JAC Advance Access published online on October 29, 2003
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkg465
© 2003 by The British Society for Antimicrobial Chemotherapy
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Original article
1 Hospital Ramon y Cajal,
Madrid, Spain;
* Corresponding author. E-mail: i.morrissey{at}grmicro.co.uk.
Received 30 June 2003
; revised 8 August 2003
; accepted 28 August 2003
Objectives: To analyse the mutations
and epidemiology associated with fluoroquinolone-resistant pneumococci
collected as part of the PROTEKT global surveillance programme during
1999-2000. Methods: Sixty-nine centres in 25 countries
submitted a total of 3362 Streptococcus pneumoniae isolates, for
which the MICs of antimicrobial agents were determined using NCCLS
methodology. Results: Levofloxacin resistance was low overall
(1% worldwide), with higher rates in: Hong Kong (14.3%), South
Korea (2.9%), USA (1.8%), Mexico (1.5%),
Canada (1.4%) and Japan (1.3%). Levofloxacin resistance was
very low or absent in European countries, and absent in Australia.
Worldwide, there was a total of 35 levofloxacin-resistant isolates,
of which 22 (63%) were resistant and 10 (29%)
were intermediate to moxifloxacin. All levofloxacin-resistant isolates
were susceptible to telithromycin ( Conclusions: Most levofloxacin-resistant isolates
possess two mutations (one in DNA gyrase and one in topoisomerase
IV). Although multilocus sequence typing demonstrated that most
of these isolates were unrelated, 12 (34%) were the Spain23F-1
clone: 10 from Hong Kong and one each from Saskatchewan, Canada and
Sao Paulo, Brazil.
Keywords: multilocus sequence typing, Spain23F-1,
topoisomerase mutations, fluoroquinolone resistance
Worldwide incidence, molecular epidemiology and
mutations implicated in fluoroquinolone-resistant Streptococcus
pneumoniae:
data from the global PROTEKT surveillance programme
2 University
of Bath, Bath;
3 GR Micro
Ltd, 7-9 William Road,
London NW1 3ER, UK
0.5
mg/L), linezolid (2 mg/L) and quinupristin/dalfopristin
(1 mg/L). One or more mutations in
the topoisomerase genes were identified in all levofloxacin-resistant
isolates; most of these isolates (33/35) had a mutation in one of
the DNA gyrase encoding genes (gyrA, gyrB)
and one of the topoisomerase IV encoding genes (parC, parE). Eighteen (51%) isolates carried
the same combination of amino acid substitutions: Ser-81
Phe
in GyrA and Ser-79Phe in ParC. Isolates
displaying a levofloxacin MIC of 2-4 mg/L generally had
no mutation or one mutation in either a DNA gyrase or a topoisomerase
IV gene, although most mutations were in parC. 
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