Variation in volatile organic compounds in Atlantic salmon mucus is associated with resistance to salmon lice infection.

Salmon lice are ectoparasites that threaten wild and farmed salmonids. Artificial selection of salmon for resistance to the infectious copepodid lice stage currently relies on in vivo challenge trials on thousands of salmon a year. We challenged 5750 salmon with salmon lice (Lepeophtheirus salmonis) from two distinct farmed strains of salmon in two separate trials. We found that volatile organic compounds (VOC), 1-penten-3-ol, 1-octen-3-ol and 6-methyl-5-hepten-2-one in the mucus of the salmon host after salmon lice infection, were significantly associated with lice infection numbers across a range of water temperatures (5 °C, 10 °C, 17 °C). Some VOCs (benzene, 1-octen-3-ol and 3,5,5-trimethyl-2-hexene) were significantly different between lines divergently selected for salmon lice resistance. In a combined population assessment, selected VOCs varied between families in the range of 47- 59% indicating a genetic component and were positively correlated to the salmon hosts estimated breeding values 0.59-0.74. Mucosal VOC phenotypes could supplement current breeding practices and have the potential to be a more direct and ethical proxy for salmon lice resistance provided they can be measured prior to lice infestation.

Persistent infections with infectious pancreatic necrosis virus (IPNV) of different virulence in Atlantic salmon, Salmo salar L.

Infectious pancreatic necrosis virus (IPNV) is a prevalent pathogen in fish worldwide. The virus causes substantial mortality in Atlantic salmon juveniles and smolts when transferred to sea water and persistent infection in surviving fish after disease outbreaks. Here, we have investigated the occurrence of the virus as well as the innate immune marker Mx in the head kidney (HK) of Atlantic salmon throughout an experimental challenge covering both a fresh and a seawater phase. The fish were challenged with a high (HV) and low virulence (LV) IPNV. Both isolates caused mortality due to reactivation of the virus after transfer to sea water. In the freshwater phase, higher levels of virus transcripts were detected in the HK of fish infected with LV IPNV compared to HV, suggesting that the HV isolate is able to limit its own replication to a level where the innate immune system is not alerted. Further, ex vivoHK leucocytes derived from fish infected with the two isolates were stimulated with CpG DNA. Significantly, higher IFN levels were found in the LV compared to the HV group in the freshwater phase. This suggests that the viruses attenuate the antiviral host immune response at different levels which may contribute to the observed differences in disease outcome.

Reference genes evaluated for use in infectious pancreatic necrosis virus real-time RT-qPCR assay applied during different stages of an infection.

The stability of 6 reference genes, 18S, beta-actin, RPS20, eEF1alpha, G6PDH and GAPDH, was examined in tissues from Atlantic salmon (Salmo salar) and Chinook salmon embryo cells (CHSE-214). The main objective of this study was to determine the most suitable reference genes for use for the normalisation of data in quantitative real-time RT-qPCR assays conducted on infected tissues. The tissue samples selected for analysis were taken from head kidney and pylorus and collected at different time points during a challenge experiment with infectious pancreatic necrosis virus (IPNV). The stability of some of the reference genes was also studied in infected CHSE-214 cells. The ranking of the genes examined was carried out using the geNorm program. This program determines the most stable genes from a set of genes tested in a given cDNA sample. The stability of the reference genes varied in different tissues and in the cell line at different stages of infection with IPNV. This study demonstrated that tissue-specific combinations of reference genes must be used to normalise real time data for use for the quantitation of IPNV.

Infectious pancreatic necrosis virus infection in Atlantic salmon Salmo salar post-smolts affects the outcome of secondary infections with infectious salmon anaemia virus or Vibrio salmonicida.

Infectious pancreatic necrosis (IPN) virus (IPNV) infection in Atlantic salmon Salmo salar L. post-smolts and its influence on the outcome of secondary infections with infectious salmon anaemia (ISA) virus (ISAV) or Vibrio salmonicida were studied. The infections with ISAV or V salmonicida were performed both in a period of acute IPN and in the following IPNV carrier stage, 3 and 6 to 8 wk after experimental IPNV challenge, respectively. An IPNV carrier condition at low virus titre did not influence the mortality rates after secondary infections. Neither the ISAV infection nor the V. salmonicida infection in experimentally induced IPNV carriers resulted in mortalities different from those observed after challenge of IPNV-free fish. At higher IPNV titres in Atlantic salmon with acute IPN, the outcome of secondary infections was quite different from that observed in IPNV-free fish and in IPNV carriers. In 2 different experiments significantly more fish died when fish with acute IPN were infected with V salmonicida than when fish were infected with V salmonicida alone. Mortality also started earlier in the double-infected group than in the group challenged with V. salmonicida alone, 3 to 4 and 8 d after V salmonicida infection, respectively. Similar results were observed independent of whether mortalities due to IPN alone were registered in the experiments. When Atlantic salmon with acute IPN were infected with ISAV, significantly fewer fish died than when fish were infected with ISAV alone. The ongoing IPNV infection seemed to provide some protection against development of ISA.

[Alzheimer's disease--considerations on the etiology and physiopathology based on a case report]. / Alzheimer's sygdom-overvejesler om aetiologi og patofysiologi på grundlag af en sygehistorie.

On the basis of a case report concerning a woman with severe dementia due to Alzheimer's disease who had a surprising mnestic comeback after mastectomy and lasting for 24 hours after operation, the hypothesis is presented that Alzheimer's disease is due to an age-related weakening in the blood-brain-barrier. Increased permeability might render a slight but constant influx of injurious endogenic substances possible. Serum cholinesterase is suggested as the primary injurious agent.