Temporal dynamics of infection of cockles Cerastoderma edule with the protistan parasite Minchinia tapetis (Rhizaria: Haplosporida) in Galicia (NW Spain).

Uninucleate and binucleate cells and multinucleate plasmodia of a haplosporidan-like protist associated with heavy haemocytic infiltration were observed in histological sections of cockles, Cerastoderma edule, from the Ría de Noia (Galicia, NW Spain) in the course of a cockle health surveillance programme. Molecular assays provided identification of this protist as Minchinia tapetis, which we thus record from a new host. Prevalence of M. tapetis as high as 93% was recorded but infection intensity was low to moderate, never heavy, and abnormally high cockle mortality was not observed in the ria by shellfishers. A significant positive correlation was found between M. tapetis prevalence and sea water temperature. Sea water temperature increase associated with climate change might contribute to increase the prevalence of this infection in cockles and, as a consequence, this parasite may be considered a threat for cockle production.

Impact of Perkinsus olseni infection on a wild population of Manila clam Ruditapes philippinarum in Ariake Bay, Japan.

Many studies have addressed the production decline of Manila clam, Ruditapes philippinarum, in Japan, but infection of clams with Perkinsus olseni has received scarce attention. To evaluate the impact of P. olseni, infection levels and host density of a wild, unexploited clam population were monitored monthly or bimonthly on a tidal flat from June 2009 to January 2013. Real-time PCR analysis discriminating P. olseni and Perkinsus honshuensis detected only P. olseni in tested clams. The prevalence of P. olseni was 100% or nearly 100% in 7 cohorts throughout the study period, except in newly recruited clams. Infection intensity remained low and seldom reached 106 cells/g wet tissue in newly recruited clams until the month of September. Infection intensity reached 106 cells/g in autumn and remained high at 104-106 cells/g until each cohort of clams disappeared. Clam density began to decrease in the autumn when the infection intensities reached ca. 106 cells/g. Density was relatively stable in winter, increased in spring and decreased again in clams aged 1 year or older during summer and autumn in the following years. Survival of clams experimentally infected with P. olseni at ca. 106 cells/g and placed in a cage in the tidal flat for 1 or 2 months was significantly lower than survival of uninfected control clams. Our results suggested that heavy infection with P. olseni was a major cause of the clam density decrease, although other environmental and biological factors also may have contributed to the decline in density. In addition, uninfected clams were deployed in cages for 1-2 months from June 2010 to January 2013 and prevalence and infection intensity were monitored. Parasite transmission and infection progression increased in summer and autumn.