Volume 16, Number 9—September 2010
Research
Determinants of Multidrug-Resistant Tuberculosis Clusters, California, USA, 2004–2007
, Elizabeth Y. Kim, S.-Y. Grace Lin, Adithya Cattamanchi, Peter Oh, Jennifer Flood, Philip C. Hopewell, and Midori Kato-Maeda
Table 2
Isoniazid and rifampin resistance–conferring mutations among 121 clustered and nonclustered MDR TB infections, California, USA, 2004–2007*
| Molecular basis for drug resistance | Nonclustered, n = 96, no. (%) | Clustered, n = 25, no. (%) |
|---|---|---|
| Isoniazid resistance | ||
| katG S315T mutation | 66 (69) | 25 (100) |
| Other katG mutation† | 8 (8) | 0 |
| inhA promoter‡ | 23 (26) | 0 |
| No katG S315T or inhA promoter mutation detected§ |
5 (5) |
0 |
| Rifampin resistance¶ | ||
| rpoB codons 511–518 | 8 (9) | 2 (8) |
| rpoB codons 523–529 | 25 (27) | 4 (16) |
| rpoB codons 529–534 | 57 (62) | 19 (76) |
| rpoB codons 515–521 | 2 (2) | 0 |
*Two isolates with otherwise complete genotyping data were unavailable for molecular beacon analysis. MDR TB, multidrug-resistant tuberculosis; S315T, serine-to-threonine substitution at position 315.
†Novel mutations detected: Y413STOP, T314T (silent), W161G, D61E (Fur A), R145P, P325L, and V633F.
‡inhA promoter mutation was concomitant with 4/91 (4%) isolates harboring the katG S315T and 2/8 (25%) isolates with katG mutations other than S315T.
§No mutations detected by molecular beacons; sequencing was not possible for these isolates because of degraded DNA.
¶Rifampin resistance–conferring mutations were not detected by the molecular beacon assay for 4 isolates.