Linking climate and infectious disease trends in the Northern/Arctic Region.

Recognition of climate-sensitive infectious diseases is crucial for mitigating health threats from climate change. Recent studies have reasoned about potential climate sensitivity of diseases in the Northern/Arctic Region, where climate change is particularly pronounced. By linking disease and climate data for this region, we here comprehensively quantify empirical climate-disease relationships. Results show significant relationships of borreliosis, leptospirosis, tick-borne encephalitis (TBE), Puumala virus infection, cryptosporidiosis, and Q fever with climate variables related to temperature and freshwater conditions. These data-driven results are consistent with previous reasoning-based propositions of climate-sensitive infections as increasing threats for humans, with notable exceptions for TBE and leptospirosis. For the latter, the data imply decrease with increasing temperature and precipitation experienced in, and projected for, the Northern/Arctic Region. This study provides significant data-based underpinning for simplified empirical assessments of the risks of several infectious diseases under future climate change.

Identifying climate-sensitive infectious diseases in animals and humans in Northern regions.

BACKGROUND: General knowledge on climate change effects and adaptation strategies has increased significantly in recent years. However, there is still a substantial information gap regarding the influence of climate change on infectious diseases and how these diseases should be identified. From a One Health perspective, zoonotic infections are of particular concern. The climate in Northern regions is changing faster than the global average. This study sought to identify climate-sensitive infectious diseases (CSIs) of relevance for humans and/or animals living in Northern regions. Inclusion criteria for CSIs were constructed using expert assessments. Based on these principles, 37 potential CSIs relevant for Northern regions were identified. A systematic literature search was performed in three databases using an explicit stepwise approach to determine whether the literature supports selection of these 37 potential CSIs. RESULTS: In total, 1275 nominated abstracts were read and categorised using predefined criteria. Results showed that arthropod vector-borne diseases in particular are recognised as having potential to expand their distribution towards Northern latitudes and that tick-borne encephalitis and borreliosis, midge-borne bluetongue and the parasitic infection fasciolosis can be classified as climate-sensitive. Many of the other potential CSIs considered are affected by extreme weather events, but could not be clearly classified as climate-sensitive. An additional literature search comparing awareness of climate influences on potential CSIs between 1997-2006 and 2007-2016 showed an increase in the number of papers mentioning effects of climate change. CONCLUSIONS: The four CSIs identified in this study could be targeted in a systematic surveillance programme in Northern regions. It is evident that climate change can affect the epidemiology and geographical range of many infectious diseases, but there were difficulties in identifying additional CSIs, most likely because other factors may be of equal or greater importance. However, climate-ecological dynamics are constantly under change, and therefore diseases may fall in or out of the climate-sensitive definition over time. There is increasing awareness in the literature of the effects of climate change on infectious diseases over time.

Discrepancies in data reporting of zoonotic infectious diseases across the Nordic countries - a call for action in the era of climate change.

Emerging infections have in recent years caused enormous health problems. About 70% of these infections are zoonotic e.g. arise from natural foci in the environment. As climate change impacts ecosystems there is an ongoing transition of infectious diseases in humans. With the fastest changes of the climate occurring in the Arctic, this area is important to monitor for infections with potentials to be climate sensitive. To meet the increasing demand for evidence-based policies regarding climate-sensitive infectious diseases, epidemiological studies are vital. A review of registered data for nine potentially climate-sensitive infections, collected from health authorities in Denmark/Greenland, Finland, Iceland, Norway and Sweden, found that performing such studies across countries is constrained by incompatible reporting systems and differences in regulations. To address this, international standardisation is recommended.

Impaired IFN-γ production after stimulation with bacterial components by natural killer cells from gastric cancer patients.

Gastric adenocarcinoma is a major health problem world-wide, as this is the second most common cause of cancer death in the world. It has been estimated that infection by Helicobacter pylori cause at least half of the gastric cancers. Previously, we have demonstrated that H. pylori antigens directly activate NK cells to secrete IFN-γ. There is also a marked synergistic effect in NK cells stimulated with bacterial lysate and low levels of IL-12, a cytokine which is produced by macrophages and dendritic cells in the H. pylori-infected stomach. The present study was designed to investigate whether NK cells from gastric cancer patients display an altered ability to respond to components from H. pylori and other bacteria. The results show that NK cells from peripheral blood of gastric cancer patients have a severely suppressed ability to produce IFN-γ after stimulation with H. pylori lysate and the synthetic bacterial lipoprotein FSL-1. Furthermore, the synergistic effect of IL-12 and lysate is absent in gastric cancer patients, unless the concentration of IL-12 is increased 10-fold. We also demonstrate that there is a similar lack of IFN-γ production from NK cells isolated from the gastric mucosa of cancer patients. In addition, we propose that the observed suppression is due to tumour-derived TGF-ß and that increased expression of the transcription factor GATA-3 may be responsible for the TGF-ß induced suppression.