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Clinical Micro > AROs > Flashcards

AROs Flashcards

1
Q

How many people die every year in the US because of AROs?

A

about 700’000

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2
Q

What are 4 resistant gram negative phenotypes that are of most concern right now?

A
  1. ESBL-producing Enterobacteriaceae
  2. MDR P. aeruginosa
  3. Carbapenem-resistant Enterobacteriaceae (e.g. KPC)
  4. Metallo-β-lactamase-producers
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3
Q

Of the 4 major resistant gram negative phenotypes, which one has NO drug at all to treat?

A

Metallo-β-lactamase-producers

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4
Q

How many/what are the classes of ß-lactamase producers in the Ambler classificiation?

A

4, A-D types

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5
Q

most of the ß-lactamase producers have what amino acid in their active site? What is the exception?

A

Serine

metallo ones that have zinc binding thiol

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6
Q

What is the most prevalent class A carbapenamase ? What ß-lactamase inhibitors is it effective against?

A

KPC-2

clavulanic acid, sulbactam, and tazobactam

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7
Q

NDM-1 is part of which class of carbapenemases?

A

Class B

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8
Q

What is the problem associated with spotting carbapenemase producers?

A

There can be a small % of overlap between them and wild type organisms that happen to show remarkable resistance

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9
Q

What are the “big 5” of carbapenemases?

A
  1. NDM (most concerning, no drugs to treat)
  2. OXA-48 (most difficult to detect)
  3. KPC
  4. VIM
  5. IMP
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10
Q

What is the MCR-1 gene?

A

Gene that encodes for colicin resistance among CRE

  • makes them legitimately impossible to treat
  • fatal in 70+% of bacterimic patients
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11
Q

MRSA is resistant to all __ and often to __

A

all ß-lactams and also often multi-drug resistant

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12
Q

CA-MRSA is responsible for what types of infections?

A

Necrotizing skin & soft tissue infections

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13
Q

What is CA-MRSA generally susceptible to?

A

TMP/SMX, doxycycline, and clindamycin

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14
Q

What are 7 risk factors for developing MRSA?

A
  1. prolonged hospitalization
  2. ICU care
  3. prolonged antimicrobial therapy
  4. surgical procedures
  5. close proximity to colonized / infected patient
  6. injection drug use
  7. implanted devices
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15
Q

What is the mechanism of resistance of MRSA?

A

Novel PBP 2a that can perform all the functions of other PBPs and is resistant to the ß-lactams due to alteration of D-ala-D-ala to D-ala-D-lac

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16
Q

What gene goes for MRSA resistance? Where did it come from?

A

mecA gene acquired by transposition from a non-staphyloccal organism but is now integrated into the genome

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17
Q

What are the two forms of MRSA expression? how are they similar/different?

A

Homogenous expression: always resistant and producing PBP 2a

Heterogenous expression: only about 1/million cells is producing PBP 2a

18
Q

What growth conditions/media are used to test for MRSA presence?

A

Mueller-Hinton agar with 4% NaCl and cefoxitin (better inducer of resistance than oxacillin)

Use a very heavy inoculum

19
Q

What are the two main differences between CA and HA MRSA?

A

CA is more virulent and also more susceptible to drugs than HA

20
Q

What is the connection genetically between CA and HA MRSA?

A

thought to have evolved separately

21
Q

CA-MRSA is spread primarily through…

A

Close contact

22
Q

What are some (5) risk factors for developing CA-MRSA?

A
  1. younger age groups
  2. IV drug use
  3. lower economic status
  4. MSM (?)
  5. crowded conditions (prisons, military etc)
23
Q

What 5 factors contribute to the spread of CA-MRSA?

A
  1. close skin to skin contact
  2. cuts and abrasions
  3. shared contaminated items / surfaces
  4. poor hygiene
  5. crowded living conditions
24
Q

What are 6 possible clinical manifestations of CA-MRSA?

A
  1. Boils or draining pimples
  2. “Spider Bites” or “bug bites”
  3. Sores that won’t heal
  4. Red areas of skin that may feel warm to the touch
  5. Abscesses
  6. Systemic infections (e.g. pneumonia, blood infections) but much less common
25
Q

What genetic element of MRSA carries the mecA gene?

A

specific integrated genetic element = staphylococcal cassette chromosome (SCC)

26
Q

How many types of SSC-mec are there?

A

5 (I-V)

27
Q

What types of SSC-mec does HA-MRSA have? What kind of resistance does this confer?

A

Has SSC-mec types I, II and III

- multidrug resistance

28
Q

What types of SSC-mec does CA-MRSA have? What kind of resistance does this confer?

A

Has type IV SCC-mec

  • doesn’t usually carry multidrug resistance
  • only usually resistant to beta-lactams and erythromycin
29
Q

What is PVL toxin and in what strains of MRSA is it found?

A

Panton-Valentine leucocidin (PVL) toxin is a cytotoxin found in 99% of CA-MRSA strains and <5% of HA-MRSA strains

30
Q

What genes encode PVL toxin?

A

lukS-PV and lukF-PV

31
Q

What is PVL capable of doing?

A

Capable of destroying WBC /severe tissue damage and associated with necrotic skin lesions /severe necrotizing pneumonia

32
Q

What is the diagnostic benefit of PVL

A

allows you to do a quick PCR test to check for the presence of the gene which will tell you fairly accurately whether or not you have CA-MRSA

33
Q

Which of HA and CA is very clonal? What does this allow you to do?

A

CA-MRSA is very clonal

Allows you to use PFGE to compare different causes of outbreaks in various locations

34
Q

What PFGE types are common for HA-MRSA? for CA-MRSA?

A

USA 100 and 200 (HA)

USA 300 and 400 (CA)

35
Q

Which two enterococci are intrinsically resistant to glycopeptides (vanco)?

A

E.gallinarum and E.casseliflavus

36
Q

What was first described in 1986 in the enterocci?

A

transferable glycopeptide resistance

37
Q

Which two enteroccoci can now be resistant to vanco? (VRE)?

A

E.faecium and E.faecalis

38
Q

What can you do to test/differentiate between E.faecium/E.faecalis, E.gallinarum and E.casseliflavus

A
  1. Glucopyranoside test
    - E.gallinarum / casseliflavus +
    - E.faecium / faecalis -
  2. If you have a positive test, then you can do a pigment test
    - E.casseliflavus has yellow pigmentwhich is not visible on plate (use white swab, see yellow pigment on swab)
39
Q

What is the motility like of the different enterococci?

A
  • E.faecium / faecalis non-motile

- E.gallinarum Motile (but 10% are not)

40
Q

What are the two VRE phenotypes we need to know? What is different about each one?

A

VanA: gene that codes for the ligase
- Highly resistant to vanco and teicoplanin

VanB: only slightly resistant to teicoplanin and vanco
- The vanco resistant can often be around the tipping point of what is resistant or not

Clinical Micro (28 decks)

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