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.

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SUMMARYA stratified and randomly-selected population sample was identified in 1990 in order to study the seroprevalence of nephropathia epidemica (haemorrhagic fever with renal syndrome) in Northern Sweden. Sera from 1538 subjects (750 men, 788 women), 25-64 years of age, were analysed for the presence of Puumala virus (PUV) specific-IgG by the indirect immunofluorescence antibody test. Specific IgG was detected in sera from 83 subjects (54%). Men and women had similar seroprevalence rates. The highest seroprevalences were found in subjects 55 years or older (8-0 %) and among farmers and forestry workers (15-9 %). The geographic distribution of seropositive individuals was uneven and there were significantly more seropositive persons in rural than in urban areas (P < 0 05).

Nephropathia epidemica (NE) is a prevalent zoonosis throughout Europe and is caused by the Puumala type of hantavirus. The incidence of NE varies in a cyclic fashion, with peaks occurring every 3rd to 4th year, coinciding with peaks in vole populations. The clinical course of NE is generally milder than haemorrhagic fever with renal syndrome caused by hantaviruses in other parts of the world. Typically, NE has a sudden onset with fever, headache, backpain and gastrointestinal symptoms. However, severe complications, e.g. gastrointestinal haemorrhage, occur and fatal cases have been reported. Renal involvement is prominent and manifests as initial oliguria and later as marked polyuria. Tests of renal function show pronounced glomerular and tubular involvement. Vaccine against Puumala virus infection as well as specific treatment for NE are still lacking.

During 1988 and 1989 > 500 cases of serious group A streptococcal infections were reported in Sweden, many with a fatal outcome. We report here on 11 consecutive patients with septic preshock/shock and multiorgan failure, including acute renal failure. 10 had verified group A streptococci (GAS) serotype T1M1 infections while 1 patient was culture negative but with clinical signs of severe infection and serological evidence of GAS infection. Presenting symptoms were high fever, relative bradycardia, edema and renal failure. In all patients the condition deteriorated despite conventional treatment including volume substitution and antibiotics. Systolic blood pressure was transiently < 80 mmHg in 10 patients and 9 of them needed infusion of inotropic agents to avoid fatal circulatory shock. In 9 patients respiratory aid was instituted and 7 were dialysed. Plasma exchange was performed in 7, while the remaining 4 received transfusions with blood and plasma without plasma exchange. 10 patients improved and were discharged within 8 weeks. One woman died within 2 days after admission to the hospital. Renal function recovered in all survivors, with a follow-up serum creatinine < 80 mumol/l. The complicated clinical picture in these patients with many simultaneous therapeutic events confounds the interpretation of the effect of single actions. The favourable outcome in these severely ill patients suggests that potent inotropic agents, immunoglobulin therapy and plasma exchange might be beneficial in severe streptococcal disease when conventional treatment fails.