ABSTRACT
In winter 2007-2008, an outbreak of pediatric pneumonia caused by serotype 5 pneumococci was identified in a northeast London suburb. Variable number of tandem repeat analyses clustered these pneumococci from the other serotype 5 pneumococci in the United Kingdom, highlighting the importance of this discriminative typing method in supporting epidemiological investigations.
Subject(s)
Bacterial Typing Techniques/methods , DNA Fingerprinting/methods , Disease Outbreaks , Pneumococcal Infections/epidemiology , Pneumococcal Infections/microbiology , Streptococcus pneumoniae/classification , Streptococcus pneumoniae/genetics , Adult , Child, Preschool , Cluster Analysis , Humans , London/epidemiology , Minisatellite Repeats , Molecular Epidemiology/methods , Streptococcus pneumoniae/isolation & purificationABSTRACT
OBJECTIVES: To investigate the incidence of levofloxacin resistance in Streptococcus pneumoniae isolates cultured by Lancashire Teaching Hospitals NHS Foundation Trust (LTHTR), and detect cases of in vivo resistance development. METHODS: During the study period (September 2004-February 2007), isolates of S. pneumoniae cultured by the LTHTR microbiology laboratory were examined by Etest to determine MICs of levofloxacin. Isolates from patients in whom there was a shift towards colonization with S. pneumoniae of reduced levofloxacin susceptibility were further characterized by serotyping, multilocus sequence typing (MLST) and sequencing of parC and gyrA genes. RESULTS: Eight hundred and sixty-five isolates were collected; however, 772 isolates from 652 patients were recoverable; 412 (53.4%) came from hospitalized patients, 12 (1.6%) were resistant to levofloxacin according to the BSAC breakpoint (>2 mg/L) and 29 (3.8%) had MICs at the breakpoint (MIC = 2 mg/L). Of six patients in whom there was a shift towards isolates with reduced levofloxacin susceptibility, five had acquired new distinct strains. One patient, who had a parC mutation (Ser79Phe) in the original susceptible isolate and an additional second-step mutation in the gyrA gene (Ser81Phe) of the later resistant one, had isolates belonging to the same pneumococcal clone. CONCLUSIONS: S. pneumoniae resistance to levofloxacin was uncommon and we managed to identify only one case of probable in vivo resistance development in the 2.5 years of the study. Strain replacement accounted for the majority of incidences where there was an apparent shift towards colonization with isolates of reduced levofloxacin susceptibility.
