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Peer-reviewed veterinary case report

Anthropogenic disturbance on island ecosystems promotes inflammation and zoonotic pathogens among invasive rats.

Journal:
The Science of the total environment
Year:
2026
Authors:
Seguel, M et al.
Affiliation:
Department of Pathobiology
Species:
rodent

Abstract

Invasive species and landscape disturbance are major drivers of emerging infectious diseases, particularly in island ecosystems where native wildlife evolved in ecological isolation. However, the mechanisms linking anthropogenic disturbance, host immune function, and pathogen transmission on island systems remain poorly understood. We investigated how small-scale anthropogenic disturbance influences host diet, body condition, immunity, and zoonotic pathogen carriage among invasive black rats (Rattus rattus) on Guafo Island, a remote island in the northern Chilean Patagonia. Using a spatial mosaic of undisturbed and disturbed habitats, we combined field ecology, immunopathology, and molecular diagnostics to assess inflammation and infection risk. Rats from human-altered habitats had access to human food sources and exhibited higher population densities and improved body condition. Although body condition was higher, rats in these human-intervened habitats had increased systemic inflammation and more marked Th2-type inflammation compared to rats in more pristine areas of the island. These immunopathological changes were associated with increased prevalence of Leptospira interrogans and Calodium hepaticum infection. These effects were independent of rat abundance and body condition, suggesting that Th2 immune skewing in rats in disturbed island habitats may independently enhance pathogen shedding. Our findings indicate that even minimal landscape disturbance in an otherwise pristine ecosystem can alter invasive species' immunity and amplify zoonotic risk, highlighting the importance of early intervention and ecological monitoring in remote island systems undergoing human encroachment.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/41364997/