Deep breaths: a reduction in the relative abundance of deer mice and update on hantavirus seroprevalence in Yosemite National Park

Yosemite Valley in August.

We arrived at Camp Curry in the heart of Yosemite Valley well past dark, two days before our long-awaited and highly-anticipated Half Dome hike in June of 2015. After collecting our key, we shined our cell phone flashlights on the uneven rooted terrain that led the way to our tent cabin. A few creaky wooden steps rose to a platform with a heavy-sided canvas structure atop. A rusty but sturdy bear-proof box for our food was situated a few steps away from the door. We unlocked the tent and flicked on the single lightbulb to inspect our rustic accommodations. Two simple cots. Several wool blankets. A tiny table. My spouse put down his bag and turned to go begin hauling the rest of our gear from the car. I hesitated, and began nervously shining my flashlight in the corners and around the edges of the floor, looking for mouse droppings. Thankfully, I saw none. As my spouse arrived with the first load of gear, I thoroughly inspected our hiking packs for any stashed away snacks to put in the bear-proof box. It wasn’t bears I was afraid of, rather a little rodent that could potentially be carrying a very big problem. 

Tent cabins in Curry Village, Yosemite Valley.
Creature comforts

In the summer of 2012, Camp Curry provided a “glamping” option when they unveiled a suite of new solid-walled tents. These cabins were well-insulated, so they were heated and sturdy enough that people were allowed to keep their food inside with them, rather than having to lock in out in the metal bear-proof box. Insulation, warmth, and food keep us humans pretty happy. Problem was, those amenities were also quite inviting to deer mice (Peromyscus maniculatus). This species is a main host of hantavirus, the cause of a highly-deadly respiratory illness transmitted by aerosolized (or made airborne when dried) feces and urine of infected mice. By the end of that summer, at least ten people who stayed in the new “glamping” cabins developed hantavirus pulmonary syndrome, and three of them died. Once the cause and locations of the infections were determined, Yosemite promptly destroyed the solid-walled tent cabins and began focusing on better rodent exclusion techniques. The infections stopped.

Tracking the disease…by tracking the mice

Continual monitoring for hantavirus in Yosemite is a high priority for the California Department of Public Health. Since the 2012 outbreak, they have conducted annual rodent trappings and serosurveys (blood testing) for the presence of the virus in the two main areas of the park where the original outbreak occurred: Yosemite Valley, a vacation hotspot, and Tuolumne Meadows, a more remote area. The researchers estimated the abundance of mice using trap success (number of mice trapped divided by the total number of traps set), collected information about the age, weight, and sex for the mice found to have immune evidence of current or past infection, and recorded environmental climate variables to understand whether these play any part in increases or decreases in mouse abundance or infection rates. Climate variables included average monthly temperatures during the trapping month, average monthly temperature in months before and after trapping, as well as precipitation at the time of trapping and in the previous year.

Deer mouse (Peromyscus maniculatus)

The vast majority of rodents captured were deer mice. The researchers found that while the infection prevalence within deer mice trapped within the camping areas in Yosemite Valley had not changed since the hantavirus outbreak in 2012, there were significantly fewer mice trapped within the more frequently visited Valley than the more remote Tuolumne Meadows camping locations. There were more hantavirus-positive mice found in Tuolumne Meadows, but interestingly researchers were unable to identify any relationship between deer mice abundance and infection rates at either site with any environmental or climate variables.


The findings suggest that the deer mouse population in Yosemite National Park appears to maintain a steady hantavirus infection rate that is not directly tied to environmental variables like temperature and precipitation. This is important because it means that officials, at least at the moment, do not have to be concerned about a spike in infection prevalence due to events like heavy rains or heat waves and their effect on deer mice populations. Another key takeaway is the evidence that efforts to prevent rodent infestation in and around Yosemite Valley appear successful due to the low relative number of deer mice captured there. Without ample shelter and food available, in addition to strategic snap-trap placement in hard-to-exclude shelters, the mice appear to have returned to a more natural habitat (like Tuolumne Meadows) where they can find typical food sources. Ongoing monitoring will be able to easily detect changes in these patterns and allow officials to adjust plans accordingly. 

The importance of public health in disease ecology

The hantavirus outbreak story reasonably strikes fear, but thorough public health investigations like this one and education campaigns can help us feel safe and continue enjoying the outdoors. My spouse and I did not see any evidence of deer mice in our tent during our stay in Curry Village, but we received ample education from park rangers about it. Awareness, not avoidance, seems to be the name of the game and for that, I’m glad. We had the time of our lives attempting the Half Dome hike that week, and though we didn’t make it to the summit due to an impending storm, we were able to enjoy our stay in one of the most beautiful wild spaces in the country.



Danforth ME, Messenger S, Buttke D, Weinburke M, Carroll G, Hacker G, et al. Long-Term Rodent Surveillance after Outbreak of Hantavirus Infection, Yosemite National Park, California, USA, 2012. Emerg Infect Dis. 2020;26(3):560-567.


Reviewed by:

Share this:

Heather Kopsco

I'm a disease ecologist interested in infectious disease emergence and spillover from wildlife to humans (and vice versa) as a result of human-induced climate and landscape alterations. I completed my PhD in May 2020 at the University of Rhode Island where I researched tick-borne disease socioecology. Currently, I am a postdoctoral research associate in the Smith lab at the University of Illinois Urbana-Champaign College of Veterinary Medicine where I am working on species distribution models of ticks and tickborne disease in Central Illinois.

Leave a Reply