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Antimicrob Agents Chemother. Triclosan Induced Aminoglycoside-Tolerant Listeria monocytogenes Isolates can appear as Small-Colony Variants.
[Source: Antimicrobial Agents and Chemotherapy, full page: (LINK). Abstract, edited.]
Triclosan Induced Aminoglycoside-Tolerant Listeria monocytogenes Isolates can appear as Small-Colony Variants.
Vicky G. Kastbjerg 1, Line Hein-Kristensen 1 and Lone Gram 2*
Author Affiliations: <SUP>1</SUP> National Food Institute, Technical University of Denmark, S?ltofts Plads bldg. 221, Dk-2800 Kgs. Lyngby, Denmark <SUP>2</SUP> Department of System Biology, Technical University of Denmark, S?ltofts Plads bldg. 221, Dk-2800 Kgs. Lyngby, Denmark
ABSTRACT
Exposure of the human food-borne pathogen L. monocytogenes to sublethal concentrations of triclosan can cause resistance to several aminoglycosides. These aminoglycoside-resistant isolates exhibit two colony morphologies: normal sized and pin-point sized colonies. The purpose of the present study was to characterize the small colonies of L. monocytogenes, and to determine if specific genetic changes could explain the triclosan-induced aminoglycoside-resistance in both pin-point and normal sized isolates. Isolates from the pin-point colonies grew poorly under aerated conditions, but growth was restored by addition of antibiotics. Pin-point isolates had decreased hemolytic activity under stagnant conditions, and a changed spectrum of carbohydrate utilization as compared to wild type and isolates from normal sized colonies. Genome sequence comparison revealed that all seven pin-point isolates had a mutation in a heme gene, and addition of heme caused the pin-point isolates to revert to normal colony size. Triclosan-induced gentamicin-resistant isolates had mutations in several different genes, and it cannot be directly concluded how the different mutations caused gentamicin-resistance. However, since many of the mutations affected proteins involved in respiration, it seems likely that the mutations affected the active transport of the antibiotic and thereby cause resistance by decreasing the amount of aminoglycoside that enters the bacterial cell. Our study emphasizes that triclosan likely has more targets than just fabI and exposure to triclosan can cause resistance to antibiotics that enters the cell via active transport. Further studies are needed to elucidate if L. monocytogenes pin-point isolates could have any clinical impact e.g. in persistent infections.
FOOTNOTES
*Corresponding author Address: Department of System Biology, Technical University of Denmark, Matematiktorvet bldg 301, DK-2800 Kgs. Lyngby, Denmark, E-mail: gram@bio.dtu.dk, Phone: +45 45252586, Fax: +45 45884774
Copyright ? 2014, American Society for Microbiology. All Rights Reserved.
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Triclosan Induced Aminoglycoside-Tolerant Listeria monocytogenes Isolates can appear as Small-Colony Variants.
Vicky G. Kastbjerg 1, Line Hein-Kristensen 1 and Lone Gram 2*
Author Affiliations: <SUP>1</SUP> National Food Institute, Technical University of Denmark, S?ltofts Plads bldg. 221, Dk-2800 Kgs. Lyngby, Denmark <SUP>2</SUP> Department of System Biology, Technical University of Denmark, S?ltofts Plads bldg. 221, Dk-2800 Kgs. Lyngby, Denmark
ABSTRACT
Exposure of the human food-borne pathogen L. monocytogenes to sublethal concentrations of triclosan can cause resistance to several aminoglycosides. These aminoglycoside-resistant isolates exhibit two colony morphologies: normal sized and pin-point sized colonies. The purpose of the present study was to characterize the small colonies of L. monocytogenes, and to determine if specific genetic changes could explain the triclosan-induced aminoglycoside-resistance in both pin-point and normal sized isolates. Isolates from the pin-point colonies grew poorly under aerated conditions, but growth was restored by addition of antibiotics. Pin-point isolates had decreased hemolytic activity under stagnant conditions, and a changed spectrum of carbohydrate utilization as compared to wild type and isolates from normal sized colonies. Genome sequence comparison revealed that all seven pin-point isolates had a mutation in a heme gene, and addition of heme caused the pin-point isolates to revert to normal colony size. Triclosan-induced gentamicin-resistant isolates had mutations in several different genes, and it cannot be directly concluded how the different mutations caused gentamicin-resistance. However, since many of the mutations affected proteins involved in respiration, it seems likely that the mutations affected the active transport of the antibiotic and thereby cause resistance by decreasing the amount of aminoglycoside that enters the bacterial cell. Our study emphasizes that triclosan likely has more targets than just fabI and exposure to triclosan can cause resistance to antibiotics that enters the cell via active transport. Further studies are needed to elucidate if L. monocytogenes pin-point isolates could have any clinical impact e.g. in persistent infections.
FOOTNOTES
*Corresponding author Address: Department of System Biology, Technical University of Denmark, Matematiktorvet bldg 301, DK-2800 Kgs. Lyngby, Denmark, E-mail: gram@bio.dtu.dk, Phone: +45 45252586, Fax: +45 45884774
Copyright ? 2014, American Society for Microbiology. All Rights Reserved.
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