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West Nile Virus Meningoencephalitis Imported into Germany - - Emerging Infectious Disease journal - CDC

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West Nile Virus Meningoencephalitis Imported into Germany - - Emerging Infectious Disease journal - CDC


Letter

West Nile Virus Meningoencephalitis Imported into Germany

Suggested citation for this article
To the Editor: West Nile virus (WNV) is a single-stranded RNA virus in the family Flaviviridae that is transmitted to humans by mosquitoes. Approximately 80% of WNV infections in humans are asymptomatic, whereas ≈20% of infected persons experience fever, often accompanied by a rash. Less than 1% of infections are manifested as neuroinvasive disease, such as meningoencephalitis, polyradiculoneuritis, and polio-like flaccid paralysis (1). WNV is endemic in Africa, southern Asia, and northern Australia, and only sporadic cases or small epidemics are seen in Europe (2). In 1999, WNV emerged in North America. By 2010, ≈1.8 million persons had become infected, with 12,852 reported cases of meningoencephalitis and 1,308 deaths (2). In Europe, the last notable outbreak of WNV infection occurred in Greece in 2010; 197 persons were infected, and 33 died (3). The Czech Republic, Denmark, France, and the Netherlands reported laboratory-confirmed WNV infections in travelers returning from North America (1).
We report a case of WNV meningoencephalitis in a 28-year-old German woman, who sought treatment the emergency department of a hospital in Potsdam, Germany, on September 7, 2011. She had a 3-day history of fever of up to 40°C and mental confusion. Six days before admission, she had returned from a 2-week holiday trip to Ottawa, Ontario, Canada. She had spent most of her time in the city of Ottawa.
The patient’s medical history was unremarkable. She was in a reduced general condition because of a severe encephalitic syndrome characterized by somnolence, meningism, fever, and mental confusion. Laboratory investigations revealed leukocytosis with 15.000 leukocytes/µL (reference range 4,400–11,300 leukocytes/µL) and elevated C-reactive protein of 14.8 mg/L (reference <3 0="0" 150="150" 1="1" 20="20" 27.6="27.6" 27="27" 430="430" 637="637" a="a" admission="admission" albumin="albumin" an="an" analysis="analysis" and="and" barrier="barrier" blood="blood" brain="brain" but="but" cells="cells" cerebrospinal="cerebrospinal" csf="csf" day="day" demonstrated="demonstrated" diagrams="diagrams" disturbance="disturbance" elevated="elevated" fluid="fluid" for="for" found.="found." granulocytes="granulocytes" iga="iga" igg="igg" igm="igm" imaging="imaging" intrathecal="intrathecal" lesions="lesions" level="level" levels="levels" lymphocytes.="lymphocytes." magnetic="magnetic" mg="mg" moderate="moderate" moderately="moderately" monocytes="monocytes" no="no" normal="normal" of="of" on="on" or="or" parenchymal="parenchymal" pleocytosis="pleocytosis" protein="protein" quotient="quotient" range="range" reference="reference" resonance="resonance" results="results" serum="serum" showed="showed" substantial="substantial" synthesis.="synthesis." synthesis="synthesis" the="the" total="total" unremarkable.="unremarkable." were="were">Antimicrobial drug therapy was initiated with ceftriaxone and ampicillin. Acyclovir was administered empirically for herpes simplex encephalitis until this diagnosis was excluded. Molecular and serologic testing of serum and CSF samples revealed no acute infection with herpesviruses, enteroviruses, alphaviruses, orthobunyaviruses, and arenaviruses or with mycobacteria, Borrelia spp., Toxoplasma gondii, Chlamydia spp., Leptospira spp., and Mycoplasma pneumoniae. CSF and blood cultures were negative for fungi and bacteria, including mycobacteria. An encephalitic syndrome caused by N-methyl-D-aspartate antibodies was also excluded. On the basis of the patient’s travel history, the clinical symptoms, and the initial laboratory findings, WNV infection was suspected. Indirect immunofluorescence assays and virus neutralization tests (VNT) for WNV and other flaviviruses were performed as described (4). IgM and IgG against WNV were detected in serum and in CSF by indirect immunofluorescence assay with an 8-fold (IgM) and 32-fold (IgG) increase in serum titer from day 4 to day 26 (Table). WNV IgG and WNV IgM titers were higher than the titers of antibodies against the other flaviviruses tested (Table), indicating that the antibodies resulted from a WNV infection. The serologic diagnosis was further substantiated by detection of WNV neutralizing antibodies at day 11 (VNT titer 640). The VNT titer further increased to 2,560 on day 26 after onset of disease. Results of reverse transcription PCR were negative for WNV and members of genus Flavivirus in serum and CSF samples taken 4 days after disease onset. Attempts to isolate WNV from serum and CSF samples in cell culture failed as well. The patient recovered slowly and was discharged from the hospital in Potsdam on September 15, 2011. She was then referred to a neurologic rehabilitation center in Berlin and was discharged from there after 2 months with a characterization of restitutio ad integrum (i.e., full recovery, restoration to original condition).
We report a case of WNV infection imported into Germany that was unambiguously confirmed by laboratory testing. WNV meningoencephalitis was diagnosed on the basis of strict serologic criteria established by the Centers for Disease Control and Prevention (Atlanta, GA, USA) (5). In 2011, 69 clinical cases of WNV infection were reported from the province of Ontario, although no cases in the city of Ottawa were reported (Public Health Agency of Canada; www.eidgis.com/wnvmonitorcaExternal Web Site Icon). This imported case adds to these cases and suggests that travelers are at risk, even if they visit only Ottawa. Physicians in Germany should be aware of the risk for WNV infection among travelers returning from Canada, especially during late summer.
Jörg Schultze-Amberger1, Petra Emmerich1, Stephan Günther, and Jonas Schmidt-ChanasitComments to Author 
Author affiliations: Klinikum Ernst von Bergmann, Potsdam, Germany (J. Schultze-Amberger); and Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany (P. Emmerich, S. Günther, J. Schmidt-Chanasit)

References

  1. Artsob H, Gubler DJ, Enria DA, Morales MA, Pupo M, Bunning ML, West Nile Virus in the New World: trends in the spread and proliferation of West Nile virus in the Western Hemisphere. Zoonoses Public Health. 2009;56:35769. DOIExternal Web Site IconPubMedExternal Web Site Icon
  2. Kilpatrick AM. Globalization, land use, and the invasion of West Nile virus. Science. 2011;334:3237. DOIExternal Web Site IconPubMedExternal Web Site Icon
  3. Danis K, Papa A, Theocharopoulos G, Dougas G, Athanasiou M, Detsis M, Outbreak of West Nile virus infection in Greece, 2010. Emerg Infect Dis. 2011;17:186872. DOIExternal Web Site IconPubMedExternal Web Site Icon
  4. Tappe D, Schmidt-Chanasit J, Ries A, Ziegler U, Müller A, Stich A. Ross River virus infection in a traveller returning from northern Australia. Med Microbiol Immunol (Berl). 2009;198:2713. DOIExternal Web Site IconPubMedExternal Web Site Icon
  5. Centers for Disease Control and Prevention. Epidemic/epizootic West Nile virus in the United States: guidelines for surveillance, prevention, and control [cited 2012 Aug 4]. http://www.cdc.gov/ncidod/dvbid/westnile/resources/wnv-guidelines-aug-2003.pdf Adobe PDF file

Table

Suggested citation for this article: Schultze-Amberger JD, Emmerich P, Günther S, Schmidt-Chanasit J. West Nile virus meningoencephalitis imported into Germany [letter]. Emerg Infect Dis [Internet]. 2012 Oct [date cited]. http://dx.doi.org/10.3201/eid1810.120204External Web Site Icon
DOI: 10.3201/eid1810.120204
1These authors contributed equally to this article.

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