3 years ago

Chronic disease in the Mojave desert tortoise: Host physiology and recrudescence obscure patterns of pathogen transmission

Chronic disease in the Mojave desert tortoise: Host physiology and recrudescence obscure patterns of pathogen transmission
Franziska C. Sandmeier, Sally DuPré, K. Nichole Maloney, C. Richard Tracy, David Hyde, Ron Marlow, Hamid Mohammadpour, Kenneth Hunter
A seminatural, factorial-design experiment was used to quantify dynamics of the pathogen Mycoplasma agassizii and upper respiratory tract disease in the Mojave desert tortoise (Gopherus agassizii) over 2 years. Groups of initially healthy animals were separated into serologically positive (seropositive), seronegative, and artificially infected groups and paired into 23 pens. We found no evidence of long-term immune protection to M. agassizii or of immunological memory. Initially seronegative, healthy tortoises experienced an equal amount of disease when paired with other seronegative groups as when paired with seropositive and artificially infected groups—suggesting that recrudescence is as significant as transmission in introducing disease in individuals in this host–pathogen system. Artificially infected groups of tortoises showed reduced levels of morbidity when paired with initially seronegative animals—suggesting either a dilution effect or a strong effect of pathogen load in this system. Physiological dynamics within the host appear to be instrumental in producing morbidity, recrudescence, and infectiousness, and thus of population-level dynamics. We suggest new avenues for studying diseases in long-lived ectothermic vertebrates and a shift in modeling such diseases. A factorial-design experiment was used to quantify dynamics of a pathogen and respiratory tract disease in the Mojave desert tortoise over 2 years, based on 23 experimental pairings of groups of animals that included ones with long-term immune responses to the pathogen, no previous evidence of disease or immune responses, and artificially infected animals. We found no evidence of long-term immune protection and found that rates of recrudescence of disease were at least as high as rates of transmission of disease. In particular, recrudescence of disease within individual, long-lived adults maintained disease within experimental groups, and similar mechanisms likely maintain disease in natural populations.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1002/ece3.3480

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