Working Group II: Impacts, Adaptation and Vulnerability

Other reports in this collection Lyme Disease

Lyme disease is caused by infection with the spirochete Borrelia burgdorferi. It is transmitted by ticks of the Ixodes ricinus complex (Dennis, 1998). Lyme disease has a global distribution in temperate countries of North America, Europe, and Asia. The transmission cycle of Lyme disease involves a range of mammalian and avian species, as well as tick species—all of which are affected by local ecology. Under climate change, a shift toward milder winter temperatures may enable expansion of the range of Lyme disease into higher latitudes and altitudes, but only if all of the vertebrate host species required by the tick vector also are able to expand their distribution. A combination of milder winters and extended spring and autumn seasons would be expected to prolong seasons for tick activity and enhance endemicity, but this would not be expected to change disease activity because humans usually are infected by the nymphal stage, which feeds at a specific time during the second year of the cycle. Tick-Borne Encephalitis

Tick-borne encephalitis (TBE) is caused by two closely related but biologically distinct viruses (Gubler and Roehrig, 1998). The eastern subtype is transmitted by Ixodes persulcatus and causes Russian spring-summer encephalitis. It occurs from China to eastern Europe and is highly focal in its distribution. The western subtype is transmitted by Ixodes ricinus and causes central European encephalitis, a milder form of the disease. It occurs within discrete foci from Scandinavia in the north to Croatia in the south, with only occasional cases further south. A related virus, Powassan, occurs in Canada and the United States and is transmitted by Ixodes scapularis. Humans usually become infected when they are exposed to ticks in habitats where the viruses are maintained. The viruses also may be transmitted directly through ingestion of raw goat milk.

It is possible that warming would extend the transmission season for TBE in Europe. The aforementioned study showed a northward extension of the tick population in Sweden in association with warmer winters, accompanied by an increase in the annual number of cases of tick-borne encephalitis reported within Sweden. Most transmission to humans is by the nymphal ticks, each of which feeds for a few days during spring-summer before dropping to the ground and molting to adult ticks, which feed primarily on deer and other large mammals. All tick stages have well-defined seasons of feeding activity, which vary geographically and may be prolonged in regions with mild winters.

Unlike Lyme disease, sustainable transmission of TBE requires a high level of coincident feeding of larval and nymphal ticks. This seasonal synchrony depends on a particular seasonal profile of land surface temperature—specifically, a rapid rate of cooling in the autumn (Randolph et al., 2000). Synchrony may be disrupted by climate change as patterns of overwinter development by ticks are changed. A statistical model, based on the current distribution of TBE, indicates significant net contraction in the geographic distribution of TBE under mid-range climate scenarios by the 2050s (Randolph and Rogers, 2000). The model indicates that although disease foci spread to higher latitudes and altitudes, current foci in central Europe largely disappear as a result of disruption of the tick seasonal dynamic by climate change. Thus, one model suggests that it is unlikely that warming would increase the incidence or net geographic distribution of TBE in Europe.

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