| Gene name | Length | Location | Length of alignment | Identity (%) | Coverage (%) | E-value |
|---|---|---|---|---|---|---|
| repA | 1101 | 89495 - 90595 (+) | 1101 | 100 | 100 | 0 |
| RHS1 | 4254 | 61276 - 65529 (+) | 4254 | 100 | 100 | 0 |
| AriB | 1156 | 119894 - 121049 (+) | 1156 | 100 | 44 | 0 |
| AriB | 640 | 112350 - 112989 (+) | 640 | 100 | 24 | 0 |
| Type match | Model name | Model type | Location | E-value | Identity | ||||
|---|---|---|---|---|---|---|---|---|---|
| Perfect | TEM-1 | protein homolog model | 56757 - 57617(-) | 0 | 100 % | ||||
|
AMR Gene Family
TEM-1 is the most commonly-encountered beta-lactamase in gram-negative bacteria. Up to 90% of ampicillin resistance in E. coli is due to the production of TEM-1. Also responsible for the ampicillin and penicillin resistance that is seen in H. influenzae and N. gonorrhoeae in increasing numbers. Although TEM-type beta-lactamases are most often found in E. coli and K. pneumoniae, they are also found in other species of gram-negative bacteria with increasing frequency. The amino acid substitutions responsible for the ESBL phenotype cluster around the active site of the enzyme and change its configuration, allowing access to oxyimino-beta-lactam substrates. Opening the active site to beta-lactam substrates also typically enhances the susceptibility of the enzyme to b-lactamase inhibitors, such as clavulanic acid. Although the inhibitor-resistant beta-lactamases are not ESBLs, they are often discussed with ESBLs because they are also derivatives of the classical TEM- or SHV-type enzymes. These enzymes were at first given the designation IRT for inhibitor-resistant TEM beta-lactamase; however, all have subsequently been renamed with numerical TEM designations. There are at least 19 distinct inhibitor-resistant TEM beta-lactamases. Inhibitor-resistant TEM beta-lactamases have been found mainly in clinical isolates of E. coli, but also some strains of K. pneumoniae, Klebsiella oxytoca, P. mirabilis, and Citrobacter freundii. Although the inhibitor-resistant TEM variants are resistant to inhibition by clavulanic acid and sulbactam, thereby showing clinical resistance to the beta-lactam-lactamase inhibitor combinations of amoxicillin-clavulanate (Co-amoxiclav), ticarcillin-clavulanate, and ampicillin/sulbactam, they normally remain susceptible to inhibition by tazobactam and subsequently the combination of piperacillin/tazobactam, although resistance has been described.
Antibiotic
Amoxicillin is a moderate-spectrum, bacteriolytic, beta-lactam antibiotic used to treat bacterial infections caused by susceptible microorganisms. A derivative of penicillin, it has a wider range of treatment but remains relatively ineffective against Gram-negative bacteria. It is commonly taken with clavulanic acid, a beta-lactamase inhibitor. Like other beta-lactams, amoxicillin interferes with the synthesis of peptidoglycan.
Antibiotic
Ampicillin is a penicillin derivative that is highly acid stable, with its activity similar to benzylpenicillin.
Antibiotic
Cefalotin is a semisynthetic cephalosporin antibiotic activate against staphylococci. It is resistant to staphylococci beta-lactamases but hydrolyzed by enterobacterial beta-lactamases.
Drug Class
Monobactams 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. Unlike penams and cephems, monobactams do not have any ring fused to its four-member lactam structure. Monobactam 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
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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| Strict | floR | protein homolog model | 113886 - 115100(+) | 0 | 99.5 % | ||||
|
AMR Gene Family
Directed pumping of antibiotic out of a cell to confer resistance. Major facilitator superfamily (MFS) transporters and ABC transporters comprise the two largest and most functionally diverse of the transporter superfamilies. However, MFS transporters are distinct from ABC transporters in both their primary sequence and structure and in the mechanism of energy coupling. As secondary transporters they are, like RND and SMR transporters, energized by the electrochemical proton gradient.
Antibiotic
Chloramphenicol is a bacteriostatic antimicrobial originally derived from the bacterium Streptomyces venezuelae. It was the first antibiotic to be manufactured synthetically on a large scale. It functions by inhibiting peptidyl transferase activity of the bacterial ribosome, binding to A2451 and A2452 residues in the 23S rRNA of the 50S ribosomal subunit and preventing peptide bond formation.
Antibiotic
Florfenicol is a fluorine derivative of chloramphenicol, where the nitro group (-NO2) is substituted by a sulfomethyl group (-SO2CH3) and the hydroxyl group (-OH), by a fluorine group (-F). The action mechanism is the same as chloramphenicol's, where the antibiotic binds to the 23S RNA of the 50S subunit of bacterial ribosomes to inhibit protein synthesis.
Drug Class
Phenicols are broad spectrum bacteriostatic antibiotics acting on bacterial protein synthesis. More specifically, the phenicols block peptide elongation by binding to the peptidyltansferase centre of the 70S ribosome.
Efflux Component
Efflux proteins that pump antibiotic out of a cell to confer resistance.
Resistance Mechanism
Antibiotic resistance via the transport of antibiotics out of the cell.
|
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| Strict | tet(A) | protein homolog model | 115700 - 116899(-) | 0 | 99.75 % | ||||
|
AMR Gene Family
Directed pumping of antibiotic out of a cell to confer resistance. Major facilitator superfamily (MFS) transporters and ABC transporters comprise the two largest and most functionally diverse of the transporter superfamilies. However, MFS transporters are distinct from ABC transporters in both their primary sequence and structure and in the mechanism of energy coupling. As secondary transporters they are, like RND and SMR transporters, energized by the electrochemical proton gradient.
Antibiotic
Tetracycline is a broad-spectrum polyketide antibiotic produced by many Streptomyces. It works by inhibiting action of the prokaryotic 30S ribosome.
Drug Class
These antibiotics are derived from tetracycline, a polyketide antibiotic that inhibits the 30S subunit of bacterial ribosomes.
Efflux Component
Efflux proteins that pump antibiotic out of a cell to confer resistance.
Resistance Mechanism
Antibiotic resistance via the transport of antibiotics out of the cell.
|
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| Strict | APH(6)-Id | protein homolog model | 118235 - 119071(-) | 0 | 99.64 % | ||||
|
AMR Gene Family
Phosphorylation of streptomycin on the hydroxyl group at position 6
Antibiotic
Streptomycin is an aminoglycoside antibiotic used to treat different types of bacterial infections. Streptomycin 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.
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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| Strict | APH(3'')-Ib | protein homolog model | 119071 - 119874(-) | 0 | 99.63 % | ||||
|
AMR Gene Family
Phosphorylation of streptomycin on the hydroxyl group at position 3''
Antibiotic
Streptomycin is an aminoglycoside antibiotic used to treat different types of bacterial infections. Streptomycin 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.
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 | sul2 | protein homolog model | 119935 - 120750(-) | 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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| Strict | catII from Escherichia coli K-12 | protein homolog model | 152385 - 153026(-) | 4.28881e-163 | 98.12 % | ||||
|
AMR Gene Family
Inactivates chloramphenicol by addition of an acyl group. cat is used to describe many variants of the chloramphenicol acetyltransferase gene in a range of organisms including Acinetobacter calcoaceticus, Agrobacterium tumefaciens, Bacillus clausii, Bacillus subtilis, Campylobacter coli, Enterococcus faecalis, Enterococcus faecium, Lactococcus lactis, Listeria monocytogenes, Listonella anguillarum Morganella morganii, Photobacterium damselae subsp. piscicida, Proteus mirabilis, Salmonella typhi, Serratia marcescens, Shigella flexneri, Staphylococcus aureus, Staphylococcus haemolyticus, Staphylococcus intermedius, Streptococcus agalactiae, Streptococcus suis and Streptomyces acrimycini
Antibiotic
Chloramphenicol is a bacteriostatic antimicrobial originally derived from the bacterium Streptomyces venezuelae. It was the first antibiotic to be manufactured synthetically on a large scale. It functions by inhibiting peptidyl transferase activity of the bacterial ribosome, binding to A2451 and A2452 residues in the 23S rRNA of the 50S ribosomal subunit and preventing peptide bond formation.
Drug Class
Phenicols are broad spectrum bacteriostatic antibiotics acting on bacterial protein synthesis. More specifically, the phenicols block peptide elongation by binding to the peptidyltansferase centre of the 70S ribosome.
Resistance Mechanism
Enzymatic inactivation of antibiotic to confer drug resistance.
|
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| Perfect | CTX-M-55 | protein homolog model | 154424 - 155299(+) | 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.
Antibiotic
Ceftazidime is a third-generation cephalosporin antibiotic. Like other third-generation cephalosporins, it has broad spectrum activity against Gram-positive and Gram-negative bacteria. Unlike most third-generation agents, it is active against Pseudomonas aeruginosa, however it has weaker activity against Gram-positive microorganisms and is not used for such infections.
Antibiotic
Ceftriaxone is a third-generation cephalosporin antibiotic. The presence of an aminothiazolyl sidechain increases ceftriazone's resistance to beta-lactamases. Like other third-generation cephalosporins, it has broad spectrum activity against Gram-positive and Gram-negative bacteria.
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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| Perfect | QnrS1 | protein homolog model | 156950 - 157606(-) | 6.836e-167 | 100 % | ||||
|
AMR Gene Family
Qnr proteins are pentapeptide repeat proteins that mimic DNA and protect the cell from the activity of fluoroquinolone antibiotics
Antibiotic
Ciprofloxacin is a bacteriocidal fluoroquinolone. It blocks bacterial DNA replication by binding to the toposiomerase II or IV-DNA complex (or cleavable complex), thereby causing double-stranded breaks in the bacterial chromosome.
Antibiotic
Levofloxacin is a synthetic chemotherapeutic antibiotic of the fluoroquinolone drug class. Its main target is topoisomerase IV, inhibiting its function and disrupting DNA replication.
Antibiotic
Moxifloxacin is a fourth generation synthetic fluoroquinolone chemotherapeutic agent, and has been shown to be significantly more active than levofloxacin (4 to 8 times more) against Streptococcus pneumoniae. It acts by inhibiting bacterial DNA topoisomerases.
Antibiotic
Gatifloxacin is an 8-methoxy, 7-piperazinyl, 6-fluoroquinolone that can be taken orally or by intravenous administration. It is active against most Gram-positive and Gram-negative bacteria, but inactive against non-fermenting Gram-negative rods including Pseudomonas aeruginosa.
Antibiotic
Nalidixic acid is a quinolone derivative of naphthyridine active against many enterobacteria, but ineffective against Ps aeruginosa, Gram-positive bacteria, and anaerobes. Acquired resistance is common in nalidixic acid treatments.
Antibiotic
Norfloxacin is a 6-fluoro, 7-piperazinyl quinolone with a wide range of activity against Gram-negative bacteria. It is inactive against most anaerobes.
Antibiotic
Sparfloxacin is a dimethylpiperazinyl difluoroquinolone that acts by inhibiting DNA gyrase. It is active against aerobic Gram-positive and Gram-negative bacteria, as well as some mycobacteria. It has moderate activity against some anaerobes.
Drug Class
The fluoroquinolones are a family of synthetic broad-spectrum antibiotics that are 4-quinolone-3-carboxylates. These compounds interact with topoisomerase II (DNA gyrase) to disrupt bacterial DNA replication, damage DNA, and cause cell death.
Resistance Mechanism
Protection of antibiotic action target from antibiotic binding, which process will result in antibiotic resistance.
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| Perfect | AAC(3)-IId | protein homolog model | 163525 - 164385(-) | 0 | 100 % | ||||
|
AMR Gene Family
Acetylation of the aminoglycoside antibiotic on the amino 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 | MCR-3 | protein homolog model | 166342 - 167967(+) | 0 | 100 % | ||||
|
AMR Gene Family
A group of mobile colistin resistance genes encode the MCR family of phosphoethanolamine transferases, which catalyze the addition of phosphoethanolamine onto lipid A, thus interfering with the binding of colistin to the cell membrane.
Antibiotic
Colistin A, or polymyxin E1, has a 6-octanoic acid lipid tail. Polymyxins disrupt the cell membrane of Gram-negative bacteria.
Antibiotic
Colistin B, or polymyxin E2, has a 6-heptanoic acid lipid tail. Polymyxins disrupt the cell membrane of Gram-negative bacteria.
Drug Class
Peptide antibiotics have a wide range of antibacterial mechanisms, depending on the amino acids that make up the antibiotic, although most act to disrupt the cell membrane in some manner. Subclasses of peptide antibiotics can include additional sidechains of other types, such as lipids in the case of the lipopeptide antibiotics.
Resistance Mechanism
Mutational alteration or enzymatic modification of antibiotic target which results in antibiotic resistance.
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