Disease Information
General Information of the Disease (ID: DIS00018)
Name |
Non-tuberculous mycobacteria infection
|
---|---|
ICD |
ICD-11: 1B21
|
Resistance Map |
Type(s) of Resistant Mechanism of This Disease
DISM: Drug Inactivation by Structure Modification
IDUE: Irregularity in Drug Uptake and Drug Efflux
UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Drug
Approved Drug(s)
24 drug(s) in total
Amikacin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Amikacin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Ampicillin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Ampicillin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Cefazolin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Cefazolin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Cefepime
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Cefepime | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Cefotaxime
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Cefotaxime | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Cefozopran
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Cefozopran | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Chloramphenicol
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Chloramphenicol | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. | |||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Lincomycin resistance efflux pump (LMRS) | [2] | |||
Resistant Disease | Superficial skin infection by Staphylococcus aureus infection [ICD-11: 1B21.3] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Chloramphenicol | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli kAM32 | 562 | ||
Staphylococcus aureus OM505 | 1280 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | LmrS is a multidrug efflux pump of the major facilitator superfamily from staphylococcus aureus. |
Ciprofloxacin XR
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Ciprofloxacin XR | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Clindamycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: ABC protein lsaC (lsaC-Unclear) | [3] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Clindamycin | |||
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. |
Co-trimoxazole
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Co-trimoxazole | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Dalfopristin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: ABC protein lsaC (lsaC-Unclear) | [3] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Dalfopristin | |||
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. |
Daptomycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Key Molecule: Cardiolipin synthase 2 (CLS2) | [4] | |||
Resistant Disease | Complicated skin infection Staphylococcus aureus infection [ICD-11: 1B21.1] | |||
Molecule Alteration | Missense mutation | p.A23V+p.T33N+p.L52F+p.F60S |
||
Resistant Drug | Daptomycin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Staphylococcus aureus isolates | 1280 | ||
Staphylococcus aureus MRSA32 [A5948] | 553567 | |||
Staphylococcus aureus RN6607 [A8115] | 553573 | |||
Staphylococcus aureus RN9120 [A8117] | 553574 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Mutation in each of these genes act similarly to reduce the net-negative charge of the cell membrane leading to electrorepulsion of daptomycin. They may act in isolation or in concert with each other, particularly for mutations in mprF and cls2. | |||
Key Molecule: Phosphatidylglycerophosphate synthase (PGSA) | [4] | |||
Resistant Disease | Complicated skin infection Staphylococcus aureus infection [ICD-11: 1B21.1] | |||
Molecule Alteration | Missense mutation | p.V59D+p.A64V+p.K75N+p.Ins.G76;Q77+p.S177F |
||
Resistant Drug | Daptomycin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Staphylococcus aureus isolates | 1280 | ||
Staphylococcus aureus MRSA32 [A5948] | 553567 | |||
Staphylococcus aureus RN6607 [A8115] | 553573 | |||
Staphylococcus aureus RN9120 [A8117] | 553574 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | Mutation in each of these genes act similarly to reduce the net-negative charge of the cell membrane leading to electrorepulsion of daptomycin. They may act in isolation or in concert with each other, particularly for mutations in mprF and cls2. |
Erythromycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Lincomycin resistance efflux pump (LMRS) | [2] | |||
Resistant Disease | Superficial skin infection by Staphylococcus aureus infection [ICD-11: 1B21.3] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Erythromycin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli kAM32 | 562 | ||
Staphylococcus aureus OM505 | 1280 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | LmrS is a multidrug efflux pump of the major facilitator superfamily from staphylococcus aureus. |
Florfenicol
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Lincomycin resistance efflux pump (LMRS) | [2] | |||
Resistant Disease | Superficial skin infection by Staphylococcus aureus infection [ICD-11: 1B21.3] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Florfenicol | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli kAM32 | 562 | ||
Staphylococcus aureus OM505 | 1280 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | LmrS is a multidrug efflux pump of the major facilitator superfamily from staphylococcus aureus. |
Gentamicin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Gentamicin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Kanamycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Lincomycin resistance efflux pump (LMRS) | [2] | |||
Resistant Disease | Superficial skin infection by Staphylococcus aureus infection [ICD-11: 1B21.3] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Kanamycin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli kAM32 | 562 | ||
Staphylococcus aureus OM505 | 1280 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | LmrS is a multidrug efflux pump of the major facilitator superfamily from staphylococcus aureus. |
Levofloxacin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Levofloxacin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Lincomycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: ABC protein lsaC (lsaC-Unclear) | [3] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Lincomycin | |||
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. |
Linezolid
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Lincomycin resistance efflux pump (LMRS) | [2] | |||
Resistant Disease | Superficial skin infection by Staphylococcus aureus infection [ICD-11: 1B21.3] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Linezolid | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli kAM32 | 562 | ||
Staphylococcus aureus OM505 | 1280 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | LmrS is a multidrug efflux pump of the major facilitator superfamily from staphylococcus aureus. |
Meropenem
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Meropenem | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Piperacillin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Piperacillin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
Streptomycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Lincomycin resistance efflux pump (LMRS) | [2] | |||
Resistant Disease | Superficial skin infection by Staphylococcus aureus infection [ICD-11: 1B21.3] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Streptomycin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli kAM32 | 562 | ||
Staphylococcus aureus OM505 | 1280 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | LmrS is a multidrug efflux pump of the major facilitator superfamily from staphylococcus aureus. |
Tiamulin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: ABC protein lsaC (lsaC-Unclear) | [3] | |||
Resistant Disease | Streptococcus agalactiae infection [ICD-11: 1B21.2] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Tiamulin | |||
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. |
Trimethoprim
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Lincomycin resistance efflux pump (LMRS) | [2] | |||
Resistant Disease | Superficial skin infection by Staphylococcus aureus infection [ICD-11: 1B21.3] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Trimethoprim | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli kAM32 | 562 | ||
Staphylococcus aureus OM505 | 1280 | |||
Experiment for Molecule Alteration |
Whole genome sequence assay; Allelic frequency measurement assay | |||
Experiment for Drug Resistance |
Broth microdilution method assay | |||
Mechanism Description | LmrS is a multidrug efflux pump of the major facilitator superfamily from staphylococcus aureus. |
Investigative Drug(s)
1 drug(s) in total
Flomoxef
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Key Molecule: OXA-23 carbapenemase (BLA OXA-23) | [1] | |||
Resistant Disease | Cutaneous bacterial infection [ICD-11: 1B21.4] | |||
Molecule Alteration | Expression | Up-regulation |
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Resistant Drug | Flomoxef | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Acinetobacter baumannii isolates | 470 | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Broth microdilution method assay; Agar dilution method assay | |||
Mechanism Description | The isolate was resistant to antibiotics other than ampicillin-sulbactam and colistin, suggesting drug resistance due to carbapenemase production by OXA-23.carbapenem resistance in the isolated carbapenem-resistant A. baumannii strain was at least partially conferred by bla OXA-23-like carbapenemase. |
References
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