Wet climate and transportation routes accelerate spread of human plague.

Currently, large-scale transmissions of infectious diseases are becoming more closely associated with accelerated globalization and climate change, but quantitative analyses are still rare. By using an extensive dataset consisting of date and location of cases for the third plague pandemic from 1772 to 1964 in China and a novel method (nearest neighbour approach) which deals with both short- and long-distance transmissions, we found the presence of major roads, rivers and coastline accelerated the spread of plague and shaped the transmission patterns. We found that plague spread velocity was positively associated with wet conditions (measured by an index of drought and flood events) in China, probably due to flood-driven transmission by people or rodents.

Reconstruction of a 1,910-y-long locust series reveals consistent associations with climate fluctuations in China.

It is becoming increasingly clear that global warming is taking place; however, its long-term effects on biological populations are largely unknown due to lack of long-term data. Here, we reconstructed a 1,910-y-long time series of outbreaks of Oriental migratory locusts (Locusta migratoria manilensis) in China, on the basis of information extracted from >8,000 historical documents. First by analyzing the most recent period with the best data quality using generalized additive models, we found statistically significant associations between the reconstructed locust abundance and indexes of precipitation and temperature at both annual (A.

Dynamics of the plague-wildlife-human system in Central Asia are controlled by two epidemiological thresholds.

Plague (caused by the bacterium Yersinia pestis) is a zoonotic reemerging infectious disease with reservoirs in rodent populations worldwide. Using one-half of a century of unique data (1949-1995) from Kazakhstan on plague dynamics, including data on the main rodent host reservoir (great gerbil), main vector (flea), human cases, and external (climate) conditions, we analyze the full ecoepidemiological (bubonic) plague system. We show that two epidemiological threshold quantities play key roles: one threshold relating to the dynamics in the host reservoir, and the second threshold relating to the spillover of the plague bacteria into the human population.

Modeling the epidemiological history of plague in Central Asia: palaeoclimatic forcing on a disease system over the past millennium.

Background: Human cases of plague (Yersinia pestis) infection originate, ultimately, in the bacterium's wildlife host populations. The epidemiological dynamics of the wildlife reservoir therefore determine the abundance, distribution and evolution of the pathogen, which in turn shape the frequency, distribution and virulence of human cases. Earlier studies have shown clear evidence of climatic forcing on contemporary plague abundance in rodents and humans.

Climatically driven synchrony of gerbil populations allows large-scale plague outbreaks.

In central Asia, the great gerbil (Rhombomys opimus) is the main host for the bacterium Yersinia pestis, the cause of bubonic plague. In order to prevent plague outbreaks, monitoring of the great gerbil has been carried out in Kazakhstan since the late 1940s. We use the resulting data to demonstrate that climate forcing synchronizes the dynamics of gerbils over large geographical areas.

Plague dynamics are driven by climate variation.

The bacterium Yersinia pestis causes bubonic plague. In Central Asia, where human plague is still reported regularly, the bacterium is common in natural populations of great gerbils. By using field data from 1949-1995 and previously undescribed statistical techniques, we show that Y.