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Volume 16, Number 9—September 2010


Determinants of Multidrug-Resistant Tuberculosis Clusters, California, USA, 2004–2007

John Z. MetcalfeComments to Author , Elizabeth Y. Kim, S.-Y. Grace Lin, Adithya Cattamanchi, Peter Oh, Jennifer Flood, Philip C. Hopewell, and Midori Kato-Maeda
Author affiliations: Author affiliations: University of California, San Francisco, California, USA (J.Z. Metcalfe, E.Y. Kim, A. Cattamanchi, P.C. Hopewell, M. Kato-Maeda); California Department of Public Health, Richmond, California, USA (S.-Y.G. Lin, P. Oh, J. Flood)

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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)
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.

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