Experimental infection and horizontal transmission of Piscirickettsia salmonis in freshwater-raised Atlantic salmon, Salmo salar L.

Experimental infections with Piscirickettsia salmonis via intraperitoneal (IF), oral (PO) and gill (GS) routes were compared, and the importance of physical contact in the horizontal transmission of this organism was investigated. Atlantic salmon, Salmo salar L., under-yearling parr raised in fresh water were used in this study. Samples of liver, kidney, spleen, gill and brain were collected weekly for 5 weeks after challenge, and were examined using the indirect fluorescent-antibody technique (IFAT). The pathogen was transmitted horizontally to fish with and without physical contact. However, transmission of P. salmonis occurred significantly more rapidly among fish with physical contact. Mortalities occurred in 50% of fish experimentally challenged with P. salmonis and their cohabitants. The estimates of the relative risk of dying demonstrated that fish challenged by the IP and GS routes had a significantly higher probability of dying than fish challenged by the PO route (P < 0.005). Contact cohabitants with infected fish had a higher probability of death than non-contact cohabitants (P < 0.005). The sequential studying using IFAT indicated that a haematogenous pattern of infection occurred among fish infected by oral and gill routes, or by cohabitation. This was different from the capsular (serosal) infection pattern observed in intraperitoneally inoculated fish. Piscirickettsia salmonis was observed within the cytoplasm of leucocytes and renal tubules, the latter indicating that elimination of this pathogen through the urine may be possible. Aeromonas salmonicida was also detected (by IFAT) in some of the fish exposed to P. salmonis, suggesting that P. salmonis may cause immunosuppression, and thus, increase the susceptibility of the host to other pathogens.PT: J; CR: *FAO, 1994, ANN STAT DAT *SAS I, 1988, SAS STAT GUID PERS C AHNE W, 1978, J FISH DIS, V1, P265 BAKKE TA, 1992, DIS AQUAT ORGAN, V13, P63 BRANSON EJ, 1991, J FISH DIS, V14, P147 BRAVO S, 1989, FHS AFS NEWSLETTER, V17, P3 BROCKLEBANK JR, 1993, CAN VET J, V34, P745 BRUNO DW, 1986, J FISH DIS, V9, P523 CHILMONCZYK S, 1980, FISH DIS 3 COOPERATI, P188 CVITANICH JD, 1991, J FISH DIS, V14, P121 EFFENDI I, 1995, B EUROPEAN ASS FISH, V15, P115 EVANS DH, 1993, PHYSL FISHES, P315 FRYER JL, 1990, FISH PATHOL, V25, P107 FRYER JL, 1992, INT J SYST BACTERIOL, V42, P120 GAGGERO A, 1995, J FISH DIS, V18, P277 GARCES LH, 1991, DIS AQUAT ORGAN, V11, P93 GRACES LH, 1994, P INT S AQ AN HLTH S HSIUNG GD, 1994, HSIUNGS DIAGNOSTIC V, P46 KANNO T, 1989, J AQUAT ANIM HEALTH, V1, P2 LANNAN CN, 1991, J AQUAT ANIM HEALTH, V3, P229 LANNAN CN, 1994, J FISH DIS, V17, P545 LEE ET, 1980, STATISTICAL METHODS MENDEZ R, 1995, AQUANOTICIAS INT, V24, P6 MURRAY CB, 1992, DIS AQUAT ORGAN, V12, P91 OLFRET ED, 1993, GUIDE CARE USE EXPT OLSEN AB, 1993, NORSK FISKEOPPDRETT, V12, P40 RODGER HD, 1993, J FISH DIS, V16, P361 TRUST TJ, 1986, ANNU REV MICROBIOL, V40, P479 WOLDEHIWET Z, 1993, RICKETTSIAL CHLAMYDI, P1; NR: 29; TC: 17; J9: J FISH DISEASES; PG: 10; GA: YK288Source type: Electronic(1