Abstract
The highest annual incidence of human tick-borne encephalitis (TBE) in Sweden ever recorded by the Swedish Institute for Communicable Disease Control (SMI) occurred last year, 2011. The number of TBE cases recorded during 2012 up to 6th August 2012 indicates that the incidence for 2012 could exceed that of 2011. In this review of the ecology and epidemiology of TBE in Sweden our main aim is to analyse the possible reasons behind the gradually increasing incidence of human TBE during the last 20 years. The main TBE virus (TBEV) vector to humans in Sweden is the nymphal stage of the common tick Ixodes ricinus. The main mode of transmission and maintenance of TBEV in the tick population is considered to be when infective nymphs co-feed with uninfected but infectible larvae on rodents. In most locations the roe deer, Capreolus capreolus is the main host for the reproducing adult I. ricinus ticks. The high number of roe deer for more than three decades has resulted in a very large tick population. Deer numbers have, however, gradually declined from the early 1990s to the present. This decline in roe deer numbers most likely made the populations of small rodents, which are reservoir-competent for TBEV, gradually more important as hosts for the immature ticks. Consequently, the abundance of TBEV-infected ticks has increased. Two harsh winters in 2009–2011 caused a more abrupt decline in roe deer numbers. This likely forced a substantial proportion of the “host-seeking” ticks to feed on bank voles (Myodes glareolus), which at that time suddenly had become very numerous, rather than on roe deer. Thus, the bank vole population peak in 2010 most likely caused many tick larvae to feed on reservoir-competent rodents. This presumably resulted in increased transmission of TBEV among ticks and therefore increased the density of infected ticks the following year. The unusually warm, humid weather and the prolonged vegetation period in 2011 permitted nymphs and adult ticks to quest for hosts nearly all days of that year. These weather conditions stimulated many people to spend time outdoors in areas where they were at risk of being attacked by infective nymphs. This resulted in at least 284 human cases of overt TBE. The tick season of 2012 also started early with an exceptionally warm March. The abundance of TBEV-infective “hungry” ticks was presumably still relatively high. Precipitation during June and July was rich and will lead to a “good mushroom season”. These factors together are likely to result in a TBE incidence of 2012 similar to or higher than that of 2011.
Highlights
In 2011, 284 people in Sweden developed tick-borne encephalitis (TBE)
We analyse how climate change with increasing environmental temperatures and changing tick host abundances have gradually increased the abundance and enlarged the geographic range of the tick Ixodes ricinus in Sweden and how these factors have resulted in gradually increasing numbers of human TBE cases since the 1980s
At least some bird species may be competent hosts for TBE-virus transmission to ticks - either by viraemic transmission or by nonviraemic transmission or by both modes. Later in this text we argue that migrating roe deer could have played and still are playing a significant role in the spread of TBE virus (TBEV) and in the founding of new foci of TBEV as well as other tick-borne pathogens
Summary
In 2011, 284 people in Sweden developed tick-borne encephalitis (TBE). This is the highest TBE incidence for any single year ever recorded by the Swedish Institute for Communicable Disease Control, Stockholm, Sweden (SMI; Figure 1). The roe deer’s spread northwards promoted the expansion to the north of the vector and the virus To understand all fundamental factors that have promoted the tick’s increasing abundance and range expansion as well as the increasing incidence of TBE both northwards and westwards in Sweden [23], it is important to know that the adult ticks most frequently feed on relatively large mammals, e.g. deer, hares, dogs and cats, and large birds such as pheasants. At high deer abundance a great proportion of the immature tick population feed on these reservoir-incompetent mammals This reduces the TBEV transmission intensity from infective nymphs co-feeding with susceptible larvae on small mammals. A large proportion of the larval and nymphal segments of the I. ricinus population succeeded in attaching to rodents This likely increased the rate of non-viraemic TBEV transmission from infective nymphs to susceptible tick larvae and of viraemic transmission [47] from TBEVinfective rodents to immature ticks. The behaviour of this tick species is more dangerous compared to I. ricinus
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