OOS 36-1 - Bighorn sheep pneumonia driving species decline: Developing an evidence base to manage infectious disease in wildlife

Friday, August 12, 2016: 8:00 AM
Grand Floridian Blrm A, Ft Lauderdale Convention Center
Raina K. Plowright, Microbiology and Immunology, Montana State University, Frances Cassirer, Idaho Dept. of Fish and Game, Lewiston, ID, Thomas E Besser, Veterinary Microbiology and Pathology, Washington State University College of Veterinary Medicine, Pullman, WA, Kezia Manlove, College of Veterinary Medicine, Washington State University, Bozeman, MT, Emily Almberg, Montana Fish, Wildlife, and Parks, Bozeman, MT, Paul Chafee Cross, Northern Rocky Mountain Science Center, US Geological Survey, Bozeman, MT and Peter J. Hudson, The Huck Institutes of Life Sciences, Penn State University, University Park, PA

Bighorn sheep pneumonia caused by Mycoplasma ovipneumoniae (M. ovi) has been a major factor driving the extirpation of bighorn sheep from their historic ranges. Efforts to recover BHS are largely failing because of ongoing mortality from pneumonia in chronically infected populations. We present the results of a long-term interdisciplinary study of bighorn sheep pneumonia incorporating nearly 20 years of population monitoring across 16 interconnected populations. Our approaches include microbiology, pathogen sequencing, longitudinal monitoring of individuals, statistical and dynamic modeling of disease dynamics, and spatial analyses of population and disease dynamics. During this period our team identified the causative pathogen and unraveled the basic epidemiological features of bighorn sheep pneumonia and the mechanisms promoting pathogen persistence.


We present clinical, pathological, and epidemiological evidence that M. ovi is the causative agent of bighorn sheep pneumonia. The initial invasion of M. ovi into naïve bighorn sheep populations typically caused mortality ranging from 30-90% across all age classes. Subsequent to invasion, surviving adults experienced low levels of sporadic mortality from pneumonia, while severe recurrent summer pneumonia outbreaks were experienced by lambs, presumably as a result of M. ovi infection from asymptomatic carrier ewes. Longitudinally sampled individual bighorn sheep were either chronic or intermittent shedders, or resistant nonshedders. Older animals were more likely to be chronic shedders. Both shedders and other adults in chronically infected populations had survival rates comparable to adults in uninfected populations. Chronically infected populations had various outcomes: Some populations recovered after a few years of summer lamb pneumonia outbreaks, while other populations experienced ongoing lamb pneumonia outbreaks, limiting recruitment for years to decades. Depending on these outcomes, some populations managed to persist with a stagnant population size, or even sustained a low rate of positive population growth, while others slowly declined and one population was driven to extinction. We present a range of hypotheses to explain this phenomenon. Bighorn sheep immunity to M.ovi may be strain specific, suggesting that domestic sheep or goats may pose ongoing risks even to bighorn sheep previously infected with other strains of M.ovi. We discuss the implications of our findings for the long-term conservation and recovery of bighorn sheep.