Demographic buffering and compensatory recruitment promotes the persistence of disease in a wildlife population

Abstract

Demographic buffering allows populations to persist by compensating for fluctuations in vital rates, including disease‐induced mortality. Using long‐term data on a badger (Meles meles Linnaeus, 1758) population naturally infected with Mycobacterium bovis, we built an integrated population model to quantify impacts of disease, density and environmental drivers on survival and recruitment. Badgers exhibit a slow life‐history strategy, having high rates of adult survival with low variance, and low but variable rates of recruitment. Recruitment exhibited strong negative density‐dependence, but was not influenced by disease, while adult survival was density independent but declined with increasing prevalence of diseased individuals. Given that reproductive success is not depressed by disease prevalence, density‐dependent recruitment of cubs is likely to compensate for disease‐induced mortality. This combination of slow life history and compensatory recruitment promotes the persistence of a naturally infected badger population and helps to explain the badger's role as a persistent reservoir of M. bovis.

Multiple mechanisms confer stability to isolated populations of a rare endemic plant

“…Some other studies have found potentially significant effects of demographic rate buffering on extinction risk (Garcia , McDonald et al. ), while others have not (Compagnoni et al. ).…”

“…, McDonald et al. ); (4) asynchronous responses to environmental fluctuations among subpopulations or individuals can stabilize numbers and thus buffer populations from extinction via the portfolio effect (e.g., Moore et al. , Schindler et al.…”

Inbreeding intensifies sex‐ and age‐dependent disease in a wild mammal

“…The analyses presented here cannot determine whether links between inbreeding, disease and age are weaker among males or are instead not evident due to the selective mortality of infected and/or inbred males. We suggest that complex multistate models of age, infection status, sex and inbreeding (sensu (McDonald et al., )) will be required to model simultaneously the processes of disease transmission, progression between disease states, survival and ageing, and how they depend on inbreeding in both sexes. Such multistate models would also help tease apart the processes of changes in exposure to and tolerance of infection with increasing age, and the cumulative and instantaneous effects of age on exposure and disease progression.…”

“…Additionally, management of TB in badgers through culling may alter the genetic structure of their populations, either by increasing levels of inbreeding through reducing density and an associated compensatory recruitment of cubs (McDonald et al., ), or by decreasing inbreeding as surviving individuals range more widely (Riordan, Delahay, Cheeseman, Johnson, & Macdonald, ), increasing mixing among remaining groups. Our results highlight the importance of considering the role that host genotype plays on disease outcomes, an area which until recently has been largely overlooked (Allen et al., ).…”

Fragile coexistence of a global chytrid pathogen with amphibian populations is mediated by environment and demography

“…Secondly, the pathogen may be parasitic but have compensatory, rather than additive, effects on the vital rates of individual hosts; that is, the individuals that die of disease would also have had higher mortality rates in the absence of the pathogen [13]. Alternatively, the parasitic pathogen may inflict additive mortality, but this is compensated at the host population level, for example through increased recruitment and a shift in age structure [4,14,15]. Understanding whether, and by what mechanisms, host populations truly coexist with a pathogen is crucial for predicting and eventually managing the potential impacts of a disease.…”