Yersinia ruckeri is a salmonid pathogen with widespread distribution in cool-temperate waters including Australia and New Zealand, two isolated environments with recently developed salmonid farming industries. Phylogenetic comparison of 58 isolates from Australia, New Zealand, USA, Chile, Finland and China based on non-recombinant core genome SNPs revealed multiple deep-branching lineages, with a most recent common ancestor estimated at 18 500 years BP (12 355–24 757 95% HPD) and evidence of Australasian endemism. Evolution within the Tasmanian Atlantic salmon serotype O1b lineage has been slow, with 63 SNPs describing the variance over 27 years. Isolates from the prevailing lineage are poorly/non-motile compared to a lineage pre-vaccination, introduced in 1997, which is highly motile but has not been isolated since from epizootics. A non-motile phenotype has arisen independently in Tasmania compared to Europe and USA through a frameshift in fliI, encoding the ATPase of the flagella cluster. We report for the first time lipopolysaccharide O-antigen serotype O2 isolates in Tasmania. This phenotype results from deletion of the O-antigen cluster and consequent loss of high-molecular-weight O-antigen. This phenomenon has occurred independently on three occasions on three continents (Australasia, North America and Asia) as O2 isolates from the USA, China and Tasmania share the O-antigen deletion but occupy distant lineages. Despite the European and North American origins of the Australasian salmonid stocks, the lineages of Y. ruckeri in Australia and New Zealand are distinct from those of the northern hemisphere, suggesting they are pre-existing ancient strains that have emerged and evolved with the introduction of susceptible hosts following European colonization.

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Aquaculture is the fastest growing animal food production industry, now producing 50% of all food fish. However, aquaculture feeds remain dependent on fishmeal derived from capture fisheries, which must be reduced for continued sustainable growth. Purple phototrophic bacteria (PPB) efficiently yield biomass from wastewater with high product homogeneity, a relatively high protein fraction, and potential added value as an ingredient for fish feeds. Here we test bulk replacement of fishmeal with PPB microbial biomass in diets for Asian sea bass ( Lates calcarifer ), a high value carnivorous fish with high protein to energy requirement. Mixed culture PPB were grown in a novel 1 m 3 attached photo-biofilm process using synthetic and real wastewater. Four experimental diets were formulated to commercial specifications but with the fishmeal substituted (0%, 33%, 66%, and 100%) with the synthetic grown PPB biomass and fed to a cohort of 540 juvenile fish divided amongst 12 tanks over 47 days. Weight and standard length were taken from individual fish at 18, 28, and 47d. No significant difference in survival was observed due to diet or other factors (94–100%). There was a negative correlation between PPB inclusion level and final weight ( p = 5.94 × 10 −5 ) with diet accounting for 4.1% of the variance over the trial (general linear model, R 2 = 0.96, p = 1 × 10 −6 ). Feed conversion ratio was also significantly influenced by diet ( p = 6 × 10 −7 ) with this factor accounting for 89% of variance. Specifically, feed conversion ratio (FCR) rose to 1.5 for the 100% replacement diet during the last sample period, approximately 1.0 for the partial replacement, and 0.8 for the nil replacement diet. However, this study demonstrates that bulk replacement of fishmeal by PPB is feasible, and commercially viable at 33% and 66% replacement.

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Summary Improving evidence for action is crucial to tackle antimicrobial resistance. The number of interventions for antimicrobial resistance is increasing but current research has major limitations in terms of efforts, methods, scope, quality, and reporting. Moving the agenda forwards requires an improved understanding of the diversity of interventions, their feasibility and cost–benefit, the implementation factors that shape and underpin their effectiveness, and the ways in which individual interventions might interact synergistically or antagonistically to influence actions against antimicrobial resistance in different contexts. Within the efforts to strengthen the global governance of antimicrobial resistance, we advocate for the creation of an international One Health platform for online learning. The platform will synthesise the evidence for actions on antimicrobial resistance into a fully accessible database; generate new scientific insights into the design, implementation, evaluation, and reporting of the broad range of interventions relevant to addressing antimicrobial resistance; and ultimately contribute to the goal of building societal resilience to this central challenge of the 21st century.

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Since 2007, 96 wild Queensland groupers, Epinephelus lanceolatus, (Bloch), have been found dead in NE Australia. In some cases, Streptococcus agalactiae (Group B Streptococcus, GBS) was isolated. At present, a GBS isolate from a wild grouper case was employed in experimental challenge trials in hatchery-reared Queensland grouper by different routes of exposure. Injection resulted in rapid development of clinical signs including bilateral exophthalmia, hyperaemic skin or fins and abnormal swimming. Death occurred in, and GBS was re-isolated from, 98% fish injected and was detected by PCR in brain, head kidney and spleen from all fish, regardless of challenge dose. Challenge by immersion resulted in lower morbidity with a clear dose response. Whilst infection was established via oral challenge by admixture with feed, no mortality occurred. Histology showed pathology consistent with GBS infection in organs examined from all injected fish, from fish challenged with medium and high doses by immersion, and from high-dose oral challenge. These experimental challenges demonstrated that GBS isolated from wild Queensland grouper reproduced disease in experimentally challenged fish and resulted in pathology that was consistent with that seen in wild Queensland grouper infected with S. agalactiae.