Abstract
Eroded swimmeret syndrome (ESS) was first described in 2014 from Swedish signal crayfish (Pacifastacus leniusculus (Dana)), and later also from Finland, with gross symptoms and disease agent candidates identified and described by 2015. The ESS was first discovered affecting alien signal crayfish in Fennoscandia. The ESS is caused by a multiple infection involving Aphanomyces astaci (Schikora) and Fusarium species complex (SC). The ESS symptoms include first melanised spots in swimmerets, then partial swimmeret erosion and finally loss of a swimmeret. There could be a total loss of all swimmerets in the most severe cases. Both females and males can be affected by the ESS. In females, the ESS lowers reproductive success while in males the ESS often causes erosion of the gonopods and thus possible partial failure in mating. The ESS is more frequent among mature females that have reproduced once compared to immature females or those that are mature but have not yet reproduced. The proportion of females with ESS has ranged from 10 to 50% among Lake Saimaa signal crayfish in Finland and in a wider survey from Sweden the range was from 0 to 38%. Among Lake Saimaa male signal crayfish, the ESS proportion has been less than 10%, while it was only 0.6% in the Swedish data. The ESS has also been observed among alien signal crayfish in Switzerland. There are recent observations of ESS affecting narrow-clawed crayfish, Pontastacus leptodactylus (Eschscholtz), in Croatia and Romania (i.e., among native European crayfish stocks). Here, we summarise current knowledge about the ESS and speculate on a few potentially crucial impacts of this syndrome.
THE DISPERSION OF THE APHANOMYCES ASTACI-CARRIER PACIFASTACUS LENIUSCULUS BY HUMANS REPRESENTS THE MAIN CAUSE OF DISAPPEARANCE OF THE INDIGENOUS CRAYFISH AUSTROPOTAMOBIUS PALLIPES IN NAVARRA
