. 2005 Feb;49(2):699–707. doi: 10.1128/AAC.49.2.699-707.2005

TABLE 4.

Evidence for emergence of spontaneous quinolone-resistant mutants from preexisting susceptible C. jejuni HS13 PT1 strains from flock 3

Treatment phase	Source	Isolate	MIC (μg/ml)^a		Genotype^b		Resistance phenotype^c
Treatment phase	Source	Isolate	CIP	NAL	gyrA	gyrB	Resistance phenotype^c
Pretreatment	Puddle	P751	0.12	8	H	A	Q^S
	Feces	P765	0.12	8	H	A	Q^S
Treatment	Litter	P762	0.12	8	H	A	Q^S
	Feces	P769	0.12	8	H	A	Q^S
	Feces	P757	0.25	64	F	ND	Nal^r Cip^s
	Feces	P753	0.5	64	F	A	Nal^r Cip^s
	Drinking water	P764	8	128	B	A	Nal^r Cip^r
	Feces	P756	16	64	B	A	Nal^r Cip^r

CIP, ciprofloxacin; NAL, nalidixic acid. The MICs of sodium dodecyl sulfate, ethidium bromide, tetracycline, chloramphenicol, kanamycin, ampicillin, trimethyprim acridine orange, and sodium deoxycholate were identical (±1 dilution) for all eight isolates.

gyrA genotypes were determined by DHPLC analysis and are designated as follows: H, His-81 (CAC→CAT); F and B, as shown in Fig. 1; a single nucleotide change in gyrA type H would give rise to an F or B genotype; gyrB genotype A, Phe-440 (TTC→TTT) and Leu-458 (CTA→TTA); ND, not done.

Nal^r Cip^r, resistant to nalidixic acid (MICs ≥ 32 μg/ml) and ciprofloxacin (MICs ≥ 2 μg/ml); Nal^r Cip^s, nalidixic acid resistant (MICs ≥ 32 μg/ml) and ciprofloxacin sensitive (MICs ≤ 1 μg/ml); Q^S, quinolone sensitive.