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INFECTIOUS DISEASE > EXAM #1- Dr Aeschlimann Material > Flashcards

EXAM #1- Dr Aeschlimann Material Flashcards

1
Q

List at least four (4) examples of Specific Activities that are part of an Antimicrobial Stewardship Program.

A

Specific Activities of ASPs
• Formulary Antimicrobial Product Selection, Use Restrictions and/or Pre-Authorizations
• Educational initiatives
• Guideline and Clinical Pathway
Development
• Prospective assessment of antimicrobial use: • Optimal therapy for each unique patient

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2
Q

What is meant by “EMPIRIC” antimicrobial therapy?

A

It means broad spectrum anti-microbial therapy.

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3
Q

What is meant by “TARGETED” or “STREAMLINED” antimicrobial therapy?

A

Therapy aimed at specific microbia.

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4
Q

What is the significance of an increased white blood cell count (WBC) when:
• There is a predominance of neutrophils?

A

Predominance of Bacterial or fungal infection

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5
Q

What is the significance of an increased white blood cell count (WBC) when:
• There is a predominance of monocytes?

A

Usually viral infection

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6
Q

What is the significance of an increased white blood cell count (WBC) when:
• There is a predominance of esosinophils?

A

Allergic response

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7
Q

What is the significance of an increased white blood cell count (WBC) when:
• There is an increase in “bands” aka
“shift to the left”?

A

That means there is an increase in the number of immature neutrophils released. It means the body is trying to fight off a very active infection and immature new red blood cells are released early to counteract the infection.
Typically associated with a bacterial infection.

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8
Q

Give at least one example of:

When the WBC count may be elevated when there is NO infectious process

A

leukemia, rheumatoid arthritis, drug therapy (lithium, steroids, G-CSF)

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9
Q

Give at least one example of:

•When the WBC count may be normal or decreased when there IS an infectious process

A

Elderly, overwhelming sepsis, chemotherapy patients, Localized, mild, ”smoldering” infections (e.g., osteomyelitis)

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10
Q

What are the strengths of Gram Staining?

A

Rapid
• Cheap, easy to perform
• Can significantly narrow down list of possible pathogens for certain
infections

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11
Q

What are the limitations of Gram Staining?

A

Issues with sensitivity & specificity:
• Can get a “negative” gram stain of a sample from a patient with a real infection
• Can get a “positive” gram stain of a sample if contaminated

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12
Q

What does the result of a Catalase Test tell you about a gram-positive cocci (Catalase “positive” vs. Catalase “negative”)?

A

It tells you wether it is STAPH or STREPTO/ENTER
Staphylococci [Catalase (+)]
Streptococci/Enterococci [Catalase (-)]

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13
Q

What does the result of a Coagulase Test tell you about a Staphylococcal isolate (Coagulase “positive” vs. Coagulase “negative”)?

A

Differentiation of Staphylococci:
• Staphylococcus aureus [Coagulase (+)]
• Staphylococcus epidermidis [Coagulase (-)]

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14
Q

What are three examples of gram-negative aerobic bacteria that are Lactose Fermenter “positive” and Oxidase “negative”?

A

E. coli, Klebsiella, and Enterobacter

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15
Q

what is one example of gram positive cocci that is catalase negative and gives BETA hemolysis?

A

Streptococcus pyogenes

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16
Q

What is one example of gram-positive cocci that is catalase negative and gives ALPHA hemolysis (Incomplete) ?

A

Streptococcus viridians, Streptococcus pneumoniae

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17
Q

What is one example of gram-positive cocci that is catalase negative and gives GAMMA hemolysis (none)?

A

E. faecalis/ E. faecium/ S.bovis

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18
Q

What is the MOST IMPORTANT gram-negative non-lactose fermenter?

A

PSEUDOMONAS

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19
Q

What is an ANTIBIOGRAM? Give an example of how you would use an antibiogram to help you to select empiric antibiotic therapy for a patient with a suspected infection.

A

ANTIBIOGRAM is an aggregated hospital, regional, and/or national epidemiologic data for trends in antibiotic susceptibility/resistance of common bacterial pathogens
It helps you to predict which antimicrobials have the best chance of being “active” against certain bacterial pathogens BEFORE you get any test results back in your specific patient…
EXAMPLE: Pt comes w a UTI infection. The top 5 organisms responsible for UTI are: E. choli, pseudomonas, Klebsiella, proteus and E, faecalis.
Until, we get more data about the specific microorganism, we can pick Zosyn (Piperacillin/tazobactam) since it covers all 5 of them.

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20
Q

What is one of the biggest draws from Cephalosporins?

A

One of the biggest draws from Cephalosporins is that they have no enterococcal activity .

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21
Q

Provide at least TWO clinical scenarios where ORAL antibiotic therapy would be preferred

A
  • Mild infections, outpatient treatment, “step-down” treatment from initial intravenous treatment • Need to assure:
  • Adherence, proper timing of administration, adequate GI absorption
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22
Q

What is the turn around for a rapid test?

A

Less than 24 hours

23
Q

What are rapid tests?

A

Gram staining, Immunologic methods (Ab or Ag detection): antibody titers (atypical bacteria: mycoplasm, chlamydia), ELISA (HIV, HSV), immunofluorescence (CMV), direct fluorescent antibody (legionella), PCR, PNA fish

24
Q

What is the golden rule for all sample collections?

A

All sample collections should be obtained prior to starting anti-microbial therapy

25
Q

whats the turn around time for “slow tests”

A 
2-4 days. Example: lab culture of specific examples and manual bbiochemical tests which can only be done after growing in the lab (1-2 days): 
• Catalase test
• Coagulase test
• Lactose Fermentation • Oxidase Test
• Hemolysis Assessments
26
Q

Provide at least TWO clinical scenarios where INTRAVENOUS antibiotic therapy would be preferred

A

Consider if:

1) inadequately absorbed drugs
2) serious infections (high concentrations needed, GI absorption may be suspect, etc…)
3) Consider if questionable adherence / complex PO regimen

27
Q

In the absence of obvious data that would indicate inappropriate therapy, what is the MINIMUM time that should elapse before considering therapy as “failing”?

A

2-3 COMPLETE DAYS OF THERAPY AT MINIMUM

28
Q

What lab tests / clinical evaluations are routinely done?

A

Vital signs, lung exam, WBC count/differential, Erythrocyte sedimentation rate (ESR), test for C-Reactive protein

29
Q

When do you start antimicrobial therapy?

A

After culture results come back

30
Q

Describe how PNA-FISH testing can help to shorten the time to definitive pathogen identification (be able to create an example case scenario)

A

PNA-FISH Benefit: allows you to switch anti-micobials a day or two later.
E. faecalis—low risk for VRE (vancomycin resistant enterococcii). The vast majority of VRE is E. faecium. If the patient is on Vancomycin and it is not a faecium, you can stop Vancomycin competently. (why-because
E. faecalis is susceptible to many other antibiotics . Hence, you can take narrow your therapy by taking off the broad spectrum Vancomycin and choosing a more streamlined therapy)
If it turns out to be E. faecium, you should look at your therapy and choose at one of the newer anti-gram + drugs to treat your patient, because it is gonna be resistant to most antibiotics except for a couple of new ones (linezolid and daptomycin).

For GRAM (-) , PNA fish allows you to differentiate between E. coli and Pseudomonas.
Pseudomonas is your typical gram negative resistant to most
antibiotics. If it is not pseudomonas, and you have pseudomonas
spectrum on board you can get rid of that. On the other hand, if you
discover it is pseudomonas and you don’t have pseudomonas
therapy, you need to do it asap as you have probably given 2
days worth of obsolete therapy.

31
Q

Describe how you could use the Hemolytic Properties of a bacterium to help you narrow down the possible causative pathogen(s) in an infection and/or to assess the appropriateness of an EMPIRIC antimicrobial regimen (and modify it, if needed

A

Beta = pyrogenes, gamma = faecalis/faecium, alpha = pneumoniae

32
Q

What does the MIC (minimum inhibitory concentration) represent?

A

Lowest concentration of antibiotic that prevents microbial growth

33
Q

Does the Kirby-Bauer (Disk Diffusion Test) provide qualitative or quantitative data on susceptibility? What is a potential limitation of this susceptibility testing method?

A

Qualitative. Potential limitation = takes long time to run, and doesn’t tell us the dose necessary to kill/inhibit the pathogen.

34
Q

What are the advantages and disadvantages of testing susceptibility with the Epsilometer Test (“E-Test”)?

A

Advantage – gives a MIC reading. Disadvantage – expensive.

35
Q 
What do the following classifications of MICs mean:
•	Susceptible (“S”)?
•	Intermediate (“I”)?
•	Resistant (“R”)?
•	No Breakpoint (“N”)?
A
  • Susceptible (“S”)? High probability of therapeutic response
  • Intermediate (“I”)? Lower probability of response, consider the dosing/site of infection. E.g. if u need to treat meningitis in the brain, need something with better classification because hard to get to that site.
  • Resistant (“R”)? High probability of therapeutic failure.
  • No Breakpoint (“N”)? Insufficient data to make a decision, or drug is completely inactive against tested organism.
36
Q

Describe how certain comorbidities such as diabetes, COPD, recurrent infections, obesity, immune deficiencies can impact your selection of antibiotic therapy (and how they generally would impact selection)

A

Diabetes Mellitus:
• Altered IM absorption (DM-associated PVD)
• Altered antibiotic penetration to infection site
COPD, Cystic fibrosis, Frequent Recent Antibiotic Usage:
• Altered pathogen spectrum [often more highly-resistant
pathogens]
Obesity, Cystic Fibrosis, Renal Replacement Therapies, Acute Critical Illness:
• Significantly altered drug pharmacokinetics • Genetic/Acquired Immune Deficiencies:
• degree and type of deficiency influence predisposition for certain types of infections

37
Q

Which types of clinical data/samples are commonly (or uncommonly) used to gauge response of an infection to treatment?

A

“Fever curve” • Vital signs
• Mental status • WBC counts
• Repeat specimen cultures: blood/CSF specimen cultures, (urine/skin/sputum: uncommon)
Radiographic findings

38
Q

When assessing and monitoring for potential antibiotic toxicities, what are at least THREE specific items that you should always consider about the potential antibiotic-related toxicity?

A
  • Know more than just “this drug causes GI upset”!!!
  • Know anticipated frequency and importance in your specific patient
  • Search for known Risk Factors
  • Know usual chronology of toxicity development
  • Know strategies for prevention / risk reduction / management
39
Q

Provide at least TWO hypothetical case examples where changing renal function could have a detrimental impact on the outcome of treating an infection (this could be related to efficacy and/or toxicity).

A

Toxicity due to decreased elimination of drug.

If renal suddenly gets better- too little of dose gets to site, low efficacy.

40
Q

Define the concept of “Class Representative” Susceptibility Testing and identify at least one limitation of this concept.

A

Basically, using one antibiotic (e.g. a fluoroquinolone) and applying that result to other drugs in same class. May miss detection of novel resistance mechanisms

41
Q

What is “Spontaneous Mutation Frequency (SMF)”? What factors influence the SMF? Explain the clinical relevance of the SMF when treating bacterial infections

A

Every bacteria has a quantifiable Spontaneous Mutation Frequency (“SM)
SMF = # of resistant cells / # total cells tested. Varies based on antibiotic type, concentration tested. Bacteria often develop resistance in a step-wise process

42
Q

What are “silent” or “first-step” resistant mutants?

A

Strain of pathogen that gains resistance to antibiotic that previously worked, without being detected.

43
Q

Explain how “first step” antibacterial resistance, coupled with a key limitation of Clinical Microbiology Susceptibility Testing, may cause poor outcomes during the treatment of bacterial infections.

A

Bacteria often develop resistance in a step-wise process… • These first steps can be below the defined breakpoint for “Resistance” via CLSI guidelines…thus giving us wrong susceptibility information and possible poor outcomes.
MIC testing may not reliably detect the presence of antibiotic-resistant subpopulations. Thus, infection may come back without warning when it seems that pt has already been cured.

44
Q

What is “MIC Creep”? Give an example of the clinical importance of MIC creep.

A

Step-wise undetected increase in resistance of pathogen to antibiotic on hospital-wide/world-wide scale. Antibiotic that may have worked for years suddenly stops working in patients at the hospital.

45
Q

Describe the three main ways that a patient can develop an antibiotic-resistant infection

A

1) Receive it as a “gift” – from infected people through direct contact, or contaminated objects, ingestion of contaminated food.
2) Random gene mutations in the pathogen.
3) Antibiotic-resistant bacteria transfer their resistance to other bacteria.

46
Q

Describe the key scientific factors that help to explain why selection of resistant mutants from a patient’s own microbiome can commonly occur upon exposure to an antibiotic

A

You kill off the weak bacteria while the resistant ones survive and grow up to higher total numbers.

47
Q

Describe the 3 specific mechanisms for common clinically-significant antibiotic resistance.

A

1) Decreasing penetration of antibiotic into the cell.
a. Loss of porin protein channels (high-level resistance, chromosomal, constitutive)
i. E.g. Carbapenem resistance in Pseudomonas due to loss of porin
b. Increased production of efflux pump proteins (low-level resistance, chromosomal, either inducible or constitutive)
i. E.g. macrolide resistance in strep pneumoniae via the “Mef” EPP
c. Alteration of cell wall/membrane (low-level resistance, chromosomal, constitutive)
i. E.g. vanco resistance in S. aureus due to thickening of cell wall that prevents penetration)
2) Alteration of antibiotic’s target (usually high-level resistance, chromosomal, inducible or constitutive)
a. E.g. penicillin resistance in S. pneumoniae due to slight alterations in the penicillin-binding proteins (PBPs)
3) Production of antibiotic-inactivating enzymes (usually high-level resistance. Chromosomal or plasmid/transposon. Chromosomal either inducible or constitutive; plasmid/transposon usually constitutive)
a. E.g. penicillin resistance in gram-positive S. aureus due to production of narrow-spectrum penicillinase.
b. E.g. Beta-lactamases in gram-negative pathogens.

48
Q

Compare and Contrast AmpC Beta-Lactamases with Extended-Spectrum Beta-Lactamases (ESBLs)

A

• CHROMOSOMAL AmpC Beta‐Lactamases found in “SPACE” pathogens:
Serratia species
Pseudomonas, Proteus, Providencia species
Acinetobacter species
Citrobacter species
Enterobacter species

ƒ AmpC can be either INDUCIBLE or CONSTITUTIVE in these “SPACE” pathogens
ƒ AmpC can inactivate all current beta‐lactams
ƒ AmpC is NOT INHIBITED by currently‐available beta‐lactamase inhibitors (i.e., clavulanic
acid, sulbactam, tazobactam)

• PLASMID‐BORNE “Extended Spectrum” Beta‐Lactamases (“ESBLs”):
ƒ Found most‐commonly in Klebsiella species and in E. coli
ƒ ESBLs can inactivate all current beta‐lactams EXCEPT CARBAPENEMS
ƒ ESBLs CAN be inhibited by currently‐available beta‐lactamase inhibitors in‐vitro

49
Q

Penicillin resistance in Streptococcus pneumoniae and Methicillin resistance in S. aureus…caused by

A

caused by PBP changes

50
Q

Carbapenem resistance in Pseudomonas aeruginosa due to

A

loss of a porin

51
Q

Macrolide resistance in Streptococcus pneumoniae

A

via the “Mef” EPP

52
Q

Resistance to nearly all clinically-used antibiotics (Multi-drug resistance) in Pseudomonas aeruginosa via…

A

via efflux pump proteins

53
Q

Resistance to Macrolides, Lincosamides, and Group B Streptogramins (“MLSB resistance”) in nearly all gram-positive bacteria (can be either INDUCIBLE or CONSTITUTIVE, occurs via…

A

methylation of the ribosomal binding site for these antibiotics)

54
Q

Fluoroquinolone resistance in nearly all gram-positive bacteria due to

A

mutations in DNA gyrase and/or Topoisomerase IV enzymes

INFECTIOUS DISEASE (6 decks)

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