• Faresh@lemmy.ml
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    10 months ago

    Does this mean we won’t have to worry about the return of bacterial infections as one of the leading causes of human mortality?

    • RedditWanderer@lemmy.world
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      10 months ago

      No, not really. It’s only a matter of time before they are resistant to this one too, and I don’t know that we can help it even if distribution antibiotics carefully.

      A war like Ukraine or a Genocide like Gaza tends to speed up bacterial resistance a lot, while breakthroughs are rare. I don’t see anything in this article that says it will be more difficult for bugs to become resistant to it. All bugs evolve constantly.

      • Pyr_Pressure@lemmy.ca
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        10 months ago

        If you alternate between uses it responsibly it would be unlikely that anything would arise to be immune to both types.

        You use type A to kill most things and then Type B to kill those resistant to type A.

        Something would need to arise to be both resistant to Type A and Type B at the same time which would be highly unlikely.

        • RedditWanderer@lemmy.world
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          10 months ago

          Name me one thing humans have been 100% reponsible with, from nuclear weapons to airplanes. Especially when it comes to antibiotics, people are going to take what they have available.

          So as was saying, it will always be a race.

    • Pup Biru@aussie.zone
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      10 months ago

      i think the key here is:

      zosurabalpin doesn’t seem to work on any other Gram-negative bacteria besides A. baumannii. The proteins in the LPS transporter complex are not conserved across different bacteria. Thus, targeting the LPS transporters of other nefarious Gram-negative bacteria will take yet more drug development research. One bright side of this, as Gugger and Hergenrother note in their commentary, is that it may produce species-specific antibiotics, which could protect patients’ microbiomes from being obliterated by broad-spectrum drugs, which we now appreciate is bad for human health.

      And, of course, with any new antibiotic, there’s the inevitability that bacteria will develop resistance. The researchers already found that select mutations in the LPS transporter machinery can knock back the drug’s potency. Also, A. baumannii doesn’t need LPS to stay alive. That said, simply blocking LPS production would leave A. baumannii more vulnerable, and it’s unclear how that trade-off will play out in clinical settings.