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Medical Bacteriostatic Drugs

  1. Mar 9, 2016 #1
    What really happens when the bacteria get exposed to a bacteriostatic drug? Bactericidal drugs cause cellular destruction but the static drugs, as per description are said to prevent the bacteria from replicating. But apart from this what happens to the bacteria, is it able to exist and function as a physiologically normal cell which has a single handicap in the form of not being able to replicate? Or is there any additional affection?

    What really happens to its metabolism? Does it still take up resources from the surrounding?
    Would be really grateful if someone can point to any specific references pertaining to this.
  2. jcsd
  3. Mar 9, 2016 #2


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    You may find the following paper to be useful: Kohanski et al. 2007. A Common Mechanism of Cellular Death Induced by Bactericidal Antibiotics Cell, 130: 797. http://dx.doi.org/10.1016/j.cell.2007.06.049 [Broken]

    Antibiotic mode-of-action classification is based upon drug-target interaction and whether the resultant inhibition of cellular function is lethal to bacteria. Here we show that the three major classes of bactericidal antibiotics, regardless of drug-target interaction, stimulate the production of highly deleterious hydroxyl radicals in Gram-negative and Gram-positive bacteria, which ultimately contribute to cell death. We also show, in contrast, that bacteriostatic drugs do not produce hydroxyl radicals. We demonstrate that the mechanism of hydroxyl radical formation induced by bactericidal antibiotics is the end product of an oxidative damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH, destabilization of iron-sulfur clusters, and stimulation of the Fenton reaction. Our results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.
    Last edited by a moderator: May 7, 2017
  4. Mar 9, 2016 #3
    That's my understanding. I know this because in the 80's I caught a urethral infection from some hooker at a strip club in downtown Honolulu :rolleyes:

    At that time on the Island there was only one community health clinic that was free, and it was a long bus ride out out Waikiki. So I took the bus out to the clinic and this 70 year old Polynesian women stuck this long cotton swab in my... Anyway, they gave me a prescription for some form of antibiotic and I was so happy that this might relieve the stinging that I read the full whitepaper on the medicine on my long bus trip back to Waikiki, complete with the contraindications and the rest of it. It was actually pretty telling and may even have been partially influential to me becoming a biologist :oldsmile:

    Basically, what the whitepaper said is that this antibiotic I was taking inhibited the replication of the bacteria. As far as you initial question, the way it works is that, pre-anti-biotics, whether you lived or died depended on whether your immune system outpaced killing the bacteria faster than it could replicate. What anti-biotics do is slow down the rate of replication.

    P.S., from what I remember the medication was a chemical that binded to a DNA sequence that was involved in or essential to the replication and prevented that from happening. So it's kind of like throwing a wooded Dutch shoe in the gears of the machine like the Luddites liked to do.
    Last edited: Mar 9, 2016
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