Unit 1 NotesJanuary 14, 2014The Story of Mrs. C Notes- How might have the MRSA entered her system?- unsterilized needle- Does methicillin resistance make the bacteria more virulent (harmful)?- Yes?- No. It makes the bacteria more resistant against the antibiotic- GonorrheaBacteria Notes- Bacteria vs. Viruses- What are antibiotics- drugs that are designed to prevent bacteria from reproducing—kill or disable bacteria- do not disable human cells- Antibiotics are different from antibodies- What is antibiotic resistance?- increased ability of bacteria to persist and reproduce in the presence of antibiotics- resistance refers to the bacteria’s resistance to the antibiotic- NOT the human body’s resistance- More resistance strains of bacteria have developed since - We want to slow down the speed of resistance- Why is resistance becoming common more quickly in hospitals?- There’s so much more bacteria in a hospital- It can spread quicker throughout the weak immune systems of the patients because the antibiotics are being used more often- The bacteria have the selective pressure to develop antibiotic resistance- Antibiotics aren’t used as frequently in the community- Antibiotic resistance is an inevitable process- Widespread use leads to widespread resistance- Methicillin became resistant more slowly than PenicillinJanuary 16, 2014Elc Assignment Review- Amoxicillin attacks which of the following cell wall components- A cell wall repair enzyme- If it attacked amino acids, it would also attack human cells and amoxicillin doesn’t do that- Human cells have a lipid bilayer- The active component that binds transpeptidase in both amoxicillin and penicillin is called - a beta lactam ring- For bacteria, the only kind of ‘spread of genetic information’ that also results in another cell is- binary fission- Learning Objectives1. describe how antibiotics act2. describe how bacteria resist the negative effects of antibiotics- If antibiotic resistance is an inevitable process, why are we so concerned?- We’re running out of antibiotics- Why aren’t drug companies designing new antibiotics?- They are spending more money than they used to on research and development, but for different, but for different kinds of drugs- They are looking to research into more long-term medication for other diseases i.e. Viagra, which is taken for a long period of time- Antibiotic resistance has always occurred- As soon as an antibiotic enters the market, populations of bacteria start to adapt to be resistant- We can take action to prevent and slow the spread of antibiotic resistance1. How does bacteria structure relate to antibiotic effectiveness?- Bacteria live everywhere and eat everything- Most bacteria are harmless/beneficial to humans- But some bacteria cause illness pathogenic bacteria- Bacteria are prokaryotes- If we wanted to damage the bacterial cell, we could attack - Cell wall- Plasmids- nucleic acids; if attacked, we’d attack eukaryotic- Ribosomes: the shape of the prokaryotic cell allows for this- Unprotected DNA-nucleic acids; if attacked, we’d attack eukaryotic2. How do antibiotics work?- Antibiotics disable a bacterium cell so that it cannot survive and/or reproduce and do not harm eukaryotic cells- Penicillin specifically attacks the cell wall: the protein is not able to bind the amino acidchains, so the peptidoglycan chains are just sliding past one another- They take advantage of the differences between structure of prokaryotes and eukaryotes- Overview of some antibiotic mechanisms3. How does resistance to antibiotics work?- generational changes within the bacteria- the bacteria may revamp the organelle that the antibiotic attacks originally- block active site - PBP would not properly bind to the beta lactum ringJanuary 21, 2014Antibiotic Resistance: the increased ability to survive and reproduce in the presence of antibioticsResistance Mechanisms:1. The Upchuck: a pump removes antibiotics from the cell; internal2. The ballistic missile/ inside job: an enzyme breaks down the antibiotic before it can act; internal3. The plastic surgeon: an enzyme alters the antibiotic before it can kill the cell; internal4. Stealth mode: the active site where the antibiotic binds is changed; external Summary Points- Antibiotic resistance is dependent upon whether it is inside or outside of the cell- Antibiotics can attack cell walls in a variety of ways- Bacteria have various mechanisms that prevent antibioticsHow do new traits (antibiotic resistance) originate?Gene expression:- DNA  transcription mRNA  translation  proteinMouse Example:- What are the differences between the two mice in the example?- phenotype- different codon that changes the protein between the two mice- White fur is advantageous in terms of camouflage- The coat color of the individual mice will NOT change; the environment doesn’t change genes- The population will change when the owl eats the dark colored mice- One cause of mutations- DNA polymerase copying errors- UV radiation- What is the effect of mutations?- difference in nucleotide sequence- phenotype/ specific characteristics- Types of Mutations- Substitution: replacement- Deletion - Insertion: add something- Inversion: mix up the order- Mutations change the genetic code of an organism which may or may not have an effect on the organismWhat kind of effect can DNA mutations have?Mutations can:- Have no effect on phenotype NEUTRAL- Have an effect on the phenotype- NEUTRAL: no effect on reproduction; they fluctuate randomly and do not die off; a small proportion may lead to them dying off- BENEFICIAL: positive effect on reproduction- HARMFUL: negative effect on reproduction- Complex traits, such as antibiotic resistance, generally require more than one random, independent mutationWhat is the origin of antibiotic resistance?- Resistance is coded for in the DNA within a bacteria cell, often on plasmids- These resistance genes DNA sequences code for proteins that produce resistance in a bacteria cell- These mutations benefit the bacteria when it is in the presence of antibiotics, but not when it is NOT in the presence of it- Complex traits like antibiotic resistance often do not result from only one mutation, but from anaccumulation of mutations over timeSummary Points:- Neutral mutations: don’t have selective pressure to increase or decrease in proportion- Antibiotic resistance results from an accumulation of mutations that are beneficial IN THE PRESENCE OF