HCAI 3 - Epidemiology Flashcards

1
Q

Way to compare bacterial genomes

A

With Single Nucleotide Polymorphisms (SNPs)

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2
Q

Phylogenetics

A

Inferring phylogeny from a set of taxa

Estimates evolutionary relationships between groups of taxa

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3
Q

Enterococcus faecium

A

Normal commensal organism
Intrinsically resistant to cephalosporins and aminoglycosides
Acquired glycopeptide resistance

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4
Q

Example of a glycopeptide antibiotic

A

Vancomycin

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5
Q

Factor transforming VSE to VRE

A

Enterococci acquire a transposon with a vancomycin resistance loci on it

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6
Q

Most common vancomycin-resistance loci in Australia

A

VanB

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7
Q

Effect of VanB

A

Encodes for a ligase

Ligase modifies peptidoglycan wall so that vancomycin can’t bind - D-ala-D-ala to D-ala-D-lac

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8
Q

Transposon with VanB locus

A

TN1549

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9
Q

Size of TN1549

A

33kb

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10
Q

E test

A

A strip of antibiotic-impregnated paper is placed on a bacterial colony.
Progressively lower concentration

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11
Q

Model A of transmission

A

Patient enters hospital with VRE, spreads it to other patients
Counter with handwashing, screening patients as they enter hospital

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12
Q

Alternative model of VanB transmission

A

VRE exist in gut as commensal flora
Transfer TN1549 to VSE
TN1549 is selected for when vancomycin is introduced into gut

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13
Q

Situation where vancomycin resistance can arise de novo

A

Broad-spectrum antibiotics are used
Lateral gene transfer is selected for (TN1549)
TN1549 transferred from bowel anaerobes to colonising VSE

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14
Q

Dominant lineage of E. faecium

A

ST203

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15
Q

How can we tell how TN1549 has been acquired?

A

Use flanking sequences to see whether it has been inserted backwards or forwards

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16
Q

Is the insertion of VanB into TN1549 random?

A

No. There are some sites where VanB is more common

17
Q

Number of VRE likely to have arisen by se novo evolution

A

18/36

18
Q

Ways to control spread of VRE

A

Test for both VRE and VSE

Control antibiotic use - A patient receiving antibiotics could become a source of VRE