An outbreak investigation was initiated in September 2019, following a notification to the Norwegian Food Safety Authority (NFSA) of an unusually high number of dogs with acute haemorrhagic diarrhoea (AHD) in Oslo. Diagnostic testing by reporting veterinarians had not detected a cause. The official investigation sought to identify a possible common cause, the extent of the outbreak and prevent spread. Epidemiological data were collected through a survey to veterinarians and interviews with dog owners. Diagnostic investigations included necropsies and microbiological, parasitological and toxicological analysis of faecal samples and food. In total, 511 dogs with acute haemorrhagic diarrhoea were registered between 1 August and 1 October. Results indicated a common point source for affected dogs, but were inconclusive with regard to common exposures. A notable finding was that 134 of 325 faecal samples (41%) cultured positive for Providencia alcalifaciens. Whole genome sequencing (WGS) of 75 P. alcalifaciens isolates from 73 dogs revealed that strains from 51 dogs belonged to the same WGS clone. Findings point to P. alcalifaciens as implicated in the outbreak, but investigations are needed to reveal the pathogenic potential of P. alcalifaciens in dogs and its epidemiology.

Aliivibrio salmonicida is the causative agent of cold-water vibriosis, a hemorrhagic septicemia of salmonid fish. The bacterium has been shown to rapidly enter the fish bloodstream, and proliferation in blood is seen after a period of latency. Although the pathogenesis of the disease is largely unknown, shedding of high quantities of outer-membrane complex VS-P1, consisting of LPS and a protein moiety, has been suggested to act as decoy and contribute to immunomodulation. To investigate the role of LPS in the pathogenesis, we constructed O-antigen deficient mutants by knocking out the gene encoding O-antigen ligase waaL. As this gene exists in two copies in the AL salmonicida genome, we constructed single and double in-frame deletion mutants to explore potential effects of copy number variation. Our results demonstrate that the LPS structure of AL salmonicida is essential for virulence in Atlantic salmon. As the loss of O-antigen did not influence invasive properties of the bacterium, the role of LPS in virulence applies to later stages of the pathogenesis. One copy of waaL was sufficient for O-antigen ligation and virulence in experimental models. However, as a non-significant decrease in mortality was observed after immersion challenge with a waaL single mutant, it is tempting to suggest that multiple copies of the gene are beneficial to the bacterium at lower challenge doses. The loss of O-antigen was not found to affect serum survival in vitro, but quantification of bacteria in blood following immersion challenge suggested a role in in vivo survival. Furthermore, fish challenged with the waaL double mutant induced a more transient immune response than fish challenged with the wild type strain. Whether the reduction in virulence following the loss of waaL is caused by altered immunomodulative properties or impaired survival remains unclear. However, our data demonstrate that LPS is crucial for development of disease.

Aliivibrio salmonicida is the causative agent of cold-water vibriosis, a septicemia of farmed salmonid fish. The mechanisms of disease are not well described, and few virulence factors have been identified. However, a requirement for motility in the pathogenesis has been reported. Al. salmonicida is motile by the means of lophotrichous polar flagella, consisting of multiple flagellin subunits that are expressed simultaneously. Here we show that flagellin subunit FlaA, but not FlaD, is of major importance for motility in Al. salmonicida. Deletion of flaA resulted in 62% reduction in motility, as well as a reduction in the fraction of flagellated cells and number of flagella per cell. Similarly, deletion of the gene encoding motor protein motA gave rise to an aflagellate phenotype and cessation of motility. Surprisingly, we found that Al. salmonicida does not require motility for invasion of Atlantic salmon. Nevertheless, in-frame deletion mutants defective of motA and flaA were less virulent in Atlantic salmon challenged by immersion, whereas an effect on virulence after i.p. challenge was only seen for the latter. Our results indicate a complex requirement for motility and/or flagellation in the pathogenesis of cold-water vibriosis, but the mechanisms involved remain unknown. We hypothesize that the differences in virulence observed after immersion and i.p. challenge are related to the immune response of the host.

In the Nordic countries, antimicrobial use in animals and the prevalence of antimicrobial resistance are among the lowest in Europe. The network “Nordic Vets Against AMR” organized a meeting in 2021, with key actors including representatives from universities, veterinary authorities and veterinary organizations in Finland, Norway and Sweden. This paper reflects the most important discussions on education, research, policy and future perspectives, including the experiences of these countries. It concludes that Nordic veterinarians are well placed to lead the way in the fight against antimicrobial resistance and that the sharing of experiences can support colleagues in other countries. Veterinary education must go hand in hand with research activities and continuously updated guidelines and legislation. There is also a need for postgraduate training on antimicrobial resistance and prudent antimicrobial use. The veterinary profession must, by any means necessary, protect the efficiency of antimicrobials for the sake of animal health, animal welfare and productivity, as well as public health. While restrictive use of antimicrobials is crucial, the ability of veterinarians to use this medical tool is also important for the sake of animal welfare and global food security.

In 2019, an outbreak of acute haemorrhagic diarrhoea (AHD) in dogs in Norway was linked to Providencia alcalifaciens . A marked increase in diarrhoeal cases in dogs during the autumn, along with the frequent identification of P. alcalifaciens in affected dogs, supports its role as a causative agent in seasonal diarrhoea in dogs in Norway. Previous phylogenetic studies have revealed two major genetic lineages of P. alcalifaciens , one of which is associated with diarrhoeal disease and carries a plasmid-borne type 3 transport system (T3SS _1a ). The aim of this study was to place Norwegian P. alcalifaciens isolates in a global phylogenetic context and to characterize the distribution of putative virulence-associated genes (VAGs) in isolates from dogs with AHD. Whole-genome sequencing was performed on 273 isolates, and 48 publicly available genomes were included for comparative analyses. Bioinformatic processing and phylogenetic analyses were conducted on the complete dataset of 321 P . alcalifaciens genomes. VAGs were identified using ABRicate and two virulence gene databases. Phylogenetic analyses revealed two main clusters, A and B. Most isolates from sick dogs belonged to cluster A, particularly to subcluster A-1 – the largest of five subclusters – which primarily contained isolates from sick dogs. All isolates in subclusters A-1 and A-4 harboured genes encoding T3SS _1a , a type II secretion system and the effector genes stcE , yopJ and cdtA-C . blast searches using closed reference genomes showed high sequence identity (>90%) to plasmid elements in 196 of 197 isolates from subclusters A-1 and A-4, suggesting plasmid-mediated acquisition of virulence factors. These findings support that specific genetic variants of P. alcalifaciens , particularly those in subclusters A-1 and A-4, exhibit increased virulence potential and are associated with AHD in dogs. The high proportion of isolates from clinically affected dogs, including many from the 2019 outbreak, further underscores the link between subcluster A-1 and disease.

The objective of this study was to evaluate welfare and health effects following single and repeated non‐lethal blood sampling from the caudal vasculature of Atlantic salmon. Two experiments were conducted at three different temperatures: a 6‐week freshwater experiment with fish weighing 50–100 g, undergoing up to four blood withdrawals, and a 4‐week seawater experiment with fish weighing 300–450 g, undergoing up to three blood withdrawals. Observed clinical signs included dark pigmentation of the skin and vascular disturbances posterior to the puncture site. Histological evaluations revealed injuries to the vasculature, vertebral column, nervous tissue and skeletal muscle. At 12°C and 15°C, fish displayed strong capacity for tissue regeneration and haematological recovery, but also an elevated risk of acute mortality. At 5°C, acute mortality was minimal, but recovery time was approximately twice as long compared with higher temperatures. Mortality rates and clinical findings decreased with increasing fish weight. These findings demonstrate that non‐lethal caudal blood sampling poses a welfare risk in salmon weighing 450 g or less. The risk factors identified here may inform future risk assessments and support the development of welfare‐compatible guidelines for non‐lethal blood sampling in Atlantic salmon.