Changing trends in mastitis

<p>Abstract</p> <p>The global dairy industry, the predominant pathogens causing mastitis, our understanding of mastitis pathogens and the host response to intramammary infection are changing rapidly. This paper aims to discuss changes in each of these aspects. Globalisation, energy demands, human population growth and climate change all affect the dairy industry. In many western countries, control programs for contagious mastitis have been in place for decades, resulting in a decrease in occurrence of <it>Streptococcus agalactiae </it>and <it>Staphylococcus aureus </it>mastitis and an increase in the relative impact of <it>Streptococcus uberis </it>and <it>Escherichia coli </it>mastitis. In some countries, <it>Klebsiella </it>spp. or <it>Streptococcus dysgalactiae </it>are appearing as important causes of mastitis. Differences between countries in legislation, veterinary and laboratory services and farmers' management practices affect the distribution and impact of mastitis pathogens. For pathogens that have traditionally been categorised as contagious, strain adaptation to human and bovine hosts has been recognised. For pathogens that are often categorised as environmental, strains causing transient and chronic infections are distinguished. The genetic basis underlying host adaptation and mechanisms of infection is being unravelled. Genomic information on pathogens and their hosts and improved knowledge of the host's innate and acquired immune responses to intramammary infections provide opportunities to expand our understanding of bovine mastitis. These developments will undoubtedly contribute to novel approaches to mastitis diagnostics and control.</p

The effect of ApoE e4 on blood pressure in patients with and without depression

Knut A Hestad,1&ndash;3 Knut Engedal,4 Jon Elling Whist,1,5 Per G Farup1,6 1Department of Research, Innlandet Hospital Trust, Brumunddal, Norway; 2Department of Psychology, Faculty of Social Sciences and Technology Management, Norwegian University of Science and Technology, Trondheim, Norway; 3Department of Public Health, Hedmark University College, Elverum, Norway; 4Norwegian Center for Aging and Health, Vestfold Health Trust, T&oslash;nsberg, Norway; 5Department of Medical Biochemistry, Innlandet Hospital Trust, Lillehammer, Norway; 6Unit for Applied Clinical Research, Department of Cancer Research and Molecular Medicine, Faculty of&nbsp;Medicine, Norwegian University of&nbsp;Science and Technology, Trondheim,&nbsp;Norway Introduction: Depression is considered an independent risk factor for hypertension, particularly for people with recurrent episodes or a long history of depression. Another risk factor for cardiovascular disease is the Apolipoprotein E e4 allele (ApoE e4). The aim of this study was to examine how ApoE e4 was related to blood pressure (BP) in patients with depression and&nbsp;a control group.Methods: A total of 78 patients, 49 with depression and 29 without, all recruited from the same hospital, underwent ApoE e genotyping (24 had at least one ApoE e4 allele) and examination of BP.Results: In the depression group, but not in the control group, both systolic and diastolic BP were significantly higher in patients with ApoE e4 than in those without. The effect of ApoE e4 on BP differed significantly between the two groups.Conclusion: Our findings showed that the effect of ApoE e4 on BP differed between the patients with depression and the control group. In patients with depression, ApoE e4 was associated with an increase in BP. We suggest that patients with depression and ApoE e4-positive status are particularly prone to develop BP elevation. Keywords: depression, blood pressure, ApoE e4, ApoE, genotypin

Patients with depression display cytokine levels in serum and cerebrospinal fluid similar to patients with diffuse neurological symptoms without a defined diagnosis

Knut A Hestad,1&ndash;3 Knut Engedal,4 Jon Elling Whist,1 P&aring;l Aukrust,5&ndash;9 Per G Farup,1,10 Tom Eirik Mollnes,9,11&ndash;13 Thor Ueland5,7,91Department of Research, Innlandet Hospital Trust, Brumunddal, 2Department of Psychology, Faculty of Social Sciences and Technology Management, Norwegian University of Science and Technology (NTNU), Trondheim, 3Department of Public Health, Hedmark University College, Elverum, 4Norwegian Centre for Aging and Health, Vestfold Health Trust, T&oslash;nsberg, 5Research Institute of Internal Medicine, 6Section of Clinical Immunology and Infectious Diseases, 7Institute of Clinical Medicine, Oslo University Hospital Rikshospitalet, 8K.G. Jebsen IRC, University of Oslo, Oslo, 9K.G. Jebsen TREC, University of Troms&oslash;, Troms&oslash;, 10Unit for Applied Clinical Research, Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, 11Centre of Molecular Inflammation Research, Norwegian University of Science and Technology (NTNU), Trondheim, 12Department of Immunology, Oslo University Hospital Rikshospitalet, Oslo, 13Research Laboratory, Nordland Hospital, Bod&oslash;, NorwayIntroduction: Several reports indicate that inflammation may play a role in depression and demonstrate enhanced systemic levels of inflammatory mediators. We hypothesized that 44 patients with a diagnosis of depression would present with a specific and different serum and cerebrospinal fluid (CSF) cytokine profile compared to 21 patients with diffuse neurological symptoms, of whom 15 had fatigue as a major symptom, but no change in emotional state.Methods: The diagnoses of the patients with depression were according to the International Classification of Diseases, tenth edition (F32&ndash;34 spectra). Cytokine profiles in serum and CSF were determined by multiplex analysis, including 27 cytokines, chemokines, and growth factors.Results: No differences could be found between the two groups studied regarding cytokine levels in serum or CSF except for serum interleukin (IL)-1 receptor antagonist that was lower in the depression group. There were only four high correlations (&gt;0.4) between serum and CSF levels of the cytokines, reflecting independent synthesis and turnover in these two compartments. In the control group, fatigue was associated with increased IL-1 receptor antagonist, IL-10, granulocyte-colony stimulating factor, and interferon-&gamma; (all P&lt;0.01).Conclusion: Patients with depression had a similar cytokine profile as nondepressive patients, both systemically and in CSF. Fatigue was associated with higher levels of some inflammatory markers in the control group. It is possible that the presence of fatigue in a large proportion of patients and controls could contribute to the lack of difference in cytokine levels between these two groups.Keywords: depression, cytokines, chemokines, inflammation, fatigue, serum, CSF, multiplex analysi