Cases reported "Hantavirus Infections"

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1/10. The incubation period of hantavirus pulmonary syndrome.

    In 1993 sin nombre virus was recognized as the cause of hantavirus pulmonary syndrome (HPS) and the deer mouse (peromyscus maniculatus) was identified as the reservoir host. Surveillance by the Centers for disease Control and Prevention and state health departments includes investigation to determine the likely site(s) and activities that led to infection, an environmental assessment of the home and workplace, and possibly rodent trappings at these sites. As of December 31, 1998, there were 200 confirmed cases from 30 states (43% case-fatality ratio). The national HPS case registry was examined to determine the incubation period of HPS. review of 11 case-patients with well-defined and isolated exposure to rodents suggests that the incubation period of HPS is 9 to 33 days, with a median of 14-17 days. Case investigations allow a better understanding of the incubation time of HPS and may define high-risk behaviors that can be targeted for intervention.
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2/10. Tula virus infection associated with fever and exanthema after a wild rodent bite.

    Reported here is the first case of human acute infection with Tula virus, which occurred in a 12-year-old boy in switzerland. This hantavirus had been considered apathogenic to humans, and in switzerland only TULV-genome sequences have been demonstrated in wild rodents to date. In this case, paronychia, fever and exanthema occurred after the patient was bitten by a wild rodent, indicating an unusual route of hantavirus transmission. Thus, Tula virus infection should be taken into account in patients with appropriate clinical symptoms and contact with rodents.
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3/10. hantavirus pulmonary syndrome in the State of Sao Paulo, brazil, 1993-1998.

    Between 1993 and 1998, 10 cases of clinical hantavirus infection were diagnosed in brazil. Hantavirus-specific IgM, or positive immunohistochemical analysis for hantavirus antigen, or positive reverse transcription-polymerase chain reaction results for hantavirus rna were used to confirm nine of these cases; eight were hantavirus pulmonary syndrome (HPS), and one was mild hantavirus disease. The remaining clinical case of hantavirus infection was fatal, and no tissue was available to confirm the diagnosis. During the first 7 months of 1998, five fatal HPS cases caused by a Sin Nombre-like virus were reported from three different regions in the State of Sao Paulo, brazil: two in March (Presidente Prudente Region), two in May (Ribeirao Preto Region), and one in July (Itapecerica da Serra Region). Epidemiologic, ecologic, and serologic surveys were conducted among case contacts, area residents, and captured rodents in five locations within the State of Sao Paulo in June of 1998. Six (4.8%) of 125 case contacts and six (5.2%) of 116 area residents had IgG antibody to sin nombre virus (SNV) antigen. No case contacts had a history of HPS-compatible illness, and only one area resident reported a previous acute respiratory illness. A total of 403 rodents were captured during 9 nights of trapping (1969 trap nights). All 27 rodents that were found to be positive for IgG antibody to SNV antigen were captured in crop border and extensively deforested agricultural areas where four of the 1998 HPS case-patients had recently worked. The IgG antibody prevalence data for rodents suggest that Bolomys lasiurus and perhaps Akodon sp. are potential hantavirus reservoirs in this state of brazil.
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4/10. First molecular identification of human Dobrava virus infection in central europe.

    Viral rna was amplified by reverse transcription-PCR from a patient suffering from hemorrhagic fever with renal syndrome (HFRS) in germany. The virus strain could be assigned to the Dobrava hantavirus (DOBV). This is the first molecular identification of human infection by DOBV in central europe and the first proof that a virus strain related to the DOBV-Aa lineage, carried by Apodemus agrarius rodents, is able to cause HFRS.
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5/10. Fatal illness associated with a new hantavirus in louisiana.

    A fatal case of hantaviral illness occurred in louisiana, outside of the range of P. maniculatus, the rodent reservoir for sin nombre virus. Hantavirus rna and antigens were detected in patient autopsy tissues, and nucleotide sequence analysis of amplified polymerase chain reaction (PCR) products identified a newly recognized unique hantavirus, provisionally named Bayou virus. Prominent features of the clinical illness are compatible with hantavirus pulmonary syndrome (HPS), but several features such as renal insufficiency and intraalveolar hemorrhage are more compatible with hemorrhagic fever with renal syndrome (HFRS), a disease associated with Eurasian hantaviruses.
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6/10. Isolation and initial characterization of a newfound hantavirus from california.

    A fatal case of hantavirus pulmonary syndrome (HPS) in northern california prompted our attempt to isolate viruses from local rodents. From tissues of two deer mice, peromyscus maniculatus, two hantaviruses (Convict Creek virus 107 and 74, CC107 and CC74) were established in cell culture. Viral antigens, proteins, and RNAs of the first and archetypical isolate (CC107) were examined, and portions of the medium (M) and small (S) genome segments of both isolates were sequenced. Antigenically, CC107 virus and the second isolate, CC74 virus, were more closely related to puumala virus than Hantaan (HTN) virus, though distinct from both. Northern blots of viral RNAs showed the large and M segments of CC107 to be the same size as those of HTN virus, whereas the S segment was larger. Protein gels did not reveal CC107 to have a substantially larger nucleocapsid protein than HTN virus. Partial nucleotide sequence comparisons of CC107 and CC74 viruses revealed their M segments to be highly similar to one another, while their S segments differed by more than 10%. Nucleotide and deduced amino acid sequence comparisons showed the california isolates to be closely related to the newfound hantaviruses first detected in the Four Corners area and since incriminated in HPS through wide areas of the United States.
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7/10. Short report: prevalence of hantavirus infection in rodents associated with two fatal human infections in california.

    Rodents living near two fatal human cases of hantavirus pulmonary syndrome in california were surveyed for evidence of hantavirus infection. Seventeen (15%) (14 peromyscus maniculatus and one each of P. truei, Eutamias minimus, and Microtus californicus) of 114 rodents tested had evidence (enzyme-linked immunosorbent assay or polymerase chain reaction) of hantavirus infection. This suggests that peromyscus mice, and P. maniculatus in particular, may be the reservoir for the virus causing this newly recognized disease in california, as previously reported for new mexico and arizona.
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8/10. hantavirus pulmonary syndrome in wisconsin.

    In the spring of 1993 an outbreak of a new illness caused by a new pathogen was identified in the southwestern united states. This infection struck relatively young, healthy individuals, was characterized by fever, myalgias, respiratory failure, and a high mortality rate. This illness was caused by a new hantavirus and has been termed hantavirus pulmonary syndrome (HPS). The virus is carried by rodents, shed in saliva, urine, and feces. Human infection occurs through inhalation of aerosolized virus. The clinical syndrome has many non-specific signs and symptoms, but does follow a typical course with characteristic laboratory and radiographic findings. Early recognition of this infection is important so maximal supportive care can be initiated. We report the first documented case of hantavirus pulmonary syndrome in wisconsin and illinois.
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9/10. High prevalence of hantavirus antibodies in bank voles (Clethrionomys glareolus) captured in the vicinity of households afflicted with nephropathia epidemica.

    puumala virus, the causative agent of nephropathia epidemica (NE), occurs endemically in europe and is spread mainly by the bank vole (Clethrionomys glareolus). In the vicinity of each of four households afflicted with NE, we studied rodents with regard to population density and prevalence of puumala virus-specific antibodies. For each case area, a control area was randomly selected 10 km away, without regard to the presence of human settlement. During 6,000 trap nights, 328 rodents were caught, of which 299 were C. glareolus. The mean rodent densities of case and control areas were 6.6 and 3.7 animals per 100 trap nights (P < 0.001). The prevalence of serum antibodies was 15.9% in case areas compared with 5.6% in control areas (P < 0.05). In three of the case areas, where NE had occurred 3-10 weeks before trapping, the rodent density and seroprevalence were much higher than in the fourth area, where NE occurred 38 weeks before trapping. In conclusion, C. glareolus seropositive for puumala virus occurred more frequently near households afflicted with NE than in control areas 10 km away.
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10/10. Genetic diversity and epidemiology of hantaviruses in argentina.

    Phylogenetic analysis of a 292-nucleotide (nt) fragment of the hantavirus M genome segment from 36 rodent and 13 human samples from three known foci of hantavirus infection in argentina was conducted. A 1654-nt fragment of the M genome segment was analyzed for 1 representative of 7 genetically distinct hantavirus lineages identified. Additionally, the nt sequence of the complete M genome segments of Lechiguanas, Oran, and Hu39694 hantavirus genotypes was determined. nt sequence comparisons reveal that 7 hantavirus lineages from argentina differ from each other by 11.5%-21.8% and from Sin Nombre, Bayou, and Black Creek Canal viruses by 23.8%-26.5%. Phylogenetic analyses demonstrate that they form a unique, separate branch within the clade containing other New World sigmodontine-borne hantaviruses. Most Oligoryzomys-borne hantavirus genotypes clearly map together. The Oligoryzomys-borne genotypes Lechiguanas, Oran, and Andes appear to be associated with human disease. Oligoryzomys longicaudatus was identified as the likely rodent reservoir for Andes virus.
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