Survival of the fittest doesn't apply. Shocking!
Natalia
http://www.world-science.net/othernews/100901_superbugs
*Drug-resistant germs found to help their brethren through the attack*
Sept. 1, 2010
Courtesy of Howard Hughes Medical Institute
and World Science <http://www.world-science.net> staff
*Confronting attack by antibiotics, some bacteria help each other
out---and unfortunately for us, they're better off for it,
researchers have found.
Though a small fraction of pathogens in a colony may have evolved the
ability to resist a drug or class of drugs, these "super bugs" were
found to help their more vulnerable peers by over-producing a
drug-fighting substance.
Prevailing wisdom held that antibiotic resistance works only on
an individual level: a bacterium acquires a mutation that
confers protection against a drug, allowing it to survive and
reproduce. Eventually, as vulnerable bacteria die, the
mutant's stronger progeny repopulate the colony. This basically
reflects how evolution is believed to work in all species: members that
are "fitter" or better adapted to prevailing conditions spread
their genes through the population at the expense of other members.
But the new study, to appear in the Sept. 2 issue of the research
journal / Nature/, indicates there are also population-wide
changes in the bacterial community at work. Faced with an
onslaught of antibiotics, resistant / Escherichichia coli/
microbes produce---at an energy cost to themselves---a protein
molecule that seeps into the communal broth and triggers a slew of
protective mechanisms in their non-resistant neighbors.
The study comes from researchers at the Howard Hughes Medical
Institute in Chevy Chase, Md.
In the past few years, the rise of "super bugs" such as
methicillin-resistant / Staphylococcus aureus/, or MRSA, has
had hospitals and medical professionals scrambling to fend off a
public health disaster. The new findings could help explain why
resistance has been so hard to curb, the researchers say.
The institute's James J. Collins and colleagues at Boston
University grew bacteria in a bioreactor---a large, capped glass
vessel with many extended arms that allow researchers precise
control over what the bugs are exposed to. "It kind of looks like a
component of a moonshine factory out in the backwoods," Collins said.
Interested in how genetically identical /E. coli/ acquire
mutations that confer resistance, the researchers trickled the
antibiotic norfloxacin into the bioreactor. As they upped the
bugs' exposure, the scientists periodically removed samples of
bacteria and measured the minimum strength of drug that stops
growth of the bug.
"That's when we were stopped in our tracks," Collins said. To their
surprise, the researchers found that the population as a whole was
much more drug-resistant than individual samples. Less than one in
a hundred individuals were typically drug-resistant.
The team then analyzed the proteins made by resistant bacteria in
the presence of norfloxacin, and found that a compound called
tryptophanase was particularly abundant. Tryptophanase breaks
down a biological molecule, the amino acid tryptophan, into
smaller bits. One of the products of this reaction is indole, a
signaling molecule that / E. coli/ produces under certain
stressful conditions.
Indole turns out to offer bacteria two kinds of protection against
norfloxacin, according to Collins' group. One is to turn on
cellular machines that pump the antibiotic out of the cell, as if
expelling a poison. Indole also turns on chemical processes that
protect the cell from oxidative stress, a chemical imbalance
that leads to the build up toxic molecules called free radicals. A
few years ago, Collins's team reported that antibiotics tend to
work by pummeling bugs with free radicals. "Here we're seeing that
indole is dampening that---turning on the sprinklers for the fire
resulting from the antibiotics," he said.
By comparing the growth of bacteria, the researchers found that
the mutants produce indole at a significant cost to themselves.
"They don't grow as well as they could, because they're producing
indole for everybody else," Collins said.
Such altruistic behavior---which appears in species throughout
the animal kingdom, including humans---presents a well-known
paradox for evolutionary biologists: if evolution favors
the fittest, why would an individual sacrifice its own fitness
for the rest of the group?
Collins said his findings bolster the "kin selection"
theory---formalized in the 1960s by the British evolutionary
biologist W.D. Hamilton---that said that organisms may behave
altruistically toward others that share their genes. By protecting
their own gene pool, they promote the spread of their genes indirectly,
even if they themselves suffer or die in the process. This principle
could have been at work in the "charitable" /E. coli,/ since they were
helping members of their own population.
"We are planning to explore whether similar strategies are used
by other bacterial species," Collins added.
Collins thinks the study is most directly pertinent to public
health. The researchers found that the same population-wide
protection occurs when bugs are exposed to other kinds of
antibiotics. What's more, many types of bacteria produce indole,
suggesting that a similar cooperative process may happen in a
host of bacterial species.
Future research on antibiotics might well focus on targeting the
indole pathway as a means to block bugs' ability to share
resistance, Collins said. More broadly, the work highlights the
pressing need for investment in new antibiotic development.
"The chance that we'll have new and dangerous super bugs emerging is
quite high, and I'm worried that our arsenal of antibiotics is
dwindling," Collins said. "We have time to respond now, but we need a
movement backed by political will to expand antibiotic
research and development."**
*
P.S. 1) The movement of the human from shared chemical communication to
the verbal communication of the individual may be the point of
fragmentation of our species. We constantly mask our senses with
additional "chemical smells" or "air cleaners" or various and sundry
items in our day-to-day lives (many of which are chronic poisons)
creating a maelstrom of information for our bodies to interpret. This
could throw the bodies defenses into play creating reactions such as
asthma or other chronic reactions that are becoming more prominent in
our societies... As with the small, so with the large. I believe that
verbal communication can keep the individual separated from the group as
a whole and more often serves ego needs more effectively for certain
individuals in the group but, reduces the chances of survival of the
group as a whole and therefore society at large. Verbal communication
can be twisted; chemical communication...not so easy, unless masked with
external scents.
2) If the "indole" molecule is used by a bacterium to fend off an
onslaught of poisons, what do our own body's cells do to protect
themselves from those same drugs? If we throw into the mix of
anti-bacterials an indole blocker, what reaction occurs in our own cells
and our own immune responses?
My only experience with the indole molecule is as part of the plant
growth hormone indoleacetic acid. Finding indole being utilized in the
above manner by single celled bacterium is, in my humble opinion,
troubling as it once more indicates the closeness with which ALL life on
this planet is related. Throwing poisons at something (no matter how
small) poisons the rest of life; whether those poisons are chemical or
verbal.
Darryl
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