Energetic and oxidative costs of microfilarial infection: evidence for fitness trade-offs in male village weavers of the Amurum Forest Reserve.

Abstract

Microfilariae contribute to a higher energetic demand that could lead to oxidative damage and reduce hosts' fitness. Yet reports about the energy status and oxidative stress‐defense mechanisms of infected wild birds are rarely documented. We investigated the relationship between microfilariae and the energy status and oxidative damage‐defense mechanisms of male village weavers Ploceus cucullatus during pre‐breeding and post‐breeding seasons (which also coincide with the birds' moult periods). Specifically, we investigated: 1) how glucose concentrations in filarial‐infected male village weavers varied during pre‐ and post‐breeding periods, and 2) how the superoxide dismutase (SOD) and malondialdehyde (MDA) levels of the infected birds varied during these two periods. A total of 117 adult male birds were trapped. During the pre‐breeding period, 53% (33 of 62) of the individuals undergoing a pre‐breeding moult were infected, and 47% (29 of 62) were non‐infected. During the post‐breeding period, 42% (23 of 55) of the individuals undergoing a post‐breeding moult were infected, and 58% (32 of 55) were non‐infected. We observed a significant positive relationship(p < 0.05) between microfilaria infection status and plasma glucose levels, as well as between infection status and the breeding phases. However, the interaction between infection status and breeding phases was negatively correlated with plasma glucose concentration. We also found that both breeding phases and infection status were positively correlated with SOD, and that the interaction between infection status and MDA correlated negatively with SOD. However, there was no direct relationship observed between MDA and SOD levels. Our findings suggest that the effect of MDA on SOD may depend on microfilaria infection status. This implies that male village weavers could be experiencing fitness costs due to oxidative imbalance – potentially through compromised antioxidant defenses during the pre‐breeding and post‐breeding periods in infected individuals.