PUUTIAISAIVOKUUME

[Bb]

Lähettäjä: Soijuv Lähetetty: 1.12.2004 10:47

Puutiaisaivokuume leviää hiljalleen nyt myös Norjaan jossa sitä ei aiemmin ole esiintynyt:


First Human Cases of Tickborne Encephalitis, Norway

Tone Skarpaas,*Comments Unn Ljøstad,* and Anders Sundøy*
*Sørlandet Hospital Kristiansand, Kristiansand, Norway

The first reported case of tickborne encephalitis (TBE) in Norway occurred in 1997. From 1997 to 2003, from zero to two cases of human TBE have been diagnosed per year in Norway, for a total of eight cases. Clinical TBE cases in dogs are not reported in Norway.

In Scandinavia, tickborne encephalitis (TBE) is endemic in the coastal areas along the Baltic Sea. The first reports of TBE from Sweden and Finland date back to1954 and 1956, but the disease was not been found in Norway until 1997. Since then, eight cases of human TBE have been reported, and five cases have been published in a Norwegian journal (1,2).

In a study of serum samples from dogs in Aust-Agder County, immunoglobulin (Ig) G antibodies to TBE virus (TBEV) were detected in 16.4% of the samples (3). Clinical TBE cases in dogs are not reported in Norway, but the disease is probably underdiagnosed because antibody testing is not usually done. We present three new cases of human TBE and summarize the clinical characteristics and laboratory findings from all eight patients.
The Study

Patient 6 is a 62-year-old man from the town of Mandal who was bitten by a tick; onset of symptoms began 2 weeks later. At the end of May, the patient was dizzy and weak, had a headache, chills, and fever. He was hospitalized on June 11, 2002.

The antibody from serum sample profiles showed previous infection with herpes simplex and varicella zoster viruses. Borrelia antibodies could not be detected in serum samples taken at 5-week intervals. IgM antibodies against Mycoplasma pneumoniae were not detected, and virus cultures were negative. Nucleic acids from herpes simplex virus, varicella-zoster virus, or enterovirus were not detected in cerebrospinal fluid (CSF).

TBEV IgM and IgG antibodies were detected in serum samples, with high levels of IgM (optical density [OD] 1.580 on June 13 to OD 0.899 on July 18 ) and high IgG levels (13.06, OD 1.235 on June 13 to OD 1.742 on July 18 ). Cut-off values were 0.250 for IgM and 0.263 for IgG on June 13 and 0.271 for IgM and 0.278 for IgG on June 18. Neutralization test antibodies in serum samples rose from <5 in samples taken on June 13 to 10 in samples from July 18. Symptoms gradually disappeared, and the patient completely recovered in 2 months.

Patient 7 is a 53-year-old man who was visiting a cabin in the coastal area near Mandal. Symptoms began at the end of June, with fever, increasing headache, nausea, and vomiting. He was hospitalized on July 20, 2002. His liver enzymes were slightly raised. Computed tomographic scan was normal. Borrelia burgdorferi antibodies were detected in serum, without intrathecal production of Borrelia antibodies. Nucleic acids from herpes simplex virus, varicella-zoster virus, or enterovirus were not detected in CSF.

The first reported case of tickborne encephalitis (TBE) in Norway occurred in 1997. From 1997 to 2003, from zero to two cases of human TBE have been diagnosed per year in Norway, for a total of eight cases. Clinical TBE cases in dogs are not reported in Norway.

In Scandinavia, tickborne encephalitis (TBE) is endemic in the coastal areas along the Baltic Sea. The first reports of TBE from Sweden and Finland date back to1954 and 1956, but the disease was not been found in Norway until 1997. Since then, eight cases of human TBE have been reported, and five cases have been published in a Norwegian journal (1,2).

In a study of serum samples from dogs in Aust-Agder County, immunoglobulin (Ig) G antibodies to TBE virus (TBEV) were detected in 16.4% of the samples (3). Clinical TBE cases in dogs are not reported in Norway, but the disease is probably underdiagnosed because antibody testing is not usually done. We present three new cases of human TBE and summarize the clinical characteristics and laboratory findings from all eight patients.
The Study

Patient 6 is a 62-year-old man from the town of Mandal who was bitten by a tick; onset of symptoms began 2 weeks later. At the end of May, the patient was dizzy and weak, had a headache, chills, and fever. He was hospitalized on June 11, 2002.

The antibody from serum sample profiles showed previous infection with herpes simplex and varicella zoster viruses. Borrelia antibodies could not be detected in serum samples taken at 5-week intervals. IgM antibodies against Mycoplasma pneumoniae were not detected, and virus cultures were negative. Nucleic acids from herpes simplex virus, varicella-zoster virus, or enterovirus were not detected in cerebrospinal fluid (CSF).

TBEV IgM and IgG antibodies were detected in serum samples, with high levels of IgM (optical density [OD] 1.580 on June 13 to OD 0.899 on July 18 ) and high IgG levels (13.06, OD 1.235 on June 13 to OD 1.742 on July 18 ). Cut-off values were 0.250 for IgM and 0.263 for IgG on June 13 and 0.271 for IgM and 0.278 for IgG on June 18. Neutralization test antibodies in serum samples rose from <5 in samples taken on June 13 to 10 in samples from July 18. Symptoms gradually disappeared, and the patient completely recovered in 2 months.

Patient 7 is a 53-year-old man who was visiting a cabin in the coastal area near Mandal. Symptoms began at the end of June, with fever, increasing headache, nausea, and vomiting. He was hospitalized on July 20, 2002. His liver enzymes were slightly raised. Computed tomographic scan was normal. Borrelia burgdorferi antibodies were detected in serum, without intrathecal production of Borrelia antibodies. Nucleic acids from herpes simplex virus, varicella-zoster virus, or enterovirus were not detected in CSF.

For Full Article see http://www.cdc.gov/ncidod/EID/vol10no12/04-0598.htm