Intro to infectious Agents HD Flashcards Preview

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Flashcards in Intro to infectious Agents HD Deck (34):
1

Most common agents that cause infectious endocarditis are:

members of normal microbiota
• Staphylococcus aureus – anterior nares
• Coagulase-negative staphylococci (e.g. S. epidermidis) – skin
• viridans streptococci (e.g. S. sanguis, S. mutans, S. mitis) – oral cavity
• enterococci (E. faecalis, E. faecium) – GI tract

2

Access to endocardium provided by

transient bacteremia

3

Properties of successful IE pathogens:

• able to survive antimicrobial components of serum
• able to adhere avidly to endocardium

4

How does viridans streptococci mediate adeherance in the endocardium?

• dextran (exopolysaccharide)
• adhesins (surface proteins; FimA, GspB, PblA, PblB) that
mediate attachment to platelets and fibrin

5

How does S.aureus mediate adherance in endocardium

• fibrinogen-binding adhesins (ClfA, coagulase)

6

What does it mean when we say infectious endocarditis bacteria 'live in a vegitation'

heterogeneous matrix of deposited bacteria, platelets, fibrin, other matrix ligands
bacteria can achieve high densities

7

Why are infectious endocarditis bacterial concerning and difficult to erradicate?

protection from immune cells
*limitations on nutrient exchange, high cell density – bacteria are not growing rapidly; most antibiotics attack rapidly growing bacteria

8

Implications for antibiotic therapy in IE?

• Bactericidal activity
• parental administration for sustained activity
• long-term treatment required

9

Thick peptidoglycan, stains purple d/t iodine and not saffron red

Gram + bacteria

10

Thin peptidoglycan wall, crosslinked to outer membrane; outer membrane has permeability layer and stains saffron red

Gram - bacteria

11

Stain/shape/ organization for streptococcus

Gram +
in Cocci
in chain
= streptococcus

12

stain/shape/organization for staphlococcus

Gram +
Cocci
Clusters

13

Antibiotics that block peptidoglycan crosslinking

B-lactams;
inhibit the L-ala--D-ala linkage

14

B lactams are bacteriostatic or bacteriocidal

bacteriostatic

15

Four basic types of β-lactam – modification at______alters properties of the
antibiotic

“R” groups
(nafcillin, peniclillin and cefazolin and ceftriaxone)

16

How do bacteria develope resistance to B-lactams?

Mutations in PBPs that prevent binding of β-lactam antibiotics
(modification of antibiotic target)

17

Most common mechanism of B- lactam resistance found in

Gram-positive bacteria, such as Streptococcus and methicillin-resistant Staphylococcus
aureus (MRSA)

18

Vancomycin is a ________
What's its mechanism?

glycopeptide
binds to D-ala-D-ala at end of peptide chain in peptidoglycan precursors... blocks PBPs from catalyzing transfer

19

Vancomycin is effective in what type of bacteria?

Gram + and in patients with bacterias resistant to (not Gram - d/t permeability barrier of Gram - outer membrane)

20

Mechanism of resistance against vancomyocin

Modification of antibiotic target - bacteria acquire genes
encoding machinery to produce altered peptidoglycan structure that lacks D-Ala-D-Ala
groups (contain D-Ala-D-Lac in place of D-Ala-D-Ala); vancomycin is unable to bind
efficiently to these modified precursors

21

How do bacteria acquire resistance to vanocmyocin?

Genes encoding vancomycin resistance are usually found on plasmids or transposons that
can be easily transferred to other bacteria

22

VRE is most common in:

hospital settings

23

thought to bind to and disrupt the cytoplasmic
membrane, possibly via loss of membrane potential, leading to death

Daptomyocin

24

Daptomycin is:
bacteriacidal/static
broad or narrow spectrum

bacteriacidal
narrow (G+)

25

used for infections caused by antibiotic-resistant bacteria because it employs a novel mechanism of action that retains activity against
resistant bacteria

Daptomycin

26

Mech of action of Rifampin

binds to and inhibits RNA polymerase to prevent gene expression (stops transcription of DNA into RNA)

27

How does bacterial develop resistance to Rifampin?

due to point mutations in the target of the drug
(RpoB subunit of RNA polymerase)

28

How do you administer Rifampin?

in synergy with other antibiotics

29

bind irreversibly to 30S ribosomal subunit and cause
misreading (incorporation of incorrect amino acid into growing protein) and
premature release of ribosome from mRNA

Aminoglycosides

30

Gentamicin is a

aminoglycoside

31

Why do we not use aminoglycosides on G+

because they don't penetrate well so give them with another antibiotic, such as a cell-wall active agent

32

adverse effects of aminoglycosides (gentamicin)

ototoxic and nephrotoxic

33

Mech of resistance of bacteria to aminoglycosides

Enzymatic modification of the antibiotic (transferases
catalyze addition of adenyl, acetyl, or phosphoryl group) to prevent aminoglycoside binding to the ribosome

34

important virulence determinants in infectious endocarditis

factors that promote adherence to heart valves (dextran, cell surface proteins)