Aminoglycoside resistance and susceptibility testing errors in Acinetobacter baumannii-calcoaceticus complex
Kevin S Akers1, Chris Chaney, Alice Barsoumian
1Infectious Disease Service, San Antonio Military Medical Center, 3851 Roger Brooke Drive, Fort Sam Houston, Texas 78234-6200, USA.
Journal of Clinical Microbiology
|January 29, 2010
Summary
Accurate antimicrobial susceptibility testing is crucial for Gram-negative bacilli. Tobramycin showed the most activity, but all tested methods had errors, highlighting the need for improved diagnostics and understanding of resistance mechanisms.
Area of Science:
- Microbiology
- Clinical Diagnostics
- Molecular Biology
Background:
- Antimicrobial resistance in Gram-negative bacilli is a growing threat, reducing treatment options.
- Accurate antimicrobial susceptibility testing (AST) is essential for effective patient management.
- The Acinetobacter baumannii-calcoaceticus complex is a significant cause of hospital-acquired infections.
Purpose of the Study:
- To evaluate the accuracy of various AST methods for amikacin, gentamicin, and tobramycin against Acinetobacter baumannii-calcoaceticus complex isolates.
- To identify aminoglycoside-modifying enzyme (AME) genes and assess their correlation with resistance.
- To investigate the prevalence and mechanisms of aminoglycoside resistance in a clinical setting.
Main Methods:
- Susceptibility testing of 107 Acinetobacter baumannii-calcoaceticus complex isolates using disk diffusion, Etest, Phoenix, Vitek 2, MicroScan, and broth microdilution.
- Detection of AME genes via multiplex PCR.
- Clonal relationship determination using pulsed-field gel electrophoresis (PFGE).
Main Results:
- Tobramycin was the most active aminoglycoside, with 27.1% susceptibility.
- Disk diffusion and Etest were generally more accurate than automated systems, though all methods exhibited errors.
- The Vitek 2 system showed significant errors, misclassifying amikacin susceptibility.
- Multiple AME genes were detected, with ant(2")-Ia statistically associated with resistance, but genotypes explained only a minority of resistance profiles.
- Resistance prevalence in a burn intensive care unit did not correlate with strain type, genotype, or consumption.
Conclusions:
- Current AST methods have limitations in accurately determining aminoglycoside susceptibility for Acinetobacter baumannii-calcoaceticus complex.
- Multiple, potentially uncharacterized, resistance mechanisms contribute to aminoglycoside resistance.
- Further research into the interplay of various resistance mechanisms is needed to improve therapeutic strategies.
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