Question about antibiotic resistance in S. aureus

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newslang

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All this talk in the media lately about MRSA got me thinking: Could oral antibiotic use in a person colonized, but not infected with S. aureus contribute to its antibiotic resistance? This is referencing nasal colonization mainly.

I am not a pharmacy student yet and I'm not trying to get anybody to answer a homework question. This is just a random thought.

Edit: see my next post in this thread for clarification of the question

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All this talk in the media lately about MRSA got me thinking: Could oral antibiotic use in a person colonized, but not infected with S. aureus contribute to its antibiotic resistance? This is referencing nasal colonization mainly.

Don't really understand the colonization and infection difference....isn't colonization infection? or do you mean as a disseminated effect.....maybe I can understand and put in a thought on your question if you could be a little explicit...
 
I think you are correct. Since S. aureus both resistant to Methacillin and not susceptible can be normal flora. If these normal pathogens i guess you could call them were to be exposed to a drug such that it could activate the gene for resistance I think it would be possible. I think it would happen at a low level though. the man problem is prescribing of medications and treatment adhearance. I did a study with Group A strep. and resistance a few years ago. our study found that there is a significant increase in resistance with this organism to erthromycin and clindamycin. In fact the only reason these drugs are used are because some people are allergic to penicillin. Now i said SOME. Penicillin G is known to be 100% effective against this bug. wouldnt it be easyer to give this out more? It would prevent the resistance from increasing. Why not ask all patients if they are allergic to pen. Most likely if they are 20 yrs or older have been exposed to pen. and know if they are allergic. I dont want to get into the ethics but theortically we need to stop this slack prescribing. GOOD question that you asked.
 
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Resistance has gone up but many medical doctors still prescribe the same dose as 20 years ago. The low dose only selects out resistance organisms and contributes to higher resistance.
 
Colonization refers to the presence of bacteria which are not causing disease. S. aureus often lives in people's noses without causing disease. Another example of a potential pathogen that can live inside us would be C. difficile, which can asymptomatically colonize the intestine. In the case of C. dif, administration of an antibiotic (at least a PO one) clearly could encourage some kind of resistance.

On the other hand, S. aureus lives most happily in the nose. This kind of colonization is normally treated with a topical antibiotic (mupirocin I think).

I guess it's a question of tissue penetration. Would any PO antibiotic have an effect on bacteria growing inside your nose? Is this surface any different from that of the skin in that regard?
 
Isn't colonization infection?

What in the hell are you talking about son??? This might be the worst question I have read in years.
 
I think you are correct. Since S. aureus both resistant to Methacillin and not susceptible can be normal flora. If these normal pathogens i guess you could call them were to be exposed to a drug such that it could activate the gene for resistance I think it would be possible. I think it would happen at a low level though. the man problem is prescribing of medications and treatment adhearance. I did a study with Group A strep. and resistance a few years ago. our study found that there is a significant increase in resistance with this organism to erthromycin and clindamycin. In fact the only reason these drugs are used are because some people are allergic to penicillin. Now i said SOME. Penicillin G is known to be 100% effective against this bug. wouldnt it be easyer to give this out more? It would prevent the resistance from increasing. Why not ask all patients if they are allergic to pen. Most likely if they are 20 yrs or older have been exposed to pen. and know if they are allergic. I dont want to get into the ethics but theortically we need to stop this slack prescribing. GOOD question that you asked.

I can't understand a word that is coming out of your mouth.

For the record, do you mean: methicillin (not capitalized of course, and has been ineffective against S. aureus since 1961 [first reported case of MRSA]), main, adherence, erythromycin, easier, theoretically.

I cannot take anyone serious who fails to spell correctly and communicate in at least semi complete sentences.
 
I think you are correct. Since S. aureus both resistant to Methacillin and not susceptible can be normal flora. If these normal pathogens i guess you could call them were to be exposed to a drug such that it could activate the gene for resistance I think it would be possible. I think it would happen at a low level though. the man problem is prescribing of medications and treatment adhearance. I did a study with Group A strep. and resistance a few years ago. our study found that there is a significant increase in resistance with this organism to erthromycin and clindamycin. In fact the only reason these drugs are used are because some people are allergic to penicillin. Now i said SOME. Penicillin G is known to be 100% effective against this bug. wouldnt it be easyer to give this out more? It would prevent the resistance from increasing. Why not ask all patients if they are allergic to pen. Most likely if they are 20 yrs or older have been exposed to pen. and know if they are allergic. I dont want to get into the ethics but theortically we need to stop this slack prescribing. GOOD question that you asked.

I'm not exactly sure which bug you are referring to but S. aureus has been known to be at least 80% resistant to penicillin since 1960. In fact, today, only 2% of S. aureus are sensitive to this drug.
 
He's a time-traveler, playa. You learn that **** in grad school.

Actually, I learned that in my microbiology class. :D Pretty cool stuff. It got me interested in infectious diseases, really.:)
 
Resistance has gone up but many medical doctors still prescribe the same dose as 20 years ago. The low dose only selects out resistance organisms and contributes to higher resistance.

IMO, doctors are too quick to prescribe newer antibiotics even though some of the older drugs are just as or even more effective than the newer drugs (Not every case need a new antibiotic). For example, in my hospital I'm noticing an increasing use of zyvox and tigecycline. I can't really say that they are improperly using these drugs because I'm not privy to why they are prescribing it in the first place. However, it seems to me that at first we would send out one or two. Now, it seems like we're sending out 5 to 10 a day.
 
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IMO, doctors are too quick to prescribe newer antibiotics even though some of the older drugs are just as or even more effective than the newer drugs (Not every case need a new antibiotic). For example, in my hospital I'm noticing an increasing use of zyvox and tigecycline. I can't really say that they are improperly using these drugs because I'm not privy to why they are prescribing it in the first place. However, it seems to me that at first we would send out one or two. Now, it seems like we're sending out 5 to 10 a day.

The thing with nosocomial MRSA is that the same strains typically get to float around the buildings and such. So it's not crazy at all that you might see a cluster of vanc resistant enterococus or something...
 
What in the hell are you talking about son??? This might be the worst question I have read in years.

Oo ma bad....I didn't understand at first...I see he meant as part of normal flora
 
Nobody has answered my question! You all just made fun of that person with the incoherent post!

Oo ma bad....I didn't understand at first...I see he meant as part of normal flora

Although S. aureus in your nose might not be considered normal flora exactly. It's not causing disease, but if you're immunocompromised or know somebody who's immunocompromised I'm guessing you'd want to treat it just to be safe.
 
Colonization refers to the presence of bacteria which are not causing disease. S. aureus often lives in people's noses without causing disease. Another example of a potential pathogen that can live inside us would be C. difficile, which can asymptomatically colonize the intestine. In the case of C. dif, administration of an antibiotic (at least a PO one) clearly could encourage some kind of resistance.

On the other hand, S. aureus lives most happily in the nose. This kind of colonization is normally treated with a topical antibiotic (mupirocin I think).

I guess it's a question of tissue penetration. Would any PO antibiotic have an effect on bacteria growing inside your nose? Is this surface any different from that of the skin in that regard?


I don't really know how to respond to your question; you seem well-intentioned but it's like you need to take multiple courses to really understand what's going on there, do you know what I mean?

C. Difficile resistance isn't a problem, I don't know where you read that. It's administration of antibiotics that wipe out the entire flora, a la clindamycin, allowing for an overgrowth of C. Difficile, which may progress to copious amounts of diarrhea, pseudomembranous colitis, and eventually be fatal. It is easily treated with metro or vanc.

You don't treat patients because they have Staph Aureus on their skin, nor do you stick topical antibiotics up your nose. And yes, oral antibiotics have a much greater tissue penetration than topical.

To answer yet another question, no you do not treat bacteria that is colonizing unless it is _impairing_ wound healing. Colonizing bacteria is not a pathogen by definition as it is not harming the host, so you don't treat.

Finally, staph aureus IS a part of the flora. That, along with staph epi, strep group A, B, etc coat your skin. Everywhere.
 
I don't really know how to respond to your question; you seem well-intentioned but it's like you need to take multiple courses to really understand what's going on there, do you know what I mean?

C. Difficile resistance isn't a problem, I don't know where you read that. It's administration of antibiotics that wipe out the entire flora, a la clindamycin, allowing for an overgrowth of C. Difficile, which may progress to copious amounts of diarrhea, pseudomembranous colitis, and eventually be fatal. It is easily treated with metro or vanc.

You don't treat patients because they have Staph Aureus on their skin, nor do you stick topical antibiotics up your nose. And yes, oral antibiotics have a much greater tissue penetration than topical.

To answer yet another question, no you do not treat bacteria that is colonizing unless it is _impairing_ wound healing. Colonizing bacteria is not a pathogen by definition as it is not harming the host, so you don't treat.

Finally, staph aureus IS a part of the flora. That, along with staph epi, strep group A, B, etc coat your skin. Everywhere.

I was just guessing about resistance in C. diff. My point was that theoretically resistance could arise because anything taken PO could reach the bacteria.

I know it's a hard question that's why I asked it in a forum frequented by pharmacy students and a couple of clinical pharmacists who seem to post prolifically. To clarify again I'm only asking if any PO antibiotic would even physically reach a bacterium in the nose, where it could, (given other variables which I'm not asking about), potentially cause resistance.

Must be a harder question than I realized, or I wasn't clear originally about how vague of a question it really was.
 
To clarify again I'm only asking if any PO antibiotic would even physically reach a bacterium in the nose, where it could, (given other variables which I'm not asking about), potentially cause resistance.

Must be a harder question than I realized, or I wasn't clear originally about how vague of a question it really was.

Dude, I answered your question. Oral antibiotics have a much greater tissue penetration than topical. Your nose is included.

Taking a PO drug doesn't cause resistance. Subtherapeutic drug levels, incomplete durations of therapies and inappropriate prescribing cause resistance.
 
And keep in mind...MRSA produces mutated PBPs with low affinity for beta-lactam antibiotics (it's not because it can now produce beta-lactamases...or otherwise the anti-staph penicillins would work).

You don't treat patients because they have Staph Aureus on their skin, nor do you stick topical antibiotics up your nose.

:eek: Sure you do!!! Bactroban ointment is oftentimes used to eradicate nasal colonization of S. aureus...it even comes in single-use intranasal tubes!

To the OP, you may be interested in reading this article:

Muller AA, Talon D, Potier A, Belle A, Cappelier G, Bertrand X. Use of intranasal mupirocin to prevent MRSA infection in intensive care units. Crit Care. 2005;9:R246–R250.

There's a commentary in the same issue as well.
 
There are plenty of articles out there detailing the use of mupirocin and chlorhexidine baths as a means of decolonizaiton. At the hospital I worked at we decolonized all patients with mupirocin and chlorhexidine undergoing elective procedures if nasal swabs came back positive. Here's the article if you are interested, "Evanston Northwestern Healthcare (ENH) is the recipient of this year’s John M. Eisenberg Patient Safety and Quality Award. ENH has been recognized for its’ methicillin-resistant Staphylococcus aureus (MRSA) Reduction Program Team.

Evanston Northwestern Healthcare was the first in the country to begin a universal MRSA surveillance program, swabbing all in-patients at its’ three hospitals for the MRSA bacteria beginning in 2005, well before any recommendations from state law-makers. ”The goal of the program was always to reduce the risk of MRSA infection to patients cared for by ENH and all our benchmarks were achieved by the end of the program’s first year,said Lance Peterson, MD, FIDSA, FASCP, Epidemiologist and a founder of the MRSA program at Evanston Northwestern Healthcare. “Everyone at ENH put a lot of effort into this initiative to benefit our patients, and it is really wonderful that ENH as a whole is recognized by this very prestigious award.”

This award, sponsored by the National Quality Forum (NQF) and The Joint Commission, recognizes ENH for local innovation when it comes to patient safety. Evanston Northwestern Healthcare’s MRSA screening program involves performing nasal swabs for colonization during the hospital admission process. A new molecular diagnostic technique called a real-time PCR is used to quickly assess MRSA infection. This allows hospital staff to promptly identify and isolate infected patients.

At its’ three hospitals, ENH has been able to reduce MRSA infection rates by 60% within the first year of the program. Universal MRSA surveillance has also decreased the risk of other patients and staff becoming infected. Peterson indicates that “The biggest risk for getting a MRSA infection is becoming colonized in the nose with it. Our program has successfully prevented nasal colonization of patients coming to ENH for their care. We want people to come here for their healthcare and not go home with something unexpected that will later cause an infection – and the program is successful in doing just that.”

The approach judged by the NQF to be easy to reproduce and cost effective in any organization, has the potential to have a positive impact on the nationally increasing mortality rates and rising costs associated with MRSA infections. Consequently, it would have a commensurate impact on the quality and safety of patient care.

Evanston Northwestern Healthcare’s MRSA Reduction Program Team will soon publish its’ findings in a peer reviewed journal. Members are offering an outreach program to long-term care facilities to help prevent MRSA infection. They are also consulting with various hospitals across the country on how to start similar MRSA surveillance programs.

The patient safety awards program, launched in 2002 by NQF and The Joint Commission, honors John M. Eisenberg, MD, MBA, former administrator of the Agency for Healthcare Research and Quality (AHRQ). Dr. Eisenberg was one of the founding leaders of the NQF and sat on its board of directors."
And keep in mind...MRSA produces mutated PBPs with low affinity for beta-lactam antibiotics (it's not because it can now produce beta-lactamases...or otherwise the anti-staph penicillins would work).



:eek: Sure you do!!! Bactroban ointment is oftentimes used to eradicate nasal colonization of S. aureus...it even comes in single-use intranasal tubes!

To the OP, you may be interested in reading this article:

Muller AA, Talon D, Potier A, Belle A, Cappelier G, Bertrand X. Use of intranasal mupirocin to prevent MRSA infection in intensive care units. Crit Care. 2005;9:R246–R250.

There's a commentary in the same issue as well.
 
I was just guessing about resistance in C. diff. My point was that theoretically resistance could arise because anything taken PO could reach the bacteria.

I know it's a hard question that's why I asked it in a forum frequented by pharmacy students and a couple of clinical pharmacists who seem to post prolifically. To clarify again I'm only asking if any PO antibiotic would even physically reach a bacterium in the nose, where it could, (given other variables which I'm not asking about), potentially cause resistance.

Must be a harder question than I realized, or I wasn't clear originally about how vague of a question it really was.

To answer your "Real Question", yes, oral antibiotics DO physically reach a bacterium in the nose, and could potentially caused resistance due to what above posters said. . . because of non compliance, under dosing, etc.
 
:eek: Sure you do!!! Bactroban ointment is oftentimes used to eradicate nasal colonization of S. aureus...it even comes in single-use intranasal tubes!
That's very true. I've seen several Bactroban scripts that indicate nare application. I don't remember a single-use tube, but I've seen them prescribe the 15g tube.
For whatever reason, there's an abundance of staph infections in this area.
 
That's very true. I've seen several Bactroban scripts that indicate nare application. I don't remember a single-use tube, but I've seen them prescribe the 15g tube.
For whatever reason, there's an abundance of staph infections in this area.

:D

p06314a1.jpg
 
You guys are both right. The single use tubes have been unavailable for awhile (over a year) and now the larger tubes are being dispensed for nasal use. (Assuming the little tubes haven't come back on the market in the last few months since I worked.)
 
You guys are both right. The single use tubes have been unavailable for awhile (over a year) and now the larger tubes are being dispensed for nasal use. (Assuming the little tubes haven't come back on the market in the last few months since I worked.)

No idea about current availability...just wanted to show her what they looked like. ;) The small tubes are nice b/c you can just split the contents into each nostril and be done with it.
 
You guys are both right. The single use tubes have been unavailable for awhile (over a year) and now the larger tubes are being dispensed for nasal use. (Assuming the little tubes haven't come back on the market in the last few months since I worked.)

I see the one gram tubes in my hospital all the time, including very recently (within the last week).
 
To answer your "Real Question", yes, oral antibiotics DO physically reach a bacterium in the nose, and could potentially caused resistance due to what above posters said. . . because of non compliance, under dosing, etc.

But what if the patient is taking an antibiotic for something unrelated to their Staph colonization, let's say oral vancomycin (who knows what for). For the purposes of treating the infection, they've completed their therapy properly. But a relatively small oral dose of vanco may not be enough to get rid of the Staph colonizing the nose.
 
But what if the patient is taking an antibiotic for something unrelated to their Staph colonization, let's say oral vancomycin (who knows what for). For the purposes of treating the infection, they've completed their therapy properly. But a relatively small oral dose of vanco may not be enough to get rid of the Staph colonizing the nose.

Are you effing kidding with some of these posts? What do you mean, "who knows what for?" Vancomycin is only given orally to treat one thing last time I checked. It also is very poorly absorbed from the gastrointestinal tract, so even high doses won't have much of an appreciable effect on Staph in the nares (i.e. eradicating bacteria or influencing resistance patterns). What school do you attend so I can be on the look out for pharmacists from wherever you are (somehow I think it must be West Virginia or somewhere close but that is just off the top of my head).
 
Are you effing kidding with some of these posts? What do you mean, "who knows what for?" Vancomycin is only given orally to treat one thing last time I checked. It also is very poorly absorbed from the gastrointestinal tract, so even high doses won't have much of an appreciable effect on Staph in the nares (i.e. eradicating bacteria or influencing resistance patterns). What school do you attend so I can be on the look out for pharmacists from wherever you are (somehow I think it must be West Virginia or somewhere close but that is just off the top of my head).

Ummmm...

I am not a pharmacy student yet and I'm not trying to get anybody to answer a homework question. This is just a random thought.
 
Are you effing kidding with some of these posts? What do you mean, "who knows what for?" Vancomycin is only given orally to treat one thing last time I checked. It also is very poorly absorbed from the gastrointestinal tract, so even high doses won't have much of an appreciable effect on Staph in the nares (i.e. eradicating bacteria or influencing resistance patterns). What school do you attend so I can be on the look out for pharmacists from wherever you are (somehow I think it must be West Virginia or somewhere close but that is just off the top of my head).

LOL I'm not in pharmacy school as I said in my OP, I'm a just a curious college sophmore working toward a bachelor's. Forgive my ignorance about what oral vanco is used to treat. All I know is that it seems to move off the shelves pretty consistently at the hospital I work at. By saying "who knows what for" I was trying to emphasize that the specifics weren't important, just the general idea.

edit: BTW thanks for all the serious replies
 
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