Antigen profiles of the fish pathogen Moritella viscosa and protection in fish

Abstract

Aims: Moritella viscosa is a Gram‐negative bacterium that causes winter ulcer disease in salmonid fish cultured in sea water below 8°C. The aim of this study was to study the antigen profiles of these bacteria and to reveal the protection which the antigens induce in fish. Methods and Results: Lipooligosaccharides (LOS) and an approximately 17–19 kDa outer membrane antigen were shown to be the major specific antigens of M. viscosa. The size of the wall antigen differed between strain groups and even between strains reacting positively in the same sera. Four different serotypes of M. viscosa were determined by producing polyclonal sera. Western blot analysis revealed that sera from vaccinated fish groups that had good or fair protection reacted against the LOS and the 17/19 kDa antigen, while no antibody response was observed with sera from groups that showed no efficacy. Conclusions: The study provides evidence that LOS and an approximately 17–19 kDa outer membrane antigen are the major specific protective antigens of M. viscosa, and that the M. viscosa species consists of many different serotypes. Significance and Impact of the Study: The results are important for the production of vaccines against winter ulcers and should also lead to better methods of verifying the bacteria and monitoring winter ulcers.

Previously unrecognised division within Moritella viscosa isolated from fish farmed in the North Atlantic

“…A degree of geographically based amplified fragment length polymorphism (AFLP) clustering within Moritella viscosa isolates has been demonstrated and the existence of 4 different serotypes was recently shown (Heidarsdóttir et al 2008). However, until the present study the Norwegian M. viscosa population had been considered relatively homogeneous, an assumption probably based on lack of evidence to the contrary, rather than direct evidence of homogeneity.…”

“…Isolates from Atlantic salmon in Norway must therefore account for the overwhelming majority of clinical M. viscosa isolates on a worldwide basis. Despite the antigenic differences identified during the present study and by Heidarsdóttir et al (2008), crossprotection has been reported between Icelandic (presumed variant) and Norwegian (typical) strains (Greger & Goodrich 1999). The previous assumption of homogeneity may therefore not have been as significant in relation to protection of vaccinated stocks as it otherwise might have been.…”

“…Although antigenic heterogeneity has been previously identified within Moritella viscosa , Heidarsdóttir et al 2008, little has been performed in the way of phenotypic and genetic comparison of this bacterium since the original species descriptions , Lunder et al 2000. Until the present study, only 2 M. viscosa 16S rRNA sequences (Lunder et al 2000, Colquhoun et , both from Norwegian farmed fish, were available in Genbank (www.ncbi.nlm.nih.gov/), and intraspecies phenotypical differences were undocumented.…”

Endobiotic bacteria and their pathogenic potential in cnidarian tentacles

“…Jellyfish Cyanea lamarckii provides the natural habitat for Moritella viscosa, which causes necrotic ''winter ulcer'' in salmons (Lunder et al 2000;Heidarsdottir et al 2008), additionally Arcobacter butzleri, a human pathogen species (Carbone et al 2003;Gugliandolo et al 2007), and finally members of group #4 (see the previous paragraph). The Lions mane jellyfish C. capillata carries the haemolytic species Shewanella waksmanii, a member of group #3 (Ivanova et al 2003), and pathogenic endobionts of the already described Photobacterium profundum and the putatively pathogenic species of groups #1 and #4 (see the previous paragraph).…”

“…Individuals of Cyanea lamarckii, Cyanea capillata, Tubularia indivisa and Sagartia elegans were collected by divers during research cruises (June/July 2005-2008) from waters around the Orkney Islands. Tips of fresh tentacles were clipped off and subjected to washing procedures and CTAB treatment ) in order to remove potentially contaminating epibiotic bacteria.…”