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Tularaemia is a zoonotic bacterial disease of the Northern hemisphere. The causative agent,Francisella tularensis, is spread to humans by direct contact with infected rodents or lagomorphs, aerogenic exposure, ingestion of contaminated food or water, or by arthropod bites. The prevalence of tularaemia shows a wide geographic variation. In some endemic regions, outbreaks occur frequently, whereas nearby rural parts of a country may be completely free.F. tularensisis a facultative intracellular pathogen and its primary mammalian target cell is the mononuclear phagocyte. When tularaemia is acquiredviathe skin, a primary ulcer is often detected and in general, regional lymph nodes become prominently enlarged. When contracted by inhalation, the disease may present with pneumonia. Nearly as frequent, however, is the development of fever and general illness with no respiratory symptoms and no pulmonary radiological changes. When present, the changes vary widely and may sometimes include hilar enlargement indistinguishable from that of lymphoma.Within an outbreak, the first case of tularaemia is not always readily diagnosed. A decade may have lapsed since the disease was encountered and its existence may be more or less forgotten. The difficulty refers especially to the respiratory form, in which symptoms are less specific. In cases of atypical pneumonia or acute febrile disease with no local symptoms, a history of exposure to hares or rodents or merely living in an endemic region should be sufficient to include tularaemia among differential diagnoses.The microbiological diagnosis of tularaemia relies mainly on serology, and the treatment on broad-spectrum antibiotics. For decades, a live vaccine has been successfully used in risk groups but is presently not available due to difficulties in standardisation.

Francisella tularensis is a potent pathogen and a cause of severe human disease. The outcome of tularemia will depend on rapid insertion of appropriate antibiotics. Until recently, effective clinical handling was hampered by shortcomings in laboratory diagnostics. No suitable direct methods were available and, because of risks and isolate recovery difficulties associated with laboratory work, culture has been rarely practiced. Due to achievements from work on modern technology, however, tularemia can now be rapidly and specifically diagnosed. Conventional PCR has been successfully applied on wound specimens of patients acquiring tularemia, and prospects for application on other human specimens are promising. Besides allowing diagnostics at high sensitivity and specificity, the PCR technology will also facilitate the identification of cases of tularemia presenting with aberrant signs and symptoms. Antibiotics for efficacious treatment of tularemia have been available for several decades. Although highly valuable, these drugs are afflicted with adverse effects and/or are available only for parenteral therapy. Recently, quinolones have been shown to afford a new valuable option for treatment of tularemia caused by F. tularensis subsp. holarctica (type B). Experience in treating more severe disease caused by F. tularensis subsp. tularensis (type A) is currently limited. In essence, the clinical handling of tularemia is currently facilitated by new achievements in molecular diagnostics and, at least with regard to type B tularemia, by the introduction of quinolones for therapy.

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Plasma levels of cytokines were measured by EIA in 15 subjects hospitalized with nephropathia epidemica, a European form of hantavirus-induced hemorrhagic fever with renal syndrome. Concentrations of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 were increased in all patients at admission, and the concentration of IL-10 was increased in most. TNF-alpha concentrations were still increased 1 week after onset of disease; levels of IL-6 and IL-10 were normalized. TNF-alpha was undetectable by the WEHI cell assay in serum samples obtained throughout the acute phase of disease. Serum levels of the two soluble TNF receptors p55 and p75 correlated with levels of the cytokine, indicating that receptor binding may be the reason for lack of bioactivity in vitro. TNF-alpha is known to induce pathophysiologic and clinical changes similar to those seen in nephropathia epidemica and in diseases caused by other hantaviruses.