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Journal of Clinical Microbiology, February 1999, p. 400-403, Vol. 37, No. 2
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Rickettsia helvetica in Ixodes ricinus Ticks in Sweden

Kenneth Nilsson,1,2,* Olle Lindquist,3 Ai Jie Liu,1 Thomas G. T. Jaenson,4 Göran Friman,1 and Carl Påhlson1,5

Section of Infectious Diseases, Department of Medical Sciences, Uppsala University Hospital, S-751 85 Uppsala,1 Unit of Forensic Medicine, Department of Surgical Sciences, Uppsala University, S-752 37 Uppsala,3 Department of Infectious Diseases, Falu Hospital, S-791 82 Falun,2 Department of Entomology, Swedish University of Agricultural Sciences, and Department of Zoology, Uppsala University, S-752 36 Uppsala,4 and Department of Biology and Chemical Engineering, Mälardalens University, S-631 05 Eskilstuna,5 Sweden

Received 20 July 1998/Returned for modification 3 September 1998/Accepted 10 November 1998

In the present study further characterization of the amplified sequence of the citrate synthase gene of the spotted fever group Rickettsia isolated from Ixodes ricinus ticks in Sweden showed that it has 100% homology with the deposited sequence of the citrate synthase gene of Rickettsia helvetica. The restriction fragment length polymorphism (RFLP) pattern of an amplified 382-bp product of the citrate synthase sequence, defined by primers RpCS877 and RpCS1258, yielded fragments for our isolate that could be visualized as a double band that migrated at approximately 44 bp, another double band at 85 bp, and a single band at nearly 120 bp after digestion with the restriction enzyme AluI. When calculating a theoretical PCR-RFLP pattern of the sequence of the citrate synthase gene of R. helvetica from the known positions where the AluI enzyme cuts, we arrived at the same pattern that was obtained for our isolate, a pattern distinctly different from the previously published PCR-RFLP pattern for R. helvetica. Investigation of 125 living I. ricinus ticks showed a higher prevalence of rickettsial DNA in these ticks than we had found in an earlier study. Rickettsial DNA was detected by amplification of the 16S rRNA gene, for which a seminested primer system consisting of two oligonucleotide primer pairs was used. Of the 125 ticks, some were pooled, giving a total of 82 tick samples, of which 20 were found to be positive for the rickettsial DNA gene investigated. When considering the fact that some of the positive samples were pooled, the minimum possible prevalence in these ticks was 20 of 125 (16%) and the maximum possible prevalence was 46 of 125 (36.8%). These prevalence estimates conform to those of other studies of spotted fever group rickettsiae in hard ticks in Europe.

* Corresponding author. Mailing address: Department of Infectious Diseases, Falu Hospital, S-791 82 Falun, Sweden. Phone: 46 (0)23 49 2861. Fax: 46 (0)23 49 2886. E-mail: knf{at}swipnet.se.

Journal of Clinical Microbiology, February 1999, p. 400-403, Vol. 37, No. 2
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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