SUOMI: TULEHDUKSELLISIA AIVOMUUTOKSIA

Voiko Borrelioosiin/lisäinfektioihin kuolla?

Valvojat:Jatta1001, Borrelioosiyhdistys, Waltari, Bb

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Liittynyt:Ke Tammi 21, 2009 14:16
SUOMI: TULEHDUKSELLISIA AIVOMUUTOKSIA

Viesti Kirjoittaja soijuv » Su Syys 06, 2009 23:01

Oksin ym tutkimus (1996): "Borreliabakteerin aiheuttamia tulehduksellisia aivomuutoksia." Kolmelta potilaalta otettiin aivoista koepala ja niissä jokaisella todettiin mm. verisuonitulehdus. Yhdellä potilaalla esiintyi laaja valkean aineen muutos - potilas menehtyi. Yhdellä lapsella ilmeni toispuolinen halvaus ja 40-vuotiaalla miehellä epileptisiä kohtauksia. Miehen tila parani useiden antibioottikuurien jälkeen. Tutkimuksessa todettiin borreliabakteerin voivan aiheuttaa aivotulehduksia ja verisuonitulehduksia.

Brain, Vol. 119, No. 6, 2143-2154, 1996
© 1996 Guarantors of Brain

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research-article


Inflammatory brain changes in Lyme borreliosis
A report on three patients and review of literature
J. Oksi1,5,7, H. Kalimo2, R. J. Marttila3, M. Marjamaki2, P. Sonninen4, J. Nikoskelainen1 and M. K. Viljanen6,7

1Departments of Internal MedicineTurku University Central Hospital Turku, Finland 2Departments of Pathology, Turku University Central Hospital Turku, Finland 3Departments of Neurology, Turku University Central Hospital Turku, Finland 4Departments of Radiology, Turku University Central Hospital Turku, Finland 5Department of Medical Microbiology, Turku University Turku, Finland 6National Public Health Institute, Department in Turku Turku, Finland 7Turku Immunology Centre Turku, Finland

Correspondence to: Correspondence to: J. Oksi, Turku University, Department of Medical Microbiology, Kiinamyllynkatu 13, FIN-20520 Turku, Finland

Despite a rapid increase in the number of patients with Lyme neuroborreliosis (LNB), its neuropathological aspects are poorly understood. The objective of this study was evaluation of neuropathological, microbiological, and magnetic resonance imaging (MRI) findings in three patients with the Borrelia burgdorferi infection and neurological disease from whom brain tissue specimens were available. Perivascular or vasculitic lymphocytic inflammation was detected in all specimens. Large areas of demyelination in periventricular white matter were detected histologically and by MRI in one patient. The disease had a fatal outcome in this patient. Brain MRI suggested malignancies in two patients before histopathological studies were carried out. One of these two patients was a child with sudden hemiparesis. Another was a 40-year-old man presenting with epileptic seizures and MRI-detected multifocal lesions, which disappeared after repeated courses of antibiotics. We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection. The presence of B. burgdorferi DNA in tissue samples from areas with inflammatory changes indicates that direct invasion of B. burgdorferi may be the pathogenetic mechanism for focal encephalitis in LNB.

Borrelia burgdorferi; Lyme disease; neuroborreliosis; neuropathology; vasculitis

Received April 30, 1996. Revised June 4, 1996. Accepted July 25, 1996.

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Oksi, Viljanen, Kalimo, Peltonen ja Marttila (1993) raportoivat kuolemantapauksen jossa henkilöllä oli sekä borrelioosi että puutiaisaivokuume.

Fatal encephalitis caused by concomitant infection with tick-borne encephalitis virus and Borrelia burgdorferi.
Oksi J, Viljanen MK, Kalimo H, Peltonen R, Marttila R, et al.
Clinical Infectious Diseases, 16(3):392-6. 1993.

Nevertheless, the coinfection might have contributed to the fatal outcome that has not been previously observed in Finnish patients with TBE.

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