Antibitoics (USMLE) PDF
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This document is a study guide focused on antibiotics, covering various classes, their mechanisms of action, uses, and potential side effects. It is designed for undergraduate medical students studying for the USMLE, and would be helpful for understanding and comparing different antibiotics' specific characteristics.
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**Penicillinase-Sensitive Penicillins** **Mechanism of Action** **Uses** **Side Effects** **Examples** \- Same as penicillin.\ - Wider spectrum; penicillinase sensitive.\ - Also combine with clavulanic acid to protect against destruction by β-lactamase.\ **[Mechanism of Resistance]**\ - Penicil...
**Penicillinase-Sensitive Penicillins** **Mechanism of Action** **Uses** **Side Effects** **Examples** \- Same as penicillin.\ - Wider spectrum; penicillinase sensitive.\ - Also combine with clavulanic acid to protect against destruction by β-lactamase.\ **[Mechanism of Resistance]**\ - Penicillinase (a type of β-lactamase) cleaves β-lactam ring. [Extended-spectrum penicillin]\ - Listeria monocytogenes\ - Proteus mirabilis\ - H influenzae,\ - Enterococci\ - Salmonella\ - Shigella\ - H pylori\ - E coli \- Hypersensitivity reactions\ - Pseudomembranous colitis\ - Rash \- Amoxicillin\ -Ampicillin\ - Aminopenicillins. **Penicillinase-resistant penicillins** **Mechanism of Action** **Uses** **Side Effects** **Examples** \- Same as penicillin.\ - Narrow spectrum; penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring.\ [ **Mechanism of Resistance**]\ - MRSA has altered penicillin-binding protein target site. S aureus (except MRSA). \- Hypersensitivity reactions\ - Interstitial nephritis \- Dicloxacillin\ - Nafcillin\ - Oxacillin **Piperacillin** **Mechanism of Action** **Uses** **Side Effects** **Examples** \- Same as penicillin.\ - Extended spectrum.\ - Penicillinase sensitive\ - Use with β-lactamase inhibitors \- Pseudomonas spp\ - Gram negative\ - Rods\ - Anaerobes \- Hypersensitivity reactions. \- Antipseudomonal penicillin **Cephalosporins (1st Generation)** **Mechanism of Action** **Uses** **Side Effects** **Examples** **[Inhibit Cell Wall Synthesis]**\ - β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.\ - Bactericidal**[\ Mechanism of Resistance\ ]**- Inactivated by cephalosporinases (a type of β-lactamase).\ - Structural change in penicillinbinding proteins (transpeptidases). \- Gram ⊕ cocci,\ - Proteus mirabilis,\ - E coli,\ - Klebsiella pneumoniae.\ - Cefazolin used prior to surgery to prevent S aureus wound infections \- Hypersensitivity reactions\ - Autoimmune hemolytic anemia\ - Disulfiram-like reaction\ - Vitamin K deficiency. \- Low rate of cross-reactivity even in penicillin-allergic patients.\ - Nephrotoxicity (when used with aminoglycosides). \- Cefa.zolin\ - Cepha.lexin **Cephalosporins (2nd Generation)** **Mechanism of Action** **Uses** **Side Effects** **Information** **[Inhibit Cell Wall Synthesis]**\ - β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.\ - Bactericidal**[\ Mechanism of Resistance\ ]**- Inactivated by cephalosporinases (a type of β-lactamase).\ - Structural change in penicillinbinding proteins (transpeptidases). \- Gram ⊕ cocci\ - H influenzae\ - Enterobacter aerogenes\ - Neisseria spp\ - Serratia marcescens\ - Proteus mirabilis\ - E coli\ - Klebsiella pneumoniae \- Hypersensitivity reactions\ - Autoimmune hemolytic anemia\ - Disulfiram-like reaction\ - Vitamin K deficiency. \- Low rate of cross-reactivity even in penicillin-allergic patients.\ - Nephrotoxicity (when used with aminoglycosides). \- Cef.aclor\ - Cef.oxitin\ - Cef.uroxime\ - Cef.otetan **Cephalosporins (3rd Generation)** **Mechanism of Action** **Uses** **Side Effects** **Information** **[Inhibit Cell Wall Synthesis]**\ - β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.\ - Bactericidal**[\ Mechanism of Resistance\ ]**- Inactivated by cephalosporinases (a type of β-lactamase).\ - Structural change in penicillinbinding proteins (transpeptidases). \- Serious gram ⊝ infections\ - Gram negative infections resistant to other β-lactams\ **[Ceftriaxone]**\ - Meningitis\ - Gonorrhea\ - Disseminated Lyme disease\ **[Ceftazidime]**\ - Pseudomonas Aeruginosa \- Hypersensitivity reactions\ - Autoimmune hemolytic anemia\ - Disulfiram-like reaction\ - Vitamin K deficiency. \- Low rate of cross-reactivity even in penicillin-allergic patients.\ - Nephrotoxicity (when used with aminoglycosides). \- Cef.triaxone -\ - Cef.podoxime\ - Cef.tazidime -\ - Cef.ixime **Cephalosporins (4th Generation)** **Mechanism of Action** **Uses** **Side Effects** **Information** **[Inhibit Cell Wall Synthesis]**\ - β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.\ - Bactericidal**[\ Mechanism of Resistance\ ]**- Inactivated by cephalosporinases (a type of β-lactamase).\ - Structural change in penicillinbinding proteins (transpeptidases). \- Gram ⊝ organisms\ - Gram ⊕ organisms.\ - Increased activity against Pseudomonas \- Hypersensitivity reactions\ - Autoimmune hemolytic anemia\ - Disulfiram-like reaction\ - Vitamin K deficiency. \- Low rate of cross-reactivity even in penicillin-allergic patients.\ - Nephrotoxicity (when used with aminoglycosides). \- Cefe.pime **Cephalosporins (5th generation)** **Mechanism of Action** **Uses** **Side Effects** **Examples** **[Inhibit Cell Wall Synthesis]**\ - β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.\ - Bactericidal**[\ Mechanism of Resistance\ ]**- Inactivated by cephalosporinases (a type of β-lactamase).\ - Structural change in penicillinbinding proteins (transpeptidases). \- Broad gram ⊕ and gram ⊝ organism coverage\ **[Unlike 1st--4th Generation Cephalosporins]**\ - Listeria\ - Atypical (chlamydia, Mycoplasma)\ - MRSA\ - Enterococcus faecalis\ - Does not cover Pseudomonas \- Hypersensitivity reactions\ - Autoimmune hemolytic anemia\ - Disulfiram-like reaction\ - Vitamin K deficiency. \- Low rate of cross-reactivity even in penicillin-allergic patients.\ - Nephrotoxicity (when used with aminoglycosides). \- Cef.taroline **β-lactamase inhibitors** **Mechanism of Action** **Uses** **Side Effects** **Examples** \- Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase.\ - β-lactamases are enzymes produced by some bacteria that break the β-lactam ring of antibiotics, rendering them ineffective.\ - By inhibiting these enzymes, β-lactamase inhibitors preserve the antibiotic\'s ability to target and kill bacteria. **[Antibiotics with Beta-Lactam Ring]**\ - Penicillins\ - Cephalosporins\ - Carbapenems\ - Monobactams (Aztreonam) \- Clavulanic acid,\ - Avibactam, \- Sulbactam,\ - Tazobactam. **Carbapenems** **Mechanism of Action** **Uses** **Side Effects** **Information** **[Imipenem]**\ - Broad-spectrum,\ - β-lactamase resistant\ P**[enicillin-Binding Proteins (PBPs)]**\ - Binds to penicillin-binding proteins (PBPs), which are crucial enzymes involved in bacterial cell wall synthesis.\ - This binding inhibits cell wall synthesis, leading to bacterial cell death (bactericidal effect).\ **[Cilastatin]**\ - Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to ? inactivation of drug in renal tubules.**[\ Mechanism of Resistance\ ]**- Inactivated by carbapenemases produced by, eg, K pneumoniae, E coli, E aerogenes \- Gram ⊕ cocci\ - Gram ⊝ rods\ - Anaerobes.\ - Wide spectrum and significant adverse effects limit use to life-threatening infections or after other drugs have failed.\ - Meropenem has a ? risk of seizures and is stable to dehydropeptidase I. \- GI distress\ - Rash\ - CNS toxicity (seizures) at high plasma levels \- Imi.penem\ - Mero.penem\ - Erta.penem **Aztreonam** **Mechanism of Action** **Uses** **Side Effects** **Examples** \- Less susceptible to β-lactamases.\ - Prevents peptidoglycan cross-linking by binding to penicillinbinding protein 3.\ - Synergistic with aminoglycosides.\ - No cross-allergenicity with penicillins \- Gram ⊝ rods only\ - No activity against gram ⊕ rods or anaerobes.\ - For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides \- Usually nontoxic\ - Occasional GI upset **Vancomycin** **Mechanism of Action** **Uses** **Side Effects** **Information** **[Inhibits Cell Wall Formation]**\ - Binds to the D-Ala-D-Ala dipeptide portion of the peptidoglycan precursors, which are essential for the construction of the bacterial cell wall.\ - Leads to bacterial cell lysis and death, especially in gram-positive bacteria, as their cell walls are more dependent on peptidoglycan.\ - Bactericidal against most bacteria (bacteriostatic against C difficile).\ - Not susceptible to β-lactamases.\ [ **Mechanism of Resistance**]\ - Occurs in bacteria (eg, Enterococcus)\ - Via amino acid modification of D-Ala \- Gram ⊕ bugs only---for serious, multidrug-resistant organisms\ - MRSA\ - S epidermidis\ - Sensitive Enterococcus species\ - Clostridium difficile (oral route) \- Well tolerated in general but not trouble free\ - Nephrotoxicity\ - Ototoxicity\ - Thrombophlebitis\ - Diffuse flushing (vancomycin infusion reaction A---idiopathic reaction largely preventable by pretreatment with antihistamines and slower infusion rate),\ - DRESS syndrome. **Protein Synthesis Inhibitors** **Mechanism of Action** **Uses** **Side Effects** **Information** \- Specifically target smaller bacterial ribosome (70S, made of 30S and 50S subunits), leaving human ribosome (80S) unaffected.\ - All are bacteriostatic, except aminoglycosides (bactericidal) and linezolid (variable). **[30S inhibitors]**\ - Aminoglycosides \- Tetracyclines\ **[50S inhibitors]**\ - Chloramphenicol, \- Clindamycin \- Erythromycin (macrolides) \- Linezolid **Aminoglycosides** **Mechanism of Action** **Uses** **Side Effects** **Information** \- Bactericidal\ - Irreversible inhibition of initiation complex through binding of the 30S subunit.\ - Can cause misreading of mRNA.\ - Also block translocation.\ - Require O2 for uptake; therefore, ineffective against anaerobes.\ **[Mechanism of Resistance]**\ - Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation. \- Severe gram ⊝ rod infections.\ - Synergistic with β-lactam antibiotics.\ - Neomycin for bowel surgery. \- Nephrotoxicity\ - Neuromuscular blockade (absolute contraindication with myasthenia gravis)\ - Ototoxicity (especially with loop diuretics)\ - Teratogenicity. \- Gentamicin\ - Neomycin\ - Amikacin\ - Tobramycin\ - Streptomycin. **Tetracyclines** **Mechanism of Action** **Uses** **Side Effects** **Information** \- Bacteriostatic\ - Bind to 30S and prevent attachment of aminoacyl-tRNA.\ - Limited CNS penetration.\ - Doxycycline is fecally eliminated and can be used in patients with renal failure.\ - Do not take tetracyclines with milk (Ca2+), antacids (eg, Ca2+ or Mg2+), or iron-containing preparations because divalent cations inhibit drugs' absorption in the gut.\ **[Mechanism of Resistance]**\ - decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps \- Borrelia burgdorferi,\ - M pneumoniae.\ - Drugs' ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia.\ - Also used to treat acne.\ **[Doxycycline]**\ - Community-acquired MRSA. \- GI distress\ - Discoloration of teeth and inhibition of bone growth in children\ - Photosensitivity.\ - "Teratocylines" are teratogenic\ - Generally avoided in pregnancy and in children (except doxycycline) \- Tetracycline\ - Doxycycline\ - Minocycline **Tigecycline** **Mechanism of Action** **Uses** **Side Effects** \- Tetracycline derivative.\ - Binds to 30S, inhibiting protein synthesis.\ - Generally bacteriostatic. \- Broad-spectrum anaerobic\ - Gram ⊝\ - Gram ⊕ coverage.\ - Multidrug-resistant organisms (eg, MRSA, VRE) \- Nausea\ - vomiting. **Chloramphenicol** **Mechanism of Action** **Uses** **Side Effects** \- Blocks peptidyltransferase at 50S ribosomal subunit.\ - Bacteriostatic\ **[Mechanism of Resistance]**\ - Plasmid-encoded acetyltransferase inactivates the drug. \- Meningitis (Haemophilus influenzae, Neisseria meningitidis,\ - Streptococcus pneumoniae)\ - Rickettsial diseases (eg, Rocky Mountain spotted fever \[Rickettsia rickettsii\]).\ - Limited use due to toxicity but often still used in developing countries because of low cost. \- Anemia (dose dependent)\ - Aplastic anemia (dose independent)\ - Gray baby syndrome (in premature infants because they lack liver UDP-glucuronosyltransferase) **Clindamycin** **Mechanism of Action** **Uses** **Side Effects** \- Blocks peptide transfer (translocation) at 50S ribosomal subunit.\ - Bacteriostatic. \- Anaerobic infections (eg, Bacteroides spp., Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections.\ - Also effective against invasive group A streptococcal infection.\ - Treats anaerobic infections above the diaphragm vs metronidazole (anaerobic infections below diaphragm). \- Pseudomembranous colitis (C difficile overgrowth)\ - Fever\ - Diarrhea **Linezolid** **Mechanism of Action** **Uses** **Side Effects** \- Inhibits protein synthesis by binding to the 23S rRNA of the 50S ribosomal subunit and preventing formation of the initiation complex.\ **[Mechanism of Resistance]**\ - Point mutation of ribosomal RNA. Gram ⊕ species including MRSA and VRE \- Myelosuppression (especially thrombocytopenia),\ - Peripheral neuropathy\ - Serotonin syndrome (due to partial MAO inhibition). **Macrolides** **Mechanism of Action** **Uses** **Side Effects** \- Inhibit protein synthesis by blocking translocation\ - Bind to the 50S ribosomal subunit.\ - Bacteriostatic.\ **[Mechanism of Resistance]**\ - Bacteria cause methylation of 23S rRNA-binding site prevents binding of drug.\ - By methylating specific adenine residues in the 23S rRNA, the binding site of the macrolides is altered, preventing the drug from effectively binding to the bacterial ribosome, thereby blocking its antimicrobial action. **[Atypical Pneumonias]**\ - Mycoplasma\ - Chlamydia\ - Legionella\ **[Other]**\ - STIs (Chlamydia)\ - Gram ⊕ cocci (streptococcal infections in patients allergic to penicillin)\ - B pertussis. \- Gastrointestinal Motility issues,\ - Arrhythmia caused by prolonged QT interval\ - Acute Cholestatic hepatitis,\ - Rash\ - Eosinophilia.\ - Increases serum concentration of theophylline\ - Oral anticoagulants.\ - Clarithromycin and erythromycin inhibit cytochrome P-450. \- Azithromycin\ - Clarithromycin\ - Erythromycin **Polymyxins** **Mechanism of Action** **Uses** **Side Effects** \- Cation polypeptides that bind to phospholipids on cell membrane of gram ⊝ bacteria.\ - Disrupt cell membrane integrity Ž leakage of cellular components Ž cell death. \- Salvage therapy for multidrug-resistant gram ⊝ bacteria (eg, P aeruginosa, E coli, K pneumoniae).\ - Polymyxin B is a component of a triple antibiotic ointment used for superficial skin infections. \- Nephrotoxicity\ - Neurotoxicity (eg, slurred speech, weakness, paresthesias)\ - Respiratory failure. \- Colistin (polymyxin E)\ - Polymyxin B **Sulfonamides** **Mechanism of Action** **Uses** **Side Effects** **[Dihydropteroate Synthase\ ]**- This enzyme is essential for bacterial to replicate\ - Inhibit dihydropteroate synthase, thus inhibiting folate synthesis, which inhibits bacterial replication\ - Bacteriostatic (bactericidal when combined with trimethoprim).**[\ Mechanism of Resistance]**\ - Altered enzyme (bacterial dihydropteroate synthase),\ - Decreased uptake\ - Increased PABA synthesis. \- Gram ⊕\ - Gram ⊝\ - Nocardia.\ - TMP-SMX for simple UTI. \- Hypersensitivity reactions\ - Hemolysis if G6PD deficient\ - Nephrotoxicity (tubulointerstitial nephritis)\ - Photosensitivity \- Stevens-Johnson syndrome\ - Kernicterus in infants\ [Drug Crowding]\ - Sulfonamides can displace other drugs from their binding sites on plasma proteins like albumin (warfarin) \- Sulfamethoxazole (SMX),\ - Sulfisoxazole\ - Sulfadiazine **Dapsone** **Mechanism of Action** **Uses** **Side Effects** \- Similar to sulfonamides, but structurally distinct agent.\ [ **Dihydropteroate Synthase\ **]- This enzyme is essential for bacterial to replicate\ - Inhibit dihydropteroate synthase, thus inhibiting folate synthesis, which inhibits bacterial replication\ - Bacteriostatic (bactericidal when combined with trimethoprim). \- Leprosy (lepromatous and tuberculoid),\ - Pneumocystis jirovecii prophylaxis\ - Treatment when used in combination with TMP \- Hemolysis if G6PD deficient\ - Methemoglobinemia\ - Agranulocytosis **Trimethoprim** **Mechanism of Action** **Uses** **Side Effects** **[Dihydropteroate Synthase\ ]**- This enzyme is essential for bacterial to replicate\ - Inhibit dihydropteroate synthase, thus inhibiting folate synthesis, which inhibits bacterial replication\ - Bacteriostatic (bactericidal when combined with trimethoprim).\ **[Combination]**\ - Used in combination with sulfonamides (trimethoprim-sulfamethoxazole \[TMPSMX\])\ - Causes sequential block of folate synthesis.\ - Combination used for UTIs \- Shigella\ - Salmonella\ - Pneumocystis jirovecii\ - Pneumonia treatment and prophylaxis\ - Toxoplasmosis prophylaxis. \- Hyperkalemia (at high doses; similar mechanism as potassium-sparing diuretics)\ - Megaloblastic anemia\ - Leukopenia\ - Granulocytopenia, which may be avoided with coadministration of leucovorin (folinic acid). **Fluoroquinolones** **Mechanism of Action** **Uses** **Side Effects** **[Inhibit topoisomerase II (DNA gyrase) and topoisomerase IV.]**\ - Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV.\ - These enzymes are crucial for bacterial DNA replication, transcription, repair, and recombination.\ - Bactericidal.\ **[Absorption]**\ - Concurrent ingestion of divalent cations (eg, dairy, antacids) markedly decreases oral absorption. ,\ **[Mechanism of Resistance]**\ - Chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps. \- Otitis externa.\ - Gram ⊕ organisms\ - Gram ⊝ rods of urinary and GI tracts\ - Pseudomonas Aeruginosa \- GI upset\ - Superinfections\ - Skin rashes\ - Headache\ - Dizziness.\ - Less commonly, can cause leg cramps and myalgias.\ - Contraindicated during pregnancy or breastfeeding and in children \< 18 years old due to possible damage to cartilage.\ - Some may prolong QT interval.\ - May cause tendonitis or tendon rupture in people \> 60 years old and in patients taking prednisone. \- Ciprofloxacin (Inhibits cytochrome P-450)\ - Ofloxacin\ - Respiratory fluoroquinolones\ - Levofloxacin\ - Moxifloxacin **Daptomycin** **Mechanism of Action** **Uses** **Side Effects** \- A cyclic lipopeptide antibiotic that primarily targets the cell membranes of Gram-positive bacteria\ - Works by inserting itself into the bacterial membrane in a calcium-dependent manner, causing rapid depolarization of the membrane potential.\ - This results in the formation of transmembrane channels, leading to the leakage of intracellular ions and molecules, and ultimately cell death without causing cell lysis. \- S aureus skin infections (especially MRSA),\ - Bacteremia\ - Infective endocarditis\ - Vancomycin-Resistant Enterococcus (VRE)\ - Not used for pneumonia (avidly binds to and is inactivated by surfactant). \- Myopathy\ - Rhabdomyolysis. **Metronidazole** **Mechanism of Action** **Uses** **Side Effects** \- Enters the bacterial or protozoal cell, where it is reduced to form highly reactive free radicals.\ - These free radicals interact with the DNA of the organism, causing damage, leading to the inhibition of DNA synthesis and cell death.\ - Bactericidal\ - Antiprotozoal. \- Giardia,\ - Entamoeba,\ - Trichomonas,\ - Gardnerella vaginalis,\ - Anaerobes (Bacteroides, C difficile).\ **[H Pylori]**\ - Can be used in place of amoxicillin in H pylori "triple therapy" in case of penicillin allergy \- Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol\ - Headache\ - Metallic taste. **Rifamycin** **Mechanism of Action** **Uses** **Side Effects** I**[nhibits DNA-Dependent RNA Polymerase]**\ - By binding to this enzyme, rifamycin prevents the initiation of transcription, thereby decreasing mRNA synthesis.\ **[Rifampin Resistance]**\ - Rifamycin resistance arises due to mutations in gene encoding RNA polymerase\ **[Information]**\ - Rifabutin favoured over rifampin in patients with HIV infection due to less CYP450 induction\ - Monotherapy rapidly leads to resistance \- Tuberculosis \- Minor hepatotoxicity\ - Drug interactions (CYP450 induction)\ - Red-orange discoloration of body fluids (non-hazardous adverse effect) \- Rifampin\ - Rifabutin\ - Rifapentine **Isoniazid** **Mechanism of Action** **Uses** **Side Effects** **[Inhibits Mycolic Acid Synthesis]**\ - inhibits the synthesis of mycolic acids, which are crucial components of the mycobacterial cell wall.\ **[Catalase-Peroxidase Enzyme]**\ - Enzyme (encoded by the katG gene) is responsible for converting isoniazid into its active form.\ - Resistance to isoniazid commonly occurs due to mutations in the katG gene, which lead to a reduction or loss of catalase-peroxidase activity.\ **[Notes]**\ - Administer with pyridoxine (vitamin B6)\ - Hepatocytes (at increased risk of risk of hepatotoxicity with increased age and alcohol overuse)\ - Different INH half-lives in fast vs slow acetylators \- Tuberculosis treatment\ - Tuberculosis prophylaxis (stand-alone) \- Vitamin B6 deficiency (peripheral neuropathy, sideroblastic anemia)\ - Hepatotoxicity\ - Drug interactions (CYP450 inhibition)\ - Drug-induced lupus INH overdose can lead to seizures (often refractory to benzodiazepines) **Pyrazinamide** **Mechanism of Action** **Uses** **Side Effects** Mechanism uncertain\ **[Notes]**\ - Works best at acidic pH (eg, in host phagolysosomes) \- Tuberculosis \- Hepatotoxicity\ - Hyperuricemia **Ethambutol** **Mechanism of Action** **Uses** **Side Effects** \- Inhibits arabinosyltransferase leading to decreased arabinogalactan synthesis resulting in decreased cell wall synthesis \- Tuberculosis \- Optic neuropathy (red-green color blindness or ? visual acuity, typically reversible) -------------------------------------------------------------------------------------------------------------------------------------- **Antimicrobial Prophylaxis** ----------------------------------------------------------------------------------- -------------------------------------------------- **Clinical Scenario** **Medication** Exposure to meningococcal infection \- Ceftriaxone,\ - Ciprofloxacin\ - Rifampin High risk for infective endocarditis and undergoing surgical or dental procedures Amoxicillin History of recurrent UTIs \- TMP-SMX Malaria prophylaxis for travelers \- Atovaquone-proguanil\ - Mefloquine\ - Doxycycline\ - Primaquine\ - Chloroquine (for areas with sensitive species) Pregnant patients carrying group B strep \- Intrapartum penicillin G or ampicillin Prevention of gonococcal conjunctivitis in newborn \- Erythromycin ointment on eyes Prevention of postsurgical infection due to S aureus \- Cefazolin; vancomycin if ⊕ for MRSA Prophylaxis of strep pharyngitis in child with prior rheumatic fever \- Benzathine penicillin G or oral penicillin V -------------------------------------------------------------------------------------------------------------------------------------- **30S inhibitors** --------------------------------- ---------------------------------------------------------------------------------------------------------------------------------------------------------------------- **- Aminoglycosides** These bind to the 30S subunit of bacterial ribosomes, causing a misreading of mRNA, leading to the production of faulty proteins. **- Tetracyclines** These inhibit protein synthesis by binding to the 30S ribosomal subunit and blocking the attachment of aminoacyl-tRNA to the ribosome. **Glycylcycline** **50S inhibitors** **- Chloramphenicol** This inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit and blocking the peptidyl transferase activity, preventing peptide bond formation. **- Clindamycin** It binds to the 50S ribosomal subunit and inhibits the early stages of protein synthesis. **- Erythromycin (macrolides)** These bind to the 50S ribosomal subunit, blocking the exit of the growing peptide chain, thus inhibiting protein synthesis. **- Linezolid** inhibits the initiation of protein synthesis by binding to the 50S ribosomal subunit and preventing the formation of the initiation complex.