Tick-borne encephalitis (TBE) is peculiar due to its unstable dynamics with profound inter-annual fluctuations in case numbers – a phenomenon not well understood to date. Possible reasons – apart from variable human contact with TBE foci – include external factors, e.g. climatic forcing, autonomous oscillations of the disease system itself, or a combined action of both. Spectral analysis of TBE data from six regions of central Europe (CE) revealed that the ostensibly chaotic dynamics can be explained in terms of four superposed (quasi-)periodical oscillations: a quasi-biennial, triennial, pentennial, and a decadal cycle. These oscillations exhibit a high degree of regularity and synchrony across CE. Nevertheless, some amplitude and phase variations are responsible for regional differences in incidence patterns. In addition, periodic changes occur in the degree of synchrony in the regions: marked in-phase periods alternate with rather off-phase periods. Such a feature in the disease dynamics implies that it arises as basically diverging self-oscillations of local disease systems which, at intervals, receive synchronizing impulses, such as periodic variations in food availability for key hosts driven by external factors. This makes the disease dynamics synchronized over a large area during peaks in the synchronization signal, shifting to asynchrony in the time in between.

The resurgence of pertussis in some countries that maintain high vaccination coverage has drawn attention to gaps in our understanding of the epidemiological effects of pertussis vaccines. In particular, major questions surround the nature, degree and durability of vaccine protection. To address these questions, we used mechanistic transmission models to examine regional time series incidence data from Italy in the period immediately following the introduction of acellular pertussis (aP) vaccine. Our results concur with recent animal-challenge experiments wherein infections in aP-vaccinated individuals proved as transmissible as those in naive individuals but much less symptomatic. On the other hand, the data provide evidence for vaccine-driven reduction in susceptibility, which we quantify via a synthetic measure of vaccine impact. As to the precise nature of vaccine failure, the data do not allow us to distinguish between leakiness and waning of vaccine immunity, or some combination of these. Across the range of well-supported models, the nature and duration of vaccine protection, the age profile of incidence and the range of projected epidemiological futures differ substantially, underscoring the importance of the remaining unknowns. We identify key data gaps: sources of data that can supply the information needed to eliminate these remaining uncertainties.