Table 4 One hundred and nine K. pneumoniae isolates classified according to their beta-lactamase phenotype including the detected resistance mechanisms against beta-lactams and aminoglycosides by LC–MS/MS.

From: Exploring antimicrobial resistance to beta-lactams, aminoglycosides and fluoroquinolones in E. coli and K. pneumoniae using proteogenomics

Phenotype

n

Antibiotics

PEN/OXA

ESBL

AmpC

CPE

16S-RMTase

AAC

CRX

CAZ

MEM

GEN

TOB

CIP

TEM

SHV

OXA-1

OXA-9

CTX-M

CMY

DHA

OXA-48

NDM

KPC

VIM

AAC(3)

AAC(6′)

WT/PEN/OXA

27

S

S

S

S

S

S/R

2

4

5

WT/PEN/OXA/AME

2

S

S

S

R

S

S

1

2

ESBL/AmpC

2

R

R

S

S

S

S/R

1

2

2

ESBL/AmpC/AME

10

R

S/R

S

R

S/R

S/R

7

2

6

10

9

6

CRE/Quin

4

R

R

S/R

S

S

R

3

2

1

1

3

CRE/AME

6

R

R

S/R

S/R

S/R

S/R

1

1

2

2

1

2

4

2

CRE/AME/Quin

58

R

R

S/R

S/R

R

R

28

18

23

5

35

6

2

13

18

19

9

15

28

29

  1. Isolates were classified based on their susceptibility (S) or resistance (R) to ceftriaxone (CRX), ceftazidime (CAZ), meropenem (MEM), gentamicin (GEN), tobramycin (TOB) and ciprofloxacin (CIP) into wild type (WT) isolates and small spectrum penicillinase (PEN) and/or oxacillinase-producing (OXA) isolates, extended-spectrum beta-lactamase producers (ESBL) in combination with isolates producing AmpC beta-lactamases (AmpC), or carbapenem resistant Enterobacterales (CRE). All CRE isolates had MEM MIC’s ≥ 0.5 mg/L. Isolates were further divided based on aminoglycoside resistance, mostly caused by aminoglycoside modifying enzymes (AME) and/or quinolone resistance (Quin). Small spectrum beta-lactamases/oxacillinases included TEM, SHV, OXA-1 and OXA-9. ESBL and AmpC were represented by CTX-M, CMY and DHA. Carbapenemase producing Enterobacterales (CPE) included OXA-48, NDM, KPC and VIM positive isolates. Mechanisms of aminoglycoside resistance included the 16S rRNA methyltransferases ArmA, RmtB, RmtC and RmtF and the acetyltransferase group AAC(3) which included AAC(3)-II, AAC(3)-IV and AAC(3)-VI and the acetyltransferase AAC(6′)-Ib.