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Disease and Defense > Unit IV > Flashcards

Unit IV Flashcards

1
Q

What is the bacterial equivalent of tubulin?

A

FtsZ

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2
Q

What is the bacterial equivalent of actin?

A

MreB

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3
Q

What is the bacterial equivalent of intermediate filament?

A

CresS

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4
Q

What is glycocalyx used for?

A

formation of microbial biofilms

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5
Q

What molecules attaches the outer membrane of gram negative bacteria to peptidoglycan?

A

Lipoproteins

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6
Q

What is another word for lipopolysaccharides?

A

Endotoxin

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7
Q

What are the three components of LPS?

A 
Lipid A (the toxic component)
core polysaccharide
O antigen that functions as a somatic antigen
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8
Q

What is the classification of enteric bacteria based on their flagella?

A

H antigens

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9
Q

What is a bacteriophage?

A

virus that infects bacteria

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10
Q

What are heterotrophic bacteria?

A

Require organic carbon for survival

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11
Q

What are autotrophic bacteria?

A

bacteria that obtain their carbon exclusively from CO2

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12
Q

What are obligate intracellular bacteria? t

A

Bacteria that can grow within eukaryotic cells but

cannot be cultivated on artificial media.

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13
Q

How do heterotrophic bacteria obtain both energy and

reducing power?

A

fermentation or respiration

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14
Q

β-lactams

A

inhibit the final transpeptidation reaction in cross-linking of peptidoglycan.

ex: penicillin, cepalosporins

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15
Q

What is the role of vancomycin?

A

inhibits utilization of lipid-linked intermediate at an

intermediate step in peptidoglycan synsthesis, e.g., elongation of the peptidoglycan chain.

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16
Q

cycloserine

A

inhibits alanine racemase, preventing formation of

muramyl pentapeptide, an early intermediate in peptidoglycan synthesis.

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17
Q

Polymyxins

A

cationic surfactants that disrupt bacterial outer and cytoplasmic membranes. They are less active on mammalian cell membranes.

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18
Q

Aminoglycosides

A

bind to specific target proteins in the 30S ribosomal subunit and inhibit protein synthesis.

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19
Q

Tetracyclines

A

reversibly bind to the 30S ribosomal subunit and inhibit

binding of aminoacyl tRNA.

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20
Q

chloramphenicol

A

binds reversibly to the 50S ribosomal subunit and inhibits peptidyl transferase and peptide bond formation.

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21
Q

Macrolides

A

bind to the 23S ribosomal RNA of the 50S subunit and inhibit peptidyl transferase.

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22
Q

Quinolones

A

inhibit DNA gyrase and topoisomerase and interfere with DNA replication

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23
Q

Rifampicin

A

inhibits RNA polymerase and interferes with the

initiation of transcription.

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24
Q

Sulfonamides

A

structural analogs of p-aminobenzoic acid (PABA), which is a component of folic acid. Sulfonamides inhibit the formation of folic acid by competing
with PABA, and this in turn prevents nucleic acid synthesis.

**humans don’t make folic acid, we get it from bacteria in our gut

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25
Q

Trimethoprim

A

interferes with folate metabolism by inhibiting
the enzyme dihydrofolate reductase. Since both bacterial and host cells both possess this enzyme, the basis of selective toxicity lies in the 50,000-fold greater sensitivity of the bacterial enzyme to this drug.

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26
Q

Isoniazid

A

inhibits lipid synthesis (probably mycolic acid synthesis) in
susceptible Mycobacteria.

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27
Q

Metronidazole

A

appears to specifically interfere with anaerobic metabolism.

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28
Q

virulence genes are often expressed under what conditions?

A

low iron conditions that are encountered IN the host

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29
Q

How does Salmonella typhimurium generate genetic diversity?

A

It has an invertible segment of DNA which includes the promoter region of H2. When reversed the H2 promoter is expressed and H2 is made. H1 is blocked .

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30
Q

How does Neisseria gonorrhoeae generate genetic diversity?

A

Recombinational exchange between the expressed and a nonexpressed copy of the pilin genes results in a new pilin gene at the expression site and production of a new antigenically distinct pili on the cell surface.

**Phase Variation

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31
Q

What are examples of mutations that are of medical importance?

A

i) increased resistance to antimicrobials in Pseudomonas and Mycobacterium tuberculosis
ii) Streptococcus pyogenes strains with an increased
likelihood of causing invasive disease due to a single amino acid change in pyogenic exotoxin B.

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32
Q

What is fermentation?

A

the catabolic process in which organic compounds serve as both electron donor and electron acceptor

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33
Q

What is respiration?

A

need a terminal electron acceptor typically O2

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34
Q

What are the two forms of energy currency for bacteria?

A
  1. ATP - biosynthetic interconversions

2. Proton Motor Force - flagellar rotation, membrane transport

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35
Q

How do you convert ATP into PMF?

A

ATPase

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36
Q

What is the active component in transformation?

A

naked DNA, probably DNA from lysing cells

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37
Q

explain transformation

A

crude extracts, and ultimately pure DNA, taken from virulent, encapsulated strains of the pneumococcus (S forms) could convert avirulent, nonencapsulated strains (R form) to the virulent phenotype.

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38
Q

How are some bacteria induced to become “competent” to transformation?

A

calcium chloride and low temperatures

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39
Q

What is transduction?

A

gene transfer mediated by a bacteriophage

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40
Q

what is a lysogenic response?

A

the host cell remains viable and the infecting phage DNA is maintained by the host cell in a noninfectious state called a “prophage”

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41
Q

What is a prophage?

A

phage DNA which is linearly inserted into the host cell genome where it becomes passively replicated as part of the bacterial chromosome.

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42
Q

How is the lysogenic stage maintained?

A

by repressor proteins that blocks expression of the

phage genes necessary for viral DNA replication and lytic development.

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43
Q

What is bacteriophage conversion (lysogenic conversion)?

A

the genes controlling the new phenotypic trait are found only as a component of the phage genome; that is, the converting genes are not found alone as normal constituents of the bacterial genome.

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44
Q

What is generalized transduction?

A

caused by error in DNA packaging where that phage mistakenly packages bacterial DNA instead of viral DNA. It can still attach to other bacterial cells and inject this DNA to cause recombination with homologous segments

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45
Q

What is bacterial conjugation mediated by?

A

bacterial plasmids

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46
Q

What often encode antibiotic resistance and virulence factors?

A

plasmids

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47
Q

What type of plasmids are self transmissible?

A

conjugative plasmids

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48
Q

The mechanism of antibiotic resistance transfer is particularly prevalent among which type of bacteria?

A

gram positive bacteria

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49
Q

The F plasmid contains genetic information encoding what traits?

A

i. Autonomous replication of the plasmid DNA
ii. Synthesis of sex pili (F pili) which are essential for mediating pair formation between donor and recipient cells
iii. Conjugative transfer of F DNA to recipient (F- ) cells
iv. Ability to integrate into the bacterial chromosome

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50
Q

What is bacterial conjugation?

A

a form of genetic transfer that is dependent upon physical

contact between the donor and recipient cells, and is usually mediated by certain types of bacterial plasmids

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51
Q

What are spores?

A

specialized cells that are produced by certain bacteria, such as Clostridium sp. and Bacillus sp.,
when the nutritional supply of carbon, nitrogen or phosphorus is limited

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52
Q

Define peritrichous?

A

Bacterial that have flagellar all around them

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53
Q

What are the three most common organisms responsible for infective bacterial endocarditis?

A

Staphylococcus aureus
Streptococci of the viridans group
coagulase negative Staphylococci **staphylcocci epidermidis

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54
Q

What bacteria is catalase positive?

A

staphylcocci

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55
Q

Which bacteria is catalase negative?

A

streptococci

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56
Q

Which bacteria is coagulase positive?

A

staphylcoccus aureus

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57
Q

What is an alternative name for staphylcocci epidermidis?

A

staph species, NOT aureus (SSNA)

coagulase negative staphylcoccus (CNS)

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58
Q

What bacteria is the causative agent of common

“strep throat”?

A

streptococcus pyogenes

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59
Q

How does streptococcus pyogenes avoid phagocytosis?

A

They are surrounded with M protein

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60
Q

Describe the distinct features of group a streptococcal lesions

A

The typical lesion is that of a SPREADING infection of the cutaneous and subcutaneous tissues (cellulitis). [Contrast with typical S. aureus infections-which are more prone to produce focal abscesses, which may be accompanied by a surrounding cellulitis]

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61
Q

What are Post-streptococcal diseases?

A

Glomerulonephritis- Streptococcal antigen-antibody complexes are deposited in the kidney and accumulate at the basement membrane.

Rheumatic fever- antibodies recognizing and binding to
specific host antigens of the myocardium and heart valves.. This leads to progressive antibody-mediated damage to these tissues.

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62
Q

What are the “big three pathogens” for antibiotic use?

A

MRSA, pseudomonas, and anaerobes

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63
Q

Which enzyme cross links peptidoglycan?

A

Penicillin Binding Proteins

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64
Q

What reactions are driven by penicillin binding proteins?

A

transpeptidase and transglycosylase

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65
Q

How do beta lactam antibiotics work?

A

they irreversibly bind and inactivate the transpeptidase reaction of penicillin binding proteins therefore, INHIBITS cross linking and synthesis of peptidoglycans

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66
Q

How do bacteria become resistant to beta lactam?

A

They produce beta lactamase which destroys the beta lactam - MODIFYING THE DRUG

Produce altered penicillin binding proteins so that the beta lactam no longer can bind - MODIFYING THE TARGET

PREVENTING DRUG TARGET INTERACTION - modifying porin channel and drug efflux mechanisms so beta lactam cannot reach its target

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67
Q

Where can beta lactamase be found?

A

in gram positive and gram negative bacteria

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68
Q

Is beta lactamase more commonly found in gram positive or gram negative bacteria?

A

Gram negative

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69
Q

How are beta lactamases encoded?

A

chromosomal or transferable genes

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70
Q

Narrow-spectrum β-lactamases are resistant to what type of antibiotics?

A

penicillins-type antibiotics (penicillin, amoxicillin, ampicillin and possibly piperacilllin)

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71
Q

Narrow-spectrum β-lactamases bacteria are sensitive to what drugs?

A

cephalosporins or carbapenems

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72
Q

extended spectrum beta-lactamases are notable for their resistance to what drugs?

A

cephalosporins

**can still be treated with beta lactamase inhibitors

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73
Q

Where are extended spectrum beta-lactamases found?

A

plasmids

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74
Q

What type of bacteria are beta lactamases?

A

gram negative

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75
Q

What are notable features of ampC-encoded β-lactamase?

A

it is chromosomally located
can hydrolyze penicillins, 1st 2nd and 3rd generation cephalosporins
NOT inhibited by beta-lactamase inhibitors

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76
Q

Which bacterias have ampC-encoded β-lactamase?

A

gram negative bacteria: enterobacter and pseudomonas

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77
Q

What are lipopolysaccarides an example of?

A

Pathogen associated molecular pattern (PAMP)

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78
Q

How are lipopolysaccarides recognized?

A

via the innate immune system -CD14 and TLR4

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79
Q

What are hemolysins?

A

erythrocyte membrane damaging toxins that kill target cells

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80
Q

cytolysins?

A

general terms for membrane damaging toxins that kill target cells.
Form pores that cause the lysis of cells

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81
Q

What are the most potent T cell activators?

A

superantigens

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82
Q

How does pseudomonas aeruginosa inhibit protein synthesis?

A

exotoxin A inactivates elongation factor 2 (EF-2) which is required for peptide chain elongation.

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83
Q

What are examples of ribosyltransferases?

A

Diphtheria toxin and pseudomonas aeruginosa exotoxin A both inactivate EF-2

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84
Q

How do shiga toxins of shigella and e.coli work?

A

they are RNA N-glycosidases that remove an adenine residue, inactivating the ribosomes

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85
Q

How does diphtheria toxins damage cells?

A

inhibits protein synthesis by inactivating EF-2

86
Q

Where is the diphtheria organism found?

A

upper respiratory tract

87
Q

Where do diphtheria toxins travel to?

A

heart, kidneys, and peripheral nerves

88
Q

Where does pseudomonas aeruginosa exotoxin A act?

A

on liver cells

89
Q

How does enterotoxin from cholerae and E.coli increase adenylate cyclase?

A

activates the stimulatory Gs regulatory protein

90
Q

How does pertussis toxin increase adenylate cyclase activity?

A

inhibits the Gi (inhibitory) regulatory protein of the cyclase complex.

91
Q

What are the two type of toxins produced by anthrax?

A

edema factor - increases cAMP

lethal factor - cleaves MAP kinase kinase proteins and inactivates their function

92
Q

What does edema factor need for enzymatic activity?

A

calmodulin and calcium

93
Q

which toxins are zinc dependent endopeptidases?

A

botulinum and tetanus toxin

94
Q

What type of bacteria uses type III secretions?

A

gram - bacteria
shigella

**needle insertion technique

95
Q

What is unique about type VI secretions?

A

can inject effectors into bacteria and eukaryotic cells

96
Q

Bacteria in the stationary phase are less susceptible to what drugs?

A

Beta lactams because there is a decrease in rate of growth and cell division. Therefore not a lot of peptidoglycan cross linking

97
Q

What bacterial structure is targeted by quinolone?

A

DNA Gyrase and topoisomerase

98
Q

What is the role of coagulase in the context of spread of infection?

A

Promotes the deposition of fibrin and walls off S. aureus

99
Q

What are the bacterial components or structures that are most commonly involved in mediating adherence of bacteria to human cells?

A

pili

100
Q

What bacteria uses m protein as its primary virulence factor?

A

streptococcus pyogenes (Group A strep)

a surface exposed protein thatninhibits phagocytosis and killing by PMNs, and enhances adherence to epithelial cells

101
Q

MacConkeys plate grows what type of bacteria?

A

Gram negative

102
Q

Which bacteria ferment lactose?

A

E. coli and Klebsiella pneumoniae

103
Q

What is a bactericidal agent?

A

kills the bacteria

104
Q

What is a bacteriostatic agent?

A

prevents the bacteria from GROWING

105
Q

Key differences between bactericidal vs bacteriostatic agent?

A

Bactericidal:
used to treat SEVERE infections
acts more QUICKLY
can compensate for patients immunocompromised
used to treat bugs that are not accessible by the immune system

106
Q

drug that is taken with food..

A

drug is stable in gastric acid but can be irritating to stomach (take with food)

107
Q

What process explains the ability of N. gonorrhoeae to express different antigenic forms of pili?

A

genetic recombination

108
Q

What type of bacteria is Klebsiella pneumoniae?

A

Gram negative rod

109
Q

What part of LPS is the toxigenic portion?

A

the inner portion that has phosphorylated sugars attached to multiple fatty acids

called Lipid A

110
Q

What is the outer portions of LPS?

A

The outer oligosaccharide polymer has the O chain that is used for recognition by host antibodies.

111
Q

What bacteria produces toxins that transfer glucose from UDP-glucose to Rho family GTPases, altering the cytoskeleton of enterocytes?

A

Clostridium difficile

112
Q

Which bacteria is a gram-negative rod with intrinsic resistance to penicillin, ceftriaxone (3rd gen cephalosporin) and erythromycin

A

pseudomonas aeruginosa

113
Q

How would enterococci appear on gram stain?

A

gram positive cocci in chains

114
Q

What is the gram stain for bacterioides fragilis?

A

gram negative bacillus

115
Q

What organisms would most likely Gram stain as Gram-negative diplococci?

A

neisseria gonorrhea

116
Q

Where in the body does clinamycin have good distribution

A

Bone for osteomylitis

117
Q

Where in the body does tetracylcins have good distribution?

A

gingival gums and sebum glands

118
Q

Where in the body do macrolides have good distributions?

A

in the lungs (pneumonia)

119
Q

What drug has rapid excretion in the kidneys and is good for UTIs?

A

Nitrofurantoin

120
Q

What drug has toxicity in developing bones and teeth/ causes discoloration in teeth?

A

tetracyclines?

121
Q

What drug has ototoxicity and renal toxicity?

A

aminoglycocides

122
Q

What is a narrow spectrum drug?

A

effective against gram positive or gram negative

123
Q

What is an extended spectrum drug?

A

effective against gram positive AND gram negative

124
Q

What is a broad spectrum drug?

A

effective against gram positive, gram negative, and atypical organisms

125
Q

What are the broad spectrum drugs?

A

macrolides: inhibits 50s
chloarmphenicol: inhibits 50s
tetracyclines: inhibits aminoacetyl t-RNA
fluorquinolones (Moxi)
sulfonamides
trimethoprim

126
Q

What are the extended spectrum drugs?

A

extended spectrum penicillins
cephalosporins
fluorquinolones (Cip, Levo)
Carbapenems

127
Q

What are the narrow spectrum drugs?

A 
aminoglycosides
penicillinase resistant penicillins
clindamycin (Gemi)
Vancomycin
Metronidazole
Penicillin G, V
128
Q

What drug increases hepatic metabolism of other drugs?

A

Rifampin is an inducers of p450

129
Q

What drug has drug drug interactions with alcohol?

A

metronidazole

130
Q

The persistent suppression of bacterial growth that may occur after limited exposure to some antibacterial drugs:

A

post-antibiotic effects

131
Q

What drugs exhibit concentration dependent killing?

A

aminoglycosides and fluroquinolones

132
Q

What drugs exhibit time dependent killing

A

Beta lactams
vancomycins
macrolides

133
Q

What drugs exhibit post antibiotic effects?

A

aminoglycosides and fluorquinolones

134
Q

What are key differences between narrow and broad spectrum drugs?

A

narrow is more effective

broad spectrum you are more likely to cause a superinfection because you kill the health bacteria

135
Q

Is amoxicillin or ampicillin better aborbed?

A

amoxicilling because it has a hydroxyl group

136
Q

What drugs affect stage 1 in bacterial cell wall synthesis?

A

cycloserines (early intermediate of peptidoglycan synthesis) and fosfomycin

137
Q

What drugs affect stage 2 in bacterial cell wall synthesis?

A

vancomycin (lipid linked intermediate step of peptidoglycan elongation) and bacitracin

138
Q

What drugs affect stage 3 in bacterial cell wall synthesis?

A

peptidoglycan cross linking - PENCILLINS AND CEPHALOSPORINS

139
Q

Are penicillins bactericidal or static?

A

bactericidal –> causes cell to lyse

140
Q

What is the role of penicillinases and cephalopsorinases?

A

bacterial resistance to beta lactams that hydrolyze beta lactams

141
Q

How is penicillin resistance acquired?

A

via plasmid - transduction

**staphylococcus

142
Q

How is pencillin best absorbed?

A

without stomach acid therefore on an EMPTY STOMACH

poor penetration into tissues

143
Q

Described distribution of penicillin

A

can enter inflamed tissue or membranes

144
Q

How is penicillin excreted?

A

renal and can be excreted via breast milk

145
Q

What is the prototypical penicillin?

A

penicillin G

146
Q

What penicillin is acid resistant?

A

penicillin V

147
Q

which penicillins are penicillinase resistant?

A

dicloxacillin, oxacillin and nafcillin *only use when penicillnase producing organisms. If not use the G spot baby (penicillin G)

148
Q

How do extended spectrum penicillins work?

A

they increase hydrophilicity allowing penetration through porins of GRAM NEGATIVE ORGANISMS

149
Q

What are the extended spectrum penicillins?

A

ampicillin and amoxicillin (better absorption because hydroxyl group)

**not resistant to penicillinas

150
Q

Which penicillins can be used against pseudomonas, enterococci, and bacteroides fragilis?

A

ticarcillin and piperacillin

151
Q

What are the beta lactamase inhibitors?

A

clavulanic acid, sulbactam, and tazobactam

152
Q

What is augmentin?

A

clavulanic acid combined with amoxicillin

153
Q

What is timentin?

A

ticarcillin combined with clavulanic acid

154
Q

What is Unasyn?

A

sulbactam with ampicillin

155
Q

What is Zosyn?

A

tazobactam with piperacillin

156
Q

What is the primary mechanism of antibacterial action of penicillins involves:

A

reactions involving transpeptidation

157
Q

What can you use to treat MRSA?

A

vancomycin, 5th generation cephalosporins, tetracyclins, and clindamycin

158
Q

What drug is not broken down by beta lactamases?

A

cephalosporins

works well for MSSA

159
Q

Which penicillins are IV only?

A

piperacillin and ticarcillin (good against pseudomonas, enteroccoci, and bacteroides fragilis)

160
Q

Between penicillin V and G which one is prescribe outpatient vs in the hospital?

A

Penicillin G - IV only in hospital

Penicillin V - oral intake/outpatient

161
Q

Ampicillin is most effective against what bug?

A

Listeria monocytogene

162
Q

what is the incidence of diarrhea with penicillins from greatest to lowest?

A

amoxicillin-clavulanate > ampicillin> amoxicillin > pen V

ampicillin>amoxicillin due to poorer oral absorption

163
Q

How is vancomycin administered?

A

IV

164
Q

if a patient has a GI infection would you use vancomycin or metronidazole

A

metronidazole is the preferred

this is the only time you would give vancomycin orally if you were to

165
Q

Are cephalosporins extended or broad spectrum?

A

extended spectrum drug

166
Q

What is unique about 3rd generation cephalosporins?

A

can penetrate into CSF

167
Q

What are the first generation cephalosporins?

A

cafazolin and cephalexin

168
Q

What is the prototype of 1st generation cephalosporins?

A

cefazolin

169
Q

Which cephalosporin has greater activity against MSSA?

A

cefazolin/cephalexin

170
Q

What is the third generation cephalosporin and what is it used against?

A

ceftriaxone good against neisseria gonorrhoeae, gram + step pneumonieae, and CNS distribution

171
Q

How is cefazoline administered?

A

IV

172
Q

How is cephalexin administered?

A

PO

173
Q

Which cephalosporin is effective against MRSA?

A

5th generation - ceftaroline

174
Q

Which drug should you NOT give if you have a patient with Type I anaphylaxis to pencillin?

A

cephalosporins

1% chance of cross reactivity

175
Q

How would you treat meningitis?

A

3rd generation cephalosporin - ceftriaxon/ ceftazidime

176
Q

What cephalosporin would you use to treat pseudomonas?

A

generation 3

177
Q

How would you treat chlamydia?

A

macrolide or tetracyclines

178
Q

Do you give cephalosporins to a patient with type I sensitivity to penicillin?

A

NO 1% CHANCE OF CROSS REACTIVITY. DO NOT TAKE RISK

179
Q

Do cephaosporins cover most anaerobes?

A

YES!

180
Q

What are the adverse reactions associated with vacomycin?

A

red man syndrome
ototoxicity
nephrotoxicity

181
Q

How is penicillin G administered?

A

IM

182
Q

Which bacteria alter the methylation of 50s ribosome to prevent macrolide binding?

A

step. pneumonia and h. influenzae

183
Q

How does resistance against macrolides occur?

A

***Methylation of target site -50S ribosome MAJOR ONE

multi-dru efflux tranporter

184
Q

Which macrolide is NOT metabolized?

A

Azithromycin

185
Q

which macrolide should you use for community acquired pneumonia due to strep penumoniae that is resistant to other antibiotics?

A

Telithromycin

186
Q

How should tetracyclines be administered?

A

on an empty stomach

187
Q

What can impair tetracycline absorption?

A

Milk products - Al, Ca, Mg, Fee

188
Q

Which tetracycline should be used for patients with renal disease?

A

Doxycycline (non-renally excreted)

189
Q

What type of spectrum drug is tetracycline?

A

broad spectrum bacteria

190
Q

What drug should be avoided during latter half of pregnancy and in children under 8 years of age?

A

tetracycline - it disrupts bone and teeth growth, also discoloration

191
Q

How are macrolides administered?

A

orally

192
Q

What is the advantage of clarithromycin over erythromycin?

A

Clarithromycin has greater duration of activity

better for treating H. pylori

193
Q

How often do you give clarithromycin (biaxin)?

A

bi daily

194
Q

How often do you give erythromycin?

A

4 times a day

195
Q

How often do you give azythromycin?

A

once a day

196
Q

What is the relationship between caffeine and macrolides?

A

they both inhibit the p450 pathway!

197
Q

Which tetracycline has the best absorption?

A

Doxycycline

198
Q

Which tetracycline is absorbed better and has a longer duration of action?

A

doxycycline - only 2 a day

199
Q

How is clindamycin absorbed?

A

Orally!

200
Q

which drug is effective against gram negative AEROBES?

A

aminoglycosides

201
Q

How are aminoglycosides administered?

A

IM

202
Q

What drugs need to be administered with supervision?

A

Vancomysin (IV)

aminoglycosides (IM)

203
Q

How is fluoroquinolone resistance acquired?

A

plasmid mediated resistance

204
Q

How is fluorquinolone administerd?

A

orally

205
Q

Is fluoroquinolone good for MRSA?

A

no because it does not have a beta lactamase

206
Q

which fluorquinolone is not good for UTIs?

A

moxifloxacin because it does not show up in urine

207
Q

what do you typically use fluorquinolones for?

A

upper respiratory and UTI infections

208
Q

what type of bugs is moxfloxacin good for?

A

anaerobes

209
Q

How can you treat pseudomonas

A

piperacillin/ticarcillin
aminoglycosides
ciprofloxin/levofloxin
ceftazidime (3rd C) and cefepime(4th C)

210
Q

How are cephalosporins administered?

A

IM/IV

Disease and Defense (4 decks)

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