Specific host factors determine resistance in a North American crayfish to the crayfish plague, Aphanomyces astaci.

The crayfish plague is caused by the oomycete Aphanomyces astaci with North American crayfish (for example Pacifastacus leniusculus and Procambarus clarkii) serving as carriers and vectors for this pathogen. This poses a constant threat to native crayfish in Europe, Asia, South America and Australia, which all are highly susceptible to this pathogen. In this study we now show how the symbiotic balance between the pathogen and its host are maintained at the molecular level. The host factors involved in this balance between the pathogen, A. astaci and the host, P. leniusculus, are one glycine-rich antimicrobial peptide (GRP) that is specifically active against A. astaci, but not to other microorganisms and two Kazal proteinase inhibitors (KPI2 and KPILA) inhibit secreted A. astaci proteases by binding to subtilisin enzymes from the pathogen. Accordingly, the expression of GRP, KPI2, KPILA, as well as proPO mRNAs increases following A. astaci infection. Silencing GRP, or KPI2 + KPILA mRNAs results in death of the crayfish from infection. Over time, this host-pathogen relationship has evolved to allow resistant crayfish to coexist with A. astaci in their cuticle for life, provided critical components remain unaltered by environmental changes or other pathogens. It is unclear whether a similar relationship could develop between currently susceptible crayfish and A. astaci.