There have been increased reports of outbreaks of enteric redmouth disease (ERM) caused by Yersinia ruckeri in previously vaccinated salmonids in Europe, with some of these outbreaks being attributed to emergent non-motile, Tween 80-negative, biotype 2 isolates. To gain information about their likely origins and relationships, a geographically and temporally diverse collection of isolates were characterised by serotyping, biotyping, pulsed-field gel electrophoresis (PFGE) and outer membrane protein (OMP) profiling. A total of 44 pulsotypes were identified from 160 isolates by PFGE, using the restriction enzyme Not I. Serotype O1 isolates responsible for ERM in rainbow trout in both the US and Europe, and including biotype 2 isolates, represented a distinct subgroup of similar pulsotypes. Biotype 2 isolates, responsible for outbreaks of the disease in rainbow trout in the UK, Denmark and Spain, had different pulsotypes, suggesting that they represented different clones that may have emerged separately. Danish biotype 2 isolates recovered since 1995 were indistinguishable by PFGE from the dominant biotype 1 clone responsible for the majority of outbreaks in Denmark and the rest of mainland Europe. In contrast, US biotype 2 isolate YRNC10 had an identical pulsotype and OMP profile to UK biotype 2 isolates, suggesting that there had been exchange of these isolates between the UK and the US in the past. UK Atlantic salmon isolates were genetically and serologically diverse, with 12 distinct pulsotypes identified among 32 isolates.KEY WORDS: Yersinia ruckeri · Pulsed-field gel electrophoresis · PFGE · Enteric redmouth disease · ERM · Biotype · Emerging strain Resale or republication not permitted without written consent of the publisherDis Aquat Org 84: [25][26][27][28][29][30][31][32][33] 2009 monovalent killed whole cell commercial vaccines, generally based on the Hagerman type strain (Horne & Barnes 1999). However, reports of ERM vaccine breakdown have emerged in Europe and the USA, which are attributed to biotype 2 (Tween 80-negative, nonmotile) isolates of Y. ruckeri (Austin et al. 2003, Fouz et al. 2006, Arias et al. 2007. Biotype 2 isolates were first described as having caused the disease in UK rainbow trout by Davies & Frerichs (1989).Farmers have also reported increasing mortalities due to yersiniosis of UK Atlantic salmon Salmo salar (L.); however, there are limited published studies regarding yersiniosis of this species (Bullock et al. 1976, Bruno & Munro 1989. Nevertheless, farmed Atlantic salmon fry in the major production areas of Europe (Scotland, Ireland and Norway) and Chile are routinely vaccinated with commercial rainbow trout ERM vaccines or autologous preparations (Bravo & Midtlyng 2007, L. A. Laidler pers. comm.). In Chile alone, up to 140 million salmon yr -1 were vaccinated against yersiniosis between and 2003(Bravo & Midtlyng 2007.Yersinia ruckeri is a highly clonal and biochemically homogeneous species (Schill et al. 1984, Stevenson & Airdrie 1984, Daly et al. 1986, Pyle et al...

Mammals are widely used by microbiologists as a model host species to study infectious diseases of humans and domesticated livestock. These studies have been pivotal for our understanding of mechanisms of virulence and have allowed the development of diagnostics, pre-treatments and therapies for disease. However, over the past decade we have seen efforts to identify organisms which can be used as alternatives to mammals for these studies. The drivers for this are complex and multifactorial and include cost, ethical and scientific considerations. Galleria mellonella have been used as an alternative infection model since the 1980s and its utility for the study of bacterial disease and antimicrobial discovery was recently comprehensively reviewed. The wider applications of G. mellonella as a model host, including its susceptibility to 29 species of fungi, 7 viruses, 1 species of parasite and 16 biological toxins, are described in this perspective. In addition, the latest developments in the standardisation of G. mellonella larvae for research purposes has been reviewed.

Our results broadly support the previous findings and the role of Etx in the aetiology of MS warrants further investigation.

Aims:  To examine the variability among environmental Vibrio parahaemolyticus (including trh+ isolates) from Norway, and to compare these to clinical isolates and isolates from imported foods. Methods and Results:  A total of 246 V. parahaemolyticus were successfully digested with NotI, and the fragments were separated by pulsed field gel electrophoresis (PFGE). The isolates could be divided into 72 clusters and 103 pulsotypes. Eleven clusters contained 4–31 environmental isolates, and the isolates within these clusters greatly varied with respect to origin. None of the trh+ and /or tdh+ isolates clustered with trh−/tdh− isolates. The trh+ environmental isolates included in the study belonged to two separate clusters. A subset of isolates was serotyped, and great serotype diversity was observed among the environmental V. parahaemolyticus. The clinical isolates included O3:K6 and O3:KUT, and these were identical or related to a pandemic reference strain by PFGE. Conclusions:  Environmental V. parahaemolyticus (including trh+) were genetically diverse, but certain variants occurred throughout the coastal environment, and some were persistent over time. Significance and Impact of the Study:  Although trh+ V. parahaemolyticus persisted in the Norwegian environment, no evidence indicated that indigenous isolates have caused disease.