Over half of the salmon consumed globally are farm-raised. The introduction of oil-adjuvanted vaccines into salmon aquaculture made large-scale production feasible by preventing infections. The vaccines that are given i.p. contain oil adjuvant such as mineral oil. However, in rodents, a single i.p. injection of adjuvant hydrocarbon oil induces lupus-like systemic autoimmune syndrome, characterized by autoantibodies, immune complex glomerulonephritis, and arthritis. In the present study, whether the farmed salmon that received oil-adjuvanted vaccine have autoimmune syndrome similar to adjuvant oil-injected rodents was examined. Sera and tissues were collected from vaccinated or unvaccinated Atlantic salmon (experimental, seven farms) and wild salmon. Autoantibodies (immunofluorescence, ELISA, and immunoprecipitation) and IgM levels (ELISA) in sera were measured. Kidneys and livers were examined for pathology. Autoantibodies were common in vaccinated fish vs unvaccinated controls and they reacted with salmon cells/Ags in addition to their reactivity with mammalian Ags. Diffuse nuclear/cytoplasmic staining was common in immunofluorescence but some had more specific patterns. Serum total IgM levels were also increased in vaccinated fish; however, the fold increase of autoantibodies was much more than that of total IgM. Sera from vaccinated fish immunoprecipitated ferritin and ∼50% also reacted with other unique proteins. Thrombosis and granulomatous inflammation in liver, and immune-complex glomerulonephritis were common in vaccinated fish. Autoimmunity similar to the mouse model of adjuvant oil-induced lupus is common in vaccinated farmed Atlantic salmon. This may have a significant impact on production loss, disease of previously unknown etiology, and future strategies of vaccines and salmon farming.

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An autopsy case of an 18 month old male infant with measles infection is reported. An autopsy revealed generalized lymphadenopathy, splenomegaly and hyperplastic thymus. Histologically, there were many Warthin-Finkeldey cells (WFC) in hyperplastic lymphoid tissues. Although viral particles and inclusions were not detected electronmicroscopically, the infection of measles virus was detected in WFC by immunofluorescent technique using anti-measles antibody. Warthin-Finkeldey cells were morphologically and immunohistochemically divided into two groups. The first type was WFC appearing in the germinal centers of lymphoid tissue, revealing many large nuclei and B cell markers. The second type was WFC appearing in the interfollicular areas and thymus, showing many small hyperchromatic nuclei and T cell markers. The data indicate that there might be a morphologic and immunophenotypic heterogeneity in WFC.

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T‐cell large granular lymphocyte (LGL) leukemia is a clonal disorder with an indolent clinical course. In July 1995, a 46‐year‐old Japanese man was admitted to our hospital because his anemia had progressed. He had a white blood cell count of 3.9 × 109/L with 75% lymphocytes, which were intermediate to large and had almost round nuclei and azurophilic granules, and anemia with a red blood cell count (RBC) of 2.69 × 1012/L, hemoglobin (Hb) of 9.5 g/dL, and hematocrit (Hct) of 28.3%. Electron microscopic examination showed that most of the lymphocytes had a parallel tubular array and dense core granules in their cytoplasm. Flow cytometry and Southern blotting of the T‐cell antigen receptor (TCR) genes using the peripheral blood species showed monoclonal proliferation of LGLs with a CD3+, TCRγδ+, CD4−, CD8−, CD16+, CD56−, CD57−, HLA‐DR+ phenotype, and a TCR γ gene rearrangement, respectively, suggesting that the patient was diagnosed as having γδ T‐cell LGL leukemia. He had no symptoms, organomegaly, or skin lesions. About 1.5 years after diagnosis, the anemia gradually improved with disappearance and appearance of a rearranged band in the TCR‐γ gene and TCR‐β gene, respectively. About 7 years after diagnosis, the anemia improved completely with a RBC of 5.01 × 1012/L, Hb of 14.8 g/dL, and Hct of 44.3%, and he was in complete remission without TCR‐β and ‐γ gene rearrangements. He had received no therapy. This is the first report of spontaneous remission of γδ T‐cell LGL leukemia. Am. J. Hematol. 75:168–172, 2004. © 2004 Wiley‐Liss, Inc.