Abstract
Acinetobacter baumannii is a prevalent nosocomial pathogen with a high incidence of multidrug resistance. Treatment of infections due to this organism with colistin, a last-resort antibiotic of the polymyxin class, can result in the emergence of colistin-resistant strains. Colistin resistance primarily occurs via modifications of the terminal phosphate moieties of lipopolysaccharide-derived lipid A, which reduces overall membrane electronegativity. These modifications are readily identified by mass spectrometry (MS). In this study, we prospectively collected Acinetobacter baumannii complex clinical isolates from a hospital system in Pennsylvania over a 3-year period. All isolates were evaluated for colistin resistance using standard MIC testing by both agar dilution and broth microdilution, as well as genospecies identification and lipid A profiling using MS analyses. Overall, an excellent correlation between colistin susceptibility and resistance, determined by MIC testing, and the presence of a lipid A modification, determined by MS, was observed with a sensitivity of 92.9% and a specificity of 94.0%. Additionally, glycolipid profiling was able to differentiate A. baumannii complex organisms based on their membrane lipids. With the growth of MS use in clinical laboratories, a reliable MS-based glycolipid phenotyping method that identifies colistin resistance in A. baumannii complex clinical isolates, as well as other Gram-negative organisms, represents an alternative or complementary approach to existing diagnostics.
| Original language | English |
|---|---|
| Article number | e01100-18 |
| Journal | Journal of clinical microbiology |
| Volume | 57 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 01-03-2019 |
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All Science Journal Classification (ASJC) codes
- Microbiology (medical)
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A prospective study of acinetobacter baumannii complex isolates and colistin susceptibility monitoring by mass spectrometry of microbial membrane glycolipids. / Leung, Lisa M.; McElheny, Christi L.; Gardner, Francesca M.; Chandler, Courtney E.; Bowler, Sarah L.; Mettus, Roberta T.; Spychala, Caressa N.; Fowler, Erin L.; Opene, Belita N.A.; Myers, Robert A.; Goodlett, David R.; Doi, Yohei; Ernst, Robert K.
In: Journal of clinical microbiology, Vol. 57, No. 3, e01100-18, 01.03.2019.Research output: Contribution to journal › Article
TY - JOUR
T1 - A prospective study of acinetobacter baumannii complex isolates and colistin susceptibility monitoring by mass spectrometry of microbial membrane glycolipids
AU - Leung, Lisa M.
AU - McElheny, Christi L.
AU - Gardner, Francesca M.
AU - Chandler, Courtney E.
AU - Bowler, Sarah L.
AU - Mettus, Roberta T.
AU - Spychala, Caressa N.
AU - Fowler, Erin L.
AU - Opene, Belita N.A.
AU - Myers, Robert A.
AU - Goodlett, David R.
AU - Doi, Yohei
AU - Ernst, Robert K.
PY - 2019/3/1
Y1 - 2019/3/1
N2 - Acinetobacter baumannii is a prevalent nosocomial pathogen with a high incidence of multidrug resistance. Treatment of infections due to this organism with colistin, a last-resort antibiotic of the polymyxin class, can result in the emergence of colistin-resistant strains. Colistin resistance primarily occurs via modifications of the terminal phosphate moieties of lipopolysaccharide-derived lipid A, which reduces overall membrane electronegativity. These modifications are readily identified by mass spectrometry (MS). In this study, we prospectively collected Acinetobacter baumannii complex clinical isolates from a hospital system in Pennsylvania over a 3-year period. All isolates were evaluated for colistin resistance using standard MIC testing by both agar dilution and broth microdilution, as well as genospecies identification and lipid A profiling using MS analyses. Overall, an excellent correlation between colistin susceptibility and resistance, determined by MIC testing, and the presence of a lipid A modification, determined by MS, was observed with a sensitivity of 92.9% and a specificity of 94.0%. Additionally, glycolipid profiling was able to differentiate A. baumannii complex organisms based on their membrane lipids. With the growth of MS use in clinical laboratories, a reliable MS-based glycolipid phenotyping method that identifies colistin resistance in A. baumannii complex clinical isolates, as well as other Gram-negative organisms, represents an alternative or complementary approach to existing diagnostics.
AB - Acinetobacter baumannii is a prevalent nosocomial pathogen with a high incidence of multidrug resistance. Treatment of infections due to this organism with colistin, a last-resort antibiotic of the polymyxin class, can result in the emergence of colistin-resistant strains. Colistin resistance primarily occurs via modifications of the terminal phosphate moieties of lipopolysaccharide-derived lipid A, which reduces overall membrane electronegativity. These modifications are readily identified by mass spectrometry (MS). In this study, we prospectively collected Acinetobacter baumannii complex clinical isolates from a hospital system in Pennsylvania over a 3-year period. All isolates were evaluated for colistin resistance using standard MIC testing by both agar dilution and broth microdilution, as well as genospecies identification and lipid A profiling using MS analyses. Overall, an excellent correlation between colistin susceptibility and resistance, determined by MIC testing, and the presence of a lipid A modification, determined by MS, was observed with a sensitivity of 92.9% and a specificity of 94.0%. Additionally, glycolipid profiling was able to differentiate A. baumannii complex organisms based on their membrane lipids. With the growth of MS use in clinical laboratories, a reliable MS-based glycolipid phenotyping method that identifies colistin resistance in A. baumannii complex clinical isolates, as well as other Gram-negative organisms, represents an alternative or complementary approach to existing diagnostics.
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U2 - 10.1128/JCM.01100-18
DO - 10.1128/JCM.01100-18
M3 - Article
VL - 57
JO - Journal of Clinical Microbiology
JF - Journal of Clinical Microbiology
SN - 0095-1137
IS - 3
M1 - e01100-18
ER -