Wednesday, November 7, 2012

Bacteria rebel against antibiotics

As we all know about bacterial infections, the simplest solution is to head to the doctor and take those prescribed antibiotics to simply kill them off. Over time though we learn that bacteria are beginning to find loop holes, or adapt to the same antibiotics that we have been taking and developed a resistance to the medications that would normally take it out. This leads towards the fact that it will be much more difficult to treat them with the same antibiotics.

There are two commonly types of bacteria that have developed a resistance to to antibiotic medications, Staphylococcus Aureus (A.K.A Staph) and Enterococcus. Over time when they do develop their resistance researchers have given them new classification names such as Methicillin-resistant Staph Aureus, and vancomycin-resistant Enterococcus. Though we know that not finishing, and repitition of antibiotics can increase the chances of the bacteria obtaining their resistance it doesnt quite answer the: How do they develop this resistance?

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Over the years we begin to figure out that those who survive will begin to obtain a resistance strain from mutation, and the rest of it is up to natural selection to run its course to populate a new colony of bacteria. Take for example this experiment using wild E.coli using different concentrations of norfloxacin (along with other various different antibiotics) with the enzyme tryptophanase. By isolating the intracellular components from the simple and high-resistance individuals leading to a discovery of mass production of a certain protein. The main job a tryptophanase was to be broken down into ammonia, pyruvate, and indole. Indole, under experimental circumstances provided antibiotic survival benefits. This caused the mutant bacteria to mass produce indole, allowing the more vulnerable non-mutated bacteria that surrounded them to survive. This would allow further more exploration of the evolving mutants that could benefit the colony to surviving, and could temporarily stop the gene from spreading.

References:
Lee, Henry H., Michael N. Molla, Charles R. Cantor and James J. Collins. "Abstract." National Center for   Biotechnology Information. U.S. National Library of Medicine, 02 Sept. 2010. Web. 07 Nov. 2012

"Life of a Lab Rat: Guest Post-Survival of the Fittest?" Life of a Lab Rat: Guest Post - Survival of the Fittest? N.p., 26 Sept. 2010. Web. 07 Nov. 2012. <http://labrat.fieldofscience.com/2010/09/guest-post-survival-of-the-fittest.html?utm_source=feedburner>

1 comment:

  1. Great! Glad to see you bringing up some important points and information.

    ReplyDelete