Cell Wall Synthesis Inhibitors

Question 1

describe gram+ bacterial cell wall

Answer 1

plasma membrane, complex peptidoglycan layering

Question 2

describe gram- bacterial cell wall

Answer 2

plasma membrane, simple peptidoglycan layer, outer lipid membrane (makes it more difficult for agents to penetrate these organisms)

Question 3

general characteristics of cell wall synthesis inhibitors

Answer 3

• -maximum selective toxicity b/c agents attack PDG layers that mammals don’t have
• -gram+ microbes are more dependent on PDG layer for organization so they’re more susceptible
• -originally narrow spectrum
• -bactericidal

Question 4

penicillin-binding proteins

Answer 4

proteins/enzymes in the plasma membrane that function in the synthesis of the PDG layer

Question 5

beta-lactamases

Answer 5

enzymes outside the cell membrane; protective, destroy antimicrobial agents like penicillins (resistance mechanism)

Question 6

porins

Answer 6

allow drugs to get into gram- microbes

Question 7

efflux channels

Answer 7

pump drugs out of cells (like in gram-)

Question 8

How does Vanc block PDG synthesis?

Answer 8

binds the D-Ala-D-Ala terminus; blocks transglycosylation rxn and blocks transpeptidation where branched peptides on different PDG chains get cross-linked together

Question 9

VRE

Answer 9

vanc resistant enterococci; vanA, vanB, vanC genes can be transmitted b/n organisms to make different cell wall substituents resistant to vanc

Question 10

VRSA

Answer 10

vanc resistant Staph aureus; overexpression of D-Ala-D-Ala that binds to vanc and neutralizes it

Question 11

How does vanc resistance occur?

Answer 11

the organism substitutes a lactate for the D-Ala end; vanc then can’t bind to block the rxns

Question 12

How do beta-lactam antibiotics work?

Answer 12

bind to penicillin binding proteins (b/c they look like D-Ala end) and block the transpeptidation