Drug Resistance Updates 13 (2010) 132–138
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Drug Resistance Updates
journal homepage: www.elsevier.com/locate/drup
Resistance to polymyxins: Mechanisms, frequency and treatment options
Matthew E. Falagas
a,b,c,*
, Petros I. Rafailidis
a,b
, Dimitrios K. Matthaiou
a,d
a
Alfa Institute of Biomedical Sciences (AIBS), Athens, Greece
b
Department of Medicine, Henry Dunant Hospital, Athens, Greece
c
Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts, USA
d
Department of Medicine, “G. Gennimatas” General Hospital, Thessaloniki, Greece
article info
Article history:
Received 27 April 2010
Received in revised form 24 May 2010
Accepted 24 May 2010
Keywords:
Colistin
Multidrug-resistance
Polymyxin
Pandrug-resistance
Fosfomycin
Tigecycline
abstract
Polymyxins act by binding to lipid A moiety of the bacterial lipopolysaccharide and subsequently disinte-
grating the bacterial membranes. The most important mechanism of resistance includes modifications of
the bacterial outer membrane structure, including lipopolysaccharide. Lipopolysaccharide modification
is mostly mediated by PmrA/PmrB and PhoP/PhoQ two-component regulatory systems. These mecha-
nisms exist with some differences in many gram-negative bacterial species. Resistance to polymyxins
is generally less than 10%. In specific regions, such as the Mediterranean basin, Korea and Singapore,
they tend to be higher. Heteroresistance to polymyxins is associated with exposure to polymyxins and
especially suboptimal therapeutic dosage. Polymyxin combination regimens, tigecycline and fosfomycin
may be useful options for the treatment of polymyxin-resistant gram-negative infections.
© 2010 Elsevier Ltd. All rights reserved.
1. Introduction
Polymyxins include polymyxin B and colistin (polymyxin E),
and are derivatives of the Bacillus polymyxa subspecies colistinus.
They belong to a diverse group of natural antimicrobials found in
eucariotic cells called cationic antimicrobial peptides. Structurally,
they are decapeptides bound to a fatty acid chain. They consist of
a seven-member cyclic ring of aminoacids with a tripeptide side
chain. The side chain links to the lipidic part of the molecule. The
heptapeptide ring is the same between the two polymyxins with
the exception of a single aminoacid, which is phenylalalanine in
polymyxin B and leucine in colistin (Kwa et al., 2007).
Polymyxins were discovered in the late 1940’s and were widely
used until the mid-1980’s when they were forsaken due to the
reported adverse events, namely nephrotoxicity. They remained in
clinical practice for the management of pseudomonal lung infec-
tions in patients with cystic fibrosis and in topical solutions with
other antimicrobials for the treatment of ear or eye infections. They
reappeared as an option for the management of gram-negative
infections (administration by the intravenous, and/or nebulized
or intrathecal route) for non-cystic fibrosis patients after the
emergence of multidrug-resistant pathogens and the subsequent
*
Corresponding author at: Alfa Institute of Biomedical Sciences (AIBS), 9
Neapoleos Street, 15 123, Marousi, Greece. Tel.: +30 694 611 0000;
fax: +30 210 683 9605.
E-mail address: m.falagas@aibs.gr (M.E. Falagas).
restriction of possible alternatives (Falagas and Kasiakou, 2005).
Despite their relatively recent reintegration in clinical practice,
resistance to polymyxins constitutes already an issue of signifi-
cance.
Polymyxins are active against gram-negative pathogens includ-
ing Pseudomonas aeruginosa, Acinetobacter baumannii, Klebsiella
spp., Escherichia coli and other enterobacteriaceae. However, there
are species possessing intrinsic resistance, such as Providencia spp.,
Neisseria spp., Proteus spp., Serratia marcescens and Burkholderia
cepacia. Polymyxins are not active against gram-positive bacteria
nor against anaerobes.
2. Mechanism of action
Lipopolysaccharide (LPS) is a structural component of the bacte-
rial outer membrane consisting of O antigen, a core polysaccharide
and lipid A, which anchors in the outer membrane (Raetz and
Whitfield, 2002). It bears negative charge and confers to the
integrity and stability of the bacterial outer membrane. Polymyx-
ins, having positive charge, displace Mg
2+
or Ca
2+
and bind on lipid
A component resulting in the destabilization and disruption of the
outer and inner membranes (Brown and Tsang, 1978; Clausell et
al., 2007; Davis et al., 1971; Newton, 1956; Schindler and Osborn,
1979). The most potent part of the polymyxin molecule is the
hydrophobic lipid tail. Polymyxin nonapeptide, which is the acyl
part remaining after the removal of the lipidic component, exerts
antimicrobial properties though to a lesser extent. It has lesser
affinity than the hydrophobic tail, but sensitizes bacteria to the
1368-7646/$ – see front matter © 2010 Elsevier Ltd. All rights reserved.
doi:10.1016/j.drup.2010.05.002