Infectious salmon anemia virus: causative agent, pathogenesis and immunity

Infectious salmon anemia (ISA) virus (ISAV), an economically important new pathogen in marine aquaculture, is classified in the family Orthomyxoviridae, genus Isavirus. The main structural properties of this genus include enveloped virions 90-140 nm in diameter with surface projections of a combined receptor-binding hemagglutinin and receptor-destroying enzyme activity demonstrated to be an esterase, hence recently designated HE, and a genome composed of eight segments of linear, single-stranded, negative sense RNA ranging in length from 1.0 to 2.4 kb, with a total size of approximately 14.3 kb. The viral genome encodes at least ten proteins, of which nine are structural and one is non-structural. Examination of more than 160 ISAV isolates has led to the identification of two hemagglutinin subtypes of ISAV, one North American and one European. The immune response against ISAV after infection or vaccination does not provide full protection against the infection. The recent discovery of antibody-mediated uptake and replication of ISAV in macrophage-like fish cell lines suggests that Fc receptor-mediated antibody-dependent enhancement of the ISA virus infection might also occur in vivo, as the virus in Atlantic salmon (Salmo salar) targets endothelial cells lining blood vessels and macrophage-like cells. Cumulative mortalities in Atlantic salmon during natural ISA outbreaks and experimental infections range from 0 to 100%. ISAV causes fatal systemic infections in marine-farmed Atlantic salmon and asymptomatic infections in feral fish. Experimentally induced fatal clinical disease in rainbow trout (Oncorhynchus mykiss) has identified a correlate of virulence of ISAV that may explain its emergence as a fish pathogen.     

Clinical outcomes,ultrastructure and immunohistochemical features of canine high‐grade olfactory neuroblastoma

Olfactory neuroblastoma (ONB) is a rare intranasal neoplasm in both dogs and humans. Similar clinical presentation and overlapping histologic and immunohistochemical features of ONB with other intranasal neoplasms can make diagnosis and treatment of intranasal neoplasia challenging. Furthermore, in part because of their rarity, there is a lack of reporting on therapeutic regimen for these neoplasms. In humans, initial debulking surgery is usually followed by radiation therapy. Here we report on the histologic, immunohistochemical, and ultrastructural characteristics of canine ONB and report on the clinical progression of cases treated with radiation therapy. In all nine canine ONB examined here, neoplastic cells were arranged in a lobular manner amidst a prominent neurofibrillary matrix and had features consistent with Grade III (high grade) ONB. The neoplastic cells demonstrated positive immunohistochemical staining for TuJ‐1, a Class III beta‐tubulin neuronal cytoskeletal protein, and variable staining for other markers, including chromogranin, synaptophysin, AE1/AE3 and MAP2. The longest surviving case was treated with a regimen similar to that used in humans, consisting of debulking surgery followed by definitive radiation therapy. Our study found that TuJ‐1 is a useful marker for ONB and that radiation therapy, even in cases of advanced disease, may result in prolonged survival.     

Equine intervertebral disk disease: A case report

Intervertebral disk disease is common in humans and dogs but is rarely reported in horses. In this case report, we describe an 11-year-old American Saddlebred gelding with a 2-month history of pain and progressive neurological abnormalities (ataxia, conscious proprioceptive deficits involving all four limbs, toe dragging, and restricted neck flexion) while being worked as a Saddleseat show horse. Radiographs of the cervical spine showed a loss of the intervertebral disk space at C₆–C₇. At necropsy, nearly complete loss of the intervertebral disk at C₆–C₇ was seen, with marked eburnation and subchondral sclerosis of the adjacent vertebral endplates that were confirmed by histopathology. Many of the marrow spaces of the affected vertebral bodies were filled with cartilage and others contained variable amounts of fibrous connective tissue (myelofibrosis). To our knowledge, these pathological lesions are rarely reported in the literature and appear to represent a chronic, end-stage phase of cervical vertebral stenosis.     

Serotonin modulates behavioral reactions to unfairness

Serotonin (5-HT) has long been implicated in social behavior and impulsivity, but the mechanisms through which it modulates self-control remain unclear. We observed the effects of manipulating 5-HT function on behavior in the ultimatum game, where players must decide whether to accept or reject fair or unfair monetary offers from another player. Participants with depleted 5-HT levels rejected a greater proportion of unfair offers, but not fair offers, without showing changes in mood, fairness judgment, basic reward processing, or response inhibition. Our results suggest that 5-HT plays a critical role in regulating emotion during social decision-making.     

Biochemical and genetic evaluation of the role of AMP-activated protein kinase in polysaccharide storage myopathy in Quarter Horses

OBJECTIVE: To evaluate whether biochemical or genetic alterations in AMP-activated protein kinase (AMPK) play a role in the development of polysaccharide storage myopathy (PSSM) in Quarter Horses. ANIMALS: 30 PSSM-affected and 30 unaffected (control) Quarter Horses. PROCEDURES: By use of an established peptide phosphotransfer assay, basal and maximal AMPK activities were measured in muscle biopsy samples obtained from 6 PSSM-affected and 6 control horses. In 24 PSSM-affected and 24 control horses, microsatellite markers identified from the chromosomal locations of all 7 AMPK subunit genes were genotyped with a fluorescent DNA fragment analyzer. Alleles of 2 of the AMPK gamma subunit genes were genotyped via DNA sequencing. Allele frequencies of DNA markers in or near the AMPK subunit genes were measured in isolated genomic DNA. RESULTS: No differences in basal or maximal muscle AMPK enzyme activities between PSSM-affected and control horses were detected. There were also no differences in allele frequencies for microsatellite markers near any of the 7 AMPK subunit genes between the 2 groups. Furthermore, previously known and newly identified alleles of 2 equine AMPK gamma subunit genes were also not associated with PSSM. CONCLUSIONS AND CLINICAL RELEVANCE: These results have provided no evidence to indicate that AMPK plays a causative role in PSSM in American Quarter Horses.     

Estimated prevalence of polysaccharide storage myopathy among overtly healthy Quarter Horses in the United States

OBJECTIVE: To estimate the prevalence of polysaccharide storage myopathy (PSSM) among Quarter Horses in the United States and evaluate possible relationships between muscle glycogen concentration, turnout time, and exercise level. DESIGN: Cross-sectional study. ANIMALS: 164 overtly healthy Quarter Horses > 2 years old from 5 states. PROCEDURES: Horses with a history of exertional rhabdomyolysis or any other muscular disease were excluded. Muscle biopsy specimens were examined histologically for evidence of PSSM and were submitted for determination of muscle glycogen concentration. A diagnosis of PSSM was made if amylase-resistant inclusions that stained with periodic acid-Schiff stain were detected. RESULTS: Prevalences of PSSM on the 2 farms with a history of PSSM were 20% (1/5) and 40.7% (11/27); mean prevalence for the other 4 farms was 6.1% (8/132). Sex was not significantly associated with a diagnosis of PSSM, and age was not significantly different between horses with and without PSSM. Total histologic score, serum creatine kinase activity, and muscle glycogen concentration were significantly higher in horses with PSSM than in horses without. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that the prevalence of PSSM among overtly healthy Quarter Horses in the United States is likely to be between 6% and 12%.     

Prevalence,intensity and pathology of the nasal parasite Nasicola hogansi in Atlantic bluefin tuna (Thunnus thynnus)

Ectoparasitic flatworms of Nasicola (Monogenoidea: Capsalidae), which infect nasal epithelium of true tunas (Thunnus spp.), are not well studied, nor have their impacts on the host's olfactory organ been evaluated. Infections of Nasicola hogansi on Atlantic bluefin tuna, Thunnus thynnus, were investigated with emphasis on the relationship between infection prevalence, abundance and mean intensity with bluefin tuna size, sex, body condition and capture month, as well as histopathological effects. Commercially caught Atlantic bluefin tuna (n = 161, 185–305 cm curved fork length) from the Gulf of Maine were sampled during June through August 2009 for infections by N. hogansi. A total of 247 specimens of N. hogansi were collected, with a prevalence of 45.3%, mean abundance of 1.57 (CI: 1.21–2.03) and mean intensity of 3.45 (CI: 2.91–4.22). Neither fish sex nor landing month had a significant effect on parasite parameters. Larger and better-conditioned Atlantic bluefin tuna had a higher mean intensity of infection. Pathology associated with infection by N. hogansi included extensive necrosis, sloughing of the nasal epithelium and associated inflammation of underlying connective tissues. Further epidemiological and pathological study of this host–parasite system is warranted since impaired olfaction, if present, could adversely affect spawning and migration of this top ocean predator.