As living organisms, bacteria are encoded by DNA, and DNA occasionally mutates. Sometimes genetic mutations render a bacterium immune to an antibiotic’s chemical tactics. The few cells that might escape antibiotic pressure then have a sudden advantage: with their counterparts wiped out, resources abound, and the remaining antibiotic-resistant bacteria proliferate. It’s a problem not only for the host—you or me when we are treated with an antibiotic and develop a resistant strain—but also for anyone with whom we happen to share our resistant bacteria, say, on a door handle or keyboard. In fact, most resistant bacteria develop not in people but in livestock fed antibiotics to promote growth; these resistant bacteria infect people through contaminated animal products. This is how even antibiotic “naive” people come to be infected with resistant strains of bacteria.

I see this all the time as a family doctor. A woman has a urinary tract infection. I tell her that her bacteria are resistant to this or that antibiotic, and she says, “But I’ve never taken any of those.” Welcome to the global human soup.

  • AnarchistArtificer@slrpnk.net
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    3 months ago

    I understand what you’re saying about drift, but I’m not sure that feels sufficient to explain the prevalence of anti-biotic resistance. You’re right to highlight that the genes for antibiotic resistance already exist and it’s just a question of how prevalent they are in different populations/generations, but I don’t think this excludes it from being evolution. I would consider the human use of antibiotics in medicine and agriculture to be a selective pressure that is increasing the prevalence of antibiotic resistant genes in bacteria, especially in combination with human activities that facilitate the global spread of antimicrobial resistance.

    I agree that “evolution” is a pretty muddy term though, which is made trickier by the fact that with how language evolves, some people use it in a different sense than what is probably strictly “correct”. I’m a biochemist, for example, and I don’t know if I could give a strictly correct definition for evolution. Along those lines, I realise I may be misinterpreting your point.

    Separate to all that, it sounds like you’re well versed on the bacteriophage stuff, are there any articles that you think cover the topic well? I’m more of a protein structure gal myself, so I only have patchy, undergrad level knowledge of microbiology stuff.

    • CeeBee@lemmy.world
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      3 months ago

      I understand what you’re saying about drift, but I’m not sure that feels sufficient to explain the prevalence of anti-biotic resistance.

      One interesting discovery was the remains of a person in Peru from something like 900 years ago. One really interesting aspect of the discovery was the gut bacteria in the remains. When they sequenced the genome of some of the bacteria they found that they were the same species as we have today. But more importantly was that the genes that encode for antibiotic resistance existed in those bacteria.

      https://www.ancient-origins.net/news-history-archaeology/ancient-peruvian-mummy-surprises-researchers-antibiotic-resistant-genes-020581

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4589460/

      The discussion here isn’t about how antibiotic resistance first came about, the discussion is about how bacteria have been reacting to modern medicine. Why are bacteria becoming harder to treat with antibiotics as time goes on?

      The point I was making is that bacteria already have antibiotic resistance in the genome, but the phenotypic expression is inversely related to bacteriophage resistance.

      Antibiotic resistance needs

      • weaker/more flexible cell walls

      • more efflux pumps

      Bacteriophage resistance needs

      • stronger/stiffer cell walls (to protect against punctures)
      • less efflux pumps (to increase material strength of cell wall)

      In any population group there’s going to be variation in the expression of genes (the phenotype). In that population there are going to be individuals with greater antibiotic resistance and others with greater bacteriophage resistance. When antibiotics are introduced it kills most of the bacteria, but there can be a few individuals with higher antibiotic resistance that can potentially repopulate a new generation with an allele frequency shifted towards higher antibiotic resistance.

      I know what I just described is “natural selection”, but that’s not evolution. Natural selection is one of the processes that is part of evolution, but it is not evolution in of itself.

      Edit: formatting

    • AmidFuror@fedia.io
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      3 months ago

      A succinct definition of evolution is “The change of allele frequencies over time.” Even “allelic drift” is evolution.

      For bacteria, population sizes are big enough that simple variants like base substitutions can occur at every single base in the genome over a short period of time. Some of these are important to the development and redevelopment of resistances. Once one allele has spread enough, compensatory mutations can bring about combinations that weren’t seen before.

      Antibiotic resistance is definitely an evolved trait, and it’s the reason why multi-resistance and resistance to brand new antibiotics is becoming such a problem.