Tell me everything about anti microbial drugs
Reading File
“Antimicrobial drugs” is a very broad pharmacology topic, covering agents against bacteria, mycobacteria, fungi, viruses, parasites, and some ectoparasites. A useful way to study it is by organism, drug target, and clinical use.
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Core principles
- Selective toxicity, spectrum, bactericidal vs bacteriostatic action
- Empiric vs definitive treatment
- Pharmacokinetics/pharmacodynamics: time-dependent and concentration-dependent killing
- Culture, susceptibility testing, combination therapy, prophylaxis
- Antimicrobial stewardship and resistance prevention
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Antibacterial drugs
- Cell-wall inhibitors: penicillins, cephalosporins, carbapenems, monobactams, glycopeptides
- Protein-synthesis inhibitors: aminoglycosides, tetracyclines, macrolides, clindamycin, linezolid, chloramphenicol
- Nucleic-acid inhibitors: fluoroquinolones, rifamycins, metronidazole, nitrofurantoin
- Antimetabolites: sulfonamides and trimethoprim
- Membrane-active and other agents: daptomycin, polymyxins, fosfomycin, mupirocin
- Adverse effects, interactions, contraindications, and resistance mechanisms
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Antitubercular and antileprosy drugs
- First-line and second-line tuberculosis regimens
- Drug-resistant tuberculosis
- Leprosy multidrug therapy and reactions
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Antifungal drugs
- Polyenes, azoles, echinocandins, flucytosine, terbinafine, griseofulvin
- Therapy for candidiasis, aspergillosis, cryptococcosis, mucormycosis, and dermatophyte infection
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Antiviral drugs
- Herpesvirus, influenza, HIV, hepatitis B/C, and COVID-19 antivirals
- Antiretroviral classes, combination treatment, resistance, and prevention
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Antiparasitic drugs
- Antimalarials
- Antiamoebic, antigiardial, antihelminthic, antileishmanial, antitrypanosomal, and antitoxoplasma drugs
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Clinical prescribing
- Choosing drugs for common syndromes such as pneumonia, UTI, meningitis, sepsis, skin infection, and intra-abdominal infection
- Dose adjustment in kidney/liver impairment, pregnancy, children, and older adults
- Therapeutic drug monitoring where required
High-level overview: Antimicrobials work by exploiting biological differences between microbes and humans, such as bacterial peptidoglycan cell walls or viral replication enzymes. The central clinical aim is to use the narrowest effective drug, at the correct dose and duration, guided by likely pathogen, infection site, patient factors, and microbiology results. Misuse promotes resistance and avoidable toxicity.
Which section should I cover in detail first?
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Choose a section for a detailed, exam-ready explanation.
“Antimicrobial drugs” is a very broad pharmacology topic, covering agents against bacteria, mycobacteria, fungi, viruses, parasites, and some ectoparasites. A useful way to study it is by organism, drug target, and clinical use.
-
Core principles
- Selective toxicity, spectrum, bactericidal vs bacteriostatic action
- Empiric vs definitive treatment
- Pharmacokinetics/pharmacodynamics: time-dependent and concentration-dependent killing
- Culture, susceptibility testing, combination therapy, prophylaxis
- Antimicrobial stewardship and resistance prevention
-
Antibacterial drugs
- Cell-wall inhibitors: penicillins, cephalosporins, carbapenems, monobactams, glycopeptides
- Protein-synthesis inhibitors: aminoglycosides, tetracyclines, macrolides, clindamycin, linezolid, chloramphenicol
- Nucleic-acid inhibitors: fluoroquinolones, rifamycins, metronidazole, nitrofurantoin
- Antimetabolites: sulfonamides and trimethoprim
- Membrane-active and other agents: daptomycin, polymyxins, fosfomycin, mupirocin
- Adverse effects, interactions, contraindications, and resistance mechanisms
-
Antitubercular and antileprosy drugs
- First-line and second-line tuberculosis regimens
- Drug-resistant tuberculosis
- Leprosy multidrug therapy and reactions
-
Antifungal drugs
- Polyenes, azoles, echinocandins, flucytosine, terbinafine, griseofulvin
- Therapy for candidiasis, aspergillosis, cryptococcosis, mucormycosis, and dermatophyte infection
-
Antiviral drugs
- Herpesvirus, influenza, HIV, hepatitis B/C, and COVID-19 antivirals
- Antiretroviral classes, combination treatment, resistance, and prevention
-
Antiparasitic drugs
- Antimalarials
- Antiamoebic, antigiardial, antihelminthic, antileishmanial, antitrypanosomal, and antitoxoplasma drugs
-
Clinical prescribing
- Choosing drugs for common syndromes such as pneumonia, UTI, meningitis, sepsis, skin infection, and intra-abdominal infection
- Dose adjustment in kidney/liver impairment, pregnancy, children, and older adults
- Therapeutic drug monitoring where required
High-level overview: Antimicrobials work by exploiting biological differences between microbes and humans, such as bacterial peptidoglycan cell walls or viral replication enzymes. The central clinical aim is to use the narrowest effective drug, at the correct dose and duration, guided by likely pathogen, infection site, patient factors, and microbiology results. Misuse promotes resistance and avoidable toxicity.
Which section should I cover in detail first?Choose one section for a detailed explanation:
- Antibacterial drugs
- Tuberculosis and leprosy drugs
- Antifungal drugs
- Antiviral drugs
- Antiparasitic drugs
Or reply “start from antibacterial drugs” and I will cover classifications, mechanisms, spectrum, adverse effects, resistance, and key clinical uses.
Start from antibacterial drugs
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antibiotic stewardship AND resistance
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WHO antimicrobial resistance antibiotic stewardship fact sheet 2025
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Antibacterial drugs
Antibacterial drugs, commonly called antibiotics, treat infections caused by bacteria. They do not treat viral illnesses such as common cold or uncomplicated influenza.
1. Principles of antibacterial therapy
Bactericidal drugs kill bacteria. Examples: beta-lactams, aminoglycosides, fluoroquinolones, vancomycin, daptomycin, metronidazole.
Bacteriostatic drugs primarily inhibit multiplication, allowing host immunity to clear infection. Examples: tetracyclines, macrolides, clindamycin, linezolid, sulfonamides.
This distinction is not absolute. Drug activity depends on organism, concentration, site of infection, and host factors.
Empiric therapy is started before culture results when a serious bacterial infection is suspected. It should be based on:
- Likely pathogens at the infection site
- Infection severity
- Patient age, allergies, pregnancy, kidney/liver function, immune status
- Recent antibiotic exposure or hospitalization
- Local hospital/community antibiogram
Definitive or directed therapy follows culture and susceptibility results. Narrowing therapy reduces toxicity, Clostridioides difficile risk, cost, and selection of resistance. Harrison’s notes that the current local antibiogram is usually more useful than national resistance data for individual prescribing decisions.
Antibiotic stewardship means using an antibiotic only when indicated, selecting the narrowest effective option, optimizing dose and duration, collecting cultures before treatment when feasible, and stopping/de-escalating treatment when bacterial infection is not supported. WHO’s AWaRe classification groups antibiotics into Access, Watch, and Reserve categories to support safer prescribing and resistance monitoring.
2. Major mechanisms of action
| Target/process | Drug classes | Main effect |
|---|---|---|
| Cell-wall synthesis | Beta-lactams, glycopeptides, fosfomycin, bacitracin | Weak cell wall, leading to bacterial lysis |
| Cell membrane | Daptomycin, polymyxins | Disrupt membrane integrity |
| 30S ribosomal subunit | Aminoglycosides, tetracyclines | Inhibit bacterial protein synthesis |
| 50S ribosomal subunit | Macrolides, clindamycin, linezolid, chloramphenicol, streptogramins | Inhibit bacterial protein synthesis |
| DNA replication | Fluoroquinolones, metronidazole | Damage DNA or inhibit DNA gyrase/topoisomerase |
| RNA synthesis | Rifampicin | Inhibits DNA-dependent RNA polymerase |
| Folate metabolism | Sulfonamides, trimethoprim | Block nucleotide synthesis |
| Other mechanisms | Nitrofurantoin, mupirocin | Multiple or specific metabolic actions |
3. Cell-wall inhibitors
A. Beta-lactam antibiotics
All beta-lactams contain a beta-lactam ring and bind penicillin-binding proteins (PBPs), inhibiting peptidoglycan cross-linking in the bacterial cell wall. They are generally bactericidal and work best against actively multiplying organisms.
Main resistance mechanisms
- Beta-lactamase production: enzyme destroys the drug.
- Altered PBP: drug no longer binds effectively, such as PBP2a in MRSA.
- Reduced permeability: especially Gram-negative bacteria with altered porins.
- Efflux pumps: bacteria expel the drug.
Resistance may be chromosomal or acquired through plasmids and other transferable genetic elements. Harrison’s groups mechanisms broadly into target alteration, reduced intracellular drug access or increased efflux, and enzymatic drug inactivation.
1. Penicillins
| Group | Examples | Usual coverage / key use | Important adverse effects |
|---|---|---|---|
| Natural penicillins | Penicillin G, penicillin V | Streptococci, syphilis, selected susceptible anaerobes | Allergy, rash, diarrhea, seizures at very high levels |
| Penicillinase-resistant anti-staphylococcal penicillins | Cloxacillin, flucloxacillin, nafcillin, oxacillin | MSSA, not MRSA | Allergy, hepatitis or cholestasis with some agents, interstitial nephritis |
| Aminopenicillins | Amoxicillin, ampicillin | Streptococci, enterococci, Listeria; some Gram-negative organisms | Rash, diarrhea, C. difficile risk |
| Antipseudomonal penicillins | Piperacillin, ticarcillin | Broad Gram-negative coverage including Pseudomonas | Allergy, electrolyte load, cytopenias |
| Beta-lactam/beta-lactamase inhibitor combinations | Amoxicillin-clavulanate, ampicillin-sulbactam, piperacillin-tazobactam | Extends coverage against many beta-lactamase producers and anaerobes | Diarrhea, cholestatic liver injury with clavulanate, allergy |
Exam points
- Penicillin G: classic therapy for susceptible streptococcal infections and syphilis.
- Cloxacillin/flucloxacillin/nafcillin: preferred for serious MSSA infections.
- Amoxicillin: frequently used for community ENT and respiratory infections when indicated.
- Ampicillin: important for Listeria monocytogenes and enterococcal infection.
- Piperacillin-tazobactam: broad hospital-use agent with antipseudomonal and anaerobic activity.
A prior mild rash does not automatically prove dangerous beta-lactam allergy. A history of anaphylaxis, angioedema, bronchospasm, or severe delayed reactions such as Stevens-Johnson syndrome requires specialist-informed antibiotic selection.
2. Cephalosporins
Cephalosporins are beta-lactams. Their spectrum generally shifts toward greater Gram-negative coverage with later generations, but individual drugs differ.
| Generation | Examples | Key coverage/use |
|---|---|---|
| First | Cefazolin, cephalexin | MSSA and streptococci; cefazolin is common surgical prophylaxis |
| Second | Cefuroxime, cefoxitin, cefotetan | More Gram-negative activity; cefoxitin/cefotetan have anaerobic activity |
| Third | Ceftriaxone, cefotaxime, ceftazidime | Serious community infections; ceftriaxone for meningitis/gonorrhea depending on guidelines; ceftazidime covers Pseudomonas |
| Fourth | Cefepime | Broad Gram-negative coverage including Pseudomonas, with good Gram-positive activity |
| Fifth | Ceftaroline | Covers MRSA through binding altered PBP2a; does not cover Pseudomonas |
Important toxicities
- Hypersensitivity reactions
- Diarrhea and C. difficile infection
- Cytopenia with prolonged therapy
- Ceftriaxone can cause biliary sludging
- Cefotetan and cefoperazone may cause hypoprothrombinemia and a disulfiram-like reaction with alcohol
3. Carbapenems
Imipenem-cilastatin, meropenem, doripenem, ertapenem
Very broad-spectrum beta-lactams, often reserved for severe infections involving resistant Gram-negative bacteria, polymicrobial infection, or ESBL-producing Enterobacterales.
- Meropenem: common choice for severe resistant Gram-negative infection and has activity against Pseudomonas.
- Imipenem: paired with cilastatin to prevent renal metabolism; seizure risk is relatively higher.
- Ertapenem: lacks activity against Pseudomonas, Acinetobacter, and enterococci.
Resistance: carbapenemases, porin loss, and efflux pumps. Carbapenem-resistant Enterobacterales are a major clinical problem.
4. Monobactam
Aztreonam
- Active only against aerobic Gram-negative bacteria, including Pseudomonas
- No useful Gram-positive or anaerobic activity
- Can be considered in selected patients with severe immediate beta-lactam allergy, though allergy assessment remains important
B. Glycopeptides and related drugs
Vancomycin
Mechanism: binds D-Ala-D-Ala terminus of peptidoglycan precursors, blocking cell-wall synthesis.
Spectrum: Gram-positive bacteria only, including:
- MRSA
- Methicillin-resistant coagulase-negative staphylococci
- Susceptible enterococci
- Severe C. difficile colitis when given orally
Adverse effects
- Nephrotoxicity
- Infusion-related flushing, erythema, and pruritus, commonly called vancomycin infusion reaction
- Neutropenia with prolonged therapy
- Ototoxicity is uncommon but risk rises with other ototoxic drugs
Resistance: substitution of D-Ala-D-Ala with D-Ala-D-Lac, as in vancomycin-resistant enterococci.
Teicoplanin
Another glycopeptide used in many countries, often with more convenient dosing and less infusion reaction.
C. Other cell-wall drugs
Fosfomycin
- Inhibits an early step in peptidoglycan synthesis.
- Often used as a single oral dose for selected uncomplicated lower UTIs, depending on local guidelines and susceptibility.
- Resistance can emerge; not a general treatment for severe kidney infection or sepsis.
Bacitracin
- Prevents transport of peptidoglycan precursors.
- Mainly topical because systemic use is nephrotoxic.
4. Protein-synthesis inhibitors
A. Aminoglycosides
Gentamicin, amikacin, tobramycin, streptomycin, plazomicin
Mechanism: irreversible binding to 30S ribosomal subunit, causing misreading of mRNA. Bactericidal.
Spectrum/use
- Aerobic Gram-negative bacilli, including some Pseudomonas
- Often combined with a beta-lactam for severe infections due to synergy
- Certain Gram-positive infections such as endocarditis, when used in selected combination regimens
- Streptomycin has special roles in tuberculosis and certain zoonotic infections
Key limitations
- Do not work against anaerobes because uptake requires oxygen-dependent transport.
- Need therapeutic drug monitoring in many settings.
Major toxicities
- Nephrotoxicity
- Ototoxicity: cochlear or vestibular, sometimes irreversible
- Neuromuscular blockade
- Fetal ototoxicity risk
Resistance: drug-modifying enzymes, reduced uptake, efflux, or ribosomal alteration.
B. Tetracyclines and glycylcyclines
Tetracycline, doxycycline, minocycline, tigecycline
Mechanism: bind 30S subunit and block attachment of aminoacyl-tRNA. Usually bacteriostatic.
Uses
- Atypical respiratory pathogens: Mycoplasma, Chlamydia, Legionella
- Tick-borne infections: rickettsial diseases, Lyme disease
- Acne and some skin infections
- Chlamydial infections
- Doxycycline is often used in malaria prophylaxis and treatment combinations
Adverse effects
- GI upset and esophagitis
- Photosensitivity
- Teeth discoloration and impaired bone growth in children
- Hepatotoxicity at high doses
- Vestibular effects, especially minocycline
- Intracranial hypertension, rarely
Avoid or use specialist guidance in pregnancy and in young children, except where benefits outweigh risks, such as severe rickettsial disease.
Tigecycline
- Broad activity including many resistant organisms and anaerobes
- Not reliable for Pseudomonas
- Low serum concentrations make it unsuitable for bacteremia
- Prominent nausea and vomiting
C. Macrolides
Azithromycin, clarithromycin, erythromycin
Mechanism: bind 50S subunit and block translocation. Usually bacteriostatic.
Uses
- Atypical respiratory infections
- Community-acquired respiratory infections in suitable patients
- Pertussis
- Chlamydial infection
- Part of combination regimens for Helicobacter pylori or mycobacterial disease in appropriate settings
Adverse effects and interactions
- GI upset, particularly erythromycin
- QT prolongation and torsades de pointes risk
- Cholestatic hepatitis, especially erythromycin estolate
- Clarithromycin and erythromycin inhibit CYP3A4 and have more interaction potential than azithromycin
Resistance: methylation of the ribosomal binding site, efflux pumps, enzymatic inactivation.
D. Lincosamide
Clindamycin
Mechanism: binds 50S subunit. Usually bacteriostatic.
Coverage/use
- Gram-positive cocci, including many streptococci and selected staphylococci
- Anaerobes, especially above the diaphragm
- Can suppress toxin production in severe group A streptococcal and clostridial toxin-mediated illness, as part of combination therapy
Important adverse effect
- High association with C. difficile colitis
E. Oxazolidinones
Linezolid and tedizolid
Mechanism: inhibit formation of the 70S initiation complex at the 50S subunit.
Uses
- MRSA, including pneumonia
- Vancomycin-resistant enterococci
Adverse effects
- Thrombocytopenia and other cytopenias, especially with longer courses
- Peripheral and optic neuropathy with prolonged therapy
- Lactic acidosis
- Serotonin toxicity risk with serotonergic medicines because linezolid is a reversible MAO inhibitor
F. Chloramphenicol
Mechanism: inhibits peptidyl transferase at the 50S ribosomal subunit.
Uses: limited because safer alternatives exist, but may be used for selected severe infections where appropriate.
Toxicities
- Dose-related reversible bone marrow suppression
- Rare idiosyncratic aplastic anemia
- Gray baby syndrome in neonates
5. Drugs acting on nucleic acids
A. Fluoroquinolones
Ciprofloxacin, levofloxacin, moxifloxacin, ofloxacin
Mechanism: inhibit DNA gyrase and topoisomerase IV. Bactericidal.
| Drug | General clinical emphasis |
|---|---|
| Ciprofloxacin | Strong Gram-negative activity, including Pseudomonas; less reliable for pneumococcus |
| Levofloxacin | Respiratory pathogens plus some Gram-negative activity |
| Moxifloxacin | Respiratory and some anaerobic activity; not appropriate for UTI because urine levels are inadequate |
Adverse effects
- Tendinitis and tendon rupture
- Peripheral neuropathy
- CNS effects, including agitation, confusion, seizures in susceptible people
- Dysglycemia
- QT prolongation
- Aortic aneurysm/dissection risk warning in predisposed patients
- C. difficile risk
Use should be restricted to situations where expected benefit outweighs these risks and other suitable options are unavailable or inappropriate.
B. Metronidazole
Mechanism: toxic free-radical metabolites damage DNA in anaerobic organisms. Bactericidal.
Uses
- Anaerobic intra-abdominal, pelvic, dental, and brain infections, usually in combination where needed
- C. difficile infection in selected circumstances, though guideline-preferred therapies have evolved
- Also active against several protozoa
Adverse effects
- Metallic taste, nausea
- Peripheral neuropathy with prolonged exposure
- Avoid alcohol during therapy and shortly after, due to possible disulfiram-like reaction
C. Nitrofurantoin
Mechanism: reactive intermediates damage bacterial DNA and proteins.
Use: lower uncomplicated UTI caused by susceptible organisms.
Do not use for
- Pyelonephritis
- Urosepsis
- Situations with inadequate kidney function where effective urinary concentrations cannot be achieved
Adverse effects
- Nausea
- Pulmonary hypersensitivity or chronic pulmonary toxicity
- Hepatotoxicity
- Peripheral neuropathy
- Hemolysis risk in G6PD deficiency
D. Rifamycins
Rifampicin (rifampin), rifabutin, rifapentine
Mechanism: inhibit DNA-dependent RNA polymerase. Bactericidal.
Uses
- Primarily used in combination regimens for tuberculosis and some nontuberculous mycobacterial infections
- Certain staphylococcal prosthetic-device infections in combination
- Chemoprophylaxis for selected meningococcal or H. influenzae contacts
Adverse effects
- Orange-red discoloration of urine, tears, and other secretions
- Hepatotoxicity
- Major drug interactions due to potent hepatic enzyme induction
Resistance develops rapidly with monotherapy, so rifampicin is rarely used alone for active infection.
6. Folate antagonists
Trimethoprim-sulfamethoxazole, TMP-SMX
Mechanism
- Sulfamethoxazole inhibits dihydropteroate synthase.
- Trimethoprim inhibits dihydrofolate reductase.
- Together they provide sequential folate-pathway blockade.
Uses
- Some uncomplicated UTIs
- Community-associated MRSA skin infections
- Pneumocystis jirovecii treatment and prophylaxis
- Nocardia and selected gastrointestinal infections
Adverse effects
- Rash, including severe cutaneous reactions
- Photosensitivity
- Bone marrow suppression
- Hyperkalemia, especially from trimethoprim
- Kidney injury
- Hemolysis in G6PD deficiency
- Avoid near term in pregnancy where possible because of neonatal bilirubin concerns
7. Cell-membrane active agents
Daptomycin
Mechanism: calcium-dependent membrane depolarization. Bactericidal against Gram-positive organisms.
Uses: MRSA bacteremia, right-sided endocarditis, complicated skin infection, VRE in some settings.
Do not use in pneumonia: it is inactivated by pulmonary surfactant.
Toxicity: myopathy and elevated creatine kinase. Monitor for muscle symptoms and CK during therapy.
Polymyxins
Colistin and polymyxin B
Mechanism: disrupt outer membrane of Gram-negative bacteria.
Uses: last-line or specialist-directed treatment for multidrug-resistant Gram-negative infections.
Toxicities
- Nephrotoxicity
- Neurotoxicity
- Neuromuscular blockade
8. Other important antibacterial drugs
| Drug | Main role | Key caution |
|---|---|---|
| Mupirocin | Topical impetigo; nasal MRSA decolonization protocols | Resistance with repeated/inappropriate use |
| Fidaxomicin | C. difficile infection | Narrow-spectrum, expensive in some settings |
| Oral vancomycin | C. difficile infection | Not absorbed systemically from gut |
| Quinupristin-dalfopristin | Selected resistant Gram-positive infections | Arthralgia, myalgia, interactions |
| Dalbavancin/oritavancin | Long-acting Gram-positive agents | Specialist use, prolonged action |
| Cefiderocol | Selected resistant Gram-negative infections | Reserved use, susceptibility-guided |
9. Antibacterial spectrum: high-yield guide
Mainly Gram-positive coverage
- Penicillin G for susceptible streptococci
- Anti-staphylococcal penicillins for MSSA
- Cefazolin
- Vancomycin
- Linezolid
- Daptomycin, except pneumonia
MRSA-active options
- Vancomycin
- Linezolid
- Daptomycin, not pneumonia
- Ceftaroline
- TMP-SMX, doxycycline, clindamycin for selected susceptible non-severe skin infections
Pseudomonas aeruginosa-active options
- Piperacillin-tazobactam
- Ceftazidime, cefepime
- Meropenem, imipenem, doripenem
- Aztreonam
- Ciprofloxacin, levofloxacin
- Tobramycin, amikacin, gentamicin
- Colistin, in selected resistant cases
Anaerobic coverage
- Metronidazole
- Clindamycin, with resistance patterns considered
- Amoxicillin-clavulanate
- Ampicillin-sulbactam
- Piperacillin-tazobactam
- Carbapenems
- Cefoxitin and cefotetan in selected settings
Atypical bacteria
- Macrolides
- Doxycycline
- Respiratory fluoroquinolones
10. Antimicrobial resistance
Major mechanisms:
- Drug destruction: beta-lactamases hydrolyze beta-lactams.
- Target modification: altered PBPs in MRSA, altered ribosomes, altered DNA gyrase.
- Reduced entry: loss of Gram-negative porins.
- Active efflux: pumps export drug from bacterial cells.
- Metabolic bypass: organisms bypass an inhibited pathway.
Resistance spreads by:
- Mutation and selection pressure
- Plasmid transfer
- Transposons and integrons
- Transformation, where bacteria take up external DNA
The WHO Global antibiotic resistance surveillance report reports resistance trends across common bacterial pathogens and highlights the growing public-health burden of resistant bloodstream, urinary, gastrointestinal, and gonococcal infections.
Recent-evidence note: a 2024 systematic review/meta-analysis on antibiotic combinations found that effects on resistance vary substantially with organism, drug combination, and context. Combination therapy should not be used simply to “prevent resistance” without a clinical indication. See PMID 39704726.
11. Practical safe-use rules
- Do not use antibiotics for clearly viral illness.
- Obtain cultures before antibiotics in severe infection if this does not delay urgent treatment.
- Use local guidelines and susceptibility results.
- Do not share leftover antibiotics or save them for future illness.
- Avoid unnecessarily prolonged courses.
- Reassess treatment within 48-72 hours when culture results and clinical response are available.
- Check allergy history carefully.
- Adjust many drugs in kidney impairment, particularly aminoglycosides, vancomycin, and several beta-lactams.
- Seek urgent medical evaluation for sepsis symptoms, severe breathing difficulty, confusion, persistent high fever, hypotension, or rapidly spreading skin infection.
Memory aid:
Cell wall: beta-lactams, vancomycin
30S: aminoglycosides, tetracyclines
50S: macrolides, clindamycin, linezolid, chloramphenicol
DNA/RNA: fluoroquinolones, metronidazole, rifampicin
Folate: sulfonamides + trimethoprim
Membrane: daptomycin, polymyxins
Cell wall: beta-lactams, vancomycin
30S: aminoglycosides, tetracyclines
50S: macrolides, clindamycin, linezolid, chloramphenicol
DNA/RNA: fluoroquinolones, metronidazole, rifampicin
Folate: sulfonamides + trimethoprim
Membrane: daptomycin, polymyxins
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