Antimicrobial Therapy & Resistance
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Why is oral vancomycin primarily used to treat local infections in the gastrointestinal tract?

  • Vancomycin is poorly absorbed in the gastrointestinal tract, leading to high local concentrations. (correct)
  • Oral vancomycin provides a broader spectrum of antibacterial activity compared to parenteral routes.
  • Vancomycin undergoes extensive first-pass metabolism, reducing its systemic bioavailability.
  • Parenteral vancomycin is contraindicated for gastrointestinal infections due to potential liver toxicity.

Considering the structural relationships between beta-lactam drugs, which of the following scenarios would MOST likely lead to cross-resistance?

  • Two drugs each have unique R1 and R2 structures with no similarities, either identical or similar.
  • Two drugs have similar, but not identical, ring structures (r1' and r1'') on their R1 substituents.
  • Two drugs share an identical R2 structure, but their R1 structures are entirely different. (correct)
  • Two drugs share an identical R1 structure, but one has an additional modification to its beta-lactam ring.

Which of the following modifications to a glycopeptide antibiotic would MOST likely enhance its ability to overcome vancomycin resistance in bacteria?

  • Increasing the drug hydrophilicity
  • Adding bulky side chains that sterically hinder binding.
  • Reducing the number of glycosidic bonds.
  • Increasing the molecule's hydrophobicity.
  • Modifying the peptide core to improve binding affinity to the altered D-Ala-D-Lac target. (correct)

A patient has a severe systemic infection that is susceptible to both vancomycin and teicoplanin. Considering the available routes of administration for glycopeptides, which treatment strategy would be MOST appropriate and why?

<p>Administer parenteral teicoplanin since it is more effectively absorbed and has a longer half-life for systemic infections. (D)</p> Signup and view all the answers

How do structural similarities and differences in R1 and R2 affect the spectrum of activity and resistance patterns?

<p>Structural differences in R1 can influence the drug's target binding affinity and resistance patterns. (B)</p> Signup and view all the answers

In the context of combination antimicrobial therapy, which scenario most accurately exemplifies a synergistic effect?

<p>Combining an antibiotic that inhibits bacterial protein synthesis with another that inhibits DNA replication, leading to a combined effect greater than the sum of their individual effects. (C)</p> Signup and view all the answers

Which of the following statements best explains the rationale for using combination antimicrobial therapy in septic shock?

<p>Combination therapy broadens the spectrum of antimicrobial coverage, increasing the likelihood of targeting the causative pathogen in empiric treatment. (B)</p> Signup and view all the answers

In which of the following clinical scenarios would combination antimicrobial therapy be most appropriate due to the likelihood of a polymicrobial infection?

<p>Surgical site infection following an appendectomy, presenting with both aerobic and anaerobic bacteria. (A)</p> Signup and view all the answers

What is the MOST important consideration when switching a patient from intravenous (IV) ciprofloxacin to oral ciprofloxacin?

<p>Ensuring the patient can tolerate oral medications and has adequate gastrointestinal absorption. (C)</p> Signup and view all the answers

Which of the following best describes the primary benefit of parenteral-to-oral switch therapy in appropriate patients?

<p>Lower healthcare costs through reduced length of stay and outpatient management. (C)</p> Signup and view all the answers

A patient is diagnosed with a hospital-acquired infection. Which of the following organisms is MORE likely to be the causative agent compared to a community-acquired infection?

<p>Vancomycin-resistant <em>Enterococcus</em> (VRE). (A)</p> Signup and view all the answers

Which of the following pathogens, known for causing community-acquired infections, is LEAST likely to exhibit multidrug resistance compared to pathogens commonly associated with hospital-acquired infections?

<p><em>Escherichia coli</em>. (B)</p> Signup and view all the answers

A patient with infective endocarditis caused by Enterococcus is being treated with Penicillin and Gentamicin. The combined effect of these antibiotics is greater than the sum of their individual effects. This is an example of:

<p>Synergism, where the combined effect is greater than the sum of their individual effects. (B)</p> Signup and view all the answers

Which of the following scenarios represents the most significant risk associated with aminoglycoside administration?

<p>An elderly patient with pre-existing mild renal impairment prescribed a prolonged course of tobramycin for a severe lung infection. (C)</p> Signup and view all the answers

A patient develops vertigo, ataxia, and hearing loss after prolonged aminoglycoside therapy. What is the most likely mechanism behind these adverse effects?

<p>Selective damage to the vestibular and auditory hair cells in the inner ear. (C)</p> Signup and view all the answers

Which of the following mechanisms best describes how tetracyclines inhibit bacterial growth?

<p>Inhibiting bacterial protein synthesis by binding to the 30S ribosomal subunit. (C)</p> Signup and view all the answers

A patient is prescribed doxycycline to treat a Mycoplasma pneumoniae infection. What is the primary reason for selecting doxycycline over penicillin in this case?

<p><em>Mycoplasma pneumoniae</em> lacks a cell wall, making it intrinsically resistant to penicillin. (B)</p> Signup and view all the answers

Which of the following tetracyclines is most likely to be administered via the parenteral (intravenous) route?

<p>Doxycycline (C)</p> Signup and view all the answers

A patient with myasthenia gravis requires antibiotic treatment. Which antibiotic class should be administered with extreme caution, and why?

<p>Aminoglycosides, due to the risk of neuromuscular blockade. (C)</p> Signup and view all the answers

A microbiology lab identifies a Gram-positive bacterial infection. Considering the provided information, which antibiotic class would be least effective as a first-line treatment?

<p>Aminoglycosides (A)</p> Signup and view all the answers

A patient is diagnosed with Bacillus anthracis. Based on the content, which antibiotic would be most appropriate?

<p>Doxycycline (A)</p> Signup and view all the answers

Which clinical scenario presents the LEAST suitable application for oral vancomycin?

<p>Eradication of methicillin-resistant staphylococci colonization in the nasopharynx. (C)</p> Signup and view all the answers

A patient develops flushing, erythema, and pruritus during a vancomycin infusion. Which action is the MOST appropriate initial step?

<p>Administer intravenous diphenhydramine and slow the infusion rate. (C)</p> Signup and view all the answers

What is the primary mechanism of action by which fosfomycin exerts its antibacterial effect?

<p>Inhibition of peptidoglycan synthesis by blocking MurA, an enolpyruvate transferase. (A)</p> Signup and view all the answers

Which antibacterial agent is MOST likely to be effective against both methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus (VRE)?

<p>Linezolid (C)</p> Signup and view all the answers

A patient with a history of end-stage renal disease develops a severe gram-negative infection. Which agent would be MOST appropriate, considering its toxicity profile and spectrum of activity?

<p>Polymyxin B (C)</p> Signup and view all the answers

What is a major limitation of using Polymyxin B compared to other antibiotics?

<p>Significant nephrotoxicity and neurotoxicity. (B)</p> Signup and view all the answers

In a patient with a severe penicillin allergy, what alternative beta-lactam antibiotic might be considered with caution for MSSA bacteremia, assuming susceptibility is confirmed?

<p>Cefazolin (C)</p> Signup and view all the answers

Which of the following is LEAST likely to be a target for antibacterial agents that inhibit cell wall synthesis?

<p>Lipopolysaccharide (LPS) transport (D)</p> Signup and view all the answers

A healthcare provider is treating a patient with a polymicrobial infection that includes both Gram-positive and Gram-negative bacteria. What approach is MOST appropriate?

<p>Prescribe a combination of antibiotics, including one primarily for Gram-positive and another for Gram-negative bacteria. (A)</p> Signup and view all the answers

What is the MOST significant consideration when deciding to switch from intravenous to oral antibiotics for a patient being treated for an infection?

<p>Availability of an oral formulation with adequate bioavailability and comparable spectrum of activity (C)</p> Signup and view all the answers

Which characteristic distinguishes Cutibacterium and Actinomyces from Clostridium difficile?

<p><em>Cutibacterium</em> and <em>Actinomyces</em> do not form spores, whereas <em>Clostridium difficile</em> is spore-forming. (B)</p> Signup and view all the answers

Why are penicillinase-resistant penicillins, such as methicillin and cloxacillin, particularly effective against Staphylococcus aureus (MSSA)?

<p>They are not degraded by beta-lactamase enzymes produced by MSSA, allowing them to inhibit cell wall synthesis. (C)</p> Signup and view all the answers

In treating a cat/dog bite wound infected with Pasteurella multocida, why might an aminopenicillin like amoxicillin be preferred over a penicillinase-resistant penicillin?

<p>Aminopenicillins provide broader coverage against the mixed flora typically found in animal bite wounds, including both Gram-positive and Gram-negative organisms such as <em>Pasteurella multocida</em>. (B)</p> Signup and view all the answers

Which statement correctly explains the limited efficacy of aminopenicillins against H. influenzae?

<p>A significant number of <em>H. influenzae</em> strains produce beta-lactamase, which inactivates aminopenicillins. (C)</p> Signup and view all the answers

A 20-year-old male presents with a fever of 39°C, severe sore throat, body aches, but no cough or nasal congestion. Physical examination reveals enlarged and tender cervical lymph nodes. Why might antibiotic treatment be considered, and what would be the MOST important factor guiding the decision?

<p>Antibiotics are warranted to target a possible bacterial infection, with the decision hinging on a rapid strep test or throat culture result. (C)</p> Signup and view all the answers

Differentiate the antimicrobial spectrum of aminopenicillins from that of penicillin, especially concerning anaerobic bacteria.

<p>Aminopenicillins offer a broader spectrum against Gram-negative bacteria while maintaining similar activity against anaerobes as penicillin. (A)</p> Signup and view all the answers

How do spirochetes like Treponema pallidum and Leptospira interrogans differ significantly from other bacteria in terms of their structural and antimicrobial susceptibility?

<p>Spirochetes have a unique outer membrane structure that prevents the entry of most beta-lactam antibiotics. (D)</p> Signup and view all the answers

In a clinical scenario involving the use of penicillin or its derivatives, what is the MOST critical consideration when prescribing for a patient with a known history of penicillin allergy?

<p>Avoiding penicillins and opting for an alternative antibiotic class with no cross-reactivity, such as macrolides or quinolones. (A)</p> Signup and view all the answers

How do beta-lactam antibiotics like penicillin disrupt bacterial cell wall synthesis?

<p>By mimicking the structure of D-Ala-D-Ala, binding to transpeptidases (PBPs), and preventing cross-linking of peptidoglycans. (C)</p> Signup and view all the answers

Which mechanism explains how quinolones interfere with bacterial DNA replication?

<p>Quinolones stabilize the DNA-topoisomerase complex, preventing DNA re-ligation, leading to DNA breakage and replication arrest. (C)</p> Signup and view all the answers

How do aminoglycosides impair bacterial protein synthesis?

<p>By causing misreading of mRNA codons, incorporating incorrect amino acids into the growing polypeptide chain. (B)</p> Signup and view all the answers

What is the primary mechanism through which sulfonamides exert their antibacterial effect?

<p>By competitive inhibition of dihydropteroate synthase, preventing the synthesis of dihydrofolic acid from PABA. (C)</p> Signup and view all the answers

How do macrolide antibiotics inhibit bacterial protein synthesis?

<p>By binding to the 23S rRNA of the 50S ribosomal subunit, blocking the exit tunnel for the nascent polypeptide. (C)</p> Signup and view all the answers

Which of the following explains the mechanism of action of glycopeptide antibiotics such as vancomycin?

<p>They bind to the D-alanyl-D-alanine terminus of the peptide chains in peptidoglycans, preventing transpeptidation. (C)</p> Signup and view all the answers

How does fosfomycin inhibit bacterial cell wall synthesis?

<p>By inhibiting the enzyme UDP-N-acetylglucosamine enolpyruvyl transferase (MurA), which is essential in peptidoglycan synthesis. (C)</p> Signup and view all the answers

What is the mechanism through which polymyxins disrupt bacterial cell membranes?

<p>They bind to lipopolysaccharides (LPS) and phospholipids in the outer membrane of Gram-negative bacteria, disrupting membrane integrity. (C)</p> Signup and view all the answers

How do oxazolidinones inhibit bacterial protein synthesis?

<p>By binding to the 23S rRNA of the 50S ribosomal subunit, preventing the formation of the initiation complex. (B)</p> Signup and view all the answers

What distinguishes beta-lactamase inhibitors (BL/BIs) from beta-lactam antibiotics in terms of their mechanism of action?

<p>BL/BIs have no direct antibacterial activity but prevent the degradation of beta-lactam antibiotics by binding to beta-lactamases. (C)</p> Signup and view all the answers

Flashcards

Combination antimicrobial therapy

Using two or more antimicrobial agents for treatment.

Synergism

When combined treatments have a greater effect than their individual effects.

Empirical treatment

Initial treatment administered before culture results are known.

Polymicrobial infection

Infection caused by multiple types of microorganisms.

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Step-down therapy

Switching from intravenous to oral antibiotics after improvement.

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Community-acquired bacteria

Bacteria typically acquired outside of healthcare settings.

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Hospital-acquired bacteria

Bacteria acquired during hospital stays, often more resistant.

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Drug-resistant organisms

Microorganisms that are not affected by typical antibiotics.

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Anaerobes

Microorganisms that thrive in low or no oxygen environments.

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Clostridium spp.

A genus of anaerobic bacteria, including pathogenic species.

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Penicillinase-resistant penicillins

Antibiotics effective against penicillinase-producing bacteria.

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Methicillin-susceptible Staphylococcus aureus (MSSA)

Staphylococcus aureus bacteria that are sensitive to methicillin.

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Aminopenicillins

A type of penicillin with a broader spectrum, effective against more Gram-negative bacteria.

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Streptococci

A genus of bacteria responsible for several illnesses, often treatable with antibiotics.

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Pasteurella multocida

Bacteria commonly found in animals, can cause infections in humans.

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Urinary tract infection (UTI)

An infection in any part of the urinary system, often caused by bacteria.

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Glycopeptides

A class of antibiotics used for treating Gram-positive bacterial infections.

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Vancomycin

A glycopeptide antibiotic given parenterally or orally for serious infections.

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Teicoplanin

Another glycopeptide antibiotic, primarily used parenterally.

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R1 and R2 structural similarities

Classification of b-lactam drugs based on certain structural components.

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b-lactam drugs

A class of antibiotics including penicillins and cephalosporins, characterized by a beta-lactam ring.

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Cefazolin

An antibiotic that reduces mortality for MSSA infections compared to vancomycin.

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Vancomycin flushing syndrome

A reaction to vancomycin marked by extreme flushing, also called Red man syndrome.

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Nephrotoxicity

The potential harmful effects of a drug on the kidneys.

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Ototoxicity

Toxicity affecting the ear or hearing, potentially caused by certain antibiotics.

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Fosfomycin

An antibiotic effective against Gram-negative bacteria by inhibiting cell wall synthesis.

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Polymyxin E (Colistin)

An antibiotic for Gram-negative bacteria, administered parenterally.

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Methicillin-resistant Staphylococcus aureus (MRSA)

A type of staphylococcus bacteria resistant to methicillin and other antibiotics.

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S.pneumoniae

A bacterium that can be drug-resistant, causing CNS infections.

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CNS infections

Infections of the central nervous system, like meningitis or encephalitis.

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Aminoglycosides

A class of antibiotics effective against Gram-negative bacteria, often used for serious infections.

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Tetracyclines

A class of antibiotics that inhibit protein synthesis and are effective against various bacteria.

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Mycobacterium tuberculosis

A bacterium that causes tuberculosis, requiring specific antibiotics for treatment.

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30S ribosomal subunit

Part of the bacterial ribosome where tetracyclines bind to inhibit protein synthesis.

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Gram-positive bacteria

Bacteria that retain the crystal violet stain used in the Gram staining protocol.

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Neuromuscular transmission blockade

Inhibition of nerve signal transmission to muscles, which can lead to paralysis.

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Beta-lactams

A class of antibiotics characterized by a beta-lactam ring in their structure.

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Penicillins

A group of beta-lactam antibiotics effective against various bacterial infections.

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Cephalosporins

Another group of beta-lactam antibiotics designed to combat resistant bacteria.

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Macrolides

A class of antibiotics that inhibit bacterial protein synthesis by blocking RNA.

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Quinolones

Antibiotics that disrupt DNA replication in bacteria.

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Sulfonamides

Synthetic antibiotics that inhibit bacterial growth by blocking folic acid synthesis.

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Polymyxins

Antibiotics that disrupt bacterial cell membranes, often used for Gram-negative bacteria.

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Study Notes

Antimicrobial Agents

  • Antimicrobial agents destroy or inhibit the growth of microorganisms, specifically pathogenic ones.
  • Antibiotics are antibacterial substances derived from microorganisms (e.g., fungi) or synthesized.
  • Antibacterial agents specifically target bacteria.
  • Alexander Fleming's accidental discovery of mold inhibiting bacterial growth led to the first antibiotic.
  • Antimicrobial therapy stages are crucial.

Outline of the Topic

  • Introduction is the initial part.
  • General principle of antibiotic treatment covers fundamentals and principles.
  • The classification of antibiotics is essential for understanding specifics.
  • Mechanisms of antibiotic resistance detail the processes.
  • How to deal with MDR (multi-drug resistant) bacteria describes strategies.
  • Exercises provide practice and application questions.

Stages of Antimicrobial Therapy

  • Time-dependent antibiotics require a duration of time above the minimum inhibitory concentration (MIC) for bacterial killing.
  • Concentration-dependent antibiotics need peak drug concentrations exceeding the MIC for effective killing.
  • AUC (area under the curve) dependent antibiotics efficacy ties to the total drug exposure above the MIC.

Pharmacodynamics

  • Time-dependent antibiotics: dosing interval must ensure T > MIC.
  • Example: Beta-lactams, need to maintain T > MIC
  • Concentration-dependent antibiotics: need a certain Cmax/MIC ratio.
  • Example: Aminoglycosides.
  • AUC-dependent antibiotics: achieving a specific AUC/MIC ratio is vital
  • Example: Vancomycin, Fluoroquinolones

Combination Antimicrobial Therapy

  • Combination therapy benefits include empirical treatment usage, polymicrobial infections, drug-resistant strains, and synergism.
  • Synergistic effect, one drug's enhancement of another's action (e.g. penicillin + aminoglycoside)
  • Additive effect, combination has a sum of individual effects (e.g., meropenem + colistin)

Parenteral to Oral Switch Therapy

  • Switching from intravenous (IV) to oral (PO) antibiotic treatment.
  • Advantages: reduced hospital-related complications, lower costs, and patient preference.
  • Key antibiotics for parenteral to oral switch: ciprofloxacin, ampicillin, and vancomycin.

Community- vs Hospital-Acquired Bacteria

  • Differentiates infections based on origin.
  • Community-acquired infections often involve less-resistant bacteria.
  • Hospital-acquired infections commonly involve more-resistant bacteria (e.g., methicillin-resistant S. aureus (MRSA), vancomycin-resistant enterococci (VRE)).

Bacterial Cell Wall Synthesis

  • Antibacterials targeting bacterial cell wall synthesis involve enzymes like transpeptidase and glucosyltransferase.

Bacterial Protein Synthesis

  • Antibacterials interfering with protein synthesis target ribosomes (e.g., 30S or 50S)

Aminopenicillins

  • Major spectrum of activity is against gram-positive (streptococci, enterococci, Listeria monocytogenes) and some gram-negative bacteria (Pasteurella multocida, H. influenzae).
  • Similar to penicillin but for respiratory tract infections, cat/dog bite wound, urinary tract infections.

Resistance Mechanisms

  • Intrinsic resistance is a result of inherent characteristics (e.g., efflux pumps).
  • Acquired resistance is due to external factors (e.g., horizontal gene transfer or mutation).
  • Modifying/degrading enzyme production is another form of resistance.

Beta-Lactamase Inhibitors

  • In combination with beta-lactams for broadening spectrum and enhancing activity against penicillinase-producing bacteria (e.g., amoxicillin/clavulanate).

Glycopeptides

  • Mechanism: Inhibit cell wall synthesis by binding to the terminal D-Ala-D-Ala end.
  • Major spectrum: gram-positive bacteria (including multidrug-resistant strains).

Macrolides

  • Mechanism: Inhibit bacterial protein synthesis by binding to 50S rRNA.
  • Spectrum: Gram-positive bacteria, atypical bacteria (e.g., Mycoplasma pneumoniae), and H. pylori.

Tetracyclines

  • Mechanism: Inhibit protein synthesis by binding to 30S ribosomal subunits.
  • Spectrum: Gram-positive bacteria, Gram-negative bacteria, Rickettsiae, Chlamydia, and some protozoa.

Fluoroquinolones

  • Mechanism: Block bacterial DNA synthesis by inhibiting topoisomerases.
  • Spectrum: Gram-positive and Gram-negative bacteria, but limited use in anaerobes, typically considered a second-line treatment.

Sulfonamides

  • Mechanism: Inhibit bacterial folic acid synthesis by inhibiting dihydropteroate synthase or dihydrofolate reductase.
  • Spectrum: Wide spectrum, but not as effective for certain bacterial and anaerobes.

Nitroimidazoles (e.g., Metronidazole)

  • Mechanism of action: Reduction of nitroimidazoles by bacterial enzymes produces nitro radicals.
  • Spectrum: Bactericidal, effective against anaerobic bacteria (e.g., Bacteroides, Clostridium).

Aminoglycosides

  • Mechanism: Inhibit bacterial protein synthesis by binding to 30S ribosomal subunits.
  • Spectrum: Primarily effective against Gram-negative bacteria, but some activity exists against Gram-positive bacteria.

Four Core Actions to Fight Resistance

  • Prevent infections (vaccination, hand hygiene).
  • Tracking emerging resistance (monitoring rates).
  • Antibiotic stewardship (appropriate use, limiting unnecessary antibiotic use).
  • New drugs and testing strategies (new treatments & diagnostics).

Emerging Non-Antibiotic Approaches

  • Monoclonal antibodies target specific bacterial antigens.
  • Antibody-antibiotic conjugates enable targeted delivery of antibiotics.
  • Antimicrobial peptides have broad-spectrum activity.
  • Bacteriophages are viruses that infect bacteria.
  • Gene therapy alters bacterial genes to prevent infection.

Alternative Approaches using Old Antibiotics

  • Combination therapy: Combination of multiple drugs.
  • Modifying drug dosing: Adjusting dosage or administration.

Exercise

  • List of Bacteria: Staphylococcus aureus, Enterococcus spp., Streptococcus pneumoniae, Enterobacteriales (e.g., E. coli, K. pneumoniae), Pseudomonas aeruginosa, Acinetobacter baumannii, and anaerobes.

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Antibacterial Agents PDF

Description

Explore antimicrobial usage, focusing on oral vancomycin's local action in the GI tract and cross-resistance in beta-lactams. Includes modifications to glycopeptides to combat vancomycin resistance and strategic use of glycopeptides. Details combination antimicrobial therapy for synergistic effects and septic shock.

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