Antibiotic Classes
Disclaimer: The antibiotics listed for each target site is NOT a comprehensive list! The listed antibiotics are those commonly seen in hospital or community settings. Please refer to the Resources section to view references that provide a more comprehensive list.
Drugs that work on the cell wall <1-2>
See the YouTube below to get a refresher about bacterial cell walls!
Penicillins
Penicillin antibiotics inhibit bacterial cell wall synthesis. Bacteria can become resistant to penicillin antibiotics by four mechanisms. First, bacteria can produce beta-lactamase to destroy the antibiotic. Second, a physical barrier can prevent penicillin antibiotics from entering bacteria (i.e. the outer membrane of gram-negative bacteria. Third, efflux pumps can push penicillin antibiotics out of the bacterial cell. Finally, bacteria can change the target site for penicillin antibiotics to prevent binding.
Penicillin antibiotics are divided into five classes. These include natural penicillin (or just 'penicillin'), anti-staphylococcal penicillin (or 'semi-synthetic pencillin'), aminopencillin, carboxypenicillin (not discussed in detail within this website), and ureidopenicillin.
Common adverse effects include nausea, vomiting diarrhea. Rarely, penicillin antibiotics can be associated with seizures and bone marrow suppression.
Penicillin antibiotics are divided into five classes. These include natural penicillin (or just 'penicillin'), anti-staphylococcal penicillin (or 'semi-synthetic pencillin'), aminopencillin, carboxypenicillin (not discussed in detail within this website), and ureidopenicillin.
Common adverse effects include nausea, vomiting diarrhea. Rarely, penicillin antibiotics can be associated with seizures and bone marrow suppression.
Cephalosporins
Cephalosporin antibiotics inhibit bacterial cell wall synthesis (in a similar way as penicillin antibiotics). Bacteria can become resistant to cephalosporin antibiotics through the same mechanisms seen with penicillin antibiotics (see previous section on 'Penicillins').
Cephalosporin antibiotics are divided into different generations depending on its spectrum of activity. First generation cephalopsorins have primarily gram-positive coverage. Second generation cephalosporins have enhanced gram-negative bacteria with respect to first generation cephalosporins. However, it is usually used for gram-positive infections. Third generation cephalosporins have significantly increased activity against gram-negative bacteria compared to the previous generations.
Common adverse effects include nausea, vomiting diarrhea. Rarely, cephalosporin antibiotics can be associated with seizures.
Cephalosporin antibiotics are divided into different generations depending on its spectrum of activity. First generation cephalopsorins have primarily gram-positive coverage. Second generation cephalosporins have enhanced gram-negative bacteria with respect to first generation cephalosporins. However, it is usually used for gram-positive infections. Third generation cephalosporins have significantly increased activity against gram-negative bacteria compared to the previous generations.
Common adverse effects include nausea, vomiting diarrhea. Rarely, cephalosporin antibiotics can be associated with seizures.
Glycopeptide
Vancomycin is the most commonly seen antibiotic in this class. Vancomycin inhibits late stages of cell wall synthesis. Bacteria can become resistant to vancomycin through expression of resistance genes.
Vancomycin antibiotics are used only for gram-positive infections (i.e. no gram-negative coverage).
Common adverse effects include nephrotoxicity, Red Man's Syndrome (if infusion rate is not prolonged). Rarely, vancomycin can be associated with ototoxicity, leukopenia, and neutropenia. The rare adverse effects are seen with prolonged use and/or high concentrations.
Vancomycin antibiotics are used only for gram-positive infections (i.e. no gram-negative coverage).
Common adverse effects include nephrotoxicity, Red Man's Syndrome (if infusion rate is not prolonged). Rarely, vancomycin can be associated with ototoxicity, leukopenia, and neutropenia. The rare adverse effects are seen with prolonged use and/or high concentrations.
Drugs that work on the cell membrane <1>
Lipopeptide
Daptomycin is the only antibiotic in this class. Daptomycin causes depolarization of the cell membrane potential to trigger a sequence of events leading to cell death. Daptomycin resistance is not common. However, bacterial can become resistant to daptomycin through mutations.
Common adverse effects include hypersensitivity reactions, creatintine phosphokinase (CPK) elevations, and myalgias.
Common adverse effects include hypersensitivity reactions, creatintine phosphokinase (CPK) elevations, and myalgias.
Drugs that work on Protein Synthesis <1-2>
See the YouTube video below to get a refresher about bacterial protein synthesis!
Macrolides
Macrolide antibiotics bind to the 50S ribosomal subunit to inhibit protein synthesis. Bacteria can become resistant to macrolide antibiotics through 2 mechanisms. First, bacteria can decrease drug uptake. Second, bacteria can produce efflux pumps.
Common adverse effects include gastrointestinal symptoms. Rarely, macrolide antibiotics can cause cholestatic hepatitis, and QT-prolongation. If macrolide antibiotics are going to be used for a prolonged period of time, monitor liver and cardiac function.
Common adverse effects include gastrointestinal symptoms. Rarely, macrolide antibiotics can cause cholestatic hepatitis, and QT-prolongation. If macrolide antibiotics are going to be used for a prolonged period of time, monitor liver and cardiac function.
Lincosamide
Clindamycin is the only antibiotic in this class. Clindamycin works similarly to macrolides by binding to the 50S ribosomal subunit to inhibit protein synthesis. Bacteria can become resistant to clindamycin by three mechanisms. First, bacteria can change the target site on the 50S ribosomal subunit to prevent binding of clindamycin. Second, mutations in the nucleic structure can cause resistance to clindamycin. Finally, bacteria can inactivate clindamycin by producing an enzyme that catalyzes the break down of clindamycin.
Common adverse effects include gastrointestinal symptoms, Clostridium difficile colitis, and hypersensitivity reaction. Antibiotic-induced C. difficile may present after antibiotic therapy. Need to monitor patients for unexplained diarrhea after antibiotic therapy.
Common adverse effects include gastrointestinal symptoms, Clostridium difficile colitis, and hypersensitivity reaction. Antibiotic-induced C. difficile may present after antibiotic therapy. Need to monitor patients for unexplained diarrhea after antibiotic therapy.
Aminoglycosides
Aminoglycoside antibiotics bind reversibly to bacterial ribosomal subunits (exact mechanism of action unknown). Bacteria can become resistant to aminoglycoside antibiotics through four mechanisms. First, bacteria can decrease drug uptake. Second, bacteria can produce efflux pumps. Third, bacteria can induce enzymatic changes of aminoglycoside antibiotics. Finally, bacteria can have mutations in 16S ribosomal RNA to cause resistance.
Common adverse effects include nephrotoxicity, ototoxicity (irreversible), and neurotoxicity.
Common adverse effects include nephrotoxicity, ototoxicity (irreversible), and neurotoxicity.
Tetracyclines
Tetracycline antibiotics bind reversibly to the 30S ribosomal subunit to stop addition of new amino acids on a peptide strand. Bacteria can become resistant to tetracycline antibiotics through three mechanisms. First, bacteria can express tetracycline resistance genes. Second, bacteria can produce efflux pumps. Third, bacteria can produce ribosomal protection proteins (RPPs) that displace tetracyclines from its target.
Tetracycline antibiotics can be classified as first- or second-generation. Second-generation tetracycline antibiotics are longer acting compared to first-generation tetracycline antibiotics.
Common adverse effects include gastrointestinal symptoms, bone/teeth staining (contraindicated during pregnancy and young children), hepatotoxicity, and photosensitivity,
Tetracycline antibiotics can be classified as first- or second-generation. Second-generation tetracycline antibiotics are longer acting compared to first-generation tetracycline antibiotics.
Common adverse effects include gastrointestinal symptoms, bone/teeth staining (contraindicated during pregnancy and young children), hepatotoxicity, and photosensitivity,
Drugs that work on DNA synthesis <1-2>
See below the YouTube video below to get a refresher about bacterial DNA synthesis!
Fluoroquinolones
Fluoroquinolone antibiotics inhibit DNA synthesis. Bacteria can become resistant to fluoroquinolone antibiotics through four mechanisms. First, bacteria can undergo mutations to prevent binding of fluoroquinolone antibiotics. Second, bacteria can limit entry of fluoroquinolone antibiotics into the bacteria. Third, efflux pumps can push fluoroquinolone antibiotics out of the bacterial cell. Finally, bacteria can produce fluoroquinolone modifying proteins to reduce antibiotic activity.
Common adverse effects include headaches, gastrointestinal symptoms, QT prolongation, photosensitivity, glycemic dysregulation, and tendon rupture. If fluoroquinolone antibiotics are going to be used for a prolonged period of time, monitor cardiac and muscle function.
Common adverse effects include headaches, gastrointestinal symptoms, QT prolongation, photosensitivity, glycemic dysregulation, and tendon rupture. If fluoroquinolone antibiotics are going to be used for a prolonged period of time, monitor cardiac and muscle function.
Drugs that inhibit folate synthesis <1-2>
Sulfamethoxazole
Sulfamethoxazole inhibits microbial folic acid synthesis by competing with a natural precursor (para-aminobenzoic acid). Bacteria can become resistant to sulfamethoxazole through two mechanisms. First, bacteria can overproduce para-aminobenozic acid. Second, bacteria can change the target site for sulfamethoxazole.
Common adverse effects include nausea, vomiting, diarrhea, anorexia, hyperkalemia, and hypersensitivity reactions.
Note: Trimethoprim and Sulfamethoxazole are commonly used together as a combination product.
Common adverse effects include nausea, vomiting, diarrhea, anorexia, hyperkalemia, and hypersensitivity reactions.
Note: Trimethoprim and Sulfamethoxazole are commonly used together as a combination product.
Trimethoprim
Trimethoprim inhibits dihydrofolate reductase and increases the activity of sulfamethoxazole. Bacteria can become resistant to trimethoprim through three mechanisms. First, bacteria can change cellular permeability to reduce intake of trimethoprim. Second, bacteria can change the target site for trimethoprim. Finally, bacteria can become resistant by overproducing dihydrofolate reductase.
Common adverse effects include nausea, vomiting, diarrhea, anorexia, renal dysfunction (dose-related), and hypersensitivity reactions.
Note: Trimethoprim and Sulfamethoxazole are commonly used together as a combination product.
Common adverse effects include nausea, vomiting, diarrhea, anorexia, renal dysfunction (dose-related), and hypersensitivity reactions.
Note: Trimethoprim and Sulfamethoxazole are commonly used together as a combination product.
References:
1. Mandell GL, Bennett JE, Dolin R. Mandell, Douglas, and Bennett's principles and and practice of infectious diseases. 9th ed. Philadelphia: Churchill Livingstone/Elsevier; 2009.
2. Gilbert DN, Mollering RC, Eliopoulos GM, et al. The sanford guide to antimicrobial therapy. 42nd ed. Sperryville: Antimicrobial Therapy; 2012.
1. Mandell GL, Bennett JE, Dolin R. Mandell, Douglas, and Bennett's principles and and practice of infectious diseases. 9th ed. Philadelphia: Churchill Livingstone/Elsevier; 2009.
2. Gilbert DN, Mollering RC, Eliopoulos GM, et al. The sanford guide to antimicrobial therapy. 42nd ed. Sperryville: Antimicrobial Therapy; 2012.