Abstract
The tick Ixodes ricinus is the main vector of the spirochaete Borrelia burgdorferi sensu lato, the causal agent of Lyme borreliosis, in the western Palearctic. Rodents are the reservoir host of B. afzelii, which can be transmitted to I. ricinus larvae during a blood meal. The infected engorged larvae moult into infected nymphs, which can transmit the spirochaetes to rodents and humans. Interestingly, even though only about 1 % of the larvae develop into a borreliae-infected nymph, the enzootic borreliae lifecycle can persist. The development from larva to infected nymph is a key aspect in this lifecycle, influencing the density of infected nymphs and thereby Lyme borreliosis risk. The density of infected nymphs varies temporally and geographically and is influenced by multi-trophic (tick-host-borreliae) interactions. For example, blood feeding success of ticks and spirochaete transmission success differ between rodent species and host-finding success appears to be affected by a B. afzelii infection in both the rodent and the tick. In this paper, we review the major interactions between I. ricinus, rodents and B. afzelii that influence this development, with the aim to elucidate the critical factors that determine the epidemiological risk of Lyme borreliosis. The effects of the tick, rodent and B. afzelii on larval host finding, larval blood feeding, spirochaete transmission from rodent to larva and development from larva to nymph are discussed. Nymphal host finding, nymphal blood feeding and spirochaete transmission from nymph to rodent are the final steps to complete the enzootic B. afzelii lifecycle and are included in the review. It is concluded that rodent density, rodent infection prevalence, and tick burden are the major factors affecting the development from larva to infected nymph and that these interact with each other. We suggest that the B. afzelii lifecycle is dependent on the aggregation of ticks among rodents, which is manipulated by the pathogen itself. Better understanding of the processes involved in the development and aggregation of ticks results in more precise estimates of the density of infected nymphs, and hence predictions of Lyme borreliosis risk.
Highlights
Borrelia burgdorferi sensu lato (s.l.), a tick-borne pathogen, can cause Lyme borreliosis in humans [1]
Borrelia burgdorferi s.l. consists of several genospecies, of which B. afzelii, B. garinii and B. burgdorferi sensu stricto (s.s.) are the main cause of Lyme borreliosis in the western Palearctic [2, 3]
Larvae can become infected with B. afzelii via a blood meal from an infected rodent or via a blood meal from an uninfected host when feeding in close vicinity of a B. afzelii-infected tick, a co-feeding infection [18,19,20,21]
Summary
Borrelia burgdorferi sensu lato (s.l.), a tick-borne pathogen, can cause Lyme borreliosis in humans [1]. Borrelia burgdorferi s.l. consists of several genospecies, of which B. afzelii, B. garinii and B. burgdorferi sensu stricto (s.s.) are the main cause of Lyme borreliosis in the western Palearctic [2, 3]. Ixodes ricinus is the principal vector of borreliae in the western Palearctic This tick has three blood-feeding stages (larva, nymph and adult), which take a single blood meal before moulting to the stage or laying eggs in the case of an adult female. It is generally believed that nymphs are responsible for infecting rodents because larvae are rarely infected and adults rarely feed on rodents. The density of infected nymphs is determined by the density of nymphs * nymphal infection prevalence
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