Viral haemorrhagic septicaemia (VHS) was diagnosed in rainbow trout in the UK in May 2006. VHS virus (VHSV) was isolated from fingerlings showing typical histopathological lesions at a single rainbow trout farm site experiencing high mortality. The virus was confirmed as VHSV by serological and molecular biological tests. Phylogenetic analysis based on the complete glycoprotein gene sequence revealed that the isolate was closely related (99% nucleotide identity) to several Danish isolates from 1991 to 2000 and was assigned to VHSV genogroup Ia. The pathogenicity of the isolate was determined in infection experiments using rainbow trout fry. Following waterborne challenge, cumulative mortalities reached 96.67-100% by 12 days post-infection. This represents the first isolation of a pathogenic freshwater VHSV in the UK.
Morbidity of intensively cultured red abalone, Haliotis rufescens, as well as experimentally stressed (elevated temperature and hyper-oxygenation) abalone, was studied using clinical, histological, immunofluorescent and bacteriological techniques. Histological study showed a typical pattern of bacterial infection from all groups studied, characterized by epithelial exfoliation or rupture and systemic growth of the bacteria along vascular sinuses and along neural sheaths. Peripheral neurons degenerated rapidly and a responsive host cellular infiltrate did not appear to effectively retard the advancement of the infection. Nine bacterial isolates from the culture system water or sick animals were characterized biochemically. All were Gram-negative, facultatively anaerobic, non-aerogenic, oxidase-positive rods with single polar flagella and thus appeared related to the Vibrio group. Further characterization showed that most isolates did not correspond to specifically characterized vibrios. Antiserum prepared to the isolates contained antibody both to common group antigens (from all nine strains) and to strain-specific antigens. Selection of antiserum and subsequent absorption permitted the use of the antiserum for specific recognition of each isolate. Immunofluorescent studies clearly demonstrated that antiserum to an isolate corresponding to Vibrio alginolyticus was the predominant antiserum producing positive staining of infecting bacteria in the typical lesions in abalone tissues. The pattern of positive staining corresponded to histopathological observations of the disease. The disease can be managed in husbandry systems by both limiting the number of potentially pathogenic bacteria and by limiting the exposure of the animals to physico-chemical stresses.
Following a reported mortality event of European flat oysters Ostrea edulis in southwestern England in December 2010, a sample of 30 oysters was examined using histology and molecular techniques. Histological examination of the oysters revealed the presence of microcell stages in the haemocytes and connective tissues of 3 out of the 30 animals examined. One animal showing marked haemocyte infiltration of the connective tissues was considered to be infected with Bonamia ostreae based on the presence of small uninucleate microcells measuring approximately 1 to 1.5 µm in diameter. Two other oysters were considered by histology to be infected with B. exitiosa. Infected haemocytes contained up to 5 microcells, measuring approximately 2 to 3 µm in diameter with a central or subcentral nucleus. Rarely, larger plasmodia-like multinucleated stages were noted in the haemocyte cytoplasm characterised by its irregular shape and increased eosinophilic cytoplasm. Haemocyte infiltration of the connective tissues surrounding the digestive gland and the mantle was noted along with necrosis of the tissues associated with the infection. Molecular analysis of the infected animals confirmed the presence of B. exitiosa in the sample. This study describes the parasite from flat oysters cultured in the UK; subsequent targeted sampling has not detected the parasite in flat oyster populations at this or other sites within the UK.
This is the first record of a fish nidovirus isolated from a consignment of goldfish at the United Kingdom (UK) border. The full-length viral genome was 25,985 nt, sharing a 97.9% nucleotide identity with the Chinook salmon bafinivirus (CSBV) NIDO with two deletions of 537 and 480 nt on the ORF Ia protein. To assess the potential impact on UK fish species, Atlantic salmon, common carp and goldfish were exposed to the virus via an intraperitoneal (IP) injection and bath challenge. Moribundity was recorded in only 8% of IP-injected goldfish. A high viral load, ≈107 of the CSBV PpIa gene, was measured in the kidney of moribund goldfish. Mild histopathological changes were observed in the kidneys of challenged carps. Ultrastructural observations in renal tubule epithelial cells of goldfish showed cylindrical tubes (≈15 nm in diameter) and tubular structures budding spherical virions (≈200 nm in diameter) with external spike-like structures. Negative staining showed both circular and bacilliform virions. Seroconversion was measured in common carp and goldfish but not in Atlantic salmon. This study reinforces the potential risk of novel and emerging pathogens being introduced to recipient countries via the international ornamental fish trade and the importance of regular full health screens at the border inspection posts to reduce this risk.
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