Year of Award

2018

Document Type

Dissertation

Degree Type

Doctor of Philosophy (PhD)

Degree Name

Fish and Wildlife Biology

Department or School/College

College of Forestry and Conservation

Committee Co-chair

L. Scott Mills, Michael K. Schwartz

Commitee Members

Mark Hebblewhite, Gordon Luikart, Angela Luis

Keywords

African lion, Canine distemper virus, Cross-species transmission, Disease spillover, Evolutionary genetics, Molecular epidemiology

Abstract

The impact of emerging infectious diseases (EIDs) on the health and persistence of wildlife populations is an increasing conservation concern. Large carnivores are particularly vulnerable to EID impacts because they often occur in small, isolated populations with demographic and genetic challenges to long-term persistence. Ecological forces that isolate carnivore populations, e.g. agricultural intensification, simultaneously increase the probability of disease exposure from domestic species and can amplify population susceptibility to infection.

Canine distemper virus emerged as a conservation threat to African lions when an explosive epizootic caused the death or disappearance of a third of the Serengeti lion population in 1994. This same lion population was exposed to CDV on several other occasions without overt clinical infection. For my dissertation, I investigated ecological, epidemiological, and evolutionary factors contributing to the emergence and outcome of CDV infection in this globally important population.

Based on phylodynamic analyses of annotated sequence data I found that the lethal outbreak in 1994 was likely catalyzed by a single spillover event from a canid reservoir, and fueled by repeated transmissions from non-canid hosts, e.g. spotted hyenas. Distinct genotypes were found in canid and non-canid hosts suggesting that there is a host barrier to CDV spillover, which might limit lethal outbreaks in lions. Expanding the spatiotemporal scope of the phylogenetic analysis I found that Serengeti lions were not epidemiologically connected to other carnivore populations at the regional or continental scale. Recurrent CDV infection in Serengeti lions was likely due to local persistence in the domestic and/or wild carnivore community. Finally, based on phylogenetic and selection analyses I identified 25 candidate markers in the CDV genome potentially associated with the pathogenicity of infection in lions during the 1994 outbreak. These were mostly found in functional domains related to transcription and replication, and viral egress, implicating these processes as possible barriers to disease in lions. Mutations at two of the markers were shared with two CDV outbreaks in North America that caused clinical infection in African lions. Surveillance for these two mutations in circulating strains may inform CDV risk assessment in lion populations of conservation concern.

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© Copyright 2018 Julie Kay Weckworth