posted
Bacteria Go Dormant To Hide From Antibiotics 26 Apr 2011
Call them the Jason Bournes of the bacteria world.
Going "off the grid," like rogue secret agents, some bacteria avoid antibiotic treatments by essentially shutting
down and hiding until it's safe to come out again, says Thomas Wood, professor in the Artie McFerrin
Department of Chemical Engineering at Texas A&M University.
This surreptitious and elaborate survival mechanism is explained in the online April edition of Nature Chemical
Biology," which details the research of Wood and his post doctoral student Xiaoxue Wang along with
colleagues Breann Brown, Wolfgang Peti and Rebecca Page of Brown University.
"Through our research, we're understanding that some bacteria go to 'sleep,' and that antibiotics only work on
bacteria that are metabolically active," Wood explains. "You need actively growing bacteria to be susceptible
to antibiotics. If the bacterium goes to sleep, the antibiotics, no matter what they do, are not effective because
the bacterium is no longer doing the thing that the antibiotic is trying to shut down."
It's an alternative method for survival, Wood says, that starkly contrasts the widely studied genetically based
approaches utilized by bacteria through which bacteria gain resistance to antibiotics as the result of mutations
experienced throughout time. This mutation-free response, however, demonstrates that some bacteria need
not mutate to survive external stressors, Wood says.
Instead, when triggered by an external stressor such as an antibiotic, a bacterial cell can render itself dormant
by triggering an internal reaction that degrades the effectiveness of its own internal antitoxins, Wood explains.
With its antitoxins damaged, the toxins present within the bacterial cell are left unchecked and damage the
cell's metabolic processes so that it essentially shuts down, he adds.
It's self-inflicted damage but with a purpose.
"The cell normally doesn't want to hurt itself; it wants to grow as fast as possible," Wood states; the raison
d'�tre for a cell is to make another cell," Wood says. "However, most bacteria have this group of proteins, and
if this group was active - if you got rid of the antitoxins - this group of toxins would either kill the cell or damage
it."
Specifically, Wood and his colleagues found that when encountering oxidative stress, their bacterial cells
initiated a process through which an antitoxin called MqsA was degraded, in turn allowing the toxin MqsR to
degrade all of the cells' messenger RNA. This messenger RNA, Wood explains, plays a critical intermediate
role in the cell's process of manufacturing proteins, so without it the cell can't make proteins. With the
protein-manufacturing factory shut down, the bacterial cell goes dormant, and an antibiotic cannot "lock on" to
the cell. When the stressor is removed, the bacterial cells eventually come back online and resume their normal
activities, Wood says.
"It was the combination of the genetic studies at Texas A&M with our structural studies at Brown University that
demonstrated that the proteins MqsR:MqsA form an entirely new family of toxin:antitoxin systems," Page says.
"Remarkably, we have shown this system not only controls its own genes, but also many other genes in E. coli,
including the gene that controls the response to oxidative stress."
This response mechanism, Wood emphasizes, does not replace the mutation-based approaches that have for
years characterized cell behavior; it's merely another method in a multifaceted approach undertaken by
bacteria to ensure survival.
"A small community of bacteria is in a sense hedging its bet against a threat to its survival by taking another
approach," Wood says. "To the bacteria, this is always a numbers game. In one milliliter you can have a trillion
bacterial cells, and they don't always do the same thing under stress.
"If we can determine that this 'going to sleep' is the dominant mechanism utilized by bacteria, then we can
begin to figure out how to 'wake them up' so that they will be more susceptible to the antibiotic. This ideally
would include simultaneously applying the antibiotic and a chemical that wakes up the bacteria. That's the goal
- a more effective antibiotic."
Source: Ryan Garcia Texas A&M University --------------------------------------------------------------------------------
Posts: 789 | From CT, | Registered: Jun 2006
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chiquita incognita
Unregistered
posted
For those who are interested, Buhner has a few simple solutions.
Knotweed, he writes, will help the delivery of abx into those areas where the bugs hide out. Skin, heart, joints, he writes, all get the abx if the knotweed is used.
Other herbs will raise CD 57 (?? is that the right number?) natural killer cells that are low in those patients who do not respond to abx, he writes.
Were it me, I would think this would be much safer than using a chemical on top of an abx to kill off bugs.
To raise the body's own defenses would take care of the bug while also averting most side effects.
Buhner also has written another book, not about lyme, but about abx-resistant bacteria. He points out that the herbs have multiple compounds that are antibiotic, whereas the abx have one. Penicillin is just that, penicillin. But herbs can have as many as 30 compounds (as with garlic, for example. Not that garlic is anti-spirochetal per se).
The point is that the bugs can adapt to a single compound, he writes, but not to the multiple compounds in the plants.
There is clinical testing to show efficacy of plants as abx, specific to certain bacteria. His book will tell you which bugs respond to which herbs (though it' s not about lyme per se). His lyme book of course will tell you which herbs are helpful with lyme.
This is not medical advice. Only information.
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Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
Interesting Al. A better antibiotic directed to addressing the short-falls of the current ones would be nice.
momindeep
Frequent Contributor (1K+ posts)
Member # 7618
posted
Wow...if this is indeed correct, it could explain A LOT.
Posts: 1512 | From Glenwood City WI | Registered: Jul 2005
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Lymeorsomething
Frequent Contributor (1K+ posts)
Member # 16359
posted
quote:Originally posted by chiquita incognita: Other herbs will raise CD 57 (?? is that the right number?) natural killer cells that are low in those patients who do not respond to abx, he writes.
What other herbs?
I know modified arabinoxylane from rice bran helps raise killer cell activity supposedly.
I'm not sure about other herbs but will say that my CD-57 came up recently while on the Cowden protocol. I'm also on abx so not sure which to attribute it to...but it never came up on abx previously.
-------------------- "Whatever can go wrong will go wrong." Posts: 2062 | From CT | Registered: Jul 2008
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map1131
Frequent Contributor (5K+ posts)
Member # 2022
posted
Oh come on Tincup. There are so few cases of Lyme & co in most areas of US. Only those in the Northeast would have any use for an abx that actually works against these super duper bacterias.
They could use our tax dollars on something more important like Bird flu, turkey flu or fowl flu.
Oh, those aren't bacterias. West Nile? I can't even find some stupid bacteria in my head right now.
Time to go. If I can't say something nice, mama said keep my mouth shut.
Pam
-------------------- "Never, never, never, never, never give up" Winston Churchill Posts: 6478 | From Louisville, Ky | Registered: Jan 2002
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