Diabetes hospitalization: some antibiotics 'raise risk'

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Main Category: Diabetes
Also Included In: Infectious Diseases / Bacteria / Viruses
Article Date: 15 Aug 2013 - 0:00 PDT Current ratings for:
Diabetes hospitalization: some antibiotics 'raise risk'

Researchers have found that, compared with other antibiotics, people with diabetes taking a class known as fluoroquinolones may be at higher risk of blood sugar-related complications.

Researchers from National Taiwan University in Taipei, carried out a population-based cohort study of around 78,000 people with diabetes.

The researchers analyzed data from the claims database for Taiwan's national insurance program, and looked at patients who had received an oral prescription of one of these three different classes of antibiotics: fluoroquinolones (levofloxacin, ciprofloxacin or moxifloxacin), second-generation cephalosporins (cefuroxime, cefaclor or cefprozil), acrolides (clarithromycin or azithromycin).

The scientists analyzed the number of emergency visits and hospitalizations related to diabetes within 30 days of the patients using the antibiotics. The visits were for dysglycemia, with blood sugars either too high (hyperglycemia) or too low (hypoglycemia).

The study, published in the journal Clinical Infectious Diseases, revealed that the patients with diabetes using fluoroquinolones had a higher risk of dysglycemia than the diabetics using other antibiotics.

The research showed that the risk was dependent on the type of antibiotic the patient was using within the class of fluoroquinolones.

The incidence, or absolute risk, of hyperglycemia cases for every 1,000 people was:

Moxifloxacin - 6.9Ciprofloxacin - 4.0Levofloxacin - 3.9.

The absolute risk of hypoglycemia cases per every 1,000 people was:

Moxifloxacin - 10.0Levofloxacin - 9.3Ciprofloxacin - 7.9.

Fluoroquinolones are a class of antibiotics with a wide number of uses against bacterial infection.

By comparison, the researchers found the absolute risks were lower among diabetes patients taking other antibiotics that can be used. The numbers were: In the macrolides class: 1.6 per 1,000 (hyperglycemia), 3.7 (hypo)For cephalosporin antibiotics: 2.1 per 1,000 (hyperglycemia), 3.2 (hypo).

The researchers say that previous research has linked fluoroquinolones to dysglycemia. They note that one of the fluoroquinolone antibiotics, gatifloxacin, was withdrawn from the US market in 2006 due, the researchers say, "to the risk of blood sugar abnormalities."

The study authors conclude that this research should prompt clinicians to consider the risks when prescribing fluoroquinolones for diabetes patients. They authors say:

"Our results showed a class effect regarding increased risk of severe dysglycemia among diabetic patients administered ?uoroquinolones in Taiwan."

"Clinicians should consider these risks when treating patients with diabetes and prescribe ?uoroquinolones cautiously."

People with diabetes can spot hypoglycemia early. Low blood sugar can, however, become serious, as listed by the Mayo Clinic: clumsiness or jerky movements, muscle weakness, difficulty speaking or slurred speech, blurry or double vision, drowsiness, confusion, convulsions or seizures, and unconsciousness.

High blood sugars, hyperglycemia, can "become severe and lead to serious complications requiring emergency care, such as diabetic coma."

Written by Honor Whiteman

Copyright: Medical News Today
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Potential for new antibiotics following finding that protein delays cell division in bacteria

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Genetics
Article Date: 14 Aug 2013 - 0:00 PDT Current ratings for:
Potential for new antibiotics following finding that protein delays cell division in bacteria

In 1958 a group of scientists working in Denmark made the striking observation that bacterial cells are about twice as large when they are cultured on a rich nutrient source than when they are cultured on a meager one. When they are shifted from a nutrient-poor environment to a nutrient-rich one, they bulk up until they have achieved a size more appropriate to their new growth conditions.

It has taken 60 years to figure out how the bacteria are able to sample their surroundings and alter their cell cycles so that they grow to a size suited to the environment.

In 2007 Petra Levin, PhD, a biologist at Washington University in St. Louis, reported in Cell that a soil bacterium named Bacillis subtilis has a protein that senses how much food is available and, when food is plentiful, temporarily blocks the assembly of a constriction ring that pinches a cell in two to create two daughter cells.

Now Norbert Hill, a graduate student in her group, reports in a recent online edition of PLoS Genetics that Escherichia coli uses a similar protein to help ensure cell size is coordinated with nutrient conditions.

Delaying division even just a little bit leads to an increase in daughter cell size. Once stabilized at the new size, cells take advantage of abundant nutrient sources to increase and multiply, doubling their population at regular intervals until the food is exhausted.

Because both the B. subtilis and E. coli proteins interact with essential components of the division machinery, understanding how they function will help in the discovery of antibiotics that block cell division permanently. A group in Cambridge, England, is already working to crystallize the E. coli protein docked on one of the essential components of the constriction ring.

If they are successful they may be able to see exactly how the protein interferes with the ring's assembly. An antibiotic could then be designed that would use the same mechanism to prevent division entirely, killing the bacteria.

Why do bacteria get bigger on a good food source?

Bacteria increase and multiply by a process called binary fission. Each cell grows and then the divides in the middle to produce two daughter cells. What could be simpler?

But the closer you look, the less simple it becomes. For binary fission to work the cell must make a copy of its circular chromosome, unlink and separate the two chromosomes to create a gap between them, assemble a constriction ring in the middle of the cell and coordinate the growth of new cell membrane as the ring cinches tight and pinches the mother cell in two. To complicate matters, bacteria don't necessarily do these steps one by one but can instead work on several steps simultaneously.

Most of the time the goal is to produce daughters the same size as the mother cell. But when food is plentiful, bacteria start making more copies of their DNA (as many as 12) in anticipation of divisions to come, and they can't easily cram all the extra DNA into standard-sized cells. So they grow bigger to accommodate the extra genetic material and remain large as long as the food lasts.

The inventory of partly copied chromosomes fuels rapid population growth, because a cell doesn't start from scratch when it needs another copy of its chromosome. Under optimum conditions, E. coli, for example, divides once every 17 minutes. If they are allowed to grow unhindered this means that in 24 hours 1 bacterium becomes about 5 x 1021 bacteria (that is 5 with 21 zeros after it.)

How do bacteria know the pickings are rich?

In B. subtilis and E. coli the signal is a modified sugar called UDP-glucose. Presumably, the richer the growth medium, the higher the level of this sugar inside the cell.

In both bacteria UDP-glucose binds to a protein and the sugar-protein complex then interferes with the assembly of the constriction ring. In the case of B. subtilis the protein is called UgtP and in the case of E. coli it is OpgH.

"It's interesting," Hill said, "that both organisms, which are more different from one another than we are from bakers' yeast, are using the same system to coordinate changing size in response to nutrient availability."

UgtP and OpgH are bifunctional proteins that are "moonlighting" as elements of the cell-division control systems. In both cases their day jobs are to help build the cell envelope. "We think they are communicating not only how much glucose there is in the cell, but also how fast the cell is growing," Levin said. "The sensor says not only is food abundant, but we're also growing really fast, so we should be bigger."

Both proteins delay division by interfering with FtsZ, the first protein to move to the division site, where it assembles into a scaffold and recruits other proteins to form a constriction ring.

"Very little is known about the assembly of the ring," Hill said. "There are a dozen essential division proteins and we don't know what half of them do. Nor do we understand how the ring develops enough force to constrict."

"We do know FtsZ exists in two states," Hill added. "One is a small monomer and the other is many monomers linked together to form a multi-unit polymer. We think the polymers bind laterally to form a scaffold and then, with the help of other proteins, make a meshwork that goes around the cell.

UgtP and OpgH both interfere with the ability of FtsZ to form the longer polymers necessary for assembly of the constriction ring.

When nutrient levels are low, UgtP and OpgH are sequestered away from the division machinery. FtsZ is then free to assemble into the scaffold supporting the constriction ring so the cell can divide. Because division proceeds unimpeded, cells are smaller when they divide.

What about other bacteria?

This control system helps to explain the 60-year-old observation that bacterial cells get bigger when they are shifted to a nutrient-rich medium.

Comparing the mechanisms that govern cell division in E. coli and B. subtilis reveals conserved aspects of cell size control, including the use of UDP-glucose, a molecule common to all domains of life, as a proxy for nutrient availability, and the use of moonlighting proteins to couple growth-rate-dependent phenomena to the central metabolism.

But much more is known about these model organisms, which many labs study, than the average bacterium. Nobody is sure how many species of bacteria there are - somewhere between 10 million and a billion at a guess - and they don't all divide the way B. subtilis and E. coli do.

The whimsically named giant bacterium Epulopiscium fiselsoni ("Fishelson's guest at a fish's banquet") that lives in the guts of sturgeonfish, has the gene for FtsZ but doesn't divide by binary fission. And then there are bacteria like the pathogen Chlamydia traachomatis that don't have a gene for anything like FtsZ. "We don't know how these bacteria divide, much less maintain an appropriate cell size," Levin said.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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When prescribing antibiotics, doctors most often choose strongest types of drugs

Main Category: MRSA / Drug Resistance
Also Included In: Primary Care / General Practice
Article Date: 05 Aug 2013 - 0:00 PDT Current ratings for:
When prescribing antibiotics, doctors most often choose strongest types of drugs

When U.S. physicians prescribe antibiotics, more than 60 percent of the time they choose some of the strongest types of antibiotics, referred to as "broad spectrum," which are capable of killing multiple kinds of bacteria, University of Utah researchers show in a new study.

Unfortunately, in more than 25 percent of such prescriptions are useless because the infection stems from a virus, which cannot be treated with antibiotics. This overuse of antibiotics has a number of downsides, including that these types of drugs kill more of the "good" bacteria found in our bodies - which may lead to more side effects - and also contribute to the growth of antibiotic-resistant bacteria, according to Adam L. Hersh, M.D., Ph.D., an infectious disease expert, assistant professor of pediatrics at the University of Utah School of Medicine and senior author on a study published July 29, 2013, in the Journal of Antimicrobial Chemotherapy.

Discerning whether an infection is viral or bacterial can be tricky, according to Hersh, which probably accounts for much of the overuse of antibiotics. "It seems that the natural bias, when there is uncertainty about an infection's cause, is to err on the side of prescribing antibiotics," he says. "Our study found that the majority of prescriptions are for antibiotics that kill a wider range of bacteria, and that they are most likely to be given when they're not needed, such as in cases of viral infections."

The types of illnesses where doctors seem to choose stronger antibiotics include respiratory problems, skin infections and urinary tract infections, which in many cases would be better treated by other antibiotics that are less likely to cause resistance.

Hersh, Andrew T. Pavia, M.D., also an infectious disease expert and professor of pediatrics at the University of Utah, Lauri A. Hicks, D.O., a medical epidemiologist at the U.S. Centers for Disease Control and Prevention, and University of California, San Francisco, medical student Daniel J. Shapiro, conducted the study using a public database with information on ambulatory care visits at physician offices and hospital-based outpatient and emergency departments nationwide. Studying data from between 2007-2009, they identified a sample of 238,624 visits by patients 18 and older at those medical facilities and found that 61 percent of antibiotic prescriptions were for broad-spectrum drugs, such as Levaquin®. Narrow-spectrum antibiotics, such as amoxicillin and doxycycline, comprised the remaining 39 percent of antibiotic prescriptions.

Based on the sample of 238,000-plus visits, the researchers estimate there was an average of 985 million annual ambulatory care visits for the 2007-2009 period, with antibiotics being prescribed in an estimated 101 million of those visits each year - 62 million in which broad-spectrum antibiotics were prescribed and 39 million that resulted in narrow-spectrum antibiotics prescriptions.

While this study looked only at adult ambulatory care visits, the prescription pattern for children is similar, according to Hersh. "Many antibiotics prescribed for children are unnecessary, particularly for conditions caused by viruses, where antibiotics don't help at all," he says. "Even when an antibiotic is indicated, such as for strep throat or some ear infection, physicians often prescribe and antibiotic such as a Z-Pak, which can be less effective than amoxicillin."

Hicks emphasizes that antibiotic overuse among children and adults is a serious problem and a threat to everyone's health. "The biggest problem with using antibiotics when they're not needed is the development of antibiotic resistance, which is when bacteria survive by outsmarting the antibiotic," she says. "Common infections become difficult to treat, and when you really need an antibiotic, it may not work."

Uncertainty about the cause of an infection is one factor in the overuse of broad-spectrum antibiotics, but there are other influences too, according to Hersh. This includes a misperception by physicians that their patients expect an antibiotic if they take the time to see the doctor. But Hersh believes this second factor is changing, due in part to major efforts to educate people about the problems associated with overuse of antibiotics, such as CDC's "Get Smart: Know When Antibiotics Work" program.

"The public is increasingly aware of the downside and side effects of antibiotics," Hersh says. "Actually, when they see their doctor, most patients just want an explanation as to what's wrong and are open to considering why an antibiotic wouldn't be helpful."

He urges patients to play a larger role by asking their doctor two questions: Do I really need this antibiotic? And, is this antibiotic the best choice for my infection?

"Both doctors and patients have a role in ensuring the effectiveness of antibiotics is preserved by using them only when needed," Pavia says.

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Reducing resistance to antibiotics via reduction campaigns not always successful

Main Category: MRSA / Drug Resistance
Also Included In: Public Health
Article Date: 31 Jul 2013 - 0:00 PDT Current ratings for:
Reducing resistance to antibiotics via reduction campaigns not always successful

Antibiotic use - and misuse - is the main driver for selection of antibiotic resistant bacteria. This has led many countries to implement interventions designed to reduce overall antibiotic consumption. Now, using methicillin resistant Staphylococcus aureus (MRSA) as an example, Laura Temime of the Conservatoire National des Arts et Metiers, Paris, and collaborators warn that simply reducing antibiotics consumption does not necessarily reduce resistance. The research is published online ahead of print in Antimicrobial Agents and Chemotherapy.

The success of antibiotic reduction programs depends on which antibiotics are reduced, because some select more strongly for resistance than others. For instance, in the case of S. aureus, reducing use of clindamycin and methicillin lead to decreased resistance, while reducing use of penicillins does not, since most S. aureus, including MRSA, are already resistant to penicillin, explains Temime.

Additionally, efforts to reduce antibiotic use must be coordinated between hospitals and the community, since either can feed resistant bacteria into the other, undermining reduction efforts, says Temime.

In 2002-2003, a national program reduced antibiotic use in France by 10 percent. However, it fell short of the full potential for reducing resistance because it failed to target those antibiotics that generate the most resistance, says Temime. She and her collaborators developed a mathematical model of MRSA circulation, which correctly simulated that reduction, post-facto. They then performed a number of simulations of reductions in antibiotic use, which demonstrated the complexities of reduction efforts.

"We found that the reduction in MRSA hospital rates could have been much larger than it actually was following the 2002 antibiotic reduction campaign," says Temime. "Our results also suggest that changes in the distribution of antibiotics prescribed for non-hospitalized patients actually limited the impact of the antibiotic reduction campaign in French hospitals."

Their research shows that class-specific changes in antibiotic use, rather than overall reductions, need to be considered in order to achieve the greatest benefit from antibiotic reduction campaigns, says Temime. "This underlines the importance of generating surveillance data on both antibiotic class-specific changes in antibiotic use and antibiotic resistance in the years following an antibiotic reduction campaign. We believe that this research may help health policy makers and physicians in the design of more efficient antibiotic reduction campaigns."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our mrsa / drug resistance section for the latest news on this subject.

Lidia Kardas-Sloma, Pierre-Yves Boëlle, Lulla Opatowski, Didier Guillemot and Laura Temime, Antibiotic reduction campaigns do not necessarily decrease bacterial resistance: the example of methicillin-resistant S. aureus, Antimicrobial Agents and Chemotherapy, Published ahead of print 1 July 2013, doi: 10.1128/AAC.00711-13

American Society for Microbiology

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'Reducing resistance to antibiotics via reduction campaigns not always successful'

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Reducing resistance to antibiotics via reduction campaigns not always successful

Main Category: MRSA / Drug Resistance
Also Included In: Public Health
Article Date: 31 Jul 2013 - 0:00 PDT Current ratings for:
Reducing resistance to antibiotics via reduction campaigns not always successful

Antibiotic use - and misuse - is the main driver for selection of antibiotic resistant bacteria. This has led many countries to implement interventions designed to reduce overall antibiotic consumption. Now, using methicillin resistant Staphylococcus aureus (MRSA) as an example, Laura Temime of the Conservatoire National des Arts et Metiers, Paris, and collaborators warn that simply reducing antibiotics consumption does not necessarily reduce resistance. The research is published online ahead of print in Antimicrobial Agents and Chemotherapy.

The success of antibiotic reduction programs depends on which antibiotics are reduced, because some select more strongly for resistance than others. For instance, in the case of S. aureus, reducing use of clindamycin and methicillin lead to decreased resistance, while reducing use of penicillins does not, since most S. aureus, including MRSA, are already resistant to penicillin, explains Temime.

Additionally, efforts to reduce antibiotic use must be coordinated between hospitals and the community, since either can feed resistant bacteria into the other, undermining reduction efforts, says Temime.

In 2002-2003, a national program reduced antibiotic use in France by 10 percent. However, it fell short of the full potential for reducing resistance because it failed to target those antibiotics that generate the most resistance, says Temime. She and her collaborators developed a mathematical model of MRSA circulation, which correctly simulated that reduction, post-facto. They then performed a number of simulations of reductions in antibiotic use, which demonstrated the complexities of reduction efforts.

"We found that the reduction in MRSA hospital rates could have been much larger than it actually was following the 2002 antibiotic reduction campaign," says Temime. "Our results also suggest that changes in the distribution of antibiotics prescribed for non-hospitalized patients actually limited the impact of the antibiotic reduction campaign in French hospitals."

Their research shows that class-specific changes in antibiotic use, rather than overall reductions, need to be considered in order to achieve the greatest benefit from antibiotic reduction campaigns, says Temime. "This underlines the importance of generating surveillance data on both antibiotic class-specific changes in antibiotic use and antibiotic resistance in the years following an antibiotic reduction campaign. We believe that this research may help health policy makers and physicians in the design of more efficient antibiotic reduction campaigns."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our mrsa / drug resistance section for the latest news on this subject.

Lidia Kardas-Sloma, Pierre-Yves Boëlle, Lulla Opatowski, Didier Guillemot and Laura Temime, Antibiotic reduction campaigns do not necessarily decrease bacterial resistance: the example of methicillin-resistant S. aureus, Antimicrobial Agents and Chemotherapy, Published ahead of print 1 July 2013, doi: 10.1128/AAC.00711-13

American Society for Microbiology

Please use one of the following formats to cite this article in your essay, paper or report:

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American Society for Microbiology. "Reducing resistance to antibiotics via reduction campaigns not always successful." Medical News Today. MediLexicon, Intl., 31 Jul. 2013. Web.
31 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Reducing resistance to antibiotics via reduction campaigns not always successful'

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View the original article here