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 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.
Highlights
Host-parasite interactions are intimate and complex – the host cannot afford to 46 overreact and risk immediate costs such as metabolic derangement and longer-term fitness costs, yet must maintain adequate defences to fight, and recover from, parasitic insult
72 c oxidase I submit (COI) 268 haplotypes were identified among the 320 individual nucleotide sequences (481 bp 269 in length) of C. maenas (Figure 1)
No significant Fst value was observed between Dock and Pier locations, indicating that the crabs from two sites were genetically similar (Supplementary Table 4)
Summary
Host-parasite interactions are intimate and complex – the host cannot afford to 46 overreact and risk immediate costs such as metabolic derangement (or self reactivity) and longer-term fitness costs, yet must maintain adequate defences to fight, and recover from, parasitic insult. The advanced colonisation of the haemolymph leads to a severe decline in the number of circulating immune cells (i.e., the haemocytes) and regional tissue necrosis (e.g., muscle) – conditions that are likely to be fatal (Rowley et al, 2015) It is the conspicuous lack of host reactivity – cellular innate immunity – that is most intriguing about this host-pathogen antibiosis. Several studies have characterised so-called co-infections of Hematodinium-positive crustaceans, including bacterial septicaemia and ciliates in tanner crabs (Chionoecetes bairdi; (Love et al, 1993; Meyers et al, 1987)), and yeast-like mycosis in edible (Cancer pagurus; (Smith et al, 2013)) and velvet swimming crabs (Necora puber; (Stentiford et al, 2003)) These co-infections elicit an immune response – leading to haemocyte-directed nodulation and melanisation events (revealed by haematology and histopathology) – but during events, Hematodinium are not targeted. These data are valuable as there are few studies on the interaction between Hematodinium sp. and crustacean innate immunity, no Hematodinium-derived effectors were identified
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