. Author manuscript; available in PMC: 2010 Mar 1.

Published in final edited form as: Expert Opin Pharmacother. 2009 Mar;10(4):555–577. doi: 10.1517/14656560902731993

Table 4.

Genetic alterations linked to Neisseria gonorrhoeae reduced susceptibility to β-lactam antimicrobials.

Gene (Amino Acid alteration)	Gene Product	Phenotype	Source
ponA (L421P)	PBP1	Altered PBP1. Requires penC for high level resistance. Role in cephalosporin resistance questioned.	150
penA (Asp-345a)	PBP2	Insertion PBP2 resulting in penicillin resistance	146
penA (mosaic PBP2)	PBP2	Oral cephalosporin resistance Possibly increased MIC for parenteral cephalosporins	108, 154
penA (A501V)	PBP2	Possibly similar effect to mosaic; 2-4 fold increase in cephalosporin MIC	112, 142
penB (porB1b)	PorB1b	Altered porin and membrane permeability to hydrophobic antibiotics and tetracycline	143, 152
pilQ (penC)	PilQ Major outer membrane protein through which pilus projects also is a porin ¹³⁵	Increases resistance to penicillin when penA, mtrR, and penB mutations are present; thought to form outer membrane pore through which antimicrobials diffuse into periplasm	143, 185
MtrR	Transcription repressor	Results in MtrC-D-E efflux pump upregulation decreased susceptibility to hydrophobic agents such as azithromycin, rifampin. Possible increased in vivo fitness	186, 187