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Questions and Answers
What distinguishes bactericidal drugs from bacteriostatic drugs?
What distinguishes bactericidal drugs from bacteriostatic drugs?
Which type of resistance is considered natural or inborn?
Which type of resistance is considered natural or inborn?
What strategy do bacteria use to develop resistance through drug inactivation?
What strategy do bacteria use to develop resistance through drug inactivation?
What is a consequence of excessive antibiotic use?
What is a consequence of excessive antibiotic use?
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Which of the following is NOT a mechanism by which bacteria develop drug resistance?
Which of the following is NOT a mechanism by which bacteria develop drug resistance?
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What is superinfection?
What is superinfection?
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What role does host defense play when bacteriostatic drugs are administered?
What role does host defense play when bacteriostatic drugs are administered?
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Why are methicillin-resistant Staphylococcus aureus (MRSA) and similar organisms a concern?
Why are methicillin-resistant Staphylococcus aureus (MRSA) and similar organisms a concern?
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What characteristic allows antibiotics to target microbial pathogens without harming the host?
What characteristic allows antibiotics to target microbial pathogens without harming the host?
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Which of the following antibiotics disrupt the bacterial cell wall?
Which of the following antibiotics disrupt the bacterial cell wall?
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Which type of antibiotic is only effective against a limited range of microorganisms?
Which type of antibiotic is only effective against a limited range of microorganisms?
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Which group of drugs is primarily responsible for lethal inhibition of bacterial protein synthesis?
Which group of drugs is primarily responsible for lethal inhibition of bacterial protein synthesis?
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What is the mechanism of action for drugs like Rifampin?
What is the mechanism of action for drugs like Rifampin?
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Which class of antimicrobial drugs is known to block the conversion of PABA to folic acid?
Which class of antimicrobial drugs is known to block the conversion of PABA to folic acid?
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What effect do broad-spectrum antibiotics have compared to narrow-spectrum antibiotics?
What effect do broad-spectrum antibiotics have compared to narrow-spectrum antibiotics?
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Which mechanism helps drugs like amphotericin B increase cell membrane permeability?
Which mechanism helps drugs like amphotericin B increase cell membrane permeability?
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Study Notes
Basic Principles of Antimicrobials
- Antimicrobials are designed to kill or suppress microbial pathogens without harming the host.
- This is achieved through differences in the cellular chemistry and biochemical processes of mammals and microbes.
- Antimicrobials can disrupt bacterial cell walls, which mammals lack.
- Some antimicrobials inhibit bacterial enzymes critical to survival, but not to the host.
- Antibiotics can also disrupt bacterial protein synthesis, as bacterial and mammalian ribosomes differ.
Characteristics of Selective Toxicity
- Antimicrobials demonstrate selective toxicity targeting bacterial processes without harming host cells.
- Differences in cellular chemistry and biochemical processes of host and microbe enable antibiotics to selectively target bacterial cells
- Disruption of bacterial cell walls is a common mechanism.
- Inhibition of unique bacterial enzymes is another strategy.
- Disruption of bacterial protein synthesis, taking advantage of differences in ribosome structure, is effective.
Classification of Antimicrobial Drugs by Susceptible Organism
- Narrow-spectrum antibiotics target only a few species of microorganisms.
- Broad-spectrum antibiotics target a wide variety of microbes.
- Antimicrobial drugs are categorized into antibacterial, antifungal, and antiviral drugs based on the susceptible organisms.
Classification by Mechanism of Action
- Drugs inhibiting bacterial cell wall synthesis (e.g., penicillins, cephalosporins).
- Drugs increasing cell membrane permeability (e.g., amphotericin B).
- Drugs causing lethal inhibition of bacterial protein synthesis (e.g., aminoglycosides).
- Drugs causing non-lethal inhibition of protein synthesis, which slows, but doesn't stop microbial growth (e.g., tetracyclines).
- Drugs inhibiting bacterial DNA or RNA synthesis, or DNA function (e.g., rifampin, metronidazole, fluoroquinolones).
- Antimetabolites that disrupt specific biochemical reactions by reducing essential cell constituents or by creating analogs of normal metabolites(e.g., trimethoprim, sulfonamides).
Classification by Mechanism of Action (Continued)
- Drugs categorized by the bacterial process they target are shown graphically
- Cell wall synthesis: beta-lactams (penicillins, cephalosporins etc), vancomycin, bacitracin.
- Nucleic Acid Synthesis: quinolones, rifampin
- Cell Membrane: polymyxins
- Protein Synthesis: macrolides, clindamycin, linezolid, chloramphenicol, tetracyclines, aminoglycosides, streptogramins.
- Folate synthesis: sulfonamides, trimethoprim.
Classification by Mechanism of Action (Continued)
- Bactericidal drugs directly kill bacteria at clinically achievable concentrations.
- Bacteriostatic drugs slow bacterial growth but do not kill them.
- Ultimately, elimination of bacteria arises from host defenses.
Innate or Acquired Resistance to Antimicrobial Drugs
- Innate resistance exists as an inborn trait of certain microbes.
- Acquired resistance develops over time as microbes adapt.
- Antibiotic resistance is associated with increased hospital stays, serious health consequences, and high mortality.
- Examples of organisms with significant antibiotic resistance issues include MRSA, Enterobacter species, P. aeruginosa, A. baumannii, Klebsiella species, and C. difficile.
Microbial Mechanisms of Drug Resistance
- Mechanisms include reduced drug uptake, increased active export, alteration of drug targets, and drug inactivation.
- Bacteria often inactivate antibiotics by producing enzymes that metabolize or break down the drugs.
- An example of drug inactivation is the bacterial production of penicillinase, an enzyme that inactivates penicillin.
- Other antibiotics similarly inactivated by drug-metabolizing enzymes are cephalosporins, carbapenems, and fluoroquinolones.
The Influence of Increased Antibiotic Use on the Emergence of Resistance
- Increased antibiotic use promotes the emergence of drug-resistant organisms.
- Normal flora, capable of transferring resistance to other organisms, and mechanisms that support resistance also contribute to the resistance development.
- Reducing inappropriate antibiotic use is paramount to lowering resistance development
Superinfection
- A superinfection is a new infection arising during treatment of a primary infection.
- Antibiotic use can eliminate the normal flora that keeps some pathogens in check, allowing other pathogens, often resistant to the treatment, to proliferate.
- Superinfections frequently happen with broad-spectrum antibiotics, as these kill more normal flora than narrow-spectrum antibiotics.
Selection of Antibiotics
- Factors considered when choosing an antibiotic include the infecting organism, the drug's sensitivity to the organism, and host factors (location of infection, immune function).
- Typically, one antibiotic is considered optimal and preferred over alternatives due to better efficacy, reduced toxicity, or a narrower spectrum of activity.
- Conditions hindering the use of a preferred antibiotic might include allergies, inadequate penetration to the infection site, or the patient's high susceptibility to antibiotic side effects.
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Description
Explore the fundamental concepts surrounding antimicrobials, including their mechanism of action and selective toxicity. This quiz covers how antimicrobials target microbial pathogens while preserving host cells, highlighting differences in cellular processes. Assess your understanding of these crucial pharmaceutical agents.
