TABLE 2.

Antimicrobial susceptibility of nalD P. aeruginosa

Strain	nalD statusa	MIC (μg/ml)b							mexA expressionc
		CAM	NAL	TET	NOV	CAR	TIC	ATM
K870	WT	16	64	8	512	128
K2346	Null	64	256	256	1,024	512
K2346(pDSK519)d	Null	64	256	256	1,024	512
K2346(pMLS003)d	WT	8	64	64	256	64
K2347	Null	64	256	256	1,024	512
PAO1	WT	32	64	32			16	8	1.00
1113(pDSK519)e	ΔT410-G433	64	256	64			64	32	1.69
1113(pMLS003)e	WT	32	32	16			8	2	0.34
WL24(pDSK519)e	?	128	>1,028	128			64	16	2.41
WL24(pMLS003)e	WT	32	>1,028f	32			16	2	0.25

^aThe indicated strains expressed wild type (WT), nalD::mini-Tn5-tet-disrupted (Null), or mutant nalD genes (specific mutations are highlighted as base changes in the gene itself). Mutations in nalD were verified following PCR amplification of the gene and nucleotide sequencing of the PCR product obtained. ?, the nalD gene could not be amplified by PCR, suggesting a possible deletion of the gene in this strain.

^bCAM, chloramphenicol; NAL, nalidixic acid; TET, tetracycline; NOV, novobiocin; CAR, carbenicillin; TIC, ticarcillin; ATM, aztreonam.

^cmexA expression (as a measure of mexAB-oprM expression) was quantitated using real-time RT- PCR and normalized to expression levels seen in wild-type strain PAO1.

^dpDSK519 is the vector without nalD; pMLS003 is pDSK519::nalD.

^eClinical isolate.

^fThe apparent lack of an impact of the cloned nalD gene on the nalidixic acid MIC likely reflects the presence of another determinant(s) of resistance to this agent in strain WL24, which may be masking any impact of mexAB-oprM expression on resistance.