Contributors
Susan A Shriner, Wildlife Disease Dynamics, Epidemiology, and Response Project, USDA APHIS WS National Wildlife Research Center. Title: Influenza infections dynamics in wild birds.
Institution/ Affiliation
Susan A Shriner, Wildlife Disease Dynamics, Epidemiology, and Response Project, USDA APHIS WS National Wildlife Research Center.
Presentation Details (date, conference, etc.)
March 24, 2022, IMAG/MSM WG on Multiscale Modeling and Viral Pandemics
- Susan A Shriner, Wildlife Disease Dynamics, Epidemiology, and Response Project, USDA APHIS WS National Wildlife Research Center. Influenza infections dynamics in wild birds. Influenza A viruses (IAVs) are endemic in wild birds but can spillover into poultry and cause serious economic harm. Quantifying infection kinetics is critical to developing predictive disease models aimed at understanding pathogen spread in an effort to prevent spillover. In this study, we evaluated whether IAV exposure dose mediates infection dynamics in mallards, a common IAV reservoir host. We experimentally inoculated 3 groups of 10 mallards with either 103, 104, or 105 EID50 of an H6N2 IAV collected from North American waterfowl during surveillance operations. Each inoculated mallard was housed with three naïve contacts. We collected fine scale viral RNA shedding information throughout the infection in a scheme designed to capture the eclipse, exponential growth, and waning phases of infection. All samples were tested by qPCR. We compared viral RNA output curves by assessing viral RNA peak load, total load, peak day, and shedding period for each dosage group. We modeled log-transformed cumulative viral loads using an exponential asymptote function. In general, viral RNA shedding patterns varied across each of the metrics evaluated with significant individual heterogeneity evident across individuals. On average, the infection curves for mallards inoculated at 104 and 105 EID50 were more similar to each other than the infection curves of the birds infected at 103, suggesting a possible saturation effect at higher exposure doses. In a subsequent experiment, we examined environmental transmission by inoculating a focal mallard and assessing infections in contact ducks added and removed at regular intervals throughout the infection. We replicated this scenario five times. Modeling results indicate that water is the primary driver of transmission and that the concentration of virus in the water is predictive of transmission. We also found that transmission probability varied over time and that mallards became infected at relatively low concentrations of virus in water. As a second follow-up experiment, we collected blood samples from 28 experimentally infected mallards for more than 18 months post exposure to test for antibodies at approximately 4-week intervals. We re-infected the same individuals with the same virus and dose after a year to investigate long-term homosubtypic immunity. After the initial infection, more than half of the ducks exhibited detectable antibodies on day 7 and all ducks were positive on day 10 and remained so through day 28. By day 56, only 39% of ducks were positive by ELISA. Only three individuals had detectable antibodies throughout the year. After the re-challenge, most ducks were antibody positive on day 4, all were antibody positive by day 10, and nearly 70% still showed detectable antibodies on day 140. These results are consistent with an anamnestic response (i.e., a more rapid production of antibodies in greater titers and persistent over a longer time period). Female mallards consistently showed a stronger ELISA response compared to males, but this difference was minor with respect to the percent of positive individuals. Overall, these results indicate antibodies may only be detectable in the short-term in many individuals, but a strong humoral memory may be present. These results have important implications for interpreting surveillance schemes based on serology and shed light on seasonal strain dynamics in mallards. Youtube.