The effects of anthropogenic global changes on immune functions and disease resistance

Abstract

Humans are changing the environmental conditions of our planet, and animal immune functions are being affected by these modifications. For instance, a diversity of chemical contaminants is entering ecosystems and modifying immune functions directly or indirectly through altered host-parasite interactions. Also, global temperature changes have caused outbreaks of disease that have decimated and even extirpated some host species, outcomes partially driven via immune alterations. Finally, some invasive species are immunologically distinct or impose stress on native species, factors that may facilitate the establishment of nonnative hosts as well as parasite transmission to native species. Here, we summarize the known and likely effects of pollutants, nonnative species introductions, and increases in ambient temperature on host immune functions and infections. We then identify future directions for research given our sparse knowledge of immune variation in natural populations. In sum, we advocate integrative, multidisciplinary work at diverse spatial and temporal scales to assess and prevent anthropogenic global changes from further compromising animal immune functions.

Linking global climate and temperature variability to widespread amphibian declines putatively caused by disease

“…Of the tested climate-based hypotheses for Atelopus declines, only the climate-variability hypothesis was supported here, consistent with previous findings that temperature variability compromises amphibian immune defenses (32) and that disease outbreaks frequently occur during extreme temperature events (33). Increases in climate variation are often linked to increases in the intensity and frequency of extreme events, which are projected to increase with anthropogenic climate change (1).…”

“…Finally, there is the climate-variability hypothesis, which proposes that temporal variability in temperature partially drives amphibian disease dynamics (32), although temperature variability could contribute directly to declines as well. This hypothesis is partly based on observations that disease outbreaks are often associated with extreme temperature events (33) and partly on evidence that temporal variability in temperature can cause suboptimal immunity in amphibians, potentially increasing their susceptibility to Bd or other infections (32). Many components of amphibian innate and adaptive immune systems depend on external temperature, but it takes time for amphibians to adjust these systems to temperature changes.…”

“…Although increases in temperature induced by global warming are expected to be small in tropical relative to temperate regions, recent evidence suggests that the greatest extinction risk from global warming might be for ectotherms in the hyperdiverse tropics because of their adaptations to relatively narrow and stable temperature ranges (46,47). Effects of temporal variation in temperature might also be generalizable across ectotherm classes, given many conserved components of ectotherm innate and adaptive immune responses (32)(33)(34). If so, elevated temperature variability caused by climate change could diminish the defenses of ectothermic hosts generally, potentially representing a common, but underappreciated, link between climate change and both disease and the loss of biodiversity.…”

Variations of transcript profiles between sea otters Enhydra lutris from Prince William Sound, Alaska, and clinically normal reference otters

“…Consistent with our findings of relatively normal transcription of AHR, Bodkin et al (2012) indicated that average annual oil encounter rates ranged from 2 to 24 times yr −1 for females, and 2 to 4 times yr −1 for males. Mitigation of detrimental effects imposes demands on animals above those normally required to sustain life and may result in reduction of fitness evidenced by decreased reproductive capability, increased susceptibility to disease, or disadvantageous behavioral changes (Graham et al 2010, Martin et al 2010. Such effects may ultimately be manifested in reduced survival rates , Monson et al 2011) that contributed to the delayed recovery of sea otters observed in areas of PWS initially oiled in 1989 (Bodkin et al 2002).…”

Host stress physiology and Trypanosoma haemoparasite infection influence innate immunity in the woylie ( Bettongia penicillata )

“…However, significant knowledge gaps remain in wildlife immunology including lack of basic species-specific data and outstanding questions surrounding factors that influence immune responses and infection patterns [2,4]. The relationship between immune function and infection has rarely been examined in wildlife despite suggestions that these processes play a part in health, population decline and extinction [5][6][7].…”