Systemic inflammation impairs recovery from hookworm-associated anemia in a wild marine mammal host

Violetta Zaitseva¹Nanami Arakawa²Carmon Co¹Aranza Gomez-Camus³Diego Perez-Venegas⁴Felipe Montalva⁵Josefina Gutierrez⁶Claudia Ulloa-Contreras⁷Ricardo Chihuailaf⁸Claudio Verdugo⁶Dorothee Bienzle¹Mauricio Seguel^3*

• ¹University of Guelph, Guelph, Canada
• ²Kagoshima University, kagoshima, Japan
• ³St George's University, Saint George's, Grenada
• ⁴Universidad Andres Bello, Santiago, Chile
• ⁵Guafo Science Research Group, Quellon, Chile
• ⁶Universidad Austral de Chile Instituto de Patologia Animal, Valdivia, Chile
• ⁷millenium institute Biodiversity of Antarctic and Subantarctic Ecosystems, Santiago, Chile
• ⁸Universidad Austral de Chile, Valdivia, Chile

Inflammation is a critical defense against pathogens but can impair iron metabolism and erythropoiesis, potentially causing or exacerbating anemia during infection. However, the ecological and evolutionary relevance of this trade-off remains poorly understood. Naturally co-evolved host–parasite systems offer a unique opportunity to explore how inflammatory responses balance the benefits of pathogen control against potential physiological costs. We examined how systemic inflammation affects recovery from hookworm-associated anemia in South American fur seal (Arctocephalus australis) pups, aiming to determine whether inflammation facilitates recovery or imposes hematological constraints. We longitudinally monitored 83 pups over approximately 3 months on Guafo Island, Northern Pacific Chilean Patagonia, measuring hookworm burden, hematological parameters, iron concentration, and blood cytokines. Seventy-two percent of the pups developed clinical hookworm infection, and 47% of these became anemic. Among anemic pups, 54% recovered from anemia 2 months after infection. Changes in inflammatory markers, but not hookworm burden, iron concentration, or body condition, predicted recovery outcome. Sustained increases in IFN-γ and neutrophils reduced the likelihood of recovery, while increased IL-10 concentration favored recovery. These effects were independent of plasma iron concentration, although IL-6 was uniquely associatednegatively correlated with lower plasma iron. Our findings show that prolonged systemic inflammation impairs recovery from anemia in a wild marine mammal, highlighting a physiological cost of inflammation in early life as a key ecological trade-off between immune defense and hematological resilience in natural host–parasite systems.