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Pergeseran paradigma dalam perlawanan multidrug .

Date:

August 20, 2015

Source:

University of California - Santa Barbara

Summary:

Menggunakan strategi Trojan horse , bakteri yang merespon terhadap antibiotik di tes laboratorium dapat menjadi sangat resisten dalam tubuh . Strategi ini mungkin menjelaskan mengapa antibiotik tidak efektif pada beberapa pasien meskipun tes laboratorium yang memprediksi sebaliknya.

........... Ini adalah contoh dari apa yang UC Santa Barbara biologi Michael Mahan sebut sebagai strategi Trojan horse . Diidentifikasi melalui penelitian baru yang dilakukan oleh Mahan dan rekan-rekannya , strategi Trojan horse mungkin menjelaskan mengapa antibiotik tidak efektif pada beberapa pasien meskipun tes laboratorium yang memprediksi sebaliknya. Temuan penelitian muncul dalam jurnal EBioMedicine .....more

Paradigm shift in multidrug resistance

Unexpected resistance mechanism found in
pathogenic bacteria that may warrant changes in the way antibiotics are
developed, tested and prescribed

Date:

August 20, 2015

Source:

University of California - Santa Barbara

Summary:

Using a Trojan horse strategy, bacteria
that respond to antibiotics in lab tests can become highly resistant in the
body. This strategy may explain why antibiotics are ineffective in some
patients despite lab tests that predict otherwise.

..............

Bacteria are pretty wily creatures. Take
for example, an organism such as Salmonella, which which are killed by
antibiotics in lab tests, but can become highly resistant in the body.

It is an example of what UC Santa
Barbara biologist Michael Mahan refers to as the Trojan horse strategy.
Identified through new research conducted by Mahan and his colleagues, the
Trojan horse strategy may explain why antibiotics are ineffective in some
patients despite lab tests that predict otherwise. The research findings appear
in the journal EBioMedicine.

"We are not petri plates, and we
need to revisit the way antibiotics are developed, tested and prescribed,"
said Mahan, a professor in UCSB's Department of Molecular, Cellular, and
Developmental Biology. Current methods for testing resistance to antibiotics do
not reflect the actual and varying environments in the body, where bacteria
fight to survive. Mahan noted that this difference can render antibiotic
susceptibility testing inaccurate.

"Prescription of the wrong
antibiotic may not only fail to clear the infection but may create the perfect
storm for the emergence of superbugs in infected patients," he added.
"Even in our most advanced hospitals, high drug doses are given to
infected patients without knowing that the body's environment may render
bacteria inherently resistant to the very antibiotics prescribed to control
them."

Mahan's research demonstrates two
important points: Bacteria become resistant only to certain antibiotics, and
they deploy this defense mechanism only in certain areas of the body. This
means that when a patient fails to respond to a particular course of
antibiotics that lab tests predict should be effective, rather than increasing
the dose or duration of treatment, a potentially more effective therapeutic
option is simply to prescribe another drug.

Mahan and his colleagues initially
worked with the aforementioned Salmonella, a bacterium that causes food and
blood poisoning. Salmonella reside within white blood cells -- the very cells
of the immune system that are involved in protecting the body against
infectious disease. When the researchers mimicked this intracellular
environment in the lab, the bacteria became highly resistant to certain
antibiotics.

Next, the researchers tested Yersinia, a
bacterium that also causes food and blood poisoning but lives outside of host
cells in the intestine. When researchers mimicked the extracellular environment
of the intestine, this bacterium also became highly resistant to certain
antibiotics. These two examples indicate that the resistance process may be
shared by many different types of bacteria.

"Our research suggests the need for
animal models to be incorporated early during the antibiotic development
process and for lab drug sensitivity testing to incorporate media that mimic
the specific biochemical environments that trigger resistance in the
body," Mahan explained. "If these additional components were added,
we'd get a more accurate reflection of what happens when a patient is treated with
a particular drug.

"An exciting potential outcome of
this research is that the next wonder drug to treat multidrug-resistant
superbugs may already exist at pharmaceutical companies, which store millions
of chemical compounds," Mahan added. "Some of these compounds may
have been excluded as antibiotics since they did not kill bugs efficiently on
petri plates, but they may work well in treating patients with
multidrug-resistant infections."







Story Source:

The above post is reprinted from materials provided byUniversity
of California - Santa Barbara.
The original item was written by Julie Cohen. Note: Materials may be
edited for content and length.







Journal Reference:

1.   
Jessica Z. Kubicek-Sutherland, Douglas
M. Heithoff, Selvi C. Ersoy, William R. Shimp, John K. House, Jamey D. Marth,
Jeffrey W. Smith, Michael J. Mahan. Host-dependent Induction of Transient
Antibiotic Resistance: A Prelude to Treatment Failure. EBioMedicine,
2015; DOI:10.1016/j.ebiom.2015.08.012

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