Letters to the Editor / International Journal of Antimicrobial Agents 36 (2010) 90–98 95 Table 1 Univariate association of patient variables with risk of ototoxicity. Variable Ototoxicity OR (95% CI) P-value a No (n = 32) Yes (n = 7) Age (years) [mean (95% CI)] 27.8 (25.9–29.6) 26.0 (21.2–30.8) – 0.41 Male sex [n (%)] 15 (46.9) 2 (28.6) 0.45 (0.08–2.69) 0.44 Caucasian [n (%)] 19 (59.4) 3 (42.9) 0.51 (0.10–2.69) 0.68 Hispanic [n (%)] 1 (3.1) 2 (28.6) 12.40 (0.94–164) 0.08 Other race [n (%)] 12 (37.5) 2 (28.6) 0.67 (0.11–3.99) 1.00 Diabetes mellitus [n (%)] 8 (25.0) 2 (28.6) 1.20 (0.19–7.44) 1.00 Renal dysfunction [n (%)] b 8 (25.0) 3 (42.9) 2.25 (0.41–12.30) 0.38 Concomitant vancomycin [n (%)] 6 (18.8) 4 (57.1) 5.78 (1.01–32.90) 0.06 Concomitant NSAIDs [n (%)] 10 (31.3) 5 (71.4) 5.50 (0.91–33.35) 0.09 Elevated troughs [n (%)] >10 mg/L (AMK) or >2 mg/L (GEN and TOB) 1 (3.1) 3 (42.9) 23.25 (1.93–280) 0.01 >5 mg/L (AMK) or >1 mg/L (GEN and TOB) 1 (3.1) 3 (42.9) 23.25 (1.93–280) 0.01 >0 mg/L (AMK, GEN and TOB) 22 (68.8) 6 (85.7) 2.73 (0.29–25.75) 0.65 No. of courses AMK c 13 8 – 0.41 GEN c 4 1 – 0.92 TOB c 58 20 – 0.30 All aminoglycoside courses c 75 29 – 0.31 Mean aminoglycoside courses [mean (95% CI)] 2.34 (1.89–2.80) 4.14 (0.2–8.08) – Cumulative dose (g) [mean (95% CI)] AMK 59.1 (17.0–101) 74.4 (-198 to 347) – 0.75 GEN 6.8 (–14.4 to 28.0) 12.6 (N/A) – 0.62 TOB 32.3 (24.4–40.1) 51.6 (20.8–82.4) – 0.06 OR, odds ratio; CI, confidence interval; NSAID, non-steroidal anti-inflammatory drug; AMK, amikacin; GEN, gentamicin; TOB, tobramycin; N/A, not applicable. a Calculated by Student’s t-test for continuous variables or by Fisher’s exact test for categorical variables. b Rise in serum creatinine of >0.5 mg/dL or 50% above baseline. c Reported as absolute number of courses per group. However, the results of this study give rise to the hypothesis that Hispanic CF patients may be predisposed to aminoglycoside- associated ototoxicity and further study of a genetic predisposition is warranted. Despite the fact that this was a small, limited study, we were able to identify two factors that may predispose adult CF patients to aminoglycoside ototoxicity, namely elevated trough concentra- tions and Hispanic race. Funding: No funding sources. Competing interests: None declared. Ethical approval: Ethical approval was obtained through the Northwestern University Institutional Review Board (project # 0273-023); informed consent was not required due to the retrospective de-identified nature of the study. References [1] Tan KH, Mulheran M, Knox AJ, Smyth AR. Aminoglycoside prescribing and surveillance in cystic fibrosis. Am J Respir Crit Care Med 2003;167:819–23. [2] Touw DJ. Clinical pharmacokinetics of antimicrobial drugs in cystic fibrosis. Pharm World Sci 1998;20:149–60. [3] Wood PJ, Ioannides-Demos LL, Li SC, Williams TJ, Hickey B, Spicer WJ, et al. Minimisation of aminoglycoside toxicity in patients with cystic fibrosis. Thorax 1996;51:369–73. [4] Mulheran M, Degg C, Burr S, Morgan DW, Stableforth DE. Occurrence and risk of cochleotoxicity in cystic fibrosis patients receiving repeated high-dose amino- glycoside therapy. Antimicrob Agents Chemother 2001;45:2502–9. [5] Mulherin D, Fahy J, Grant W, Keogan M, Kavanagh B, FitzGerald M. Amino- glycoside induced ototoxicity in patients with cystic fibrosis. Ir J Med Sci 1991;160:173–5. [6] Tang HY, Hutcheson E, Neill S, Drummond-Borg M, Speer M, Alford RL. Genetic susceptibility to aminoglycoside ototoxicity: how many are at risk? Genet Med 2002;4:336–45. [7] Fischel-Ghodsian N, Prezant TR, Chaltraw WE, Wendt KA, Nelson RA, Arnos KS, et al. Mitochondrial gene mutation is a significant predisposing factor in aminoglycoside ototoxicity. Am J Otolaryngol 1997;18:173–8. E. Paul O’Donnell ∗ Midwestern University, Chicago College of Pharmacy, 555 31st Street, Downers Grove, IL 60515, USA Kimberly K. Scarsi Northwestern University Feinberg School of Medicine, Division of Infectious Diseases, 645 N. Michigan Avenue, Suite 900, Chicago, IL 60611, USA Marc H. Scheetz a,b a Midwestern University, Chicago College of Pharmacy, 555 31st Street, Downers Grove, IL 60515, USA b Northwestern Memorial Hospital, 251 E. Huron Street, Feinberg LC-700, Chicago, IL 60611, USA Michael J. Postelnick Northwestern Memorial Hospital, 251 E. Huron Street, Feinberg LC-700, Chicago, IL 60611, USA Joanne Cullina Cystic Fibrosis Center, Children’s Memorial Hospital, 2300 Children’s Plaza, #43, Chicago, IL 60614, USA Manu Jain Northwestern University Division of Pulmonary & Critical Care Medicine, 240 E. Huron Street, McGaw M300, Chicago, IL 60611, USA ∗ Corresponding author. Tel.: +1 630 515 7264. E-mail address: podonn@midwestern.edu (E.P. O’Donnell) 17 January 2010 doi:10.1016/j.ijantimicag.2010.02.018 Antimicrobial susceptibility of pneumococcal isolates causing bacteraemic pneumococcal pneumonia: analysis using current breakpoints and fluoroquinolone pharmacodynamics Sir, We undertook a prospective, observational study in the pub- lic sector (Charlotte Maxeke Johannesburg Academic Hospital) and the private sector (private hospitals in Johannesburg and Preto-