UCLA

Urbanization has profound ecological impacts that reach beyond city boundaries. Obvious ecological consequences of urbanization include habitat loss and fragmentation. Anthropogenic barriers reduce habitat connectivity, impede gene flow between populations and accelerate the loss of genetic diversity in populations due to drift. Urbanization may have also cryptic consequences such as the effects of human-introduced toxicants on wildlife populations. Toxicants are a leading cause of population decline for a variety of animal species worldwide and may directly threaten animal populations by causing direct mortalities, or indirectly through sublethal, chronic effects such as reproductive impairment, decreased immune competence, and increased disease susceptibility or emergence. If population-level impacts occur as a result of toxicant exposure, genetic consequences may also accompany reduced population sizes and connectivity. These include inbreeding depression that may increase the probability of population extinction and the loss of adaptive potential that reduces the ability of populations to respond to novel selection regimes. Overall, urbanization presents wildlife with many novel stressors to which they must adapt or perish. Urbanization is increasing at an unprecedented pace; understanding both the obvious and the cryptic threats to wild animal populations persisting near urban areas will be vital to promoting conservation and the maintenance of global biodiversity.

To address the consequences of urbanization on wildlife populations, I focused on a well-studied population of bobcats (Lynx rufus) living in and around Santa Monica Mountains National Recreation Area (SMMNRA). This region comprises a collection of protected park areas near downtown Los Angeles. Bobcats inhabiting SMMNRA have been monitored by National Park Service (NPS) biologists since 1996. Within a localized region of SMMNRA, the NPS has demonstrated that a major freeway (US-101) acts not only as a barrier to movement for bobcat and coyote (Canis latrans) populations, but potentially also as a social barrier. Further, from 2002-2005, a notoedric mange epizootic associated with secondary anticoagulant rat poison exposure was the greatest source of mortality for bobcats. During this period, the annual survival rate for radio-collared animals fell by > 50% and in 2003 the mange mortality rate reached a high of 51%. Long-term samples were collected from this population from 1996-2012, allowing the rare opportunity to make direct comparisons before, during, and after the population decline.

Using these data as a foundation, my research focused on three main objectives. First, I characterized neutral and adaptively relevant genetic diversity in bobcat populations across SMMNRA in both fragmented urban and protected natural areas. Second, I examined anticoagulant rodenticide exposure in bobcats across southern California, contrasting seasonal, demographic and spatial risk factors in both natural and urbanized areas. Third, I characterized physiological and immunological parameters in bobcats across SMMNRA to evaluate the effects of disease and toxicant exposure on bobcat health in an urban, fragmented landscape.

I found that two freeways are significant barriers to gene flow. Further, the 3-year disease epizootic, associated with secondary anticoagulant rodenticide exposure, caused a population bottleneck that led to significant genetic differentiation pre- and post-disease populations that was greater than that between populations separated by major freeways for > 60 years. However, balancing selection acted on immune-linked loci during the epizootic, maintaining variation at functional regions. With respect to anticoagulant rodenticide exposure, I detected high prevalence of exposure (89%, liver; 39%, blood) and found that for individuals with paired liver and blood data (N = 64), 92% were exposed most frequently to greater than or equal to 3 compounds. Prevalence and the amounts of contaminants were associated with human activities that included commercial, residential, and agricultural development. I found a strong association between AR exposure to greater than and equal to 0.25 ppm or greater than and equal to 2 compounds and an ectoparasitic disease, notoedric mange. Finally, I observed that AR exposure has both immune stimulatory and suppressive effects that may explain increased bobcat susceptibility to notoedric mange as a result of chronic exposure to anticoagulant rodenticides. Bobcats exposed to ARs had elevated lymphocyte, and specifically B cell counts, and decreased percentages of neutrophils. Overall, these data highlight that even for free-ranging animals that are considered relatively adaptable to urbanization, habitat fragmentation and toxicant exposure can have profound population level effects that threaten the long-term stability of wildlife populations in an increasingly urbanized landscape.