Nuclear inclusion X (NIX), the etiological agent of bacterial gill disease in Pacific razor clams Siliqua patula, was associated with host mortality events in coastal Washington State, USA, during the mid-1980s. Ongoing observations of truncated razor clam size distributions in Kalaloch Beach, Washington, raised concerns that NIX continues to impact populations. We conducted a series of spatial and longitudinal NIX surveillances, examined archived razor clam gill tissue, and used population estimates from stock assessments to test whether (1) the prevalence and intensity of NIX infections is higher at Kalaloch Beach relative to nearby beaches, (2) infected gill tissue has features consistent with historical descriptions of NIX-associated histopathology, and (3) annual clam survival is inversely related to NIX infection prevalence and intensity. NIX prevalence exceeded 85% at all sampled locations, and infection intensity was the highest at Kalaloch Beach by 0.9-2.6 orders of magnitude. Kalaloch Beach clams revealed histopathology consistent with previous NIX epidemics, including enlarged and/or rupturing branchial epithelial cells, branchial necrosis, and high hemocyte densities. Estimated annual survival was 22% at Kalaloch Beach, and ranged between 57 and 99% at other study sites. NIX infection intensity (via quantitative PCR) was not significantly correlated with annual survival; however, annual survival was lowest at Kalaloch Beach, where infection intensities were highest, suggesting that clams can tolerate infections up to a lethal threshold. Collectively these data support the hypothesis that high NIX intensities are associated with host mortality. NIX-associated mortality appears to be more pronounced at Kalaloch Beach relative to other Washington beaches.
Keywords: Fisheries management; Gammaproteobacteria; NIX; Nuclear inclusion X; Pacific razor clam; Siliqua patula.