The genus Hantavirus of the family Bunyaviridae comprises to the retroperitoneal space, and the kidneys are usually not affected [7]. at least 15 viruses, including those that cause hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary Slovenia is situated in the northern part of the Balkan Peninsula. Evidence of the circulation of PUU and DOB viruses syndrome. Each hantavirus is carried primarily by a specific throughout the Balkans has been collected recently [5, 8]. The rodent or insectivore host and is transmitted by inhalation of presence of HFRS in Slovenia was first reported in 1954 [9]. virus-contaminated aerosols of rodent excreta [1, 2]. Because Since then, 110 cases occurring sporadically or in small epiof the virus-rodent association, each hantavirus has a characterdemics have been documented [authors' unpublished data]. istic geographic distribution. HFRS, which is caused by HanBoth severe and mild clinical courses of the disease are seen, taan (HTN), Seoul (SEO), Dobrava (DOB), and Puumala with an overall mortality rate of 4.5% [10]. The presence of (PUU) viruses, occurs endemically on the Eurasian continent, two different hantaviruses responsible for human infections in whereas hantavirus pulmonary syndrome caused by Sin NomSlovenia has already been reported [11]. Broad epidemiological bre and related viruses occurs in the Americas [3 -5]. Both studies have shown that 10% to 35% of the rodents captured syndromes involve a sudden onset of high fever, headache, and in areas in Slovenia where HFRS is endemic have antibodies myalgia. HFRS may appear as a mild, moderate, or severe to hantavirus [12]. disease with renal impairment as the predominant organ maniIn 1988, DOB virus was isolated from the lungs of a yellowfestation. The mortality rate varies from õ0.5% for HFRS necked field mouse (Apodemus flavicollis) captured in the vilcaused by PUU virus to Ç5% to 10% for HFRS caused by HTN lage of Dobrava (Dolenjska region, Slovenia) where a number virus [6]. Hantavirus pulmonary syndrome is characterized by of cases of severe HFRS had occurred. Complete genetic and acute noncardiac pulmonary edema and is associated with a antigenic characterization identified DOB virus as a unique mortality rate of Ç50%; capillary leakage in hantavirus pulmohantavirus [13]. Recent reports have shown that DOB virus is nary syndrome is localized exclusively to the lungs, rather than the etiologic agent of the severe form of HFRS that occurs in the Balkans [5, 8,14]. In this report, we describe the clinical presentation of patients with HFRS who were hospitalized from 1985 to 1995 at the

Genetic analysis was performed of wild-type (wt) Dobrava hantavirus (DOB) strains from Slovenia, the country where the virus was first discovered and where it was found to cause haemorrhagic fever with renal syndrome (HFRS), with a fatality rate of 12 %. Two hundred and sixty mice of the genus Apodemus, trapped in five natural foci of DOB-associated HFRS during 1990-1996, were screened for the presence of anti-hantavirus antibodies and 49 Apodemus flavicollis and four Apodemus agrarius were found to be positive. RT-PCR was used to recover partial sequences of the wt-DOB medium (M) and small (S) genome segments from nine A. flavicollis and one A. agrarius. Sequence comparison and phylogenetic analysis of the Slovenian wt-DOB strains revealed close relatedness of all A. flavicollis-derived virus sequences (nucleotide diversity up to 6 % for the M segment and 5 % for the S segment) and the geographical clustering of genetic variants. In contrast, the strain harboured by A. agrarius showed a high level of genetic diversity from other Slovenian DOB strains (14 %) and clustered together on phylogenetic trees with other DOB strains harboured by A. agrarius from Russia, Estonia and Slovakia. These findings suggest that the DOB variants carried by the two species of Apodemus in Europe represent two distinct genetic lineages.

In Europe, the zoonotic cycle of Babesia microti has not been determined so far. Recently, B. microti was detected in Ixodes ricinus ticks in Slovenia by using molecular methods. In order to investigate the mammalian hosts of B. microti in Slovenia we collected 261 small mammals representing 11 species. They were tested for the presence of babesial parasites with a PCR assay based on the nuclear small subunit rRNA gene (nss-rDNA). The bank vole (Clethrionomys glareolus) and yellow-necked mouse (Apodemus flavicollis) were infected with B. microti. The prevalence rate was 15.9% for C. glareolus and 11.8% for A. flavicollis. Nucleotide sequences of amplified portions of B. microti nss-rDNA from C. glareolus and A. flavicollis were indistinguishable from each other and identical with those previously described in I. ricinus ticks collected in Slovenia. The results of this study represent molecular evidence of B. microti in small mammals in Europe.

An evaluation of the clinical outcome and the duration of the antibody response of patients with human granulocytic ehrlichiosis (HGE) was undertaken in Slovenia. Adult patients with a febrile illness occurring within 6 weeks of a tick bite were classified as having probable or confirmed HGE based on the outcome of serological or PCR testing. Thirty patients (median age, 44 years) were enrolled, and clinical evaluations and serum collection were undertaken at initial presentation and at 14 days, 6 to 8 weeks, and 3 to 4, 6, 12, 18, and 24 months. An indirect immunofluorescence assay (IFA) was performed, and reciprocal titers of >128 were interpreted as positive. Patients presented a median of 4 days after the onset of fever and were febrile for a median of 7.5 days; four (13.3%) received doxycycline. Seroconversion was observed in 3 of 30 (10.0%) patients, and 25 (83.3%) showed >4-fold change in antibody titer. PCR results were positive in 2 of 3 (66.7%) seronegative patients but in none of 27 seropositive patients at the first presentation. IFA antibody titers of >128 were found in 14 of 29 (48.3%), 17 of 30 (56.7%), 13 of 30 (43.4%), and 12 of 30 (40.0%) patients 6, 12, 18, and 24 months after presentation, respectively. Patients reporting additional tick bites during the study had significantly higher antibody titers at most time points during follow-up. No long-term clinical consequences were found during follow-up.Human granulocytic ehrlichiosis (HGE) is an emerging tickborne disease described for the first time in 1994 in the United States (4). The first European case of acute HGE was uncovered in Slovenia in 1996 and reported in 1997 (20). Through September 2000, nine patients with acute HGE confirmed by positive PCR results and/or at least fourfold change in antibody titers contracted their illness in Central Europe, in Slovenia (15,16,24; S. Lotric-Furlan, M. Petrovec, T. AvsicZupanc, T. Lejko-Zupanc, and F. Strle, Abstr. II Croatian Congr. Infect. Dis. Int. Participation, abstr. 71, p. 30, 2000).The epidemiology and ecology of HGE have not been completely elucidated. The etiological agent of HGE is closely related to the veterinary pathogen Ehrlichia phagocytophila, which has been a recognized cause of disease among ruminants in Europe for decades (25). In Europe, E. phagocytophila is transmitted by Ixodes ricinus ticks (21).The clinical presentation of HGE is generally nonspecific and usually consists of fever, headache, malaise, myalgias, and/or arthralgias. A history of tick bite or tick exposure, while suggestive, is not diagnostic. Similarly, clinical laboratory findings of leukopenia, thrombocytopenia, and elevated liver enzymes are typical but relatively nonspecific, making the diagnosis problematic.Infection with E. phagocytophila in the acute stage has been confirmed by identification of morulae in granulocytes, positive PCR results using whole blood as a substrate, and/or isolation of E. phagocytophila from the blood. Serological tests, particularly indirect immunofluorescence assay (IFA), ar...

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