2018 ESA Annual Meeting (August 5 -- 10)

COS 44-5 - A within-host perspective of URTD dynamics: Infection resistance and tolerance linked to variable host roles in mycoplasma transmission

Tuesday, August 7, 2018: 2:50 PM
335-336, New Orleans Ernest N. Morial Convention Center
Christina M. Aiello1,2, Todd C. Esque1, Kenneth E. Nussear3, Patrick G. Emblidge2 and Peter J. Hudson4, (1)Western Ecological Research Center, U.S. Geological Survey, Henderson, NV, (2)Biology, Pennsylvania State University, University Park, PA, (3)Geography, University of Nevada, Reno, Reno, NV, (4)Biology, Pennsylvania State University, State College, PA
Background/Question/Methods

The epidemiology of infectious diseases depends on many characteristics of disease progression and the degree of heterogeneity expected in these processes between hosts. Following infection, within-host dynamics can influence whether and to what extent pathogens impact host fitness and in turn, whether hosts contribute to pathogen fitness via onward transmission. For many wildlife diseases, these host-pathogen interactions can be difficult to study in detail, particularly for chronic and intermittent diseases within long-lived hosts. North American tortoises in the genus Gopherus face numerous threats, including a pathogenic mycoplasma associated with chronic Upper Respiratory Tract Disease (URTD). Many studies of this disease and its role in host declines produce ambiguous results that may be better interpreted with more data describing the basic features of the infection over longer time periods. To that end, we characterized numerous attributes of M. agassizii infection in 14 captive desert tortoises following horizontal transmission events. We collected data relative to clinical signs of disease, infection intensity, pathogen shedding, and antibody production for nearly 4 years after initial exposure to a donor host.

Results/Conclusions

All tortoises showed evidence of infection establishment (within 10 weeks) and infection persistence at the end of the study (202 weeks), but experienced variable timing and severity of clinical disease and patterns of pathogen resistance and shedding. A measure of host resistance and nasal discharge severity explained 90% of the variation in cumulative pathogen shed during the study. Greater host resistance was also associated with shorter infectious periods. Tortoises appeared to fall into three fairly distinct response categories associated with different infection dynamics: 1) hosts with early and often severe clinical signs, highly successful pathogen reduction (often below detection), and cessation of clinical signs and shedding; 2) hosts with delayed clinical signs, moderate success in pathogen reduction, and slowly dissipating clinical signs and shedding; 3) hosts with mild or often absent clinical signs, no evidence of pathogen reduction, and persistent shedding. These results have important implications for the epidemiology of URTD and the study of disease in wild populations. Temporal and host variation in infection response could underlie many confounding results from URTD studies in Gopherus hosts and explain the widespread distribution of this pathogen despite limited observations of overt disease outbreaks.