Molecule Information
General Information of the Molecule (ID: Mol01173)
Name |
ABC protein lsaC (lsaC-Unclear)
,Streptococcus agalactiae
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Molecule Type |
Protein
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Gene Name |
lsaC
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Sequence |
MSTIKIENLTFSYYGYVKPVFENVSFSFDTNWKTGLIGRNGIGKSTLFKLLLNQEVYKGK
ISKSVDFIKFPPNLSDTSKLGIELYRELISDEEEWKLFRELHLLKVDESLIYRKFETLSK GEQTKILLAILFTREDGFLLIDEPTNHLDMDGRKIVSEYLKNKKGFLLISHDRDFLDGCI NHIISINRNSIDVQSGNFTSWYENKLMKDQFEISQNEKLRKDIKRLKEAARQSQIWSDKV ENTKNGVKVSGVKPDKGHIGHQSAKMMKKSKNLENRQNKAIEEKQNLLKDIETKESLLLH PLHHHKNPLISVCDLSSYYGKKQILSNISFDIKQGDIVAIYGGNGSGKSTLIKILLGLNH EYSGDVKLASNLKISYVPQDTSNLTGSLNEYIHKQGVDETLCKTILRKLDFARELFEIDM KNYSDGQKKKVLIAVSLSKSAHIFIWDEPLNYLDVISRIQIEEIIKEANPTLIFVEHDKS FVEDIANKIIRL Click to Show/Hide
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Click to Show/Hide the Complete Species Lineage | |||||
Type(s) of Resistant Mechanism of This Molecule
IDUE: Irregularity in Drug Uptake and Drug Efflux
Drug Resistance Data Categorized by Drug
Approved Drug(s)
4 drug(s) in total
Clindamycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Clindamycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Clindamycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Clindamycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Clindamycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Clindamycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Klebsiella pneumoniae | [1] | |||
Resistant Disease | Klebsiella pneumoniae [ICD-11: CA40.0] | |||
Resistant Drug | Clindamycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Clindamycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae inection | [1] | |||
Resistant Disease | Streptococcus agalactiae inection [ICD-11: FB84.0] | |||
Resistant Drug | Clindamycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. |
Dalfopristin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Dalfopristin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Dalfopristin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Dalfopristin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Dalfopristin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Dalfopristin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Klebsiella pneumoniae | [1] | |||
Resistant Disease | Klebsiella pneumoniae [ICD-11: CA40.0] | |||
Resistant Drug | Dalfopristin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Dalfopristin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae inection | [1] | |||
Resistant Disease | Streptococcus agalactiae inection [ICD-11: FB84.0] | |||
Resistant Drug | Dalfopristin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. |
Lincomycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Lincomycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Lincomycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Lincomycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Lincomycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Lincomycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Klebsiella pneumoniae | [1] | |||
Resistant Disease | Klebsiella pneumoniae [ICD-11: CA40.0] | |||
Resistant Drug | Lincomycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Lincomycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae inection | [1] | |||
Resistant Disease | Streptococcus agalactiae inection [ICD-11: FB84.0] | |||
Resistant Drug | Lincomycin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. |
Tiamulin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Tiamulin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Tiamulin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Tiamulin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Tiamulin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Tiamulin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Klebsiella pneumoniae | [1] | |||
Resistant Disease | Klebsiella pneumoniae [ICD-11: CA40.0] | |||
Resistant Drug | Tiamulin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae infection | [1] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Resistant Drug | Tiamulin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. | |||
Disease Class: Streptococcus agalactiae inection | [1] | |||
Resistant Disease | Streptococcus agalactiae inection [ICD-11: FB84.0] | |||
Resistant Drug | Tiamulin | |||
Molecule Alteration | Expression | Up-regulation |
||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli TOP10 | 83333 | ||
Staphylococcus aureus ATCC 29213 | 1280 | |||
Streptococcus agalactiae UCN70 | 1311 | |||
Streptococcus agalactiae isolates | 1311 | |||
Streptococcus agalactiae BM132 | 1319 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 ug/ml), clindamycin (0.03 to 2 ug/ml), dalfopristin (2 to >32 ug/ml), and tiamulin (0.12 to 32 ug/ml), whereas no change in MICs of erythromycin (0.06 ug/ml), azithromycin (0.03 ug/ml), spiramycin (0.25 ug/ml), telithromycin (0.03 ug/ml), and quinupristin (8 ug/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. |
References
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