<i>Hematodinium</i> sp. infection does not drive collateral disease contraction in a crustacean host.

Abstract

Host, pathogen, and environment are determinants of the disease triangle, the latter being a key driver of disease outcomes and persistence within a community. The dinoflagellate genus <i>Hematodinium</i> is detrimental to crustaceans globally - considered to suppress the innate defences of hosts, making them more susceptible to co-infections. Evidence supporting immune suppression is largely anecdotal and sourced from diffuse accounts of compromised decapods. We used a population of shore crabs (<i>Carcinus maenas</i>), where <i>Hematodinium</i> sp. is endemic, to determine the extent of collateral infections across two distinct environments (open-water, semi-closed dock). Using a multi-resource approach (PCR, histology, haematology, population genetics, eDNA), we identified 162 <i>Hematodinium-</i>positive crabs and size/sex-matched these to 162 <i>Hematodinium-</i>free crabs out of 1191 analysed. Crabs were interrogated for known additional disease-causing agents; haplosporidians, microsporidians, mikrocytids, <i>Vibrio</i> spp., fungi, <i>Sacculina</i>, trematodes, and haemolymph bacterial loads. We found no significant differences in occurrence, severity, or composition of collateral infections between <i>Hematodinium</i>-positive and <i>Hematodinium</i>-free crabs at either site, but crucially, we recorded site-restricted blends of pathogens. We found no gross signs of host cell immune reactivity towards <i>Hematodinium</i> in the presence or absence of other pathogens. We contend <i>Hematodinium</i> sp. is not the proximal driver of co-infections in shore crabs, which suggests an evolutionary drive towards latency in this environmentally plastic host.