Data from: Detecting signals of chronic shedding to explain pathogen persistence: Leptospira interrogans in California sea lions

Identifying mechanisms driving pathogen persistence is a vital component
of wildlife disease ecology and control. Asymptomatic, chronically
infected individuals are an oft-cited potential reservoir of infection but
demonstrations of the importance of chronic shedding to pathogen
persistence at the population level remain scarce. Studying chronic
shedding using commonly collected disease data is hampered by numerous
challenges, including short-term surveillance that focuses on single
epidemics and acutely ill individuals, the subtle dynamical influence of
chronic shedding relative to more obvious epidemic drivers, and poor
ability to differentiate between the effects of population prevalence of
chronic shedding versus intensity and duration of chronic shedding in
individuals. We use chronic shedding of Leptospira interrogans serovar
Pomona in California sea lions (Zalophus californianus) as a case study to
illustrate how these challenges can be addressed. Using
leptospirosis-induced strands as a measure of disease incidence, we fit
models with and without chronic shedding, and with different seasonal
drivers, to determine the timescale over which chronic shedding is
detectable and the interactions between chronic shedding and seasonal
drivers needed to explain persistence and outbreak patterns. Chronic
shedding can enable persistence of L. interrogans within the sea lion
population. However, the importance of chronic shedding was only apparent
when surveillance data included at least two outbreaks and the intervening
inter-epidemic trough during which fadeout of transmission was most
likely. Seasonal transmission, as opposed to seasonal recruitment of
susceptibles, was the dominant driver of seasonality in this system, and
both seasonal factors had limited impact on long-term pathogen
persistence. We show that the temporal extent of surveillance data can
have a dramatic impact on inferences about population processes, where the
failure to identify both short- and long-term ecological drivers can have
cascading impacts on understanding higher-order ecological phenomena, such
as pathogen persistence.