MCB 4934 FINAL EXAM QUESTIONS WITH ANSWERS
2025/2026 GRADED A+
Chloramphenicol MOA - Binds to 50s and inhibits peptidyl transferase (peptidyl
transferase facilitates peptide bond formation)
Lincosamides MOA - Bind to 23S subunit of the 50S bacterial ribosome and lead to
bacteriostatic inhibition of protein synthesis
Mupirocin MOA - Non-ribosomal translational inhibitor
Binds to and inhibits isoleucyl-tRNA synthetase
Tetracycline MOA - Bind to 30s and inhibit translation
Tetracycline binding site overlaps partially with the aminoacyl-tRNA binding site leading
to tRNA dissociation from the ribosome consequently blocking translation
Central Dogma - DNA Synthesis, RNA synthesis, or protein synthesis
Clinical resistance - multiple factors such as type of bacteria, infection site, antibiotic
pharmacokinetics, growth on a petri dish, and the immune response affecting clinical
outcomes of antibiotic treatment
Why are STDs a big threat to AMR? - intracellular bacterial pathogens
undetectable by the immune system
high selection for resistance
always treated with antibiotics
easily transmissible
may be asymptomatic
highly prevalent
Carriers - Mainly environmental, with high capacity to acquire and transfer by horizontal
gene transfer clinically relevant ARG
Vectors - Ubiquitous human-commensal and clinically relevant bacteria with high
capacity to receive clinically relevant ARG by horizontal gene transfer
MDR pathogens - Vectors that may combine ARG'S with virulence factors and that have
a high capacity to infect and cause disease
,Reservoirs - Mainly strictly environmental, harbour ARG that occasionally may be
transferred, directly or indirectly, to clinically relevant bacteria
Did humans develop AMR? - Humans did not develop AMR, but we did select for it.
Is soil the largest resistome? - Soil is the origin of all clinically-relevant antibiotic
resistant genes (does not come from the healthcare environment)
The bacteria that live in the soil started selecting for material that helped them survive
against antibiotic producing bacteria
MRSA - Pathogen that most commonly colonizes our skin therefore most common
activities that decrease transmission is personal hygiene that is related to our skin.
Antimicrobial resistance mechanisms of biofilms - 1. Physical barrier
2. Antibiotic degradation
3. Persister cells
4. Biofilm-specific/Efflux pumps
5. Stress responses
Biofilm mechanisms of AMR:
1. Thick DNA, protein, exopolysaccharide matrix: Physical barrier, outer cells absorb
damage
2. Cells within biofilms are not as metabolically active. Such non-growing (persister)
cells are resistant to antibiotics
3. Unfavorable condition (low O2, pH, hydration)
Vertical Gene Transfer - Transfer of genetic material from parental organism(s)
Horizontal Gene Transfer - Transfer of genetic materials between organisms
Horizontal Gene Transfer: Conjugation F Factor Transfer, Conjugation Hfr transfer - The
temporary union of two bacteria or unicellular organisms for the exchange of genetic
material
Horizontal Gene Transfer: Transduction - the transfer of genetic material from one
microorganism to another by a viral agent (such as a bacteriophage)
Horizontal Gene Transfer: Transformation - Uptake of "naked" DNA from the outside
environment
Requires competent cells (able to uptake DNA)
Incorporation of foreign DNA into own genomic DNA
, Efflux pumps - Pump molecules out of cells; antibiotic-specific or broad (MDR); provide
intrinsic resistance against antibiotic-producing bacteria; all pumps require energy to
move molecules across the membrane (active transport)
Porins - Allow small molecules( B-lactams, chloramphenicols, quinolones, tetracyclines)
into cells; reduce the concentration of antibiotics even before pumps get a chance to
pump them out; provide the first line of defense against toxic compounds; intrinsic
resistance of gram negative (P. aeruginosa)
Two-component regulatory system (TCRS) - A signaling cascade that allows a cell to
sense the outside environment and respond accordingly
If you have two components A & B, 1 senses and the other one responds
Target replacement: Methicillin resistance - The resistance to methicillin was not
dependent on typical b-lactamases, but was encoded by mecA, a gene coding for
PBP2a, a PBP homolog that exhibits low affinity for all clinically used B-lactam
antibiotics. The source of the resistance and the mechanism of acquisition are unknown
Structural basis for the b-lactam resistance of PBP2a from methicillin-resistant
staphylococcus aureus - Structural work revealed that resistance to B-lactams is not
due to antibiotics poor fit into the active site, but is due to inefficient formation of the
acyl-PBP intermediate. The intermediate formation between methicillin and PBP2a is
1000 less efficient.
Why is PBP2a a major problem? - Confers resistance to methicillin which means it
confers resistance to other beta lactams
One of the major problems of PBP2a is that it is encoded on a plasmid
Antibiotic target protection: Quinolone Binding Protein - 1. MfpA expression in M.
tuberculosis leads to fluoroquinolone resistance2. Mimics B-form DNA3. MfpA binds to
DNA gyrase and inhibits its activity4. MfpA binding protects DNA gyrases from
quinolone binding whenever they are not bound to bacterial DNA
The purpose of antibiotic surveillance is to - 1. Better understand AMR patterns2.
Provide appropriate response
Global Antimicrobial Resistance Surveillance System (GLASS): Goal - To enable
standardized, comparable, and validated data on AMR to be collected, analyzed, and
shared with countries in order to inform decision-making, drive local, national, and
regional action and provide the evidence based for action and advocacy.
GLASS (Objectives) - 1. Foster national surveillance systems and harmonized global
standards
2. Estimate the extent and burden of AMR globally by selected indicators
2025/2026 GRADED A+
Chloramphenicol MOA - Binds to 50s and inhibits peptidyl transferase (peptidyl
transferase facilitates peptide bond formation)
Lincosamides MOA - Bind to 23S subunit of the 50S bacterial ribosome and lead to
bacteriostatic inhibition of protein synthesis
Mupirocin MOA - Non-ribosomal translational inhibitor
Binds to and inhibits isoleucyl-tRNA synthetase
Tetracycline MOA - Bind to 30s and inhibit translation
Tetracycline binding site overlaps partially with the aminoacyl-tRNA binding site leading
to tRNA dissociation from the ribosome consequently blocking translation
Central Dogma - DNA Synthesis, RNA synthesis, or protein synthesis
Clinical resistance - multiple factors such as type of bacteria, infection site, antibiotic
pharmacokinetics, growth on a petri dish, and the immune response affecting clinical
outcomes of antibiotic treatment
Why are STDs a big threat to AMR? - intracellular bacterial pathogens
undetectable by the immune system
high selection for resistance
always treated with antibiotics
easily transmissible
may be asymptomatic
highly prevalent
Carriers - Mainly environmental, with high capacity to acquire and transfer by horizontal
gene transfer clinically relevant ARG
Vectors - Ubiquitous human-commensal and clinically relevant bacteria with high
capacity to receive clinically relevant ARG by horizontal gene transfer
MDR pathogens - Vectors that may combine ARG'S with virulence factors and that have
a high capacity to infect and cause disease
,Reservoirs - Mainly strictly environmental, harbour ARG that occasionally may be
transferred, directly or indirectly, to clinically relevant bacteria
Did humans develop AMR? - Humans did not develop AMR, but we did select for it.
Is soil the largest resistome? - Soil is the origin of all clinically-relevant antibiotic
resistant genes (does not come from the healthcare environment)
The bacteria that live in the soil started selecting for material that helped them survive
against antibiotic producing bacteria
MRSA - Pathogen that most commonly colonizes our skin therefore most common
activities that decrease transmission is personal hygiene that is related to our skin.
Antimicrobial resistance mechanisms of biofilms - 1. Physical barrier
2. Antibiotic degradation
3. Persister cells
4. Biofilm-specific/Efflux pumps
5. Stress responses
Biofilm mechanisms of AMR:
1. Thick DNA, protein, exopolysaccharide matrix: Physical barrier, outer cells absorb
damage
2. Cells within biofilms are not as metabolically active. Such non-growing (persister)
cells are resistant to antibiotics
3. Unfavorable condition (low O2, pH, hydration)
Vertical Gene Transfer - Transfer of genetic material from parental organism(s)
Horizontal Gene Transfer - Transfer of genetic materials between organisms
Horizontal Gene Transfer: Conjugation F Factor Transfer, Conjugation Hfr transfer - The
temporary union of two bacteria or unicellular organisms for the exchange of genetic
material
Horizontal Gene Transfer: Transduction - the transfer of genetic material from one
microorganism to another by a viral agent (such as a bacteriophage)
Horizontal Gene Transfer: Transformation - Uptake of "naked" DNA from the outside
environment
Requires competent cells (able to uptake DNA)
Incorporation of foreign DNA into own genomic DNA
, Efflux pumps - Pump molecules out of cells; antibiotic-specific or broad (MDR); provide
intrinsic resistance against antibiotic-producing bacteria; all pumps require energy to
move molecules across the membrane (active transport)
Porins - Allow small molecules( B-lactams, chloramphenicols, quinolones, tetracyclines)
into cells; reduce the concentration of antibiotics even before pumps get a chance to
pump them out; provide the first line of defense against toxic compounds; intrinsic
resistance of gram negative (P. aeruginosa)
Two-component regulatory system (TCRS) - A signaling cascade that allows a cell to
sense the outside environment and respond accordingly
If you have two components A & B, 1 senses and the other one responds
Target replacement: Methicillin resistance - The resistance to methicillin was not
dependent on typical b-lactamases, but was encoded by mecA, a gene coding for
PBP2a, a PBP homolog that exhibits low affinity for all clinically used B-lactam
antibiotics. The source of the resistance and the mechanism of acquisition are unknown
Structural basis for the b-lactam resistance of PBP2a from methicillin-resistant
staphylococcus aureus - Structural work revealed that resistance to B-lactams is not
due to antibiotics poor fit into the active site, but is due to inefficient formation of the
acyl-PBP intermediate. The intermediate formation between methicillin and PBP2a is
1000 less efficient.
Why is PBP2a a major problem? - Confers resistance to methicillin which means it
confers resistance to other beta lactams
One of the major problems of PBP2a is that it is encoded on a plasmid
Antibiotic target protection: Quinolone Binding Protein - 1. MfpA expression in M.
tuberculosis leads to fluoroquinolone resistance2. Mimics B-form DNA3. MfpA binds to
DNA gyrase and inhibits its activity4. MfpA binding protects DNA gyrases from
quinolone binding whenever they are not bound to bacterial DNA
The purpose of antibiotic surveillance is to - 1. Better understand AMR patterns2.
Provide appropriate response
Global Antimicrobial Resistance Surveillance System (GLASS): Goal - To enable
standardized, comparable, and validated data on AMR to be collected, analyzed, and
shared with countries in order to inform decision-making, drive local, national, and
regional action and provide the evidence based for action and advocacy.
GLASS (Objectives) - 1. Foster national surveillance systems and harmonized global
standards
2. Estimate the extent and burden of AMR globally by selected indicators
