On 31 of July 2019, the Public Health Agency of Sweden was alerted about an increasing number of tularaemia cases in Gävleborg, a county in central Sweden. The number of cases increased thereafter peaking at about 150 reports of illnesses every week. As at 6 October, a total of 979 cases (734 laboratory-confirmed) have been reported, mainly from counties in central Sweden. The outbreak is now considered over (as at 14 October).

Background. We aimed to evaluate the potential association of mosquito prevalence in a boreal forest area with transmission of the bacterial disease tularemia to humans, and model the annual variation of disease using local weather data. Methods. A prediction model for mosquito abundance was built using weather and mosquito catch data. Then a negative binomial regression model based on the predicted mosquito abundance and local weather data was built to predict annual numbers of humans contracting tularemia in Dalarna County, Sweden. Results. Three hundred seventy humans were diagnosed with tularemia between 1981 and 2007, 94% of them during 7 summer outbreaks. Disease transmission was concentrated along rivers in the area. The predicted mosquito abundance was correlated (0.41, P < .05) with the annual number of human cases. The predicted mosquito peaks consistently preceded the median onset time of human tularemia (temporal correlation, 0.76; P < .05). Our final predictive model included 5 environmental variables and identified 6 of the 7 outbreaks. Conclusions. This work suggests that a high prevalence of mosquitoes in late summer is a prerequisite for outbreaks of tularemia in a tularemia-endemic boreal forest area of Sweden and that environmental variables can be used as risk indicators.

Transfusion MedicineVolume 21, Issue 3 p. 211-213 Successful management of a planned pregnancy in severe congenital thrombotic thrombocytopaenic purpura: the Upshaw–Schulman syndrome J. Richter, Corresponding Author J. Richter Department of Hematology, Skåne University Hospital, LundJohan Richter, Department of Hematology, Skåne University Hospital, 221 85 Lund, Sweden. Tel.: +46 46 2220587; fax: +46 46 2220568;e-mail: [email protected]Search for more papers by this authorK. Strandberg, K. Strandberg Department of Clinical Chemistry, University and Regional Laboratories Region Skåne, MalmöSearch for more papers by this authorA. Lindblom, A. Lindblom Section of Hematology, Department of Medicine, Malmö University Hospital, MalmöSearch for more papers by this authorH. Strevens, H. Strevens Department of Obstetrics and Gynecology, Skåne University Hospital, LundSearch for more papers by this authorD. Karpman, D. Karpman Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, SwedenSearch for more papers by this authorD. Wide-Swensson, D. Wide-Swensson Department of Obstetrics and Gynecology, Skåne University Hospital, LundSearch for more papers by this author J. Richter, Corresponding Author J. Richter Department of Hematology, Skåne University Hospital, LundJohan Richter, Department of Hematology, Skåne University Hospital, 221 85 Lund, Sweden. Tel.: +46 46 2220587; fax: +46 46 2220568;e-mail: [email protected]Search for more papers by this authorK. Strandberg, K. Strandberg Department of Clinical Chemistry, University and Regional Laboratories Region Skåne, MalmöSearch for more papers by this authorA. Lindblom, A. Lindblom Section of Hematology, Department of Medicine, Malmö University Hospital, MalmöSearch for more papers by this authorH. Strevens, H. Strevens Department of Obstetrics and Gynecology, Skåne University Hospital, LundSearch for more papers by this authorD. Karpman, D. Karpman Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, SwedenSearch for more papers by this authorD. Wide-Swensson, D. Wide-Swensson Department of Obstetrics and Gynecology, Skåne University Hospital, LundSearch for more papers by this author First published: 11 January 2011 https://doi.org/10.1111/j.1365-3148.2010.01067.xCitations: 6Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume21, Issue3June 2011Pages 211-213 RelatedInformation

Thrombotic microangiopathy can be caused by several conditions which are difficult to diagnose from the clinical presentation alone. Deficient enzyme activity of a newly-discovered enzyme, ADAMTS-13, can lead to thrombotic thrombocytopenic purpura (TTP). Lack of ADAMTS-13 activity causes increased concentrations of high molecular weight von Willebrand factor forms and increased platelet aggregation. Measurement of ADAMTS-13 activity is useful for the diagnosis of TTP and may also be relevant as a prognostic test for recurrent TTP.

BACKGROUND:Many strategies are currently being pursued in order to generate mature dendritic cells (DC) to be used for immunotherapy. A potent anti-tumour influence by extracorporeal photopheresis has been documented for cutaneous T-cell lymphoma, and a major mechanism of action has been suggested to be generation of DC presenting tumour antigens. PURPOSE:To determine the potential of a simple clinical photopheresis protocol for large-scale development of mature DC. METHODS:A standard monocyte-enriched leukapheresis preparation of 10(9)-10(10) cells was derived during each of five consecutive treatment sessions of a patient with cutaneous T-cell lymphoma. The cells were incubated overnight in autologous plasma with no addition of growth medium. Cell surface lymphocyte, monocyte and DC markers were determined using multi-colour flow cytometry. RESULTS:We find signs of activation of the CD14+ monocytes, as well as the appearance of a minor population of mature DC negative for CD14 but with strong CD83 expression. CONCLUSIONS:With a procedure appropriate for routine clinical use, a total number of 10(6)-10(7) DC ready for patient reinfusion can be prepared within 24 h. Our findings indicate the need to further explore the capacity of photopheresis to stimulate cancer patients' anti-tumour defence reaction.

This double-blind, multicentre study was performed at nine centres on a total of 171 patients who presented with fever (> 38.5 degrees C) and signs of acute pyelonephritis. All were initially treated with intravenous cefuroxime. After 2-3 d, when the fever had subsided and urinary culture had revealed growth of Gram-negative bacteria ( > 10(7) colony-forming units per litre), treatment was changed to oral administration of ceftibuten 200 mg b.i.d. or norfloxacin 400 mg b.i.d. for 10 d. The patients were followed for signs of bacterial or clinical relapse 7-14 d after the end of treatment. The initial clinical and bacteriological cure was excellent in both groups, but there were significantly fewer bacterial relapses after oral treatment with norfloxacin than with ceftibuten in acute febrile pyelonephritis initially treated with intravenous cefuroxime. The causal strain was eradicated in 75% of patients (73% of males, 76% of females) in the ceftibuten group and in 89% of patients (94% of males, 85% of females) in the norfloxacin group. The relative frequency of eradication was 0.84 (p < 0.05; 95%, confidence interval 0.74-0.97). Adverse events were reported by 47% of the patients in the ceftibuten group and by 38% in the norfloxacin group. This difference was not significant, but diarrhoea or loose stools occurred more frequently in the ceftibuten group.