Geology topics

Bruce Rideout

Publications and source records attributed to Bruce Rideout.

4 recordsLinked to original sources

USGS2026

Improving the use of expert opinion in disease risk analysis for conservation translocations

Conservation translocations are subject to considerable uncertainty and risk, of which disease is one of the most recognized. To address disease risks, several protocols for qualitative disease risk analysis (qDRA) exist and are used for responsible conservation translocation planning. Existing qDRA protocols usually rely on expert judgment, but they lack quantitative aggregation of elicited estimates, transparent treatment of uncertainty, and explicit comparison of alternative disease risk management pathways. We added these factors to a qDRA for translocation of a charismatic species that is extinct in the wild, the sihek (Guam kingfisher) ( Todiramphus cinnamominus ). We asked a panel of seven independent experts to quantify their judgment of risks of pathogen release, exposure, and consequences for seven pathogen hazards under three translocation management scenarios. Experts suggested that implementing a full biosecurity protocol would reduce risk for several pathogen hazards but would have variable effectiveness (11–65% depending on the hazard). There was substantial uncertainty associated with individual experts and noise among different experts, showing the potential for error if decisions are based on single-point judgments (i.e., providing judgment of a central tendency without accounting for uncertainty) from one expert or on collaborative consensus of multiple experts, as is current practice.

Conservation Biology↗

USGS2021

Assessment of disease risk associated with potential removal of anthropogenic barriers to Mojave desert tortoise (Gopherus agassizii) population connectivity

The Mojave Desert tortoise ( Gopherus agassizii ), federally listed as threatened, has suffered habitat loss and fragmentation due to human activities. Upper respiratory tract disease (URTD), a documented health threat to desert tortoises, has been detected at the Large-Scale Translocation Study Site (LSTS) in southwestern Nevada, US, a fenced recipient site for translocated animals. Our study aimed to 1) estimate prevalence of URTD and Mycoplasma infection at LSTS and three nearby unfenced sites; 2) assess whether Mycoplasma infection status was associated with developing clinical signs of URTD; and 3) determine whether such an association differed between LSTS and unfenced areas. We sampled 421 tortoises in 2016 to describe the current status of these populations. We evaluated three clinical signs of URTD (nasal discharge, ocular discharge, nasal erosions) and determined individual infection status for Mycoplasma agassizii and Mycoplasma testudineum by quantitative PCR and enzyme-linked immunosorbent assay. In 2016, LSTS had the highest prevalence of M. agassizii (25.0%; 33/132), M. testudineum (3.0%; 4/132), and URTD clinical signs (18.9%; 25/132). Controlling for other factors, clinical sign(s) were positively associated with M. agassizii infection (odds ratio [OR]=7.7, P =0.001), and this effect was similar among study sites ( P >0.99). There was no association with M. testudineum status ( P =0.360). Of the 196 tortoises in a longitudinal comparison of 2011–14 with 2016, an estimated 3.2% converted from M. agassizii -negative to positive during the study period, and incidence was greater at LSTS ( P =0.002). Conversion to positive M. agassizii status was associated with increased incidence of clinical signs in subsequent years (OR=11.1, P =0.018). While M. agassizii and URTD are present outside the LSTS, there is a possibility that incidence of Mycoplasma infection and URTD would increase outside LSTS if these populations were to reconnect. Population-level significance of this risk appears low, and any risk must be evaluated against the potential long-term benefits to population viability through increased connectivity.

Journal of Wildlife Diseases↗

USGS2012

Serologic and molecular evidence for testudinid herpesvirus 2 infection in wild Agassiz’s desert tortoise, Gopherus agassizii

Following field observations of wild Agassiz’s desert tortoises ( Gopherus agassizii ) with oral lesions similar to those seen in captive tortoises with herpesvirus infection, we measured the prevalence of antibodies to Testudinid herpesvirus (TeHV) 3 in wild populations of desert tortoises in California. The survey revealed 30.9% antibody prevalence. In 2009 and 2010, two wild adult male desert tortoises, with gross lesions consistent with trauma and puncture wounds, respectively, were necropsied. Tortoise 1 was from the central Mojave Desert and tortoise 2 was from the northeastern Mojave Desert. We extracted DNA from the tongue of tortoise 1 and from the tongue and nasal mucosa of tortoise 2. Sequencing of polymerase chain reaction products of the herpesviral DNA-dependent DNA polymerase gene and the UL39 gene respectively showed 100% nucleotide identity with TeHV2, which was previously detected in an ill captive desert tortoise in California. Although several cases of herpesvirus infection have been described in captive desert tortoises, our findings represent the first conclusive molecular evidence of TeHV2 infection in wild desert tortoises. The serologic findings support cross-reactivity between TeHV2 and TeHV3. Further studies to determine the ecology, prevalence, and clinical significance of this virus in tortoise populations are needed.

California;Nevada↗

USGS2005

Pathology and proposed pathophysiology of diclofenac poisoning in free-living and experimentally exposed oriental white-backed vultures (Gyps bengalensis)

Oriental white-backed vultures ( Gyps bengalensis ; OWBVs) died of renal failure when they ingested diclofenac, a nonsteroidal anti-inflammatory drug (NSAID), in tissues of domestic livestock. Acute necrosis of proximal convoluted tubules in these vultures was severe. Glomeruli, distal convoluted tubules, and collecting tubules were relatively spared in the vultures that had early lesions. In most vultures, however, lesions became extensive with large urate aggregates obscuring renal architecture. Inflammation was minimal. Extensive urate precipitation on the surface and within organ parenchyma (visceral gout) was consistently found in vultures with renal failure. Very little is known about the physiologic effect of NSAIDs in birds. Research in mammals has shown that diclofenac inhibits formation of prostaglandins. We propose that the mechanism by which diclofenac induces renal failure in the OWBV is through the inhibition of the modulating effect of prostaglandin on angiotensin II-mediated adrenergic stimulation. Renal portal valves open in response to adrenergic stimulation, redirecting portal blood to the caudal vena cava and bypassing the kidney. If diclofenac removes a modulating effect of prostaglandins on the renal portal valves, indiscriminant activation of these valves would redirect the primary nutrient blood supply away from the renal cortex. Resulting ischemic necrosis of the cortical proximal convoluted tubules would be consistent with our histologic findings in these OWBVs.

Punjab Province↗