The
treatment of serious infections caused by Staphylococcus aureus (Golden
Staph) is complicated by the development of antibiotic resistance.
Seriously ill patients, vulnerable to infections can be at additional
risk if antimicrobial agents become less effective in fighting
infections.
Published
today in the journal PLoS Pathogens, a new piece has been added to the
puzzle, making the picture clearer. By using whole genome DNA sequencing
of strains obtained from patients during persistent blood stream
infections, Dr. Timothy Stinear and Associate Professor Ben Howden,
senior research fellows from the Department of Microbiology and
Immunology at the University of Melbourne, Australia, have discovered how Staph can make one small change to its
DNA and then develop resistance to the last-line antibiotic, vancomycin.
“We
have applied the latest genome sequencing technology to show that Staph
can readily become vancomycin (antibiotic) resistant by acquiring a
single mutation in its DNA. When the bacteria mutate, they are
reprogramming themselves, changing their cell walls to resist the action
of our antibiotics” said Stinear.
Associate
Professor Howden, who is also the head of Microbiology at Austin
Health, is concerned by the implications of this discovery for patients.
“Worryingly,
this mutation also makes Staph more resistant to another last-line
antibiotic, daptomycin, even though this drug had never been used for
treatment. These last-line therapies are more toxic and cause additional
side-effects in already compromised patients,” said Howden.
“This
study highlights the high adaptability of Staph in the face of
antimicrobial treatment and suggests we need to improve the way in which
we use antibiotics to treat serious bacterial infections,” he said.
