| Gene name | Length | Location | Length of alignment | Identity (%) | Coverage (%) | E-value |
|---|---|---|---|---|---|---|
| repA | 1101 | 1 - 1101 (+) | 1101 | 99 | 100 | 0 |
| ORF1832 | 5500 | 50897 - 56395 (+) | 5500 | 91 | 100 | 0 |
| I2 | 121 | 30946 - 31065 (+) | 121 | 96 | 26 | 1.1941E-51 |
| RHS1 | 3679 | 74787 - 78449 (+) | 3679 | 94 | 86 | 0 |
| RHS1 | 2295 | 108065 - 110357 (+) | 2295 | 96 | 54 | 0 |
| RHS1 | 325 | 81756 - 82079 (+) | 325 | 92 | 8 | 4.73081E-129 |
| RHS1 | 356 | 85685 - 86038 (+) | 356 | 86 | 8 | 4.90115E-104 |
| RHS1 | 239 | 83795 - 84032 (+) | 239 | 86 | 6 | 1.43188E-69 |
| RHS1 | 185 | 87311 - 87494 (+) | 185 | 89 | 4 | 3.12149E-61 |
| RHS1 | 89 | 111328 - 111416 (+) | 89 | 100 | 2 | 8.92801E-42 |
| RHS1 | 63 | 85185 - 85246 (+) | 63 | 92 | 1 | 1.98804E-18 |
| RHS2 | 3919 | 74787 - 78689 (+) | 3919 | 92 | 92 | 0 |
| RHS2 | 2527 | 108065 - 110591 (+) | 2527 | 95 | 59 | 0 |
| RHS2 | 431 | 83795 - 84225 (+) | 431 | 90 | 10 | 3.51261E-160 |
| RHS2 | 363 | 81756 - 82117 (+) | 363 | 92 | 8 | 3.58795E-145 |
| RHS2 | 238 | 87311 - 87548 (+) | 238 | 91 | 6 | 6.4898E-88 |
| RHS2 | 272 | 85685 - 85956 (+) | 272 | 88 | 6 | 8.39508E-87 |
| RHS2 | 67 | 85178 - 85244 (+) | 67 | 96 | 2 | 1.52926E-24 |
| Type match | Model name | Model type | Location | E-value | Identity | ||||
|---|---|---|---|---|---|---|---|---|---|
| Perfect | CTX-M-2 | protein homolog model | 88408 - 89283(-) | 0 | 100 % | ||||
|
AMR Gene Family
These enzymes were named for their greater activity against cefotaxime than other oxyimino-beta-lactam substrates (eg, ceftazidime, ceftriaxone, or cefepime). Rather than arising by mutation, they represent examples of plasmid acquisition of beta-lactamase genes normally found on the chromosome of Kluyvera species, a group of rarely pathogenic commensal organisms. These enzymes are not very closely related to TEM or SHV beta-lactamases in that they show only approximately 40% identity with these two commonly isolated beta-lactamases. Despite their name, a few are more active on ceftazidime than cefotaxime. CTX-M-15 was recently found in bacterial strains expressing NDM-1 and were responsible for resistance to aztreonam.
Drug Class
Cephalosporins are a class of beta-lactam antibiotics, containing the beta-lactam ring fused with a dihydrothiazolidine ring. Together with cephamycins they belong to a sub-group called cephems. Cephalosporin are bactericidal, and act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls. The peptidoglycan layer is important for cell wall structural integrity, especially in Gram-positive organisms.
Resistance Mechanism
Enzymatic inactivation of antibiotic to confer drug resistance.
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| Strict | ANT(3'')-IIa | protein homolog model | 97921 - 98826(+) | 0 | 87.71 % | ||||
|
AMR Gene Family
Nucleotidylylation of streptomycin at the hydroxyl group at position 3''
Drug Class
Aminoglycosides are a group of antibiotics that are mostly effective against Gram-negative bacteria. These molecules consist of aminated sugars attached to a dibasic cyclitol. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit (some work by binding to the 50S subunit), inhibiting the translocation of the peptidyl-tRNA from the A-site to the P-site and also causing misreading of mRNA, leaving the bacterium unable to synthesize proteins vital to its growth.
Resistance Mechanism
Enzymatic inactivation of antibiotic to confer drug resistance.
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| Perfect | AAC(6')-Iae | protein homolog model | 98912 - 99463(+) | 6.49108e-136 | 100 % | ||||
|
AMR Gene Family
Acetylation of the aminoglycoside antibiotic on the amino group at position 6'.
Antibiotic
Neomycin is an aminoglycoside antibiotic used to treat different types of bacterial infections. Neomycin works by binding to the bacterial 30S ribosomal subunit, causing misreading of mRNA and leaving the bacterium unable to synthesize proteins vital to its growth.
Antibiotic
Dibekacin is an aminoglycoside antibiotic used to treat different types of bacterial infections. Dibekacin works by binding to the bacterial 30S ribosomal subunit, causing misreading of mRNA and leaving the bacterium unable to synthesize proteins vital to its growth.
Antibiotic
Amikacin is an aminoglycoside antibiotic that works by binding to the bacterial 30S ribosomal subunit, causing misreading of mRNA and leaving the bacterium unable to synthesize proteins vital to its growth.
Antibiotic
Sisomicin is an aminoglycoside antibiotic used to treat different types of bacterial infections. Sisomicin works by binding to the bacterial 30S ribosomal subunit, causing misreading of mRNA and leaving the bacterium unable to synthesize proteins vital to its growth.
Antibiotic
Netilmicin is a member of the aminoglycoside family of antibiotics. These antibiotics have the ability to kill a wide variety of bacteria by binding to the bacterial 30S ribosomal subunit, causing misreading of mRNA and leaving the bacterium unable to synthesize proteins vital to its growth. Netilmicin is not absorbed from the gut and is therefore only given by injection or infusion. It is only used in the treatment of serious infections particularly those resistant to gentamicin.
Antibiotic
Kanamycin is an aminoglycoside antibiotic used to treat different types of bacterial infections. Kanamycin works by binding to the bacterial 30S ribosomal subunit, causing misreading of mRNA and leaving the bacterium unable to synthesize proteins vital to its growth.
Antibiotic
Tobramycin is an aminoglycoside antibiotic used to treat different types of bacterial infections. Tobramycin works by binding to the bacterial 30S ribosomal subunit, causing misreading of mRNA and leaving the bacterium unable to synthesize proteins vital to its growth.
Antibiotic
A semi-synthetic derivative of gentamicin B (hydroxyamino propionyl genamicin B). It is modified to combat microbial inactivation and has a slightly larger spectrum of activity compared to other aminoglycosides, including Ser marcescens, Enterobacteria, and K pneumoniae.
Antibiotic
A synthetic derivative (1-N-(4-amino-2-hydroxybutyryl) of dibekacin used in Japan. It is active against methicillin-resistant Staph. aureus and shows synergy with ampicillin when treating gentamicin and vancomycin resistant enterocci.
Antibiotic
Gentamicin B is a semisynthetic aminoglycoside antibacterial.
Drug Class
Aminoglycosides are a group of antibiotics that are mostly effective against Gram-negative bacteria. These molecules consist of aminated sugars attached to a dibasic cyclitol. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit (some work by binding to the 50S subunit), inhibiting the translocation of the peptidyl-tRNA from the A-site to the P-site and also causing misreading of mRNA, leaving the bacterium unable to synthesize proteins vital to its growth.
Resistance Mechanism
Enzymatic inactivation of antibiotic to confer drug resistance.
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| Perfect | sul1 | protein homolog model | 99978 - 100817(+) | 0 | 100 % | ||||
|
AMR Gene Family
The sul genes encode forms of dihydropteroate synthase that confer resistance to sulfonamide.
Antibiotic
Sulfadiazine is a potent inhibitor of dihydropteroate synthase, interfering with the tetrahydrofolic biosynthesis pathway. Tetrahydrofolic acid is essential for folate synthesis, a precursor to many nucleotides and amino acids.
Antibiotic
Sulfadimidine is an alkaline sulfonamide antibiotic that inhibits dihydropteroate synthase, and enzyme in the tetrahydrofolic acid biosynthesis pathway. This interferes with the production of folate, which is a precursor to many amino acids and nucleotides.
Antibiotic
Sulfadoxine is an inhibitor of dihydropteroate synthase, interfering with the tetrahydrofolic biosynthesis pathway. Tetrahydrofolic acid is essential for folate synthesis, a precursor to many nucleotides and amino acids.
Antibiotic
Sulfamethoxazole is a sulfonamide antibiotic usually taken with trimethoprim, a diaminopyrimidine antibiotic. Sulfamethoxazole inhibits dihydropteroate synthase, essential to tetrahydrofolic acid biosynthesis. This pathway generates compounds used in the synthesis of many amino acids and nucleotides.
Antibiotic
Sulfisoxazole is an inhibitor of dihydropteroate synthase, interfering with the tetrahydrofolic biosynthesis pathway. Tetrahydrofolic acid is essential for folate synthesis, a precursor to many nucleotides and amino acids.
Antibiotic
Sulfacetamide is a very soluable sulfonamide antibiotic previously used to treat urinary tract infections. Its relatively low activity and toxicity to those with Stevens-Johnson syndrome have reduced its use and availability.
Antibiotic
Mafenide is a sulfonamide used topically for treating burns.
Antibiotic
Sulfasalazine is a derivative of the early sulfonamide sulfapyridine (salicylazosulfapyridine). It was developed to increase water solubility and is taken orally for ulcerative colitis.
Antibiotic
Sulfamethizole is a short-acting sulfonamide that inhibits dihydropteroate synthetase.
Drug Class
Sulfonamides are broad spectrum, synthetic antibiotics that contain the sulfonamide group. Sulfonamides inhibit dihydropteroate synthase, which catalyzes the conversion of p-aminobenzoic acid to dihydropteroic acid as part of the tetrahydrofolic acid biosynthetic pathway. Tetrahydrofolic acid is essential for folate synthesis, a precursor of many nucleotides and amino acids. Many sulfamides are taken with trimethoprim, an inhibitor of dihydrofolate reductase, also disturbing the trihydrofolic acid synthesis pathway.
Resistance Mechanism
Replacement or substitution of antibiotic action target, which process will result in antibiotic resistance.
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| Perfect | KHM-1 beta-lactamase | protein homolog model | 113186 - 113911(+) | 0 | 100 % | ||||
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AMR Gene Family
KHM beta-lactmases are Class B beta-lactamases that can confer resistance to all classes of beta-lactams, except the monobactams.
Drug Class
Carbapenems are a class of beta-lactam antibiotics with a broad spectrum of antibacterial activity, and have a structure which renders them highly resistant to beta-lactamases. Carbapenem antibiotics are bactericidal, and act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls. The peptidoglycan layer is important for cell wall structural integrity, especially in Gram-positive organisms.
Drug Class
Cephalosporins are a class of beta-lactam antibiotics, containing the beta-lactam ring fused with a dihydrothiazolidine ring. Together with cephamycins they belong to a sub-group called cephems. Cephalosporin are bactericidal, and act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls. The peptidoglycan layer is important for cell wall structural integrity, especially in Gram-positive organisms.
Drug Class
Cephamycins are a group of beta-lactam antibiotics, very similar to cephalosporins. Together with cephalosporins, they form a sub-group of antibiotics known as cephems. Cephamycins are bactericidal, and act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls. The peptidoglycan layer is important for cell wall structural integrity, especially in Gram-positive organisms. The 7-alpha-methoxy group increases resistance to beta-lactamases.
Drug Class
Penams, often referred to as penicillins, are a group of antibiotics derived from Penicillium fungi. Penicillin antibiotics are historically significant because they are the first drugs that were effective against many previously serious diseases such as syphilis and Staphylococcus infections. Penicillins are still widely used today, though many types of bacteria are now resistant. All penicillins are beta-lactam antibiotics in the penam sub-group, and are used in the treatment of bacterial infections caused by susceptible, usually Gram-positive, organisms.
Drug Class
Penems are a class of unsaturated beta-lactam antibiotics with a broad spectrum of antibacterial activity and have a structure which renders them highly resistant to beta-lactamases. All penems are all synthetically made and act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls. They are structurally similar to carbapenems, however, where carbapenems have a carbon, penems have a sulfur.
Resistance Mechanism
Enzymatic inactivation of antibiotic to confer drug resistance.
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