Posts Tagged ‘antibiotics’
Antibiotics May Be Permanently Altering the Guts of Humanity
Our microbiomes are the collection of bacterial microbes that we carry around with us all the time, those symbiotic little bugs that live on our skin and in our esophagi and--very importantly--in our guts. And while we’ve long known that a cycle of antibiotics prescribed to kill off an infection can also kill off some of our most important beneficial microorganisms, the general line of thinking is that once the cycle of antibiotics ends our microbiomes correct themselves and the natural order of things returns.
Blaser presents arguments otherwise in an editorial that suggests that our gut bacteria is permanently affected by a cycle of antibiotics, and that the impact is so profound that it might be time to seriously consider not giving antibiotics to anyone other than very young children and pregnant women. Quoted by Maryn McKenna in :
Early evidence from my lab and others hints that, sometimes, our friendly flora never fully recover. These long-term changes to the beneficial bacteria within people’s bodies may even increase our susceptibility to infections and disease. Overuse of antibiotics could be fueling the dramatic increase in conditions such as obesity, type 1 diabetes, inflammatory bowel disease, allergies and asthma, which have more than doubled in many populations.
He then goes on to present some disconcerting correlations between the absence of certain bacteria and the rise in incidences of things like allergy, asthma, and weight gain. He points to evidence that children are getting too many doses of antibiotics before adulthood and that their microbiomes are never the same for it--specifically that the damage to our gut bacteria populations is permanent from that point forward.
Which leads to an eventual conclusion that when our children are sick we shouldn’t give them what we know will make them better. And that’s a tough pill to swallow.
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Scientists Mine Dormant Bacterial Genes For New Antibiotics
To produce the antibiotic, scientists identify idle genome segments in the bacteria, isolate the repressor gene that keeps those segments dormant, and delete it from the genome—in effect, switching on the potentially antibiotic-producing segment. The team, led by Eriko Takano, hopes to find compounds that are effective against fungi and cancerous human cells, providing further treatment options for immune-compromised and cancer patients.
Cockroach Brains Could Hold the Key to Next Generation of Antibiotics
The researchers identified nine different molecules found in the insects' nervous system tissues that are toxic to bacteria but harmless to human cells. Those tissues could be used to engineer new kinds of antibiotics that are effective in treating infections that are resistant to conventional drugs.
For strains of infectious bacteria like MRSA, that could be huge. MRSA is highly-resistant to the usual battery of antibiotics used to treat bacterial infections and is particularly troublesome in hospital environments where it can take up residence and be particularly difficult to eradicate -- kind of like an infestation of cockroaches. When conventional drugs don't work, doctors have to reach deeper into their medicine bags, and some of the treatments they are forced to fall back on have very unpleasant side effects on healthy human tissue.
Considering the pharmaceutical industry is having a hard time finding novel (or profitable) ways of combating drug-resistant bacteria like MRSA, this new method could provide a cheap source of effective antimicrobial drugs. So before you go crushing that tiny little pharma factory skittering across your living room floor, think twice. Then go ahead and do it. Cockroaches are disgusting, dude.
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To Fight Drug-Resistant MRSA, Algorithm Predicts Bacteria’s Future Mutations
Some bacteria, including MRSA (methicillin-resistant Staphylococcus aureus), evolve mutations to change the shape of the active site of their enzymes, which is what antibiotics are after. The algorithm, called K* (pronounced K-star), tries to anticipate those changes.
The team modeled mutations in an MRSA enzyme called dihydrofolate reductase, which is targeted by several drugs. Almost every living thing has a version of DHFR, because it helps turn folic acid into thymidine, the "T" among the DNA nucleotides.
The K* algorithm helped the researchers find DHFR mutation candidates that would be able to block new antibiotics. This knowledge could be incorporated into a drug-design strategy -- anticipating how bacteria would mutate to fight antibiotics, and designing antibiotics around those predicted mutations.
When the team studied the mutant enzymes, they realized their structures were one reason why they were able to evade antibiotics, according to a Duke news release.
Donald's team has also studied using the K* algorithm to diagnose cancer and to design enzymes that could improve antibiotics' efficacy.
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Scientists Crack Chemical Code that Controls Bacterial Swarms
When infecting tissue in the body, bacteria swarm collectively across the surface like an 18th-century army on the march, growing into a massive colony that produces toxins that cause damage to the tissue. The mechanism by which bacteria organize this mass movement has remained a mystery to researchers, but now scientists at the Universitat Autònoma de Barcelona (UAB) have identified the chemical courier that makes this possible.
A protein called CheW is essential for swarming, catalyzing the mass movement of bacteria across the surface of an organ. But when bacteria encounter antibiotics, the drugs initiate a DNA repair system in bacteria known as SOS response, which is supposed to stop the infection. But the Spanish researchers found that when SOS response kicks in, levels of another protein known as RecA begin to increase. RecA interferes with CheW, causing the colony to stop moving forward. As a result, only the front line of the colony is affected by the antibiotics; the rest of the colony stops marching until the concentration of antibiotics decreases, at which point RecA concentrations fall and the colony starts attacking again.
It's a clever play by the bacteria, but it could open up new treatment options to deal with bacterial infections. If antibiotics could be augmented with something that stops RecA from halting the forward progress of the swarm, current drugs could become more effective in neutralizing infections.
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