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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  Hematodinium  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 ( Carcinus maenas ), where  Hematodinium  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  Hematodinium- positive crabs and size/sex-matched these to 162  Hematodinium- free crabs out of 1191 analysed. Crabs were interrogated for known additional disease-causing agents; haplosporidians, microsporidians, mikrocytids,  Vibrio  spp., fungi,  Sacculina , trematodes, and haemolymph bacterial loads. We found no significant differences in occurrence, severity, or composition of collateral infections between  Hematodinium -positive and  Hematodinium -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  Hematodinium  in the presence or absence of other pathogens. We contend  Hematodinium  sp. is not the proximal driver of co-infections in shore crabs, which suggests an evolutionary drive towards latency in this environmentally plastic host.

Hematodinium sp. infection does not drive collateral disease contraction in a crustacean host