Islamabad, Jan 11 :
Genetic resistance to antibiotics is not the only trick bacteria use to resist
eradication- they also have a second defence strategy known as persistence that
can kick in.
Researchers reporting in the Journal of Medical Microbiology
have now demonstrated for the first time that interplay occurs between the two
mechanisms to aid bacterial survival. The findings could lead to novel,
effective approaches to treat multi-drug resistant (MDR)
infections.
'Persister' bacterial cells are temporarily hyper-resistant
to all antibiotics at once. They are able to survive (normally) lethal levels of
antibiotics without being genetically resistant to the drug. These cells are a
significant cause of treatment failure yet the mechanism behind the persistence
phenomenon is still unclear.
Scientists from Centre of Microbial and
Plant Genetics, at the Katholieke Universiteit Leuven, Belgium found that the
number of persister cells isolated from Pseudomonas aeruginosa infections
decreases when the bacterial population shows genetic resistance to the
antibiotic fosfomycin.
P. aeruginosa is an opportunistic human pathogen
and a significant cause of hospital-acquired infections. It can cause fatal
infections in people suffering from cystic fibrosis. The bacterium is notorious
for its ability to develop resistance against commonly-used antibiotics and
treatment failure is common.
Professor Jan Michiels who led the study
explained that persister cells are a major contributor to treatment failure.
"Persister cells are produced in low numbers, but nevertheless make it almost
impossible to completely remove the bug from the patient. As a result,
eradication of infections through antibiotic treatment usually takes a long
time," he said. "Our work shows that antibiotic treatment may also influence the
number of persisters formed."
Co-administration therapies are being
developed to treat MDR infections, in which drugs targeting non-essential
cellular functions are combined with antibiotics. Professor Michiels explained
that targeting persistence is an attractive option. "Ideally both susceptible
and persistent cells would be targeted in a single therapy, but firstly we need
to understand more about the interplay between genetic resistance and
persistence to avoid stimulating one or the other. Unravelling the mechanism
behind bacterial persistence is really important to enable us to optimise
treatments of chronic bacterial
infections."
Ends
SA/EN
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