An Epizootic in Chinook Salmon (Oncorhynchus Tshawytscha) Caused by a Sorbitol-Positive Serovar 2 Strain of Yersinia Ruckeri

Cipriano, Rocco C.; Schill, William B.; Pyle, Stephen W.; Horner, Rodney

doi:10.7589/0090-3558-22.4.488

Cited by 16 publications

(8 citation statements)

References 10 publications

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“…Sorbitol-negative and positive strains from the same farms in the present study were capable of causing clinical signs in stressed fish, which suggests that the sorbitol test is not essential when evaluating the pathogenicity of Y. ruekeri. The same opinion is expressed by Stevenson & Airdrie (1984) and Cipriano et al (1986), who stated that sorbitol fermentation is not eonneeted with the serotype or the pathogenicity of Y, ruekeri.…”

Section: Discussionmentioning

confidence: 65%

“…The connection between stress and y. ruekeri outbreaks was also obvious in northern Finland; for example, brood brown trout were found to have K. ruekeri infection associated with ulcers after artificial spawning. Cipriano, Sehill, Pyle & Horner (1986) reported that the sorbitol-fermenting serovar 2 of Y. rtickeri was pathogenic for both brook trout, Salvelinus fontinalis Mitchell, and salmon, while Michel et al (1986) found that minnows from the USA also had a sorbitol-positive strain pathogenic for salmon. Sorbitol-negative and positive strains from the same farms in the present study were capable of causing clinical signs in stressed fish, which suggests that the sorbitol test is not essential when evaluating the pathogenicity of Y. ruekeri.…”

Section: Discussionmentioning

confidence: 99%

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Occurrence and pathogenicity of Yersinia ruckeri at fish farms in northern and central Finland

Valtonen

Rintamäki

Koskivaara

1992

Journal of Fish Diseases

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Salmonid fish at fish farms in northern and central Finland and perch, Perca fluviatitis L., roach. Rutilus rutilus (L.), and whitefish, Coregonus sp., from four lakes in central Finland were studied between 1985 and 1990 for the occurrence of Yersinia ruckeri. The bacteria were found in fish from both areas, but in most cases, only single diseased salmon, Salmo salar L., brown trout, S. trutta L., rainbow trout, Oncorhynchus mykiss (Walbaum), whitefish and pereh were encountered and were always connected with stress conditions. One chnical outbreak occured in salmon fingerlings in northern Finland, and the fish were successfully treated with trimethoprim-sulpha. Monthly monitoring of lake fish revealed two symptomless carrier perch in two lakes. Outwith the main study a moribund perch with yersiniosis was found in a polluted lake, and for the first time in Finland, a rainbow trout was also found to have contracted yersiniosis in a small private pond. Sorbitol-positive and negative isolates have been found to occur in both moribund and carrier farmed fish, indicating that the sorbitol test is not essential when evaluating the pathogenicity of Y. ruckeri.

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Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Occurrence and pathogenicity of Yersinia ruckeri at fish farms in northern and central Finland

Valtonen

Rintamäki

Koskivaara

1992

Journal of Fish Diseases

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“…This method of biotyping was abandoned when the current Davies (1991) typing scheme was introduced. Moreover, sorbitol fermentation was also attributed to disease outbreaks caused by Y. ruckeri in chinook salmon, Oncorhynchus tshawytscha (Walbaum), and brook trout, Salvelinus fontinalis (Mitchell) Cipriano, Schill, Pyle & Horner 1986). Sorbitol fermentation was found to be a characteristic of serogroup O1 biotype 1, OMP type 4 and clonal group 6 isolates as based on the Davies (1991) scheme.…”

Section: Discussionmentioning

confidence: 99%

Novel non‐motile phenotypes of Yersinia ruckeri suggest expansion of the current clonal complex theory

Tinsley

Austin

Lyndon

et al. 2011

Journal of Fish Diseases

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The biochemical and cell surface characteristics of 63 non-motile isolates of Yersinia ruckeri from various sources were compared using the API 20E rapid identification system and conventional phenotypic methods. Eight individual phenotypic groups from a variety of fish species were observed from the data set. Non-motile isolates were not exclusively observed from serogroup O1; membership of biotype 2 was recorded for representatives from serogroups O2-O7. Variations in phenotypes highlights that new clonal groups are arising and that the current typing scheme requires expansion. Previously, it was hypothesized that disease was caused by a few virulent clones; data in this paper suggests that this assumption is not the case. The lipopolysaccharide (O antigen) type in the non-motile biotype was different from other isolates of Y. ruckeri.

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“…Major differences between the virulence of different Y. ruckeri isolates to salmon and trout were shown, particularly when administered by a more natural exposure route (bath challenge), than by injection. Davies (1991b) also demonstrated host tropism in Y. ruckeri, with isolates reportedly virulent to chinook salmon (Onchorhynchus tshawytscha L.) and brook trout Salvelinus fontinalis (Mitchill, 1814) (Cipriano et al 1986;Cipriano and Ruppenthal 1987), avirulent to (rainbow) trout, when tested in that species by experimental bath challenge. The organisms that typically cause ERM in rainbow trout represent a closely-related subgroup of O1 serotype Y. ruckeri , the Hagerman Type strain ATCC T -like clonal complex (Davies 1991b;Wheeler et al 2009).…”

Section: Discussionmentioning

confidence: 94%

Comparative susceptibility of Atlantic salmon and rainbow trout to Yersinia ruckeri: Relationship to O antigen serotype and resistance to serum killing

Haig

Davies

Welch

et al. 2011

Veterinary Microbiology

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A study was undertaken to compare the virulence and serum killing resistance properties of Atlantic salmon and rainbow trout Yersinia ruckeri isolates. Five isolates, covering heat-stable O-antigen O1, O2 and O5 serotypes, were tested for virulence towards fry and juveniles of both species by experimental bath challenge. The sensitivity of 15 diverse isolates to non-immune salmon and rainbow trout serum was also examined. All five isolates caused significant mortality in salmon fry. Serotype O1 isolate 06059 caused the highest mortality in salmon (74% and 70% in fry and juveniles, respectively). Isolate 06041, a typical ERM-causing serotype O1 UK rainbow trout strain, caused mortalities in both rainbow trout and salmon. None of the salmon isolates caused any mortalities in 150-250 g rainbow trout, and only serotype O2 isolate 06060 caused any significant mortality (10%) in rainbow trout fry. Disease progression and severity was affected by water temperature. Mortality in salmon caused by the isolates 06059 and 05094 was much higher at 16 °C (74% and 33%, respectively) than at 12 °C (30 and 4% respectively). Virulent rainbow trout isolates were generally resistant to sera from both species, whereas salmon isolates varied in their serum sensitivity. Convalescent serum from salmon and rainbow trout that had been infected by serotype O1 isolates mediated effective classical pathway complement killing of serotype O1 and O5 isolates that were resistant to normal sera. Overall, strains recovered from infected salmon possess a wider range of phenotypic properties (relative virulence, O serotype and possession of serum-resistance factors), compared to ERM-causing rainbow trout isolates.

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An Epizootic in Chinook Salmon (Oncorhynchus Tshawytscha) Caused by a Sorbitol-Positive Serovar 2 Strain of Yersinia Ruckeri

Cited by 16 publications

References 10 publications

Occurrence and pathogenicity of Yersinia ruckeri at fish farms in northern and central Finland

Occurrence and pathogenicity of Yersinia ruckeri at fish farms in northern and central Finland

Novel non‐motile phenotypes of Yersinia ruckeri suggest expansion of the current clonal complex theory

Comparative susceptibility of Atlantic salmon and rainbow trout to Yersinia ruckeri: Relationship to O antigen serotype and resistance to serum killing

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