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Hoffner, S.

Publications and source records attributed to Hoffner, S..

3 recordsLinked to original sources

First records of invasive Vespa velutina nigrithorax Buysson, 1905 (Hymenoptera: Vespidae) and Megachile sculpturalis Smith, 1853 (Hymenoptera: Megachilidae) in Slovakia

Biological invasions are an increasing threat to ecosystems; early identification of invasive species and rigorous monitoring are prerequisites to minimize environmental damage. Currently, two large hymenopterans of Asian origin are spreading across Europe: the yellow-legged hornet Vespa velutina nigrithorax Buysson, 1905 and the giant resin bee Megachile sculpturalis Smith, 1853, populations of which have been gradually being discovered across Europe since 2004 and 2008, respectively. Considering the current distribution of both species in Europe, further spread through Central Europe is expected in recent years. In July 2024, the first record of M. sculpturalis was documented in Slovakia, followed by more reports from 11 localities. Less than two months later, the second invasive hymenopteran, V. velutina nigrithorax, was also detected. Utilising multiple methods, their nest was discovered as well. On-site observations showed that the yellow-legged hornets (workers) were active almost two days after colony eradication. The finding of both species was accompanied by an intensive campaign using citizen science.

zoology↗

Rare alternative second line injectable drug resistance markers identified by gene-wise genome wide association in M. tuberculosis with unexplained resistance

Point mutations in the rrs gene and eis promoter are known to confer resistance to second-line injectable drugs (SLIDs) amikacin (AMK), capreomycin (CAP), and kanamycin (KAN). While mutations in these canonical genes confer a majority of SLID-resistance, alternative mechanisms of resistance are not uncommon and threaten effective treatment decisions when using conventional molecular diagnostics. In total, 1184 clinical M. tuberculosis isolates from 7 countries were studied for genomic markers associated with phenotypic resistance. The markers rrs:A1401G and rrs:G1484T were associated with resistance to all three SLIDs, and three known markers in the eis promoter (eis:G-10A, eis:C-12T, and eis:C-14T) were similarly associated with kanamycin resistance (KAN-R). Among 325, 324, 270 AMK-R, CAP-R, and KAN-R isolates, 264 (81.2%), 250 (77.2%), and 249 (92.3%) harbored canonical mutations, respectively. Thirteen isolates harbored more than one canonical mutation. Canonical mutations did not account for 111 of the phenotypically resistant isolates. A gene-wise method identified three genes and promoters with mutations that, on aggregate, associated with unexplained resistance to at least one SLID. Our analysis associated whiB7 promoter mutations with KAN resistance, supporting clinical relevance for the previously demonstrated role of whiB7 overexpression in KAN resistance. We also provide evidence for the novel association of ppe51 (a gene previously associated with various antimicrobial compounds) with AMK resistance, and for the novel association of thrB with AMK and CAP resistance. The use of gene-wise association can provide additional insight, and therefore is recommended for identification of rare mechanisms of resistance when individual mutations carry insufficient statistical power.

genomics↗

Pyrazinamide action is driven by the cell envelope stress response in Mycobacterium tuberculosis

Pyrazinamide (PZA) plays a crucial role in first-line tuberculosis drug therapy. Unlike other antimicrobial agents, PZA is only active against Mycobacterium tuberculosis at low pH. The basis for this conditional drug susceptibility remains undefined. In this study, we utilized a genome-wide approach to interrogate potentiation of PZA action. We find that mutations in numerous genes involved in central metabolism as well as cell envelope maintenance and stress response are associated with PZA resistance. Further, we demonstrate that constitutive activation of the cell envelope stress response can drive PZA susceptibility independent of environmental pH. Consequently, treatment with peptidoglycan synthesis inhibitors, such as beta-lactams and D-cycloserine, potentiate PZA action through triggering this response. These findings illuminate a regulatory mechanism for conditional PZA susceptibility and reveals new avenues for enhancing potency of this important drug through targeting activation of the cell envelope stress response.

microbiology↗