Bell's palsy and sudden deafness associated with Rickettsia spp. infection in Sweden. A retrospective and prospective serological survey including PCR findings
Article first published online: 21 JUN 2013
© 2013 The Author(s) European Journal of Neurology © by John Wiley & Sons Ltd on behalf of EFNS
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European Journal of Neurology
Volume 21, Issue 2, pages 206–214, February 2014
How to Cite
Nilsson, K., Wallménius, K., Hartwig, S., Norlander, T. and Påhlson, C. (2014), Bell's palsy and sudden deafness associated with Rickettsia spp. infection in Sweden. A retrospective and prospective serological survey including PCR findings. European Journal of Neurology, 21: 206–214. doi: 10.1111/ene.12218
- Issue published online: 13 JAN 2014
- Article first published online: 21 JUN 2013
- Manuscript Accepted: 16 MAY 2013
- Manuscript Received: 19 JAN 2013
- Uppsala-Örebro-Regional Research. Grant Number: 25021
- Center of Clinical Research Dalarna. Grant Number: 9028
- Olle Engqvist Byggmästare Stiftelse. Grant Number: 11877
- Bell's palsy;
- PCR ;
- spotted fever rickettsia
Background and purpose
Sixty patients with facial palsy and 67 with sudden deafness were retrospectively or prospectively examined for serological evidence of rickettsial infection; in six cases where cerebrospinal fluid was available, patients were also examined for presence of rickettsial DNA.
Rickettsial antibodies were detected in single or paired serum samples using immunofluorescence with Rickettsia helvetica as the antigen and in four cases also using western blot. Using PCR and subsequent direct cycle sequencing, the nucleotide sequences of the amplicons (17 kDa protein gene) in cerebrospinal fluid were analysed.
Five out of 60 (8.3%) patients with facial palsy and eight of 67 (11.9%) with hearing loss showed confirmative serological evidence of infection with Rickettsia spp. An additional three and four patients in the facial palsy and hearing loss groups, respectively, showed evidence of having a recent or current infection or serological findings suggestive of infection. In four cases, the specificity of the reaction was confirmed by western blot. An additional 70 patients were seroreactive with IgG or IgM antibodies higher than or equal to the cut-off of 1:64, whereas 37 patients were seronegative. Only two of 127 patients had detectable antibodies to Borrelia spp. In three of six patients, rickettsial DNA was detected in the cerebrospinal fluid, where the obtained sequences (17 kDa) shared 100% similarity with the corresponding gene sequence of Rickettsia felis.
These results highlight the importance of considering Rickettsia spp. as a cause of neuritis, and perhaps as a primary cause of neuritis unrelated to neuroborreliosis.