TABLE 3.
Mutations resulting in amino acid substitutions in H. influenzae mutants exceeding the CLSI breakpoint for moxifloxacin
| Strain | Mutated gene(s)a (corresponding amino acid substitution[s]) |
|---|---|
| SMHi4-H | acrB (A813V), asd (A371V), atpB (I255V), ccmH (R20V), fabA (M145I), lexA (P91S), mlaE (G24S), pdxY (T257fs), rfaF (Y324fs), rpoB (L1102P), torY (A197fs), acetyltransferase (S61A), UPF0701 protein (V269A), six hypothetical proteins,b integrase (P63L), lysozyme (E152G), putative acyl-coenzyme A thioester hydrolase (Δ20R), putative glycosyltransferase (Y210fs) |
| SMHi18-H | artM (T59fs), ompP2 (V37fs), putative HTH-type transcriptional regulator (G86S), hypothetical protein (T22fs) |
| SMHi2-H | ompP2 (T132K), fabH (G38S), rpoD (P520S), tadA (R157C), 5′–3′ exoribonuclease (H10fs) |
| SMHi6-H | secD (R599C), udk (L115fs), glycosyl transferase family 1 (P335fs) |
| SMHi17-H | corA (S231L), ompP2 (E278fs) |
| SMHi23-H | fmt (D37_K38insN), putative HTH-type transcriptional regulator (D161fs) |
| SMHi15-H | fabZ (E49G), ompP2 (Val161fs) |
| SMHi9-H | dnaK (G221S), infC (D107E), dusB (I3fs) |
| Hui436-H | adk (G80S) |
| SMHi22-H | None |
a
Mutations in genes other than gyrA, gyrB, parC, and parE (shown in Table 2) in the in vitro-derived H. influenzae mutants with the highest moxifloxacin MIC determined are shown. The mutations were determined by sequence comparison with the parental H. influenzae clinical isolate. fs, frameshift.
b
Six hypothetical proteins with one mutation each (Table S3).