To the Editor—Since the invasion of Afghanistan in October 2001, Walter Reed Army Medical Center (WRAMC) has been a destination for service members wounded in Iraq and Afghanistan. For reasons that have yet to be fully elucidated, their wounds are commonly colonized or infected with multidrug-resistant (MDR), gram-negative bacilliform bacteria, including Acinetobacter baumannii-calcoaceticus (ABC). Indeed, 96% of the ABC organisms isolated at WRAMC since 2000 were isolated within the past 4 years; this increasing prevalence has been matched by increasing resistance to antibiotics (especially resistance to ceftazidime, fluoroquinolones, gentamicin, imipenem, and piperacillin/tazobactam). To treat infections with MDR ABC, physicians increasingly resort to an intravenous formulation of a polymyxin, such as colistin (0 g dispensed for inpatient use at WRAMC in 2001 vs. 350 g dispensed in 2006), to which 98.6% of our ABC isolates remain susceptible. Moreover, polymicrobial infections with MDR ABC and other MDR gram-negative bacteria are increasingly common, most notably with extended-spectrum β-lactamase (ESBL)–producing Escherichia coli and Klebsiella pneumoniae and AmpC β-lactamase–producing Enterobacter species. Although the polymyxins are generally effective against gram-negative bacteria [1], data are lacking regarding their efficacy against MDR β-lactamase–producing Enterobacteraceae. Faced with a polymicrobial infection involving both a carbapenem-resistant ABC organism (39% of ABC organisms isolated from our inpatients) and ESBL- or AmpC β-lactamase–producing gram-negative bacteria, physicians may opt for dual therapy with a polymyxin and a carbapenem. Potentially, however, monotherapy with a polymyxin might be adequate against both organisms. One hundred fifty clinical ESBL- and AmpC β-lactamase–producing clinical isolates composed of Enterobacter cloacae (28 isolates), Enterobacter aerogenes (2 isolates), Enterobacter hormachei (1 isolate), E. coli (48 isolates), and K. pneumoniae (71 isolates) were identified using the Phoenix System ID/AST (BD Diagnostic Systems) and were tested for in vitro colistin susceptibility using the E-test (AB Biodisk). Specimen sources included blood (for 23 samples), bronchoalveolar lavage fluid (for 4 samples), an intravenous catheter tip (for 1 sample), sputum (for 12 samples), sterile fluids (for 3 samples), sterile sites (for 38 samples), tracheal aspirates (for 8 samples), urine (for 39 samples), and wounds (for 22 samples). MICs were determined for all specimens (table 1). In accordance with established guidelines, an isolate was considered to be susceptible to colistin if the MIC was <4 µg/mL and resistant to colistin if the MIC was >8 µg/mL [2]. All but 2 (98.7%) of the isolates that were tested were considered to be susceptible to colistin using the E-test. One isolate each of E. cloacae and K. pneumoniae were colistin resistant, with an MIC of 32 µg/mL and 12 µg/mL, respectively. The former was isolated from a sample of BAL fluid, the latter from a urine sample. Among the Enterobacter species tested, 30 (96.8%) of 31 were susceptible to colistin (median MIC, 0.19 µg/mL). Seventy (98.6%) of 71 K. pneumoniae isolates were susceptible to colistin (median MIC, 0.25 µg/mL), as were all 48 E. coli isolates (100%) that were tested (median MIC, 0.38 µg/mL). In vitro susceptibility of extended-spectrum β-lactamases and AmpC β-lactamase–producing Enterobacteraceae clinical isolates. Polymicrobial wound infections caused by MDR ABC and β-lactamase–producing gram-negative bacteria are increasingly common at WRAMC [3]. Our data suggest that colistin has fairly reliable in vitro activity against the ESBL- and AmpC β-lactamase–producing Enterobacteriaceae, and it might be useful in the treatment of coinfection with these organisms and MDR ABC. Potential conflicts of interest. All authors: no conflicts.
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Paolino et al. (2007) studied this question.
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