make a detailed structured note on different classes of antibiotics with examples & how they work, when to use as per diferent types of bacterial infection. Make sure to use valid & latest guidelines
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I now have all the information needed to compile a thorough, well-structured antibiotic reference note. Here it is:
Antibiotic Classes: Mechanisms, Spectrum, and Clinical Use
Sources: Medical Microbiology 9e (Murray et al.), Jawetz Melnick & Adelberg's Medical Microbiology 28e, The Washington Manual of Medical Therapeutics; guidelines from IDSA 2024-2026, ATS 2026 CAP Guideline (PMID: 40679934), SIS 2024 (PMID: 38990709)
Overview: Sites of Antibiotic Action
Fig. 17.1 - Medical Microbiology 9e. Antibiotics grouped by their intracellular target.
All antibiotics work through one of five major mechanisms:
- Cell wall synthesis inhibition
- Protein synthesis inhibition (30S or 50S ribosome)
- Nucleic acid synthesis inhibition (DNA/RNA)
- Cell membrane disruption
- Antimetabolite action (folate pathway blockade)
CLASS 1: Beta-Lactams
Mechanism
Beta-lactams bind penicillin-binding proteins (PBPs) - enzymes responsible for cross-linking peptidoglycan in the bacterial cell wall. This leads to defective wall synthesis, osmotic lysis, and bactericidal activity. They share a core beta-lactam ring; structural modifications determine spectrum and stability.
Resistance: Over 200 beta-lactamases have been described. ESBLs (extended-spectrum beta-lactamases) are class A enzymes on transferable plasmids - a major clinical problem in E. coli and Klebsiella. Class B metalloenzymes (e.g., NDM, VIM) hydrolyze carbapenems. - Medical Microbiology 9e, p.199
1A. Penicillins
| Subgroup | Examples | Spectrum |
|---|---|---|
| Natural penicillins | Penicillin G (IV), Penicillin V (oral) | Narrow: streptococci, spirochetes, Neisseria, anaerobic gram-positives |
| Penicillinase-resistant | Methicillin, Nafcillin, Oxacillin, Cloxacillin | MSSA; NOT for MRSA |
| Aminopenicillins | Ampicillin, Amoxicillin | Broader: E. coli, Proteus, H. influenzae (non-beta-lactamase strains); enterococci |
| Anti-pseudomonal | Piperacillin | Gram-negatives including Pseudomonas aeruginosa |
| +BLI combinations | Amoxicillin-clavulanate, Ampicillin-sulbactam, Piperacillin-tazobactam, Ceftolozane-avibactam | Restore activity against ESBL-producing organisms |
Clinical Use:
- Penicillin G/V: Streptococcal pharyngitis (GAS), syphilis (Treponema pallidum), pneumococcal pneumonia (susceptible strains), actinomycosis
- Nafcillin/Oxacillin: MSSA bacteremia, native valve endocarditis (drug of choice over vancomycin for MSSA)
- Amoxicillin: Otitis media (1st line, IDSA/AAP), dental infections, uncomplicated UTI (susceptible E. coli)
- Amoxicillin-clavulanate: Human/animal bite wounds, sinusitis, diabetic foot infections (mild-moderate), community pneumonia with aspiration concern
- Piperacillin-tazobactam (Pip-Tazo): Complicated intra-abdominal infections, hospital-acquired pneumonia, febrile neutropenia (combination)
1B. Cephalosporins (& Cephamycins)
Classified by generation; each successive generation has improved gram-negative coverage and (generally) reduced gram-positive activity, except 5th generation.
| Generation | Examples | Key Coverage |
|---|---|---|
| 1st | Cefazolin (IV), Cefalexin (oral) | MSSA, streptococci; limited GNR |
| 2nd | Cefuroxime, Cefaclor; Cephamycins: Cefoxitin, Cefotetan | H. influenzae, Moraxella; cephamycins add anaerobes (B. fragilis) |
| 3rd | Ceftriaxone, Cefotaxime, Ceftazidime | Most Enterobacterales, N. gonorrhoeae, meningitis-penetrating; Ceftazidime covers Pseudomonas |
| 4th | Cefepime | Gram-positive + broad GNR including Pseudomonas; AmpC-stable |
| 5th | Ceftaroline | MRSA activity + gram-negatives |
Clinical Use:
- Cefazolin: Surgical prophylaxis (gold standard), MSSA skin/soft tissue infections, native/prosthetic valve endocarditis (MSSA)
- Ceftriaxone: Community-acquired pneumonia (CAP), bacterial meningitis (+ vancomycin empirically), gonorrhea (IM single-dose 500mg per CDC 2021), typhoid fever, Lyme neuroborreliosis
- Ceftazidime / Cefepime: Pseudomonal infections, hospital-acquired/ventilator-associated pneumonia (HAP/VAP), febrile neutropenia
- Ceftolozane-tazobactam, Ceftazidime-avibactam: MDR/ESBL and carbapenem-resistant Pseudomonas (IDSA AMR Guidance 2024)
- Ceftaroline: MRSA skin infections, CAP
Per ATS 2026 CAP Guideline (PMID: 40679934): Amoxicillin or Doxycycline remain 1st-line for outpatient CAP; Ceftriaxone + Azithromycin (or Respiratory fluoroquinolone alone) for inpatients.
1C. Carbapenems
| Drug | Notes |
|---|---|
| Imipenem-cilastatin | Broadest spectrum; covers Pseudomonas and many anaerobes; cilastatin prevents renal tubular degradation of imipenem |
| Meropenem | Similar to imipenem; preferred for CNS infections (lower seizure risk) |
| Ertapenem | No Pseudomonas / Acinetobacter coverage; useful for ESBL infections in stable outpatients |
| Doripenem | Similar to meropenem |
Mechanism: Bind PBPs with high affinity; resist most (but not all) beta-lactamases. Carbapenem-resistant organisms (CRE, CRPA) are treated with novel combinations (ceftazidime-avibactam, meropenem-vaborbactam, imipenem-relebactam).
Clinical Use:
- ESBL-producing gram-negative infections (sepsis, pyelonephritis) - preferred over pip-tazo in bacteremic ESBL cases per IDSA 2024
- Febrile neutropenia with risk of resistant GNR
- Intra-abdominal infections with risk of resistant organisms (SIS 2024 guideline, PMID: 38990709)
- Nocardia infections (imipenem)
1D. Monobactams
- Aztreonam: Active only against aerobic gram-negative rods (including Pseudomonas). No gram-positive or anaerobic coverage. Safe in IgE-mediated penicillin allergy (does not cross-react meaningfully with most penicillins; minor cross-reaction with ceftazidime).
CLASS 2: Glycopeptides
Mechanism
Bind the D-Ala-D-Ala terminus of the lipid-PP-disaccharide-pentapeptide peptidoglycan precursor, preventing cross-linking - distinct from beta-lactam binding site. Bactericidal against gram-positives only (too large to penetrate gram-negative outer membrane).
| Drug | Notes |
|---|---|
| Vancomycin | Prototype; IV for serious MRSA; oral for C. difficile colitis (acts locally, not absorbed) |
| Teicoplanin | Similar spectrum; once-daily dosing |
| Dalbavancin, Oritavancin | Long-acting (single or 2-dose course); used for ABSSSI (acute bacterial skin/skin structure infections) |
Clinical Use:
- MRSA infections: Bacteremia, endocarditis, HAP/VAP, osteomyelitis, meningitis
- C. difficile colitis (oral vancomycin): 1st-line (equal to fidaxomicin per IDSA/SHEA 2021 guideline)
- Penicillin-allergic patients with serious streptococcal/enterococcal infections
- VRE (Vancomycin-resistant enterococci): requires linezolid or daptomycin
Therapeutic Drug Monitoring (TDM): Vancomycin AUC/MIC-guided dosing now preferred over trough-only monitoring (ASHP/IDSA/SIDP consensus 2020).
CLASS 3: Aminoglycosides
Mechanism
Enter bacteria via energy-dependent process; irreversibly bind 30S ribosomal proteins (16S rRNA). This causes:
- Misreading of mRNA -> aberrant/non-functional proteins
- Premature release of ribosomes from mRNA -> interruption of elongation
Bactericidal. Concentration-dependent killing. Anaerobes are intrinsically resistant (no aerobic energy for uptake).
| Drug | Key Use |
|---|---|
| Gentamicin | Synergy with beta-lactams/vancomycin for enterococcal/streptococcal endocarditis; gram-negative infections |
| Tobramycin | Slightly more active vs. Pseudomonas than gentamicin; inhaled form for cystic fibrosis |
| Amikacin | Most active; stable against many aminoglycoside-inactivating enzymes; reserved for resistant GNRs |
| Streptomycin | Tuberculosis (2nd line), plague, tularemia, brucellosis, enterococcal endocarditis (synergy) |
Clinical Use:
- Synergistic therapy in enterococcal endocarditis (gentamicin + ampicillin or vancomycin)
- Serious gram-negative infections (Enterobacterales, Pseudomonas, Acinetobacter), especially when beta-lactams cannot be used
- TB regimen (streptomycin or amikacin in resistant TB)
- Inhaled tobramycin for Pseudomonas in cystic fibrosis
Toxicity: Nephrotoxic + ototoxic. TDM mandatory. Extended-interval dosing (once-daily) reduces nephrotoxicity and exploits concentration-dependent killing. - Medical Microbiology 9e, p.202
CLASS 4: Macrolides (and Ketolides)
Mechanism
Reversibly bind 23S rRNA of the 50S ribosomal subunit -> block polypeptide elongation. Generally bacteriostatic (bactericidal at high concentrations against some organisms). Excellent intracellular penetration.
| Drug | Notes |
|---|---|
| Erythromycin | Prototype; significant GI side effects; inhibits CYP3A4 |
| Azithromycin | Longer half-life (once daily); concentrated in phagocytes; less GI intolerance |
| Clarithromycin | Better GI tolerance; used in H. pylori regimens and MAC prophylaxis |
| Telithromycin (Ketolide) | Overcomes macrolide-resistant pneumococci; reserved due to hepatotoxicity concerns |
Clinical Use:
- CAP (outpatient): Azithromycin or Doxycycline (ATS 2026)
- Atypical pneumonia: Mycoplasma pneumoniae, Legionella pneumophila, Chlamydophila pneumoniae
- Pertussis: Azithromycin (drug of choice, all ages)
- MAC (disseminated): Clarithromycin + ethambutol ± rifabutin
- STIs: Azithromycin for Chlamydia trachomatis (single 1g dose); alternative in gonorrhea
- Campylobacter enteritis: Azithromycin (fluoroquinolone resistance now common)
- H. pylori eradication: Clarithromycin-based triple therapy (where clarithromycin resistance <15%)
Resistance mechanism: Methylation of 23S rRNA (MLSB phenotype) is the most common mechanism. Rising macrolide-resistant Mycoplasma is a concern globally (2024-2025 surveillance data).
CLASS 5: Tetracyclines (and Glycylcyclines)
Mechanism
Bind reversibly to 30S ribosomal subunit -> block aminoacyl-tRNA attachment to the ribosomal acceptor (A) site -> prevent polypeptide elongation. Bacteriostatic.
| Drug | Notes |
|---|---|
| Doxycycline | Most widely used; once/twice daily; low renal excretion (safe in mild CKD) |
| Minocycline | Good CNS/tissue penetration; Acinetobacter activity |
| Tetracycline | Older; used for H. pylori quadruple therapy |
| Tigecycline (glycylcycline) | Semisynthetic derivative of minocycline; broader spectrum; avoids efflux pumps; covers MRSA, VRE, Acinetobacter, anaerobes; NOT for Pseudomonas, Proteus, Providencia |
Clinical Use:
- CAP (outpatient): Doxycycline (ATS 2026 - equal to amoxicillin)
- Atypical organisms: Chlamydia, Mycoplasma, Rickettsia (drug of choice), Coxiella burnetti (Q fever)
- Lyme disease: Doxycycline (early Lyme, ILADS/IDSA)
- Malaria prophylaxis and treatment (with quinine)
- Brucellosis: Doxycycline + rifampin (standard regimen)
- MRSA SSTI (outpatient): Doxycycline or TMP-SMX (IDSA SSTI 2014 guideline)
- Acne vulgaris / rosacea: Doxycycline (dermatology)
- Tigecycline: MDR gram-negative infections (last resort), complicated skin/intra-abdominal infections
Avoid in: Children <8 years (dental/bone effects), pregnancy, concurrent antacids/dairy (chelation reduces absorption).
CLASS 6: Fluoroquinolones
Mechanism
Inhibit bacterial DNA topoisomerase II (gyrase) and topoisomerase IV - enzymes essential for DNA supercoiling, replication, recombination, and repair. Bactericidal. Concentration-dependent.
- Gram-negatives: primary target = DNA gyrase (GyrA subunit)
- Gram-positives: primary target = topoisomerase IV
| Drug | Generation | Notable Features |
|---|---|---|
| Ciprofloxacin | 2nd | Best gram-negative activity (including Pseudomonas); limited pneumococcal coverage |
| Levofloxacin | 3rd (respiratory) | Broader; good pneumococcal coverage; suitable for CAP |
| Moxifloxacin | 4th (respiratory) | Enhanced gram-positive + anaerobic coverage; no Pseudomonas; no UTI use (low urinary excretion) |
| Delafloxacin | Newer | MRSA activity; ABSSSI and CAP |
Clinical Use:
- UTI (uncomplicated/complicated): Ciprofloxacin, Levofloxacin (IDSA 2025 cUTI guideline - 3rd/4th gen cephalosporins preferred to preserve quinolone class; FQs as alternatives)
- CAP: Respiratory quinolone (Levofloxacin/Moxifloxacin) - monotherapy equivalent to beta-lactam + macrolide (ATS 2026)
- HAP/VAP: Ciprofloxacin or Levofloxacin (with anti-pseudomonal beta-lactam)
- Anthrax: Ciprofloxacin (drug of choice, post-exposure prophylaxis and treatment)
- Traveler's diarrhea / enteric infections (decreasing role due to resistance): Ciprofloxacin for Salmonella, Shigella (where susceptible)
- Prostatitis: Ciprofloxacin or Levofloxacin (4-6 weeks)
- TB (drug-resistant): Levofloxacin or Moxifloxacin are Group A drugs in WHO 2022 MDR-TB regimen
Caution: FDA Black Box Warning - tendinopathy/tendon rupture (especially Achilles), peripheral neuropathy, CNS effects, QTc prolongation. Use conservatively - antibiotic stewardship programs restrict broad empiric use. Resistance develops rapidly in Pseudomonas, oxacillin-resistant staphylococci, enterococci.
CLASS 7: Sulfonamides and Trimethoprim
Mechanism
Antimetabolites - block the folate synthesis pathway sequentially:
- Sulfonamides: Competitive inhibitors of dihydropteroate synthase (DHPS) - prevent para-aminobenzoic acid (PABA) incorporation -> block dihydrofolic acid synthesis
- Trimethoprim: Inhibits dihydrofolate reductase (DHFR) -> blocks conversion of dihydrofolate to tetrahydrofolate
- TMP-SMX (Co-trimoxazole): Sequential blockade = synergistic bactericidal effect
Clinical Use (TMP-SMX):
- Uncomplicated UTI: First-line (where resistance <20% locally) - IDSA guideline
- MRSA SSTI (outpatient): Drug of choice along with doxycycline (IDSA SSTI guideline)
- Pneumocystis jirovecii pneumonia (PCP): Drug of choice (prophylaxis and treatment) in HIV/immunocompromised
- Nocardiosis: TMP-SMX (first-line)
- Toxoplasmosis prophylaxis (in AIDS)
- Traveler's diarrhea (largely replaced by fluoroquinolones)
Avoid in: G6PD deficiency (hemolysis risk), late pregnancy (neonatal kernicterus), severe renal impairment.
CLASS 8: Lincosamides (Clindamycin)
Mechanism
Binds 50S ribosomal subunit (23S rRNA) -> inhibits peptide bond formation/translocation. Bacteriostatic. Excellent anaerobic coverage; good tissue penetration.
Clinical Use:
- Anaerobic infections (lung abscess, aspiration pneumonia, pelvic infections, intra-abdominal) - alternative to metronidazole
- MRSA SSTI (community-acquired, if susceptible; check D-zone/inducible resistance)
- Streptococcal necrotizing fasciitis: Add clindamycin to beta-lactam to suppress toxin production
- Dental/odontogenic infections in penicillin-allergic patients
- Osteomyelitis (gram-positive pathogens)
- Malaria (severe falciparum, with quinine)
Risk: Clostridioides difficile colitis - clindamycin is among the highest-risk antibiotics for CDI.
CLASS 9: Metronidazole (Nitroimidazoles)
Mechanism
A prodrug - reduced by intracellular electron transport proteins (ferredoxin, nitroreductase) in anaerobic environments to toxic nitro radical anions that cause DNA strand breakage. Active ONLY against anaerobes and microaerophiles.
Clinical Use:
- Clostridioides difficile colitis: Oral fidaxomicin or oral vancomycin preferred (IDSA/SHEA 2021); metronidazole reserved for mild CDI when oral vancomycin/fidaxomicin unavailable
- Bacterial vaginosis / Trichomoniasis: 1st-line (oral or topical)
- Anaerobic infections: Intra-abdominal, pelvic, lung abscess, brain abscess (with ceftriaxone)
- H. pylori eradication: Part of quadruple bismuth therapy
- Amebiasis/Giardiasis: Drug of choice
- Diverticulitis (+ cephalosporin for gram-negative coverage)
CLASS 10: Oxazolidinones (Linezolid, Tedizolid)
Mechanism
Bind 50S ribosomal subunit -> prevent formation of the 70S initiation complex (blocks mRNA-tRNA-ribosome assembly). Unique mechanism = no cross-resistance with other protein synthesis inhibitors. Bacteriostatic.
Clinical Use:
- VRE infections (primary indication): Linezolid is a cornerstone
- MRSA pneumonia: Linezolid may be superior to vancomycin (better lung penetration, inhibits toxin production)
- MRSA SSTI (oral option - excellent bioavailability ~100%)
- MDR-TB / XDR-TB: Linezolid is a Group A drug (WHO 2022)
- Tedizolid: Fewer myelosuppression concerns; once-daily; used for ABSSSI
Toxicity (linezolid): Myelosuppression (thrombocytopenia - monitor CBC weekly), serotonin syndrome (avoid with SSRIs/MAOIs), lactic acidosis with prolonged use.
CLASS 11: Polymyxins (Colistin/Polymyxin E, Polymyxin B)
Mechanism
Cationic polypeptides that bind to lipopolysaccharide (LPS) and phospholipids in the gram-negative outer membrane, causing membrane disruption and cell death. Active only against gram-negatives (E. coli, Klebsiella, Acinetobacter, Pseudomonas). Bactericidal.
Clinical Use:
- Carbapenem-resistant Acinetobacter baumannii (CRAB), Pseudomonas aeruginosa (CRPA), Klebsiella pneumoniae (CRKP) - last-resort agents (IDSA AMR Guidance 2024)
- Used in combination (with carbapenems, rifampin, or fosfomycin) to enhance activity and reduce resistance emergence
- Inhaled colistin for Pseudomonas in CF (adjunctive)
Toxicity: Nephrotoxicity (dose-dependent), neurotoxicity (paresthesias, neuromuscular blockade). TDM and renal monitoring mandatory.
CLASS 12: Daptomycin (Cyclic Lipopeptide)
Mechanism
Inserts into gram-positive cytoplasmic membrane in a calcium-dependent manner -> causes depolarization and disruption of ionic concentration gradients -> membrane instability and rapid bactericidal killing.
Clinical Use:
- MRSA bacteremia and right-sided endocarditis (FDA-approved; 6mg/kg/day IV)
- VRE bacteremia
- MRSA/MRSE skin/soft tissue infections
- NOT for pneumonia (daptomycin is inactivated by pulmonary surfactant)
CLASS 13: Rifamycins (Rifampin, Rifabutin, Rifaximin)
Mechanism
Bind beta subunit of bacterial DNA-dependent RNA polymerase -> inhibit initiation of RNA transcription. Bactericidal for M. tuberculosis and active against gram-positive cocci.
Clinical Use:
- Tuberculosis: Rifampin is a core drug in the 2HRZE/4HR standard regimen (WHO, CDC)
- Rifabutin: Substitute for rifampin in HIV patients on antiretroviral therapy (less CYP450 induction)
- Staphylococcal biofilm infections (prosthetic joint, device-associated): Add rifampin to base regimen to penetrate biofilm
- Leprosy: Rifampin in multidrug therapy (WHO)
- Meningococcal prophylaxis (close contacts)
- Rifaximin: Non-absorbed oral form for traveler's diarrhea (E. coli), hepatic encephalopathy, IBS-D
NEVER use as monotherapy - resistance emerges rapidly (single-step mutations in rpoB gene).
INFECTION-SPECIFIC Antibiotic Selection Guide
Respiratory Infections
| Infection | Pathogen(s) | Preferred Agent | Guideline |
|---|---|---|---|
| Outpatient CAP (no comorbidities) | S. pneumoniae, M. pneumoniae, C. pneumoniae | Amoxicillin OR Doxycycline | ATS 2026 (PMID: 40679934) |
| Outpatient CAP (comorbidities/risk factors) | + gram-negatives | Amoxicillin-clavulanate + macrolide OR Respiratory FQ alone | ATS 2026 |
| Inpatient CAP (non-ICU) | S. pneumoniae, gram-negatives | Beta-lactam + Azithromycin OR Respiratory FQ | ATS 2026 |
| Inpatient CAP (ICU/severe) | Broad coverage | Beta-lactam + Azithromycin + consider Vancomycin if MRSA risk | ATS 2026 |
| HAP / VAP | Pseudomonas, MRSA, Enterobacterales | Anti-pseudomonal beta-lactam ± vancomycin/linezolid | IDSA/ATS 2016 (update pending) |
| Atypical pneumonia | Mycoplasma, Legionella, Chlamydophila | Azithromycin or Doxycycline or Respiratory FQ | - |
Urinary Tract Infections
| Infection | Preferred Agent | Notes |
|---|---|---|
| Uncomplicated cystitis (women) | Nitrofurantoin x5d, TMP-SMX x3d, Fosfomycin x1d | Fluoroquinolones/beta-lactams - avoid when alternatives available (IDSA) |
| Complicated UTI (no sepsis) | 3rd/4th gen cephalosporin (oral/IV), TMP-SMX | 4-step IDSA 2025 framework |
| cUTI with sepsis (no shock) | 3rd/4th gen cephalosporin (IV) or carbapenem if ESBL risk | IV to oral switch as early as day 3 if improving |
| cUTI with ESBL risk | Ertapenem (stable) or Meropenem (septic/unstable) | IDSA 2025 (PMID: 41419448) |
| Prostatitis | Ciprofloxacin or Levofloxacin x4-6 weeks | - |
Skin and Soft Tissue Infections
| Infection | Preferred Agent |
|---|---|
| Non-purulent cellulitis (beta-Strep) | Penicillin V or Amoxicillin; IV Penicillin G (severe) |
| Purulent SSTI / Furuncle (CA-MRSA) | I&D + TMP-SMX or Doxycycline (outpatient) |
| Severe MRSA SSTI (inpatient) | IV Vancomycin or Daptomycin |
| Necrotizing fasciitis (Type I - polymicrobial) | Pip-Tazo + Vancomycin + Clindamycin (toxin suppression) |
| Necrotizing fasciitis (Type II - GAS) | IV Penicillin G + Clindamycin |
| Diabetic foot infection (moderate-severe) | Amoxicillin-clavulanate or Pip-Tazo; add MRSA coverage if risk |
Intra-Abdominal Infections
| Setting | Preferred Regimen | Guideline |
|---|---|---|
| Community-acquired, mild-moderate | Amoxicillin-clavulanate OR Cefoxitin | SIS 2024 (PMID: 38990709) |
| Community-acquired, severe / ICU | Pip-Tazo OR Ceftriaxone + Metronidazole | SIS 2024 |
| Healthcare-associated / post-operative | Pip-Tazo OR Carbapenem (if resistant organism risk) | SIS 2024 |
| Empiric anaerobic coverage | Always include (Metronidazole or Pip-Tazo or Cephamycin) | - |
CNS Infections (Bacterial Meningitis)
| Scenario | Empiric Regimen |
|---|---|
| Community-acquired (adult) | Ceftriaxone + Vancomycin + Dexamethasone |
| Age >50 or immunocompromised (add Listeria coverage) | + Ampicillin |
| Hospital-acquired/post-procedural | Vancomycin + Cefepime or Meropenem |
| Brain abscess | Ceftriaxone + Metronidazole (± Vancomycin if MRSA risk) - ESCMID 2024 (PMID: 37648062) |
Sexually Transmitted Infections
| Infection | Preferred Agent |
|---|---|
| Gonorrhea | Ceftriaxone 500mg IM x1 (CDC 2021; 1g if >150kg) |
| Chlamydia | Doxycycline 100mg BD x7d (preferred) or Azithromycin 1g x1 |
| Syphilis (primary/secondary) | Benzathine Penicillin G 2.4MU IM x1 |
| BV / Trichomoniasis | Metronidazole |
| Pelvic inflammatory disease | Ceftriaxone + Doxycycline ± Metronidazole |
Resistant Organism-Specific Treatment (IDSA AMR Guidance 2024)
| Organism | Preferred Treatment |
|---|---|
| MRSA (serious/bacteremia) | Vancomycin (AUC-guided) or Daptomycin |
| MRSA pneumonia | Linezolid or Vancomycin |
| VRE | Linezolid or Daptomycin |
| ESBL-producing Enterobacterales | Ertapenem or Meropenem; Ceftolozane-tazo (UTI) |
| CRE (KPC-producing) | Ceftazidime-avibactam ± Aztreonam |
| CRPA (carbapenem-resistant Pseudomonas) | Ceftolozane-tazobactam or Ceftazidime-avibactam |
| CRAB (carbapenem-resistant Acinetobacter) | Sulbactam-durlobactam (preferred, 2024) or Colistin-based combination |
| MDR-TB | Levofloxacin/Moxifloxacin + Bedaquiline + Linezolid (WHO 2022 BPaL/BPaLM regimen) |
Antibiotic Resistance Mechanisms (Summary)
| Mechanism | Examples |
|---|---|
| Enzymatic inactivation | Beta-lactamases (ESBLs, carbapenemases), aminoglycoside-inactivating enzymes, chloramphenicol acetyltransferase |
| Efflux pumps | Fluoroquinolone, macrolide, tetracycline resistance |
| Reduced permeability | Porin loss in GNRs (imipenem resistance in Pseudomonas) |
| Target modification | PBP2a in MRSA (mecA gene), altered 23S rRNA (macrolide/linezolid), GyrA mutation (FQ resistance) |
| Bypass pathway | DHPS/DHFR overexpression (sulfonamide resistance) |
| Target protection | Tet(M) ribosome protection proteins (tetracycline) |
- Medical Microbiology 9e, Box 17.2, p.199-205
Key Antibiotic Stewardship Principles (CDC 2025)
- De-escalate from broad-spectrum to targeted therapy once culture/susceptibility results are available
- IV-to-oral switch as soon as clinically appropriate (reduces line complications, costs)
- Shortest effective duration - most infections do not require >5-7 days (IDSA 2025 cUTI: 7 days for most cases)
- Culture before starting antibiotics whenever possible (do not delay treatment for sepsis)
- Avoid high-CDI-risk agents (clindamycin, fluoroquinolones, broad-spectrum cephalosporins) when alternatives exist
- Check local antibiogram before choosing empiric therapy - resistance patterns vary significantly by region and institution
Sources: Medical Microbiology 9e (Murray et al.) | Jawetz Melnick & Adelberg's Medical Microbiology 28e | ATS 2026 CAP Guideline (PMID: 40679934) | IDSA 2025 cUTI Guideline (PMID: 41419448) | SIS 2024 Intra-Abdominal Infection Guideline (PMID: 38990709) | ESCMID 2024 Brain Abscess Guideline (PMID: 37648062) | IDSA AMR Guidance 2024 | CDC Antibiotic Stewardship Report 2025
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