Volunteer Angling and Technology-Based Solutions Provide the First Estimate of Sea Lice Infections for Wild Coastal Cutthroat Trout (Oncorhynchus Clarkii Clarkii)

Anadromous Coastal Cutthroat Trout Oncorhynchus clarkii clarkii are one of the least studied salmonids but are a highly prized target in sport fisheries in coastal waters of the Pacific Northwest. Despite an observed high prevalence of ectoparasite infections, described by sport anglers as "sea lice," there is a paucity of data available on the spatial and temporal occurrence of infections on Coastal Cutthroat Trout. We collaborated with the angling community through social media engagement and an online application to report ectoparasites observed on sport catch. In 2018, we received voluntary reports for 1,493 Cutthroat Trout and 416 salmon catch events in marine waters from the province of British Columbia and the states of Washington, Oregon, and California. These data demonstrated that the number of argulids and copepods per trout varied according to body size, capture month, and area. To evaluate accuracy of voluntary parasite counts, we compared results to parasite counts on cutthroat from sampling events conducted by trained biologists. For both voluntary angler reports and those of biologists, spring months had a lower prevalence of argulids and copepods, argulids were common on trout, but absent on salmon, and larger trout were associated with an increased number of argulid and copepod infections

Dispersal of brown trout (Salmo trutta L.) fry in a low gradient stream - implications for egg stocking practices

Stocking of eggs is a common strategy to support declining or reintroduce extirpated salmonid populations. Data on how juveniles disperse from stocking points is crucial to be able to design efficient stocking programs. Detailed information of dispersal is limited for many salmonids, for example, brown trout. In this study, dispersal distance was measured at the end of the first growing season in a low gradient (0.7%) stream in Sweden where the trout population had been depleted. Eggs from 17 separate sets of parents were stocked as eyed eggs in March. During the following fall fry were sampled throughout the stream. The majority of the fry dispersed downstream and remained within a distance of 200 m from the stocking point with no difference between sizes of fry and the presence of a competing cohort or not. There was no dissimilarity in dispersal distances across offspring originating from different parents indicating absence of genetic influence. Our results suggest that, in streams similar to our study site, stocking points should be separated by approximately 330 m in order to avoid overlap in habitat use of fry from different stocking points and that the presence of competing cohorts, fry size and within population variability in dispersal can be neglected

Pacific Salmon in Puget Sound: abundance, survival and body size (1970-2015)

Pacific salmon and trout (Oncorhynchus spp.) inhabiting Puget Sound marine waters have experienced both recent and long-term variability in abundance while supporting robust commercial, tribal, and sport fisheries. In recent years, numerous species-specific status reports have been completed, though formal comparisons among all five species of salmon and steelhead trout are not available. We compared spatial and temporal patterns of abundance, survival, productivity, and body size between hatchery-origin and naturally-produced adult salmon and steelhead trout returning to marine waters of Puget Sound, Washington, USA. Stock-specific total run size (of fish at the entrance to Puget Sound) was calculated for pink (O. gorbuscha), chum (O. keta), coho (O. kisutch), sockeye (O. nerka), and Chinook (O. tshawytscha) salmon for years 1970-2015 by combining estimates of escapement (spawners) with stock-specific estimates of harvest (catch) in Puget Sound marine and fresh waters. In general, trends in abundance varied by species and origin (hatchery vs naturally produced) with increased abundance, survival, and productivity associated with species exhibiting “fry” (vs. “smolt”) life history types. Overall, average weight of salmon and steelhead has decreased significantly since 1970 with the exception of coho salmon. Information presented here will allow fishery managers to evaluate recovery plans and harvest objectives as well as identify trends in abundance, survival, and productivity related to climate and life history expression

Structural and Magnetic Properties of [(CH₃)₃NH] CuCl₃2H₂O

The crystal structure at room temperature and the low-temperature heat capacity and magnetic susceptibilities of single crystals of [(CH3)3 NH]CuCl3 2H2O are reported. The monoclinic crystals belong to the space group P21c with a=7.479(10), b=7.864(11), c=16.730(23), =91.98(3)°, and Z=4. The structure consists of chains of edge-sharing [CuCl4(OH2)2] octahedra running along the a axis. Each copper atom is coordinated in a square plane by two water molecules and two chlorine atoms, with two more chlorine atoms at a longer distance. The susceptibility data can be fitted adequately between 1.5 and 20°K by a CurieWeiss law [ga=2.080.01, gb=2.020.01; gc=2.110.01; a=(0.380.03)°K, b=(0.360.03)°K, c=(0.410.03)°K], but the susceptibility parallel to the chain can be better fitted as an Ising linear chain. Measurements perpendicular to the chain are not as well fitted by the Ising model. The heat capacity, which consists primarily of a lattice contribution above 3°K, begins to rise as the temperature falls below 3°K, but long-range order does not set in above 1°K, the lowest temperature attained in this work. Both Ising and Heisenberg linear-chain models fit the low-temperature data with |Jk| \u3c1°K. The results are compared with those reported for the compounds CuCl2 2H2O and CuCl2 2NC5H5. © 1972 The American Physical Society

Comparison of triploid and diploid rainbow trout (Oncorhynchus mykiss) fine-scale movement, migration and catchability in lowland lakes of western Washington

Fisheries managers stock triploid (i.e., infertile, artifcially produced) rainbow trout Oncorhynchus mykiss in North American lakes to support sport fsheries while minimizing the risk of genetic introgression between hatchery and wild trout. In Washington State, the Washington Department of Fish and Wildlife (WDFW) allocates approximately US $3 million annually to stock hatchery-origin rainbow trout in>600 lakes, yet only about 10% of them are triploids. Many lakes in Washington State drain into waters that support wild anadromous steelhead O. mykiss that are listed as threatened under the U.S. Endangered Species Act. As a result, there is a strong interest in understanding the costs and benefts associated with stocking sterile, triploid rainbow trout as an alternative to traditional diploids. The objectives of this study were to compare triploid and diploid rainbow trout in terms of: (1) contribution to the sport fshery catch, (2) fne-scale movements within the study lakes, (3) rate of emigration from the lake, and (4) natural mortality. Our results demonstrated that triploid and diploid trout had similar day-night distribution patterns, but triploid trout exhibited a lower emigration rate from the lake and lower catch rates in some lakes. Overall, triploid rainbow trout represent a viable alternative to stocking of diploids, especially in lakes draining to rivers, because they are sterile, have comparable home ranges, and less often migrat

Evaluation of Visible Implant Elastomer Tags in Wild Coastal Cutthroat Trout in the Marine Environment

We evaluated the detectability of visible implant elastomer (VIE) tags in Coastal Cutthroat TroutOncorynchus clarkii clarkiiin the marine environment by comparing visually identified recaptures from VIE tags with known recaptures that were identified through genotype matching. A total of 89 individual Coastal Cutthroat Trout were marked in the lower jaw with colored VIE tags, sampled for genetics, and recaptured across 12 months in 2015. The rate of correspondence between the VIE tags and genetic matches was 92% (82/89) of the recaptured Coastal Cutthroat Trout in the nearshore marine environment. We found that red- and blue-colored VIE tags were detected at a higher rate (100%) than were yellow- and orange-colored tags (87.3% and 90.6%, respectively). In contrast, tag type (single or double), tag location (left or right), fish length (FL, mm), and time (days) since tagging had no effect on tag detectability during the study period. All of the tag colors were recovered for the maximum life of the study (up to 342 days). In all of the cases of nondetections (5/89), the tags were not identified upon initial recapture or subsequent capture events, suggesting that they were lost or not visible immediately upon insertion in the field-as opposed to being unidentified due to the degradation of tag detectability over time. The results of this study suggest that VIE tags have the potential to be detectable in juvenile and adult Coastal Cutthroat Trout for at least 12 months after insertion, with blue and red performing the best. Additional monitoring extending beyond 12 months after tagging would be necessary to identify the maximum life of VIE tags

Teixobactin kills bacteria by a two-pronged attack on the cell envelope

Antibiotics that use novel mechanisms are needed to combat antimicrobial resistance1–3. Teixobactin4 represents a new class of antibiotics with a unique chemical scaffold and lack of detectable resistance. Teixobactin targets lipid II, a precursor of peptidoglycan5. Here we unravel the mechanism of teixobactin at the atomic level using a combination of solid-state NMR, microscopy, in vivo assays and molecular dynamics simulations. The unique enduracididine C-terminal headgroup of teixobactin specifically binds to the pyrophosphate-sugar moiety of lipid II, whereas the N terminus coordinates the pyrophosphate of another lipid II molecule. This configuration favours the formation of a β-sheet of teixobactins bound to the target, creating a supramolecular fibrillar structure. Specific binding to the conserved pyrophosphate-sugar moiety accounts for the lack of resistance to teixobactin4. The supramolecular structure compromises membrane integrity. Atomic force microscopy and molecular dynamics simulations show that the supramolecular structure displaces phospholipids, thinning the membrane. The long hydrophobic tails of lipid II concentrated within the supramolecular structure apparently contribute to membrane disruption. Teixobactin hijacks lipid II to help destroy the membrane. Known membrane-acting antibiotics also damage human cells, producing undesirable side effects. Teixobactin damages only membranes that contain lipid II, which is absent in eukaryotes, elegantly resolving the toxicity problem. The two-pronged action against cell wall synthesis and cytoplasmic membrane produces a highly effective compound targeting the bacterial cell envelope. Structural knowledge of the mechanism of teixobactin will enable the rational design of improved drug candidates

Teixobactin kills bacteria by a two-pronged attack on the cell envelope

Antibiotics that use novel mechanisms are needed to combat antimicrobial resistance1–3. Teixobactin4 represents a new class of antibiotics with a unique chemical scaffold and lack of detectable resistance. Teixobactin targets lipid II, a precursor of peptidoglycan5. Here we unravel the mechanism of teixobactin at the atomic level using a combination of solid-state NMR, microscopy, in vivo assays and molecular dynamics simulations. The unique enduracididine C-terminal headgroup of teixobactin specifically binds to the pyrophosphate-sugar moiety of lipid II, whereas the N terminus coordinates the pyrophosphate of another lipid II molecule. This configuration favours the formation of a β-sheet of teixobactins bound to the target, creating a supramolecular fibrillar structure. Specific binding to the conserved pyrophosphate-sugar moiety accounts for the lack of resistance to teixobactin4. The supramolecular structure compromises membrane integrity. Atomic force microscopy and molecular dynamics simulations show that the supramolecular structure displaces phospholipids, thinning the membrane. The long hydrophobic tails of lipid II concentrated within the supramolecular structure apparently contribute to membrane disruption. Teixobactin hijacks lipid II to help destroy the membrane. Known membrane-acting antibiotics also damage human cells, producing undesirable side effects. Teixobactin damages only membranes that contain lipid II, which is absent in eukaryotes, elegantly resolving the toxicity problem. The two-pronged action against cell wall synthesis and cytoplasmic membrane produces a highly effective compound targeting the bacterial cell envelope. Structural knowledge of the mechanism of teixobactin will enable the rational design of improved drug candidates

Teixobactin kills bacteria by a two-pronged attack on the cell envelope

Antibiotics that use novel mechanisms are needed to combat antimicrobial resistance1–3. Teixobactin4 represents a new class of antibiotics with a unique chemical scaffold and lack of detectable resistance. Teixobactin targets lipid II, a precursor of peptidoglycan5. Here we unravel the mechanism of teixobactin at the atomic level using a combination of solid-state NMR, microscopy, in vivo assays and molecular dynamics simulations. The unique enduracididine C-terminal headgroup of teixobactin specifically binds to the pyrophosphate-sugar moiety of lipid II, whereas the N terminus coordinates the pyrophosphate of another lipid II molecule. This configuration favours the formation of a β-sheet of teixobactins bound to the target, creating a supramolecular fibrillar structure. Specific binding to the conserved pyrophosphate-sugar moiety accounts for the lack of resistance to teixobactin4. The supramolecular structure compromises membrane integrity. Atomic force microscopy and molecular dynamics simulations show that the supramolecular structure displaces phospholipids, thinning the membrane. The long hydrophobic tails of lipid II concentrated within the supramolecular structure apparently contribute to membrane disruption. Teixobactin hijacks lipid II to help destroy the membrane. Known membrane-acting antibiotics also damage human cells, producing undesirable side effects. Teixobactin damages only membranes that contain lipid II, which is absent in eukaryotes, elegantly resolving the toxicity problem. The two-pronged action against cell wall synthesis and cytoplasmic membrane produces a highly effective compound targeting the bacterial cell envelope. Structural knowledge of the mechanism of teixobactin will enable the rational design of improved drug candidates