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Notre Dame (Indiana) – Anthropogenic change is contributing to the increase in emerging infectious diseases. Not only humans are affected, but also flora and fauna. Protecting natural biodiversity and reducing environmental pollution from chemicals would be effective countermeasures, emphasize American life scientists in their in Nature published meta-analysis (2024; DOI: 10.1038/s41586-024-07380-6).
Human socioeconomic and ecological interests are causing changes in the landscape, biodiversity, climate and infection rates caused by new pathogens around the world. In a meta-analysis, American life scientists tried to answer which anthropogenic drivers most favor infectious diseases.
To this end, the literature was searched for infectious diseases and parasitism in plant, animal and human host organisms and evaluated for global changes. 2,938 observations resulting from infectious diseases that were documented in connection with global change were taken into account. These included 1,497 cases of parasite-host relationships.
Key parameters for the increase in infectious diseases were, for example, reductions in the biological diversity of flora and fauna, introduced neozoa and environmental pollution from chemicals.
Possible other factors such as urbanization, natural biodiversity gradients, deforestation and forest fragmentation were less important as disease drivers, say the study authors. Overall, the results were consistent with regard to infectious diseases in humans, plants and animals.
The results of this meta-analysis should help to keep a close eye on the main infection drivers in the wake of global change. The study authors emphasize that more emphasis should be placed on reducing greenhouse gas emissions even further.
In addition, existing ecosystems should be protected above all from other species invading them. Biological invasions and the loss of endemic biodiversity were main factors for the increase in (parasitic) infectious diseases in the plant and animal world and also in humans. © cw/aerzteblatt.de
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