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Deana L. Clifford

Publications and source records attributed to Deana L. Clifford.

4 recordsLinked to original sources

Antibody response of endangered riparian brush rabbits to vaccination against rabbit hemorrhagic disease virus 2

Rabbit hemorrhagic disease virus 2 (RHDV2; Caliciviridae , Lagovirus europaeus ), the cause of a highly transmissible and fatal lagomorph disease, has spread rapidly through the western United States and Mexico, resulting in substantial mortality in domestic and wild rabbits. The disease was first detected in California in May 2020, prompting an interagency/zoo/academia/nonprofit team to implement emergency conservation actions to protect endangered riparian brush rabbits ( Sylvilagus bachmani riparius ) from RHDV2. Prior to vaccinating wild rabbits, we conducted a vaccine safety trial by giving a single SC dose of Filavac VHD K C+V (Filavie) vaccine to 19 adult wild riparian brush rabbits captured and temporarily held in captivity. Rabbits were monitored for adverse effects, and serum was collected before vaccination, and at 7–10, 14–20, and 60 d post-vaccination. Sera were tested using an ELISA to determine antibody response and timing of seroconversion. Reverse-transcription quantitative real-time PCR (RT-qPCR) was performed on rectal swabs to evaluate infection status. No adverse effects from the vaccine were observed. Before vaccination, 18 of 19 rabbits were seronegative, and RHDV2 was not detected by RT-qPCR on any rectal swabs. After vaccination, all rabbits developed an antibody response, with titers of 1:10–1:160. Seroconversion generally occurred at 7–10 d. The duration of antibody response was ≥60 d in 12 of 13 rabbits. Sixteen animals were released and 4 were recaptured several months later, offering a glimpse into longer duration immune response. Our study has informed vaccination strategies for this species and serves as a model for protecting other vulnerable lagomorphs against RHDV2.

California

Modeling the response of an endangered rabbit population to RHDV2 and vaccination

Rabbit hemorrhagic disease virus 2 (RHDV2), recently detected in the western United States, has the potential to cause mass mortality events in wild rabbit and hare populations. Currently, few management strategies exist other than vaccination. We developed a spatially explicit model of RHDV2 for a population of riparian brush rabbits ( Sylvilagus bachmani riparius ), a subspecies of brush rabbit classified as endangered in the United States, on a subsection of the San Joaquin River National Wildlife Refuge. The goal of our model was to provide guidance regarding vaccination strategies for an endangered rabbit species. Our model predicts that increased interactions between rabbits (a proxy for landscape connectivity) and disease transmission rates among susceptible hosts (individual brush rabbits and conspecifics) have the greatest influence on the outcome of a potential vaccination campaign. Our model projects that across a range of parameter estimates (given an RHDV2 incursion), the median estimated population size with a 0%–10% vaccination rate after 1 year is 538 rabbits (95% Confidence Interval [C.I.] 69–1235), approximately 36% of the expected size of the study population of 1470 rabbits without an RHDV2 introduction. With a 10%–20%, 20%–30%, or 30%–40% vaccination rate, the median estimated population size increased to 628 rabbits (95% C.I. 130–1298), 723 rabbits (95% C.I. 198–1317), and 774 rabbits (95% C.I. 228–1410), respectively. These estimates represent 43%, 49%, and 53% of the expected population size without an RHDV2 introduction. Overall, a 1% increase in vaccination rate was associated with a six rabbit (95% C.I. 5–7) increase in total remaining population size. This result is dependent on assumptions regarding environmental transmission, home range size (and contact rates of rabbits). Given the relatively short lifespan of rabbits and the potential need for boosters, vaccination programs are most likely to be successful for small target populations where relatively high vaccination rates can be maintained.

California

Marine fog inputs appear to increase methylmercury bioaccumulation in a coastal terrestrial food web

Coastal marine atmospheric fog has recently been implicated as a potential source of ocean-derived monomethylmercury (MMHg) to coastal terrestrial ecosystems through the process of sea-to-land advection of foggy air masses followed by wet deposition. This study examined whether pumas ( Puma concolor ) in coastal central California, USA, and their associated food web, have elevated concentrations of MMHg, which could be indicative of their habitat being in a region that is regularly inundated with marine fog. We found that adult puma fur and fur-normalized whiskers in our marine fog-influenced study region had a mean (±SE) total Hg (THg) (a convenient surrogate for MMHg) concentration of 1544 ± 151 ng g −1 (N = 94), which was three times higher ( P < 0.01) than mean THg in comparable samples from inland areas of California (492 ± 119 ng g −1 , N = 18). Pumas in California eat primarily black-tailed and/or mule deer ( Odocoileus hemionus ), and THg in deer fur from the two regions was also significantly different (coastal 28.1 ± 2.9, N = 55, vs. inland 15.5 ± 1.5 ng g −1 , N = 40). We suggest that atmospheric deposition of MMHg through fog may be contributing to this pattern, as we also observed significantly higher MMHg concentrations in lace lichen ( Ramalina menziesii ), a deer food and a bioindicator of atmospheric deposition, at sites with the highest fog frequencies. At these ocean-facing sites, deer samples had significantly higher THg concentrations compared to those from more inland bay-facing sites. Our results suggest that fog-borne MMHg, while likely a small fraction of Hg in all atmospheric deposition, may contribute, disproportionately, to the bioaccumulation of Hg to levels that approach toxicological thresholds in at least one apex predator. As global mercury levels increase, coastal food webs may be at risk to the toxicological effects of increased methylmercury burdens.

California

Serum chemistry, hematologic, and post-mortem findings in free-ranging bobcats ( Lynx rufus ) with notoedric mange

Notoedric mange was responsible for a population decline of bobcats ( Lynx rufus ) in 2 Southern California counties from 2002–2006 and is now reported to affect bobcats in Northern and Southern California. With this study we document clinical laboratory and necropsy findings for bobcats with mange. Bobcats in this study included free-ranging bobcats with mange (n = 34), a control group of free-ranging bobcats without mange (n = 11), and a captive control group of bobcats without mange (n = 19). We used 2 control groups to evaluate potential anomalies due to capture stress or diet. Free-ranging healthy and mange-infected bobcats were trapped or salvaged. Animals were tested by serum biochemistry, complete blood count, urine protein and creatinine, body weight, necropsy, and assessment for anticoagulant rodenticide residues in liver tissue. Bobcats with severe mange were emaciated, dehydrated, and anemic with low serum creatinine, hyperphosphatemia, hypoglycemia, hypernatremia, and hyperchloremia, and sometimes septicemic when compared to control groups. Liver enzymes and leukocyte counts were elevated in free-ranging, recently captured bobcats whether or not they were infested with mange, suggesting capture stress. Bobcats with mange had lower levels of serum cholesterol, albumin, globulin, and total protein due to protein loss likely secondary to severe dermatopathy. Renal insufficiency was unlikely in most cases, as urine protein:creatinine ratios were within normal limits. A primary gastrointestinal loss of protein or blood was possible in a few cases, as evidenced by elevated blood urea nitrogen, anemia, intestinal parasitism, colitis, gastric hemorrhage, and melena. The prevalence of exposure to anticoagulant rodenticides was 100% (n = 15) in bobcats with mange. These findings paint a picture of debilitating, multisystemic disease with infectious and toxic contributing factors that can progress to death in individuals and potential decline in populations.

Journal of Parasitology