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Unfortunately, we do see examples of bacteria and viruses evolving vaccine resistance. For instance, vaccine resistant strains of polio and pertussis have recently been identified. Yet these seem like the exception rather than the rule. One thing that makes it harder for pathogens to evolve resistance is that vaccines usually generate antibodies to ...


6

Yes, many times. For just one example, see this paper; you could also see this review for numerous examples. These are examples of spontaneous mutations that lead to antibiotic resistance, so this is sort of an extreme version of evolution of antibiotic resistance. You could also say that antibiotic resistance "evolves" in terms of selection any time an ...


6

Natural selection is environment-dependent. A mutation that makes an individual more fit in one context, might make it less fit in a different context. The mutations that make bacteria more fit in an environment where they're exposed to antibiotics generally make them less fit in a "natural" environment where they don't have to deal with antibiotics. That ...


5

There are physical limits to the existance of life forms, wether temperature, pressure, osmolarity, etc. But these are usually physicochemical fields acting over a wide spatial structure. In the case of drugs, they are physically localized molecular entities. They are usually very tiny, even compared to the smallest microbes. Even though the genome of any ...


4

If we assume all of these things could be practically done at least at some point in the future, here are the problems I see with the suggestions, and why they might not work (others may spot additional ones). 1 Translocation of a sabotaging 'agent' via the conjugation apparatus. This basically already exists, look up the various secretion systems of ...


4

You're correct, this is extremely relevant, and it's unfortunate that your medical education didn't include good instruction about evolution. You point to some very useful and interesting studies. I'm particularly fond of the studies that demonstrate the early existence of antibacterial resistance genes, e.g., in ancient permafrost. Now to your question ...


3

The mutations are random, the survival and spread of bacteria with said mutations is NOT random. Evolution and selection are situational. The careless use of antibiotics causes those mutations and bacteria to spread because they out compete others without resistance. However, often these will not outcompete without antibiotics being present. Often ...


3

Resistance to antiviral therapy is a problem in the treatment of many viral illnesses. Influenza is particularly significant given the epidemiological characteristics of the disease. This Nature Medicine article gives a good overview of oseltamivir resistant pandemic H1N1, which is a useful example, since our assumption that resistant virus would not ...


3

It is possible due to the fact that some antimicrobial resistance genes are induced by the presence of antibiotics themselves and are not promoted in the absence of a specific antibiotic, so the production of certain antimicrobial structures (enzymes, pumps, etc.) will be reduced once the bacterial medium is antibiotic free for enough time. This is sometimes ...


3

Antibiotics ARE compounds, and they kill or inhibit the growth of bacteria by specific mechanisms. Each class of antibiotics has specific mechanism of actions. Given enough exposure to these antibiotics compounds, bacteria can develop specific molecular mechanism to nullify their effect, and hence antibiotics resistance. Antibiotics resistance will ...


3

does long term use of antibiotics breed these strains in the bodies of antibiotic users[,] and increase the risk of various bodily infections? Yes to the first question (although I would use the words select for). No, not usually for the second question in the individual(*), yes in the population. This should be looked at as a problem in populations of ...


2

As anongoodnurse has mentioned in the comments, an incomplete course can allow weakly resistant stains to expand their population. As you mentioned, the antibiotic does not cause the bacteria to mutate but it kills all strains that do not carry the mutation that provides the resistance. This mutation arises randomly (in certain cases it can be acquired by ...


2

For some classes of antiseptics the effect is more simple chemistry or even physics than biochemical toxicity. Ethanol will just denature proteins and dissolve the membrane, and the used concentration of ethanol is so high that no amount of efflux pumps is going to save the bacterium. Some other compounds work in a similar brute force way: QACs will break ...


2

I will assume the mutation is not under some kind of balancing selection such as negative frequency dependent selection. As fitness is conditional upon the environment, I will assume a constant environment (heterogeneous environment can also lead to balancing selection). Is WT expected to be the ONLY strain to persist in the long run? Yes. In fact, even ...


2

Check out phage therapy. For more details check out the reviews by Levin & Bull (2004) and Skurnik & Strauch (2006). The idea was around for quite some time and there is active ongoing research in this field. However, this idea just involves killing the bacteria using bacteriophages and not reducing their resistance to antibiotics. The bacteria that ...


2

Could plasmids and conjugation mechanisms be used against antibiotic-resistant bacteria? Apparently yes. At least, it's plausible. The study is very new and, even though it was conducted in vivo, it was still under artificial conditions. We'll have to see what comes out of it. Most important modern antibiotic resistance genes spread between such species ...


1

It's possible and certain engineered solutions might be even more potent than just phage therapy on its own. For example, imagine if you could deliver CRISPR-Cas with a lysogenic bacteriophage (that is, the phage delivers a CRISPR-Cas payload, and that payload gets integrated into the host genome without immediately killing the bacteria). The CRISPR-Cas ...


1

This is a very interesting topic. Indeed, historically, it might seem that "phage therapy" research is in a dormant state. But there are some groups actively doing theoretical research on the synergy between phage treatments and the immune system, as well as research on how the appearance of antibiotic resistance could be attenuated by the use of phages. ...


1

The answer is no. The antibiotic will kill all the bacteria it's intended to target, unless a special resistive variant cell(s) exist. What this means is that it is possible that non-resistive cells are not present. Also bear in mind that it's not the drug that induces the mutation, rather it just isolates and funnels the randomly generated mutant (if ...


1

Yes. It is down to mutations. DNA replication is not 100% accurate, there will be mistakes that are not corrected in the progeny produced. Antibiotics works like a bit of gunk wedging itself into the machine of a bacteria cell but avoids jamming a human cell due to that very same shape. Gunk that wedges into both human and bacteria machines is just a ...


1

As @swbarnes says: Every time you expose a population of bacteria to an antibiotic, you select for organisms with resistance-granting genes. But you're asking about the situation where you're not 'sick' when you're taking them, and how it affects future infections. To understand why that's a bad thing, you need to understand a couple more things. ...


1

Every time you expose a population of bacteria to an antibiotic, you select for organisms with resistance-granting genes. Bacteria can pass plasmids full of genes back and forth. So if you get a nasty E.coli infection, do you really want one of your usual bacteria with a resistance-granting gene sitting right next to it? Let's say you are so sick you go ...


1

This is not a proper answer as such and it's based on a bit of an 'educated guess' but it was too long for a comment. I did however, find this article. Unsurprisingly, one of the big drivers of using surrogate antibiotics is down to availability and cost. Some antibiotics, while known about, may not be produced commercially at scale, or be widespread enough ...


1

The answer is actually a lot simpler. Antibacterials are the most commonly used antimicrobials by far and a consequence of this is that many people use antimicrobrial and antibacterial interchangably. You're right that antimicrobials are substances that target microorganisms such as bacteria, archaea, viruses, and eukaryotes. As stated earlier, the reality ...


1

The relative placement of genes on a plasmid should not affect their expression. Both will be expressed and to what extent is dependent on the strength of the promoters and a few other factors like codon availability. However where you ultimately plan to express these genes can be an important consideration in plasmid design. For example, if you are ...


1

Of course bacteria can evolve resistance against antiseptics. Usually antiseptics inflict direct damage to the cell rather than interfering in some biochemical pathway. Also, antiseptics are used in very high concentrations which usually leads to complete elimination of the microbes. Moreover, different antiseptic/disinfectant agents have different toxicity ...


1

The major effect of drugs or antibiotics on bacterium is on its cell wall. Gram positive bacteria have a thick outer layer of a polymer called peptidoglycan (formed by repeated units of a disaccharide: NAG-NAM) which has many cross-linkages. Beta-lactam antibiotics such as penicillin, cephalosporin etc. competitively inhibit an enzyme called transpeptidase (...


1

I assume from your question (and your pseudonym) that you are confused by terminology. Our adaptive immune system does not make antibiotics, it makes antibodies. Antibiotics are small molecules that interfere with bacterial metabolism. Antibodies are proteins that recognise foreign macromolecules. (You could regard both as “anti-bacterials” — perhaps this is ...


1

Since people and animals routinely get sick, it is obvious that our immune system (which includes but isn't limited to antibodies) doesn't always protect against pathogens. There are many reasons for this, far too many to summarize here, but one common reason is that it takes several days for the adaptive part of the immune system (which includes antibodies,...


1

One possibility is that these antibiotics could disrupt your normal gut bacteria. Given that your gut has the surface area of a tennis court and is typically coated with symbiotic microbes, antimicrobial therapies could dramatically change the population dynamics of your gut ecosystem. One might imagine that the immune system of the gut is in homeostasis ...


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