Researchers Find "Achilles Heel" of Drug Resistant Bacteria

Rambo Tribble writes Researchers in Britain are reporting that they have found a way to prevent bacteria from forming the "wall" that prevents antibiotics from attacking them. “It is a very significant breakthrough,” said Professor Changjiang Dong, from the University of East Anglia's (UAE) Norwich Medical School. “This is really important because drug-resistant bacteria is a global health problem. Many current antibiotics are becoming useless, causing hundreds of thousands of deaths each year. Many bacteria build up an outer defence which is important for their survival and drug resistance. We have found a way to stop that happening," he added. This research provides the platform for urgently-needed new generation drugs.

HOPE to exploit it

[kae77]

From TFA ... researchers have discovered what causes anti-biotic resistance, and HOPE to use that to discover how to stop them from becoming resistant.

The summary suggests that they already have. The summary will be perfect in "a few years time" when the researchers hope to have the solution.

Re:e. coli and salmonella?

[theshowmecanuck]

They are talking about the class of bacteria that can form the barrier they mention. That is, "Gram-negative bacteria" [wikipedia.org] which includes "Escherichia coli (E. coli), Salmonella, Shigella, and other Enterobacteriaceae, Pseudomonas, Moraxella, Helicobacter, Stenotrophomonas, Bdellovibrio, acetic acid bacteria, Legionella etc.". (Courtesy of Wikipedia)

Re:e. coli and salmonella?

[MrBingoBoingo]

The mention of MRSA in the article was probably erroneous and sloppy reporting. Gram Negative bacteria tend to resist chemotherapy due to robust cell walls. Gram Positive bacteria like MRSA, VRSA, VRE, et al... resist drug therapy by other means. This covers nothing of the most concerning drug resistant bacteria, but merely offers a way to make some bacteria vulnerable to drugs that they were not vulnerable to before.

Re:What's with the quotes around "gram-negative?"

[MrBingoBoingo]

Seems to only work on bacterial that are only inherently resistant to some antibiotics to because they are gram negative, so some bacterial that were hard to kill because they were gram negative get easier. The rest stay hard targets.

Re:Easier

[rsmith-mac]

Stop disinfecting and over-cleaning everything. Remove the Purell crap

Purell is alcohol based (good ole' ethanol). That has nothing to do with antibiotics and the antibiotic resistant bacteria in TFA.

Antibiotic resistance

[Anonymous Coward]

One of the main mechanisms for antibiotic resistance is efflux pumping. Drug makes it across the membrane and then is pumped out before it can reach a lethal concentration. If you can attack the cell from outside then you can sidestep this mechanism.

There are a natural class of antimicrobials called Protegrins that usually insert into the membrane from outside and combine to form a pore, spilling the cell contents. If you modify these you can make them lethal without forming a pore and in this state the protein they bind to (with low nanomolar affinity) is LptD (http://www.ncbi.nlm.nih.gov/pubmed/20167788) - one of the protein structures discussed. With a structure of the target there is a bit more information to guide development of these.

Re:The Reason...

[Overzeetop]

Yeah, don't think so. I suggest this chart: http://www.infoplease.com/ipa/... [infoplease.com]

The age of mortality for non-infants (those living past age 10) has increased by 20-25 years, a 50% increase in life expectancy, in the past century. Even if you look at "adults", or those who make it to age 20, there is still a 17-23 year increase. Again, a 50% increase in longevity for adults.

Re:e. coli and salmonella?

[dfm3]

As a microbiologist, I agree that the Telegraph article is rife with errors. The original article is paywalled, but from the abstract it sounds as if the researchers described a mechanism by which lipopolysaccharide, a component of the gram-negative cell wall which provides some degree of antibiotic resistance, is exported from the cell. I understand Dong, et al to be suggesting that a compound which prevents proper transport of LPS could be used synergistically with another drug which would otherwise be blocked from entry into the cell by LPS.

Further, the use of the term "immunity" to describe antibiotic resistance is a pet peeve of mine, as these terms do not mean the same thing!