(centres A and F) (Figure 1). The remaining 10 isolates were unique types by PFGE. These data indicate that qnrA-positive E. cloacae isolates are widely scattered in SE England, at least, and that one strain with the mechanism has spread among three hospitals. Equally sig- nificant, however, was the absence of qnrA from the large number of CTX-M b-lactamase-positive Escherichia coli and Klebsiella investigated, although virtually all of these were also quinolone-resistant. Many of these latter isolates have fluoroqui- nolone resistance co-mediated by plasmids that encode the ami- noglycoside/ciprofloxacin modifying enzyme AAC(6 )-Ib-cr along with the CTX-M-15 b-lactamase. 8 Acknowledgements We would like to acknowledge Nicola Potz and the 2004 South East England ESBL survey for providing strains for this study. Parts of this work were presented at the Forty-fifth Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC), Washington, DC, 2005 (Ellington MJ, Hope R, Turton J, Livermore DM, Woodford N. In: Abstracts of the Forty-fifth Interscience Conference on Antimicrobial Agents and Chemotherapy, Washington, DC, 2005. Abstract C2-786, p. 119. American Society for Microbiology, Washington, DC, USA). Funding This work was supported by the Health Protection Agency. Transparency declarations None to declare. References 1. Wang M, Tran JH, Jacoby GA et al. Plasmid-mediated quinolone resistance in clinical isolates of Escherichia coli from Shanghai, China. Antimicrob Agents Chemother 2003; 47: 2242–8. 2. Jacoby GA. Mechanisms of resistance to quinolones. Clin Infect Dis 2005; 41: S120–6. 3. Nordmann P, Poirel L. Emergence of plasmid-mediated resist- ance to quinolones in Enterobacteriaceae. J Antimicrob Chemother 2005; 56: 463–9. 4. Cheung TKM, Chu YW, Chu MY et al. Plasmid-mediated resis- tance to ciprofloxacin and cefotaxime in clinical isolates of Salmonella enterica serotype Enteritidis in Hong Kong. J Antimicrob Chemother 2005; 56: 586–9. 5. Corkill JE, Anson JJ, Hart CA. High prevalence of the plasmid- mediated quinolone resistance determinant qnrA in multidrug-resistant Enterobacteriaceae from blood cultures in Liverpool, UK. J Antimicrob Chemother 2005; 56: 1115–7. 6. Andrews JM. BSAC standardized disc susceptibility testing method (version 4). J Antimicrob Chemother 2005; 56: 60–76. 7. Mammeri H, Van De LM, Poirel L et al. Emergence of plasmid- mediated quinolone resistance in Escherichia coli in Europe. Antimicrob Agents Chemother 2005; 49: 71–6. 8. Karisik E, Ellington MJ, Pike R et al. Molecular characterization of plasmids encoding CTX-M-15 b-lactamase from Escherichia coli strains in the United Kingdom. J Antimicrob Chemother 2006; 58: 665–8. Journal of Antimicrobial Chemotherapy doi:10.1093/jac/dkm343 Advance Access publication 6 September 2007 Is Bordetella pertussis susceptibility to erythromycin changing? MIC trends among Australian isolates 1971 – 2006 Vitali Sintchenko 1,2 *, Mitchell Brown 1 and Gwendolyn L. Gilbert 1,2 1 Centre for Infectious Diseases and Microbiology, Institute of Clinical Pathology and Medical Research, Sydney West Area Health Service, Sydney, Australia; 2 Western Clinical School, The University of Sydney, Sydney, Australia Keywords: pertussis, antibiotic therapy, resistance *Corresponding author. Tel: þ61-2-9845-6255; Fax: þ61-2- 9893-8659; E-mail: vitalis@icpmr.wsahs.nsw.gov.au Sir, Pertussis is a highly contagious respiratory tract infection caused by Bordetella pertussis and, less frequently, by Bordetella para- pertussis. There is the suggestion that vaccination programmes over the last century may have led to genetic changes in B. per- tussis. 1 However, the extent of genetic diversity in different countries remains debatable. Macrolide antibiotics have been used for treatment and prophylaxis of pertussis for over 50 years, but occasional reports of resistance to erythromycin, the traditional antibiotic of choice, highlight the need for continued surveillance of pertussis. 2,3 Unfortunately, widespread replace- ment of culture with direct nucleic acid amplification, for diag- nosis of pertussis, has dramatically decreased the availability of clinical isolates for testing and resulted in a lack of data on the antimicrobial susceptibility of B. pertussis and its temporal trends. This study reports susceptibility to erythromycin of clini- cal isolates of B. pertussis collected from patients in New South Wales between 1971 and 2006. A convenience sample of 99 isolates of B. pertussis and 5 of B. parapertussis from our laboratory collection was used. All isolates had been recovered from respiratory specimens by culture on selective agar plates and stored in nutrient broth con- taining 10% glycerol at 2708C. Suspensions of the isolates from a master stock were subcultured onto charcoal blood agar without antibiotics (Oxoid, Australia) and incubated in a moist, closed ambient air environment at 358C for 72 h. The bacterial cells were then harvested and suspended in 2 mL of PBS and the turbidity adjusted to be equivalent to that of a 0.5 McFarland standard. All isolates were tested using 15 mg erythromycin discs. The plates were incubated at 358C in high humidity, and zones of growth inhibition were measured on days 3 and 5. Isolates with growth inhibition of more than 40 mm in diameter after 3 days of incubation were considered as susceptible. 4 Plates were incubated for 7 days to exclude heterogeneous phe- notypes as indicated by resistant colonies appearing within the zone after extended incubation. 5 The MIC of erythromycin was determined by Etest (AB BIODISK, Solna, Sweden), performed Correspondence 1178 Downloaded from https://academic.oup.com/jac/article/60/5/1178/2359066 by guest on 18 August 2022