Bobcat with moderate mange. Photo: V. Subramanyan

What happens when disease and poisons collide in a wildlife population? In the outskirts of Los Angeles, California, an unexpected outbreak of notoedric mange- a typically benign skin condition- drastically reduced the annual survival rate of radio-collared bobcats from over 75% to less than 30% within just a few years. Deeper investigation by State veterinary pathologists revealed that all of the bobcats that died of mange were exposed to high levels of anticoagulant rat poisons. This startling discovery led my colleagues at the National Park Service and I to hypothesize that these anticoagulant rat poisons might impair bobcat immune systems, making them more vulnerable to fatal mange. This intriguing potential connection became the focus of my Phd research, in which I explored how exposure to these toxicants and disease influences immunity, and the genetic impacts of urbanization and the disease outbreak.

To tackle this pressing issue, I began by examining both living and dead bobcats. I personally captured 60 bobcats, and with the help of my National Park Service colleagues, we sampled more than 125 in total. We collected blood samples from the captured bobcats to analyze for immunological markers, toxicant exposure, and genetic information. Working alongside National Park Service and U.S. Geological Survey biologists, we gathered samples from 172 dead bobcats, most of which died of vehicle collisions and mange. My initial findings were startling: a staggering 92% of bobcats in the study were exposed to the rat poisons. Delving further, I discovered a strong link between exposure levels and proximity to residential areas, highlighting the influence of human environmentals on wildlife health. Read the publication here.

In the next stage of my research, I investigated the immune health of bobcats that were exposed to rat poisons compared to those that weren’t. To ensure accurate results, I excluded bobcats suffering from notoedric mange, as their immune response to the disease could skew the findings. I developed novel immune assays to characterize and quantify different types of lymphocytes in the blood samples of bobcats that I captured. I also conducted comprehensive veterinary diagnostic tests to gather further health data. What emerged was revealing: bobcats exposed to rat poisons showed a clear and predictable pattern of immune dysfunction which could explain heightened susceptibility to mange. Our findings also echoed results of laboratory experiments on rodents showing immune dysfunction linked to exposure to anticoagulant rat poisons. This connection was not entirely new, but it reinforced evidence that these poisons can disrupt immune systems, not just in lab settings but in wildlife as well. Read the bobcat publications here and here.

In the final phase of my research, I turned to population genetics to explore how urban infrastructure and the disease outbreak impacted genetic structure and genetic diversity in urban bobcats. I analyzed two types of genetic markers: neutral microsatellite markers and microsatellites linked with immune genes. The results were striking. Both the disease outbreak and the presence of freeways influenced the genetic makeup of the bobcat population. Surprisingly, the disease outbreak, despite lasting only a few years, had a more significant impact than the freeways, which have been around for over 60 years.

The disease outbreak caused a genetic bottleneck in the population, which was not surprising considering that we estimated the population declined by approximately 90% during the disease outbreak. Additionally, my research showed that natural selection, specifically balancing selection, was at work during the disease outbreak. While genetic diversity at immune markers stayed stable, no population structure emerged, and the inbreeding coefficient at immune markers fell by half– even as it increased 10-fold in neutral markers. Moreover, the genetic difference between bobcats before and after the outbreak was negligible at immune markers, yet notable at neutral markers. Read the publication here.