Losses from infectious diseases are an important component of natural mortality among marine fish species, but factors controlling the ecology of these diseases and their potential responses to anthropogenic changes are poorly understood. We used viral hemorrhagic septicemia virus (VHSV) and a laboratory stock of Pacific herring Clupea pallasii to investigate the kinetics of viral shedding and its effect on disease transmission and host mortality. Outbreaks of acute disease, accompanied by mortality and viral shedding, were initiated after waterborne exposure of herring to concentrations of VHSV as low as 10 1 plaque-forming units (pfu) ml -1 . Shed virus in flow-through tanks was first detected 4 to 5 d post-exposure, peaked after 6 to 10 d, and was no longer detected after 16 d. Shedding rates, calculated from density, flow and waterborne virus titer reached 1.8 to 5.0 × 10 8 pfu fish -1 d -1. Onset of viral shedding was dose-dependent and preceded initial mortality by 2 d. At 21 d, cumulative mortality in treatment groups ranged from 81 to 100% and was dependent not on challenge dose, but on the kinetics and level of viral shedding by infected fish in the tank. Possible consequences of the viral shedding and disease kinetics are discussed in the context of epizootic initiation and perpetuation among populations of wild Pacific herring. KEY WORDS: Viral shedding · VHSV · Pacific herring · Clupea pallasii · Disease ecology Resale or republication not permitted without written consent of the publisherMar Ecol Prog Ser 400: [187][188][189][190][191][192][193] 2010 herring populations in Prince William Sound, Alaska, involves excess mortality from disease (Marty et al. 1998(Marty et al. , 2003, although the precise role of VHS remains controversial (Elston & Meyers 2009).Factors contributing to the onset of VHS epizootics in populations of wild marine fishes are not well understood, but initial infection occurs following direct contact with exogenous waterborne virus (Kocan et al. 2001a). Laboratory studies show that epizootics are readily initiated in naïve stocks of Pacific herring after a 1 h waterborne exposure to moderate levels (10 3 plaque-forming units [pfu] ml -1 ) or greater of VHSV (Kocan et al. 1997). However, field surveys have detected only low titers of virus (5 to 15 pfu ml -1 ) in samples of marine water collected in the vicinity of free-ranging schools of herring (Hershberger et al. 1999).The objectives of this study were to determine the minimum exposure thresholds required to initiate epizootics of VHS in Pacific herring and to quantify the kinetics of viral shedding from infected fish. These empirically deduced infection thresholds and virus shedding rates are discussed in the context of disease initiation and perpetuation in wild marine fishes. MATERIALS AND METHODSMinimum exposure levels required to initiate VHS epizootics in groups of 1+ yr old (mean length = 100 mm, SD = 7.2 mm), specific pathogen-free (SPF) Pacific herring (Hershberger et al. 2007) were determined by immer...

Laboratory challenges using specific-pathogen-free Pacific herring Clupea pallasii from three distinct populations indicated that stock origin had no effect on susceptibility to viral hemorrhagic septicemia (VHS). All of the populations were highly susceptible to the disease upon initial exposure, with significantly greater cumulative mortalities occurring in the exposed treatment groups (56.3-64.3%) than in the unexposed control groups (0.8-9.0%). Interstock differences in cumulative mortality were not significant. The virus loads in the tissues of fish experiencing mortality were 10-10,000 times higher during the acute phase of the epizootics (day 13 postexposure) than during the recovery phase (days 30-42). Survivors of the epizootics were refractory to subsequent VHS, with reexposure of VHS survivors resulting in significantly less cumulative mortality (1.2-4.0%) than among positive controls (38.1-64.4%); interstock differences in susceptibility did not occur after reexposure. These results indicate that data from experiments designed to understand the ecology of VHS virus in a given stock of Pacific herring are broadly applicable to stocks throughout the northeastern Pacific.

Avian influenza A viruses (IAVs) in different species of seals display a spectrum of pathogenicity, from sub-clinical infection to mass mortality events. Here we present an investigation of avian IAV infection in a 3- to 4-month-old Grey seal (Halichoerus grypus) pup, rescued from St Michael’s Mount, Cornwall in 2017. The pup underwent medical treatment but died after two weeks; post-mortem examination and histology indicated sepsis as the cause of death. IAV NP antigen was detected by immunohistochemistry in the nasal mucosa, and sensitive real-time reverse transcription polymerase chain reaction assays detected trace amounts of viral RNA within the lower respiratory tract, suggesting that the infection may have been cleared naturally. IAV prevalence among Grey seals may therefore be underestimated. Moreover, contact with humans during the rescue raised concerns about potential zoonotic risk. Nucleotide sequencing revealed the virus to be of subtype H3N8. Combining a GISAID database BLAST search and time-scaled phylogenetic analyses, we inferred that the seal virus originated from an unsampled, locally circulating (in Northern Europe) viruses, likely from wild Anseriformes. From examining the protein alignments, we found several residue changes in the seal virus that did not occur in the bird viruses, including D701N in the PB2 segment, a rare mutation, and a hallmark of mammalian adaptation of bird viruses. IAVs of H3N8 subtype have been noted for their particular ability to cross the species barrier and cause productive infections, including historical records suggesting that they may have caused the 1889 pandemic. Therefore, infections such as the one we report here may be of interest to pandemic surveillance and risk and help us better understand the determinants and drivers of mammalian adaptation in influenza.

Background Mycoplasma species have been associated with economically important diseases affecting ruminants worldwide and include contagious bovine pleuropneumonia (CBPP), contagious caprine pleuropneumonia (CCPP) and contagious agalactia, listed by the World Organisation for Animal Health (OIE). The Mycoplasma Team at the Animal and Plant Health Agency provides an identification service for Mycoplasma and Ureaplasma species of veterinary importance to the United Kingdom (UK), supporting the detection of new and emerging pathogens, as well as contributing to the surveillance of endemic, and the OIE listed diseases exotic to the UK. Mycoplasma and other Mollicutes species were identified from diagnostic samples from farmed ruminants in England and Wales using a combination of culture and 16S rRNA gene-based PCR-denaturing gradient gel electrophoresis, submitted between 2005 and 2019. Results A total of 5578 mollicutes identifications, which include mycoplasmas and the related acholeoplasmas and ureaplasmas, were made from farmed ruminant animals during the study period. Throughout the study period, the pathogen Mycoplasma bovis was consistently the most frequently identified species, accounting for 1411 (32%) of 4447 molecular identifications in cattle, primarily detected in the lungs of pneumonic calves, followed by joints and milk of cattle showing signs of arthritis and mastitis, respectively. M. bovirhinis, M. alkalescens, M. dispar, M. arginini and Ureaplasma diversum, were also common. Mixed species, principally M. bovis with M. alkalescens, M. arginini or M. bovirhinis were also prevalent, particularly from respiratory samples. The non-cultivable blood-borne haemoplasmas Candidatus ‘Mycoplasma haemobos’ and Mycoplasma wenyonii were identified from cattle, with the latter species most often associated with milk-drop. M. ovipneumoniae was the predominant species identified from sheep and goats experiencing respiratory disease, while M. conjunctivae preponderated in ocular samples. The UK remains free of the ruminant mycoplasmas listed by OIE. Conclusions The continued high prevalence of M. bovis identifications confirms its ongoing dominance and importance as a significant pathogen of cattle in England and Wales, particularly in association with respiratory disease. M. ovipneumoniae has seen a general increase in prevalence in recent years, notably in coughing lambs and should therefore be considered as a primary differential diagnosis of respiratory disease in small ruminants.

This focus article was prepared by Amanda Carson, Rudolf Reichel, Suzie Bell, Rachael Collins and Jasmine Smith of the APHA Small Ruminant Species Expert Group, and Dave Bartley from the Moredun Research Institute.