a Department of Microbiology, Level 7, John Radcliffe Hospital, Headington, Oxford OX3 9DU; b Directorate of Public Health and Health Policy, Richards Building, Oxfordshire Health Authority, Old Road, Headington, Oxford OX3 7LG, UK
Sir,
Recent publications have highlighted the increasing rate of trimethoprim resistance in organisms causing community-acquired urinary tract infection (UTI) and have identified associated risk factors.1,2 We have monitored resistance rates among urinary isolates from the Oxford area and, in accordance with Department of Health recommendations, have reassessed data to ensure relevant treatment advice.3 We wish to alert colleagues to the potential for misinterpreting laboratory-generated data and stress the need for caution.
In an attempt to improve immediate patient management and develop more rational use of the laboratory, we promoted the use of biochemical reagent strips for screening urine and introduced guidelines for result interpretation in both community and hospital settings. Clinical criteria were used to allocate patients into high or low UTI risk groups which, together with the result of strip tests for the presence of urinary leucocyte esterase and nitrite, guided clinicians on the need for empirical therapy and use of the laboratory for urine culture (see Table). Trimethoprim was advised for first-line empirical therapy for UTI uncomplicated by the sepsis syndrome or pregnancy in both the community and hospital settings.
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In addition to monitoring laboratory workload we also reviewed the antimicrobial susceptibility of urinary tract pathogens pre- and post-intervention. Escherichia coli accounted for the majority of all significant urinary isolates (74%) and most E. coli were recovered from community samples (80%).
During 19951996, immediately before guideline introduction, resistance rates in 13311 E. coli isolates were: 44.3% for ampicillin, 17.9% for cefradine, 6.4% for augmentin, 0.8% for ciprofloxacin and 28.1% for trimethoprim. Post-guideline introduction, 20002001, resistance rates in 10260 E. coli were (percentage change in brackets): 51.2% (6.9% increase) for ampicillin, 17.3% (0.6% decrease) for cefradine, 5.1% (1.3% decrease) for augmentin, 2.3% (1.5% increase) for ciprofloxacin and 62.5% (34.4% increase) for trimethoprim. The dramatic increase in trimethoprim resistance compared with the pre-guideline introduction rate was not reflected in the changing rates of other commonly prescribed antimicrobial agents.
We attribute the fall in urines cultured to more selective use of the laboratory based on the guidelines. For patients with uncomplicated UTI, empirical therapy with trimethoprim is advised without the need for urine culture. Culture is reserved for recurrent, relapsing and other forms of complicated UTI, situations where previous therapy with trimethoprim is likely. The rise in trimethoprim resistance may be explained in part by more selective use of the laboratory for patients who are more likely to have been exposed to trimethoprim. It cannot be due to increased use because the weight of trimethoprim prescribed either alone or as co-trimoxazole in our catchment population dropped from 164 g/1000 patients in the year ending April 1995 to 116 g/1000 patients in the year ending April 2001.
Variation in both national and regional resistance rates of E. coli to trimethoprim have recently been documented4,5 and highlight the need to base local policy on the relevant local population. When using laboratory data to help formulate policy it is important to recognize the changing way in which laboratories are used and to take into account such changes when interpreting data. We believe that the adoption of guidelines for the diagnosis of UTI may have influenced not only workload but also the level of trimethoprim resistance in E. coli isolated from the urinary tract because the laboratory is now sampling from a different patient population. It is important that decisions about choice of empirical antimicrobial therapy are informed by data on antimicrobial resistance derived from the appropriate patient population.
Notes
* Corresponding author. Tel: +44-1865-220868; Fax: +44-1865-220890; E-mail: barry.batchelor{at}orh.nhs.uk
References
1
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Steinke, D. T., Seaton, R. A., Phillips, G., MacDonald, T. M. & Davey, P. G. (2001). Prior trimethoprim use and trimethoprim-resistant urinary tract infection: a nested casecontrol study with multivariate analysis for other risk factors. Journal of Antimicrobial Chemotherapy 47, 7817.
2
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Howard, A. J., Magee, J. T., Fitzgerald, K. A. & Dunstan, F. D. J. (2001). Factors associated with antibiotic resistance in coliform organisms from community urinary tract infections in Wales. Journal of Antimicrobial Chemotherapy 47, 30513.
3 . Standing Medical Advisory Committee Sub-group on Antimicrobial Resistance. (1998). The Path of Least Resistance. Department of Health, London.
4
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Kanhlmeter, G. (2000). The ECO SENS project: a prospective, multinational, multicentre epidemiological survey of the prevalence and antimicrobial susceptibility of urinary tract pathogensinterim report. Journal of Antimicrobial Chemotherapy 46, Suppl. 1, 1522.
5
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Livermore, D. M., Stephens, P., Weinberg, J., Johnson, A. P., Gifford, T., Northcott, D. et al. (2000). Regional variation in ampicillin and trimethoprim resistance in Escherichia coli in England from 1990 to 1997, in relation to antibacterial prescribing. Journal of Antimicrobial Chemotherapy 46, 41122.