How to beat the new superbug NDM-1

[Rob060870]

Hello Members,

I have read the disturbing reports in the various media outlets. . .

"A new gene, NDM-1, emerged which allows bacteria to be highly resistant to almost all antibiotics, scientists have said"

I remember a program which followed a scientist who used Phage therapy, as I understand it bacteriophages evolve unlike antibiotics so, instead of continually trying to find evermore powerfull antibiotics why not use bacteriophages that evolve with and can beat harmfull bacteria?

could anyone on here please explain the processes involved to the layman ie. . me!. and also why its use isn't more widespread?

Thanks

Robert

 

[Borek]

Have you read wikipedia article?

http://en.wikipedia.org/wiki/Phage_therapy

While wiki is not the ultimate source of all knowledge, on a layman's level it usually gives enough basic information. I think the article linked to should answer some of your questions.

 

[physi-man]

Phages aren't as simple as a wonder virus that attacks any bacteria. Like any virus they are specific, so this can be an advantage and disadvantage. Also just because they are also capable of evolving along with bacteria, this does not mean they will evolve along the same path. Bacteria may go one direction on the evolution chain and the phage won't necessarily follow the same path of evolution and keep up.

This isn't the first time a drug resistant bacteria mutation has occured.

 

[nismaratwork]

There are also new therapies targeting the means by which bacteria communicate with each other, and program "healthy" cells. Bacteria evolve, and so do antibiotics (albeit, slower than the former). I see a lot of hope in targeting Secretion Systems however, so I wouldn't invest in the hermetic bubble just yet...

 

[Rob060870]

I was thinking along the lines of an international bacteriophage bank which is constantly updated with information on which phages treat what viruses so that any new ones discovered are able to be put to good use.
Thanks for the interesting input. it just shows how powerfull evolution really is doesn't it?

 

[nismaratwork]

I was thinking along the lines of an international bacteriophage bank which is constantly updated with information on which phages treat certain what viruses so that any new ones discovered are able to be put to good use.
Thanks for the interesting input. it just shows how powerfull evolution really is doesn't it?

Adaptation is a ***** when it comes to pathogens, no doubt.

 

[alxm]

Find an inhibitor that targets the NDM-1 beta-lactamase mutant.
(It actually has reduced catalytic activity, but the antibiotics bind more strongly to it, leading to an overall higher turnover)

 

[nismaratwork]

Find an inhibitor that targets the NDM-1 beta-lactamase mutant.
(It actually has reduced catalytic activity, but the antibiotics bind more strongly to it, leading to an overall higher turnover)

That could definitely be easier said than done, especially given the process to approve and assure that such an inhibitor isn't toxic. Really, that's the problem with all of these solutions; the "bugs" mutate rapidly, and more often we play catch-up.

 

[madcat8000]

The problem with phages is that by the time you have narrowed down the specific kind of phages that would be of benifit to the patient, the doctor could already have used a antibiotic to start treatment. Just not economical.

There are other antibiotics that would be completely immune because they don't attack the cell wall. But in the end we are going to get smacked in the face with these things until every single person in the medical industry learns to observe proper antiseptic techniques. These genes probably pre-exsisted our use of antibiotics. Our overuse of antibiotics and shoveing all the sick people into one building in every city have meerly provided the bacteria that harbor them room to thrive.

 

[nismaratwork]

The problem with phages is that by the time you have narrowed down the specific kind of phages that would be of benifit to the patient, the doctor could already have used a antibiotic to start treatment. Just not economical.

There are other antibiotics that would be completely immune because they don't attack the cell wall. But in the end we are going to get smacked in the face with these things until every single person in the medical industry learns to observe proper antiseptic techniques. These genes probably pre-exsisted our use of antibiotics. Our overuse of antibiotics and shoveing all the sick people into one building in every city have meerly provided the bacteria that harbor them room to thrive.

That is precisely why attacking universal signaling mechanisms is most advantageous, because alterations in the cell wall are far more likely to occur than novel signaling mechanisms.

 

[madcat8000]

LOL I know many nurses who would love for a signaling drug to come along that would down regulate Clostridium difficile bacteria. Poor poor CNA's.

 

[nismaratwork]

LOL I know many nurses who would love for a signaling drug to come along that would down regulate Clostridium difficile bacteria. Poor poor CNA's.

Amen to that.

 

[alxm]

That could definitely be easier said than done, especially given the process to approve and assure that such an inhibitor isn't toxic. Really, that's the problem with all of these solutions; the "bugs" mutate rapidly, and more often we play catch-up.

I'm aware of that. But there's little evidence or reason to believe that the active site of beta-lactamase mutates rapidly.

 

[bobze]

I'm aware of that. But there's little evidence or reason to believe that the active site of beta-lactamase mutates rapidly.

...Ever been in a long term care hospital in the last couple decades?

ESBL (extended spectrum beta-lactamase) is precisely a reason to suspect that BL genes mutate rapidly

In fact, that is completely wrong. BL genes are carried on plasmids that have higher mutations than other plasmids. Prokaryotes go to great lengths to exchange plasmids like a cheap party favor and do all sorts of whacky things to modify those plasmids.

I'm not a bacteriologist, so maybe one can give more explicit detail here, but I'm pretty sure I remember reading that some bacteria use an almost viral-like-stuttering mechanism when copying antibiotic resistance plasmids--Which increases mutation rate, but more importantly enzyme diversity.Edit: Don't forget too that these guys will develop resistance to inhibitors. We see lots of that now with amp-clavulanate and others.