Other ATB
BROAD SPECTRUM ATB
Macrolides, lincosamides, aminoglycosides, tetracyclines
Macrolides
Active Agents:
15-member lactone ring (azalides): Azithromycin
16-member lactone ring: Spiramycin
14-member lactone rings: Erythromycin, Roxithromycin, Clarithromycin
Ketolide: Telithromycin
Produced by various Streptomyces strains
Mechanism of Action:
Reversible binding to the 50S subunit
Inhibition of peptidyl transferase and protein chain elongation
Bacteriostatic effect
Macrolides Antimicrobial Spectrum
General:
Gram-positive bacteria:
Similar to penicillins (e.g., Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes)
Gram-negative bacteria:
Corynebacterium diphtheriae, Bordetella pertussis, Campylobacter jejuni, Helicobacter pylori, Haemophilus influenzae, Neisseria catarrhalis
Anaerobic pathogens (except Bacteroides fragilis)
Intracellular Pathogens:
Mycoplasma, Legionella pneumophila, Chlamydia pneumoniae, Chlamydia trachomatis, Toxoplasma gondii
Spirochetes:
Borrelia burgdorferi, Leptospira, Treponema pallidum
Mycobacteria:
Mycobacterium avium complex (MAC)
Enterobacteriaceae, Pseudomonas - many isolates of methicillin-resistant staphylococci
MLSB Resistance:
Macrolide-lincosamide-streptogramin B resistance via rRNA methylation/mutation leading to decreased affinity for the 50S subunit
Mechanisms: efflux, enzymatic inactivation
Macrolides PK, SE, Interactions
Acid Stability:
Erythromycin < Azithromycin < Clarithromycin
Absorption: Varies based on formulation, number of doses, and gastrointestinal filling
Tissue Penetration: Excellent except for CNS; concentrated in phagocytes
Excretion: Primarily in bile and stool; no dosing modifications required for kidney disease
Interactions:
Irreversible CYP450 inhibition leading to increased plasma levels of drugs metabolized by this pathway.
Common side effects (SE): Nausea, diarrhea, abdominal pain; ototoxicity with erythromycin and high-doses clarithromycin; rare skin allergic reactions.
Liver concentration increases leading to risk for QT interval prolongation events like "torsades de pointes".
Macrolides Therapeutic Use
General Use: Not indicated for life-threatening infections due to slow onset
Specific Uses:
Atypical pneumonia (Mycoplasma, Legionella)
Streptococci and sensitive staphylococci infections
Dental infections (Spiramycin enters saliva)
Chlamydia trachomatis and rickettsia infections
Treatment of toxoplasmosis in immunocompromised and pregnant women (Spiramycin)
Helicobacter pylori eradication in combination with amoxicillin and PPI
Mycobacterium avium infections, typically a three-drug regimen
Previous usage in colorectal surgery prophylaxis combined with neomycin.
Clarithromycin PK and Spectrum
Characteristics:
Semisynthetic macrolide, lipophilic, tissue concentrations 10x greater than serum
Oral bioavailability 55%; plasma half-life 3x longer than erythromycin
Inhibits CYP3A, can increase plasma levels of concurrently applied drugs.
Spectrum of Activity:
Effective against a range of G+ and G- bacteria, including atypical mycobacteria and Mycoplasma, Chlamydia.
Clarithromycin Principal Indications
Treats:
Respiratory tract infections, HP infections, skin and soft tissue infections
Second-line agent for Lyme disease, Toxoplasmosis, MAC infections
Bacterial endocarditis prophylaxis in penicillin allergy cases.
Azithromycin Spectrum and PK
Characteristics:
Azalide related to erythromycin, slightly less potent against G+ but superior against G- bacilli.
Absorption ~37%; affected by food intake
Extensive tissue distribution and intracellular accumulation; hepatic metabolism predominates.
Indications:
Effective for acute exacerbations of COPD, community-acquired pneumonia, and other infections.
Spiramycin Spectrum and PK
Antimicrobial Spectrum:
Broad spectrum against G+ and G- bacteria, not effective against E. coli
Excellent tissue and saliva diffusion, with significant levels in infected tissues.
Pharmacokinetics:
Rapid but incomplete absorption, 30-39% bioavailability; plasma half-life about 8 hours.
Telithromycin MOA and Indications
Mechanism of Action:
First ketolide, dual binding to bacterial ribosomal RNA enhances efficacy against resistant strains.
Indications: Effective for community-acquired respiratory infections.
Macrolides Summary
Uses: Effective for otitis media, upper/lower respiratory tract infections, pneumonia, Mycobacterium avium complex, and STDs.
Pharmacokinetics: 3-day half-life for Azithromycin, 500 mg dosage regimen for H. pylori treatment often includes Clarithromycin.
Mechanism: Binds to 50S, blocking translocation in protein synthesis.
Adverse Effects: Nausea, vomiting, diarrhea, liver toxicity, P450 interactions, and QT prolongation risks.
Lincosamides: Clindamycin
Bacteriostatic Action: More effective than lincomycin, inhibits 50S ribosomal subunit.
Spectrum: Effective against anaerobic G– bacteria (excluding Bacteroides fragilis) and resistant G+ strains.
Resistance: Mainly via target site modification.
Clindamycin PK and Therapeutic Use
Pharmacokinetics: Good absorption and tissue penetration, metabolized in liver, excreted in bile.
Indications: Useful for anaerobic infections, G+ infections post-surgery, dentistry, and gynecological infections.
Resistance and Side Effects
Resistance: Significant presence of MLSB and other resistance mechanisms.
Side Effects: Potential for CDI, nausea, hypersensitivity, transient blood count changes.
Aminoglycosides
Mechanism: Irreversible binding to the 30S subunit, bactericidal effect, sensitive to aerobic bacteria, including G− and select G+ infections.
Active Agents: Streptomycin, Gentamicin, Amikacin, Tobramycin, Neomycin.
Aminoglycosides Therapeutic Use and SE
Indications: Used for severe infections involving aerobic G- bacteria; often combined with other antibiotics for efficacy.
Side Effects: Include nephrotoxicity, ototoxicity, and potential neuromuscular issues.
Tetracyclines and Their Spectrum
Active Agents: Doxycycline, Tigecycline, among others.
Mechanism: Reversible binding to the 30S subunit, inhibiting protein synthesis.
Spectrum: Broad activity against G+/G− bacteria, effective for intracellular pathogens.
Doxycycline PK and Indications
Pharmacokinetics: High absorption, good tissue penetration, long half-life, renal/biliary excretion.
Indications: Used for respiratory infections, genital infections, GIT infections, and skin infections.
Chloramphenicol Review
Mechanism: Binds to the 50S subunit, bacteriostatic effect but with serious toxicity.
Uses: Very limited use due to adverse effects like aplastic anemia and gastrointestinal issues.
Rifaximin Action and Applications
MOA: Inhibition of bacterial RNA synthesis.
Indications: Treatment of hepatic encephalopathy, IBS, and traveler's diarrhea.
Resistance to Antibiotics
Key Resistance Issues: Resistance in pneumococci, Staphylococcus aureus (MRSA), and several other pathogens.
ESKAPE Pathogens: Notable multidrug-resistant organisms.
Staphylococcal Infections Overview
Common Pathogen: Staphylococcus aureus.
Effects: Causes various pyogenic infections, foodborne illness, and toxic syndromes.
MRSA Concerns and Management
Origins: Resistance attributed to antibiotic use in health settings.
Management: Increasing awareness of historical origins and resistance mechanisms involving the mecA gene.
Antistaphylococcal Antibiotics
Active Agents: Include multiple penicillins, cephalosporins, and unique agents for MRSA treatment.
Glycopeptide Antibiotics Action
Mechanism: Inhibition of cell wall synthesis, effective against G+ organisms.
Key Agents: Vancomycin, Teicoplanin, Dalbavancin.
Vancomycin Details
MOA: Peptidoglycan synthase inhibitor; key for life-threatening infections.
Spectrum and Applications: Critical for MRSA, enterococcal infections, demonstrated synergy with aminoglycosides.
Side Effects of Vancomycin
Common Reactions: Nephrotoxicity, ototoxicity, and local irritation. Monitoring important due to narrow therapeutic window.
Linezolid MOA and Applications
Mechanism: Binds to the 50S ribosomal subunit, effective against a variety of G+ pathogens including MRSA.
Side Effects: Notable hematologic effects, potential interactions with MAO inhibitors.
Fusidic Acid Overview
Mechanism: Bacteriostatic action against G+ microorganisms, commonly used locally for infections.
Daptomycin Overview
Mechanism: Binds to bacterial membranes; utilizes rapid depolarization; effective against MRSA and resistant enterococci.
Quinupristin/Dalfopristin Summary
Mechanism: Streptogramin class, effective for complex resistant infections, administered via IV infusion.