TABLE 3.
In vitro and in vivo mutation frequenciesa
| Strain | Mutation frequency |
|||||||
|---|---|---|---|---|---|---|---|---|
| TSA |
MHII agar |
RPMI agar |
RPMI+AA agar |
|||||
| RFB (8 mg/L) | RIF (8 mg/L) | RFB (8 mg/L) | RIF (8 mg/L) | RFB (8 mg/L) | RIF (8 mg/L) | RFB (8 mg/L) | RIF (8 mg/L) | |
| In vitro | ||||||||
| A. baumannii HUMC1 | 1.28E−08 | 1.44E−08 | 2.20E−09 | 9.19E−09 | 5.49E−06 | 9.89E−06 | 6.30E−07 | 1.71E−06 |
| A. baumannii ABNIH1 | 5.95E−09 | 1.75E−08 | 8.85E−09 | 4.17E−08 | 1.40E−05 | 4.84E−05 | 6.83E−06 | 5.75E−06 |
| A. baumannii ATCC 17978 | 8.49E−10 | 7.95E−09 | 5.72E−09 | 5.14E−09 | 2.12E−06 | 2.20E−05 | 7.57E−06 | 2.60E−05 |
| A. baumannii LAC-4 | 7.41E−09 | 1.76E−08 | 1.29E−08 | 2.62E−08 | 1.79E−06 | 6.72E−06 | 1.06E−06 | 6.65E−06 |
| S. aureus LAC | 1.10E−07 | 9.49E−08 | 1.11E−07 | 1.08E−07 | 1.43E−06 | 8.60E−06 | 6.05E−06 | 3.09E−06 |
| E. coli JJ1886 | 3.89E−08 | 2.21E−08 | 1.48E−07 | 1.95E−07 | 7.06E−07 | 1.06E−05 | 4.53E−07 | 5.70E−06 |
| In vivo | Blood (TSA) | Kidney (TSA) | Blood (RPMI agar) | Kidney (RPMI agar) | ||||
| A. baumannii HUMC1 | <1.7E−09 | 8.4E−08 | <3.7E−08 | 1.2E−07 | <8.3E−09 | 4.1E−07 | 3.7E−07 | 1.6E−06 |
| A. baumannii LAC-4 | <4.1E−09 | <4.1E−09 | <2.2E−09 | <2.2E−09 | <4.1E−09 | <4.1E−09 | <2.2E−09 | <2.2E−09 |
a
For matched medium conditions, there was no significant difference in the emergence frequency of resistant A. baumannii mutants (Mann-Whitney test; P > 0.05). However, there was a significant difference when the A. baumannii mutants selected on TSA and RPMI were compared for rifampin (Kruskal-Wallis, P = 0.014) and rifabutin (Kruskal-Wallis, P = 0.028). C3H mice (n = 3) were infected with 1.3E7 to 2.7E7 CFU of A. baumannii HUMC1 or 4.6E6 CFU of A. baumannii LAC4. Blood and kidneys were collected 16.5 h postinfection, and samples were plated on TSA or RPMI agar plates alone or supplemented with 8 mg/L rifampin or rifabutin.