antimicrobial_resistance_micro5

Antimicrobial Drug Resistance Overview

Page 1: Introduction

• Title: Antimicrobial Drug Resistance

• Course: MICRO 5

Page 2: Learning Goals

• Understand mechanisms of antibacterial resistance in bacteria.

• Relate antibiotic resistance to natural selection and discuss mutation origins.

• Identify overuse/misuse of antibiotics as a contributor to resistance.

• Describe prevention strategies for the spread of antibiotic-resistant bacteria.

Page 3: Key Terms

• Virulence Factor vs. Antibiotic Resistance Gene:

  • Virulence factor: Proteins aiding pathogen’s ability to cause disease.

  • Antibiotic resistance gene: Genes enabling pathogens to resist antibiotics.

Page 4: Definitions

• Virulence Factors: Specific proteins that help pathogens invade, establish, or damage the host.

• Antibiotic Resistance Genes: Genes that confer resistance to specific antibiotics, allowing survival in hostile environments.

Page 5: Darwinian Model of Resistance

• Resistance and virulence traits that improve chances for survival become selected within populations.

• Positive traits (increased resistance + virulence) are rapidly favored.

Page 6: Mutation Origins

• Q: Can bacteria develop antibiotic resistance mutations without exposure?

  • Answer: True.

Page 7: Spontaneous Mutations

• Mutations arise from:

  • Errors in DNA replication

  • Presence of mutagens.

• Example of mutation representation to include DNA sequences and changes.

Page 8: Natural Selection in Action

• Advantages of certain traits (like moth color) provide grounds for natural selection.

• Adaptive traits are passed on through successful reproduction.

Page 9: Fitness Distribution

• Normal distribution trends shift during selection, affecting the average value of traits found within populations.

Pages 10-12: Antimicrobial Drug Mechanisms

1. Inhibition of Cell Wall Synthesis: e.g., Penicillins.

2. Inhibition of Protein Synthesis: e.g., Tetracyclines, Erythromycin.

3. Inhibition of Nucleic Acid Replication: e.g., Quinolones.

4. Injury to Plasma Membrane: e.g., Polymyxin B.

5. Inhibition of Essential Metabolite Synthesis: e.g., Sulfanilamide.

Pages 13-14: Resistance Mechanisms

• Key mechanisms of resistance:

  • Blocking entry: Limiting access of antibiotic to bacteria.

  • Inactivation by enzymes: Enzymes that break down antibiotics.

  • Altered target molecule: Changes in target sites so antibiotics no longer work.

  • Efflux of antibiotic: Pumps that expel antibiotics from bacteria.

Page 15: Specific Resistance Strategies

• Bacteria may develop strategies like altering porin proteins or using efflux pumps to expel drugs, enhancing resistance.

Page 16: Superbugs

• Definition: Multi-drug resistant organisms (e.g., MRSA).

• Common humorous personification to highlight their resilience against antibiotics.

Page 17: Resistance Trends Over Time

• 60% of MRSA infections reported in certain years.

• Timeline noting the increase in resistance since 1981.

Page 18: Resistance Development Timeline

• Average duration of 8 years for antibiotic resistance to develop post antibiotic introduction for various drugs.

Pages 19-20: Antibiotic Exposure Effects

• Bacterial growth is influenced by exposure to antibiotics, leading to survival of resistant strains.

• No exposure leads to simple growth without resistance.

Page 21: Evolutionary Mechanism of Resistance

• Development of antibiotic resistance is driven by selective pressures resulting from antibiotic exposure.

Page 22: Hereditary Resistance

• Resistant traits are already present due to genetic variation prior to antimicrobial exposure.

Page 23: Resistance Characteristics

• Discussion on predicted outcomes for different bacterial species under treatment pressures and early termination of treatment.

Page 24: Post-Treatment Resistance Dynamics

• Antibiotic usage favors survival of pre-existing resistant bacteria, leading to population-wide resistance.

Page 25: Rapid Reproduction of Bacteria

• Bacteria reproduce quickly causing genetic diversity to increase rapidly despite low mutation rates.

Page 26: Gene Transfer Mechanisms

• Mechanisms of horizontal gene transfer include:

  • Transformation, Conjugation, Transduction.

Page 27: Prokaryotic Diversity and Evolution

• Prokaryotes thrive due to rapid reproduction and genetic diversity.

• Metabolic and structural adaptations allow survival in varied environments.

Page 28: Causes of Resistance

• Emphasis on overuse and misuse as primary causes of developing resistance.

Page 29: Inappropriate Antibiotic Use

• Use inappropriately (e.g., viral infections) or low doses can lead to resistance.

• Usage in livestock contributes to resistance development in humans.

Page 30: Spread of Resistance

• Tracked examples of how resistant bacteria spread from animals to humans through food and care facilities.

Page 31: Acquired Infections

• Healthcare Associated Infections (HAI): Infections from healthcare settings, often resistant.

• Community Acquired Infections (CAP): Infections outside healthcare settings.

Page 32: CAP vs. HAP Comparison

• Distinction between community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP) based on various clinical features and risk factors.

Page 33: HAI Characteristics

• HAIs are prevalent in compromised hosts, with various transmission routes increasing infection risk.

Page 34: Prevention Strategies

• Strategies to combat antibiotic resistance:

  • Completing prescribed antibiotic courses.

  • Avoiding leftover antibiotics for new illnesses.

  • Prescribing narrow-spectrum antibiotics whenever possible.