Immunization with bacterial antigens: piscirickettsiosis.

Piscirickettsiosis is a septicaemic disease of salmonid fish caused by the obligated intracellular rickettsia, Piscirickettsia salmonis. This disease was first reported in 1989 in salmon cultured in sea water netpens in southern Chile where it is still a major problem causing high mortality among cultured salmonids. In recent years related agents have been reported in farmed salmonids from Ireland, Canada and Norway. Mortality, however, at these locations has been reported to be low. Because of the recent description of piscirickettsiosis and its aetiological agent, knowledge about the immune response of fish against this organism is limited. At present, there is only one paper in the literature dealing with this subject. To standardise challenge methods for testing the efficacy of vaccination, lethal dose 50% and infectivity dose 50% were determined for coho salmon (Oncorhynchus kisutch) and rainbow trout (O. mykiss) using intraperitoneal (i.p.) injections of P. salmonis. Experiments using bath challenge methods failed to reproduce the disease using rainbow trout although low levels of infection in their tissues were found. In a field trial, using formalin killed bacterins injected i.p. into pre-smolt coho salmon, the fish were naturally challenged by placing them in sea water where endemic piscirickettsiosis occurred. The results showed that some of the vaccinated fish groups experienced lower cumulative mortality than the non-vaccinated control group (X < 0.05), suggesting an immunoprotective response in these animals. A trial was also conducted with formalin-killed bacterins in rainbow trout using different antigen concentrations with and without booster injections. Fish were challenged by IP injection of P. salmonis. Vaccinated fish showed less mortality than their respective infected control. Unfortunately the challenge was not strong enough because mortality in the infected control fish was low (20%). Antibody levels measured by radio-immuno-assay increased until day 40 post vaccination. The highest levels of antibody were obtained in the sera of fish vaccinated with concentrated antigen using booster injections.

[Pathogenesis of spontaneous chronic polyarthritis in MRL mice]. / Beitrag zur Pathogenese der spontanen chronischen Polyarthritis der MRL-Mäuse.

In a sequential study the pathogenesis of chronic polyarthritis occurring spontaneously in MRL mice was analysed by light microscopy. A total of 128 MRL mice of both substrains (MRL/Mp-lpr/lpr and +/+) and different age groups was studied. In 50 lpr/lpr mice, tinctorial and histochemical methods were applied for the identification of fibrin/fibrinoid, iron compounds, amyloid, and proteoglycan. The earliest lesions seen in mice of substrain lpr/lpr at the age of 2 months were proliferation of synovial lining cells and loss of tinctorially demonstrable proteoglycan in the articular cartilage. Beginning at 3 months, severe joint destruction associated with pannus formation was encountered usually in knee, carpal and tarsal joints. Besides inflammatory processes in tendons, nerves and musculature fibrinoid-necrotising panarteritis occurred in the intra- and extraarticular tissue. Furthermore, fibrin-containing exudations and deposits of fibrinoid material, occurred in the synovium of large joints and in the periarticular connective tissue of phalangeal joints. The occurrence of these morphological changes, destructive arthritis, vasculitis and periarticular inflammatory changes, was, at the age of 3 months, associated with a highly significant increase of circulating immune complexes. In mice of substrain +/+ aged 1 year and older, arthritic changes with synovial lining cell proliferation, cartilage destruction and inflammatory periarticular lesions developed.