Microbiology-Antibiotics against cell wall Flashcards Preview

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Flashcards in Microbiology-Antibiotics against cell wall Deck (18)
1

What are the repeating disaccharide linkages in peptidoglycan?

MurNac gets the 5 D amino acid tail (tail ends in D-Ala-D-Ala

2

A patient comes to see you with a multiple resistant staph infection. You have tried several antibiotics before and decide to go with the "last ditch" antibiotic. What is the drug and how does it affect bacteria?

Vancomycin. It bind to the D-Ala-D-Ala residues on the MurNAc tail. It is a huge molecule and sterically hinders transglycosylation and thus peptidoglycan synthesis.

3

Your patient does not respond to Vancomycin therapy. What mechanism has the bacteria employed to evade the effects of Vancomycin?

They have likely undergone mutation to express a weaker peptidoglycan cell wall with linkages other than D-Ala-D-Ala.

4

How does transpeptidization differ between gram + and gram - bacteria?

Gram + bacteria have an extra 5 glycine residues that link residue 4 of MurNac to residue 3 of GlcNac. Gram - bacteria simply bind residue 4 to residue 3.

5

In the 1940s a patient was seen for a secondary bacterial infection. She said in the past she had gotten antibiotics to treat it and it went away. What drug was likely given and what effect does this drug have on the bacteria?

Penicillin has a beta-lactam ring structure analogous to the D-Ala-D-Ala structure, which allows it to bind to transpeptidases and disable cross-linking in peptidoglycan synthesis.

6

What are the beta-lactam antibiotics?

*

7

How do bacteria become resistant to beta-lactam antibiotics?

Cleavage by bacterial beta-lactamase

8

Your patient complains they have not been relieved of their symptoms after taking cephalosporin for a whole week. What enzyme might the bacteria have that is causing her infection?

Extended-spectrum Beta-lactamases

9

Klebsiella pneumoniae was originally very susceptible to antibiotics, however, last year news came out that it has become a superbug because it makes a carbapentamase and ESBLs. How did it become so resistant?

R-plasmid transfer in conjugation

10

1st generation penicillin

Penicillin G

11

2nd and 3rd generation penicillins

Amp, Amox, Meth, Oxacillin, Nafcillin, Carbenicillin, Ticarcillin, Piperacillin

"Double A Mon' CTP"

12

Generations of Cephalosporins

1st: Cephalothin, Cephalexin, Cefazolin 2nd: Cefaclor, Cefuroxime, Cefotetan, Cefoxitin 3rd: Cefotaxime, Ceftriaxone, Ceftazidime 4th: Cefepime

"1st, I loathe Alex the Azhole. 2nd, Ur Ox is Aclor o'tet. 3rd, Taz Tri to Taxime"

13

How did bacteria gain methicillin resistance?

The transposon mecA gene codes for PBP2 that actually alters the structure of transpeptidase so it is no longer a target of methicillin

14

How can we evade beta-lactamase when we give antibiotics?

Clavulanic acid competitively inhibits beta-lactamase and is given in combination with Amoxicillin in Augmentin.

15

You run a gram stain on a patient and find that they have gram - bacteria. You determine that he has an acinetobacter infection and prescribe antibiotics. What do you prescribe and how does it work?

You prescribe a polymixin (Colistin). It is an amphipathic antibiotic that targets the gram - bacterial membrane and is a bactericidal.

16

What are the membrane inhibiting antibiotics?

Daptomycin (gram +) and Polymixin (gram -)

17

What are the bactericidal drugs?

Bactericidal drugs act on actively growing cells. "Pops Can't Cook, Mom Bakes Veil Pretty Good."

18

Why are bactericidal drugs less effective if you prescribe a bacteriostatic drug?

Bacteriostatic drugs prevent growth and do not kill the microbe. The bacteriostatic drug will have no effect because they require actively growing cells in order to inhibit cell wall synthesis.