Sophie.cerys
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Will one antibiotic kill all different types of bacteria? I.e. would penicillin and vancomycin for example both cure tuberculosis? Or does each antibiotic have a specific disease it cures?
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username2998742
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(Original post by Sophie.cerys)
Will one antibiotic kill all different types of bacteria? I.e. would penicillin and vancomycin for example both cure tuberculosis? Or does each antibiotic have a specific disease it cures?
I'm not 100% sure of this but I'm following this thread coz I'm doing tuberculosis antibiotic resistance for my EPQ. As far as I know Rifampicin, Isoniazid, Pyrazinamide and Ethambutol are used to treat TB but I'm not sure so I'll leave it to someone else to properly answer.
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Jpw1097
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(Original post by Sophie.cerys)
Will one antibiotic kill all different types of bacteria? I.e. would penicillin and vancomycin for example both cure tuberculosis? Or does each antibiotic have a specific disease it cures?
There is no antibiotic that kills all different types of bacteria. Different antibiotics target different types of bacteria, for example, some antibiotics are good at killing gram-positive bacteria while not so good at killing gram-negative bacteria and vice versa. However, certain infections are typically treated using a particular antibiotic or antibiotic family (penicillin is a family of antibiotics). Using your example of penicillin, cellulitis (a skin infection) is usually treated with flucloxacillin (a type of penicillin) as it is good at killing staphylococcal aureus - the organism that usually causes cellulitis, as well as other skin infections. Bacterial tonsillitis is usually treated with phenoxymethylpenicillin (another type of penicillin) as it is good at killing streptococcus pyogenes, the bacterium that usually causes bacterial tonsillitis. Amoxicillin is usually used to treat pneumonia and middle ear infections as it is good at killing streptococcus pneumoniae - the usual culprit in these infections. Amoxicillin would be no good at treating tonsillitis or cellulitis as it doesn't work against these organisms.
The choice of antibiotic depends on the causative organism. And just because a particular type of antibiotic works against one strain of bacteria, that does not mean it will work against all strains as different bacteria within the same species can be resistant to a particular antibiotic. For example, as I've mentionned, flucloxacillin is used to treat most cases of cellulitis. However, some strains of staphylococcus aureus are resistant to flucloxacillin, and these bacteria are known as methicillin-resistant staph aureus, or MRSA (which you've probably heard of), which is treated with vancomycin instead.
So antibiotic choice is not only guided by the causative organism, but it also depends on what antibiotics the particular strain is sensitive to. So one antibiotic can potentially kill many different species of bacteria, and one species of bacteria can be killed by several different antibiotics.
Also, penicillin and vancomycin would not work against TB; TB is quite an odd bacterium requiring several atypical antibiotics.
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Jpw1097
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(Original post by HowToBeABlobfish)
I'm not 100% sure of this but I'm following this thread coz I'm doing tuberculosis antibiotic resistance for my EPQ. As far as I know Rifampicin, Isoniazid, Pyrazinamide and Ethambutol are used to treat TB but I'm not sure so I'll leave it to someone else to properly answer.
Yes, you're right. The standard regimen for TB is isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months followed by 4 months of just isonazid and pyrazinamide, assuming the particular strain of TB is susceptible to these agents. If the strain is resistant to both rifampicin and isoniazid, it is known as multi-drug resistant TB (MDR-TB) which is usually treated with pyrazinamide, ethambutol as well as other drugs such as moxifloxacin/levofloxacin, amikacin, kanamycin, capreomycin, etc. for at least 20 months, though there is now a shorter regimen lasting 9 months. If the strain is resistant to rifamipicin, isoniazid, a fluoroquinolone (i.e. levofloaxin, moxifloxacin or gatifloxacin) and an injectable aminoglycoside (e.g. capreomycin, amikacin, etc.) it is classed as extensively drug resistant TB (XDR-TB) and is treated with various other strange agents in addition to whatever agents I've already mentionned that it is susceptible to.
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username2998742
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(Original post by Jpw1097)
Yes, you're right. The standard regimen for TB is isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months followed by 4 months of just isonazid and pyrazinamide, assuming the particular strain of TB is susceptible to these agents. If the strain is resistant to both rifampicin and isoniazid, it is known as multi-drug resistant TB (MDR-TB) which is usually treated with pyrazinamide, ethambutol as well as other drugs such as moxifloxacin/levofloxacin, amikacin, kanamycin, capreomycin, etc. for at least 20 months, though there is now a shorter regimen lasting 9 months. If the strain is resistant to rifamipicin, isoniazid, a fluoroquinolone (i.e. levofloaxin, moxifloxacin or gatifloxacin) and an injectable aminoglycoside (e.g. capreomycin, amikacin, etc.) it is classed as extensively drug resistant TB (XDR-TB) and is treated with various other strange agents in addition to whatever agents I've already mentionned that it is susceptible to.
Thanks for doing half of my EPQ research for me!

Seriously though, that makes sense, thanks a lot
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macpatgh-Sheldon
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Excellent answer by our young medic @Jpw1097! May I add a few points that might help both @Sophie.cerys and @HowToBeABlobfish, Sophie cos she seems to have an eye for detail like JPW and myself, and Fish cos he/she needs detail for EPQ.A)
A) When a patient presents to the clinician with symptoms + signs of an infection, especially when it is not easy to tell which organism might be causing the infection, and whether or not it might be resistant to certain antibiotics, the clinician will FIRST TAKE A SAMPLE of the affected tissue (blood, urine, sputum, etc.) and send it off to the lab, then prescribe a broad-spectrum antibiotic (which is known to be effective against a range of gram +ve and -ve bacteria, NOT ALL AS JPW pointed out) e.g. ampicillin, amoxycillin, etc to get some antibacterial activity started off [empirical therapy].Once the result from the lab provides detail of the offending bacterium [which is NOT killed off as the sample was taken before empirical therapy commenced] AND ITS SENSITIVITY to various antibiotics [determined by the size of the area of inhibition on the culture plate] are known, then the best antibiotic specific for that infection [depending on identity of bacterium, sensitivity and several other factors] is added [definitive therapy].
B) The effects of several drugs in clinical pharmacology, in particular the use of more than one agent, depend on the fact that the 2 drugs will have different mechanisms of action, and the joint effects are synergistic (where 2+2 is not 4 BUT is 5 or 6, i.e. the effect is more than summative) e.g. sulphamethoxazole (a sulphonamide) and trimethoprim are two antibiotics that block different steps in bacterial dihydrofolate metabolism, and the two together (cotrimoxazole) have an enhanced antibacterial activity.
C) Some antibiotics are bactericidal (kill bacteria - cide = killing as in homicide OR suicide), others are bacteriostatic (just prevent multiplication and growth). It is important not to prescribe a combination of these two types, as the action of one is hampered by the other.
D) Bacteria develop resistance to antibiotics in various ways, mostly through mutations that provide selective survival of resistant strains e.g. some staphylococci and other bacteria produce a variant version of PBP [penicillin binding protein] that prevents entry of the drug into the bacterial cell, thus making it ineffective.Hope this adds to the superb info provided by JPW.

M
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RegisteredBMS
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(Original post by macpatgh-Sheldon)
Excellent answer by our young medic @Jpw1097! May I add a few points that might help both @Sophie.cerys and @HowToBeABlobfish, Sophie cos she seems to have an eye for detail like JPW and myself, and Fish cos he/she needs detail for EPQ.A)
A) When a patient presents to the clinician with symptoms + signs of an infection, especially when it is not easy to tell which organism might be causing the infection, and whether or not it might be resistant to certain antibiotics, the clinician will FIRST TAKE A SAMPLE of the affected tissue (blood, urine, sputum, etc.) and send it off to the lab, then prescribe a broad-spectrum antibiotic (which is known to be effective against a range of gram +ve and -ve bacteria, NOT ALL AS JPW pointed out) e.g. ampicillin, amoxycillin, etc to get some antibacterial activity started off [empirical therapy].Once the result from the lab provides detail of the offending bacterium [which is NOT killed off as the sample was taken before empirical therapy commenced] AND ITS SENSITIVITY to various antibiotics [determined by the size of the area of inhibition on the culture plate] are known, then the best antibiotic specific for that infection [depending on identity of bacterium, sensitivity and several other factors] is added [definitive therapy].
B) The effects of several drugs in clinical pharmacology, in particular the use of more than one agent, depend on the fact that the 2 drugs will have different mechanisms of action, and the joint effects are synergistic (where 2+2 is not 4 BUT is 5 or 6, i.e. the effect is more than summative) e.g. sulphamethoxazole (a sulphonamide) and trimethoprim are two antibiotics that block different steps in bacterial dihydrofolate metabolism, and the two together (cotrimoxazole) have an enhanced antibacterial activity.
C) Some antibiotics are bactericidal (kill bacteria - cide = killing as in homicide OR suicide), others are bacteriostatic (just prevent multiplication and growth). It is important not to prescribe a combination of these two types, as the action of one is hampered by the other.
D) Bacteria develop resistance to antibiotics in various ways, mostly through mutations that provide selective survival of resistant strains e.g. some staphylococci and other bacteria produce a variant version of PBP [penicillin binding protein] that prevents entry of the drug into the bacterial cell, thus making it ineffective.Hope this adds to the superb info provided by JPW.

M
Can I add to this as somebody who works in this area. It's not possible to tell, clinically, what the organism is, nor whether it will or won't be resistant to certain antibiotics. They will know what organisms usually cause said type of infection. This is very varied and can include a mixture of gram positive and negative bacteria which both require very different antibiotics and can have various resistance mechanisms including intrinsic resistance. Treatment is blind until a laboratory result is sought hence the use of broad spectrum treatment.

"Whether it might or might not be resistance to certain antibiotics" it's more that some bacteria are 'built' in a way in which certain antibiotics won't work such as the cell wall difference between gram pos/neg bacteria.
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nexttime
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(Original post by Sophie.cerys)
Will one antibiotic kill all different types of bacteria? I.e. would penicillin and vancomycin for example both cure tuberculosis? Or does each antibiotic have a specific disease it cures?
There are literally hundreds of doctors who have trained for >12 years whose entire profession consists of deciding which antibiotic to use for which patients. Don't let them hear you ask that! :p:

(Original post by Jpw1097)
Using your example of penicillin, cellulitis (a skin infection) is usually treated with flucloxacillin (a type of penicillin) as it is good at killing staphylococcal aureus - the organism that usually causes cellulitis, as well as other skin infections.
And a whole variety of other non-skin infections!

Amoxicillin would be no good at treating tonsillitis or cellulitis as it doesn't work against these organisms.
Actually yes it would probably be fine for both! :p:

Its generally reserved though as amoxicillin is very broad spectrum and we want to try to limit the already widespread resistance to it. It also isn't quite as good against S.Aureus as fluclox, but it will do the job in most cases.

So antibiotic choice is not only guided by the causative organism, but it also depends on what antibiotics the particular strain is sensitive to.
It can also depend on site directly, of course. For example, mitrofuratoin gets concentrated in the urine, so its only used for UTIs. Daptomycin is very broad spectrum with great resistance profiles, but its inactivated by lung surfactant so can't be used for chest infections. Many antibiotics don't cross the blood-brain barrier, etc.

(Original post by macpatgh-Sheldon)
C) Some antibiotics are bactericidal (kill bacteria - cide = killing as in homicide OR suicide), others are bacteriostatic (just prevent multiplication and growth). It is important not to prescribe a combination of these two types, as the action of one is hampered by the other.
I mean, not really. I've never seen that be of relevance in clinical practice.

For example probably the most common combination of antibiotics used nationwide is amoxiciliin and clarithromycin for pneumonia - the former being bacteriocidal and the latter being bacteriostatic.

Biology examiners do love the distinction though and it was worth pointing out!
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RegisteredBMS
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(Original post by nexttime)
I mean, not really. I've never seen that be of relevance in clinical practice - whether its dead or just not reproducing... same difference really.

For example probably the most common combination of antibiotics used nationwide is amoxiciliin and clarithromycin for pneumonia - the former being bacteriocidal and the latter being bacteriostatic.
I missed that bit of his post. The combination of cidal and static antibiotics is important. If you give somebody a static antibiotic then, as long as they're healthy, their immune system will do the rest in most cases. The combination of cidal and static antibiotics is vital in the cases of immunocomprimised patients and is an area it is commonly used. I'm unsure where the idea that it should be avoided as come from, it's a common tactic where treatment is failing or predicted to fail.
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nexttime
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(Original post by RegisteredBMS)
The combination of cidal and static antibiotics is vital in the cases of immunocomprimised patients and is an area it is commonly used.
? No its not. Nationwide the most common regimen for neutropenic sepsis is tazocin monotherapy i.e. bacteriocidal only.

You could possibly argue that using bacteristatic therapy alone might not be a good idea. I am not aware of any actual evidence though - most bacteriostatic agents don't lend themselves very well spectrum-wise, side effect-wise or administration-wise to treating infected, potentially septic immunocompromised patients!

I'm unsure where the idea that it should be avoided as come from...
It does make logical sense (many bacteriocidal antibiotics still work in areas that will be more prominently used if the bacteria are replicating) and I think it might even have some experimental data. However in practice its just entirely secondary to locally observed resistance profiles and other factors.
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RegisteredBMS
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(Original post by nexttime)
? No its not. Nationwide the most common regimen for neutropenic sepsis is tazocin monotherapy i.e. bacteriocidal only.

You could possibly argue that using bacteristatic therapy alone might not be a good idea. I am not aware of any actual evidence though - most bacteriostatic agents don't lend themselves very well spectrum-wise, side effect-wise or administration-wise to treating infected, potentially septic immunocompromised patients!



It does make logical sense (many bacteriocidal antibiotics still work in areas that will be more prominently used if the bacteria are replicating) and I think it might even have some experimental data. However in practice its just entirely secondary to locally observed resistance profiles and other factors.
I work with a Trust that is one the largest cancer treatment centres in Europe, static and cidal is commonly used for the reasons I stated.
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(Original post by RegisteredBMS)
I work with a Trust that is one the largest cancer treatment centres in Europe, static and cidal is commonly used for the reasons I stated.
In the UK I take it.

I ask as NICE specifically recommends using tazocin alone, so it would be odd for such a large specialist centre to be operating outside of guidance!

I did another quick check and I can't find any recent publications which advocate combination therapy. UpToDate, which is normally pretty good at picking up niche/emerging ideas, doesn't mention it at all. It does talk about combination therapy, but from a resistance standpoint. It says "Numerous combination antibiotic regimens have been studied as initial empiric therapy in neutropenic fever, but none has been shown to be clearly superior to others or to monotherapy". American sources agree, with all suggested regimes being monotherapy.

So yeah, your hospital seems to be doing something quite atypical. Do you know the specific evidence their approach is based on? When you say they use "static and cidal" - do you know what the 1st line empirical guidance is?

Edit: Oh and here is a paper about why using both static and cidal is bad due to pharmacological antagonism https://aac.asm.org/content/58/8/4573
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Jpw1097
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(Original post by nexttime)
And a whole variety of other non-skin infections!
Of course, fluclox is a good anti-staph agent.

(Original post by nexttime)
Its generally reserved though as amoxicillin is very broad spectrum and we want to try to limit the already widespread resistance to it. It also isn't quite as good against S.Aureus as fluclox, but it will do the job in most cases.
I accept your point about amoxicillin for strep pyogenes. However, beta-lactamse producing staph aureus are quite prevalent and so I can't imagine amoxicillin would be very effective in most cases - in fact, I think most strains are resistant to penicillins (with the exception of the beta-lactamase stable penicillins).
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nexttime
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(Original post by Jpw1097)
I accept your point about amoxicillin for strep pyogenes. However, beta-lactamse producing staph aureus are quite prevalent and so I can't imagine amoxicillin would be very effective in most cases - in fact, I think most strains are resistant to penicillins (with the exception of the beta-lactamase stable penicillins).
Quite prevalent = about 25% in the community, so "most cases" is not wrong!

Its also not wrong because most infections will resolve themselves even without antibiotics, of course!

But I agree it would be a weird choice. I have only seen it a handful of times, all by GPs.
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Jpw1097
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(Original post by nexttime)
Quite prevalent = about 25% in the community, so "most cases" is not wrong!

Its also not wrong because most infections will resolve themselves even without antibiotics, of course!

But I agree it would be a weird choice. I have only seen it a handful of times, all by GPs.
An Australian study of hospital inpatients showed that 80-90% of MSSA isolates are resistant to penicillin:
https://www.researchgate.net/publica...ial_Resistance

I'm not sure what the resistance rate is in the community in the UK, I'm struggling to find specific figures, but I can't imagine it would be as low as 25% but I could be wrong.
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TheGraduateMedic
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There’s a good ted talk on spider venom being the future of combating MRSA - quite interesting!
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