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(Health) Antibiotics: Flora Horror

 
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PostPosted: Sat Feb 18, 2006 8:33 am    Post subject: (Health) Antibiotics: Flora Horror Reply with quote






What are antibiotics? These are substances that we take to kill bacteria. It is important to take note that antibiotics are used against bacteria. These are not for viruses. Most of the common illnesses such as colds and flu are caused by viruses. Antibiotics are not meant for this type of illness and taking antibiotics improperly leads to serious undesirable effects. Bacteria when exposed to antibiotics can develop resistance. Taking antibiotics in an unprescribed fashion provides an environment for bacteria to develop resistance. Noncompliance to dosage instructions (for example, discontinuing antibiotic treatment earlier than prescribed) likewise can lead to resistance. Once bacteria become immune to antibiotics, these drugs will no longer work, leading to an even more serious problem not just to the individual, but to the society as a whole.

This lesson introduces us to antibiotics and microbes. The following link is a good place to start (it likewise provides links to sites that provide an introduction to terms and concepts related to microbes and antibiotics):

http://www.bacteriamuseum.org/.....tics.shtml



Science News Online
Week of Feb. 18, 2006; Vol. 169, No. 7

Flora Horror
Hospitals struggle with a serious new gut microbe
Ben Harder

About 3 years ago, physicians in Quebec noticed an alarming pattern in patients with diarrhea. "All of a sudden, we were having patients so sick that they needed the ICU [intensive-care unit]," says doctor and epidemiologist Sandra Dial. The same illness was also sending patients to the morgue as never before. They weren't succumbing to the ailment that brought them to the hospital. Instead, they seemed to have gotten sick from their antibiotic treatment.

As an antibiotic attacks its target, it can also kill harmless flora, the term for the billions of bacteria that live in healthy intestines. Invaders, mainly the pathogen Clostridium difficile, can flock to the colon's open real estate.

Doctors treat C. difficile by suspending the culpable antibiotic therapy and administering a different one. While usually curable, the diarrheal disease recurs repeatedly in some patients and occasionally causes life-threatening inflammation of the colon.

C-diff, as it's called, is a rising problem across North America and in parts of Europe. A virulent, once-rare strain has driven a string of recent outbreaks and is suspected to be responsible for much of the overall increase in the disease. New resistance to widely used antibiotics seems to have made the microbe more likely to cause diarrhea in sick and elderly people.

At the same time, scattered cases of C. difficile among people not normally susceptible to it have researchers concerned.

Before December 2002, Dial had seen only three cases of C. difficile in 8 years at the McGill University–affiliated ICUs where she works. Then, she says, "we had five patients in 1 month."

Parallel epidemics were soon under way elsewhere in the region. More than 7,000 C. difficile cases occurred in Quebec hospitals in 2003, affecting up to 2.5 percent of patients. By early 2005, 30 centers in the province were seeing at least five times as many cases as they had identified in previous years.

In the United States, "the rate of C-diff in hospital patients doubled between 2000 and 2003," says L. Clifford McDonald of the Centers for Disease Control and Prevention (CDC) in Atlanta.

In response, researchers have identified unique characteristics of the newly virulent strain—and have revealed a grimmer picture of C. difficile than the one familiar to most physicians.

"Ten years ago, we didn't believe people died of this," Dial says. "It was very unusual. Now, unfortunately, it's not unusual."


Unprecedented illness
Previously, elderly people staying in health care facilities and nursing homes were virtually the only targets of C. difficile. Now, the bacterium is gaining notoriety for illnesses in seemingly vigorous people.

Last year, for instance, the pathogen felled a 31-year-old Pennsylvania woman who was pregnant with twins. Early in her second trimester, she went to the emergency room with worsening diarrhea. Despite treatment that night and during two subsequent hospital stays, within a month she delivered stillborn fetuses and died of complications of colon inflammation.

In the Dec. 2, 2005 Morbidity and Mortality Weekly Report, McDonald and his collaborators in four states describe this case and 34 other recent illnesses caused by C. difficile contracted outside health care facilities.

To tease out the changing characteristics of C-diff, Jacques Pépin and his colleagues at the University of Sherbrooke Hospital Center in Quebec combed through data on 5,619 hospital patients treated between January 2003 and June 2004. Nearly 300 of the patients had developed the disease.

Compared with the other patients, those who'd contracted C. difficile tended to be older and to have had longer hospital stays. Those infected were also more likely to have recently used an antibiotic of the cephalosporin family, the team found.

Those antibiotics had been previously linked to outbreaks. The diarrhea-causing bacterium is usually resistant to cephalosporins, but normal colon bacteria are not. Therefore, the drugs create a wide-open opportunity for C. difficile. Swallowing a spore of the bacterium during cephalosporin therapy could result in an infection that otherwise wouldn't have gained a foothold.

In the Nov. 1, 2005 Clinical Infectious Diseases, the Sherbrooke researchers also link C. difficile to a class of antibiotics that had only infrequently turned up in earlier work. Fluoroquinolones, the most widely used antimicrobials in the United States, fight infections of the respiratory and urinary tracts, the skin, and other tissues. Ciprofloxacin is the main drug in this class.

In early 2004, researchers at Sherbrooke and 11 other Quebec hospitals joined forces to investigate what they regarded as the province's plague. Led by microbiologist Vivian G. Loo of McGill, they ultimately studied 1,703 patients who acquired C. difficile during the first half of that year.

The infected patients represented 2.25 percent of all people hospitalized at the 12 centers during the study. That reflects an infection rate four times as high as that in earlier data.

Almost 7 percent of the 2004 infections were fatal. That rate, too, is at least four times as high as that found in the past, Loo says.

As in the Sherbrooke study, patients who developed C-diff were more likely than other patients to have used fluoroquinolones while hospitalized, the researchers report in the Dec. 8, 2005 New England Journal of Medicine (NEJM).

More than 80 percent of the infected patients had acquired a single, fluoroquinolone-resistant form of the pathogen, making that strain primarily responsible for the Quebec outbreaks, Loo's team concludes.


A novel mutant
To characterize the guilty strain, Pépin, McDonald, and six collaborators analyzed 124 C. difficile samples taken from Sherbrooke patients in 2004 and early 2005. They also looked at 30 recent samples from other patients in Quebec, the United States, and the United Kingdom.

Disease-causing C. difficile produce at least two colon-inflaming substances, called toxin A and toxin B. Rare strains that make neither toxin don't result in illness. Scientists have occasionally identified strains that produce a third toxin, called binary toxin.

The new outbreak strain always produces binary toxin, the researchers determined. Furthermore, they found, it produces 16 times as much toxin A and 23 times as much toxin B as typical hospital strains of C. difficile do.

Genetic traits also set apart the dangerous strain. For example, the researchers identified a standard C. difficile gene that was uniformly mutated in the samples. The mutation may account for the excess production of toxins A and B, the team suggested in the Sept. 24, 2005 Lancet. Extra toxin may lead to more severe diarrhea, and, therefore, greater spread of the pathogen in hospitals.

The mutant strain, which the researchers labeled NAP1/027, had infected patients in all three countries in the study.

It has also caused recent outbreaks in the Netherlands and Belgium, says Dale N. Gerding of Hines Veterans Affairs Medical Center in Illinois.

Until recently, NAP1/027 was rare, he says. "It was definitely present in other hospitals 20 years ago, but it wasn't causing epidemics," he says.

Gerding, McDonald, and their collaborators made that assessment after comparing 187 recent samples of C. difficile, collected between 2001 and 2003, with more than 6,000 older samples. About half of the recent samples were NAP1/027.

Genetic similarities indicated that 14 older samples dating to 1984 were of the same, newly troublesome strain. NAP1/027 made binary toxin in the 1980s, but it was not resistant to most fluoroquinolones before 2001, the researchers report in the Dec. 8, 2005 NEJM.

"Fluoroquinolone resistance is unusual and new for this strain," Gerding says. Use of those antibiotics in hospitals has increased tremendously over the past 2 decades, which could explain the success of the newly resistant variant, he says.

But Dial suggests that antibiotics aren't the only medications contributing to the epidemic. She and three McGill colleagues have found possible links between C. difficile infection and some commonly used drugs, particularly acid reducers that treat heartburn, indigestion, and stomach ulcers in millions of people.

In studying a U.K. database that doesn't track individual strains, Dial's team found that people who acquired C. difficile outside the hospital were three times as likely as uninfected people to use proton pump inhibitors (PPIs), such as Prilosec, and twice as likely to use H2 blockers, an older class of acid reducers.

Dormant C. difficile spores are resistant to acid, but replicating cells are susceptible. So, normal concentrations of stomach acid could suppress the organism's activity—until a person takes an acid reducer, Dial says.

Use of nonsteroidal anti-inflammatory drugs is also slightly elevated among the people with C. difficile, her team reports in the Dec. 21, 2005 Journal of the American Medical Association.

Gerding, along with doctors from a Portland, Maine, hospital, separately found an association between PPIs and C. difficile. Robert C. Owens Jr. of the Maine Medical Center presented that finding at the Interscience Conference on Antimicrobial Agents and Chemotherapy in Washington, D.C., last December.

But Gerding says that it's "an open question" whether the acid reducers contribute to infection. Data sets analyzed by Loo and by Pépin don't suggest a link.

In any case, says Gerding, "antibiotics are still the overwhelming risk factor."


Manifold responses
In the United States, the newly troublesome strain continues to spread. "CDC has documented the strain in 16 states," McDonald says.

In Quebec, the worst-hit Canadian province, diligent efforts in hospitals have brought the new bug under control—to a degree. Compared with the epidemic's early&150;2003 peak, says Loo, "our rates are halved." But they're still significantly elevated from pre-epidemic rates, she notes.

Hospitals employed a multifaceted approach to rein in the epidemic. First, they increased the frequency of cleanings. Rooms with C. difficile–infected patients now get scrubbed down twice a day, Loo says. And to fight C. difficile's hardy spores, bleach has been substituted for gentler agents.

Second, hospitals spent new funds from the Canadian government to buy more of their most frequently used medical items, such as blood pressure cuffs, so that equipment that might pick up spores doesn't get shuttled from room to room. "We also eliminated rectal thermometers," Loo says.

Furthermore, hospitals installed more sinks to encourage hand washing and created new rooms to reduce patient crowding in some older hospitals.

"We also changed our hand-hygiene practice," Loo says. "Alcohol hand rinses decrease the concentration of the bacteria, but washing at the sink was still better."

Finally, she says, the hospitals made an effort to educate physicians and medical residents on appropriate antibiotic use. That effort has somewhat reduced unnecessary administration of fluoroquinolones and other drugs, but more progress is needed, says Loo.


Fire with fire
At the December conference on antimicrobial agents, Gerding described new tests conducted on a strain of C. difficile that might prevent, rather than cause, disease.

Scientists had previously observed that hospitalized people who already carry a harmless form of the bacterium are unlikely to pick up a disease-causing strain. So, Gerding and his team took a non–toxin-making strain from a healthy person and introduced it into laboratory hamsters. Then, they exposed the animals to a strain that normally kills hamsters within 48 hours. The hamsters stayed healthy.

Gerding says that he is seeking the Food and Drug Administration's permission to test the protective strain in people.

While the approach is "counterintuitive," says McDonald, "there's a couple of lines of evidence to suggest it holds promise."

Other experimental approaches aim to strengthen the gut's defenses. The closest to fruition, according to McDonald, is a strategy in which a polymer binds to and inactivates the bacterium's toxins. Genzyme Corp. of Cambridge, Mass., developed the polymer, which it calls tolevamer. After promising preliminary results, the company launched a treatment trial that it projects will include more than 1,000 C. difficile–infected volunteers by the end of this year.

A positive outcome could lead to the first treatment for the antibiotic-associated illness that does not employ an antibiotic.

*************************************************************

Questions to explore further this topic:

What is Clostridium Difficile?

http://www.amm.co.uk/newamm/fi....._cdiff.htm
http://www.cmaj.ca/cgi/content/full/171/1/51
http://healthlink.mcw.edu/article/954992292.html
http://www.aboutibs.org/Public.....icile.html
http://www.phac-aspc.gc.ca/c-difficile/index.html
http://www.hpa.org.uk/infectio.....n_info.htm
http://www.cdc.gov/ncidod/dhqp.....neral.html
http://www.wsufftrust.org.uk/I.....icille.htm
http://kidshealth.org/parent/i.....idium.html
http://www.cfpc.ca/cfp/2004/No.....-cme-1.asp

Images of Clostridium Difficile

http://distans.livstek.lth.se:2080/C_difficile.htm

Photo gallery of bacteria

http://library.thinkquest.org/26260/pg1.html

An audiovisual presentation of Clostridium Difficile

http://microbiology.mtsinai.on.....cdiff.html

How are Clostridium Difficile infections treated?

http://path.upmc.edu/cases/case153/dx.html
http://news.bbc.co.uk/1/hi/pro.....680919.stm

Are there harmless bacteria?

http://www.msnbc.msn.com/id/10...../newsweek/
http://news.bbc.co.uk/1/hi/health/3208290.stm
http://www.actionbioscience.or.....enaar.html
http://www.bacteriamuseum.org/.....sals.shtml
http://www.pnas.org/cgi/content/full/103/3/732

What are antibiotics?

http://www.cyh.com/HealthTopic.....mp;id=2376
http://www.hhmi.org/biointerac.....meset.html
http://users.rcn.com/jkimball......otics.html
http://www.lung.ca/antibiotics/
http://textbookofbacteriology......obial.html
http://www.accessexcellence.org/HHQ/HLC/HNA/
http://www.bacteriamuseum.org/.....tics.shtml

History of antibiotics

http://www.molbio.princeton.ed.....iotics.htm

When do antibiotics work?

http://www.cdc.gov/drugresista...../index.htm
http://www.mayoclinic.com/heal.....cs/FL00075
http://www.cdc.gov/ncidod/op/antibiotics.htm

What is antibiotic resistance?

http://www.nimr.mrc.ac.uk/mill.....crobes.htm
http://www.niaid.nih.gov/factsheets/antimicro.htm
http://www.tufts.edu/med/apua/.....ction.html
http://www.doctorsforadults.co.....a_anti.htm
http://www.mayoclinic.com/heal.....ea/DS00454
http://kidshealth.org/parent/g.....eruse.html
http://www.fda.gov/fdac/features/795_antibio.html

An animation of antimicrobial resistance

http://www.fda.gov/cvm/antiresistvideo.htm

Antibiotics and Clostridium Difficile

http://www.wndu.com/news/mommo....._47622.php
http://www.discover.com/issues.....s-killing/

GAMES

http://www.dobugsneeddrugs.org/kidsarea/index.html


Last edited by adedios on Sat Jan 27, 2007 4:48 pm; edited 3 times in total
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PostPosted: Tue Mar 07, 2006 3:43 pm    Post subject: Antibiotic-resistant Community-acquired Staph Infections Reply with quote

Source: Emory University Health Sciences Center

Posted: March 7, 2006

Study Indicates Dramatic Rise In Antibiotic-resistant Community-acquired Staph Infections

Staph infections resistant to antibiotics, previously only associated with hospitalization or prior contact with the healthcare system, are now widespread in the community and coming home. A new study from Emory University School of Medicine and Grady Memorial Hospital, featured in the March 7, 2006 Annals of Internal Medicine, reports on a dramatic rise in antibiotic resistant community-acquired methicillin-resistant Staphylococcus aureus (MRSA), making it the primary cause of skin and soft tissue infections. An editorial accompanying the article notes, "the number of populations at risk for community-acquired MRSA infections is steadily expanding", making it a "remarkable epidemic."

The bacterium Staphyloccus aureus (staph) normally resides on skin and in noses, and typically infects tissues through cuts or rashes. Those infections can remain minor, or lead to illnesses ranging from boils or abscesses to necrotizing skin infections, pneumonia and sometimes blood stream infections. The Centers for Disease Control and Prevention (CDC) reports that staph is one of the leading causes of skin infections in the United States.

Previously, scientists have categorized staph into two main types: antibiotic resistant (MRSA), and methicillin-susceptible Staphyloccus aureus (MSSA), which can be treated by antibiotics in the penicillin or related groups (i.e, beta-lactam antibiotics). Previously, MRSA infections were usually restricted to hospital or healthcare-associated infections. This is clearly no longer the case.

Henry M. Blumberg, MD, is the senior author of the study, and professor of medicine and program director of the Division of Infectious Diseases at Emory University School of Medicine and hospital epidemiologist at Grady Memorial Hospital. He says, "We have seen an explosion of community-acquired MRSA infections among the urban patient populations served by the Grady Health System. Community-acquired MRSA infections are no longer restricted to certain risk groups but appear to be wide spread in the Atlanta community."

The study demonstrated that 72 percent of community-onset Staph skin and soft tissue infections among patients receiving care at the Grady Health System (Grady Memorial Hospital and its affiliated outpatient clinics in Atlanta) are now due to MRSA. The vast majority of these MRSA skin and soft tissue infections are due to a single clone or strain of MRSA called USA300. As noted in the accompanying editorial, MRSA appears to have emerged as a cause of community-acquired skin infections in other U.S. communities as well.

As noted by Dr. Blumberg and other Emory and Grady authors, "Empirical use of antibiotics active against community-acquired MRSA is warranted, especially for patients presenting with serious skin and soft-tissue infections." This represents a major change in prescribing practices for community-onset skin and soft tissue infections.

Dr. Blumberg's team included first author Mark King, MD, MSc, previously an infectious diseases fellow and faculty member at Emory as well as Dr. Susan Ray, an associate professor of medicine in the Emory Division of Infectious Diseases and Dr. Wayne Wang, a member of the Emory Department of Pathology and Laboratory Medicine and director of the Grady Clinical Microbiology Laboratory.

The Emory scientists began their research in response to observations about increasing number of community-acquired skin and soft tissue infections that were due to MRSA. Dr. Blumberg notes, "In recent years there have been reports of outbreaks of community-acquired infections due to MRSA. Our study now shows that these community-acquired infections are no longer just restricted to certain risk groups but are widespread and now endemic."

The recognition of community-acquired MRSA as a primary cause of skin and soft tissue infections offers implications for prevention and treatment. In the past, Dr. Blumberg says, "skin and soft tissue infections occurring in the community were generally MSSA, and that is how antibiotic therapy was targeted." Currently, many doctors may assume that community-acquired staph infections will not be resistant to antibiotics similar to methicillin and patients may be prescribed ineffective antibiotics.

Implications of the study include that healthcare professionals who diagnose skin or soft tissue infections should prescribe drugs that are active against MRSA. As Dr. Blumberg says, "selection of empiric antibiotics should focus on covering MRSA," and doctors should work toward confirming the diagnosis by obtaining appropriate material for culture in order to achieve a definitive diagnosis and ensure appropriate treatment is given. At Grady Memorial Hospital, where the study took place, Dr. Blumberg reports that his team has already started following up on the findings: "We have worked hard on educating physicians, including those in training, about the need to consider community-acquired MRSA infections," he says. "There have been changes in recommendations for empiric therapy for skin and soft tissue infections."

Dr. Blumberg and his fellow researchers are now conducting follow-up studies at Grady Memorial Hospital and in the community, and hope other scientists might implement clinical trials to definitively determine which antibiotic agents work best for the treatment of community acquired MRSA infections. In the meantime, the CDC's fact sheet on MRSA suggests that preventing MRSA may be as simple as employing the tried and true cure of soap and water: "Practice good hygiene," is its primary advice.



###
The study was funded by the Emory Medical Care Foundation, Emory Mentored Clinical Research Scholars Program (supported by a grant from the National Institutes of Health, National Center for Research Resources), and the NIH/National Institute of Allergy and Infectious Diseases.
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PostPosted: Sat Mar 18, 2006 2:52 pm    Post subject: Bacteria vs. Bacteria: The New Fight Against Salmonella Reply with quote

Bacteria vs. Bacteria: The New Fight Against Salmonella
By Robert Roy Britt
LiveScience Managing Editor
posted: 17 March 2006
09:19 am ET

Salmonella and other potentially deadly bacteria in poultry face a new enemy, as scientists develop more effective ways to fight fire with fire.

As they've been doing since the 1970s, researchers put "good" bacteria into the chickens on purpose to fight bad bacteria. Now one group has cooked up a culture of the beneficial variety that preliminary studies show is more effective in combating salmonella.

The good bacteria is sprayed on chicks or introduced into their water.

It's all okay with the Food and Drug Administration, so long as the bacteria is what researchers call a "defined culture," one that's derived from a single defined group of known bacteria.

"They're known organisms, specific isolates that are well characterized," explained Billy Hargis University of Arkansas's Food Safety Consortium project.

Yogurt science

Work in the United States and in other countries over the past three decades has led to undefined cultures of good bacteria, which contain strains that aren't identified. Researchers here worry that those cultures could contain emerging pathogens that would only make matters worse, so use is sometimes restricted.

The new cocktail of good bacteria—including things like enterobacteriaceae and lactic acid bacteria—is what's known as a probiotic culture. Probiotic bacteria have also been found effective in fighting human diseases. Yogurt is the classic probiotic food item, and the bacteria are available in dietary supplements, too.

The good bacteria work by exclusion—they get into the intestinal track of the bird and set up shop, leaving no room for the bad bacteria. The probiotic is given to newly hatched chicks so it can go to work before the bad bacteria take hold.

"The newly hatched chick's gut is essentially sterile and highly susceptible to pathogen colonization, whereas the mature bird can be resilient to pathogen colonization," explained Annie Donoghue of the Poultry Science Center at the University of Arkansas. "The biggest challenge is determining the correct types and quantity of probiotics because of the numbers and diversity of microbes and the poorly understood interactions between the microbes and the intestine."

You don't want this

Salmonella infection causes diarrhea, fever, and abdominal cramps for up to seven days and in extreme cases can be deadly. Some 40,000 cases are reported each year in the United States, but the Centers for Disease Control and Prevention estimates that perhaps 30 times that many mild cases go unreported. About 600 people die from it each year.

Thorough cooking kills the bacteria, but they can be introduced to raw vegetables or cooked food if a cook does not wash his hands after using the restroom.

Hargis and colleagues think their approach will help, however.

"Salmonella does not occur by spontaneous generation in a processing plant," he said. "It comes in with the live animals. I think it's a pretty good bet that reducing salmonella in live animals will end up reducing salmonella in food."

Much of the research is being done at a handful of labs around the country, which like Hargis' are supported by the U.S. Department of Agriculture.

Hargis said several companies have begun using the new product.

"Our cultures are different because they can be truly defined and they can be reproduced from specific isolates that are stored back in the freezer," Hargis said. "Then they can be propagated virtually forever."

And are they safe for humans?

"These are all considered GRAS organisms—Generally Recognized As Safe," Donoghue said in an email interview. "These are similar to the bacteria found in yogurts."
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PostPosted: Mon Apr 17, 2006 11:38 am    Post subject: Less antibiotic use in food animals leads to less drug resis Reply with quote

Infectious Diseases Society of America
17 April 2006

Less antibiotic use in food animals leads to less drug resistance in people, study shows

Australia's policy of restricting antibiotic use in food-producing animals may be linked with lower levels of drug-resistant bacteria found in its citizens, according to an article in the May 15 issue of Clinical Infectious Diseases, now available online.
Campylobacter jejuni is a leading bacterial cause of foodborne illness in industrialized countries. Drug resistance can make Campylobacter infections difficult for physicians to treat, and can result in longer bouts of diarrhea and a higher risk of serious or even fatal illness. Bacterial resistance to drugs is generally attributed to inappropriate prescribing or overuse of antibiotics.

An Australian solution to the drug resistance problem has been to prohibit the use of certain antibiotics, called fluoroquinolones, in food animals such as poultry. Such a policy puts Australia in a relatively unique position, since its animal and food production levels are comparable to those of other industrialized nations, but it has avoided using the antibiotics that have been standard in the other countries' food animal production.

To evaluate whether the country's restrictive antibiotic policy has affected bacterial drug resistance, Australian researchers examined C. jejuni isolates collected from 585 patients in five Australian states. None of the patients had received fluoroquinolone treatment within the month prior to becoming ill. The researchers discovered that only 2 percent of the locally acquired Campylobacter isolates were resistant to ciprofloxacin, a type of fluoroquinolone. Countries that allow fluoroquinolone use in animals may have a drug resistance prevalence of up to 29 percent. Ciprofloxacin can be used to treat severe Campylobacter disease, so a low level of bacterial drug resistance should lead to better treatment efficacy.

"There are different causes that lead to bacterial antibiotic resistance, and use of antibiotics in food animals is only one of the multiple causes," said lead author Leanne Unicomb, an epidemiologist with OzFoodNet and Australia National University. However, the evidence indicates that "use of fluoroquinolones in food animals in other countries has increased the risk of resistance in [Campylobacter] isolates infecting humans," she said. The researchers concluded that the low drug resistance they found "probably reflects Australia's policy of prohibiting fluoroquinolones for animal use."

Other industrialized nations have also realized the apparent benefits of restricting antimicrobial use in animals. Sweden prohibited the use of fluoroquinolones for food animals in 1986, Norway has never licensed their use in food animals, and both countries have reported low trends--similar to Australia's--in fluoroquinolone-resistant Campylobacter infecting humans. The United States, in a recent effort to reduce American levels of Campylobacter drug resistance, has taken a cue from other countries' success. The U.S. Food and Drug Administration proposed banning fluoroquinolones in poultry in 2000, but one drugmaker fought the ban until it was finally enacted in September 2005.

Reducing the use of antibiotics in food animals, coupled with the authors' additional recommendation of "sensible use of fluoroquinolones in clinical settings," seem to be steps in the right direction toward curbing harmful foodborne bacterial drug resistance.


###
Founded in 1979, Clinical Infectious Diseases publishes clinical articles twice monthly in a variety of areas of infectious disease, and is one of the most highly regarded journals in this specialty. It is published under the auspices of the Infectious Diseases Society of America (IDSA). Based in Alexandria, Virginia, IDSA is a professional society representing about 8,000 physicians and scientists who specialize in infectious diseases. For more information, visit www.idsociety.org.
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PostPosted: Wed Apr 26, 2006 6:41 pm    Post subject: Aspirin shows promise in combating antibiotic-induced hearin Reply with quote

University of Michigan Health System
26 April 2006

Aspirin shows promise in combating a common, antibiotic-induced hearing loss

University of Michigan, Chinese hospital find high success rate at preserving hearing when aspirin is paired with widely used antibiotic
ANN ARBOR, Mich. -- Around the world, inexpensive antibiotics known as aminoglycosides have been used for the past 60 years in the battles against acute infections and tuberculosis as antibacterial prophylaxis in cystic fibrosis patients and in other conditions. But for all of the good they do, the drugs also have been widely linked to irreversible hearing loss.
Now, researchers at the University of Michigan's Kresge Hearing Research Institute and their Chinese colleagues, working under the leadership of Jochen Schacht, Ph.D., and Su-Hua Sha, M.D., have found that the hearing loss can be prevented in many people with the use of another inexpensive, widely available medication: aspirin. The results appear in the April 27 issue of the New England Journal of Medicine.

The researchers studied 195 patients in China who received 80 to 160 milligrams of gentamicin (a type of aminoglycoside) intravenously twice daily, typically for five to seven days. Of those, 89 patients were given aspirin along with the antibiotic, and 106 were given placebos along with the antibiotic. The results were dramatic: The incidence of hearing loss in the group that was given placebos was 13 percent, while in the aspirin group it was just 3 percent, or 75 percent lower.

"We would like to see the word get around to the medical community around the world that you can take some precautions to minimize the risk to your patients. Aspirin is available everywhere, and it's cheap," says senior author Schacht, professor of biological chemistry in otolaryngology at the University of Michigan Medical School and director of the U-M Health System's Kresge Hearing Research Institute. Gentamicin is not commonly used in the United States.

He notes that this research builds on earlier U-M studies that showed promise in combating drug-induced hearing loss in the laboratory. "Previously we found that such a treatment works well in mice, but I am very excited that this worked so well in humans," says Schacht. "Translating animal studies into clinical practice is not an easy thing to do. We were fortunate that our extrapolation from mice to men and women worked in the first trial."

The research is exciting, says lead author Sha, because hearing loss caused by these antibiotics is so prevalent. The incidence of aminoglycoside-induced hearing loss averages 8 percent but the numbers may be higher in developing countries, she notes, where aminoglycosides are frequently the only affordable antibiotics and are sold over the counter. No therapy currently exists to prevent ototoxicity.

This research began in 1999 with a collaboration with Chinese hospitals. Working with Schacht, Sha – associate laboratory director of U-M's Kresge Hearing Research Institute's Biochemistry Laboratory – got in touch with her colleagues in China. The two traveled to China and presented their ideas, and ultimately began a partnership with the Fourth Military Medical University in Xi'an, China. The third author on the paper, Jian-Hua Qiu, M.D., represents the colleagues of the Fourth Military Medical University.

After receiving approvals from institutional review boards at U-M and the Fourth Military Medical University, the otolaryngology department in Xi'an conducted the prospective, randomized, double-blind trial at Xijing Hospital and Airforce Chengdu Hospital from 1999 to 2003. All of the participants were ages 18 to 65, and were inpatients who were scheduled for treatment with gentamicin. Hearing damage, or ototoxicity, was defined as a shift from a person's baseline hearing by at least 15 decibels at both the 6 and 8 kHz frequencies, which are the first affected by the drugs. The effectiveness of the gentamicin as an antibiotic did not lessen when it was paired with aspirin.

Schacht notes that even though gentamicin has been linked widely with hearing loss, and its use has been declining in industrial countries, it is not practical to think that it will be replaced in the near future by other antibiotics because it has specific applications and is so inexpensive and available, especially in poor countries. While aspirin shows promise, and he hopes that health care providers pair it with gentamicin, he also notes it is not yet the perfect solution because of the potential side effects of aspirin, including gastric bleeding. And he notes that this is an off-label use of aspirin, which may inhibit some practitioners from giving it to patients in such instances.

He hopes that further studies will lead to the development of new and safer antibiotics, or another drug that can be paired with gentamicin that has fewer side effects than aspirin. He and Sha are exploring partnerships with other countries to conduct future research.


###
Funding for the research came from George and Christine Strumbos and the Kent and Carol Landsberg Foundation.

Citation: New England Journal of Medicine, Volume 354, Issue 17: April 27, 2006.
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PostPosted: Mon Sep 11, 2006 1:41 pm    Post subject: antibiotic drug development Reply with quote

University of Minnesota
11 September 2006

Minnesota and Michigan reseachers discover new insights for antibiotic drug development


Discovery will help in fight against 'superbugs'
University of Minnesota and University of Michigan researchers have discovered a new method of developing antibiotics, an important step in fighting the growing number of drug-resistant infections.

In two articles published in the current online issue of Nature Chemical Biology, researchers describe an approach that is more efficient--and environmentally friendly--in developing new antibiotics, those needed to kill the increasing number of infections resistant to multiple drugs.

"We're striving to create new drugs that can have a positive impact on the growing threat of infectious diseases," says Robert Fecik, Ph.D., an assistant professor of Medicinal Chemistry at the University of Minnesota College of Pharmacy and one of the lead authors of the study. "This type of research can help us make new antibiotic molecules."

Officials at the Centers for Disease Control and Prevention have called antibiotic resistance one of the world's most pressing public health problems. Once only found in hospitals, these "superbugs" are now being found in community settings, including schools, nursing homes, and locker rooms.

These infections don't respond to common antibiotics such as erythromycin, which belong to a ring-shaped class of antibiotics called macrolides. Nearly all antibiotics in use today are natural molecules made by bacteria to kill their enemies. The bacteria use specialized proteins called enzymes to carry out the chemical steps in making these ring-shaped antibiotic molecules.

One way to increase the number of antibiotics for fighting infections is to start where nature stopped and engineer the enzymes to produce new molecules, and thus new antibiotics. But to do this more effectively, scientists need a clearer picture of how the enzyme molecules act upon the precursor to the antibiotic.

The interdisciplinary team of scientists, including research professors David H. Sherman and Janet L. Smith from the University of Michigan's Life Sciences Institute and Fecik of University of Minnesota College of Pharmacy, is the first to crystallize an enzyme in the process of closing the antibiotic ring, which illustrates exactly how the ring is formed.

Their work creates important opportunities for drug discovery to stay one step ahead of the superbugs.

"Having the tools to make the next generation of macrolide antibiotics is crucial because these drugs are so well tolerated and have so few side effects," Smith said. "They are really a great class of antibiotics, so we need more of them."

These macrolide antibiotics are of particular interest because bacteria make them in a way that potentially allows for thousands of slightly different compounds to be synthesized and tested for antibiotic activity.

The structure of macrolides is a large ring, itself constructed from a linear molecule, which is built in an assembly-line fashion from smaller molecules. An enzyme at the end of the chain triggers the ring formation that results in antibiotic formation.

"These findings are likely to enable the development of powerful new methods to build structural diversity into large ring systems that are a key component of many types of macrolide antibiotic molecules. This will provide yet another strategy to stay ahead of the emerging and persistent antibiotic resistance threat," Sherman said.

In traditional drug development, researchers start with an existing antibiotic and chemically manipulate it to develop a new version of the original drug. With the new approach outlined in the article, researchers describe a method that can be used to get the bacteria itself to produce new compounds that turn into the ring structure and may be useful as new drugs.

Typical drug development involves chemical manipulations that result in chemical waste, which can be difficult to dispose of and is hazardous to the environment.

This research implies it is realistic to develop a more environmentally friendly way to discover more potential drug compounds with less chemical manipulation, and thus less chemical waste.
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PostPosted: Mon Oct 23, 2006 11:16 am    Post subject: DNA Found in Drinking Water Could Aid Germs Reply with quote

DNA Found in Drinking Water Could Aid Germs

By Charles Q. Choi
Special to LiveScience
posted: 23 October 2006
08:28 am ET

DNA that helps make germs resistant to medicines may increasingly be appearing as a pollutant in the water.

This DNA was found "even in treated drinking water," researcher Amy Pruden, an environmental engineer at Colorado State University in Fort Collins, told LiveScience.

The spread of this DNA could exacerbate the already growing problem of drug resistance among potentially infectious microbes. Diseases once considered eradicated, such as tuberculosis, are making alarming comebacks. Currently, more than two million Americans are infected each year by resistant germs, and 14,000 die as a result, the World Health Organization reports.

"I personally have known people with antibiotic-resistant infections, and they can be very scary," Pruden said.

For the full article:

http://www.livescience.com/hum.....pread.html
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PostPosted: Mon Nov 27, 2006 11:22 am    Post subject: Fostering a new medical life for a forgotten antibiotic Reply with quote

Fostering a new medical life for a forgotten antibiotic
Journal of the American Chemical Society
27 November 2006

The increasing need for new antibiotics to combat multidrug-resistant bacteria has led chemists to develop the first method for synthesizing a potentially valuable antibiotic that has been sidelined from clinical use for 40 years. Harvard University's Daniel E. Kahne and colleagues report the first total synthesis of the antibiotic, moenomycin A, in an article in the Nov. 15 issue of the Journal of the American Chemical Society, a weekly publication.

Kahne points out that moenomycin is a broad-spectrum antibiotic with unusual promise. It has strong antibacterial activity against a large group of bacteria that cause pneumonia, urinary tract infections, gastritis, stomach ulcers, food poisoning and other disorders. Moenomycin also kills bacteria in an unusual way; it binds directly to enzymes that bacteria need to form a cell wall.

Although used as a growth promoter in animals, moenomycin has never been developed for medical use in humans because it is poorly absorbed into the body. Discovery of a method to synthesize moenomycin is important because it will allow scientists to better understand the antibiotic and make variants of the natural antibiotic that may be suitable for medical use.

ARTICLE #2
"The Total Synthesis of Moenomycin A"

DOWNLOAD PDF http://pubs.acs.org/cgi-bin/sa.....65907x.pdf
DOWNLOAD HTML http://pubs.acs.org/cgi-bin/sa.....5907x.html
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PostPosted: Fri Dec 29, 2006 8:46 am    Post subject: New Approach Disarms Deadly Bacteria Reply with quote

New Approach Disarms Deadly Bacteria

By LiveScience Staff

posted: 29 December 2006
08:21 am ET

A warmer, gentler approach to controlling bacteria may be the answer for the emerging menace of drug-resistant diseases.

For more than 50 years antibiotics, such as penicillin, have been the ammunition in war against a rogues gallery of scourges from tonsillitis to typhoid fever. Recently, however, antibiotics have begun to lose their mojo.

So many strains of bacteria now shrug off garden-variety antibiotics that scientists at the U.S. Food and Drug Administration have tagged drug resistance as a growing threat to human and animal health. Just some of the diseases that are increasingly hard to treat are tuberculosis, gonorrhea, malaria, and the ear infections that plague little kids.

Health experts warn that if bacteria keep toughening up, some deadly diseases that have been treatable for the last five-plus decades again will have no cure.

For the full article:

http://www.livescience.com/hum.....teria.html
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PostPosted: Sat Mar 10, 2007 8:13 am    Post subject: Bacterial Walls Come Tumbling Down Reply with quote

March 09, 2007
Bacterial Walls Come Tumbling Down
HHMI

The first detailed images of an elusive drug target on the outer wall of bacteria may provide scientists with enough new information to aid design of novel antibiotics. The drugs are much needed to treat deadly infections initiated by Staphylococcus aureus and other bacterial pathogens.

The research team, led by Natalie Strynadka, a Howard Hughes Medical Institute (HHMI) international research scholar at the University of British Columbia in Vancouver, Canada, published its findings in the March 9, 2007, issue of the journal Science.

For the full article:

http://www.hhmi.org/news/strynadka20070309.html
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PostPosted: Thu May 03, 2007 11:02 am    Post subject: Maggots rid patients of MRSA Reply with quote

University of Manchester
3 May 2007

Maggots rid patients of MRSA

University of Manchester researchers are ridding diabetic patients of the superbug MRSA - by treating their foot ulcers with maggots.

Professor Andrew Boulton and his team used green bottle fly larvae to treat 13 diabetic patients whose foot ulcers were contaminated with MRSA and found all but one were cured within a mean period of three weeks, much quicker than the 28-week duration for the conventional treatment.

Professor Boulton, who published the results in the journal Diabetes Care, has now been awarded a £98,000 grant by Diabetes UK to carry out a randomized controlled trial to compare this treatment with two others.

"Maggots are the world's smallest surgeons. In fact they are better than surgeons - they are much cheaper and work 24 hours a day," Professor Boulton jokingly said.

"They have been used since the Napoleonic Wars and in the American Civil War they found that those who survived were the ones with maggots in their wounds: they kept them clean. They remove the dead tissue and bacteria, leaving the healthy tissue to heal.

"Still, we were very surprised to see such a good result for MRSA. There is no reason this cannot be applied to many other areas of the body, except perhaps a large abdominal wound."

Professor Boulton and his team, including senior nurse Ann Knowles, have used maggots to treat diabetic foot ulcers of patients attending the Manchester Diabetes Centre and foot clinics, as well as in in-patients at the Manchester Royal Infirmary, for ten years. More recently they found that many of their patients were suffering from MRSA-contaminated foot ulcers, with the rate doubling in a three year period, possibly due to overuse of antibiotics and the selection of broad rather than narrow-spectrum antibacterial agents. This led to their first study, funded by Central Manchester and Manchester Children's University Hospitals NHS Trust (CMMC) Chairman's Prize Award.

They treated 13 patients, aged 18-80 years with chronic foot ulcers that had suffered loss of feeling and reduced blood supply, with sterile free-range larvae of the green bottle fly Lucilia Sericata. They applied the larvae between two and eight times, depending on the size of the ulcer, for four days at a time, with pressure relieving dressings to protect them. No topical antimicrobial agents or growth factors were used on the study ulcer.

All but one of the patients was cleared of the superbug. During the treatment period, no adverse reactions were reported and there was a reduction in sloughy necrotic tissue and an increase in healthy, growing tissue on removal of the last larval application.

In their second study, he and his team will compare larval treatment with antibacterial silver dressings and the biogun treatment, which uses ionized air to create superoxide radicals and eradicate bacteria.

Professor Boulton said: "This is very exciting. We have demonstrated for the first time the potential of larval therapy to eliminate MRSA infection of diabetic foot ulcers. If confirmed in a randomized controlled trial, larval treatment would offer the first non-invasive and risk-free treatment of this increasing problem and a safe and cost-effective treatment in contrast to the expensive and potentially toxic antibiotic remedies."


###
For more information, a copy of the paper, moving and still images or an interview with Professor Andrew Boulton please contact Media Relations Officer Mikaela Sitford on 0161 275 2111.

Editors Note:

The paper 'Larval Therapy: A Novel Treatment in Eliminating Methicillin-Resistant Staphylococcus aureus From Diabetic Foot Ulcers' is in Diabetes Care, Volume 30, Number 2, February 2007.

Professor Andrew Boulton leads the Manchester DIALEX (Diabetes Lower Extremity Research Group), which has been actively researching clinical aspects of diabetic foot disease over the last 15 years. Over 200 peer reviewed research articles have been published as a result of research in this group. His clinical research group in Diabetic Nephropathy, in collaboration with Professor Gokal, has been active in researching clinical aspects of the management of diabetic nephropathy at all stages. He is a member of the Institute of Health Sciences Diabetes and Obesity Research Network and has been Chairman of Postgraduate Education for the European Diabetes Association and Honorary Secretary / Programme Chair for the EASD in the last 5 years. He also has strong links with American centres of research. The University of Manchester School of Medicine is one of the largest in the country, with almost 2000 undergraduates, 700 postgraduates and 1300 staff. The University's four teaching hospitals, together with affiliated hospitals and community practices across the North West, provide excellent facilities for clinical training and research. The School is a major contributor to the University's research profile and external grant income, with annual expenditure on research amounting to £30-35 million. This funding is obtained from research councils, medical charities, the health services and industry. The School was rated 5 in both hospital-based and community-based clinical subjects in the last RAE.

The Central Manchester and Manchester Children's University Hospitals NHS Trust (CMMC) has a strong commitment to research. Excellent facilities and researchers allow for world-class research in diverse areas such as cancer, cardiovascular disease, genetics and human development. The Trust has 14 major programmes of research, 675 ongoing research projects (at 2005/06) and 600 peer reviewed publications per year. Long-standing and successful partnerships with The University of Manchester and other collaborators are rapidly establishing Manchester as a centre of research excellence.

Diabetes UK is the largest charity in the UK devoted to the care and treatment of people with diabetes in order to improve the quality of life for people with the condition. It is one of the largest funders of diabetes research in the UK - investing £6M to develop better treatment, prevent diabetes and to find a cure.
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PostPosted: Fri May 11, 2007 6:33 am    Post subject: Researchers discover how antibiotic inhibits bacterial growt Reply with quote

University of Illinois at Chicago
11 May 2007

Researchers discover how antibiotic inhibits bacterial growth

Researchers at the University of Illinois at Chicago, in collaboration with research teams from Pharmacia & Upjohn and Pfizer, have discovered precisely how the antibiotic linezolid inhibits bacterial growth.

Scientists have known that the drug linezolid -- the first new antibiotic to enter the marketplace in 30 years -- works by binding to ribosomes, the protein production factory of the cell. But exactly where the binding occurred and how the drug worked was not known. Until now.

"Linezolid targets ribosomes, inhibits protein synthesis, and kills bacteria," said Alexander Mankin, professor and associate director of UIC's Center for Pharmaceutical Biotechnology and lead investigator of the study. "If we know exactly where the drug binds, we can make it better and learn how to use it more effectively."

Linezolid is a synthetic antibiotic used for the treatment of infections caused by pathogens such as staph and strep, including multi-drug-resistant bacteria. Skin infections, pneumonia, and other diseases can be treated with linezolid. It is marketed in the United States as Zyvox.

Mankin and his colleagues managed not only to crosslink the drug to its target in the living cell, but to precisely characterize the mode of binding of the drug to the ribosome.

"It was a combined effort of excellent chemists, structural biologists and biochemists," Mankin said.

"We now understand much better how the drug works, how it can be improved, and how bacteria can become resistant to linezolid."

A second part of the study involved learning why, in rare cases, the drug can have side effects causing a decrease in the production of blood cells. By crosslinking linezolid to its target in human cells, the researchers showed that the drug may be toxic to mitochondria -- the power generators of the cell -- which contain ribosomes that resemble the ribosomes of bacteria.

"This is the first time such detailed information about the linezolid target in the living cell has been obtained," Mankin said.


###
The findings are published in the May 11 issue of the journal Molecular Cell.

For more information about UIC, visit www.uic.edu
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PostPosted: Wed May 23, 2007 7:52 am    Post subject: Resistance genes in our food supply Reply with quote

American Society for Microbiology
23 May 2007

Resistance genes in our food supply

Could the food we eat be contributing to the continuing rise of antibiotic-resistant infections? Harmless and even beneficial bacteria that exist in our food supply may also be carrying genes that code for antibiotic resistance. Once in our bodies, could they transmit the resistance genes to disease-causing bacteria?

"The data indicate that food could be an important avenue for antibiotic-resistant bacterial evolution and dissemination. The role of commensals, especially food-borne microbes, in transmitting resistance genes are becoming a concern to the scientific community," says Hua Wang of the Ohio State University, presenting May 23, 2007 at the 107th General Meeting of the American Society for Microbiology (ASM) in Toronto.

The culprit is a process known as horizontal gene transfer, in which bacteria in close proximity to each other can share genetic information, including genes that code for antibiotic resistance. Horizontal gene transfer between disease-causing bacteria in the hospital setting has already been recognized as an important avenue for the exchange of antibiotic-resistance genes among pathogens.

Research has also already demonstrated that pathogenic bacteria have the ability to engage in horizontal gene transfer with various commensal bacteria and even beneficial bacteria, including those from the food chain. What concerns scientists is that the size and diversity of the gene pool represented by commensal bacteria increases the likelihood of gene transfer and some commensals possess high frequency gene transfer mechanisms.

"We have demonstrated not only that organisms carrying such intrinsic mechanisms have the potential to become an important reservoir for antibiotic resistance genes but, more importantly, that these intermediate organisms can disseminate antibiotic resistance genes in subsequent events much more effectively than the parental donor strain," says Hua.

"Once we no longer limit ourselves to foodborne pathogens and look at commensal bacteria, we will find that the magnitude of antibiotic-resistant bacterial contamination in the food chain is tremendous," says Hua.

In a study published last year, she and her colleagues tested a variety of ready-to-eat food samples including seafood, meats, dairy, deli items and fresh produce purchased from several grocery chain stores. With the exception of processed cheese and yogurt, antibiotic-resistance gene-carrying bacteria were found in many food samples examined.,

"Despite the fact that this study only screened for a limited number of resistance markers, it illustrated the prevalence of antibiotic-resistant commensals and antibiotic-resistance genes in retail foods," says Hua. "While further research is needed to establish the direct correlation between the antibiotic-resistant microbes from foods and the antibiotic-resistant population in host ecosystems, it is evident that a constant supply of antibiotic-resistant bacteria, partnered with occasional colonization and horizontal gene transfer, are at least partially responsible for the increased antibiotic resistance profiles seen in humans."

Antibiotic resistant infections are an increasing public health problem, says Marilyn Roberts of the University of Washington. Depending on the disease and the patient, an antibiotic-resistant infection could triple a hospital stay. A methicillin-resistant Staphylococcus aureus infection in a hospital patient can cost thousands of dollars more to treat. In some cases, such as the new extensively resistant tuberculosis, antibiotics are no longer effective, forcing doctors to take extreme measures like removing an infected lung.

The problem is not just confined to the food supply. Recent studies have shown antibiotic resistance genes in bacteria in the digestive tract of young infants. Since these children were still breast- or formula-feeding and had not eaten solid food yet, they must have acquired these genes somewhere other than the food supply. This suggests that resistance genes from the environment might have played an important role, says Hua.

"Antibiotics and the contamination of the environment is a medical problem, an agricultural problem and a human problem. Everybody plays a role in it. They also have a stake in it," says Roberts.

But there are things that can be done to minimize resistance genes in our food. Hua is currently working on characterizing the optimum conditions and processing parameters to minimize the emergence of these genes in fermented products. In time, and with a little help, she hopes to expand this research to other food industries as well.

"Given the proper investment of money, effort and time we can identify the steps that need to be taken at the processing level to minimize the emergence of antibiotic resistance genes in our food supply," says Hua.
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PostPosted: Thu May 24, 2007 11:45 am    Post subject: Understanding why C. difficile causes disease -- it's hungry Reply with quote

American Society for Microbiology
24 May 2007

Understanding why C. difficile causes disease -- it's hungry

Researchers studying the genetics behind why C. difficile causes disease have come to a simple conclusion -- the bacteria do it because they are starving. That just might help them find a new treatment for what can sometimes be a very difficult disease to treat.

"The genes responsible for toxin production only seem to be expressed during periods of nutrient deprivation. This is consistent with the view that most disease-causing bacteria express their pathogenicity when they are hungry," says Abraham Sonenshein, professor at the Sackler School of Graduate Biomedical Sciences at Tufts University and at Tufts University School of Medicine, at the 107th General Meeting of the American Society for Microbiology (ASM) on May 24, 2007.

C. difficile bacteria are everywhere — in soil, air, water, human and animal feces, and on most surfaces in hospital wards. The bacteria don't cause problems until they grow in abnormally large numbers in the intestinal tract. This can happen when the benign bacteria that normally inhabit the intestinal tract are reduced such as when people take antibiotics or other antimicrobial drugs. Then, C. difficile can cause symptoms ranging from diarrhea to life-threatening inflammations of the colon.

In 2002 a new, more virulent strain began appearing in hospitals in the United States and Canada. Recently, this strain was shown to be responsible for more than half of all cases in a representative sampling in Quebec. The highly virulent strain has a much higher toxin production which leads to more destructive and deadly disease, says Vivian Loo of McGill University.

Sonenshein is studying a five-gene region of the bacterium’s chromosome known as the tcd locus. Two of the genes code for the toxins the bacterium produces that cause disease and a third gene codes for a protein that makes a hole in the organism’s cell envelope to let the toxins out. The last two genes are of greatest interest to Sonenshein and his colleague, Bruno Dupuy from the Institut Pasteur. One codes for a protein, known as R, that is necessary for the expression of the first three genes and the other codes for a protein called C that prevents R from acting.

A mutation in the C protein gene, leaving R unchecked, is the cause of the hypervirulent strain. Sonenshein and his colleagues are currently working to identify a protein that might shut down the gene that codes for R. By identifying such a protein, Sonenshein hope to find a way to change the appetite of the bacteria. "If we find a way to shut down toxin production in the hypervirulent strain, we might have a new way to treat the disease," says Sonenshein.
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PostPosted: Tue Jun 26, 2007 10:50 am    Post subject: Deadly Superbug More Widespread than Thought Reply with quote

Deadly Superbug More Widespread than Thought
By Mike Stobbe, Associated Press

posted: 25 June 2007 04:27 pm ET

ATLANTA (AP) -- A dangerous, drug-resistant staph germ may be infecting as many as 5 percent of hospital and nursing home patients, according to a comprehensive study.

At least 30,000 U.S. hospital patients may have the superbug at any given time, according to a survey released Monday by the Association for Professionals in Infection Control and Epidemiology.

The estimate is about 10 times the rate that some health officials had previously estimated.

Some federal health officials said they had not seen the study and could not comment on its methodology or its prevalence. But they welcomed added attention to the problem.

For the full article:

http://www.livescience.com/hea.....erbug.html
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PostPosted: Wed Jul 11, 2007 8:19 am    Post subject: Antibiotics don't prevent future urinary tract infections, m Reply with quote

Children's Hospital of Philadelphia
10 July 2007

Antibiotics don't prevent future urinary tract infections, may cause resistance in future infections

After a first childhood urinary tract infection (UTI), daily antibiotics may not prevent another such infection, and may actually increase the risk that the next urinary tract infection is caused by resistant bacteria, according to a new study in the July 11 issue of the Journal of the American Medical Association.

In the first large study of children diagnosed with UTI in a primary care pediatric setting, researchers from The Children’s Hospital of Philadelphia reviewed the electronic health records of 74,974 children with at least two clinic visits in The Children’s Hospital of Philadelphia’s pediatric healthcare network between July 2001 and May 2006. The researchers found that 611 children had a first urinary tract infection and 83 had a recurrent UTI. Children between ages three and five, Caucasians, and those with severe vesicoureteral reflux had the highest risk of recurrent UTI. Receiving a daily dose of preventive antibiotics was not associated with a lower risk of recurrent UTI.

“The majority of children with first UTI were female, Caucasian and two through six years old. Most did not have an imaging study performed and did not receive daily antibiotics to prevent infections,” said Patrick Conway, M.D. M.Sc., primary investigator of the study. “We found that daily antibiotic treatment was not associated with a decreased risk of recurrent UTIs, but was associated with an increased risk of resistant infections.” Currently at Cincinnati Children’s Hospital Medical Center, Dr. Conway conducted the research while at The Children’s Hospital of Philadelphia and a Robert Wood Johnson Clinical Scholar at the University of Pennsylvania.

“More definitive studies, such as clinical trials, are needed to look at this issue.” said Ron Keren, M.D., M.P.H., a general pediatrician at The Children’s Hospital of Philadelphia and senior author on this study. “But given these findings, it is appropriate for pediatricians to discuss with families the risks and unclear benefits of daily preventive antibiotic treatment after a child has had a first UTI.”

UTIs are common in children. In fact, of all the children born in one year, 70,000 to 180,000 will have a UTI by age six.

The American Academy of Pediatrics (AAP) practice guideline for management of children after a first UTI recommends an imaging study to evaluate the presence and degree of vesicoureteral reflux (VUR), a condition found in approximately 30 to 40 percent of children who have had a UTI. If the child has VUR, daily antibiotic treatment is recommended in an attempt to prevent recurrent UTIs.

Vesicoureteral reflux (VUR) occurs when urine in the bladder flows back into the ureters or kidneys during urination. It is thought that a child who has VUR is at risk for developing recurrent kidney infections, which, over time, can cause damage to the kidneys. However, Dr. Conway summarized, “The majority of children have lower grade VUR and this lower grade VUR was not associated with an increased risk of recurrent UTI in our study.”

###
Grants from the National Institutes of Health, the Robert Wood Johnson Foundation Clinical Scholars Training Program and the University of Pennsylvania Center for Education and Research on Therapeutics supported this study.

Dr. Conway and Dr. Keren’s coauthors were Avital Cnaan, Ph.D.; Theoklis Zaoutis, M.D., M.S.C.E.; Brandon V. Henry; and Robert W. Grundmeier, M.D., all of The Children’s Hospital of Philadelphia and the University of Pennsylvania School of Medicine.

About The Children's Hospital of Philadelphia: The Children's Hospital of Philadelphia was founded in 1855 as the nation's first pediatric hospital. Through its long-standing commitment to providing exceptional patient care, training new generations of pediatric healthcare professionals and pioneering major research initiatives, Children's Hospital has fostered many discoveries that have benefited children worldwide. Its pediatric research program is among the largest in the country, ranking third in National Institutes of Health funding. In addition, its unique family-centered care and public service programs have brought the 430-bed hospital recognition as a leading advocate for children and adolescents. For more information, visit http://www.chop.edu
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PostPosted: Thu Sep 06, 2007 11:34 am    Post subject: New insight into how antibiotics kill might make them deadli Reply with quote

Cell Press
6 September 2007

New insight into how antibiotics kill might make them deadlier

Scientists have what could be some very bad news for disease-causing bacteria. All three major classes of antibiotics that kill infectious bacteria do so in part by ramping up the production of harmful free radicals, researchers report in the September 7, 2007, issue of Cell, a publication of Cell Press. Because those different types of antibiotics each initially hit different targets, it had been believed they worked by independent means.

The findings could point the way to new classes of antibiotics and to a common method by which existing antibiotics could be made to stamp out bacteria even better, according to the Boston University researchers. Such advances are particularly critical at a time when, according to the Centers for Disease Control and Prevention, nearly all significant bacterial infections in the world are becoming resistant to the most commonly prescribed antibiotic treatments.

“Hydroxyl radicals damage DNA, which turns on the S.O.S. repair response,” said James Collins. “Therefore, our findings suggest that if you could shut off the bacteria’s repair response, you might make all bactericidal antibiotics more effective and effective at lower doses. You could in essence create a super-Cipro, super-mycins, and so on.”

Current antimicrobial therapies fall into two general categories: (1) bactericidal drugs, which kill bacteria with almost complete efficiency, and (2) bacteriostatic drugs, which inhibit their growth, allowing the immune system to clear the infection, Collins’s group explained. The targets of bactericidal antibiotics are well studied and predominantly fall into three classes: (1) those that hit DNA, (2) those that hit proteins, and (3) those that hit the bacterial cell wall. In contrast, most bacteriostatic drugs work by blocking the function of ribosomes, which are the sites of protein synthesis. While antibiotics’ ability to kill bacteria had been attributed solely to those class-specific drug-target interactions, “our understanding of many of the bacterial responses that occur as a consequence of the primary drug-target interaction remains incomplete,” the researchers said.

Collins and his colleagues recently uncovered some evidence that at least some antibiotics might have some other deadly tricks. They showed that one type of antibiotics, including quinolones, which block DNA’s replication and transcription into messenger RNA, also causes a breakdown that leads to the production of free radicals. Moreover, they found that those highly reactive chemicals help finish the bacteria off.

In the new study, the researchers wanted to know whether other antibiotics also drive the toxic brew. Indeed, they show, drugs that kill bacteria all do cause a rise in free radicals, and all in the same manner. This is not so for drugs that only stunt bacteria’s growth, they report.

“The ever-increasing prevalence of antibiotic-resistant strains has made it critical that we develop novel, more effective means of killing bacteria,” the researchers concluded. “Our results indicate that targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response… is a viable means of potentiating all three major classes of bactericidal drugs. Moreover, pathway analyses and systems biology approaches may uncover druggable targets for stimulating hydroxyl radical formation, which could result in new classes of bactericidal antibiotics.”

###
The researchers include Michael A. Kohanski of Boston University and Boston University School of Medicine in Boston and Daniel J. Dwyer, Boris Hayete, Carolyn A. Lawrence, and James J. Collins of Boston University in Boston.

This work was supported by the National Science Foundation FIBR and Department of Energy GTL programs and NSF award EMSW21-RTG to J.J.C.

Kohanski et al.: “A Common Mechanism of Cellular Death Induced by Bactericidal Antibiotics.” Publishing in Cell 130, 797–810, September 7, 2007. DOI 10.1016/j.cell.2007.06.049 http://www.cell.com
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PostPosted: Tue Oct 30, 2007 12:36 pm    Post subject: The Truth About Deadly 'Superbugs' Reply with quote

The Truth About Deadly 'Superbugs'
By Dave Mosher, LiveScience Staff Writer

posted: 30 October 2007 08:54 am ET

NEW YORK – Armies of invisible creatures are spreading across the planet, infesting local communities and claiming the lives of innocent children in their wake. And the attackers are immune to some of the world's best weaponry.

It sounds more like a sci-fi movie plot than reality, but "superbugs"—deadly microbes that can resist drugs designed to wipe them out—are far from imaginary. Schoolchildren in several states recently have died from infections caused by MRSA bacteria, otherwise known as methicillin-resistant Staphylococcus aureus, and medical recordkeeping shows such cases are increasing annually.

For the full article:

http://www.livescience.com/hea.....erbug.html
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PostPosted: Sat Nov 03, 2007 7:06 am    Post subject: Clay That Kills: Ground yields antibacterial agents Reply with quote

Week of Nov. 3, 2007; Vol. 172, No. 18 , p. 276

Clay That Kills: Ground yields antibacterial agents
Sarah C. Williams

A fistful of slimy green clay may be just what the doctor ordered. Researchers studying a special type of French clay found that it smothers a diverse array of bacteria, including antibiotic-resistant strains and a particularly nasty pathogen that causes skin ulcers in some parts of the world.

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http://sciencenews.org/articles/20071103/fob4.asp
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