Biocides, such as herbicides, are routinely tested for toxicity but not for sublethal effects on microbes. Many biocides are known to induce an adaptive multiple-antibiotic resistance phenotype. This can be due to either an increase in the expression of efflux pumps, a reduced synthesis of outer membrane porins, or both. Exposures of Escherichia coli and Salmonella enterica serovar Typhimurium to commercial formulations of three herbicides—dicamba (Kamba), 2,4-dichlorophenoxyacetic acid (2,4-D), and glyphosate (Roundup)—were found to induce a changed response to antibiotics. Killing curves in the presence and absence of sublethal herbicide concentrations showed that the directions and the magnitudes of responses varied by herbicide, antibiotic, and species. When induced, MICs of antibiotics of five different classes changed up to 6-fold. In some cases the MIC increased, and in others it decreased. Herbicide concentrations needed to invoke the maximal response were above current food maximum residue levels but within application levels for all herbicides. Compounds that could cause induction had additive effects in combination. The role of soxS, an inducer of the AcrAB efflux pump, was tested in β-galactosidase assays with soxS-lacZ fusion strains of E. coli. Dicamba was a moderate inducer of the sox regulon. Growth assays with Phe-Arg β-naphtylamide (PAβN), an efflux pump inhibitor, confirmed a significant role of efflux in the increased tolerance of E. coli to chloramphenicol in the presence of dicamba and to kanamycin in the presence of glyphosate. Pathways of exposure with relevance to the health of humans, domestic animals, and critical insects are discussed.

Beak and feather disease virus (BFDV) infections are often fatal to both captive and wild parrot populations. Its recent discovery in a wild population of native red-fronted parakeets has raised concerns for the conservation of native parrots, all of which are threatened or endangered. The question of a recent introduction versus a native genotype of the virus poses different conservation-management challenges, and thus, a clear understanding of the molecular phylogeny of BDFV is a crucial step towards integrated management planning. This study represents the first comprehensive attempt to screen New Zealand's endangered and threatened psittacines systematically for BFDV. We sampled and screened kakapos (Strigops habroptilus), kakas (Nestor meridionalis), keas (N. notabilis), Chatham parakeets (Cyanoramphus forbesi), Malherbe's parakeets (Cyanoramphus malherbi), yellow-crowned parakeets (C. auriceps) and red-fronted parakeets (Cyanoramphus novaezelandiae), as well as eastern rosellas (Platycercus eximius), an introduced species that is now common throughout the North Island, for BFDV. Out of all species and populations sampled (786 individuals), we found 16 BFDV-positive red-fronted parakeets from Little Barrier Island/Hauturu, seven eastern rosellas from the Auckland region, and eight yellow-crowned parakeets from the Eglinton Valley in the South Island. The full genomes of the viral isolates from the red-fronted parakeets share 95-97 % sequence identity to those from the invasive eastern rosellas and 92.7-93.4 % to those isolates from the South Island yellow-crowned parakeets. The yellow-crowned parakeet BFDV isolates share 92-94 % sequence identity with those from eastern rosellas. The low level of diversity among all BFDV isolates from red-fronted parakeets could suggest a more recent infection among these birds compared to the yellow-crowned parakeets, whereas the diversity in the eastern rosellas indicates a much more established infection. Pro-active screening and monitoring of BFDV infection rates in aviaries as well as in wild populations are necessary to limit the risk of transmission among threatened and endangered parrot populations in New Zealand.

The conjugative multiple antibiotic resistance plasmid pIP501 can be transferred and stably maintained in a variety of Gram-positive genera, including multicellular Streptomyces lividans, as well as in Gram-negative Escherichia coli. The 15 putative pIP501 transfer (tra) genes are organized in an operon-like structure terminating in a strong transcriptional terminator. This paper reports co-transcription of the pIP501 tra genes in exponentially growing Enterococcus faecalis JH2-2 cells, as shown by RT-PCR. The tra genes are expressed throughout the life cycle of Ent. faecalis, and the expression level is independent of the growth phase. Electrophoretic mobility shift assays indicated that the TraA relaxase, the first gene of the tra operon, binds to the tra promoter P tra , which partially overlaps with the origin of transfer (oriT ). DNase I footprinting experiments further delimited the TraA binding region and defined the nucleotides bound by TraA. b-Galactosidase assays with P tra -lacZ fusions proved P tra promoter activity, which was strongly repressed when TraA was supplied in trans. Thus, it is concluded that the pIP501 tra operon is negatively autoregulated at the transcriptional level by the conjugative DNA relaxase TraA.

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