Abstract
Individual host immune responses to infectious agents drive epidemic behavior and are therefore central to understanding and controlling infectious diseases. However, important features of individual immune responses, such as the strength and longevity of immunity, can be challenging to characterize, particularly if they cannot be replicated or controlled in captive environments. Our research on bighorn sheep pneumonia elucidates how individual bighorn sheep respond to infection with pneumonia pathogens by examining the relationship between exposure history and survival in situ. Pneumonia is a poorly understood disease that has impeded the recovery of bighorn sheep (Ovis canadensis) following their widespread extirpation in the 1900s. We analyzed the effects of pneumonia-exposure history on survival of 388 radio-collared adults and 753 ewe-lamb pairs. Results from Cox proportional hazards models suggested that surviving ewes develop protective immunity after exposure, but previous exposure in ewes does not protect their lambs during pneumonia outbreaks. Paradoxically, multiple exposures of ewes to pneumonia were associated with diminished survival of their offspring during pneumonia outbreaks. Although there was support for waning and boosting immunity in ewes, models with consistent immunizing exposure were similarly supported. Translocated animals that had not previously been exposed were more likely to die of pneumonia than residents. These results suggest that pneumonia in bighorn sheep can lead to aging populations of immune adults with limited recruitment. Recovery is unlikely to be enhanced by translocating naïve healthy animals into or near populations infected with pneumonia pathogens.
Highlights
The population-level dynamics of infectious diseases in both time and space are shaped by individual-level responses to infection: how long an individual is infectious, how many individuals she or he infects, and how that host develops resistance to subsequent exposures
Past exposure was significantly associated with a decrease in relative risk of pneumonia, as were the number of previous exposure events (Count)
Without directly identifying the pathogen, we found that ewes develop some level of protective immunity following exposure; protection may wane in the absence of exposure or be boosted by repeated exposures; protective immunity is not effectively transferred from ewes to lambs; and unexposed animals translocated near infected populations have a high risk of developing pneumonia
Summary
The population-level dynamics of infectious diseases in both time and space are shaped by individual-level responses to infection: how long an individual is infectious, how many individuals she or he infects, and how that host develops resistance to subsequent exposures. A high R0 (basic reproductive rate of a disease) [1] coupled with lifelong immunity drives diseases like measles to become so-called childhood diseases characterized by an early age of infection and an adult population mostly resistant to infection but with a small proportion of susceptible individuals protected by herd immunity [2] Infections with these characteristics can persist within populations larger than a critical community size, where births introduce a sufficient number of susceptible hosts to keep the effective R0 above unity [3], or by reinvasion of smaller populations within a metapopulation [4]. M. ovipneumoniae impairs mucociliary clearance and increases the probability of multiple opportunistic lung infections that are the proximate cause of death [11,12,13]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
