AROs Flashcards

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1
Q

What mechanism of resistance do most ARO problems revolve around?

A

Beta-lactamases

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2
Q

What are the four classes of the amber classification for beta-lactamases? What is the active site for each class and which one is the most problematic in terms of drugs available for treatment?

A

A, B, C, D. All are serine based active sites except for B which is a metallo based active site. Metallo class beta lactamases are the most worrying because there is no drug currently available to treat them.

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3
Q

What is the most prevalent class beta lactamase in the world? What can it do?

A

The most prevalent class A beta lactamase is KPC-2, which is a carbapenemase that can hydrolyze beta-lactamase inhibitors such as clavulanic acid.

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4
Q

What is a CRE? What does it produce to confer resistance?

A

Carbapenemase resistant enterobacteriaceae. It produces a carbapenemase.

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5
Q

What are the big 5 carbapenemases? Which one is the most problematic and which one is the most difficult to detect?

A

KPV, VIM, NDM, IMP, OXA-48
OXA-48 most difficult to detect
NDM most worrying

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6
Q

What are 3 characteristics of MRSA?

A

Resistant to all beta-lactams, usually multi-drug resistant, nosocomial pathogen that is easily transmissable

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7
Q

How is CA-MRSA different from HA-MRSA? How can it be treated?

A

CA-MRSA is more virulent but less resistant than HA-MRSA. It can cause necrotizing skin and soft tissue infections. It can be treated with TMP/SMX, doxycycline and clindamycin

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8
Q

How has MRSA become resistant to beta lactams? What gene is resistance encoded on?

A

It produces a novel PBP, PBP-2a which has reduced affinity for beta lactams and can perform the functions of all other PBPs. It is encoded on the mecA gene, carried on the acquired staphylococcal chromosomal cassete (SCC)

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9
Q

How is the mecA gene usually expressed in strains of MRSA?

A

It is normally expressed heterogenously meaning that 1 in every 1,000,000 cells may express it.

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10
Q

How can MRSA be detected in the lab? (2)

A

On Mueller Hinton agar with 4% NaCl and oxicillin or with the cefoxitin screen test.

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11
Q

What are the risk factors for CA-MRSA? (4)

A

Crowded conditions, IV drug use, younger age groups, lower economic status

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12
Q

What is PVLT and what strains of Staph carry it?

A

Panton-Valentine Leucocidin toxin. Capable of destroying WBCs, severe tissue damage, necrotic skin lesions, necrotizing pneumonia. Usually carried by MSSA and CA-MRSA, not often by HA-MRSA

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13
Q

What are VREs? What are they resistant to?

A

Vancomycin resistant enterococci with intrinsic glycopeptide resistance. They have a very high propensity to spread because they can survive for a long time on fomites.

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14
Q

What are the 2 species of enterococcus associated with disease? How can they be diffentiated from other enterococcus?

A

E. faecium and E. faecalis. Both are non-motile whereas E. gallinarum is. Both are glucopyranoside negative.

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15
Q

How does vancomycin work?

A

Inhibits cell wall synthesis by complexing with the D-ala-D-ala portion of the cell wall precursor, sterically inhibiting it from binding the rest of the peptidoglycan precursor

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16
Q

What makes the spread of vancomycin resistance slow?

A

An entire operon of genes is used to encode resistance to the drug and thus transfer of an entire operon is unlikely and therefore resistance is forming slowly.