The influence of parasite infection on host thermal tolerance remains poorly understood. To address this, we investigated how infection with the trematode Himasthla elongata affects survival and heat shock protein expression in the blue mussel Mytilus edulis following repeated exposure to heat stress in a simulated intertidal environment. Two groups of mussels with experimentally induced low (55. 3 ± 35. 6 metacercariae per mussel) and high (148. 6 ± 78. 2 metacercariae per mussel) infection levels were exposed to air (31°C, 33°C or 35°C) for 2 h over 10 days to simulate a tidal cycle. Survival was assessed daily. In addition, the mRNA expression level of three heat shock genes (hsp24, hsp70 and hsp90) was assessed in mussels exposed to 17°C and 33°C for 2 h over a three-day period. Dissection confirmed clear differences in infection levels between groups. Survival decreased significantly with increasing air temperature, but in the 35°C treatment, mussels with high infection levels exhibited a near-significant increase in survival. Expression of hsp24, hsp70 and hsp90 increased with rising air temperatures, and high infection levels significantly upregulated hsp90. Although trematode infection did not significantly increase survival, our results suggest that trematode infection can protect against thermal stress by upregulating specific heat shock proteins in M. edulis. The hsp responses point to a parasite-induced tolerance mechanism, potentially through stress priming or frontloading, and highlight an overlooked role of parasitism in mediating thermal resilience in intertidal ecosystems.
Greve et al. (Mon,) studied this question.