Rising imports of oysters and domestic production problems for seed oysters indicated a need to analyze mortality causes of seed oysters. The economic impact of the severe and persistent oyster seed mortality problem is large, and estimated at about $16.5 M on the west coast alone. Serious losses of juvenile oyster due to poorly defined causes are known on both the east and west coast of the U.S. The objectives of this study were to (1) Determine seed mortality causes from west coast production facilities, (2) Compare diploid and triploid seed performance, (3) Prepare a guide to seed anatomy and summarize and recommend (4) procedures to prevent seed mortality. Four oyster seed nurseries in Washington and California that produced commercial quantities of Pacific oyster (Crassostrea gigas), kumomoto (C. sikamea) oyster and flat oyster (Ostrea edulis) seed were the study sites. Histological analysis of tissues was the primary aim of the study but growth and mortality data were systemically collected from study areas. Selected sequential samples representing developmental sequences were used to study and develop a description of the normal anatomical development of juvenile oysters. Seed growth was high in fall and spring but flat during winter months. Overall, seed survival was highly variable on nursery beds. Significant causes of seed loss were bacterial infections originating in the adductor muscle, predation, heavy sedimentation in certain locations during a high rainfall period and sunburn inseed planted at a small size in the summer. A benign systemic protozoan infection was found in seed planted on certain nursery beds and oysters outgrew the infection. For cultchless seed cultivated in upwelling systems, the most significant causes of mortality losses were chronic bacterial infections of the subpallial space, ciliate infections of very early stage juvenile oysters, loss of digestive gland epithelium, and ingestion of cultch material infested with a variety of microorganisms that appeared to interfere with normal digestive processes. This study showed for the first time that ciliates cause primary infections and must be managed to prevent losses to early stage juvenile oyster cultures. Both the ciliate and extrapallial bacterial infections result from the ability of the microorganisms to pass between the outer lobe of the mantle and the inner shell surface. Ingestion of degrade cultch material resulted in growth inhibition and degradation of the digestive gland epthelium. No differences were found in growth or dieases of triploid and diploid oysters. Survival in both groups was low but related to site characteristics rather than to triploidy or diploidy. The normal developmental anatomy of juvenile oysters anatomy and a review and management analysis of juvenile oyster diseases will be published as a book, based on work performed in this study.