TABLE 1.
Group | Origin | No. of strains | Resistance phenotypea | Resistance genotype | Class 1 integronb | Origin (no. of isolates)c | PFGE profile |
Plasmid sizes (no. of isolates)d | ||
---|---|---|---|---|---|---|---|---|---|---|
XbaI | BlnI | No. | ||||||||
1 | Turkey baseline study feces samples (2006 and 2007) | 16 | [R]e | [R′]f | [I]g | NI (13) | X1 | B1 | 4 | 7 kb, two ≤6 kb (2); 7 kb, ≤6 kb; NP |
X1 | B2 | 8 | NP (7); 41 kb, 16 kb | |||||||
X1 | B1b | 1 | 28 kb | |||||||
[R]-TET | [R′]-tet(A) | [I] | MV | X1 | B1 | 1 | ≤6 kb | |||
NI | X5 | B2 | 1 | NP | ||||||
[R]-TET | [R′]-tet(A) | [I] + 1,000 bp/aadA1 | NI | X1 | B2a | 1 | 100 kb, 16 kb | |||
2 | Turkey diagnostic feces samples (2002 and 2003, 2005 and 2006) | 17 | [R] | [R′] | [I] | BW | X1 | B1 | 1 | 16 kb |
BW, ST (3) | X1 | B2 | 4 | NP (3); 54 kb | ||||||
Unknown | X1a | B2 | 1 | ≤6 kb | ||||||
B | X14 | B3 | 1 | NP | ||||||
HE | X3 | B10 | 1 | ≤6 kb | ||||||
B | X4 | B4 | 1 | 16 kb | ||||||
[R] | [R′] | [I] + 1,000 bp/aadA1 | B | X4 | B4 | 1 | 100 kb, 49 kb | |||
[R]-TET | [R′]-tet(B) | [I] | NRW | X1 | B2 | 1 | 47 kb, ≤6 kb | |||
BW, NI | X4 | B4 | 2 | 49 kb, ≤6 kb; 62 kb, ≤6 kb | ||||||
[R]-CHL | [R′]-sul3-cmlA | [I] | SN | X1 | B2 | 1 | 69 kb, 16 kb | |||
[R]-CHL-TMP/SXT | [R′]-blaPSE-1-sul3-cmlA-(unknown)h | [I] | B | X2 | B2c | 1 | 100 kb, 16 kb | |||
Susceptible | BW (2) | X13a | B5 | 2 | 12 kb, three ≤6 kb (2) | |||||
3 | Turkey-derived food diagnostic samples (2000 to 2007) | 22 | [R] | [R′] | [I] | NI | X1 | B1 | 1 | NP |
NRW | X1 | B1a | 1 | NP | ||||||
NI, NRW | X1 | B2 | 2 | NP (2) | ||||||
[R]i | [R′] | 1,600 bp/dfrA1-aadA1 | ST | X4 | B4 | 1 | ≤6 kb | |||
NI | X4 | B14 | 1 | ≤6 kb | ||||||
[R] | [R′] | [I] + 1,000 bp/aadA1 | B | X4 | B4 | 1 | 100 kb, 16 kb | |||
[R]-TET | [R′]-aphA1-strA-(unknown)j | [I] | B | X11 | B11 | 1 | 138 kb, 70 kb, 9 kb, 7 kb, three ≤6 kb | |||
[R]-TET-TMP/SXT | [R′]-aphA1-sul2-tet(A)-dfrA14 | [I] | B | X11 | B11 | 1 | 174 kb, 77 kb, 37 kb | |||
[R]-CHL-TET-TMP/SXT | [R′]-catA1-tet(B)-dfrA1-like | [I] | BW, RP | X8 | B2b | 2 | 28 kb, ≤6 kb; ≤6 kb | |||
AMP-TET-STR/SPE-SUL-TMP/SXT | blaTEM-1-tet(A)/tet(B)-aadA1-like-sul1-dfrA1-like | 1,950 bp/estX-aadA1 + 700 bp/estX | B | X6 | B6 | 1 | 41 kb, three ≤6 kb | |||
TET-STR/SPE-SUL | tet(B)-aadA1-like-sul1 | 1,950 bp/estX-aadA1 + 700 bp/estX | NRW | X6 | B6 | 1 | Three ≤6 kb | |||
TET-STR/SPE-SUL | tet(B)-aadA1-like-sul1 | 1,950 bp/estX-aadA1 | B (2) | X6 | B6 | 2 | Three ≤6 kb; 70 kb, three ≤6 kb | |||
AMP-CHL-TET-STR-SUL-TMP/SXT | blaTEM-1- catA1-tet(A)-strA/aadA1-like-sul1/sul2-dfrA1-like | 1,600 bp/dfrA1-aadA1 | SH | X10 | B8 | 1 | NP | |||
AMP/AMC(i/r)-NAL-TET-STR-SUL | blaTEM-1-gyrASer83→Tyr83-tet(A)-strA-sul2 | 200 bp/without gene cassettes | NRW | X7 | B7 | 1 | 100 kb, two ≤6 kb | |||
NAL | gyrASer83→Tyr83 | BW | X7a | B7 | 1 | 16 kb, two ≤6 kb | ||||
GEN-NAL-TET-STR/SPE-SUL | gyrASer83→Glu83-tet(B)-aadA1-like-sul1 | 1,000 bp/aadA1 | TH | X9 | B9 | 1 | 138 kb, 70 kb | |||
Susceptible | RP | X13a | B5 | 1 | 12 kb, three ≤6 kb | |||||
NRW | X12 | B12 | 1 | 74 kb | ||||||
SN | X13 | B13 | 1 | Two ≤6 kb |
Resistance phenotypes were assessed by the broth microdilution method as described by Schroeter et al. (37) by following the guidelines of the CLSI (13). The breakpoints used for ampicillin (AMP), amoxicillin-clavulanic acid (AMC), ceftiofur (XNL), chloramphenicol (CHL), ciprofloxacin (CIP), gentamicin (GEN), kanamycin (KAN), sulfonamides (SUL), and tetracycline (TET) were the CLSI breakpoints (14). For ciprofloxacin, the MIC breakpoints were as follows: resistant, ≥4 μg/ml; intermediate, 2 μg/ml; and susceptible, ≤1 μg/ml (decreased susceptibility, 1 to 0.12 μg/ml; fully susceptible, ≤0.06 μg/ml). The breakpoints used for colistin (COL) (resistant, ≥16 μg/ml; susceptible, ≤8 μg/ml), florfenicol (FLO) (resistant, ≥32 μg/ml; susceptible, ≤8 μg/ml), nalidixic acid (NAL) (resistant, ≥32 μg/ml; susceptible, ≤16 μg/ml), spectinomycin (SPE) (resistant, ≥128 μg/ml; susceptible, ≤64 μg/ml), and trimethoprim (TMP) (resistant, ≥16 μg/ml; susceptible, ≤8 μg/ml) were the DANMAP breakpoints (17). And the breakpoints used for neomycin (NEO) (resistant, ≥16 μg/ml; susceptible, ≤4 μg/ml), streptomycin (STR) (resistant, ≥32 μg/ml; susceptible, ≤8 μg/ml), and trimethoprim-sulfamethoxazole (SXT) (resistant, ≥4 and ≥76 μg/ml respectively; susceptible, ≤2 and ≤38 μg/ml, respectively) were the breakpoints of Schroeter et al. (37).
Variable regions of class 1 integrons; indicated are their lengths (determined using the 5′CS and 3′CS primers [28]) and the inserted gene cassettes.
B, Berlin; BW, Baden-Württemberg; HE, Hesse; MV, Mecklenburg Western Pomerania; NI, Lower Saxony; NRW, North Rhine-Westphalia; RP, Rhineland-Palatinate; SH, Schleswig-Holstein; SN, Saxony; ST, Saxony-Anhalt; TH, Thuringia. Unless indicated otherwise, the number of isolates was one.
NP, no plasmid detected. Unless indicated otherwise, the number of isolates was one.
[R], core resistance phenotype [AMP/AMC(i/r)-GEN(i/r)-KAN(i/r)-NAL-CIP(i/ds)-STR/SPE-SUL], where (i/r) indicates intermediate or full resistance and (i/ds) indicates intermediate or decreased susceptibility.
[R′], core resistance genotype [blaTEM-1-aadB-gyrASer83→Glu83-aadA1-like/aadA2-sul1].
[I], class 1 integron with the 1,700 bp/aadB-aadA2 variable region.
None of the genes encoding trimethoprim resistance tested were detected in the strain.
The strain exhibited the core resistance pattern, but the class 1 integron with the 1,700 bp/aadB-aadA2 variable region was not detected by PCR.
None of the genes encoding tetracycline resistance tested were detected in the strain.