Antibiotics And Pathogenicity

Front 1

Inhibitors of Peptidoglycan Synthesis
-B-Lactam Antibiotics?
-Other Antibiotics?

Back 1

B-lactam Antibiotics:
-penicillins
-cephalosporins
-carbapenems
-monobactams

Other Antibiotics:
-vancomycin
-bacitracin

Front 2

Inhibitors of Acid Fast Wall Synthesis
-Mode of action? (for 2 of them)

Back 2

-isonaizid - blocks incorporation of mycolic acid into cell walls
-ethionamide
-ethambutol - blocks incorporation of arabinoglactan
-cycloserine

Front 3

B-Lactam:
-Mode of action?
-Bactericidal/Bacteriorstatic?

Back 3

-inhibits penicillin-binding proteins (e.g. transpeptidase, transglycosylase) weakening the cell wall
-bactericidal

Front 4

Vancomycin:
-Mode of action?
-Bactericidal/Bacteriorstatic?

Back 4

-inhibits bacterial cell wall synthesis by binding to the peptidoglycan precursor at the Ala terminus, thereby preventing both the formation of glycosidic bonds and the formation of pentaglycine peptide bonds.
-bactericidal
*note: inactive against gram- due to outer mb

Front 5

Bacitracin:
-Mode of action?

Back 5

-prevents the peptidoglycan monomers from being transported across the cell membrane by inhibiting bactoprenol

Front 6

Acid Fast Bacteria:
-5 Layers of the Waxy Layer (above the cell wall)?

Back 6

-arabinoglactan
-phosphatidylinositol mannoside
-mycolic acid
-outer lipids
-lipoarabinomannan (LAM)

Front 7

Polymyxins:
-Mode of action?
-Gram+/Gram-?
-Bactericidal/Bacteriorstatic?

Back 7

-binds mb phospholipids and causes openings in mb
-effective against gram- (gram+ too thick)
-bactericidal
*note: limited to topical use

Front 8

Inhibitors of Protein Synthesis:
-30S Binding?
-50S Binding?

Back 8

30S:
-aminoglycosides
-tetracyclines

50S:
-chloramphenical
-clindamycin
-macrolides
-oxazolidinones

Front 9

Aminoglycosides:
-Mode of action?
-Bactericidal/Bacteriorstatic?

Back 9

-irreversibly binds to 30S subunit (but needs O2 to get thru outer mb)
-bactericidal (ONLY prot synth inhibitor)

Front 10

Tetracyclines:
-Mode of action?
-Bactericidal/Bacteriorstatic?

Back 10

-reversibly binds to 30S subunit blocking tRNA binding
-bacteriostatic

Front 11

Quinolone:
-Mode of action?
-Synthetic/natural?

Back 11

-DNA replication inhibitor
-synthetic

Front 12

Inhibitors of Biosynthesis Pathways:
Folic Acid Synthesis Inhibitors?
-Bactericidal/Bacteriorstatic?

Back 12

-sulfonamide
-trimethoprim
-both are bacteriostatic

Front 13

Sensitivity Testing

Back 13

-disk diffusion
-MIC/MBC measurement thru dilution
-E-test
See lecture 3, slides 16-21

Front 14

MIC vs. MCB

Back 14

-MIC: min. inhibitory [] - min [] that inhibits visual growth
-MBC: min. bactericidal [] - min. [] that completely kills bact.

Front 15

Mechanisms of Antibiotic Resistnce

Back 15

-reduced drug accumulation: decreased permeability or increased efflux
-drug inactivation or modification
-alteration of drug target site
-alteration of biosynthesis pathway

Front 16

2 Mechamisms of B-lactams Resistance

Back 16

-B-lactamases hydrolyze B-lactam ring in drug
-alteration of penicillin binding prots causing decreased affinity of drug

Front 17

2 Mechanisms of Vancomycin Resistance

Back 17

-gram- are inherently resistant due to outer mb
-change ala terminus on tetrapeptide so vancomycin cant bind

Front 18

2 Factors that Contribute to Tissue Specificity b/w Bacterial Flora and Host

Back 18

-tissue tropism: factors for bacterial growth
-specific adherence

Front 19

Benefits of Normal Flora

Back 19

-synthesize and excrete vitamins
-prevent colonization of pathogens
-produce substances that can inhibit or kill pathogens
-stimulate the development of certain tissues
-stimulation of immune system

Front 20

Stages of Bacterial Infection

Back 20

1. colonization/adhesion
2. invasion
3. multiplication

Front 21

Adhesins:
-Fxn?
-Utilized to Cure Infections by?

Back 21

-bacterial surface proteins that bind specific receptors on surface host cells (can be nonspecific)
-since they are on the surface, they are common vaccine candidates

Front 22

Invasins:
-Fxn?

Back 22

-act locally to damage host cells (break down defenses of body) and/or facilitate growth and spread of pathogen

Front 23

Phagocytosis:
4 Steps?

Back 23

1. engulfment
2. phagosome formation
3. phagosome fuses with lysosome to form phagolysosome
4. digested by lysozyme and exocytosed

Front 24

Complement System:
3 End Results?

Back 24

-opsonization (coating with c3b)
-inflammation (mediated by histamine)
-cytolysis (transmb channel formation)

Front 25

Ways a Pathogen Inhibits Phagocytosis

Back 25

-glycocalyx prevents opsonization
-lyse phagosome mb to escape
-resistant to lysosomes
-make prots that kill/damage phagocytes

Front 26

Ways a Pathogen Destroys Normal Immune Fxn

Back 26

-changes antigens to escape host Ab response
-produce proteases that degrade complement prots and Abs

Front 27

Intracellular Growth

Back 27

some bacteria multiplicate inside of host cells thereby avoiding immune clearance

Front 28

Toxigenesis:
Exotoxins vs. Endotoxins

Back 28

-exotoxins: released by bacterial cells
-endotoxins: substances that are part of cell walls e.g. lipid A in LPS

Front 29

3 Types of Exotoxins

Back 29

-toxins that act on cell surface: bind to receptors (e.g. superantigens); form pores in mb
-toxins that need to enter cell (e.g. A/B toxins)
-toxins delivered into host cells (type III/IV secretion systems)

Front 30

Superantigens

Back 30

usually t cell needs to bind to antigen+MHC II perfectly. superantigens stimulate t-cells independently of antigen/MHC binding causing massive release of cytokines

Front 31

A/B Toxins:
-Mode of Action?

Back 31

1. B subunit binds to receptor
2. A toxin enters the interior of the cell