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Boards: SIRS/sepsis/MODS > Bacterial infections and Abx > Flashcards

Bacterial infections and Abx Flashcards

1
Q

Describe the layers of gram positive and gram negative bacterias’ cell wall

A

gram positive:
* thick outer peptidoglycan wall and one inner phospholipid membrane

gram negative
* thin peptidoglycan wall surrounded by an inner and an outer phospholipid membrane
* lipopolysacchardie layer on the outside

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2
Q

What are the most common Staph bacteria isolated from dogs and cats?

A

dogs: Staphylococcus pseudointermedius, S. schleiferi
cats: S. pseudointermedius

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3
Q

Which Staph species indicates transfer from people?

A

Staphylococcus aureus

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4
Q

What are the most common bacteria to cause postsurgical infections?

A

Staphylococcus

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5
Q

Name 2 bacteria producing urease enzymes, leading to struvite infections

A

S pseudointermedius
Proteus mirabilis

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6
Q

Which S species are coagulase positive versus negative? What does this indicate?

A

S pseudointermedius - coagulase positive
S schleiferi - depending on subsp can be either
S aureus - most coagulase positive

virulence factor - low virulence if negative
coagulase induces blood clotting and fibrin clots covering bacteria can help avoid phagocytosis

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7
Q

How do Staph appear microscopically?

A

perfectly round and clustered

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8
Q

How do Streptococcus bacteria appear on cytology?

A

round and in chains

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9
Q

What does usually determine the virulence of Streptococci?

A

differentiate between
* alpha (partial) hemolytic
* beta (complete) hemolytic
* gamma (non) hemolytic

beta hemolytic bacteria most virulent

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10
Q

What is the most common Streptococcus species isolated in dogs and cats?

A
  • Streptococcus canis

beta-hemolytic
part of the normal canine flora
can cause pneumonia, UTIs, wound infections

associated with toxic shock syndrome and necrotizing fasciitis

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11
Q

Why are Fluoroquinolones use contraindicated in Streptococcus canis infections?

A

can induce bacteriophage and increase the risk of toxic shock syndrome and necrotizing fasciitis

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12
Q

What bacteria has been associated with outbreaks of hemorrhagic pneumonia in dogs in shelter setting?

A

Streptococcus equi subsp zooepidemicus

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13
Q

What are the most common Enterococcus isolates in dogs and cats, where are they normal inhabitants?

A

E faecalis
E faceium

gastrointestinal tract

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14
Q

What are infections caused by Enteroccous and how are they treated?

A

UTIs, cholangiohepatitis, wound infections

E. faecalis - less resistant, tx of choice penicillin
E. faecium - more resistant

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15
Q

What classes of abx are enteroccus species generally resistant to?

A
  • cephalosporins
  • fluoroquinolones
  • low dose aminoglycosides
  • sulfonamides
  • macrolides
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16
Q

What are 3 members of the Actinomycetales order?

A
  • Actinomyces
  • Nocardia
  • Mycobacterium

Actinomyces - normal oral flora
Nocardia and Mycobacterium - environemnt

Actinomyces/Nocardia common pyothorax isolates
Mycobacterium infections rare

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17
Q

What is the treatment of choice for Actinomyces, Nocardia, or Mycobacterium?

A

Actinomyces - Penicillin, high dose and frequency
Nocardia - TMS
Mycobacterium - macrolide (clarithromycin)

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18
Q

What predisposes to Clostridium difficile diarrhea?

A

previous abx tx

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19
Q

What is caused by adherent-invasive E.coli? How is the condition treated?

A

Granulomatous colitis
enrofloxacin at 10-20 mg/kg q24h for 8 weeks

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20
Q

What is Pseudomonas aeruginosa resistant to and how are infections treated?

A

Resistant to:
* aminopenicillins
* most cephalopsorins
* TMS
* chloramphenicol
* tetracyclines
* often acquired resistance to aminoglycosides and fluoroquinolones

treatment with anti-pseudomonal beta-lactams i.e., ceftazidime, pipercaillin => reserve for life-threatening systemic infections

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21
Q

What Pasteurella spp. are isolated in dogs and cats and what kind of infections do they usually cause?

A

P. multicide, P. canis => normal flora of oral cavity and upper respiratory tract

can cause bite wound infections and pneumonia

best tretment: penicillins or aminopenicillins

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22
Q

What is the most sensitive diagnostic for Bartonellosis?

A

PCR followng enrichment culture

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23
Q

What is increaesed time to antibiotic therapy in sepsis associated with?

A
  • increased mortality
  • increased rate of AKI
  • increased rate of organ dysfunction
  • increased length of hospitalization
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24
Q

Explain how to use the MIC information for dosing regiments of time-dependent or concentration dependent antibiotics

A

Minimum inhibitory concentration - i.e., the lower the MIC the more susceptible

time-dependent abx - reversibly act on abx - i.e., want to minimize the time the plasma cc is less than MIC
* fT > MIC is the percent of time the plasma drug concentration is above the MIC
* ideally 100% for critically ill patients
* non critically ill: 50-60% penicillins, 60-70% cephalosporins, 30-40% carbapenems

concentration-dependent abx - irreversibly bind to abx
* want Cmax to be over MIC
* post-antibiotic effect
* Cmax:MIC should be 8 in critically ill patients

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25
Q

Explain how fluid overload may alter the PK of antibiotics and how to address this

A

increases the Vd - especially for hydrophilic antibiotics (e.g., beta lactams)
=> lower plasma cc => lower target tissue cc

  • increase dose and frequency for time-dependent abx
  • increase dose for concentration-dependent abx
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26
Q

Explain how hypoalbuminemia may affect the PK of abx

A
  • increases the volume of distribution for hydrophilic abx
  • increases renal clearance for abx that are usually mostly protein-bound
  • increases fraction of free/active compound

net effect of hypoalbuminemia
* time-dependent => decreased efficacy because of fast elimination
* concentration-dependent => increased efficancy due to increased Cmax

  • time-dependent antibiotics => increase dose or frequency
  • concentration-dependent => no change needed
  • not highly protein-bound => no change needed
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27
Q

In what ways can kidney disease affect antimicrobial PK?

A

AKI
* decreased renal clearance
* incresed fT>MIC
* higher risk of toxicity
* if high therapeutic index => likely safe, if narrow therapeutic index => frequency reduction or avoid drug overdose

Augmented renal clearance (ARC)
* may need to increase dose and frequency
* difficult to identify - need to measure renal creatinine clearance (>120-150 mL/minute people)

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28
Q

How does hepatic disease affect antimicrobial PK?

A

hepatic dysfunction would need reduction of at least 90% of metabolic capacity to substantially alter antimicrobial clearance

unlikely to play a role in most patients

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29
Q

Which group of beta lactams is MRSA resistant to?

A

all, except 5th gen cephalosporin (ceftaroline)

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30
Q

Name 4 classes of beta lactams

A
  • penicillins
  • cephalosporins
  • monobactams
  • carbapenems
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31
Q

Are beta lactams bacteriostatic or bactericidal?

A

bactericidal

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32
Q

Describe how beta lactams excert antibiotic properties

A

beta-lactam rings binds to penicillin-binding protein (PBP) –> inactivates transpeptidase enzymes –> bacteria can not build peptidoglycan layer –> defects –> permeability –> lysis

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33
Q

Name 4 ways of beta lactam resistance by bacteria

A
  • antimicrobial efflux pump
  • changes to porins in cell walls
  • PBP mutation
  • beta-lactamases
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34
Q

Name 4 systems of beta-lactamases

A
  • penicillinases
  • AmpC-type cephalosporinases
  • extended spectrum beta-lactamases
  • carbapenemases
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35
Q

How does MRSA exert its resistance

A

PBP2a mutation - beta-lactam ring cannot bind

MacA gene

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36
Q

Explain how beta lactams distribute in tissues. Which tissues do not typically achieve high concentration?

A

hydrophilic weak acid => cannot cross cell membranes, stays in EC space but with high Vd - interstitial cc will reach same as serum levels

tissue exceptions: ocular, reproductive, CNS

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37
Q

How are beta lactams excreted?

A

urine - high cc in urine!

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38
Q

Name 2 beta-lactams with a higher half-life

A

cefpodoxime
cefovecin

high protein-binding

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39
Q

Compare the spectrum of:
* penicillin
* aminopenicillins
* 1st through 5th gen Cephalosporins

A
  • Penicillin - gram positive and anaerobic but minimal gram negative
  • aminopenicillins - same gram positive and anerobic but better gram negative than penicillin
  • 1st gen ceph: good gram positive, gram neg similar to aminopenicillins
  • 2nd gen ceph: moderate gram pos and neg coverage, increased anerobe spectrum compared to 1st gen ceph
  • 3rd gen ceph: broad spectrum, resistant against many beta-lactamases, ceftazidime covers P. aeroginosa and can reach CSF
  • 4th gen ceph: good against enteric organism
  • 5th gen ceph: covers MRSA
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40
Q

List examples for the 5 generations of cephalosporins

A
  • 1st gen: cefazolin, cephalexin
  • 2nd gen: cefoxitan
  • 3rd gen: cefpodoxime, cefovecin, ceftiofur, ceftazidime
  • 4th gen: cefquinome
  • 5th gen: ceftaroline
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41
Q

What is the coverage of monobactams?

A

gram negative

poor gram pos or anaerobe coverage

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42
Q

List 2 examples of carbapenems and compare their risks of adverse effects

A

imipenem
maropenem

imipenem nephrotoxic and can cause seizures

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43
Q

Compare the efficacy of clavulanic acid and sulbactam

A

clavulanic acid is significantly more effective than sulbactam

44
Q

Are aminoglycosides bactericidal or bacertiostatic?

A

bactericidal

45
Q

What is the general coverage of aminoglycosides?

A

good gram negative, some gram positive, no anaerobes

46
Q

What class of antibiotics combines well with aminoglycosides (synergistic effects)?

A

beta-lactams - break the cell membrane and help aminoglycosides reach the intracellular space of bacteria faster

47
Q

Describe how aminoglycosides kill bacteria

A

binding to ribosome 30S subunit - specifically high affinity for the A site on the 16S ribosomal RNA => alters its conformation => tRNA binds => causes mRNA misreading

=> lead to faulty protein synthesis => cessation of ribosomal activity

48
Q

Describe how aminoglycosides cross the cell membranes of bacteria

A

three phases of aminoglycosides crossing cell membrane

Stage I:
positively charged aminoglycosides binding with the negatively charged lipopolysaccharide layer => ionic binding increases wall permeability
(gram pos => ionic binding to phospholipids)

Stage II: small amounts have reached cell and caused faulty protein synthesis => these proteins insert themselves into the cytoplasmic membranes => membrane channels => more aminoglycoside entering
ATP-dependent process

Stage III: large amount of aminoglycosides enter bacterial cells via previously formed channels

49
Q

List the ways bacteria can use to build resistance against aminoglycosides

A
  • aminoglycoside efflux pumps
  • intrinsically resistant: anaerobes - aminoglycosides need O2 for active cell membrane crossing
  • enzymatic mutation of aminoglycosdies - AME (intracellular aminoglycoside modifying enzymes) causing structural modifications rendering aminoglycosides unable to bind to the A site
  • target modification - change of the 16S rRNA - either via mutation or enzymatic modificaiton
50
Q

describe the Vd, bioavailability, protein-binding, and chemical properties of aminoglycoside

A

low volume of distribution
low protein binding
weak base, polar, hydrophilic/water-soluble
poor bioavailability

51
Q

Explain the PK/PD targets for aminoglycosides

A

concentration-dependent abx
want Cmax 8-10 times MIC
or AUC over MIC ration >75

post-antibiotic effect - suspected to be partially from enhancing leukocyte activity

52
Q

Describe how aminoglycosides excert renal damage

A

freely filtered by the glomerulus - some reabsorbed in the proximal tubules - enter cells via pinocytosis => causes necrosis of the tubular cells due to changes in water and solute transport

sloughing tubular cells create casts –> can obstruct tubules and increased pressure within the bowman’s space –> decreasing GFR

53
Q

List the following by most to least nephrotoxic: amikacin, gentamicin, tobramycin

A

dog: gentamicin, tobyamycin, amikacin
cats: tobramycin, gentamicin, amikacin

54
Q

What conditions can increase the risk of nephrotoxicity from aminoglycosides?

A
  • preexisting renal disease, e.g., CKD
  • concurrent drug administration with renal effects (e.g., NSAIDs)
  • conditions lowering GFR (pregnancy or old age)
  • metabolic acidosis - will increase tubular uptake
55
Q

What are the recommended trough concentrations for amikacin and gentamicin?

A

amikacin < 2.5 mcg/mL
gentamicin < 1 mcg/mL

56
Q

list ways to monitor patients for nephrotoxicity when receiving aminoglycosides

A
  • UA - glucosuria (w/o hyperglycemia) or proteinuria
  • granular casts

biomarkers: uNGAL, uNGAL to creatinine ratio, urinary cystatin C

57
Q

Other than the kidneys, what other organ systems may be affected by adverse effects from aminoglycosides?

A
  • ototoxicity - taken up by cells in the ears and causing necrosis,
  • CSN - impairment of Ca release at the neuromuscular junction - neuromuscular blockage
58
Q

Are fluoroquinolones bacteriostatic or bactericidal?

A

bactericidal

59
Q

Describe in detail how Fluoroquinolones affect bacteria. Which effect targets gram neg versus pos bacteria?

A

DNA gyrase and Topoisomerase IV inhibition - * DNA gyrase needed for DNA supercoiling regulation => unable to transcript DNA normally
* Topoisomerase needed for unlinking DNA following replication (daughter cell replication)

  • DNA gyrase inh - gram neg
  • Tropoisomerase IV inh - gram pos
60
Q

Describe the coverage by fluoroquinolones

Discuss sepcifically:
* gram pos/neg/anaerobes
* Pseudomonas aeruginosa
* Staph and Strep
* tick-borne diseases
* Mycoplasma

A

good against gram neg
some gram pos
no anaerobes except pradofloxacin

  • some efficacy against P aeruginosa - but develops resistance fast
  • Staph susceptible, most Strep resistant
  • tick-borne commonly resistant
  • cane move IC –> so okay for IC bacteria like Mycoplasma
61
Q

What is the oral bioavailability of fluoroquinolones, how are they metabolized, and excreted?

A

great bioavailability

metabolized by the liver - cytochrome P450 pathway
excreted some in bile, mostly in urine

62
Q

Are fluoroquinolones hydrophilic or lipophilic, how is their protein-binding and volume of distribution?

A

lipophilic
high Vd - i.e., distributes well into tissues
protein-binding variable (18%-35%)

63
Q

How do antiacids affect enrofloxacins bioavailability?

A
  • Sucralfate dose not affect it
  • polyvalent cation antacids (e.g., mg, aluminum, Ca, etc.) can interfere
64
Q

What are the PK targets of fluoroquinolones?

A

AUC24/MIC > 125
Cmax:MIC >10
AUC/MPC > 32-39 (depending on which fluoroquinolones)

MPC mutant prevention concentration

65
Q

What are mechanisms by which bacteria become resistant to fluoroquinolones?

A
  • increased efflux
  • alterations of the antimicrobial targets (point mutations)
66
Q

In what conditions are fluoroquinolones acceptable first-line agents?

A
  • pyelonephritis
  • prostatitis
  • say pneumonia here, but check with consensus
  • hepatobiliary infection suspected to not be anaerobe (unless prado used in cats) and neither Enterococcus induced
67
Q

List adverse effects of fluoroquinolones

A
  • GI
  • seizures/tremors
  • cartilage defects in juveniles
  • irreversible blindness in cats
68
Q

How are fluoroquinolones suspected to cause seizures

A

competitively inhibit GABA binding

69
Q

What can too rapid IV infusion of fluoroquinolones cause?

A

histamine release

70
Q

What is the primary metabolite of enrofloxacin?

A

cirpofloxacin

71
Q

What is a specific adverse effect of pradofloxacin in dogs?

A

bone marrow suppression

72
Q

What is mitronidazole’s Vd, bioavailability and tissue penetration?

A

high bioavailability (50-100%)
good tissue penetration and high Vd (reaches CSF and crosses BBB)

73
Q

What class of antibiotic does Metronidazole belong to?

A

nitroimidazoles

74
Q

Is metronidazole
* time-dependent/concentratio-dependent?
* bacteriostatic/bactericidal?

A

cc-dependent
bactericidal

75
Q

How does metronidazole assert its action on bacteria?

A
  • reduced by enzymes in the bacteria => produced product incoorporates into the DNA => cell death
76
Q

What is the spectrum of metronidazole?

A

only anaerobes - nitrous reduction of metronidazole can only happen in anaerobic bacteria

also protozoals - but higher dosages (i.e., risk of CNS signs)

77
Q

List the adverse effects of Metronidazole

A
  • GI upset
  • CNS toxicity (ataxia, nystagmus, tremors, etc.)
78
Q

What is the mechanism of action of Chloramphenicol, is it bacteriostatic or bactericidal?
What other classes of antibiotics have the same mechanism of action?

A

bacteriostatic (time-dependent)
binds to the 50S ribosomal subunit - blocks elongation

same binding site: clindamycin, macrolides

79
Q

What is the reason for Chloramphenicol’s high risk of toxicity?

A

it inhibits mitochondrial protein synthesis in mammalian cells (especially erythropoietic cells)

80
Q

What is the spectrum of Chloramphenicol?

A

gram +/- and anaerobes

but common resistancies

81
Q

What is the bioavailability, Vd and metabolism/excretion of Chloramphenicol?

A

good bioavailability, high Vd, most tissues except prostate only 60%
metabolized by liver - glucuronidation –> cats more sensitive to toxicities
renal excretion - inactive form

82
Q

What class of antiobitics is clindamycin? Is is bacteriostatic/bactericidal, concentration/time dependent?

A

Lincosamide

bacteriostatic, time-dependent

83
Q

What is the spectrum of clindamycin?

A

gram positives
anaerobes
Myocplasma

84
Q

How is the tissue distribution of Clindamycin?

A

good distribution - therapeutic levels in CNS (toxoplasmosis!) - penetrates BBB

85
Q

What is the mechanism of action of tetracyclines?

A

binds to the ribosomal 30S subunit - blocks tRNA bindings and elongation

86
Q

Name an additional effect of doxycycline besides antimicrobial

A

inhibits matrix metalloproteinases - can potentially help in delayed wound healing but not proven

87
Q

List the spectrum of tetracyclines

A

Gram pos, neg
vector-borne rickettsial
anaerobes
intracellular bacteria (E.g., mycoplasma)

88
Q

What is the bioavailability, Vd, lipophilic/hydrophilic, and protein-binding of tetracyclines? How are they eliminated?

A

high bioavailability
high Vd
lipophilic
high protein-binding (99%)

unknown elimination (suspect hepatobiliary and enteric), only 19% in urine

89
Q

List adverse effects of tetracyclines

A

esophagitis with subsequent strictures
GI upset
enamel discoloration of erupting teeth
thrombophlebitis from IV
rare: hepatotoxicity

90
Q

What is the mechanism of action of TMS, is it bacteriostatic or bactericidal?

A

bactericidal in combination (time-dependent)
sulfadiazine and trimethoprim each alone would be bacteriostatic

causes inhibition of the folic acid production
* sulfonamide => competetive analog to P aminobenzoic acid (PABA)
* trimethoprim inhibits folic acid reduction

target different parts of the folic acid pathway

91
Q

What is the ratio of TMS combination products?

A

1:5 trimethoprim to sulfonamide

92
Q

What is the spectrum of TMS? How does it distribute in tissue?

A

gram +/-, anaerobes
ineffective against mycoplasma, P aeruginosa, rickettsial disease

good tissue distribution - sulfonamide reaches CNS, trimethoprim reaches prostate

93
Q

How is TMS excreted?

A

renally - good for UTIs

94
Q

List the adverse effects of TMS

A
  • KCS
  • immune-mediated disease
  • hypersensitivity reactions (fever, pancreatitis, glomerulonephritis, etc.)
95
Q

What are the most concerning adverse effects of nitrofurantoin?

A

dogs - irreversible neuropathy, severe, occurs delayed
cats - causes glutathione instability and can cause hemolysis

96
Q

How should rifampin be administered?

A

always with another antibiotic! - otherwise resistance develops quickly (within 2 days)

97
Q

What are the three types of resistance?

A
  • inherent resistance (e.g., anaerobes to aminoglycosides)
  • circumstantial resistance - i.e., culture says susceptible but not effective in vivo
  • acquired resistance - phenotypic changes
98
Q

How are multidrug resistant organisms (MDRO) defined?

A

resistant to at least 1 agent in 3 or more classes of antibiotics

99
Q

What are XDR and PDR drugs?

A

XDR - extensively drug resistant - susceptible to only one or two classes of antimicrobials
PDR - pan drug resistant - resistant to all known licensed antimicrobials

100
Q

What are risk factors for MDR infections?

A
  • previous antimicrobial administration
  • hospitalization
  • duraiton of ICU stay
  • surgical procedures
  • MV
  • predisposing diseases
101
Q

What is the primary mechanism of acquired resistance by MRS?

A

acquisition of the mecA gene

102
Q

What are MRS resistant to and what are options for empirical abx tx?

A
  • all beta lactams except cetaroline (5th gen)
  • frequently resistant to: clindamycin, fluoroquinolone, macrolides, TMS

empiric: vancomycin, aminoglycosides (but not good at penetrating purulent material or cellular debris)

103
Q

What are Enterococci typically resistant to?

A
  • cephalosporins
  • clindamycin
  • aminoglycosides
  • Fluoroquinolones
  • Carbapenems (E. faecium)
104
Q

What are treatment options for Enterococcus spp.?

A
  • Vancomycin
  • combination of gentamycin and ampicillin

Note: Enterococcus spp. are not highly pathogenic, so treatment may not be always necessary
Note: don’t use amikacin or tobramycin with ampicillin - not synergistic

105
Q

Which antibiotics is Pseudomonas aeruginosa most susceptible to?

A
  • meropenem
  • amikacin
106
Q

What antibiotics is Pseudomonas aeruginosa typically resistant to?

A

almost all beta-lactams except piperacillin, ceftazidime, carbapenem

107
Q

Compare the resistance of beta-lactamases versus ESBLs

A

beta-lactamases: penicillins, aminopenicillins, carboxypenicillins, narrow-spectrum cephalosporins

ESBLs: also third-gen cephalosporins

Tx of choice: carbapenems

Boards: SIRS/sepsis/MODS (9 decks)

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