Ignitions explain more than temperature or precipitation in driving Santa Ana wind fires.

Autumn and winter Santa Ana wind (SAW)-driven wildfires play a substantial role in area burned and societal losses in southern California. Temperature during the event and antecedent precipitation in the week or month prior play a minor role in determining area burned. Burning is dependent on wind intensity and number of human-ignited fires. Over 75% of all SAW events generate no fires; rather, fires during a SAW event are dependent on a fire being ignited. Models explained 40 to 50% of area burned, with number of ignitions being the strongest variable. One hundred percent of SAW fires were human caused, and in the past decade, powerline failures have been the dominant cause. Future fire losses can be reduced by greater emphasis on maintenance of utility lines and attention to planning urban growth in ways that reduce the potential for powerline ignitions.

Acquisition of rifabutin resistance by a rifampicin resistant mutant of Mycobacterium tuberculosis involves an unusual spectrum of mutations and elevated frequency.

BACKGROUND: Mutations in a small region of the rpoB gene are responsible for most rifamycin resistance in Mycobacterium tuberculosis. In this study we have sequentially generated resistant strains to first rifampicin and then rifabutin. Portions of the rpoB gene were sequenced from 131 randomly selected mutants. Second round selection resulted in a changed frequency of specific mutations. METHODS: Mycobacterium tuberculosis (strain Mtb72) rifamycin resistant mutants were selected in vitro with either rifampicin or rifabutin. One mutant R190 (rpoB S522L) selected with rifampicin had a rifampicin MIC of 32 microg/ml but remained sensitive to rifabutin (MIC<0.8 microg/ml). This mutant was subjected to a second round of selection with rifabutin. RESULTS: All 105 first round resistant mutants derived from the parent strain (Mtb72) screened acquired mutations within the 81 bp rpoB hotspot. When the rifampicin resistant but rifabutin sensitive S522L mutant was subjected to a second round of selection, single additional rpoB mutations were identified in 24 (92%) of 26 second round mutants studied, but 14 (54%) of these strains contained mutations outside the 81 bp hotspot (codons 144, 146, 148, 505). Additionally, spontaneous rifabutin resistant mutants were produced at >10 times the frequency by the S522L mutant than the parent strain. CONCLUSION: First round selection of mutation S522L with rifampicin increased the frequency and changed the spectrum of mutations identified after selection with rifabutin.