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PHRM 865 > Introduction to Infectious Diseases Part 2 > Flashcards

Introduction to Infectious Diseases Part 2 Flashcards

1
Q

Gram stain used to

A

differentiate bacteria

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2
Q

Gram positive bacteria

A

appear purple due to thick peptidoglycan cell wall

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3
Q

Gram negative bacteria

A

appear red/pink due to thin peptidoglycan cell wall

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4
Q

Atypical bacteria

A

do not stain using gram-stain

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5
Q

Acid-fast bacilli

A

resistant to acids/ethanol based decolorization procedures
ex. mycobacterium species

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6
Q

Gram positive - cocci anaerobic

A

anaerobic: peptococcus peptostreptococcus

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7
Q

Gram positive - cocci aerobic - clusters

A

clusters (catalase +) –> coagulase (+) —> staphylococcus aureus
clusters (catalase +) –> coagulase (-) –> CoNS (staphylococcus epidermidis)

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8
Q

Gram positive - cocci aerobic - pairs/chains

A

pairs/chains (catalase -) –> alpha-hemolysis –> streptococcus pneumoniase, viridans streptococci
pairs/chains (catalase -) –> beta-hemolysis –> streptococcus pyogens (group A), streptococcus afalactiae (group B)
pairs/chains (catalase -) –> gamma-hemolysis (nonhemolytic) –> enterococcus faecium, enterococcus faecalis

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9
Q

Gram positive - bacilli anaerobic

A

anaerobic –> spore forming –> clostridium spp, clostridioides difficile
anaerobic –> non-spore forming –> cutibacterium, actinomyces

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10
Q

Gram positive - bacilli aerobic

A

aerobic –> spore forming –> bacillus spp
aerobic –> non-spore forming –> corynebacterium, lactobacillus spp, listeria monocytogenes

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11
Q

Hemolysis patterns

A

alpha, beta, gamma

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12
Q

Gram positive morphology

A

most medically important pathogens are cocci rather than bacilli
gram positive bacilli should be interpreted within clinical context

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13
Q

Gram positive colony clustering

A

staphylococcus form clusters
streptococci and enterococci appear in pairs or chains

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14
Q

Gram positive biochemistry testing

A

catalase test: staphylococci from streptococci
coagulase test: staphylococcus aureus from coagulase-negative staphylococcus

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15
Q

Gram positive agar appearance

A

oral flora: alpha-hemolytic
skin, pharnyx, genitourinary: beta-hemolytic
gastrointestinal: gamma-hemolytic

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16
Q

Gram negative - aerobic

A

cocci –> neisseria spp, moraxella catarrhalis
coccobacilli –> haemophilus

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17
Q

Gram negative - anaerobic

A

cocci –> veillonella spp
bacilli –> bacteroides spp, fusobacterium spp, prevotella spp

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18
Q

Gram negative - aerobic bacilli

A

aerobic bacilli –> enterobacterales –> lactose fermenters (oxidase negative) –> citrobacter spp, enterobacter spp, E. coli, klebsiella spp
aerobic bacilli –> enterobacterales –> non-lactose fermenters –> morganella morganii, proteus spp, providencia spp, salmonella spp, serratia marcescens, shigella spp

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19
Q

Gram negative - aerobic bacilli (non enterobacterales)

A

aerobic bacilli –> lactose-fermenters (oxidase positive) –> aeromonas hydrophila, pasteurella multocida, vibrio cholerae
aerobic bacilli –> non-lactose fermenters –> pseudomonas spp, acinetobacter spp, alcaligenes spp, burkholderia cepacia, stenotrophomonas maltophilia
aerobic bacilli –> fastidious –> campylobacter, helicobacter, bartonella, HACEK organisms

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20
Q

Gram negative atypical

A

chlamydia pneumoniae, chlamydia trachomatis, legionella pneumophila, mycoplasma pneumoniae

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21
Q

Gram negative spirochetes

A

treponema pallidum, borrelia burgdorferi

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22
Q

Gram negative morphology

A

bacilli predominate pathogen

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23
Q

Gram negative lactose fermentation

A

helps identify enterobacterales from non-fermenting gram negative rods
oxidase test helps distinguish between enteric vs non-enteric lactose fermenters

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24
Q

Gram negative fastidious organisms

A

slow growers, require special supplemental media

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25
Q

Gram positive and gram negative cell overview

A

gram positive: thick peptidogylcan wall, semi-permeable membrane, beta-lactamases located in extracellular space
gram negative: thin peptidoglycan wall, contain porins to let drugs through, beta-lactamases in periplasmic space, contain lipopolysaccharides (endotoxins)

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26
Q

Bacterial structure composed of

A

cytoplasmic membrane, peptidoglycan layer, outer membrane, periplasmic space

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27
Q

Cytoplasmic membrane

A

acts as selective barrier
certain drugs must pass through to reach target site

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28
Q

Peptidoglycan layer (cell wall)

A

GP: thick, GN: thin
permeability barrier for large molecules
PBPs: proteins essential for cell-wall synthesis

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29
Q

Outer membrane (gram-negative)

A

lipopolysaccharides: mediator of immune response and sepsis
porins: hydrophilic chanels the permit diffusion of essential nutrients and small hydrophilic molecules

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30
Q

Periplasmic space

A

compartment between cell membrane and cell wall (GP) or between cell membrane and outer membrane (GN)
vital for bacterial protein secretion, folding, quality control; acts as reservoir for virulence factors

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31
Q

Penicillin binding proteins (PBPs)

A

these are enzymes vital for cell wall synthesis, cell shape, and structural integrity - transpeptidases, carboxypeptidases, endopeptidases
differ from one bacterial species to another
binding to PBPs 1A, 1B, 2, and 3 result in bactericidal effect
transpeptidase most important PBP - catalyzes the final cross linking in the peptidoglycan structure

32
Q

Intrinsic resistance

A

always resistant to given antibiotic (naturally resistant)
MOA: absence of target site, bacterial cell impermeability
ex. cephalosporins vs enterococci; beta-lactams vs mycoplasma

33
Q

Acquired resistance

A

initially susceptible but develop resistance due to some mechanism
MOA: mutation in bacterial DNA (spontaneously vs selective pressure); asquisition of new DNA (chromosomal or extrachromosomal plasmid)
ex. stable depression of AmpC; acquisition of KPC gene in GNRs

34
Q

Acquired resistance - plasmids

A

self-replicating, extrachromosomal DNA; transferable between organisms

35
Q

Acquired resistance - transposons

A

genetic elements capable of translocating from one location to another; move from plasmid to chromosome or vice versa

36
Q

Acquired resistance - phages

A

viruses that can transfer DNA from organism to organism

37
Q

Acquired resistance - conjugation

A

direct contact or mating via sex pili
most common

38
Q

Acquired resistance - transduction

A

transfer of genes between bacteria by bacteriophage

39
Q

Acquired resistance - transformation

A

transfer or uptake of “free floating” DNA from the environment

40
Q

Mechanisms of antibiotic resistance

A

4 different mechanisms:
1. altered cell wall protein/decreased porin production
2. efflux pump (pump it out)
3. drug-inactivating enzyme
4. modified drug target
don’t let it in, pump it out, chew it up, change it up

41
Q

Enzymatic inactivation: beta-lactamase

A

enzymes that hydrolyze beta-lactam ring by splitting amide bond: inactivates drugs
two classification systems: ambler class, bush-jacoby medeiros

42
Q

Two types of beta-lactamase

A

serine beta-lactamase: serine residue at active site
metallo-beta lactamases: zinc residue at active site

43
Q

Serin beta-lactamase MOA

A

serine active site creates acyl-enzyme complex through acylation –> through de-acylation, we open up the beta-lactam ring –> opening it up inactivates the beta-lactam antibiotic
restores beta-lactamase

44
Q

Metallo-beta-lactamase MOA

A

open up the ring and inactivate the beta-lactam antibiotic

45
Q

Beta-lactamase types

A

extended spectrum beta lactamases (ESBL)
serine carbapenemases
metallo-beta-lactamases
cephalosporinases
OXA-type

46
Q

Extended spectrum beta lactamases (ESBL) enzyme example

A

CTX-M-15
hyrdolyze narrow and extended spectrum beta-lactam antibiotics
(bacteria that carry these enzymes are resistant to these antibiotics)

47
Q

Serine carbapenemases enzyme example

A

KPC-1, KPC-2, KPC-3
hydrolyze carbapenems, cephalosporins, and penicillins

48
Q

Metallo-beta-lactamases enzyme example

A

NDM-1
hydrolyze carbapenems

49
Q

Cephalosporinases enzyme example

A

Amp-C
inducible

50
Q

OXA-type enzyme example

A

OXA-48
hydrolyze oxacillin, oxyimino beta-lactams, and carbapenems

51
Q

Ambler class A: ESBLs

A

Plasmid-mediated enzymes that hydrolyze most penicillins, cephalosporins, and monobactams - Do not inactivate non-beta-lactam agents (eg. ciprofloxacin, doxycycline, gentamicin); Organisms with ESBL genes often harbor additional resistance genes
CTX-M enzyme most common: Most prevalent in Escherichia coli, Klebsiella pneumoniae/oxytoca, and Proteus mirabilis; Ceftriaxone non-susceptibility
Treatment of choice: Carbapenems (meropenem, imipenem, doripenem, ertapenem) Piperacillin/tazobactam an option for urinary source only

52
Q

Ambler class A: carbapenemase

A

Most frequent cause of Carbapenem-resistant Enterobacterales (CRE) - Resistance to whole beta-lactam class
Klebsiella pneumonia carbapenemase (KPC) - Plasmid-mediated enzyme; KPC-2 & KPC-3 most common variants; Found in: K. pneumoniae, K. oxytoca, E.coli, E. cloacae, E. aerogenes, P. mirabilis
Treatment options:
◦ β-lactam: ceftazidime/avibactam, meropenem/vaborbactam,
imipenem/cilastatin/relebactam
◦ Non β-lactam: Plazomicin, eravacycline, omadacycline

53
Q

Ambler class B: metallo-beta-lactamases

A

Confer resistance to all β-lactams except monobactams (aztreonam) - Harbor additional antibiotic-resistance genes to other antimicrobial classes
Examples: New Delhi MBL (NDM) - Present in P. aeruginosa, Acinetobacter spp, and Enterobacterales
Treatment options: Limited!; Not inhibited by any current β-lactamase inhibitors; Cefiderocol; aztreonam + ceftazidime/avibactam

54
Q

Ambler class D: OXA-type

A

Large heterogenous group often accompanied by other beta-lactamase classes (e.g., co-expression of ESBLs and AmpC)
Primarily found in Acinetobacter baumannii (A. baumannii), Pseudomonas aeruginosa and some Enterobacterales, such as Klebsiella pneumonia
Treatment options: Extremely limited; Cefiderocol; Sulbactam/durlobactam

55
Q

Ambler class C: AmpC

A

Three different mechanisms:
◦ 1) inducible via chromosomally encoded AmpC genes
◦ 2) Non-inducible chromosomal resistance via mutations (rare)
◦ 3) Plasmid-mediated resistance
Not inhibited by older β-lactamase inhibitors (clavulanic acid, tazobactam, sulbactam); Inhibited by newer β-lactamase inhibitors: avibactam, vaborbactam, relebactam
Found in: Hafnia alvei, Enterobacter cloacae, Citrobacter freundii, Klebsiella aerogenes, Yersinia enterocolitica (HECK-YES); Also in Serratia marcescens, Morganella morganii, Aeromonas hydrophilaà HECK-YES Ma’aM
Referred to as AmpC or inducible organisms

56
Q

AmpC induction mechanism

A

Transient elevation in enzyme production in the presence of certain beta-lactam agents
Initially, gene for beta-lactamase production is repressed –> inducer –> gene derepressed –>
increased beta-lactamase production
Remove inducer –> gene repressed –> beta-lactamase production back to low level
Genetic mutation –> gene derepressed –> stable derepression –> high level beta-lactamase production continuously
Different beta-lactams induce AmpC beta-lactamases to varying degrees

57
Q

AmpC inducers

A

ceftriaxone is a weak inducer, with high susceptibility to ampC hydrolysis
cefepime is a weak inducer, with low susceptibility to ampC hydrolysis
carbapenems (imipenem, meropenem, ertapenem) are strong inducers, with low susceptibility to ampC hydrolysis
cefepime is 1st line –> carbapenems

58
Q

Selection and treatment of stably derepressed mutants

A

Treatment: Cefepime(1st-line), Carbapenems, Non-β-lactams (Fluoroquinolones, trimethoprim/sulfamethoxazole, tetracyclines)

59
Q

Enzymatic inactivation: aminoglycoide-modifying enzymes

A

Most common method of aminoglycoside resistance
3 mechanisms: Acetylation, Nucleotidylation, Phosphorylation
Modify aminoglycoside structure by transferring the indicated chemical group to a specific side chain –> impairs cellular uptake and/or binding to ribosome
Nomenclature based on chemical group transferred and site of transfer
Bifunctional enzyme –> acetylation and phosphorylation of aminoglycoside
Seen in Enterococci –> high level of gentamicin resistance

60
Q

Altered target site: cell wall precursor

A

Mechanism of vancomycin resistance in Enterococci species
Vancomycin binds to D-Alanine-D-Alanine terminus of peptidoglycan precursors: Inhibits cell wall synthesis
Resistance alters D-Ala-D-Ala to D-Ala-D-Lac or D-Ala-D-Ser: Mediated by VanA or VanB gene –> most common; Produces vancomycin-resistant enterococcus (VRE)
Treatment: Daptomycin or linezolid

61
Q

Altered target site: penicillin binding proteins (PBPs)

A

Alterations in PBPs leads to β-lactam resistance
Due to decreased affinity of PBPs for antibiotic or change in amount of PBP produced by bacteria - Addition of β-lactamase inhibitor is ineffective in restoring activity of β-lactam antibiotic
Methicillin-resistant Staphylococcus aureus (MRSA): Resistance due to expression of mecA gene (mecA + = PBP2A + = MRSA)
◦ Encodes for PBP2A –> low affinity for beta-lactam antibioticsà resistance to β-lactam class with 2 exceptions (see below)
Treatment: Ceftaroline, Ceftobiprole; vancomycin, daptomycin, linezolid
Streptococcus pneumoniae: Alteration in PBP confers penicillin and cephalosporin resistance

62
Q

Altered target site: ribosomal target

A

Responsible for macrolide resistance in S. pneumoniae: ermB gene –> cross resistance with clindamycin
Aminoglycoside resistance in Gram negatives Clindamycin resistance

63
Q

Altered target site: DNA gyrase/topoisomerase IV

A

Responsible for Fluoroquinolone (ciprofloxacin, levofloxacin) resistance in Gram-negative and S. pneumoniae

64
Q

Efflux pumps

A

actively transport antibiotics OUT of periplasmic space: overexpression can lead to high-level of resistance; Efflux is important for a range of antibiotic classes
Important resistance mechanism for P. aeruginosa against carbapenems & S. pneumoniae against macrolide antibiotics

65
Q

Porin channels

A

are hydrophilic diffusion channels
Rate of antibiotic diffusion depends on porin & antibiotic physiochemical characteristics - smaller, more hydrophilic antibiotics pass easier than larger, hydrophobic antibiotics
Mutations result in loss of specific porins –> leads to antibiotic resistance - Most commonly seen with Enterobacterales and carbapenem-resistant P. aeruginosa

66
Q

Cidal vs static

A

In vitro terms not based on linkage to any predictive ability in vivo
Not always a clear distinction: some bactericidal drugs may be static against certain organism and vice versa
Bactericidal agents still preferred for certain infections (meningitis, endocarditis)
Important to optimize dose based on patient factors, site of infection, and organism

67
Q

Concentration dependent

A

Exert effect when concentrations well above organism’s MIC: ↑Cmax/MIC = greater killing –> correlates with increased AUC
Some agents, such as fluoroquinolones and aminoglycosides exhibit PAE: Gram-positive and Gram-negative bacteria
Fluoroquinolones (Levofloxacin, Ciprofloxacin): Concentration-dependent bactericidal activity –> fAUC0-24/MIC
Aminoglycosides (Gentamicin, Tobramycin, Amikacin): Concentration-dependent bactericidal activity –> Cmax/MIC; Optimal dosing achieved through TDM and use of high dose extended interval

68
Q

Time-dependent

A

All β-lactam antibiotics (penicillin, cephalosporin, carbapenem, monobactam)
Time that free drug concentrations remain above MIC correlates with clinical and
microbiological outcomes (fT>MIC)
fT>MIC Penicillin: 50%
fT>MIC Cephalosporin: 60-70%
fT>MIC Carbapenem: 40%
Antibacterial properties: Not rapidly bactericidal; Time-dependent bactericidal activity; Little to no PAE

69
Q

Beta-lactam dosing optimization

A

Maximize fT>MIC (as a % of dosing interval): Gram-negatives: Carbapenems: ≥40%; Penicillins: ≥50%; Cephalosporins: ≥ 60%; Gram-positive: ≥40-50%
Strategies to maximize fT>MIC: Increase dose, same interval (1g Q8h vs. 2g q8h); Same dose, shorter interval (1g Q12h vs. 1g Q6h); Continuous infusion: Stability issues; need dedicated IV line
Prolonged infusions: Infuse dose over 3-4 hours; Provides longer T>MIC than traditional infusions

70
Q

AUC/MUC dependent (vancomycin)

A

Time-dependent bactericidal activity; very long PAE for Gram-positive organisms
PD Target: AUC0-24/MIC
Goal AUC0-24/MIC ≅ 400-600
Prolonged, elevated AUC0-24/MIC ≥ 600-700 mg*h/L is a risk factor for nephrotoxicity
Dosing is patient-specific and achieved through TDM using Bayesian programs

71
Q

Aminoglycosides PK/PD

A

concentration dependent
predictive PK/PD parameter: peak/MIC, AUC/MIC
cidal

72
Q

Beta-lactams PK/PD

A

time-dependent
predictive PK/PD parameter: T>MIC
cidal

73
Q

Daptomycin PK/PD

A

concentration-dependent
predictive PK/PD parameter: AUC/MIC, peak/MIC
cidal

74
Q

Fluoroquinolones PK/PD

A

concentration dependent
predictive PK/PD parameter: AUC0-24/MIC
cidal

75
Q

Vancomycin PK/PD

A

time dependent
predictive PK/PD parameter: AUC0-24/MIC
cidal (slowly)

PHRM 865 (12 decks)

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