Increased susceptibility of polar bears to zoonotic pathogens due to prolonged starvation

Dear Editor,

While reading this article (1), my mind went to another recently published work, focused on the links between the Arctic Sea ice melting and the climate change-driven, prolonged starvation experienced by polar bears (Ursus maritimus) (2).

Indeed, the progressively declining Arctic Sea ice thickness represents a leading cause of the profound ecological, behavioural, feeding and dietary pattern modifications reported with an increased frequency in this highly threatened apex predator (2).

Within this framework, polar bears’ stress arising from chronic starvation is of further concern.

Indeed, besides being a powerful and efficient machinery allowing us and all the other living organisms to cope with a huge number of environmental stressors, chronic stress responses are invariably characterized by immunosuppression, originating from enhanced cortisol production (3).

Therefore, while increased cortisol levels would be plausibly expected to occur in the blood of these undernourished polar bears (2), it should be additionally emphasized that they could also become, at the same time, more susceptible to microbial pathogens impacting their already threatened health and conservation status.

This could hold true also for zoonotic agents like Toxoplasma gondii, a cosmopolitan protozoan parasite infecting humans alongside a huge number of terrestrial and aquatic vertebrates, including polar bears. In this respect, anti-T. gondii antibodies were reported in almost half of the polar bears from Svalbard, Norway, with male individuals exhibiting higher seroprevalence values than females and with the infection’s frequency turning out to have doubled in comparison to another study previously carried out in the same area (4).

Furthermore, the well-known top predator position occupied by polar bears within the marine food chain makes these animals prone to bioaccumulate and biomagnify a huge number of persistent environmental pollutants within their body tissues, including immunotoxic heavy metals like methyl mercury (methyl Hg) (5).

Summarizing, the immunosuppression synergistically induced by the chronic stress response deriving from prolonged starvation as well as by the high tissue concentrations of immunotoxic environmental xenobiotics, may render polar bears more sensitive to the acquirement and subsequent development of various infectious disease processes (of both viral and non-viral nature) impacting their already threatened health and conservation status, including SARS-CoV-2 infection, for which a progressively expanding wild and domestic animal host range has been clearly documented (6).

Once again, therefore, a multidisciplinary and One Health-based approach would be strongly recommended in order to get proper insight into, and adequately counteract also, the alarming risk of getting another so iconic “biodiversity piece” irreversibly lost!

References

1) Dyer, O. Alaskapox: First human death from zoonotic virus is announced. BMJ 384, q415 (2024).
doi: 10.1136/bmj.q415.

2) Pagano, A.M., Rode, K.D., Lunn, N.J., et al. Polar bear energetic and behavioral strategies on land with implications for surviving the ice-free period. Nat. Commun. 15, 947 (2024). https://doi.org/10.1038/s41467-023-44682-1.

3) O’Leary, A. Stress, emotion, and human immune function. Psychol. Bull.108, 363-382 (1990). doi: 10.1037/0033-2909.108.3.363.

4) Jensen, S.K., Aars, J., Lydersen, C., et al. The prevalence of Toxoplasma gondii in polar bears and their marine mammal prey: evidence for a marine transmission pathway? Polar. Biol. 33, 599-606 (2010). https://doi.org/10.1007/s00300-009-0735-x.

5) St Louis, V.L., Derocher, A.E., Stirling, I., et al. Differences in mercury bioaccumulation between polar bears (Ursus maritimus) from the Canadian high- and sub-Arctic. Environ. Sci. Technol. 45, 922-928 (2011). doi: 10.1021/es2000672.

6) Di Guardo, G. The SARS-CoV-2 pandemic at the wildlife-domestic animal-human interface. Pathogens 12(2), 222 (2023). doi: 10.3390/pathogens12020222.