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NUNA 679 - ANP Pharm > Cell Wall Synthesis Inhibitors > Flashcards

Cell Wall Synthesis Inhibitors Flashcards

1
Q

Describe the cell wall architecture of a gram-positive bacteria.

A

A thick murein wall outside the cytoplasmic membrain.

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2
Q

Describe the cell wall architecture of a gram-negative bacteria.

A

An outer lipopolysaccharide layer, outer membrane layer (both of these containing pores), a thin murein layer, and then an inner cytoplasmic membrane.

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3
Q

Describe the cell wall architecture of a mycobacteria.

A

From outside to in: extractable phospholipids, mycolic acids, and arabinogalactan (all three layers transversed by a pore), thin murein layer, and cytoplasmic mebrane.

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4
Q

Murein chains are cross-linked to one another by ___________ (__), also known as ________________.

A

transpeptidases; TP; penicillin-binding proteins

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5
Q

______________ (__) forms linkages between NAM & NAG residues.

A

glycosyltransferase; GT

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6
Q

Beta-lactams bind to & inhibit _____.

A

PBP (cross-linking)

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7
Q

Glycopeptides bind to terminal __________ residues, prevent cross-linking and polymerization.

A

D-alanine

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8
Q

What are the 4 major subclasses of beta-lactam antibiotics?

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

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9
Q

Describe the structure of beta-lactam antibiotics and how this impacts the MOA.

A

They contain a “beta-lactam” ring which mimics the shape of the terminal D-alanine-D-alanine of peptidoglycan in the bacterial wall.

The antibiotic binds covalently (permanently) to the PBP.

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10
Q

Beta-lactam antibiotics are active only in ________ bacteria actively ________ cell wall.

A

growing; synthesizing

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11
Q

True/false: Highly hydrophobic agents have an increased ability to penetrate the outer membrane of GNB.

A

FALSE! Hydrophilic agents penetrate GNB via membrane pores. Hydrophilic and hydrophobic agents are able to penetrate the cell wall of GPB/GNB.

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12
Q

Name 3 types of beta-lactamases.

A

Penicillinases
Extended-Spectrum Beta-Lactamases (ESBLs)
Carbapenemases

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13
Q

What does a penicillinase inactivate?

A

Penicillins

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14
Q

What does an ESBL inactivate?

A

Penicillins, cephalosporins, and monobactams; they are produced by GNB.

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15
Q

What kind of bacteria produce ESBLs?

A

GNB

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16
Q

What do carbapenemases inactivate?

A

All beta-lactams and beta-lactamase inhibitors

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17
Q

Where do beta-lactamases distribute in GPB and GNB? Which is more problematic?

A

Outside the cell wall of GPB and around the cell wall between the membranes of GNB. The latter is more problematic because they are more concentrated and produce more of an effect.

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18
Q

What are the two types of beta-lactamase inhibitors?

A

Beta-lactam beta-lactamase inhibitors

Non beta-lactam beta-lactamase inhibitors

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19
Q

Name 3 beta-lactam beta-lactamase inhibitors

A

Clavulanic acid, sulbactam, tazobactam

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20
Q

Name 3 non beta-lactam beta-lactamase inhibitors.

A

Avibactam, vaborbactam, relebactam

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21
Q

True/false: Beta-lactamase inhibitors have extensive anti-bacterial activity.

A

FALSE! They are combined with certain beta-lactams to protect against beta-lactamases (rodeo clowns) but have limited to no antibacterial activity themselves.

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22
Q

Name 4 mechanisms of resistance to beta-lactams (besides beta-lactamases).

A

Penetration - inability to reach transpeptidases
Bacteria does not have cell wall (mycoplasma)
Bacterial efflux pumps (specifically GNB)
Transpeptidase (PBP) mutation - reduced binding (ex., MRSA)

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23
Q

Name the 4 classes of penicillins.

A

Natural penicillins
Anti-staph penicillins
Aminopenicillins
Anti-psudomonal penicillins

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24
Q

Name 2 natural penicillins.

A 
Benzyl Penicillin (Pen G)
Phenoxymethyl Penicillin (Pen V)
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25
Q

Name 4 anti-staph penicillins.

A

Dicloxacillin
Oxacillin
Methicillin
Nafcillin

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26
Q

Name 2 aminopenicillins.

A

Ampicillin

Amoxicillin

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27
Q

Name an anti-psudomonal penicillin.

A

Piperacillin

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28
Q

List the penicillin classes in order from more GPB activity to GNB activity.

A

Natural penicilins, anti-staph penicillins, aminopenicillins, anti-pseudomonal penicillins

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29
Q

Penicillins do NOT cover ____ or _______ bacteria.

A

MRSA; atypical

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30
Q

Describe the coverage of natural penicillins.

A

Streptococci, enterococci, GP anaerobes (mouth flora)
VERY LIMITED GP coverage: treponema pallidum (syphilis)
DO NOT cover staphylococci (resistance)

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31
Q

Describe the coverage of anti-staph penicillins.

A

Streptococci, MSSA

Do NOT cover enterococci, GNB, or anaerobes

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32
Q

Describe the coverage of aminopenicillins.

A

Streptococci, enterococci, GP anaerobes (mouth flora)
GNB - Haemophilus, Neisseria, Proteus, E. coli, Klebsiella (HNPEK)
With beta-lactamase inhibitor: MSSA, resistant HNPEK strains, and B fragilis (GN anaerobe)

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33
Q

Describe the coverage of anti-pseudomonal penicillins.

A

Streptococci, enterococci, MSSA, GP anaerobes (mouth flora), HNPEK and HNPEK resistant strains
B fragilis
Other GNB: citrobacter, acinetobacter, serratia (CAPES), Pseudomonas aeruginosa

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34
Q

The natural penicillins, Benzyl Penicillin (Pen G) and Phenoxymethyl Penicillin (Pen V) are susceptible to ___________.

A

beta-lactamases

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35
Q

Pen G is unstable in ____________, necessitating administration by?

A

gastric acid; IV or IM

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36
Q

IV or IM Pen G comes in a ________ ______ formulation, therefore, monitoring which lab is important?

A

potassium salt; potassium

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37
Q

Which Pen G formulations are IM administration only?

A

Procaine (Wycillin) or benzathine (Bicillin L-A) salts

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38
Q

Which formulation of Pen G has a loner duration of action: procaine or benzathine?

A

Benzathine is more insoluble, producing a slow release; makes this formulation good for peds because they can get one shot and be done.

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39
Q

Which natural penicillin is stable in gastric acid, making it appropriate for oral administration?

A

Pen V

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40
Q

By what route is dicloxacillin taken?

A

Oral

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41
Q

By what routes is nafcillin taken?

A

IV & IM; a vesicant so give thru CVL

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42
Q

By what route is oxacillin taken?

A

IV

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43
Q

True/false: Anti-staphylococcus penicillins have GNB coverage.

A

False! They have none.

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44
Q

Anti-staphylococcus penicillins are resistant to _________ produced by _____________.

A

beta-lactamases; staphylococcus spp

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45
Q

Anti-staphylococcus penicillins are preferred for what 4 kinds of infections?

A

MSSA, bone and joint, endocarditis, and bloodstream

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46
Q

Anti-staphylococcus penicillins are primarily eliminated by what means? What is the implication?

A

Bile; no renal dose adjustment!

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47
Q

Compare/contrast the routes of administration for amoxicillin and ampicillin.

A

Amoxicillin is only given orally and has better PO absorption than ampicillin which is available PO, IV, and IM.

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48
Q

Amoxicillin is the drug of choice for what 3 conditions?

A

Acute otitis media, endocarditis prophylaxis (dental procedures), and H. pylori (ulcers)

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49
Q

How does the coverage of aminopenicillins compare to anti-staph penicillins?

A

Some GN coverage for aminopenicillins, but they are still susceptible to beta-lactamases, therefore they are combined with beta-lactamase inhibitors.

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50
Q

What are Augmentin and Unasyn?

A

Amoxicillin + clavulanic acid (a beta-lactamase inhibitor); PO
Ampicillin + sulbactam; IV

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51
Q

What is the drug of choice for acute otitis media and sinus infections?

A

Augmentin (amoxicillin + clavulanic acid)

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52
Q

What is the dose-related side effect of clavulanic acid?

A

Diarrhea

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53
Q

Piperacillin is always combined with what beta-lactamase inhibitor? Describe its activity.

A

Tazobactam (together as Zosyn); IV

Enhanced activity against GNB with increased resistance to GNB beta-lactamases; ACTIVE AGAINST PSEUDOMONAS AERUGINOSA!!!!!

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54
Q

Pencillins: static or cidal?

A

Bactericidal

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55
Q

Penicillins: time or concentration dependent?

A

Time-dependent: frequent dosing!

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56
Q

How are most penicillins eliminated? What is the exception?

A

Renally; anti-staph penicillins are eliminated in the bile.

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57
Q

What is the relative half-life of penicillins?

A

short; requires frequent dosing

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58
Q

Penicillins generally have poor CNS penetration, but what conditions can improve it?

A

Inflamed meninges
High doses
Reduced renal elimination (Prevenacid)

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59
Q

Name 6 potential side effects of penicillins.

A 
Diarrhea
Changes to gut flora
Allergic interstitial nephritis
Hematological reactions
Neurotoxicity
Seizures (antagonize GABA-A receptors)
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60
Q

Compare and contrast a type I and type IV allergic reaction/hypersensitivity.

A

Type I: Immediate, IgE mediated; within minutes to an hour; pruritis, flushing, urticaria, angioedema, wheezing, laryngeal edema, hypotension, anaphylaxis

Type IV: Delayed, T-cell mediated; appears after MULTIPLE doses of treatment, typically after days or weeks of administration; maculopapular cutaneous eruptions or delayed urticarial eruptions (as severe as SJS)

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61
Q

What is the rationale for attempting treatment with penicillin in patients who have had a previous reaction?

A

Less than 1% of reactions are IgE mediated; most patients lose their sensitivity after 10 years; other broad-spectrum antibiotics are more costly and put the patient at risk for resistance/suboptimal therapy.

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62
Q

What structural component increases the risk of cross-reactivity for patients with a penicillin/beta-lactam allergy?

A

Similar side chains

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63
Q

Name 5 types of drugs that have interactions with penicillins.

A

Anticoagulants/antiplatelets
Drugs that undergo renal tubular excretion
Methotrexate
Potassium sparing diuretics/drugs that increase potassium, or patients with renal dysfunction with potassium salt formulations
Aminoglycosides

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64
Q

Are cephalosporins bacteriostatic or bactericidal?

A

Bactericidal

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65
Q

Are cephalosporins time-dependent or concentration-dependent?

A

Time-dependent

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66
Q

Cephalosporins do NOT cover…(2)

A

Enterococcus and atypical

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67
Q

Name 2 drug classes that have cross-allergenicity.

A

Cephalosporins and penicillins

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68
Q

All cephalosporins are renally eliminated except?

A

Ceftriaxone (renal-biliary excretion)

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69
Q

Which 5 cephalosporins have CNS penetration?

A

Cefuroxime, Ceftriaxone, Cefotaxime, Ceftazidine, Cefepime

70
Q

Which 2 cephalosporins have seizure risk due to antagonizing GABA-A receptors?

A

Cefazolin and cefepime

71
Q

Discuss cephalosporins and enzymatic resistance.

A

More resistant to beta-lactamases than penicillins, but there is increasing prevalence of cephalosporinases.

72
Q

What are the 1st generation cephalosporins?

A

Cefazolin, cephalexin

73
Q

What are the 2nd generation cephalosporins?

A

Cefuroxime, cefotetan

74
Q

What are the 3rd generation cephalosporins?

A

Cefdinir, ceftriaxone, cefotaxime, ceftazidime

75
Q

What is the 4th generation cephalosporin?

A

Cefepime (“Hank Pim has 4 in the family)

76
Q

What is the 5th generation cephalosporin?

A

Ceftaroline (“Caroline was 5th in line”)

77
Q

What cephalosporin generations have the highest GP activity?

A

1 and 5

78
Q

What cephalosporin generation has the highest GN activity?

A

4th generation

79
Q

What are the routes/primary uses for cefazolin (Ancef)?

A

IV/IM

Surgical prophylaxis

80
Q

What are the routes/primary uses for cephalexin (Keflex)?

A

Oral

Strep throat, MSSA skin infections

81
Q

Describe the general activity of 1st generation cephalosporins.

A

Great GP cocci activity/MSSA infections

Limited GN activity; PEK only (Proteus, E. coli, Klebsiella)

82
Q

What is HNPEK?

A

Haemophilus, Neissera, Proteus, E. Coli, Klebsiella

83
Q

What are the routes/primary uses for cefuroxime (Ceftin)?

A

Oral, IV, IM

Acute otitis media, CAP, sinus infections (bacterial)

84
Q

What are the routes/primary uses/AEs for cefotetan (Cefoten)?

A

IV, IM
Surgical prophylaxis (COLORECTAL)
Bleeding risk
Disulfiram-like rxn with ETOH

85
Q

Describe the general coverage of 2nd generation cephalosporins.

A

Better coverage of strep pneumoniae RESISTANT strains, plus HNPEK coverage
Cefotetan also covers GN anaerobes (B fragilis as in the gut)

86
Q

All 3rd generation cephalosporins are IV/IM except ______ whichis PO only?

A

Cefdinir (Omnicef) is PO

Ceftriaxone (Rocephin), Cefotaxime, Ceftaizidime (Fortaz) are IV/IM

87
Q

What are common uses for oral 3rd generation cephalosporins (cefdinir)?

A

CAP, sinus infections (bacterial)

88
Q

What are common uses for parenteral 3rd generation cephalosporins?

A

CAP, meningitis, spontaneous bacterial peritonitis, pyelonephritis

89
Q

The 3rd generation cephalosporins (SPECIFICALLY cefdinir, ceftriaxone, and cefotaxime) are good for what kind of infections?

A

Resistant streptococci strains, MSSA, GP anaerobes (mouth flora), and resistant HNPEK strains

90
Q

Which 3rd generation cephalosporin has minimal GP activity but covers Pseudomonas aeruginosa?

A

Ceftazadime

91
Q

What 3rd generation-beta-lactam-inhibitor combo treats MDR Pseudomonas and GN rods?

A

Ceftazadime with avibactam (Avycaz)

92
Q

Things to know about ceftriaxone, a 3rd generation cephalosporin? (3)

A

Renal and hepatic elimination; NO renal adjustment needed
High doses required for MSSA infections
CI in neonates!! - biliary sludging, kernicterus, interacts with Ca++-containing products (crystals precipitate in lungs, kidneys)

93
Q

How is the CSF penetration of the 4th generation cephalosporin cefepime?

A

Good! (High)

94
Q

By what routes is cefepime administered?

A

IV/IM

95
Q

Describe the relative bacterial coverage of the 4th generation cephalosporins (cefepime).

A

Increased GN activity (HNPEK, CAPES, Pseudomonas aeruginosa)

Increased staphylococci activity

96
Q

Cefepime should be reserved for what kind of infections/population?

A

Febrile, neutropenic patients

Nosocomial infections

97
Q

What is a notable adverse effect of cefepime?

A

Neurotoxicity - nonconvulsive status epilepticus

98
Q

What is the only beta-lactam that covers MRSA? By what mechanism?

A

Ceftaroline (5th generation cephalosporins)

High affinity for mutated PBP (type 2)

99
Q

By what route is ceftaroline given?

A

IV

100
Q

What 3rd generation cephalosporin does ceftaroline share GN activity with?

A

Ceftriaxone

101
Q

Name the carbapenems (4)

A

Doripenem
Imipenem
Meropenem (Merrem)
Ertapenem (Invanz)

102
Q

Describe the coverage of the carbapenems.

A

Most GPB, GN (including ESBL-producing bacteria), and anaerobes

103
Q

What is NOT covered by the carbapenems?

A

Atypicals, MRSA, VRE, C diff, Stenotrophomonas

Ertapenem in particular: NO pseudomonas, acinetobacter, enterococcus

104
Q

Common uses for carbapenems?

A

Polymicrobial infections (as with GI perf), MDR infections (as with diabetic foot ulcers)

105
Q

What is the route of administration for carbapenems?

A

IV

Ertapenem must be diluted with NS and can also be given IM

106
Q

What is the carbapenem + renal dehydropeptidase blocker combo?

A

Imipenem with cilastatin (Primaxin)

107
Q

Name 2 carbapenem/beta-lactamase inhibitor combinations, name the route of administration, and describe the coverage.

A

Imipenem/cilastatin/relebactam (Recabrio) and meropenem/vaborbactam (Vabomere)
IV
Beta-lactamase inhibitor extends coverage to GNB that have developed resistance to carbapenems

108
Q

By what route are carbapenems eliminated?

A

Renal

109
Q

Carbapenems can penetrate the ___.

A

CNS (good for meningitis)

110
Q

Under which conditions does the administration of carbapenems put the patient at highest risk for seizures? (4)

A

Imipenem, patients with renal dysfunction, preexisting CNS disease/infection, and large doses

111
Q

What drug interaction increases seizure risk with carbapenems?

A

Valproic acid (reduces plasma levels)

112
Q

Side effects of carbapenems? (3)

A

Diarrhea, rash, BM suppression with prolonged use

113
Q

What lab should be monitored with carbapenems?

A

CBC (for bone marrow suppression)

114
Q

What is a beta-lactam drug of significance that is a monobactam?

A

Aztreonam (Azactam)

115
Q

What characteristics make aztreonam a good drug of choice for CF patients?

A

Inhalation route and activity against Pseudomonas aeruginosa!

116
Q

What are the 2 routes of administration for aztreonam?

A

IV and inhalation

117
Q

Aztreonam does/does not penetrate CNS??

A

Does!

118
Q

How does aztreonam measure up against beta-lactamases?

A

Relatively resistant

119
Q

Aztreonam is only active against _____ ___.

A

aerobic GNB

120
Q

Aztreonam has cross-reactivity with ________ due to same side-chain.

A

ceftazidime

121
Q

What is the drug class of vancomycin?

A

Glycopeptide

122
Q

Describe the MOA/physical characteristics of vancomycin.

A

Large and bulky
Active against GPB ONLY (can’t get thru porins) and only during active wall building
Binds D-alanine residues and takes up a lot of space, blocking the cross-linking of peptidoglycan layers
Blocks the linking of NAG-NAM polymers

123
Q

Describe the MOA of Enterococci resistance to vancomycin.

A

D-Alanine residue is replaced with D-Lac(???) residue so the Vancomycin cannot bind

124
Q

Vancomycin is bactericidal/static and concentration-/time-dependent.

A

Bactericidal; time-dependent

125
Q

Describe the antibacterial activity of vancomycin.

A 
All GPB (INCLUDING MRSA!!!)
GP anaerobes (INCLUDING C. DIFF taken PO!!!!)
Moderate activity toward enterococci (though increased resistance with VRE)
126
Q

Discuss routes of vancomycin administration

A

IV except PO for C. diff

127
Q

How is vancomycin cleared from the body?

A

Renally

128
Q

Vancomycin is the drug of choice for _____ and an alternative for _________ with IgE-mediated allergy.

A

MRSA; penicillin

129
Q

What are the 2 infusion-related adverse events associated with vancomycin?

A 
Histamine release ("Red Man Syndrome") - rash, flushing, tachycardia, hypotension
Phlebitis
130
Q

How can you prevent histamine release with vancomycin?

A

Dilute and give over 60 min; premedicate with diphenhydramine

131
Q

What are 2 other non-histamine-related vancomycin adverse effects associated with high and prolonged dosage?

A

Nephrotoxicity and auditory nerve damage

Consider renal function, previous hearing loss, and other nephro/ototoxic drug use

132
Q

From what drug are lipoglycopeptides derived?

A

Vancomycin

133
Q

Describe MOA/spectrum of lipoglycopeptides.

A

GPB only

Same as MOA (bind to D-Alanine and take up space) but ALSO disrupt membrane

134
Q

How are lipoglycopeptides cleared?

A

Renally

135
Q

Lipoglycopeptides are bactericidal/static and concentration-/time-dependent?

A

Bactericidal; concentration-dependent

136
Q

What potential reaction do lipoglycopeptides have in common with vanc?

A

Infusion reactions

137
Q

What is the spectrum of activity of lipoglycopeptides?

A

GPB including MRSA!!!!
Vanc-SENSITIVE enterococci
GP anaerobes (NOT C DIFF!!!)

138
Q

Name 3 lipoglycopeptides.

A

Televancin (Vibativ)
Dalbavancin (Dalvance)
Oritavancin (Orbactiv)

“Telemachus had a dalliance with Rita; he gave her an LG tv”

139
Q

Televancin is given how often?
What is the boxed warning?
Potentially harmful to what population?
Affects ______ tests.

A

Once daily IV
Nephrotoxic
Teratogenic
Coagulation

140
Q

Dalbavancin has a half-life of how long?

Admin how often over what time frame?

A

10 days!!!

Once per week over 30 minutes

141
Q

Oritavancin has a half-life of how long (same as dalbavancin)?
Given how often over what time frame?
Affects what tests?

A

10 days!!
Once a week over 3 hours
Coagulation

142
Q

What is the MOA of fosfomycin (Monurol)?

A

Covalently (irreversibly) inhibits UDP-N-acetylglucosamine enopyruvyl transfurase (MurA), blocking the FIRST step in bacterial cell wall synthesis and affecting the formation of NAM

143
Q

Fosfomycin is transported into bacterial cells by (2)

A

Glycerol-3-phosphate transporter (GlpT)

Glucose-6-phostphate transporter (UhpT)

144
Q

Route of administration for fosfomycin?

A

Oral

145
Q

Fosfomycin is bactericidal/static?

A

Bactericidal

146
Q

Fosfomycin’s primary route of elimination is in ______ and makes it ideal for treatment of __________ ____.

A

Urine; uncomplicated UTIs

147
Q

Fosfomycin is reliably active against what 4 organism species?

A

E. coli (including ESBL producing)
Proteus spp
Klebsiella spp
Citrobacter spp

148
Q

What two antibiotics are selective for mycobacteria such as M. tuberculosis and M. intracellulare?

A

Isoniazid

Ethambutol

149
Q

What is the MOA of isoniazid against mycobacteria?

A

Blocks synthesis of mycolic acid, a major component of the mycobacterial cell wall

150
Q

Is isoniazid bactericidal/static?

A

Trick question!! It is bactericidal in ACTIVELY growing mycobacteria and bacteriostatic in RESTING mycobacteria.

151
Q

What is the MOA of ethambutol?

A

Inhibits arabinosyl transferase leading to the polymerization of arabinogalactan which is a key component of the mycobacterial cell wall.

152
Q

Is ethambutol bactericidal/static?

A

Bacteriostatic but does work against actively growing mycobacteria

153
Q

Isoniazid absorption can be decreased by _____ and ____________ _______.

A

food; aluminum-containing antacids

154
Q

Describe the metabolism/excretion of isoniazid.

A

Acetylation by NAT2; metabolites and unchanged drug are eliminated in the urine.

155
Q

Isoniazid can cause ______toxicity and competes with vit __, leading to what side effects?

A

hepato; neurotoxicity - peripheral neuropathy, ataxia, paresthesia

You can take vit B6 to minimize neurotoxicity :)

156
Q

How is ethambutol metabolized/eliminated?

A

Eliminated in urine unchanged

157
Q

Major SE of ethambutol?

A

Optic neuropathy - visual acuity or red-green color blindness

158
Q

Name a cyclic lipopeptide.

A

Daptomycin (Cubicin)

159
Q

What is the MOA of daptomycin?

A

Rapid depolarization of bacterial cell membrane

Affects synthesis of DNA, RNA, and protein

160
Q

Daptomycin is bactericidal/static and concentration-/time-dependent?

A

Bactericidal; concentration-dependent

161
Q

What organisms is daptomycin active against?

A

GPB only - including MRSA!!!, VRE, and GP anaerobes EXCEPT C diff

162
Q

Daptomycin is given by what route and is incompatible with what?

A

IV; dextrose

163
Q

How is daptomycin cleared?

A

Renally

164
Q

Daptomycin is inactivated by __________ __________ and consequently not useful for what condition?

A

pulmonary surfactant; pneumonia

165
Q

Daptomycin can affect what tests?

A

Coagulation

166
Q

The combination of daptomycin with _____ can increase risk of what MSK/renal conditions? Monitor what labs?

A

statins; myopathy/rhabdomyolysis; CK

167
Q

Daptomycin can also cause peripheral ___________.

A

Neuropathy

168
Q

By what MOA can daptomycin cause breathing problems?

A

Accumulation of eosinophils in the lungs (2-4 weeks after starting treatment)

169
Q

Name 2 polypeptides.

A

Polymyxin B

Polymyxin E

170
Q

What is the MOA of polypeptides?

A

Bind lipopolysaccharides in the membrane of the GNB (detergent-like effect), breaking membrane open

171
Q

What is the route of administration for polypeptides?

A

IV

172
Q

What are the uses of polypeptides? What is Colistin preferred for? What are polypeptides used off-label for?

A

Serious infections caused by MDR GNB
UTIs
Pseudomonas in CF patients

NUNA 679 - ANP Pharm (9 decks)

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