Abstract

Authors' reply Sir—Sarah Randolph challenges our findings that increases in TBE incidence since the mid-1980s in Stockholm County, Sweden, are related to changes in climate during the same period. We hope that such misunderstandings and misinterpretations of the results of our report will be further avoided by the following clarifications. First, the criticism is based on weak historical European data. We used incidence data from Stockholm County, a high TBE endemic area in Sweden, which has a continuing TBE surveillance programme that includes epidemiological data since the late 1950s. All cases of encephalitis admitted in the area have been, when clinically relevant, serologically tested for TBE virus. Epidemiological information has been obtained from confirmed cases. In the rest of Europe, including other parts of Sweden, the registration of TBE cases has been non-existent or inconsistent, or affected by other non-causative factors. TBE data from the early 1940s and 1950s are difficult to compare with later data. During this time, various viral encephalitis, including poliovirus, causing neurological symptoms were flourishing in Sweden and the former Czechoslovakia. Similarities in the clinical picture could have led to over-reporting of TBE cases, since the serological methods used at the time (IgM detection was not available) could not distinguish between acute and previous TBE infections, and the latter were frequently subclinical since only one of four TBE infections develop symptoms in the central nervous system. Reanalyses of Swedish national data from 1956 and 1958 showed that only 50% of these cases could be completely confirmed. This type of serological method was used until the mid 1970s in Sweden, but the clinical and epidemiological follow-up of positive TBE cases in our study region made the degree of over-reporting from 1960 to the mid-70s low. Over-reporting of TBE cases from this early part of our study period would, however, further strengthen our results. Second, the design of our study did enable us to not only look at the direct climatic effects on the tick's life cycle dynamics, but also to cover indirectly other climate dependent factors of interest for disease transmission, such as host animal availability and human leisure activities. Third, Randolph criticises our graphs. There are different ways of designing the illustrations, but the observations made, and the conclusions, remain unchanged. Remarks based on comparisons of one explanatory variable at a time may be interesting, but since our results show that the combined effects of five explanatory variables during 2-year cycles are accompanied by the variations in TBE incidence, these remarks are not relevant to the results. Finally, our results are in concordance with previous findings showing that the northward spread of ticks in Sweden and the increased tick abundance in Stockholm County during the 1980s and 1990s are related to similar changes in seasonal climatic conditions.1Lindgren E Tälleklint L Polfeldt T Impact of climatic change on the northern latitude limit and population density of the disease-transmitting European tick.Ixodes ricinus. Environ Health Perspect. 2000; 108: 119-123Crossref PubMed Google Scholar Tick-borne encephalitis in EuropeElisabet Lindgren and Rolf Gustafson (July 7, p 16) 1 give the false impression of a simple causal relation between the increased incidence of tick-borne encephalitis (TBE) in Sweden since 1984 and climate change, specifically more warm (5–8°C) spring days and fewer cold (−10 to −7°C) winter days. Full-Text PDF

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