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Climate change - a threat to pathogen life

CLIMATE is changing the life behavior of living organisms including human, domestic animals, wildlife, and domestic crops. These changes are strongly proportional to solar radiations that enter every day into the earth’s biosphere. The radiations are reflected back and filtered by dust particles, clouds, aerosols, and atmospheric gases. But gases like CO2 are chief source of absorbing harmful radiations from sun and trapping in earth’s atmosphere, thus producing an elevated mean temperature which leads towards an adverse “Greenhouse Effect.” Strong evidences of such effects were found during droughts and floods of Australia and other countries.     
The Intergovernmental Panel on Climate Change (IPCC) has reported in 2007 that increase in global mean temperatures, droughts of mid-continents, rising sea levels, and changed patterns of global precipitation are all due to unpredicted abrupt changes in global climate. These changes have enormously affected the health of biological organisms. Human activities (e.g. uncontrolled population growth, demands of land and water resources) are involved in habitat destruction of many beneficial living organisms and shifting of pathogens from wild species to field crops. Once the host destroyed the pathogens may die up to maximum levels but some of them find a new host for their next generations.           
Recently, researches on zoonotic diseases (which are transferable from animals to humans and vice versa like West Nile virus and the Lyme disease), have proved a strong relationship of changes in lifestyle of human, domestic animals, and pathogens. In case of plants, the pathogenic rusts fungi can cause diseases to both Lolium and Festuca whenever temperature rises in winters whereas leaf beetle of bean found a new host soybean for winter high temperatures. These diseases have vectors as wild insects (like mosquitoes, ticks, arachnids, aphids, moths and white flies) and wild birds. Attack of such diseases occurs according to “Disease Triangle” (host-environment-pathogen) and components of triangle are related to each other. The actual dependence of disease epidemics depend on the climatic conditions as found by the Duveiller & Legreve.
Reproduction rate of pathogens is determined as time interval required to produce as much generations necessary for species survival and this rate is directly related to favorable climate such as high temperature which is provided as a result of more CO2 accumulation in atmosphere which is advantageous for pathogenic reproduction.
Numerous changes in climate are useless for pathogens because of the complete stalling of reproductive cycles. Pathogens do not find any alternate host during sudden changes if conditions prevail for a long time. This makes them to be less in numbers occasionally.    
Effects on wildlife diseases and pathogen life by vector unavailability 
The phenology (biological cycles during which one specie finds a host or food source that is necessary for its survival) of many birds when studied showed that birds mostly migrate as a result of climatic changes (weather shifts and delayed seasons). These birds get new migration patterns and change their time of arrival and sometimes the areas for new habitat. These migrations results in a remarkable loss of birds population whenever arrival is deferred because of late plant emergence from dormant conditions. So, the vector’s availability is decreased for early survival of plant without any alien disease attack. 
Some plants use structural changes against certain abiotic stresses like drought and salinity. These structural or morphological changes e.g. changes in leaf chemistry and reduced opening of stomata make the plant as unavailable host or vector for pathogens that could attack through stomata, for example phyllosticta minima. 
During start of warmer temperatures in spring in Europe, humans become more vulnerable to tick-borne encephalitis (TBE) because of availability of an overlapping host for ticks. Ticks larvae of castor bean uninfected with TBE virus could also become infected when they feed with virus-infected migrated ticks’ nymph during their overlap feeding. As a result, the disease also transfers to small rodents who are tick-infected. So, this contact of virulent and non-virulent strain could increase the risk of TBE in human. But during low temperatures of spring, the overlapping in feeding is reduced so the virus-infected rodents can recover themselves without passing disease to humans. 
Similar effect of seasonal temperature is observed at sites in North America, where the Lyme disease is common and transmitted by the overlap feeding of infected nymphs of black-legged ticks with uninfected larvae ticks through pathogenic Borrelia burgdorferi bacterium. But the climate changes could easily limit the natural cycles of these pahogens.
Changing patterns of wildlife disease
Diseases are either transmitted through direct contacts or through intermediated hosts (a biting insect or an infected prey). These intermediate hosts are climate dependent and could decrease or increase the transmission cycle of pathogen to actual host. High temperatures are found along with continuous rainfalls, to be associated with more infection of intermediate hosts or sometimes infected host challenging survival. For example, lung nematode of Arctic region has found an intermediate host, the marsh slug, for warmer summer temperatures and could easily infect the muskoxen within the same year thus reducing transmission cycle to half. Study proved the same case with another nematode, the brain worm of white-tailed deer, having intermediate host a snail, and actual host as moose. This nematode attacks during warmer temperatures and milder winters in southern Canada and North America. From these examples we are able to understand the global impact of climate change on biological organisms and their pathogens. So it is clear that pathogens may reduce and become non-virulent when the climatic conditions have sudden changes but sometimes they become more virulent and climate resistive.


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