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This article from the WHO states:

If you stop treatment early, there is a risk the antibiotics won’t have killed all the bacteria that made you sick and that it will mutate and become resistant. This will not happen to everyone – the problem is that we don’t know who can safely stop treatment early.

By taking the full course prescribed by your doctor, even if you start to feel better earlier, you increase the chances of killing all of the bacteria and reduce the risk of resistance.

  1. A clarification: When the WHO says “[bacteria] will mutate and become resistant,” they are implying that using antibiotics will create a selective pressure for bacteria with antibiotic resistance, arising most likely through mutations, correct? Bacteria don’t mutate into antibiotic resistant strains in direct response to a drug; rather, antibiotic resistance is a phenomenon of natural selection. I’ve seen so many articles about antibiotic resistance worded this way and I feel it’s simply wrong.
  2. Presuming I am correct about my first point, here’s my true question: Say you’re prescribed a course of antibiotics. It kills the bacteria that are not resistant to the drug and leaves those that have developed resistance behind. What does it matter if you finish the whole course? Taking more of the drug is not going to affect the resistant strain. The only rationale I can think of is that it would kill off any residual non-resistant bacteria and prevent them from gaining resistance (via conjugation) from the resistant kind. However, is this the only mechanism whereby completing the course prevents the rise of antibiotic resistance? How effective is this at all at preventing the rise of antibiotic resistance in the bacterial population in general (i.e. beyond the host)?
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    $\begingroup$ Good points. Yes, it is worded misleadingly. Resistant bacteria are selected for in the presence of antibiotic. when you stop an antibiotic, levels are still present for a while and it may select for more weakly resistant bacteria (that can survive at low levels of the antibiotic - very common.) Stopping your antibiotic early mainly means you've left a lot of bacteria behind (that colonized part of your body) and reinfection is possible, requiring yet another course of antibiotics. It's the "yet another course" that confers the increased possibility of selection of a resistant strain. $\endgroup$
    – anongoodnurse
    Commented Jul 10, 2016 at 12:14
  • $\begingroup$ "it will mutate" could also be read where "it" is the population of bacteria and not the individual bacterium. $\endgroup$
    – Ashafix
    Commented Jul 10, 2016 at 12:37

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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 other mechanisms such as lateral gene transfer).

Many antibiotics may not kill the resistant strains but may still impose some burden on their growth. Now, with a complete course you would have eradicated a lot of strains and only a few resistant strains would be left. The probability of extinction/eradication depends on how many individuals are present in a population. When you do a complete course, then the chances of extinction of the resistant strains due to random birth-death process (and attack by the immune system) would be high because of their low numbers. However, with an incomplete course these bacteria would quickly expand their population once the antibiotic is gone. Now, with the next round of antibiotic treatment you would have more number of resistant cells to kill. As again pointed out by anongoodnurse, this will lead to further selection of resistant strains.

There are additional factors:

  • Microbial community (colony) is more than just a bunch of cells. They can protect each other.
  • There are some cells called persisters which are not really genetically resistant strains but tolerate the drug because of adaptive phenotypes. Again, the microbial community plays some role here.
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  • $\begingroup$ Furthermore, resistance comes in many strengths. A weakly resistant strain is less likely to die from an incomplete course of antibiotics. But a weakly resistant strain is many more times likely to become a strongly resistant strain... $\endgroup$
    – Aron
    Commented Jul 12, 2016 at 6:21
  • $\begingroup$ @Aron "a weakly resistant strain is many more times likely to become a strongly resistant strain” Why is that so? $\endgroup$
    – lightweaver
    Commented Jul 12, 2016 at 10:45
  • $\begingroup$ @lightweaver Imagine one strain randomly mutates an enzyme that breaks down the antibiotic. But it's a very weakly binding enzyme. Then imagine how much it would take to optimise the enzyme. $\endgroup$
    – Aron
    Commented Jul 12, 2016 at 12:02
  • $\begingroup$ @Aron Could you give an example? Maybe it’s the lack of experience but I’m not quite imagining it. $\endgroup$
    – lightweaver
    Commented Jul 12, 2016 at 14:31
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    $\begingroup$ @lightweaver An enzyme that can break down the antibiotic could requires thousands of mutations. But it might only be good enough to break down half the antibiotic in your blood. So if you take a full course, the bacteria that makes it still dies. However, if it survives a half course...all its rivals are dead. It multiplies, and all the bacteria has a weak immunity. All of them mutates...maybe 10 or so mutations. But out of the trillions of bacteria ONE hits the jack pot, and evolves the 10 mutations required for FULL strong immunity. Congrats, you just killed man kind. $\endgroup$
    – Aron
    Commented Jul 12, 2016 at 14:40

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