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100 Cards in this Set

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broad coverage of antibiotics is best during:
early stage of the inf's

- narrow, targeted treatment is important to minimize the risk of bacterial R
whether static or cidal sometimes depends on:
time course of a drug

distribution - lipophilicity, prot. binding, CNS penetraition
4 general mech's of R:
1. cleave the drug

2. alter the drug r's

3. activate special membrane proteins => drug efflux

4. circumvent the blocked pathway by using an alternative pathway
treating pneumonia: antimicrobial chosen depends on:

1. suspected pathogen

2. likely etiology

3. where pt. developed inf.

4. pattern of signs and symptoms
most common causes pneumonia:

1. S. penumoniae

2. H. influ
3. SA
4. Klebsiella pneumoniae
treating CAP: if ambulatory, give:
a macrolide
treating CAP: comorbidities within 3 months:

1. FQ

2. BL + macrolide
treating CAP: if inpatient:
1. FQ

2. BL + macrolide

(same as with comorbidities)
treating CAP: in ICU:

1. BL


EITHER macrolide or FQ
treating CAP: if concerned about Pseudomonas, add:
antiPseudomonas BL
treating CAP: if concerned about CA MRSA, add:

1. Vancomycin


2. linezolid
"nosocomial" penumonias =
wrt HCAP's, 2 inf's of particular concern:
1. Pseudomonas

if pneumonia is late-onset or MDR is suspected, use:
broad-spectrum antibiotics
these 3 species form biofilms on medical equipment, door handles, and computer keys, and cause HCAP:
1. acinetibacter

2. Kleb pneumonia

3. En. faecium
***4 BL/B-lactamase inhibitor combo drugs:***
1. Augmentin

2. Unasyn

3. Zosyn

4. Timentin
Augmentin =
Clavulanic acid + amoxicillin
Unasyn =
Sulbactam + ampicillin
Zosyn =
tazobactam + pipercillin
Timentin =
Clavulanic acid + ticarcillin
GP's feature =
THICK peptidoglycan wall,

one membrane
GN features:

1. OUTER membrane

2. thin peptidoglycan wall
when bacteria-static drugs are removed,
growth resumes
**bacteria-static drugs are NOT given to:**
imm-comp pts,

since they require an immunologic response to work properly
***cidal drugs require ____________________ to work***
bacterial GROWTH

=> cidal and static drugs are NOT combined
lowest conc. that prevents growth
MIC's are specific for:
BOTH drug AND organism

- a LAB value - can be different in vivo
lower MIC =
better antibiotic
concentration-dependent killing

~~ how certain antib's like AG's and FQ's show inc. in killing as their dose inc's

=> given at HIGHER doses for SHORTER periods of time
time-dependent killing
TDK is seen with:

1. BL's

2. vancomycin
TDK drugs kill bacteria at:
the same rate, as long as their conc. is above the MIC

- dosing tries to maximize time above MIC
PAE = post-antibiotic effect =
time required for the antibiotic-treated cultures to return to log growth following removal of antibiotic
PAE allows:
once-daily dosing

=> dec in toxicity, cost
superinfection =
growth of regularly-stable *pathogenic* organisms

that are normally held in check by normal flora,

following antibiotic admin
which kind of antibiotics are more likely to kill normal flora?
3 mech's of MDR:
1. mutation/selection

2. uptake of extracellular DNA from related commensal bact/recombination

3. plasmid-mediated acquisition of R-factors
(can have 5 or more R factors on a single plasmid)
4 inhibitors of nucleic acid synthesis:
1. Sulfo's

2. TMP's

3. Q's

4. FQ's
neither Sulfonamides nor Trimethoprims are used:
SMZ = sulfamethoxazole
bacteria MUST synthesize:
folate to grow
what do bacteria need to synthesize folic acid?

1. pteridine


3. glutamate
how do Sulfonamides inhibit folic acid synthesis?
**structural analogs of PABA**

TMP/SMZ has a *limited toxicity*, b/c:
it's got a 50K-fold preference for BACT. DHFR over mammalian DHFR
what does TMP/SMZ do?
inhibits DHFR
what does DHFR do?
converts DHF to TetraHF, which is then used as a cofactor for DNA, RNA, and prot synth
2 examples of TMP/SMZ:
1. Septra

2. Bactrim
kernicterus =
prot-bound bilirubin in the BG of newborns
"selective toxicity" =
targeting bacteria-specific pathways/enzymes/factors
what kinds of pts are usually folic acid-deficient?

1. alcoholics

2. malnourished
during DNA replication, positive supercoils preclude:
further replication
2 enzymes to solve positive supercoiling:
1. gyrA

2. parC

- both make double-strand breaks, relieve supercoil, and reseal
inhibition of gyrA and parC by FQ's =>
cell death

(in other words, what do FQ's do? inhibit gyrA and parC)
use of FQ's is limited by:
increasing R
FQ's are selectively toxic b/c they:
inhibit bact. gyrA at much lower rates than they do the mammalian version
2 older agents for the treatment of uncomplicated UTI's:
1. Nalidixic acid
(a Q that acts like a FQ)

2. Nitrofurantoin
**Nalidixic acid and Nitrofurantoin:**

should NEVER be combined
what do BL's do?
inhibit cross-linking of peptide chains at the D-Ala-D-Ala

=> no peptidoglycan wall
***bacterial PBP's are either:***

1. essential (high-mlclr)


2. non-essential
***the efficacy of a BL is a function of:***

1. its affinity for any ONE of the essential PBP's
(an antibiotic that inhibits >1 is even better)

2. its ability to reach PBP's by getting inside GN's periplasm
(greater ability to reach periplasm = lower MIC)
*intrinsic R of bacteria = *
its ability to maintain keep PBP's unbound by inhibitors, either through wall or otherwise
extrinsic R of bacteria to antibiotics is NOT found in wild-type strains and include:

1. expression of B-lactamases

2. dec. permeability to drugs

3. inc. efflux

4. mut's in essential PBP's that dec. affinity of drug for PBP
how do B-lactamases worK?
like PBP's, they bind BL's

=> knock them out of use with rapid hydrolysis
B-lactamases can be either:
1. chromosomally encoded


2. plasmid-encoded
"chromosomally encoded" =
expression is INDUCED by sensing B-lactam or disruption in recycled cell wall materials
in which type of bacteria are B-lactamases more effective, and why?
in GN's, b/c they stay in the periplasmic space

- in GP's, they are excreted to the outside world
what are ESBL's?
extended-spectrum B-lactamases,

expressed by certain types of SA of hospitals,

which hydrolyze previously unhydrolyzable B-lactams
Staph. aereus often express B-lactamases, so SA inf's are treated with lactamase-R antibiotics, which are:

1. oxacillin

2. nafcillin

3. 2nd/3rd cephalosporins

4. carbapenems

- but ESBL's are becoming R to even these
NDM-1 B-lactamase does NOT form:
acyl-enzyme complex with B-lactams

=> VERY wide spectrum

=> hydrolyzes nearly ALL B-lactams

- essentially eliminates the use of BL's for treatment
dec. in outer membrane permeability is a function of:
mutated porins that have constricted channels
mut's in essential PBP's are seen most often in:

1. SA

2. SP

3. H. influ

4. N. gonorrhea
***pen-R SP contains mutations in:***
ALL the essential PBP's

- also R to many other antibiotics
pen-R SP is currently treated with:

1. Vancomycin + cefotaxime

2. linezolid

3. Streptogramins
Neisseria becomes R to penicillin in 2 ways:
1. plasmid-mediated production of B-lactamases

2. chromosomal mutations of endogenous genes (much more common)
what determines whether a strain is ceftriaxone-R?
the mut's in PBP2

(which is the target of both penicillin AND ceftriaxone)
what's the deal with MRSA?
have acquired ***NEW PBP, called PBP2a, from Staph fleuretti

=> **PBP2a becomes the ONLY essential PBP**

=> BL's CANNOT be used to treat MRSA
MRSA is also cross-resistant to:
other antibiotics
MRSA is currently treated with:

1. Vancomycin

2. linezolid

3. Streptogramins (Dalfopristin/Quinipristin)
CA-MRSA is increasing; a high % of such strains cause:
severe necrotizing hemorrhagic pneumonia
B-lactamase-R penicillins are used only against:

Carbapenem-R Enterobacteriaceae are emerging; Iminepem is hydrolyzed by a:
renal dispeptidase, so it's given with a

renal dispeptidase inhibitor, cilistatin
mut's in B-lactamases can mitigate both:
Augmentin and Unasyn
normally, BL tubular secretion is RAPID; one exception =
ceftriaxone, whose half life is 8 hours

(compared to 30-120 minutes)
the half-life of BL's can be increased by giving:
probenizid, which blocks renal secretion, concurrently
if a pt has a hyperS rxn to one penicillin, he will:
probably have a rxn to another
the only BL that doesn't cause a hperS rxn =
aztreonam, a monobactam
***B-lactams must NEVER be used in pts who:***
exhibit anaphylaxic rxns
some cephalosporins cause:
bleeding disorders

- given Vit K concurrently
2 mech's of R to Vancomycin:
1. induced directly by Vanco

2. plasmid-mediated
bacteria that is most commonly R to Vaoncomycin =
E. faecium
VISA appears after:
prolonged exposure to Vanco

(25 days to 18 weeks)

=> cell wall thickens, trapping the antibiotic in the outer layers
VRSA have obtained:
VanA,/others by transposon-mediated horizontal transfer

- still rare and susceptible to other antibiotics
4 cidal protein synthesis inhibitors:
1. AG's

2. Streptogramins

3. metronidazole

4. daptomycin
5 bacteria-static protein synthesis inhibitors:
1. Tetracyclins

2. Chloramphenicol

3. macrolides

4. clindamycin

5. linezolide
AG binding to negative sites of the inner membrane is inhibited by:
presence of divalent cations like Ca2+. Mg2+
AG's can only reach the cytoplasmic membrane of GP's if:
BL's are present

=> often combined

- presence of BL also improves AG's against GN's
**uptake of AG's is ___________- dependent

=> AG's are USELESS against strict anaerobes
AG's are great for:

=> once-daily dose
AG + penicillin treats:
E. facium, a GP

- neither is effective against E. faecium by itself => ALWAYS combined to treat enteroccoci inf's