Table 1.
Characterization of the low-virulence L. monocytogenes strains
Strains |
Sub-cutaneous test |
Phenotypic Groupc | Mutations | Genotypic Groupd |
MLST |
PFGE types |
||
---|---|---|---|---|---|---|---|---|
Mean (log spleens) ± S.D.a | I/Tb | Sequence types | ApaI | AscI | ||||
CHU 860776 e |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
2 |
2 |
CNL 895803 e |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
2 |
2 |
CNL 895804 e |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
2 |
2 |
CNL 895806 e |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
2 |
2 |
CNL 895809 e |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
2a |
2 |
CNL 895793 e |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
2a |
2 |
SO49 e |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
3 |
23 |
AF10 e |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
3 |
23 |
99EB24LM |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
3 |
23 |
99EB04LM |
0 |
0/5 |
I |
PrfA K220T, truncated InlA (76 AA) |
Ia |
13 |
3 |
23 |
BO18 e |
1.31 |
1/5 |
I |
PrfAΔ174-237, truncated InlA (188 AA) |
Ib |
31 |
77a |
61b |
BO38 e |
0 |
0/5 |
I |
PrfAΔ174-237, truncated InlA (188 AA) |
Ib |
31 |
77a |
61b |
AF95 e |
0 |
0/5 |
I |
PrfAΔ174-237, truncated InlA (188 AA) |
Ib |
31 |
77a |
61c |
99EB15LM |
0 |
0/5 |
I |
PrfAΔ174-237, truncated InlA (188 AA) |
Ib |
31 |
21a |
20 |
NP 26 |
0 |
0/5 |
I |
PrfA K130Q |
Ic |
2 |
61a |
3 |
454 e |
3.26 ± 0.53 |
3/20 |
II |
mutated PC-PLC (D61E, L183F, Q126K, A223V) |
|
10 |
9 |
11 |
CNL 895807 e |
3 |
1/25 |
III |
truncated InlA (25 AA), mutated InlB (A117T, V132I), PI-PLC T262A |
IIIa |
193 |
1 |
1 |
416 e |
0 |
0/5 |
III |
truncated InlA (25 AA), mutated InlB (A117T, V132I), PI-PLC T262A |
IIIa |
193 |
1 |
1 |
417 e |
2.81 ± 1.47 |
2/20 |
III |
truncated InlA (25 AA), mutated InlB (A117T, V132I), PI-PLC T262A |
IIIa |
193 |
1 |
1 |
BO43 e |
2.53 |
1/5 |
III |
truncated InlA (25 AA), mutated InlB (A117T, V132I), PI-PLC T262A |
IIIa |
193 |
1a |
1a |
CNL 895795 e |
0 |
0/5 |
III |
truncated InlA (25 AA), mutated InlB (A117T, V132I), PI-PLC T262A |
IIIa |
193 |
1a |
1a |
DSS794AA1 |
0 |
0/5 |
III |
truncated InlA (25 AA), mutated InlB (A117T, V132I), PI-PLC T262A |
IIIa |
193 |
144 |
33a |
DSS1130BFA2 |
0.47 |
1/5 |
III |
truncated InlA (25 AA), mutated InlB (A117T, V132I), PI-PLC T262A |
IIIa |
193 |
143 |
129 |
DPF234HG2 |
2.76 ± 0.04 |
2/5 |
III |
truncated InlA (25 AA), mutated InlB (A117T, V132I), PI-PLC T262A |
IIIa |
193 |
145 |
33b |
AF105 e |
0 |
0/5 |
III |
truncated InlA (576 AA) |
IIIb |
9 |
81 |
64 |
442 e |
0 |
0/5 |
IV |
|
|
1 |
6 |
7 |
02-99 SLQ 10c Al |
2.9 ± 0.05 |
2/5 |
IV |
|
|
1 |
11 |
7 |
3876 |
3.42 ± 0.2 |
3/5 |
IV |
|
|
1 |
142 |
113 |
3877 |
2.7 ± 0.2 |
3/5 |
IV |
|
|
1 |
142 |
113 |
N2 |
3.59 ± 0.48 |
2/5 |
IV |
|
|
10 |
11 |
4b |
CR282 e |
3.01 ± 0.61 |
2/10 |
IV |
|
|
195 |
158 |
85 |
LSEA 99–23 f |
4.49 ± 0.89 |
3/5 |
IV |
truncated InlA (576 AA) |
|
9 |
21a |
20 |
LSEA 99-4f |
3.67 ± 0.81 |
3/5 |
IV |
|
|
198 |
48 |
101 |
09-98 SRV 10a Al1 |
0 |
0/5 |
IV |
|
|
4 |
37 |
38b |
449 e |
0 |
0/5 |
V |
3 AA deletion at position 742 in InlA |
|
194 |
8 |
6 |
BO34 e |
3.63 ± 0.56 |
5/10 |
V |
|
|
2 |
4a |
3 |
464 e |
2.59 ± 0.39 |
9/15 |
V |
|
|
1 |
9c |
4a |
09-98 SRV 10b Al2 |
3.54 ± 0.27 |
3/5 |
V |
|
|
54 |
135 |
124 |
11-99 SRV 1a Al |
0 |
0/5 |
V |
|
|
4 |
37 |
38b |
09-98 HPR 50a Al1 |
0 |
0/5 |
V |
3 AA deletion at position 742 in InlA |
|
6 |
67a |
98a |
436 e |
2.81 ± 0.68 |
12/20 |
VI |
|
|
2 |
4 |
3 |
LSEA 00–14 f |
0 |
0/5 |
VI |
|
|
2 |
106 |
3a |
04-99 EBS 1 lb Al | 2.53 ± 1.76 | 2/5 | VI | 54 | 139 | 125 |
a Log numbers of Listeria recovered from spleens three days after sub-cutaneous injection into the left hind footpads of immunocompetent Swiss mice with 104 CFU in 50 μL. Values are from infected mice.
b Ratio of infected mice to inoculated mice in sub-cutaneous test.
c These groups are based on combined values of cell invasion, plaque formation, and phospholipase activities.
d These groups are based on sequencing of prfA, plcA, plcB, inlA and inlB genes.
e Results already published in Roche et al. [7].
f Results already published in Kerouanton et al. [10].