Over the past 30 years, the California condor (Gymnogyps californianus) population has rebounded from 22 individuals to over 200 birds living in the wild. Historical impacts to the population have been largely anthropogenic. In this study, we explore mortality and cause of death data from condors that died during the years 2010-2014 and compare these to mortality data described by Rideout et al. in 2012, covering the years 1992-2009. In addition, morphologic and genetic analysis of the contents of the upper gastrointestinal (GI) tract was performed on the 2010-2014 condor mortalities to determine animal origins of the last meal eaten. The maximum population at risk within this time frame was 329 birds. During this time, 88 condors died and underwent post-mortem examination, and 41 birds were lost to tracking efforts and presumed dead (crude mortality rate of 39%; 129/329). A cause of death was determined for 66 of the 88 necropsied birds. Lead toxicosis remained a significant negative factor in condor population recovery, being related to the deaths of 37 adult and juvenile condors (proportional mortality rate 56%). Compared to condors succumbing to other causes of death, cattle were less often part of the last meal of lead-intoxicated condors. Based on these data, continued efforts to mitigate the impact of lead on California condors should be pursued.
Chronic wasting disease (CWD) is a fatal, highly transmissible spongiform encephalopathy caused by an infectious prion protein. CWD is spreading across North American cervids. Studies of the prion protein gene (PRNP) in white-tailed deer (WTD; Odocoileus virginianus) have identified non-synonymous substitutions associated with reduced CWD frequency. Because CWD is spreading rapidly geographically, it may impact cervids of conservation concern. Here, we examined the genetic vulnerability to CWD of two subspecies of WTD: the endangered Florida Key deer (O. v. clavium) and the threatened Columbian white-tailed deer (O. v. leucurus). In Key deer (n = 48), we identified three haplotypes formed by five polymorphisms, of which two were nonsynonymous. The polymorphism c.574G>A, unique to Key deer (29 of 96 chromosomes), encodes a nonsynonymous substitution from valine to isoleucine at codon 192. In 91 of 96 chromosomes, Key deer carried c.286G>A (G96S), previously associated with substantially reduced susceptibility to CWD. Key deer may be less genetically susceptible to CWD than many mainland WTD populations. In Columbian WTD (n = 13), two haplotypes separated by one synonymous substitution (c. 438C>T) were identified. All of the Columbian WTD carried alleles that in other mainland populations are associated with relatively high susceptibility to CWD. While larger sampling is needed, future management plans should consider that Columbian WTD are likely to be genetically more vulnerable to CWD than many other WTD populations. Finally, we suggest that genetic vulnerability to CWD be assessed by sequencing PRNP across other endangered cervids, both wild and in captive breeding facilities.
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