Detection of humoral antibodies to Renibacterium salmoninarum in rainbow trout Oncorhynchus mykiss and Atlantic salmon Salmo salar challenged by immersion and in naturally infected populations

Chinook salmon Oncorhynchus tshawytscha are highly susceptible to Renibacterium salmoninarum, the causative agent of bacterial kidney disease (BKD). Previously we demonstrated that introduced Chinook salmon from Lake Michigan, Wisconsin (WI), USA, have higher survival following R. salmoninarum challenge relative to the progenitor stock from Green River, Washington, USA. In the present study, we investigated the pathological and immunological responses that are associated with differential survival in the 2 Chinook salmon stocks following intra-peritoneal R. salmoninarum challenge of 2 different cohort years (2003 and 2005). Histological evaluation revealed delayed appearance of severe granulomatous lesions in the kidney and lower overall prevalence of membranous glomerulopathy in the higher surviving WI stock. The higher survival WI stock had a lower bacterial load at 28 d post-infection, as measured by reverse-transcriptase quantitative polymerase chain reaction (RT-qPCR). However, at all other time points, bacterial load levels were similar despite higher mortality in the more susceptible Green River stock, suggesting the possibility that the stocks may differ in their tolerance to infection by the bacterium. Interferon-γ, inducible nitric oxide synthase (iNOS), Mx-1, and transferrin gene expression were up-regulated in both stocks following challenge. A trend of higher iNOS gene expression at later time points (≥28 d post-infection) was observed in the lower surviving Green River stock, suggesting the possibility that higher iNOS expression may contribute to greater pathology in that stock.

Section: Introductionmentioning

confidence: 99%

Pathological and immunological responses associated with differential survival of Chinook salmon following Renibacterium salmoninarum challenge

Metzger¹,

Elliott²,

Wargo³

et al. 2010

“…The effective bacterial concentration, however, may depend on the challenge conditions. The R. salmoninarum concentrations measured in the current study were several orders of magnitude lower than those used successfully for relatively short (30 min) immersion challenges in other studies (Murray et al 1992, Jansson & Ljungberg 1998. Murray et al (1992) recommended that the challenge suspension contain 1 X 106 or more R. salmoninarum if the evaluation is to be based on relative survival.…”

mentioning

confidence: 65%

Shedding of Renibacterium salmoninarum by infected chinook salmon Oncorhynchus tschawytscha

McKibben¹,

Pascho²

1999

Laboratory studies of the transmission and pathogenesis of Renlbactenurn salmonmarum may descnbe more accurately what is occurring in the natural environment if test fish are infected by waterborne R salmoninarum shed from Infected flsh To quantify bacterial sheddlng by chinook salmon Oncorhynchus tschawytscha at 13°C in freshwater, groups of fish were injected mtrapentoneally wlth R salmoninarum at either 1 3 X 106 colony formlng unlts (('FU) fish-' (high-dose injection group) or 1 5 X 103 CFU fish (low-dose ~nlection group) R salmoninarum Infection levels were measured in the exposed flsh by the enzyme-l~nked imrnunosorbent assay (BKD-ELISA) At regular intervals for 30 d , the numbers of R salmoninarum shed by the injected fish were calculated on the basis of testlng water samples by the membrane f~ltration-fluorescent ant~body test (MF-FAT) and bacteriological culture Mean BKD-ELISA optical dens~ties (ODs) for flsh in the low-dose injection group were not different from those of control fish ( p > 0 05) and no R salmon~narum were detected in water samples taken up to 30 d after inlection of fish in the low-dose group By 12 d after inlection a proportion of the flsh from the high-dose Infection group had high (BKD-ELISA OD 2 1000) to severe (BKD-ELISA OD 2 2 000) R salmonlnarurn infection levels, and bactena were detected In the water by both tests However, measurable levels of R salmonlnarum were not consistently detected in the water u n t~l a proportion of the fish maintained high to severe infection levels for an additional 8 d The concentrations of R salmoninarum in the water samples ranged from undetectable up to 994 cells ml-' on the b a s~s of the MF-FAT, and up to 1850 CFU m1 ' on the basis of bactenological cultureThe results suggest that chinook salmon infected with R salmonlnarum by inlection of approx~mately 1 X lob CFU fish-' can be used as the source of infection In cohabitat~on challenges beginning 20 d after ~nlection

“…Several exposed white seabass harbored P. salmonis DNA as detected by PCR, but there was no apparent correlation between PCR-positive fish and the concentration of serum anti-P. salmonis antibodies. This lack of correlation may result from the dramatic difference observed between fish in the response to bacterial antigens whether administered by vaccination or active infection (Jansson & Ljungberg 1998). The presence of serum anti-P. salmonis antibodies does not confirm the presence of live P. salmonis cells and thus an active carrier state in white seabass.…”

mentioning

confidence: 75%

“…However, in following antibody levels in fish that had been vaccinated against the nodavirus, they found high variations in individual responses to immunization, particularly following boosting at 4 and 6 wk. Individual fish-to-fish antibody variation has been documented for other bacterial and viral pathogens, including Vibrio anguillarum (Thorburn & Jansson 1988), infectious pancreatic necrosis virus (Dixon 1996), and Renibacterium salmoninarum (Jansson & Ljungberg 1998). …”

mentioning

confidence: 99%

Persistence of Piscirickettsia salmonis and detection of serum antibodies to the bacterium in white seabass Atractoscion nobilis following experimental exposure

Arkush

Edes²,

McBride³

et al. 2006

White seabass Atractoscion nobilis surviving experimental exposure to Piscirickettsia salmonis harbored the bacterium for periods up to at least 123 d post injection (dpi). Intraperitoneal injections of juvenile white seabass with 1.26 × 10 2 TCID 50 P. salmonis fish -1 resulted in a 29% cumulative mortality over a 27 d period. Both molecular and histologic methods provided evidence for persistence of the bacterium in fish sampled sequentially from the surviving population. Throughout the period of acute mortality, the bacterium was detected in all impression smears of liver tissue stained with Giemsa and was reisolated in cell cultures from all dead fish sampled. Polymerase chain reaction (PCR) assays detected P. salmonis-specific DNA in 13.3 to 50% of the fish sampled at time points between 28 and 123 dpi, while cell culture reisolation was largely ineffective in detecting the bacterium. An enzyme-linked immunosorbent assay (ELISA) detected serum anti-P. salmonis antibodies in 48 of 59 white seabass exposed to P. salmonis but not in fish which were not exposed to the bacterium. At the end of the 4 mo experiment, microscopic lesions consisting of single to multiple and coalescing granulomas were found in liver and kidney tissues of 9 of 10 fish examined from the exposure group, while no lesions were detected in the fish from the control group. Immunohistochemical staining with anti-P. salmonis polyclonal antibodies detected bacterial antigens in some but not all granulomas examined from the exposure group at 4 mo. This study demonstrates that P. salmonis may persist among white seabass following infection and thus provide a potential reservoir of infection contributing to transmission both within and between fish species in the marine environment. KEY WORDS: Piscirickettsia salmonis · White seabass · Persistent infection · Carrier state Resale or republication not permitted without written consent of the publisherDis Aquat Org 73: [131][132][133][134][135][136][137][138][139] 2006 with lesser amounts in visceral organs (Comps et al. 1996, Grant et al. 1996, Skarmeta et al. 2000, McCarthy et al. 2005. P. salmonis and P. salmonis-like bacteria have been detected from a variety of marine and freshwater fish (Mauel & Miller 2002). Two of these bacteria from marine fish recently have been confirmed to be P. salmonis by phylogenetic comparisons of the small and large subunit ribosomal (16S and 23S) DNA and the internal transcribed spacer (ITS) (Arkush et al. 2005, McCarthy et al. 2005. Arkush et al. (2005) demonstrated that P. salmonis causes a disease similar to piscirickettsiosis in white seabass Atractoscion nobilis. Experimental infections with the bacterium caused mortality similar to that of P. salmonis infections in salmon, with granulomatous lesions principally in the liver and to a lesser extent in the spleen, kidney, intestine and gills. McCarthy et al. (2005) also confirmed P. salmonis as a pathogen in European sea bass Dicentrarchus labrax. Interestingly, in their report, as in an earlier rep...