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
Inhibition of Cell Wall Synthesis: e.g., Penicillins.
Inhibition of Protein Synthesis: e.g., Tetracyclines, Erythromycin.
Inhibition of Nucleic Acid Replication: e.g., Quinolones.
Injury to Plasma Membrane: e.g., Polymyxin B.
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.