Midterm Flashcards
What is Antibiotic Resistance?
- Occurs when bacteria, viruses, fungi and parasites no longer respond to antimicrobial medicines
- antimicrobial medicines become ineffective & infections become difficult or impossible to treat
Biological Resistance Vs. Clinical Resistance
- Biological - refers to changes that result in reduced susceptibility of an organism to a particular antimicrobial agent
- Clinical - when this susceptibility is lost to an extent that the drug is no longer effective for clinical use
What is Environmentally mediate Antimicrobial resistance?
- Resistance directly resulting from physical or chemical characteristics of the envmt that either directly altered the antimicrobial agent or alter the microorganism’s normal physiologic response to the drug
Microorganism-mediated Antimicrobial Resistance
- Microorganism-mediated antimicrobial resistance refers to antimicrobial resistance that results from genetically encoded traits of the microorganism
Intrinsic Resistance
- Naturally resistant to a certain antibiotic or family of antibiotics, w/out the need for mutation or gain or further genes
- Ex. Aerobic bacteria are NOT able to anaerobically reduce metronidazole to its active form
Acquired Resistance
- Bacteria can acquire resistance through a new genetic mutation or by getting DNA from a resistant bacteria
- Resistance genes are often on plasmids or transposons (mobile genetic elements) that can be transferred horizontally b/w bacteria
Steps in Transduction by a Bacteriophage
- Phage infects donor cell
- Phage DNA & proteins are made, bacterial chromosome is broken into pieces
- Pieces of bacterial DNA are packaged into phage capsid, when cell lyses it releases the phage carrying bacterial DNA
- A phage carrying bacteria DNA can infect a new host recipient cell
- Recombination can occur producing a recipient cell that has a genotype different from both the original recipient and host cells
What are the 4 Mechanisms of Drug Resistance
- Modifications or destruction of the antimicrobial molecule
- Preventing the antibiotic from reaching its target
- Changes and/or bypass of target sites
- Resistance due to global cell adaptive processes
Modifications of the Antimicrobial molecules
Mechanisms of Drug Resistance
- Chemical conjugation of Abx - Acetylation, Phosphorylation, Adenylation
- Destruction/deactivation of Abx - B-lactamases
Preventing the Abx from reaching its target
Mechanisms of Drug Resistance
- Decreased permeability - decreasing amount of drug in bacteria can prevent cell death (changes in porins)
- Efflux pumps
Changes in Target Site
Mechanisms of Drug Resistance
- Target Protection - Tet(M) dislodges tetracycline bound to ribosome
- Modification of Target - mutations of target site, enzymatic alteration of target, complete replacement or bypass of target site
Changes in Global Cell Adaptive Processes
Mechanisms of Drug Resistance
- gene clusters that can work together to make Abx less effective
Resistance to B-lactams Mechanism
- Enzymatic destruction of Abx
- Decreased uptake to B-lactams
- Altered target
Resistance to Glycoproteins Mechanism
- Acquired high level resistance to vancomycin has been commonly encountered among enterococci
- The main resistance mechanism: change to target site, production of altered cell wall precursors that do not bind vancomycin w/ sufficient avidity to allow inhibition of peptidoglycan
Resistance to Aminoglycosides Mechanisms
- Enzymatic modification - modifying enzymes causes affinity for binding ribosomal subunit to diminsh so protein synthesis can continue
- Altered target - changes in ribosomal binding site, aminoglycoside can’t bind
- Decreased uptake pathways - changes in # or characteristics of outer membrane porins
Why is Abx Resistance on the Rise?
- Using Abx for common cold & other viral infections
- Using Abx in animal feed
- Using someone else’s leftover prescription
What is Binary Fission?
- cell division in Prokaryotes
- similar to mitosis
- DNA replicates -> cell wall & PM constrict -> cell wall forms completely separating 2 DNA copies -> cells separate
Gram +ve vs. Gram -ve cell components
- gram +ve - cell wall, plasma membrane
- gram -ve - cell wall, plasma membrane, outer membrane, periplasm
Composition of Cell wall in gram +ve
- MANY peptidoglycan layers
- lipoteichoic & teichoic acid (surface Ags) - usually what our body targets in response
Composition of Cell wall in gram -ve
- FEW layers of peptidoglycan
- Outer membrane - consists of lipopolysaccharide (LPS) & porins
- LPS has Lipid A attached to polysaccharide
What has better Antibiotic Resistance Gram +ve or Gram -ve? why?
- Gram -ve
- outer membrane has porins, only small hydrophilic molecules can pass
- Large Abx molecules penetrate outer membrane SLOWLY
Functions of the Cell wall
- protection against osmotic damage
- cell division (target this, can’t reproduce)
- responsible for shape
- target sites for Abx, lysozymes & bacteriophages
What are Mycoplasma?
- naturally occurring bacteria which lack cell wall (ex. Mycoplasma pneumoniae)
Gram +ve Gram Stain Colour
purple