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  • 1.
    Ahlm, Clas
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Thelin, Anders
    Elgh, Fredrik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Juto, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Stiernström, E L
    Holmberg, S
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Prevalence of antibodies specific to Puumala virus among farmers in Sweden1998Ingår i: Scandinavian Journal of Work, Environment and Health, ISSN 0355-3140, E-ISSN 1795-990X, Vol. 24, nr 2, s. 104-108Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Serological evidence confirmed that the exposure of humans to Puumala virus is firmly restricted to the northern and central parts of Sweden. In addition the evidence indicated that, in this region, farming is associated with an increased risk of contracting hantavirus infection.

  • 2.
    Ahlm, Clas
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Wallin, Kjell
    Skoglig zooekologi, SLU, Umeå.
    Lundkvist, Åke
    Smittskyddsinstitutet.
    Elgh, Fredrik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Juto, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Merza, Malik
    Virologi, SVA, Uppsala.
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Serologic evidence of Puumala virus infection in wild moose in northern Sweden2000Ingår i: American Journal of Tropical Medicine and Hygiene, ISSN 0002-9637, E-ISSN 1476-1645, Vol. 62, nr 1, s. 106-111Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Puumala (PUU) virus is the causative agent of nephropathia epidemica, the Scandinavian form of hemorrhagic fever with renal syndrome. The infection is acquired by airborne transmission of PUU virus from its rodent reservoir, the bank vole. Besides serologic data indicating that the virus may spread also to heterologous rodents, there is little information on the susceptibility of wild living animals to PUU virus. We studied the occurrence of antibodies to PUU virus in serum samples from 427 wild-living moose, of which 260 originated from the PUU virus-endemic northern and central parts of Sweden and 167 originated from the southern, nonendemic part of Sweden. Samples from 5 animals showed reactivity in an ELISA for recombinant PUU virus nucleocapsid protein, an immunofluorescent assay, and a neutralization test. These 5 animals all originated from the PUU virus-endemic northern part of Sweden. In conclusion, 5 of 260 moose from the endemic region showed convincing serologic evidence of past PUU virus infection. The seroprevalence was low, suggesting that the moose is subjected to endstage infection rather than being part of an enzootic transmission cycle.

  • 3.
    Alexeyev, Oleg A
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Ahlm, Clas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Elgh, Fredrik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Aava, Birgitta
    Skoglig Zooekologi, SLU, Umeå.
    Palo, Thomas
    Skoglig Zooekologi, SLU, Umeå.
    Settergren, Bo
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Wadell, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Juto, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    A minority of seropositive wild bank voles (Clethrionomys glareolus) show evidence of current Puumala virus infection1998Ingår i: Epidemiology and Infection, ISSN 0950-2688, E-ISSN 1469-4409, Vol. 121, nr 2, s. 419-425Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Bank voles (Clethrionomys glareolus) serve as the reservoir for Puumala (PUU) virus, the aetiologic agent of nephropathia epidemica. The animals are believed to be persistently infected and the occurrence of serum antibodies is usually taken as an evidence of active infection. We found serum antibodies to PUU virus in 42 of 299 wild bank voles captured in a PUU virus endemic area. PUU virus RNA was demonstrated in lung specimens of 11 of these 42 animals and in 2 of them antigen was also found. Thus in the lungs of 31 of 42 seropositive animals neither PUU virus RNA nor antigen was detected. In 2 of 257 seronegative animals, lung specimens showed presence of PUU virus antigen and RNA. Isolation of PUU virus from lung tissue was successful in all 4 antigen-positive bank voles but in none of 16 tested antigen-negative animals. In conclusion, only a minority of bank voles with serum antibodies to PUU virus showed evidence of current infection.

  • 4.
    Eneslätt, Kjell
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Rietz, Cecilia
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Rydén, Patrik
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för matematik och matematisk statistik.
    Stöven, Svenja
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    House, Robert V
    Wolfraim, Lawrence A
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Sjöstedt, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Persistence of cell-mediated immunity three decades after vaccination with the live vaccine strain of Francisella tularensis2011Ingår i: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 41, nr 4, s. 974-980Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The efficacy of many vaccines against intracellular bacteria depends on the generation of cell-mediated immunity, but studies to determine the duration of immunity are usually confounded by re-exposure. The causative agent of tularemia, Francisella tularensis, is rare in most areas and, therefore, tularemia vaccination is an interesting model for studies of the longevity of vaccine-induced cell-mediated immunity. Here, lymphocyte proliferation and cytokine production in response to F. tularensis were assayed in two groups of 16 individuals, vaccinated 1-3 or 27-34 years previously. As compared to naïve individuals, vaccinees of both groups showed higher proliferative responses and, out of 17 cytokines assayed, higher levels of MIP-1β, IFN-γ, IL-10, and IL-5 in response to recall stimulation. The responses were very similar in the two groups of vaccinees. A statistical model was developed to predict the immune status of the individuals and by use of two parameters, proliferative responses and levels of IFN-γ, 91.1% of the individuals were correctly classified. Using flow cytometry analysis, we demonstrated that during recall stimulation, expression of IFN-γ by CD4(+) CCR7(+) , CD4(+) CD62L(+) , CD8(+) CCR7(+) , and CD8(+) CD62L(+) cells significantly increased in samples from vaccinated donors. In conclusion, cell-mediated immunity was found to persist three decades after tularemia vaccination without evidence of decline.

  • 5.
    Kroca, Michal
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Johansson, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
    Sjöstedt, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Vγ9Vδ2 T cells from individuals undergoing Pontiac fever or tularemia respond at a similar extent to phosphoantigen from Francisella tularensis or Legionella micdadei.Manuskript (Övrig (populärvetenskap, debatt, mm))
  • 6.
    Lindgren, Helena
    et al.
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi. Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Klinisk bakteriologi. Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Infektionssjukdomar.
    Stenman, Linda
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi. Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Klinisk bakteriologi.
    Tärnvik, Arne
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Infektionssjukdomar.
    Sjöstedt, Anders
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi. Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Klinisk bakteriologi.
    The contribution of reactive nitrogen and oxygen species to the killing of Francisella tularensis LVS by murine macrophages.2005Ingår i: Microbes and infection, ISSN 1286-4579, E-ISSN 1769-714X, Vol. 7, nr 3, s. 467-475Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Intracellular killing of Francisella tularensis by macrophages depends on interferon-gamma (IFN-gamma)-induced activation of the cells. The importance of inducible nitric oxide synthase (iNOS) or NADPH phagocyte oxidase (phox) for the cidal activity was studied. Murine IFN-gamma-activated peritoneal exudate cells (PEC) produced nitric oxide (NO), measured as nitrite plus nitrate, and superoxide. When PEC were infected with the live vaccine strain, LVS, of F. tularensis, the number of viable bacteria was at least 1000-fold lower in the presence than in the absence of IFN-gamma after 48 h of incubation. PEC from iNOS-gene-deficient (iNOS-/-) mice killed F. tularensis LVS less effectively than did PEC from wild-type mice. PEC from phox gene-deficient (p47phox-/-) mice were capable of killing the bacteria, but killing was less efficient, although still significant, in the presence of NG-monomethyl-L-arginine (NMMLA), an inhibitor of iNOS. A decomposition catalyst of ONOO-, FeTPPS, completely reversed the IFN-gamma-induced killing of F. tularensis LVS. Under host cell-free conditions, F. tularensis LVS was exposed to S-nitroso-acetyl-penicillamine (SNAP), which generates NO, or 3-morpholinosydnonimine hydrochloride (SIN-1), which generates NO and superoxide, leading to formation of ONOO-. During 6 h of incubation, SNAP caused no killing of F. tularensis LVS, whereas effective killing occurred in the presence of equimolar concentrations of SIN-1. The results suggest that mechanisms dependent on iNOS and to a minor degree, phox, contribute to the IFN-gamma-induced macrophage killing of F. tularensis LVS. ONOO- is likely to be a major mediator of the killing.

  • 7.
    Lindgren, Helena
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi. Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Stenmark, Stephan
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Chen, Wangxue
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Sjöstedt, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
    Distinct roles of reactive nitrogen and oxygen species to control infection with the facultative intracellular bacterium Francisella tularensis.2004Ingår i: Infection and Immunity, ISSN 0019-9567, E-ISSN 1098-5522, Vol. 72, nr 12, s. 7172-7182Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Reactive nitrogen species (RNS) and reactive oxygen species (ROS) are important mediators of the bactericidal host response. We investigated the contribution of these two mediators to the control of infection with the facultative intracellular bacterium Francisella tularensis. When intradermally infected with the live vaccine strain F. tularensis LVS, mice deficient in production of RNS (iNOS(-/-) mice) or in production of ROS by the phagocyte oxidase (p47(phox-/-) mice) showed compromised resistance to infection. The 50% lethal dose (LD(50)) for iNOS(-/-) mice was <20 CFU, and the LD(50) for p47(phox-/-) mice was 4,400 CFU, compared to an LD(50) of >500,000 CFU for wild-type mice. The iNOS(-/-) mice survived for 26.4 +/- 1.8 days, and the p47(phox-/-) mice survived for 10.1 +/- 1.3 days. During the course of infection, the serum levels of gamma interferon (IFN-gamma) and interleukin-6 were higher in iNOS(-/-) and p47(phox-/-) mice than in wild-type mice. Histological examination of livers of iNOS(-/-) mice revealed severe liver pathology. Splenocytes obtained 5 weeks after primary infection from antibiotic-treated iNOS(-/-) mice showed an in vitro recall response that was similar in magnitude and greater secretion of IFN-gamma compared to cells obtained from wild-type mice. In summary, mice lacking expression of RNS or ROS showed extreme susceptibility to infection with F. tularensis LVS. The roles of RNS and ROS seemed to be distinct since mice deficient in production of ROS showed dissemination of infection and died during the early phase of infection, whereas RNS deficiency led to severe liver pathology and a contracted course of infection.

  • 8. Palo, Thomas R
    et al.
    Ahlm, Clas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Climate variability reveals complex events for tularemia dynamics in man and mammals2005Ingår i: Ecology & society, ISSN 1708-3087, E-ISSN 1708-3087, Vol. 10, nr 1, artikel-id 22Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tularemia is caused by the bacterium Francisella tularensis, but the natural reservoir is unknown and environmental conditions for outbreaks in mammals and man are poorly understood. The present study analyzed the synchrony between the North Atlantic Oscillation (NAO) index, the number of human cases of tularemia reported in Sweden, and the density of hares. Climate variation at a lag of 2 yr explained as a single factor similar to 27% of the variation in the number of tularemia cases over time. A low NAO index, indicating cold winters, and low water flow in rivers during the coming summer were associated with high numbers of human cases of tularemia 2 yr later. The number of mountain hares was not related to NAO or to the number of cases of tularemia. The change in mountain hare numbers was negatively associated with the number of human cases, showing the sensitivity of this species to the disease. Low turnover in water environments may at some point in time trigger a chain of events leading to increased replication of F. tularensis via unknown reservoirs and/or vectors that affect humans and mammals. A possible increase in the NAO index with a future warmer climate would not be expected to facilitate a higher frequency of tularemia outbreaks in Sweden.

  • 9.
    Stenmark, Stephan
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Lindgren, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Sjöstedt, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
    Specific antibodies contribute to the host protection against strains of Francisella tularensis subspecies holarctica2003Ingår i: Microbial Pathogenesis, Vol. 35, nr 2, s. 73-80Artikel i tidskrift (Refereegranskat)
  • 10.
    Stenmark, Stephan
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Lindgren, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Sjöstedt, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
    T-cell-dependent and independent protection against Francisella tularensisManuskript (preprint) (Övrigt vetenskapligt)
  • 11.
    Tärnvik, Arne
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Infektionssjukdomar.
    [Importance of non-graded student case discussions]2004Ingår i: Lakartidningen, ISSN 0023-7205, Vol. 101, nr 45, s. 3620-Artikel i tidskrift (Övrigt vetenskapligt)
  • 12.
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Management of complicated skin and skin structure infections: a call for infectious disease specialists2018Ingår i: Infectious Diseases, ISSN 2374-4235, E-ISSN 2374-4243, Vol. 50, nr 2, s. 117-118Artikel i tidskrift (Övrigt vetenskapligt)
  • 13.
    Tärnvik, Arne
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Infektionssjukdomar.
    Revival of the case method: a way to retain student-centred learning in a post-PBL era.2007Ingår i: Medical Teacher, ISSN 1466-187X, Vol. 29, nr 1, s. e32-6Artikel i tidskrift (Refereegranskat)
  • 14.
    Tärnvik, Arne
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Infektionssjukdomar.
    [The case method--engaging teaching method. Realistic exercises make practical training of the medical profession possible]2004Ingår i: Lakartidningen, ISSN 0023-7205, Vol. 101, nr 43, s. 3314-6, 3319Artikel i tidskrift (Övrigt vetenskapligt)
  • 15.
    Tärnvik, Arne
    et al.
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Infektionssjukdomar.
    Chu, May C
    New approaches to diagnosis and therapy of tularemia.2007Ingår i: Annals of the New York Academy of Sciences, ISSN 0077-8923, Vol. 1105, s. 378-404Artikel i tidskrift (Refereegranskat)
  • 16.
    Tärnvik, Arne
    et al.
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Infektionssjukdomar.
    Priebe, Heidi-Sabrina
    Grunow, Roland
    Tularaemia in Europe: an epidemiological overview.2004Ingår i: Scandinavian Journal of Infectious Diseases, ISSN 0036-5548, Vol. 36, nr 5, s. 350-5Artikel i tidskrift (Refereegranskat)
  • 17.
    Tärnvik, Arne
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Stenberg, Berndt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Suitability of the multiple case method when applied on dermatology and infectious diseases at the clinical stage of medical education2010Ingår i: The Internet Journal of Medical Education, ISSN 2155-6725, Vol. 1, nr 1Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: By mimicking situations relevant to future work conditions, the multiple case method aims to trigger student interest in a subject and to induce familiarity with subject knowledge. Objectives: Our main aim was to assess the suitability of the multiple case method when applied at the clinical stage of medical education. Moreover, we wished to define the maximum group size with which students felt comfortable. Methods: Between 2001 and 2007, during 24 runs of a course in dermatology and infectious diseases, student assessments of the multiple case method were rated. Between 1993 and 2007, 1323 student evaluations were scrutinized for comments on group size. Results: On a 1-5 scale (1= value poor, 5= value high), student ratings of the multiple case method remained consistent at 4.4 to 4.7. When the number of participants in the discussion groups was 18 - 25, no comments on group size occurred. When size increased to 26 - 33 participants, 4/605 (0.7%) commented spontaneously that they would prefer discussing in a smaller group. At a size of 34 – 37, 20/396 (5.1%) expressed such a concern.

  • 18.
    Tärnvik, Arne
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
    Sundqvist, G
    Gothefors, Leif
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Gustafsson, H
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Öron- näs- och halssjukdomar.
    Meningitis caused by Fusobacterium necrophorum.1986Ingår i: European Journal of Clinical Microbiology and Infectious Diseases, ISSN 0934-9723, E-ISSN 1435-4373, Vol. 5, nr 3, s. 353-355Artikel i tidskrift (Refereegranskat)
  • 19.
    Wiström, Johan
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Ahlm, Clas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Lundberg, Sonia
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Settergren, Bo
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Booster vaccination with recombinant hepatitis B vaccine four years after priming with one single dose1999Ingår i: Vaccine, ISSN 0264-410X, E-ISSN 1873-2518, Vol. 17, nr 17, s. 2162-2165Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We here studied the antibody response to a booster dose four years after the administration of one single dose of recombinant HB vaccine. Before receiving the booster dose, levels of protective antibodies (anti-HBs) were generally low and 24/41 (59%) individuals lacked detectable antibodies (< 1 IU/L). Within 14 d of booster vaccination, 36/38 (95%) vaccinees showed levels of antibodies > 100 IU/L. Notably, these levels were at least as high as those of a reference group 12 months after initiation of vaccination according to the standard three-dose vaccination at intervals of 0, 1 and 6 months. In conclusion, one single dose of HB vaccine seemed to confer on young healthy individuals a well preserved B cell memory, disclosed as a rapid and strong antibody response to a second dose four years later.

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