Why do we tell patients to finish antibiotics even after symptoms resolve?

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

ldiot

Full Member
7+ Year Member
Joined
Oct 7, 2015
Messages
1,640
Reaction score
971
I'm told it's to prevent resistant bugs from proliferating and resuming the infection.... but if the bugs are resistant how would continuing the antibiotic that they are resistant to prevent this? If anything wouldn't increasing exposure to antibiotics after the infection has cleared actually increase the incidence of resistance by selecting for resistant bacteria?

Every pharmacist jumps all over this like it's some major counseling point to complete the course of antibiotics but in terms of resistance I think taking unnecessary antibiotics would do more harm than good.

Perhaps symptoms may resolve before all of the infectious bacteria is killed in which case it would make sense to continue the antibiotics... but this has absolutely NOTHING to do with resistance. Using resistance as the rationale seems completely ass backwards. One of the ID physicians says patients should stop taking them as soon as symptoms resolve, while other professors say the opposite.

Members don't see this ad.
 
Does your school not teach you things?
 
  • Like
Reactions: 11 users
Just because you don't have symptoms, doesn't mean the bacteria has been completely annihilated.
 
  • Like
Reactions: 3 users
Members don't see this ad :)
In other words I'm correct, it has nothing to do with resistance.

No need to be a ****ing dick
 
It does have to do with resistance...the antibiotics kill susceptible organisms while your body's immune system fights off the rest. You are selecting for the mutans. Not killing all the bacteria allows them to multiply and mix their genomes...
 
  • Like
Reactions: 2 users
In other words I'm correct, it has nothing to do with resistance.

No need to be a ****ing dick
Think of it this way, if you take half the antibiotic course you will kill the bacteria that is most susceptible and leave the lesser susceptible bacteria alive. That's why we say it can increase resistance. You need to kill all the bacteria on the first course to avoid needing a second course.

In truth it really is more about effectiveness than resistance but resistance still plays a role. If you think it through it makes sense.

Also what prescriber told you it's okay to stop when symptoms resolve? That dude is way out in left field.

Sent from my SAMSUNG-SM-G920A using SDN mobile
 
  • Like
Reactions: 1 users
Think of it this way, if you take half the antibiotic course you will kill the bacteria that is most susceptible and leave the lesser susceptible bacteria alive. That's why we say it can increase resistance. You need to kill all the bacteria on the first course to avoid needing a second course.

In truth it really is more about effectiveness than resistance but resistance still plays a role. If you think it through it makes sense.

Also what prescriber told you it's okay to stop when symptoms resolve? That dude is way out in left field.

Sent from my SAMSUNG-SM-G920A using SDN mobile

ID physician that gave the lecture. Also said that switching to more narrow spectrum once you get a culture is pointless if the susceptibility is the same. Guy is a professor at an ivy league med school.
 
Last edited:
Let's say the symptoms resolve halfway through your course. You've knocked out the majority of your infection (susceptible bacteria), but have left a few more (intermediate bacteria). You could finish the course and kill them, or take your chances. If the infection takes hold again, you may now be dealing with an intermediate colony that could take a longer course of antibiotics to clear up. More exposure to the drug over a longer period of time increases the chances of resistance forming, especially when dealing with large populations over time.

Just tell them it's to make sure you completely clear away the infection and call it a day.
 
  • Like
Reactions: 3 users
ID physician that gave the lecture. Also said that switching to more narrow spectrum once you get a culture is pointless if the susceptibility is the same. Guy is a professor at an ivy league med school.
He was either trolling or severely misinformed. I will say that ID physicians are often some of the most negligent when it comes to antibiotic stewardship.

Then again there are pharmacist who think that antibiotic resistance is a myth to begin with so you can find Coco's on both sides. Or pharmacist who think that vaccines are a scam.

Sent from my SAMSUNG-SM-G920A using SDN mobile
 
  • Like
Reactions: 1 users
There was a new study recently published in JAMA pushing towards discontinuing therapy after symptoms resolve. If you follow idstewardship on social media he posts some pretty interesting stuff regarding antibiotics.
 
  • Like
Reactions: 3 users
ID physician that gave the lecture. Also said that switching to more narrow spectrum once you get a culture is pointless if the susceptibility is the same. Guy is a professor at an ivy league med school.
Not switching to narrow spectrum would be fine if there was only one bacterial genome being exposed to the antibiotic. That is very unlikely to be the case.
 
  • Like
Reactions: 1 users
There was a new study recently published in JAMA pushing towards discontinuing therapy after symptoms resolve. If you follow idstewardship on social media he posts some pretty interesting stuff regarding antibiotics.
What was the rationale? Preventing superinfection?
 
I'm not sure why people got so hostile in this thread. There's still a lot of things we do in medicine that don't have the strongest evidence (or in many cases, any evidence at all), and there's nothing wrong with asking about the actual evidence for the suggestions we make. If it's solid medicine, there should be plenty of evidence to back it up.

Ideas in medicine change all the time; even things that we think make sense often change and we find out that our hunches were wrong. Everyone's favorite example of this is probably beta blockers being contraindicated in heart failure.

A quick search turned up this:
https://www.mja.com.au/journal/2015/202/3/knowing-when-stop-antibiotic-therapy
which seems to indicate that this is a controversial topic, and it may be a misconception that stopping therapy early leads to resistance. I'm not an expert in ID, so maybe someone who is can comment more on this.
 
  • Like
Reactions: 2 users
Members don't see this ad :)
Microorganisms evolve fast. There are new ones emerging all the time. Even if the older ones are already resistant, you don't want to challenge the new guys but not kill them. By the way, why are you so angry? It's okay there are things you don't understand.


In other words I'm correct, it has nothing to do with resistance.

No need to be a ****ing dick
 
There was a new study recently published in JAMA pushing towards discontinuing therapy after symptoms resolve. If you follow idstewardship on social media he posts some pretty interesting stuff regarding antibiotics.

My DI skills have clearly diminished since school- link please?
 
I'll be an angry person for 2 more week... then this class will be over :D
 
Not to nit-pick, but they actually did not stop therapy as soon as symptoms resolved, right? They stopped after 5 days if the symptoms were resolved for at least 48 hours. So yes the duration was shorter but it still wasn't "stop once symptoms resolve". (If I am reading the abstract correctly)
 
  • Like
Reactions: 1 users
Not to nit-pick, but they actually did not stop therapy as soon as symptoms resolved, right? They stopped after 5 days if the symptoms were resolved for at least 48 hours. So yes the duration was shorter but it still wasn't "stop once symptoms resolve". (If I am reading the abstract correctly)

I was thinking about this some more... I guess this may apply more to hospitals where resistance is more a problem but if you treat with multiple antibiotics wouldn't this lower resistance? Say for example you have a bug that is susceptible to everything. You could give the patient a beta lactam + a quinolone... if the bug has a mutation in the penicillin binding protein or produces beta lactamases it would still be killed the the quinolone and therefore the beta lactam resistance would not be selected for. An added bonus would be more coverage for empiric treatments. Maybe they already do this, I have no idea. I guess if the method of resistance was lower permeability of the cell wall or capsule it wouldn't help... and I suppose a lot of the resistance already exists and is transmitted from bug to bug so the problem now is treating already resistant bugs as opposed to just preventing their emergence. In other words the problem isn't that the bacteria are mutating so much as the resistance genes already exist and are transmitted by plasmid, not only from cell to cell but even from species to species in some cases.
 
I was thinking about this some more... I guess this may apply more to hospitals where resistance is more a problem but if you treat with multiple antibiotics wouldn't this lower resistance? Say for example you have a bug that is susceptible to everything. You could give the patient a beta lactam + a quinolone... if the bug has a mutation in the penicillin binding protein or produces beta lactamases it would still be killed the the quinolone and therefore the beta lactam resistance would not be selected for. An added bonus would be more coverage for empiric treatments. Maybe they already do this, I have no idea. I guess if the method of resistance was lower permeability of the cell wall or capsule it wouldn't help... and I suppose a lot of the resistance already exists and is transmitted from bug to bug so the problem now is treating already resistant bugs as opposed to just preventing their emergence. In other words the problem isn't that the bacteria are mutating so much as the resistance genes already exist and are transmitted by plasmid, not only from cell to cell but even from species to species in some cases.
The problem then is while you're treating only one bug, the human body has however many hundreds of other kinds that will be "treated". So you might not select for resistance in the exact bug causing your infection, but you might select for resistance in another bug. Also, multiple antibiotics encourages things like c.diff, which is ****ty.
 
  • Like
Reactions: 1 users
I have noticed a gradual shift towards lower duration of treatment. The IDSA, for example, now only suggests 7 days for sinus infections, 3-5 days for UTI depending on whether its macrobid or not, and some new evidence that says 5 days for uncomplicated cellulitis.
 
  • Like
Reactions: 1 user
I was thinking about this some more... I guess this may apply more to hospitals where resistance is more a problem but if you treat with multiple antibiotics wouldn't this lower resistance? Say for example you have a bug that is susceptible to everything. You could give the patient a beta lactam + a quinolone... if the bug has a mutation in the penicillin binding protein or produces beta lactamases it would still be killed the the quinolone and therefore the beta lactam resistance would not be selected for. An added bonus would be more coverage for empiric treatments. Maybe they already do this, I have no idea. I guess if the method of resistance was lower permeability of the cell wall or capsule it wouldn't help... and I suppose a lot of the resistance already exists and is transmitted from bug to bug so the problem now is treating already resistant bugs as opposed to just preventing their emergence. In other words the problem isn't that the bacteria are mutating so much as the resistance genes already exist and are transmitted by plasmid, not only from cell to cell but even from species to species in some cases.

There's two problems essentially with multi-antibiotic treatment after you've already received cultures and sensitivities. First is obviously cost: why have the patient pay for more when usually one will suffice. This doesn't necessarily mean the drug alone but also testing and monitoring that may be required for certain antiobiotics (vanc is usually ~$4 a bag but ~$100 for the blood levels). Second is side effects: more antibiotics mean more likelihood of having adverse effect from a drug. Getting C. diff is definitely not fun.

But yes, some disease states do require multiple drug regimens due to inherent resistances. Why you wouldn't want to do this regularly, in terms of "decreasing mutations", is that we don't live in an ideal world. Patients don't always stay on their meds, now instead of now being resistant to 1 med, they're now resistant to two. Sometimes patients don't fix whatever situation cause their infection in the first place (wiping the wrong way, unsanitary beds, ect). Maybe even the nurses of pharmacists miss a dose or give the wrong antibiotic.
 
  • Like
Reactions: 1 users
I have noticed a gradual shift towards lower duration of treatment. The IDSA, for example, now only suggests 7 days for sinus infections, 3-5 days for UTI depending on whether its macrobid or not, and some new evidence that says 5 days for uncomplicated cellulitis.

Many ID HCPs both domestically and internationally are now leaning towards NOT giving instructions to "finish the course no matter what." Instead, we've adjusted to saying "do not stop taking your abx without permission from your hcp" (also problematic for several reasons). But the rationale is that many of the durations of therapy are arbitrary and unnecessary, even for the purpose of slowing abx resistance.
 
I was thinking about this some more... I guess this may apply more to hospitals where resistance is more a problem but if you treat with multiple antibiotics wouldn't this lower resistance? Say for example you have a bug that is susceptible to everything. You could give the patient a beta lactam + a quinolone... if the bug has a mutation in the penicillin binding protein or produces beta lactamases it would still be killed the the quinolone and therefore the beta lactam resistance would not be selected for. An added bonus would be more coverage for empiric treatments. Maybe they already do this, I have no idea. I guess if the method of resistance was lower permeability of the cell wall or capsule it wouldn't help... and I suppose a lot of the resistance already exists and is transmitted from bug to bug so the problem now is treating already resistant bugs as opposed to just preventing their emergence. In other words the problem isn't that the bacteria are mutating so much as the resistance genes already exist and are transmitted by plasmid, not only from cell to cell but even from species to species in some cases.
This is the basis for HIV and TB regimens. When our drug choices are very limited and resistance occurs easily we work harder to prevent it.
 
  • Like
Reactions: 1 user
I have noticed a gradual shift towards lower duration of treatment. The IDSA, for example, now only suggests 7 days for sinus infections, 3-5 days for UTI depending on whether its macrobid or not, and some new evidence that says 5 days for uncomplicated cellulitis.
7 days for HAP/VAP as well regardless of the causative organism.
 
Another thought is the harm of leftover abx being used. For example, if the 7 day course is stopped on day 5, who knows what becomes of those 2 days of remaining pills? I'm certain that taking a few extra days to make a longer course of therapy would select for less resistance than a short course followed by an even shorter, not prescribed, completely unsupervised course.
 
  • Like
Reactions: 1 user
Remember, medicine is art as much as it is a science. A great deal of the standards we go by are not supported by more than clinical experience. That being said, we should not arbitrarily change what we have observed over the years without good clinical data. It's not like we made up this stuff (though maybe we did 50 years ago). I once asked my kids pediatrician about the need for 10 days of Penicillin for strep throat and was told the throat was probably cleansed of strep in 48 hours, but the he had no data to backup a reduction of risk of SBE or other sequale of strep so stay with the 10 days. That was 25 years ago. I don't know what he would say today. Acute vaginal candidiasis was treated with Miconazole for 14 days. Once that data showed that 7 days was sufficient, we had Monistat-7. (1/2 the size, only 40% less in price, drug companies have always been pigs.)

Unless you have the diagnosis and good hard data to back it up, it's best to stick with current recommendations until we have good clinical data to back up our ideas. UTI is a perfect example. It certainly appears 3 days is enough, but I would be hard pressed to assert that someone who was prescribed 5 days to 10 days should stop once they no longer have symptoms.

In the abstract, this is a good question to kick around. Where the rubber meets the road, stick with the tried and true until we have more and better information.
 
  • Like
Reactions: 2 users
But yes, some disease states do require multiple drug regimens due to inherent resistances. Why you wouldn't want to do this regularly, in terms of "decreasing mutations", is that we don't live in an ideal world. Patients don't always stay on their meds, now instead of now being resistant to 1 med, they're now resistant to two. Sometimes patients don't fix whatever situation cause their infection in the first place (wiping the wrong way, unsanitary beds, ect). Maybe even the nurses of pharmacists miss a dose or give the wrong antibiotic.
Not to be picky, but patients do not become resistant, bacteria become resistant.
 
  • Like
Reactions: 1 user
Top