There
could be an explanation for how the most common strain of methicillin-resistant
Staphylococcus aureus (MRSA) rapidly rose to prominence. Research published in
mBio®, suggests that the strain recently acquired a number of genes from common
skin bacteria that allow it to grow and thrive on the skin where other strains
of MRSA cannot.
Since
it was first identified in the late 1990s the USA300 strain of MRSA has
undergone an extremely rapid expansion across the United States. It is now the
predominant cause of community-acquired MRSA skin and soft tissue infections
and has been implicated in MRSA outbreaks among professional football teams.
The strain is genetically distinguished from other strains by a cluster of
genes known as the arginine catabolic mobile element (ACME.)
Using
phylogenetic analysis researchers have shown that the modular segments of ACME
were assembled into a single genetic locus in Staphylococcus epidermidis (a relatively harmless bacterium
typically found on human skin) and then horizontally transferred to the common
ancestor of USA300 strains in an extremely recent event that coincided with the
emergence and spread of this strain.
The
researchers identified one ACME gene in particular, called speG, that conferred
on USA300 strains the ability to withstand high levels of polyamines, compounds
produced by the skin that are toxic to other strains of MRSA. Polyamine
tolerance also gave MRSA multiple advantages including enhanced biofilm
formation, adherence to host tissues and resistance to certain antibiotics,
according to the study.
The
findings suggest that these properties gave USA 300 a major selective advantage
during skin infection and colonization, contributing to the evolutionary
success of this clone.
For
further details see:
Posted by Tim Sandle
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