Hiramatsu also demonstrated that strains
from the same area that were vancomycin susceptible
could become intermediate at relative high frequency
[12]. Further investigation revealed that the bacteria had
increased their cell wall production and now had a much
thicker cell wall than the parent strains, which provided
some barrier to vancomycin [13]. Infections caused by
these strains, now known as VISA (vancomycin-intermediate
Staphylococcus aureus) could still be treated. An
in vitro experiment 10 years ago demonstrated that the
much more efficient vancomycin resistance mechanism of
the vanA operon from VRE could transfer and survive in
MRSA [14]; fortunately this was not found in clinical
strains. The situation changed in 2002 when the first
MRSA strain harbouring a vanA operon was found in a
patient in Michigan [15]. This was followed by reports
of a strain in Pennsylvania [16,17] and later in New York.
Courvalin recently described at the 14th European Congress
of Clinical Microbiology and Infectious Diseases
(ECCMID) in Prague that the vanA operon is very similar
to that in VRE but that the mobile element on which it is
located is not stable in S. aureus. To survive, Tn1546 had
to have sufficient opportunity to ‘jump’ into a more stable
replicon in S. aureus. The rarity of reports of vancomycinresistant
S. aureus strains around the world, despite the
pressure that there must be to select them, suggests that
this operon has yet to find a sufficiently stable genetic
environment in MRSA, but surely it will.
De