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Background: In Scandinavia, the incidence of cystic echinococcosis (CE) and alveolar echinococcosis (AE) is low and almost exclusively an imported disease following the trends of immigration. The aim of the study was to review available data on clinical management and outcome for patients treated at Oslo University Hospital, a referral centre for echinococcosis in Norway, with special emphasis on surgical treatment., Methods: All patients admitted with echinococcosis between January 2000 and December 2020 were identified. Medical records were reviewed retrospectively concerning patient demographics, treatment strategy, surgical procedures, complications and outcomes., Results: A total of 92 patients with median age 37 years (range 4-85) were identified. Sixty-eight patients (74%) were symptomatic. All patients, except for two, were immigrants to Norway and born in endemic areas. Ninety patients were diagnosed with CE and two with AE. Location of the cysts was most commonly in the liver (86%) followed by peritoneum, lungs, and spleen. All patients with active cysts were treated with albendazole. Surgical treatment was performed in 51 (56%) patients. The most common reason for abstaining from surgical treatment was that the diagnostic work-up revealed inactive cysts or interventional radiology was performed. Of the 51 patients who underwent surgery, a radical procedure was performed in 32 (64%) cases, a conservative procedure in 12 (24%), and a combination in six (12%). Clavien Dindo grade ≥3 complications occurred in 30%, and 90-day mortality was 2%. Bile leakage occurred in seven patients and was treated successfully with endoscopic retrograde cholangiopancreatography with biliary stent placement in all patients., Conclusion: In a low-endemic area like Norway, management of echinococcus includes medical therapy, surgery, and/or interventional radiology. Surgical intervention seems to be effective, and is associated with acceptable morbidity rates.

We present a Norwegian female in her thirties who acquired dengue fever caused by dengue virus serotype 2 while travelling to Mexico. When hospitalised 3 days after symptom onset, the patient had severe headache, fever, rash and a positive tourniquet test, but did not fulfil the criteria of dengue haemorrhagic fever (DHF). Five days later she developed a fatal subarachnoidal haemorrhage. A post-mortem examination failed to reveal any intracranial arterial aneurysm. Our case was consistent with so called 'dengue fever with haemorrhages', a recently described entity that mainly affects adults and may cause severe bleedings also in the absence of DHF.

We present the first 3 cases of confirmed scrub typhus imported to Scandinavia. The patients were infected in Thailand, Laos and Sri Lanka, respectively. Treatment with ciprofloxacin and doxycycline lead to rapid cure in 2 of the patients, while the third patient, who was not treated, had a prolonged convalescence. Specific antibodies against Orientia tsutsugamushi, the causative agent of scrub typhus, were detected in all 3 cases.

African tick bite fever (ATBF) caused by Rickettsia africae is an emerging health problem in travellers to sub-Saharan Africa. We here present 6 patients with evidence of long-lasting sub-acute neuropathy following ATBF contracted during safari trips to southern Africa. Three patients developed radiating pain, paresthaesia and/or motor weakness of extremities, 2 had hemi-facial pain and paresthaesia, and 1 developed unilateral sensorineural hearing loss. When evaluated 3-26 months after symptom onset, cerebrospinal fluid samples from 5 patients were negative for R. africae PCR and serology, but revealed elevated protein content in 3 and mild pleocytosis in 1 case. Despite extensive investigations, no plausible alternative causes of neuropathy could be identified. Treatment with doxycycline in 2 patients had no clinical effect. Given the current increase of international safari tourism to sub-Saharan Africa, more cases of sub-acute neuropathy following ATBF may well be encountered in Europe and elsewhere in the y to come.

We report 3 cases of fascioliasis imported to Norway: a 24-y-old male Vietnamese immigrant and a 51-y-old female Vietnamese immigrant with acute fascioliasis, and a 2-y-old male Ethiopian adoptee with chronic fascioliasis. Diagnosis was confirmed by detection of specific antibodies to Fasciola hepatica in the 2 first cases and by demonstration of Fasciola hepatica eggs in stool samples in the latter case. Treatment with oral triclabendazole led to prompt cure in all 3 patients. Imported fascioliasis is rarely reported but should be suspected in patients with a travel history to endemic areas, abdominal symptoms and hypereosinophilia of the blood.

Rickettsia africae is the causative agent of African tick bite fever (ATBF), an acute febrile illness frequently accompanied by inoculation eschars, regional lymphadenitis, myalgia and severe headache. Recently, ATBF has been recognized as an emerging health problem for international travellers to rural sub-Saharan Africa. To estimate the incidence, risk factors for and proportion of symptomatic cases of travel-associated R. africae infection, we performed a seroepidemiological study of 152 first-time Norwegian travellers to rural areas in sub-Equatorial Africa. Seropositivity was based on the detection of specific antibodies to R. africae in microimmunofluorescence and/or Western blotting assays. Thirteen (8.6%) travellers were seropositive to R. africae. Eight (62%) seropositive travellers reported symptoms consistent with ATBF; of these, 2 had received antirickettsial therapy. Using multiple logistic regression, the following factors were found to be significantly associated with seropositivity: hunting as the purpose of travel [odds ratio (OR) 10.1; 95% confidence interval (CI) 1.5-69; p=0.019] and stay in rural areas of > 7 d (OR 6.0; 95% CI 1.5-24; p=0.012). This first seroepidemiological study on travel-associated R. africae infection suggests that the infection may be common in international travellers to rural sub-Saharan Africa but that most cases are asymptomatic or clinically mild and self-limited.

We describe a case of culture-proven Brucella spondylitis in a 28-y-old Turkish male asylum seeker who had arrived to Norway 6 months earlier. Several diagnostic difficulties, including rapid in vitro growth and misidentification of the causative microorganism in biochemical gallery strip tests, resulted in late diagnosis.

We performed a retrospective study of 222 cases of falciparum malaria diagnosed in Oslo and Akerhus counties, Norway, from January 1988 to December 1997. Except for 12 cases, all had acquired the disease in sub-Saharan Africa. Sixty-four (28.8%) cases occurred in assumed non-immune individuals; of these, 41 (64.1%) were compliant to recommended antimalarial chemoprophylaxis. The mean time lag from first symptom to diagnosis (total diagnosis delay) was 4.6 d (median 3 d, range 0-30 d) and the mean time from presentation to diagnosis (doctor's delay) was 1.3 d (median 0 d, range 0-25 d). There were no fatal cases, and only 8 (3.6%) had a complicated course. The following factors were significantly associated with development of complicated disease: higher age, non-immunity combined with chemoprophylaxis non-compliance, prolonged doctor's delay and prolonged total diagnosis delay (p < or = 0.05). Our data suggest that complicated disease in imported falciparum malaria may largely be prevented by high chemoprophylaxis compliance rates in non-immune travellers and a high index of suspicion in physicians evaluating febrile travellers.

We report on 8 Norwegian travellers to Southern Africa with African tick-bite fever (ATBF), a recently described spotted fever group rickettsiosis. All patients had acute flu-like symptoms and developed I or multiple inoculation eschars. The patients were treated with either doxycycline or ciprofloxacin, and all recovered. The diagnosis of ATBF was confirmed by the detection of specific IgM antibodies to Rickettsia africae by microimmunofluoroscence in convalescent-phase serum samples.

From April to June 1996, an outbreak of hepatitis A virus (HAV) infection affecting 15 nurses, patients and household contacts occurred in the Department of Internal Medicine at Aker University Hospital, Oslo. The index case was a homeless alcoholic who was hospitalized in March 1996 with pneumonia while simultaneously incubating HAV infection. Four secondary cases were infected by the index case, while another 10 cases were caused by a continuous spread of infection within the department during the following months. Sequence of the VP1/P2A junction of HAV was obtained from 9 patients, including the index case, and all sequences were identical to each other. Mass vaccination of hospital employees with a formalin-inactivated HAV-vaccine took place in late May, and following this the outbreak stopped. Several factors probably combined to account for this unusual outbreak, e.g. an index case unsuspected of incubating with HAV infection, and a low prevalence rate of protective antibodies to HAV among the hospital staff.