Intro to infectious Agents HD

Question 1

Most common agents that cause infectious endocarditis are:

Answer 1

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

Question 2

Access to endocardium provided by

Answer 2

transient bacteremia

Question 3

Properties of successful IE pathogens:

Answer 3

• able to survive antimicrobial components of serum

* able to adhere avidly to endocardium

Question 4

How does viridans streptococci mediate adeherance in the endocardium?

Answer 4

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

Question 5

How does S.aureus mediate adherance in endocardium

Answer 5

• fibrinogen-binding adhesins (ClfA, coagulase)

Question 6

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

Answer 6

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

Question 7

Why are infectious endocarditis bacterial concerning and difficult to erradicate?

Answer 7

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

Question 8

Implications for antibiotic therapy in IE?

Answer 8

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

Question 9

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

Answer 9

Gram + bacteria

Question 10

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

Answer 10

Gram - bacteria

Question 11

Stain/shape/ organization for streptococcus

Answer 11

Gram +
in Cocci
in chain
= streptococcus

Question 12

stain/shape/organization for staphlococcus

Answer 12

Gram +
Cocci
Clusters

Question 13

Antibiotics that block peptidoglycan crosslinking

Answer 13

B-lactams;

inhibit the L-ala–D-ala linkage

Question 14

B lactams are bacteriostatic or bacteriocidal

Answer 14

bacteriostatic

Question 15

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

Answer 15

“R” groups

nafcillin, peniclillin and cefazolin and ceftriaxone

Question 16

How do bacteria develope resistance to B-lactams?

Answer 16

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

Question 17

Most common mechanism of B- lactam resistance found in

Answer 17

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

Question 18

Vancomycin is a ________

What’s its mechanism?

Answer 18

glycopeptide

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

Question 19

Vancomycin is effective in what type of bacteria?

Answer 19

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

Question 20

Mechanism of resistance against vancomyocin

Answer 20

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

Question 21

How do bacteria acquire resistance to vanocmyocin?

Answer 21

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

Question 22

VRE is most common in:

Answer 22

hospital settings

Question 23

thought to bind to and disrupt the cytoplasmic

membrane, possibly via loss of membrane potential, leading to death

Answer 23

Daptomyocin

Question 24

Daptomycin is:
bacteriacidal/static
broad or narrow spectrum

Answer 24

bacteriacidal

narrow (G+)

Question 25

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

Answer 25

Daptomycin

Question 26

Mech of action of Rifampin

Answer 26

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

Question 27

How does bacterial develop resistance to Rifampin?

Answer 27

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

Question 28

How do you administer Rifampin?

Answer 28

in synergy with other antibiotics

Question 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

Answer 29

Aminoglycosides

Question 30

Gentamicin is a

Answer 30

aminoglycoside

Question 31

Why do we not use aminoglycosides on G+

Answer 31

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

Question 32

adverse effects of aminoglycosides (gentamicin)

Answer 32

ototoxic and nephrotoxic

Question 33

Mech of resistance of bacteria to aminoglycosides

Answer 33

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

Question 34

important virulence determinants in infectious endocarditis

Answer 34

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