Drug resistant bacteria and hope on the horizon - page 2
Becoming a problem
So how do antibiotic-resistant bacteria become a problem down the road? Well, this generally happens when a patient takes a broad-spectrum antibiotic. This antibiotic mows down the body’s own normal flora (the “good” bacteria) along with the bug that the drug was originally prescribed for in the first place. When this happens, the overall amount of bacteria in the body is decreased. What’s left is some normal, healthy bacteria, and some drug-resistant bacteria. Because these resistant bacteria are immune to most antibiotics, they survived largely unscathed, and with the competition over resources with the healthy bacteria suddenly decreased, they are given a chance to flourish and multiply, choking out the healthy bacteria like weeds can choke a garden. This is what happens in the case of illnesses like C. Diff, where the organism Clostridium difficile takes over the colon because there’s no healthy bacteria to check its growth.
More typical medical issues that can arise from antibiotic overuse are vulnerability to bacterial pneumonia after something like a bad cause of the flu; greater risk of secondary infection following surgery or other body trauma; and drug-resistant urinary tract infections which can require multiple antibiotics to treat. (This last one I’ve personally seen a lot of in the last few years.) Research has shown, time and again, that reducing antibiotic usage leads to fewer incidences of resistant strains.
But doctors are finally beginning to come around, and it’s generally subtleties that aid them in persuading patients that it might not be a good idea to prescribe an antibiotic. People are more easily persuaded when they don’t realize that they’re being led. Brochures in patient waiting rooms educate patients on what sorts of symptoms may be caused by viruses, and which symptoms may be bacterial. Letting patients know the treatment for viruses before they even hit the doctor’s examination room prepares them for possibly not getting a prescription, and opens the door for the placebo effect.
Hope on the horizon
Despite the progress being made in patient waiting rooms, there is also progress being made finding new antibiotics, using both old and new approaches.
A spin off an older type of antibiotic, the cephalosporins, offers promise by confusing drug-resistant bacterial cells into thinking that the drug is part of the bacterial wall, which destroys the cell. This experimental new drug was effective even against vancomycin-resistant MRSA. Vancomycin has long been considered the last line of defense against bacteria, so this is excellent news. (Though Zyvox/linezolid is also gaining in popularity.)
Staph aureus is not the only bacteria that is resistant to antibiotics, and the new drugs show promise against non-staph bacteria as well.
Mobashery’s group recently discovered, in a study published in the Feb. 16 issue of the Journal of the American Chemical Society, that the enzyme interacts with certain components of the bacterial cell wall and that targeting these components might deactivate the enzyme, making the bacteria vulnerable to attack. Subsequently, the group identified a set of three novel cephalosporin antibiotics that appear to interact with the enzyme and also contain protein components that are similar to those of the bacterial cell wall.
The researchers then added the antibiotics to vancomycin-resistant MRSA and compared the results to those of another set of antibiotics belonging to a similar drug class (beta-lactams). The new antibiotics killed the bacteria, whereas the others did not, they say.
Based on lab studies, Mobashery believes that the novel antibiotics gained access to the enzyme’s active site by mimicking chemical components of the bacterial cell wall, which is largely composed of a polymer called peptidoglycan. Upon contact with the cell wall components, the antibiotics appear to trigger the enzyme to open. Once open, the antibiotics deactivate the enzyme, setting in motion a chain of events that eventually kills the bacteria, the researcher says.
Basically, the cells lys, as happens with most other antibiotics — the trick was finding the right chemical key to unlock the bacterial wall.
I would also expect other novel approaches to new antibiotics, perhaps borrowing a page from some experimental antiviral drugs, utilizing metals as a means to destroy bacteria, but the issue with these is tailoring them enough to be useful against specific bacteria, and engineering them in such a way that they do not harm the body’s own cells.
Conclusion
Regardless of what happens in the future, expect to see Big Pharma look at antibiotics again. As the current strains of bacteria become more invulnerable, there will be money in developing new cures. Unfortunately for the public, this wake-up call might come too late for families of loved ones who will have died as a result of secondary nosocomial infections. If a financial incentive could be made for pharmaceutical companies today, the pain of tomorrow might be lessened. Non-profit pharmaceutical companies, such a OneWorldHealth, are also working on cures for some of these historically unprofitable causes.
I don’t believe that it is fair to blame Big Pharma for focusing mainly those conditions which offer the greatest profit. Businesses are in business to make money, and so pursuing the lifestyle conditions makes good financial sense using modern business models. One can hope that a company like Napo Pharmaceuticals comes along with a radically different business model, and can turn a decent profit combating killer diseases. If this does happen, it’ll happen first in the third world, and then trickle back to the US. This seems strange given that most pharmaceutical breakthroughs and advances are made in the US.
Comments
Page 1
polyscience.org home
No Comments »
No comments yet.
RSS feed for comments on this post.
| TrackBack URI
You can also bookmark
this on del.icio.us or check the cosmos