
Antibiotic Breakthrough Ends 25-Year Discovery Drought - uptown
http://www.bloomberg.com/news/2015-01-07/antibiotic-breakthrough-ends-25-year-discovery-drought.html
======
spanktar
I think the real meat of this article is here:

"...strikes multiple targets, including cell walls...Since the lipid
structures it attacks don’t evolve as quickly as frequently mutating proteins,
it may take the bacteria longer than usual to develop a survival tactic."

Proteins change often and quickly, but basic cell structures may take longer
or never adapt.

But I'm not a pathobiologist, I just play one on the Internet

~~~
hga
So do the β-Lactam antibiotics (e.g. penicillin), but that doesn't stop a host
of unrelated resistance mechanisms: enzymes that directly attack it, mutations
to the protein(s) that are necessary for entry into the bacteria, and probably
the pumps that actively remove various antibiotics.

Given that this was discovered from existing bacteria, there's a significant
chance nature has already done the first and last of those. The middle
mechanism is likely possible for any bacteria, if you have enough to start
with (there's nothing I could find with Google in a minute to describe
teixobactin's transport mechanism).

In general there was a rule of thumb when I was doing microbiology of this
exact nature (an antibiotic created by some strains of _E. Coli_ ), if you
exposed a million bacteria cells to a generic antibiotic, 1 would would
survive due to a mutation (a useful number in microbiology, likely dead meat
in the body). Streptomycin was more effective, 1 in a billion.

ADDED: it's implied by the _Nature_ abstract that the researchers have tried
this general approach, that they were not able to find spontaneous resistance
mutations in a couple of the standard nasties. But extending on the above
thesis, ecologically, there's a respectable chance some bacteria out there
have developed defenses. It's a jungle out there, and e.g. in your gut, that's
why fungi and bacteria developed antibiotics in the first place. They aren't
expending resources just to allow us to kill the inconvenient ones.

~~~
pcrh
From the Nature article, the claim that resistance to teixobactin is hard is
based on an attempt by the authors to induce resistance by culturing _S.
aureus_ or _M. tuberculosis_ in the presence of sub-lethal concentrations of
teixobactin for 27 days and seeing if resistant clones evolved. They did not
observe any. That doesn't mean it's impossible, though. Plasmids for example
are a source of resistance that doesn't require mutations.

Edit: deleted incorrect information about b-lactamase.

~~~
hga
[ Deleted β-Lactam stuff. ]

 _Nature_ asked me for $$$ to read the article, so ... from your description,
that's leaving out the hard, fast test of just culturing several billion of
those, adding a lethal concentration and seeing if there are any survivors.
Which is how I gather one found spontaneous transport mutations, at least
circa 1977. The state of the art has likely improved, and these guys used
novel microbiological methods to find the bacteria that produce teixobactin in
the first place.

ADDED: thanks to betatim's link to the full text, I've skimmed it and read the
discussion, and teixobactin sound quite promising. They haven't found any
protein to which it binds, and they think it binds to an "Achilles's heel" in
the outer cell wall. The method described to generate resistance was their
most extreme attempt, so I assume they tried the fast way, and I can see why
it didn't work.

Ecologically, they believe there's little gene (e.g. plasmid) transfer between
these soil bacteria and human pathogens, and the "30 year" bit came from
experience with vancomycin, to which it has a lot of similarity. And they've
done lots of tests for human toxicity and effectiveness in mammals. It's still
early in the process, but a degree of fuss is warranted, especially due to
their discovery method.

~~~
pcrh
Here are the pertinent bits regarding resistance, in summary it implies that
_spontaneous_ resistance will be difficult, But... "life has a way":

>We were unable to obtain mutants of S. aureus or M. tuberculosis resistant to
teixobactin even when plating on media with a low dose (4 X MIC [minimal
inhibitory concentration]) of the compound. Serial passage of S.aureus in the
presence of sub-MIC levels of teixobactin over a period of 27 days failed to
produce resistant mutants as well (Fig. 2d, Supplementary Discussion)

From the Supplementary information:

>Cells were added to teixobactin present at 0.25xMIC, 0.5xMIC,1xMIC,2xMIC and
224xMIC. At 24 hour intervals, the cultures were checked for growth. Cultures
from the second highest concentrations that allowed growth (OD600≥2) were
diluted 1:100 into fresh media containing 0.25xMIC, 0.5xMIC,1xMIC,2xMIC and
4xMIC of teixobactin. This serial passaging was repeated daily for 30 days.
Any cultures that grew at higher than the MIC levels were passaged on drug
free MHA plates and the MIC was then determined by broth microdilution. No
resistant mutants were obtained. This experiment was repeated, and produced
the same negative result. In order to maximize the chance of obtaining a
resistant mutant, we performed an additional experiment with very small
incremental increases in the drug concentration. Cells were added to a series
of tubes with small differences in the concentration of teixobactin (0.06xMIC,
0.25xMIC, 0.5xMIC, 0.75xMIC,1xMIC, 1.25xMIC, 1.5xMIC, and 2xMIC). At 24 hour
intervals, cultures from the highest concentration that allowed growth to a
minimum OD600 of 0.2 were diluted 1:100 into fresh medium containing 0.06xMIC,
0.25xMIC, 0.5xMIC, 0.75xMIC,351xMIC, 1.25xMIC, 1.5xMIC, and 2xMIC. This
passaging was repeated for 27 days. Cultures that grew at levels higher than
the MIC were passaged on drug free MHA plates, and the MIC was determined. For
teixobactin, there were no mutants with an MIC greater than the parent S.
aureus ATCC 29213.

~~~
timr
What they're describing here is an _intensive_ selection process for
resistance. It's debatably much more intensive than nature would ever perform:
they're growing bacteria in the presence of various dilutions of the
antibiotic, taking a sample of the culture, diluting it 100-fold, and
repeating the selection many (~30) times. Then they look for any bugs that
develop resistance. None were found. Even if you had a truly pathological
patient (i.e. someone who was doing his level best to mis-use an antibiotic),
it wouldn't come close to this level of selective pressure for antibiotic
resistance.

Moreover, there's a strong biochemical argument against resistance: the region
that the antibiotic targets is highly conserved, which means that it's
probably functionally necessary. The bug is therefore unlikely to evolve away
from the threat. This is important, because it's that most likely avenue for
antibiotic resistance, energetically speaking: it doesn't cost anything for an
organism to mutate a weakly conserved gene, so they do it once, and pass it on
to every subsequent generation with no penalty.

The antibiotic is just a peptide, so _in theory_ you could see some sort of
specialized peptidase evolve from an existing gene...but the problem is that
the bug would have to then carry around that gene and _express it constantly_
(or even less likely: evolve a sensing system that allows for selective
expression). It's a highly unlikely thing, and virtually impossible to
maintain over multiple generations without constant selective pressure.
Bacteria do not like to hold on to genes that they don't need.

Nothing is impossible over evolutionary time, of course, but the researchers
don't seem to be overstating their case here.

~~~
fraserharris
Removed anthropomorphising:

It's a highly unlikely thing, and virtually impossible to maintain over
multiple generations without constant selective pressure. Bacteria are quickly
out-competed by genetic variants with fewer expressing genes that they don't
need.

BTW: do you have any links/data re the relative 'cost' of expressing unneeded
genes?

~~~
Fomite
"Bacteria are quickly out-competed by genetic variants with fewer expressing
genes that they don't need." This has not been true for MRSA, where
transmission of resistant organisms in the community was sustained despite
there not being particularly intense selective pressure in the community. Last
I checked (I don't work in community transmission as much) we don't have a
firm handle on why that's true, but I'd caution against simply assuming that
resistant organisms will be out competed absent selective pressure.

Beyond that, even if they _are_ out competed, that's not sufficient. They need
to be out competed to extinction.

~~~
timr
MRSA is due to the _mecA_ gene, which is integrated into the _S. Aureus_
genome. It's not plasmid-mediated resistance, which means that it's less
likely to disappear from bacterial populations, even in the absence of
selective pressure:

[http://www.eurekaselect.com/68849/article](http://www.eurekaselect.com/68849/article)

~~~
Fomite
True - but the post I was responding to wasn't talking about plasmid-mediated
resistance, but rather a broad assertion that a competitive disadvantage will
take care of things. That's a strong assumption for which we have a counter
example.

------
betatim
Full text for free: [http://rdcu.be/bVbR](http://rdcu.be/bVbR)

This is a link to nature's new "share it for everyone to read if you have paid
access to the article" version of 'open-access'.

A new antibiotic kills pathogens without detectable resistance, Nature,
January, 2015. DOI: 10.1038/nature14098

------
TomAnthony
They author's state "it should be used, if it gets successfully developed, as
broadly as possible" \- because they believe it is robust against bacteria
developing resistance.

Knowing nothing about this area... isn't this a bad idea because board use
would increase the risk of resistance appearing and would mean those bacteria
resistant to this would be extremely resistant to most other treatments aw
well (given this drug has multiple modes of attack)?

~~~
mseebach
Apparently they have a very plausible reason to think it will be robust: It
attacks cell walls, which are structural, rather than receptors (I think I'm
using the term correctly) that are proteins and prone to mutations.

It's basically the same reason we don't fear bacteria to develop resistance to
boiling or alcohol disinfectant.

~~~
gus_massa
I tempted to write "What could go wrong?" or "Life finds a way.".

A fast Google search gives this paper: " Relatively Alcohol-Resistant
Mycobacteria Are Emerging Pathogens in Patients Receiving Acupuncture
Treatment"
[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC140401/](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC140401/)

There are some archeas (and a few bacterias) that support boiling temperature,
but IIRC they don't like meatware because it's too cold for them.
[http://en.wikipedia.org/wiki/Hyperthermophile](http://en.wikipedia.org/wiki/Hyperthermophile)

~~~
jobu
> I tempted to write "What could go wrong?" or "Life finds a way.".

My thoughts exactly. Try using it in large scale animal farms for a couple
decades and I'm betting something will become resistant.

~~~
platz
I thought some bacteria had developed double walls with an insulating fluid,
so that they could expunge bad chemicals.

------
_craft
The nytimes article mentions:

"The research was paid for by the National Institutes of Health and the German
government (some co-authors work at the University of Bonn). Northeastern
University holds a patent on the method of producing drugs and licensed the
patent to a private company, NovoBiotic Pharmaceuticals, in Cambridge, Mass.,
which owns the rights to any compounds produced. Dr. Lewis is a paid
consultant to the company."

If the research was paid for by the National Institutes of Health, why is the
patent privately owned? This does not seem fair to taxpayers.

~~~
skosuri
This is not only allowed, it's encouraged by legislation called the Bayh-Dole
Act. The general thought is that there would be no incentive for anyone to do
clinical trials on the drug, which can get quite expensive, if they don't have
some protection for exclusive use. Many, if not most drugs proceed starting
from academic research funded by governmental support.

~~~
_craft
Thanks for the informative response! Do you know how expensive clinical trials
would be for this kind of drug?

~~~
skosuri
$100M-500M gets thrown around [1] but it's hard to find good data. This might
seem not too high, but many drugs fail, and often fail at the most costly step
(phase III). So you have to be sure to factor that failure rate in.

[1] [http://www.manhattan-institute.org/html/fda_05.htm](http://www.manhattan-
institute.org/html/fda_05.htm)

------
dbcooper
The _Nature_ publication seems to be open access:

[http://www.nature.com/nature/journal/vaop/ncurrent/full/natu...](http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14098.html)

 _The Scientist_ has quite a nice write up:

[http://www.the-
scientist.com/?articles.view/articleNo/41850/...](http://www.the-
scientist.com/?articles.view/articleNo/41850/title/New-Antibiotic-from-Soil-
Bacteria/)

Details on the cell culture device (open access):

[http://aem.asm.org/content/76/8/2445.full.pdf+html](http://aem.asm.org/content/76/8/2445.full.pdf+html)

~~~
pcrh
That device is a smart and clever approach! It will undoubtedly get used for
many other applications.

------
baldfat
While there are new strains this would be a new class WHICH means AWESOME if
it works out. Since this is so early I am not hoping for much.

My son had cancer and he had a staph infection that was septic (AKA in his
blood through out his body). Non-resistant = 95% cure rate resistant strain
and if you have a compromised immune system less then 50% cure rate. Good news
for cancer patients and glad to see it coming down the track.

~~~
AceJohnny2
I had a friend die from a lung infection from a compromised immune system
because of leukemia.

Very glad to hear your son made it, and I echo your sentiment.

------
refurb
This is a bit of an odd article. The FDA has approved a number of different
antibiotics over the past year. Most are not new mechanisms of action, but
they are new products that have different profiles against different resistant
bacteria.

The other issue is that this is _very_ early in development. I really hope it
gets through trials, but there are graveyards full of promising antibiotics
that failed.

~~~
baldfat
This in fact would be a different class. So it is a HUGE deal.

~~~
refurb
There are a _number_ of different antibiotic class currently in development
(in clinical trials already). This certainly isn't the "end of a drought".

~~~
baldfat
There has been exactly 2 new classes since 1962.
[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085877/](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085877/)

Now if this actually works then yes great, and I hope it does.

~~~
refurb
I think the reliance on new classes is a bit excessive. There are numerous new
beta-lactams that have come out that are still in the same class, but have
overcome (some of) the resistance issues.

A new class would be great, but even different drugs from the same class would
be great as well.

------
Gatsky
Their experimental approach was interesting and hopefully will lead to more
discoveries. I feel like this drug is already being overhyped however. It
doesn't work for gram negative bacteria, which are responsible for most of the
serious and scary multi drug resistant infections.

Also, assuming it doesn't have weird toxicity in people, or unfavourable
pharmacokinetics, the author's suggestion that we should give it to everyone
is a bit cute, given that it will almost certainly cost north of $200 per day
if it gets to market...

Peptide antibiotics can have some issues. A recent new peptide antibiotic
called Daptomycin [1] can't be used for pneumonia for example, because it is
inhibited by pulmonary surfactant.

[1]
[http://en.m.wikipedia.org/wiki/Daptomycin](http://en.m.wikipedia.org/wiki/Daptomycin)

~~~
scarmig
Is $200/day a lot for a highly effective antibiotic?

Genuine question--my experience is that a serious hospital stay racks up
charges starting in the high five figures (and the sky's the limit), and if
there's an antibiotic that's merely a couple thousand a day, it'd certainly be
very cost effective.

~~~
ajuc
> my experience is that a serious hospital stay racks up charges starting in
> the high five figures (and the sky's the limit)

This is USA specific. Day in hospital in Poland costs around 100-400 USD (and
that's for people without insurance, so for >95% of population it's free).
It's probably worse quality, but still..

I don't understand how you get so outrageus prices for healthcare in USA.

------
ars
When they made roundup they expected plants would never be able to be
resistant to it[1].

And in fact plants did not become resistant in the way they expected. Trouble
is plants found a completely different way to resist roundup that no one
expected.

Their claim that bacteria would not become resistant to this antibiotic is
rubbish. They do have the ability to determine that.

If they actually want to know then deliberately try to (carefully) create
resistant bacteria by continuously giving them low levels of antibiotic and
slowly increasing it.

[1] [http://www.npr.org/blogs/thesalt/2012/03/11/148290731/why-
mo...](http://www.npr.org/blogs/thesalt/2012/03/11/148290731/why-monsanto-
thought-weeds-would-never-defeat-roundup)

~~~
duskwuff
> If they actually want to know then deliberately try to (carefully) create
> resistant bacteria by continuously giving them low levels of antibiotic and
> slowly increasing it.

That's precisely what they did while investigating teixobactin, and they
didn't see any resistance develop:

[https://news.ycombinator.com/item?id=8853232](https://news.ycombinator.com/item?id=8853232)

~~~
ars
That's quite impressive!

Was there a control? i.e. same procedure, but with a different antibiotic?

~~~
cowsandmilk
Yes. They used ofloxacin as a control. Figure 2d in the paper.

Kim Lewis, the senior author on this publication, is one of the world's
foremost experts on antibiotic resistance. This isn't amateur hour.

------
Houshalter
All of the comments are by armchair biologists about how the scientists are
wrong and all bacteria strains will become resistant to it in 2 days.

But anyways, if it is an issue, why can't we just require antibiotics be taken
intravenously? The vast majority of bacteria exposed to antibiotics are in
your digestive system and that is where resistance develops. Or at least
that's how I understand it.

~~~
robbiep
IV antibiotics generally mean hospital, which generally means severe life-
threatening infection. Outpatient IV antibiotics are done but it's complicated
and carry further risk of infection through having a line in situ for long
periods of time.

IV antibiotics do have an effect on gut bacteria as well, it's not as simple
as just not giving oral; additionally (and, perhaps the crux of the issue) is
that gut bacteria exposure to antibiotics is not how resistance develops; and
certainly aren't the main problem. It is the more common infective agents that
cause the problems - Gram positive organisms (Strep Viridians, Staph Aureus
etc) that usually enter from cuts or abscesses and, in the immunocompromised,
cause significant disability.

~~~
Houshalter
>IV antibiotics do have an effect on gut bacteria as well, it's not as simple
as just not giving oral;

How so? And more importantly how much antibiotics make it to the gut, vs if
you take it orally? I would guess it would be a lot less.

>It is the more common infective agents that cause the problems

I know that, but as I understand it the resistance first evolves in gut
bacteria, then spreads through horizontal gene transfer. Wikipedia cites this
as the main cause of antibiotic resistance:
[https://en.wikipedia.org/wiki/Horizontal_gene_transfer](https://en.wikipedia.org/wiki/Horizontal_gene_transfer)

~~~
robbiep
> How so? And more importantly how much antibiotics make it to the gut, vs if
> you take it orally? I would guess it would be a lot less.

I have no idea what figure or percentage it would be, but for most common
antibiotics which end up distributed in total body water, there will be a
component that leaks into the gut through capillary action; if it is
metabolised in the liver then a proportion of it will end up in bile (if fat
soluble) and then enter the gut that way; either itself or a metabolite of it
- it would be impossible for me to quantify and likely depends on many many
factors such as molecular weight, structure and a host of other features.

Patients on IV antibiotics develop diarrhoea from IV antibiotics at a similar
rate (from what I have experienced) to those on orals. hence it undoubtedly
kills bacteria in a similar fashion.

And we use IV antibiotics to kill bad infections of the gut. So whatever the
mechanism, if I have elucidated it or simply done some hand-waving, it clearly
affects it significantly.

The only instance of antibiotic use that touches on what I feel you are
pushing for is the use of oral vancomycin (It is almost always IV) for severe
bacterial infections of the gut - we use it oral because it is not absorbed
systemically (as opposed to other specifically oral antibiotics) so doesn't
cause systemic effects.

> then spreads through horizontal gene transfer.

Sure. But if you look at how they tested this particular antibiotic for the
ability to develop resistance, they exposed TB and Staph to sub-theraputic
doses for 27 days, or (for Staph) or 810generations (assuming a rough rate of
division somewhere around 40 min to 1 hr in ideal conditions). An epic number
of cell divisions if you work it out (and I can't).

The commonly accepted knowledge, as far as I understand it and as far as I
have been taught it, whether or not bowel bacteria have a significant role to
play or not, is that exposure of antibiotics to sub-lethal doses for long
periods of time promote the survival of strains that have a competitive
advantage against the agent in use, which over time allows the strain to
survive in otherwise-lethal doses, and that gene becomes incorporated into a
plasmid and then ends up spreading to every other organism capable of
horizontal gene transfer.

Anyway, I am at home and not going to see the next MD, PhD in Infectious
Diseases until tomorrow but when I do I will ask him and reply here. So, check
back in 24 hours if you're interested

~~~
robbiep
On the off-chance that you read this I apologise for not delivering, I wasn't
able to speak to ID but will on Monday so if this thread is locked by then
then shoot me an email

~~~
Houshalter
It's fine you don't have to. The responses to my question were phenomenal.

------
NoMoreNicksLeft
> “It should be used, if it gets successfully developed, as broadly as
> possible, because it is exceptionally well-protected from resistance
> development,” said Kim Lewis, one of the study’s authors and a professor at
> Northeastern University in Boston. Lewis estimated that it may take more
> than 30 years for bacteria to become resistant to teixobactin. He is also a
> co-founder of NovoBiotic Pharmaceuticals LLC, which is developing the drug.

I'd much rather get two or three more that all use different mechanisms, and
use them as a cocktail.

Let the bugs try to develop 3 different kinds of resistance at once.

~~~
Fomite
Multiple antibiotics often carry fairly serious medical risks. "Cured of your
infection" is somewhat less heartening when we boxed your kidneys doing it.

------
kileywm
Can anyone clarify the core causes of antibiotic resistance over the last
several decades?

I've _heard_ the following causes, but I cannot substantiate them:

[1] Improper patient usage. Primarily, not taking the prescribed dosage long
enough to eradicate all of the target bacterium, leaving (enough) survivors to
meaningfully propagate their resistance. Typical to the "Hey I think my sinus
infection is gone already! Adios remaining pills."

[2] Improper targeting. A functional antibiotic used on the wrong type of
bacterium, or even usage against viruses.

Are there any others? Are my [1] and [2] debunked?

~~~
Fomite
1\. This is a major problem - patients start feeling better and discontinue
therapy, which promotes resistance, save partially consumed prescriptions for
"if this happens again", etc.

2\. This is also a thing - broad spectrum antibiotics, difficulty in
diagnosing, patients wanting _something_ even if their infections are viral,
etc. all lead to mistargeting of antibiotics for a number of reasons.
Antimicrobial stewardship has become a major part of hospital infection
control.

3\. The widespread use of antibiotics in livestock. The agricultural use of
antibiotics is _staggering_

~~~
VLM
"patients wanting something even if their infections are viral"

What the market needs is a placebo anti-biotic. One thats totally wasted by
resistance so it won't hurt anything, and is reasonably cheap. Give it some
nasty digestive system "effects" as a special gift to patients dumb enough to
demand a pill against medical advice. Something that is, in fact, an
antibiotic, so when they go home and look it up on wikipedia they don't freak
out when they find out what a sucrose pill is. Maybe a homeopathic dose of it,
so counter-reactions are rare and minimal.

~~~
jrockway
"First, do no harm" is somewhat incompatible with dumb, demanding patients,
unfortunately.

~~~
Fomite
Medical ethics are also very patient focused - it's hard to deal with
situations that are good for _this patient_ but bad for _hypothetical future
patients_.

------
emmanueloga_
The mention of the "25 year discovery drought" made me think about this
documentary I saw once about bacteriophages ("viruses that infect and
replicate within bacteria") [1].

I don't remember the specific documentary but here is a wikipedia link [2]
"Although extensively used and developed mainly in former Soviet Union
countries circa 1920, the treatment is not approved in countries other than
Russia and Georgia."

1:
[http://en.wikipedia.org/wiki/Bacteriophage](http://en.wikipedia.org/wiki/Bacteriophage)

2:
[http://en.wikipedia.org/wiki/Phage_therapy](http://en.wikipedia.org/wiki/Phage_therapy)

------
shanev
I think we'll be seeing more research like this in the future, where we
develop drugs by mimicking nature instead of starting from scratch in the lab.
Nature has had a few millions of years more to build and test things.

~~~
nkozyra
Nature (at least in terms of natural antibiotic sources like fungi and
bacteria) also has a relatively quick turnaround in terms of adaptation.

Ultimately, developing antibiotics is a cat-and-mouse game, and eventually
nanotech will render it archaic, but in the mean time the more we can do to be
responsive and quick to adjust, the better, and that means new antibiotics.

I do worry about this "30 year projection" and what that's based on. Is that a
historical norm?

~~~
shanev
I think nanotech will bring about it's own problems.

What we should be doing is addressing the cause of antibiotic resistance in
the first place, namely the overprescription of antibiotics, and their
improper use in industrial farming.

~~~
nkozyra
The over-prescription of antibiotics isn't the cause of antibiotic resistance,
it's the cause of accelerated antibiotic resistance.

Which for all practical purposes might be the same thing, if we're talking 80
years versus 30 years for propagation of resistance.

Nanotech will be a very, very arduous and slow process. "Its own problems" is
putting it lightly. People will die due to nanotech approaches to anti-
pathogenics, no question about it. We're talking about programmable biology,
something will go wrong.

The biggest problem is what happens when we've eliminated human pathogens?
What happens when we've extended the average life expectancy by 10 years -
after all, many cancers are caused by pathogens. What happens to the ecosystem
when herpesviridae is effectively gone? What are the side effects, the
unintended consequences?

------
tokenadult
A very interesting submission about the big medical news story of the day. The
news suggests that we can all enjoy significant gains in finding effective
treatments for dangerous infections. The era of antibiotics is probably not
over yet, by a long way.

As noted in another comment, the underlying _Nature_ article is up on the
World Wide Web, [after edit:] and now shared to all of us by a subscriber who
posted a subscriber's-sharing link in this thread.[1] I searched for some
other news stories about this preliminary research finding to link to others
based on independent reporting as well as the authors' press release and the
_Nature_ article. I found a story in _Financial Times_ [2] reporting,
"Teixobactin quickly kills Gram-positive bacteria, which are prominent in
discussions of antibiotic resistance, including _Clostridium difficile,_
_Mycobacterium tuberculosis_ and _Staphylococcus aureus._

"Neil Woodford, head of the antimicrobial resistance unit at Public Health
England, commented:

"'The rise in antibiotic resistance is a threat to modern healthcare as we
know it, so this discovery could potentially help to bridge the ever
increasing gap between infections and the medicines we have available to treat
them.'

"But Prof Woodford added: 'Although it is a step forward, this new discovery
would not be suitable for treating infections caused by _E. coli,_
_Klebsiella_ or other Gram-negative bacteria.'"

The _Washington Post_ reports,[3] "But all good things must eventually come to
an end.

"'They didn't find resistance in a couple of simple tests, so it won’t happen
in a minute, but there is no compound on this planet that bacteria will not
develop resistance to,' Said Richard Novick, an NYU Langone Medical Center
professor who wasn't involved in the study. 'But it would certainly happen
more slowly with this one.'

"And unfortunately, the drug's genius mechanism is also its biggest flaw. It
can only target so-called gram-positive bacteria, like staph, strep, and TB,
because they're unprotected once their cell wall starts to break down. Gram-
negative bacteria like _E. coli_ and the organisms that cause many sexually
transmitted infections have an outer membrane that Teixobactin can't
penetrate. That's probably a safety mechanism built-in by the gram-negative
bacteria that created Teixobactin in the first place."

That expert also comments that he would strictly limit application of this
antibiotic at first to hospital settings, and that would be my policy
recommendation too, to reduce the chance of producing selection pressure for
resistant strains of bacteria. But this does look like it could be a big
advance in clinical treatment of gram-positive bacterial infections resistant
to other antibiotics.

The reporting in _The Scientist_ ,[4] already linked by an earlier
participant, includes a comment on the laboratory technique used to find the
microorganism that produces this new antibiotic: "'This is a very clever
technique,' added Robert Austin, a physicist at Princeton University who
studies the evolution of microbes and was not involved in the current study.
'The bacteriology community needs to get away from culturing bacteria on agar
plates, because this will not lead to new antibiotics.'" That's a familiar
principle in science: look in a new place, and make new discoveries.

The reporting in _The Guardian_ [5] picks up on that idea in the words of
another expert: "'What most excites me is the tantalising prospect that this
discovery is just the tip of the iceberg,' said Mark Woolhouse, professor of
infectious disease epidemiology at the University of Edinburgh. 'It may be
that we will find more, perhaps many more, antibiotics using these latest
techniques.'"

It's very likely that there are more antibiotics yet to be discovered, because
all microorganisms live in a world full of other microorganisms, and haphazard
adaptation to that environment must have produced selection pressure for many
microorganisms to produce natural chemicals ("antibiotics") that kill off
other kinds of microorganisms. Putting those chemicals into human bodies
applies human knowledge to take advantage of the variety of life that has
arisen from evolution.

[1] [http://rdcu.be/bVbR](http://rdcu.be/bVbR)

"A new antibiotic kills pathogens without detectable resistance"
[http://www.nature.com/nature/journal/vaop/ncurrent/full/natu...](http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14098.html)

DOI: 10.1038/nature14098

[2]
[http://www.ft.com/intl/cms/s/0/701a3c36-95be-11e4-a390-00144...](http://www.ft.com/intl/cms/s/0/701a3c36-95be-11e4-a390-00144feabdc0.html#axzz3OAXfp1y4)

[3] [http://www.washingtonpost.com/news/speaking-of-
science/wp/20...](http://www.washingtonpost.com/news/speaking-of-
science/wp/2015/01/07/new-class-of-antibiotic-found-in-dirt-could-prove-
resistant-to-resistance/)

[4] [http://www.the-
scientist.com/?articles.view/articleNo/41850/...](http://www.the-
scientist.com/?articles.view/articleNo/41850/title/New-Antibiotic-from-Soil-
Bacteria/)

[5] [http://www.theguardian.com/science/2015/jan/07/antibiotic-
dr...](http://www.theguardian.com/science/2015/jan/07/antibiotic-drug-
resistance-teixobactin)

------
briantakita
I'm skeptical that this is a good thing given how the profit motive motivates
people to "externalize" side effects; Environmental damage from antibacterial
soaps, disrupting natural biological processes, disease-resistant bacteria,
are a few effects.

> Scientists have discovered an antibiotic capable of fighting infections that
> kill hundreds of thousands of people each year

Given it's potential as a medicine, the media will hype it into public
consciousness. Marketers & Entrepreneurs will use this social inertia to sell
it in places where it is dangerous to use. The FDA has a history of revolving
doors with big pharma & playing loose in pandering to corporate interests, at
the expense of the public & environment.

I'm merely presenting a minority view here on Hacker News. It's good to have
all your t's crossed and i's dotted.

------
hga
Derek Lowe has his usual great analysis of this paper and the antibiotic:
[https://news.ycombinator.com/item?id=8862148](https://news.ycombinator.com/item?id=8862148)

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stevewilhelm
Company's press release [http://s831.us/1Dml4G5](http://s831.us/1Dml4G5)

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jalada
Headline should read: Zombie apocalypse averted for now.

