therefore accelerate the development of new resistance.

- The rising level of integrons after 1990 in manured soil could indicate that through our efforts to reduce antibiotic resistance, we have unintentionally increased resistance gene exchange and more study is needed on the use of animal manure, says Prof Graham from Newcastle University.

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Tuesday, March 8, 2016 1:02 AM

6IXSTRINGJACK

That's so much boring shit to read. I'll read it when I'm dead from whatever disease you were talking about :)

lol... j/k...

No I won't.

Every single thing I do is in a passive-agressive effort to end my own life anyhow.

I'd get a huge kick out of "everybody dying along side of me"...

It's kind of the definition of "Serendipity", which is not only my favorite word of all time, but my favorite short-story our teachers made us read back in early grade school :)

Burn the Air and Boil the Sea.....

Do Right, Be Right. :)

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Tuesday, March 8, 2016 2:16 PM

1KIKI

Goodbye, kind world (George Monbiot) - In common with all those generations which have contemplated catastrophe, we appear to be incapable of understanding what confronts us.

Some people think it's boring. Personally, I've been interested in biology and medicine since I was a little kid. What could be more interesting than studying yourself by studying about how people work inside? And I just got interested in other things, even chemistry and physics, because they were connected.

Do you play any instruments, Jack? I used to get home and take an hour or so each evening playing guitar to wind down. They can be more calming and less destructive than drugs. ETA: You don't have to be good to enjoy it. I never had music lessons as a child, consequently I never learned to read music. Most of what I learned as a mid-20's young adult was by watching others play in my spare time, which I never had much of. Or by picking it out by ear. So my repertoire was never extensive. And I was OK but not great. I still enjoyed playing immensely. Perhaps you might enjoy it.

SAGAN: We are releasing vast quantities of carbon dioxide, increasing the greenhouse effect. It may not take much to destabilize the Earth's climate, to convert this heaven, our only home in the cosmos, into a kind of hell.

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