NAAS Score 2020

                   5.36

UserOnline

Free counters!

Previous Next

Effects of Climate Change on Animal Health and Diseases

M. I. Yatoo Pankaj Kumar U. Dimri M. C. Sharma
Vol 2(3), 15-24
DOI- http://dx.doi.org/10.5455/ijlr.20120930051739

Climate change and global warming now being accepted facts have affected all the ecosystems and will do so if left uncontrolled. Impacts on some components have gained more attention while others have been neglected. Animals belong to latter. Even among the aspects relating to impacts of climate change on animals, production related impacts have gained attention when the impacts on health in general and on infectious diseases in particular are neglected.Despite not being studied in depth, it can be assumed that as in the case of humans, climate change, in particular global warming, is likely to greatly affect the health of animals, both directly and indirectly. Direct effects include temperature-related illness and death, and the morbidity of animals during extreme weather events. Indirect impacts follow more intricate pathways and include those deriving from the attempt of animals to adapt to thermal environment or from the influence of climate on microbial populations, distribution of vector-borne diseases, host resistance to infectious agents, feed and water shortages, or food-borne diseases.


Keywords : Climate change Animal Health Disease

Introduction  

Climate change and global warming now being accepted facts have affected all the ecosystems and will do so if left uncontrolled. Impacts on some components have gained more attention while others have been neglected. Animals belong to latter. Even among the aspects relating to impacts of climate change on animals, production related impacts have gained attention when the impacts on health in general and on infectious diseases in particular are neglected.

Despite not being studied in depth, it can be assumed that as in the case of humans, climate change, in particular global warming, is likely to greatly affect the health of animals, both directly and indirectly. Direct effects include temperature-related illness and death, and the morbidity of animals during extreme weather events. Indirect impacts follow more intricate pathways and include those deriving from the attempt of animals to adapt to thermal environment or from the influence of   climate on microbial populations, distribution of vector-borne diseases, host resistance to infectious agents, feed and water shortages, or food-borne diseases.

Infectious diseases especially vector-borne diseases and diseases having a stage in the environment are likely to be more affected by climate change than other diseases, but may vary depending on different factors.

There are in general many factors operating, and considerably more work is needed on disease dynamics and how these may adapt to a changing climate. These things make impact assessment of animal diseases (in developing countries) particularly challenging. By assessing the risk of potential disease through the identification of potential pathogens and routes of disease spread, can generate forecasts of disease risk areas and implement surveillance efforts to monitor spread and plan intervention efforts in order to reduce the risk of animal disease. From the years 1906 to 2005, global average temperature has warmed by 0.74°C, and since 1961, sea level has risen on average by approximately 2 mm per year. Arctic sea ice extent has declined by 7.4% per decade and snow cover and glaciers have diminished in both hemispheres. The rate of change in climate is faster now than in any period in the last 1000 years. According to the United Nations Intergovernmental Panel on Climate Change, in 90 years, average global temperatures will increase between 1.8°C and 4.0°C and sea level will rise between 18 and 59 cm. Extremes of the hydrologic cycle (e.g, floods and droughts) are also expected to accompany global warming trends.

Impact of Climate Change on Animal Health

As mentioned earlier climate change affects the health of farm animals, both directly and indirectly. Under the changing climate animals tend to undergo acclimation.

Acclimation is a phenotypic response developed by the animal to an individual source of stress within the environment. The acclimation of the animals to meet the thermal challenges results in the reduction of feed intake and alteration of many physiological functions that are linked with impaired health and the alteration of productive and reproductive efficiency. Acclimation to high environmental temperatures involves responses that lead to reduce heat load. The immediate responses are the reduction of feed intake, increase in respiration rate and water intake and changes in hormonal signals that affect target tissue responsiveness to environmental stimuli. The decrease in energy intake due to reduced feed intake, results in a negative energy balance (NEB), and partially explains why cows lose significant amounts of body weight and body score when subjected to heat stress. If exposure to high air temperature is prolonged, lower feed intake is followed by a decline in the secretion of calorigenic hormones (growth hormone, catecholamines and glucocorticoids in particular), in thermogenic processes of digestion and metabolism, and metabolic rate. All these events together (lower feed intake, change in endocrine status and lower metabolic rate) tend to reduce metabolic heat production and might be responsible for modifications of energy, lipids, protein and mineral metabolism, and liver function. Previous studies (Lacetera et al., 1996; Nardone et al., 1997; Ronchi et al., 1995, 1997, 1999) and studies done by others (Itoh et al., 1998a,b; Moore et al., 2005; O’Kelly, 1987; Sano et al., 1983, 1985; Vizcarra et al., 1997) clearly demonstrated the alteration of glucose, protein and lipid metabolism and alteration of liver functionality in heat stressed subjects.

Blood glucose is usually reduced in heat-stressed subjects and this reduction is not all attributable and justified by the lower feed intake occurring in a hot environment. Also, non-esterified fatty acids (NEFA) are usually reduced under hot conditions. The changes of plasmatic concentrations of NEFA under hot environment are in contrast with NEB and loss of BCS, which generally occur in very hot conditions. Considering, these facts, the lower values of plasma NEFA in heat-stressed animals would not seem explainable by the lower feed intake. Recently Baumgard et al. (2007) and Wheelock et al. (2006) described lower glucose and lower NEFA in heat stressed cows compared with pair-fed cows. In addition, these authors demonstrated that glucose disposal (rate of cellular glucose entry) was greater in heat-stressed compared to thermal neutral pair-fed cows, and heat-stressed cows had a much greater insulin response to a glucose challenge when compared to underfed cows. The consequence of the reduction of hepatic glucose synthesis, the alteration of glucose turnover and the increased glucose demand for energy need is the lower availability of glucose for mammary gland lactose synthesis. Since, lactose production is the primary osmo regulator and thus determinant of milk yield, reduction of glucose availability leads to the reduction of milk yield and may account the reduction of milk yield not explainable by the reduction of feed intake under hot conditions. Our research evidenced the alteration of liver functions in heat stressed subjects. The reduction of cholesterol and albumin secretion and liver enzyme activities clearly indicated a reduction in liver activity in heat-stressed cattle. We also demonstrated that hot conditions, capable of producing moderate or severe heat stress, cause oxidative stress in transition dairy cows. More recently, Lin et al. (2006) concluded that the oxidative stress should be considered as part of the stress response of broiler chickens to heat exposure. Alteration of glucose and lipid metabolism, liver function and oxidative status may be responsible for the increased sensitivity of heat-stressed animals to metabolic diseases with negative consequences on production, reproduction and infectious disease sensitivities in intensive and extensive livestock production systems. The increased respiration rate results in enhanced CO2 being exhaled. Under a hot environment, hyperventilation induces a decrease in blood CO2 and the kidney secretes HCO3 − to maintain this ratio. This reduces the availability of HCO3 − that can be used (via saliva) to buffer and maintain a healthy rumen pH. In addition, panting ruminants drool and drooling reduces the quantity of saliva that would have normally been deposited in the rumen. Furthermore, due to reduced feed intake and reduced forage/ concentrate ratio, heat-stressed ruminants ruminate less and therefore produce less saliva. The reduction in the amount of saliva produced and salivary HCO3 − content, the decreased amount of saliva entering the rumen and the reduced forage intake make the heat-stressed cow much more susceptible to sub-clinical and acute rumen acidosis , which indirectly enhances the risk of other concurrent health and productive problems (laminitis, milk fat depression, etc.). These circumstances are more typical for intensive cattle production systems (dairy and beef). In a recent retrospective study carried out for years 2001– 2006 in the geographic area known as the Po Valley, and including the regions Lombardia and Emilia Romagna (Italy), it was analyzed seasonal variations of mortality rate in dairy cows . For all these years and for both regions, the analysis of the standard mortality rate showed that during the summer season the observed deaths (OD) were significantly higher than the expected deaths (ED). In the summer season the OD overcame ED by values ranging from +14% (year 2002, Emilia Romagna) to +60% (year 2003, Lombardia); the corresponding 95% confidence intervals were 1.10–1.18 and 1.57–1.64 for the years 2002 and 2003, respectively. Results of an epidemiology study carried out in California documented higher mortality rates in summer calves. Others have reported that heat stress may be responsible for impairment of the protective value of colostrum both in cows and pigs, and also for alteration of passive transfer of immunoglobulin in neonatal calves. On the other hand, results on the negative influence of heat stress on colostral immunoglobulin is likely to explain the higher mortality rate of newborns observed during hot months .

A series of studies carried out in dairy cows indicated a higher incidence of mastitis during periods of hot weather. However, the mechanisms responsible for the higher occurrence of mammary gland infections during summer months have not been elucidated. The hypothesis advanced to explain these observations include the possibility that high temperatures may facilitate survival and multiplication of pathogens or their vectors, or a negative action of heat stress on defensive mechanisms.

Several studies have assessed the relationships between heat stress and immune responses in cattle, chickens or pigs. However, results of those studies are conflicting. In particular,

some authors reported an improvement (Beard and Mitchell, 1987; Regnier and Kelley, 1981; Soper et al., 1978), others described an impairment (Elvinger et al., 1991; Kamwanja et al., 1994; Morrow-Tesch et al., 1994; Regnier and Kelley, 1981), and others indicated no effects (Bonnette et al., 1990; Donker et al., 1990; Kelley et al., 1982; Lacetera et al., 2002; Regnier et al., 1980) of high environmental temperatures on immune function. Recently, in a field study carried out in Italy during the summer 2003, which was characterized by the occurrence of at least three severe heat waves, we observed a profound impairment of cell-mediated immunity in high yielding dairy cows. The large variety of experimental conditions in terms of species, breeds, severity and length of heat stress, recovery opportunities, and also of the specific immune functions taken into consideration are likely to explain the discrepancy among results of different studies.

For instance, in a recent in vitro study we observed that peripheral blood mononuclear cells from Brown cows are less tolerant to chronic heat exposure than those from Holstein cows, and that the lower tolerance is associated with higher expression of heat shock proteins 72 kDa, suggesting that the same level of hyperthermia may be associated with a differential decline of immune function in the 2 breeds. As already reported above, global warming will also affect the biology and distribution of vector-borne infections. Wittmann et al. (2001) simulated an increase of temperature values by 2 °C, and under these conditions, their model indicated the possibility of an extensive spread of Culicoides imicola, which represents the major vector of the bluetongue virus. Another mechanism through which climate change can impair livestock health is represented by the favourable effects that high temperatures and moisture have on growth of mycotoxin-producing fungi. With regard to the alteration of animal health, mycotoxins can cause acute disease episodes when animals consume critical quantities of these toxins. Specific toxins affect specific organs or tissues such as the liver, kidney, oral and gastric mucosa, brain, or reproductive tract. In acute mycotoxicoses, the signs of disease are often marked and directly referable to the affected target organs. Most frequently, however, concentrations of mycotoxin in feeds are below those that cause acute disease. At lower concentrations, mycotoxins reduce the growth rate of young animals, and some interfere with native mechanisms of resistance and impair immunologic responsiveness, making the animals more susceptible to infections. Studies have shown that some mycotoxins can alter lymphocyte function in domestic ruminants through alteration of DNA structure and function

Impact of Climate Change on Animal Diseases

The impacts of changes in ecosystems on infectious diseases depend on the ecosystems affected, the type of land-use change, disease specific transmission dynamics, and the susceptibility of the populations at risk the changes wrought by climate change on infectious disease burdens may be extremely complex. Climate change will affect not only those diseases that have a high sensitivity to ecological change, but there are also significant health risks associated with flooding. The major direct and indirect health burdens caused by floods are widely acknowledged, but they are poorly characterized and often omitted from formal analyses of flood impacts There is quite a large literature on the prospective impacts of climate change on health and disease, but much of it is devoted to human health and vector-borne disease, unsurprisingly. The effects of climate change on livestock and non-vector-borne disease have received only limited attention, however (e.g., Cook, 1992; Harvell et al., 1999, 2002). As Baylis and Githeko (2006) note, given the global burden of disease that is not vector-borne, and the contribution of animal diseases to poverty in the developing world, this needs to be rectified. In their review, Baylis and Githeko (2006) discuss several ways in which climate change may affect infectious diseases:

Effects on Pathogens: higher temperatures may increase the rate of development of pathogens or parasites that spend some of their life cycle outside their animal host, which may lead to larger populations (Harvell et al., 2002). Other pathogens are sensitive to high temperatures and their survival may decrease with climate warming. Similarly, those pathogens and parasites that are sensitive to moist or dry conditions may be affected by changes to precipitation, soil moisture and the frequency of floods. Changes to winds could affect the spread of certain pathogens and vectors. Effects on hosts: Baylis and Githeko (2006) mention that mammalian cellular immunity can be suppressed following heightened exposure to ultraviolet B radiation, which is an expected outcome of stratospheric ozone depletion. So greenhouse-gas emissions that affect ozone could have an impact on certain animal diseases, although this link has not been studied in livestock. A more important effect may be on genetic resistance to disease. While animals often have evolved genetic resistance to disea ses to which they are commonly exposed, they may be highly susceptible to ‘‘new” diseases. Climate change may bring about substantial shifts in disease distribution, and outbreaks of severe disease could occur in previously unexposed animal populations (possibly with the breakdown of endemic stability).

Effects on Vectors: there may be several impacts of climate change on the vectors of disease (midges, flies, ticks, mosquitoes and tsetse are all important vectors of livestock disease in the tropics). Changes in rainfall and temperature regimes may affect both the distribution and the abundance of disease vectors, as can changes in the frequency of extreme events (outbreaks of some mosquito-borne diseases have been linked to El Niño-Southern Oscillation (ENSO), for example). It has also been shown that the ability of some insect vectors to become or remain infected with viruses (such as bluetongue) varies with temperature. The feeding frequency of arthropod vectors may also increase with rises in temperature. As many vectors must feed twice on suitable hosts before transmission is possible (to acquire and then to transmit the infection), warmer temperatures may increase the likelihood of successful disease transmission.

Effects on Epidemiology: climate change may alter transmission rates between hosts not only by affecting the survival of the pathogen or parasite or intermediate vector but also by other means. Future patterns of international trade, local animal transportation, and farm size are factors that may be driven in part by climate change, and may affect disease transmission.

Other Indirect Effects: climate change may also affect the abundance and/or distribution of the competitors, predators and parasites of vectors themselves, thus influencing patterns of disease. It may also be that changes in ecosystems, driven by climate change and other drivers that affect land-use, could give rise to new mixtures of species, thereby exposing hosts to novel pathogens and vectors and causing the emergence of new diseases (WHO, 1996).

The impacts of climate change on livestock disease may be very complex, and studying them needs to go well beyond any simple assessment of rainfall and temperature effects on distribution, although that is a start. Examples of this type of analysis have been done for several diseases of livestock in developing countries. Rogers (1996) looked at possible climate change impacts on the distribution of the brown-ear tick, Rhipicephalus appendiculatus, and the primary vector of East Coast Fever, a disease that affects both grazing (LG) and mixed (MR) systems in eastern and southern Africa. By the 2050s, suitable habitat is projected to have largely disappeared from the south-eastern part of its existing range (southeastern Zimbabwe and southern Mozambique), although its range may expand in western and central parts of southern Africa. In another study that looked at possible impacts of climate change on a major disease of livestock in African livestock systems, cattle Trypanosomiasis, Thornton et al. (2006a) investigated climate-driven changes in habitat suitability for the tsetse fly vector. While climate will modify habitat suitability for the tsetse fly, the demographic impacts on trypanosomiasis risk through bush clearance are likely to outweigh those brought about by climate change. A similar result was found in a modelling study of changes in malaria distribution in Africa by Hay et al (2006). Climate change may increase the numbers of people at risk from this disease, but that these increases are small when compared with the likely impacts of demographic changes. Randolph (2010) cautions that there are no a priori reasons for expecting that climate change will necessarily lead to increases in disease risk in general, and in general a multitude of interacting factors determine infection risk and exposure of livestock and humans to that risk. More integrated assessments have been attempted, that go beyond the distributional effects of the vector of disease, although to date these have tended to have a developed-country focus. White et al. (2003) simulated the increased vulnerability of the Australian beef industry to the cattle tick (Boophilus microplus). They calculated economic losses in relation to tick populations and productivity reductions, and assessed switching breeds as an adaptation option. Their results are perhaps more interesting in relation to the uncertainties and assumptions made, and their key conclusion that risk assessments of climate change should extend to all relevant variables, where this is possible. AR4 does not have much to say on plant and animal diseases. It notes that new studies are focusing on the spread of animal diseases and pests from low to mid-latitudes due to warming. Models project that bluetongue, which mostly affects sheep and occasionally goat and deer, will spread from the tropics to mid-latitudes. Most assessments do not explicitly consider the impacts on livestock health as a function of CO2 and climate combined. Whether CO2 impacts are important or not in this regard, is essentially unknown. Perhaps more than other livestock-related impacts, climate change effects on livestock disease suffer intrinsic problems of predictability. This is due in part to the nature of disease. As Baylis and Githeko (2006) note, climate change-driven alterations to livestock husbandry in Africa, if they occur, could have many indirect and unpredictable impacts on infectious animal disease in the continent. It has been observed that combinations of drought followed by high rainfall have led to wide-spread outbreaks of diseases such as Rift Valley Fever and bluetongue in East Africa and of African horse sickness in the Republic of South Africa. The predictability of events such as ENSO in current GCMs is poor, so while it is likely that outbreaks of certain vector-borne diseases will become more common in parts of Africa, we are very limited when it comes to predicting when and where these are likely to occur. In addition to this, Kovats et al. (2001) note that there has been a tendency to over simplify the mechanisms by which climate change may affect disease transmission. There are in general many factors operating, and considerably more work is needed on disease dynamics and how these may adapt to a changing climate. These things make impact assessment of livestock diseases in developing countries particularly challenging.

Climate Variability and Change Effects on Vector and Rodent-Borne Diseases

The transmission dynamics and geographic distribution of most insect- or rodent borne (vector-borne) diseases are highly climate sensitive. Vector-borne pathogens spend part of their life cycle in cold-blooded arthropods that are subject to many environmental factors. Changes in weather and climate that can affect transmission of vector-borne diseases include temperature, rainfall, wind, extreme flooding or drought, and sea level rise. Rodent-borne pathogens can be affected indirectly by ecologic determinants of food sources affecting rodent population size, and floods can displace and lead them to seek food and refuge. The extrinsic incubation time of an infective agent within its vector organism is typically sensitive to changes in temperature and humidity.

Some of the Common and Frequently Occurring Diseases As Affected By Climate Change

Malaria

Malaria kills between 700,000 and 2.7 million persons each year, mostly children in sub-Saharan Africa. Although malaria’s resurgence involves multiple factors, from climate and land use change to drug resistance, variable disease-control efforts, and other socio demographic factors, malaria is an extremely climate-sensitive tropical disease, and one of the most important climate change/health questions to resolve.

Vector Survival can decrease or increase, depending on the species. Some vectors have higher survival at higher latitudes and altitudes with higher temperatures.

Changes are possible in the susceptibility of vectors to some pathogens (eg, higher temperatures reduce the size of some vectors but reduce the activity of others).

Changes occur in the rate of vector population growth.

Changes occur in feeding rate and host contact (which may alter the survival rate).

Changes occur in the seasonality of populations.

Pathogen

Extrinsic incubation period of pathogen is decreased in vector at higher temperatures,

Changes occur in the transmission season.

Changes occur in distribution.

Viral replication is decreased.

Examples of effects of changes in precipitation on selected vector-borne pathogens

Vector

Increased rain may increase larval habitat and vector population size by creating a new habitat.

Excess rain or snow pack can eliminate habitat by flooding, thus decreasing the vector population size.

Low rainfall can create habitat by causing rivers to dry into pools (dry season malaria).

Decreased rain can increase container-breeding mosquitoes by forcing increased water storage.

Epic rainfall events can synchronize vector host seeking and virus transmission.

Increased humidity increases vector survival; decreased humidity decreases vector survival.

Pathogen

Few direct effects are evident but some data indicate humidity effects on malarial parasite development in the anopheline mosquito host.

Vertebrate host

Increased rain can increase vegetation, food availability, and population size.

Increased rain can also cause flooding and decrease population size but increase contact with humans.

Decreased rain can eliminate food and force rodents into housing areas, increasing human contact, but it can also decrease population size.

Increased sea level

Increased levels alter estuary flow and change existing salt marshes and associated mosquito species, decreasing or eliminating selected mosquito breeding sites (e.g, reduced habitat for Culiseta melanura).

The relationship between ambient weather conditions and vector ecology is complicated by the natural tendency for insect vectors to seek out the most suitable ‘‘microclimates’’ for their survival (eg, resting under vegetation or pit latrines during dry or hot conditions or in culverts during cold conditions).

Dengue fever

The peridomestic urban mosquito, Aedes aegypti, is also strongly influenced by climate, including variability in temperature, moisture, and solar radiation. Similar to the extrinsic incubation period of the malaria parasite, the rate of dengue virus replication in A aegypti mosquitoes increases directly with temperature in the laboratory. When linked to future climate change projections, biologic models of dengue transmission suggest that small increases in temperature, given viral introduction into a susceptible human population, could increase the potential for epidemics. For small countries with presumably some climate uniformity, a climate-based Aedes mosquito population model strongly correlates climate conditions with the variability in dengue cases reported at the national level.

West Nile Virus

Climate variability has an effect on West Nile virus (WNV), a disease that rapidly spread across the Western hemisphere. Reisen and colleagues found that the strain of WNV that entered New York (during the record hot July of 1999) differed from the South African strain in that it required warmer temperatures for efficient transmission. The investigators concluded that during the epidemic summers of 2002 and 2004 in the United States, epicenters of WNV were linked to above-average temperatures. Temperature influences other important components of the WNV transmission cycle, such as the development rate and fitness of immature mosquitoes and the biting rate and survival of adult female mosquitoes. Anomalously hot summer temperatures are also linked to international WNV outbreaks in South Africa and Russia. Variability of precipitation may affect WNV transmission by inducing a large increase in disease-transmitting mosquito abundance or killing mosquito predators and competitors vector–avian host contact. Multiple North American WNV vector mosquito population sizes tend to mirror the total amount of summer season precipitation. Above-average summer precipitation likely activates new larval breeding habitats and temporarily increases the number of disease vectors, which may increase the level of WNV transmission. This mechanism appears to be behind the 1974 South African WNV epidemic, which infected more than 18,000 people. In the United States, below-average rainfall the previous year tended to increase WNV transmission the following year. Drought over multiple time periods has inconsistently been reported as a potential driver of multiple individual WNV outbreaks.61,67,68 Disease transmitting mosquito populations recover more rapidly than mosquito competitors and predators from a disturbance like drought, which may increase disease transmission. In humid Florida, spring drought increases vector and avian host contact and WNV transmission, and wet summer conditions foster mosquito dispersal and subsequent disease transmission. Similar to WNV, Saint Louis encephalitis virus (SLEV) is also associated with climatic factors. In Florida, SLEV appearance in sentinel chicken flocks is preceded by a wet period followed by drought.

Chikungunya

During July 2004, amidst a severe drought in East Africa, an epidemic of chikungunya virus erupted in Lamu, Kenya, where an estimated 13,500 people (75% of the population) were infected. Climate analysis showed that unseasonably warm and dry conditions, especially over coastal Kenya, occurred during May 2004. Such conditions may have led to unsafe domestic water storage practices and infrequent changing of water storage and hastened viral development in the Aedes mosquito. The virus spread to islands of the western Indian Ocean, then to India, and most recently to Italy during the summer of 2007. Although the role of climatic conditions in Italy is not clear, southern Europe was experiencing an unusually warm and dry summer.

Rift Valley Fever

All known Rift Valley fever virus outbreaks in East Africa from 1950 to May 1998, and probably earlier, followed periods of abnormally high rainfall. Analysis of this record and Pacific and Indian Ocean sea surface temperature anomalies, coupled with satellite normalized difference vegetation index data, shows that prediction of Rift Valley fever outbreaks may be made up to 5 months in advance of outbreaks in East Africa. Concurrent near–real-time monitoring with satellite normalized difference vegetation data may identify actual affected areas. Dams and irrigation can increase breeding sites, exacerbating the effect of extreme rainfall. Extensive human disease outbreaks were not reported until 1951, when an estimated 20,000 persons were infected during an epidemic in cattle and sheep in South Africa. Outbreaks were reported exclusively from sub-Saharan Africa until 1977–78, when 18,000 persons were infected and 598 deaths were reported in Egypt.

Lyme disease

Lyme disease is a prevalent, tick-borne disease in North America that new evidence suggests has an association with temperature and precipitation. In the field, temperature and vapor pressure contribute to maintaining populations of the tick Ixodes scapularis which, in the United States, is the microorganism’s secondary host. A monthly average minimum temperature above 7c is required for tick survival.The northern boundary of tick-borne Lyme disease is limited by cold temperature effects on the tick, I. scapularis. The northern range limit for this tick could shift north by 200 km by the 2020s, and 1000 km by the 2080s (based on projections from the CGCM2 and HadCM3 atmosphere-ocean global circulation models under the Special Report on Emissions Scenarios A2 emissions scenario).

Rodent-Borne Diseases

For Hantavirus pulmonary syndrome, which newly emerged in the Southwest in 1993, weather conditions led to a growth in rodent populations and subsequent disease transmission, all following unusually heavy El Nino–driven rainfall. Hantavirus infections are transmitted largely by exposure to infectious excreta, and may cause serious disease in humans and a high fatality rate.

Extreme flooding or hurricanes can lead to outbreaks of leptospirosis. In Nicaragua, for example, an epidemic of leptospirosis followed heavy flooding in 1995. From a case-control study, a 15-fold risk for disease was associated with walking through flooded waters.

Plague is another climate-sensitive disease that is carried by fleas, and it is associatedwith populations of rodents, the primary reservoir hosts of the Yersinia pestis bacterium.

In the desert southwestern United States, plague bacterial levels in rodents have been found to increase in the wake of wet climate conditions following El Nino and Pacific Decadal Oscillation–driven wet weather conditions. Historically, according to tree-ring proxy climate data, during the major plague epidemics of the Black Death period (1280–1350), climate conditions were becoming warmer and wetter.

Bluetongue

Bluetongue disease, a viral illness that is fatal to sheep and other ruminants, is spread by Culicoides spp (midges) and historically, only rarely reached north into Europe. But since 1998, several strains of bluetongue virus have advanced 800 km further into Europe than previously reported. Warming temperatures in the region have allowed enhanced survival of viruses through winter and a northern expansion of the insect vector of the disease. Warmer winter temperatures projected for the future may further the geographic range of this serious livestock disease; the warm temperatures of 2007 already have allowed establishment of bluetongue in Northern Europe.

Aproaches to Be Followed

Every attempt should be made to prevent climate change-global, regional or national level.

Guidelines of national and international agencies like IPCC, UNEP, OIE, WHO should be followed.

Assemble, preserve and characterize animal genes and research on alternative animals (Resource: genetic diversity)

As veterinarian we should play a greater role.

 

Conclusion

Climate change will affect animal health; infectious diseases will be no different. Climate change will affect the distribution and incidence of VBD globally. Impacts will vary from region to region. Current evidence suggests impacts on some diseases may already be occurring. Risk assessments constrained by complex transmission cycles and multiple determinants. Impacts may include unanticipated emergence of new pathogens/diseases or re-emergence. By assessing the risk of potential disease through the identification of potential pathogens and routes of disease spread, can generate forecasts of disease risk areas and implement surveillance efforts to monitor spread and plan intervention efforts in order to reduce the risk of animal disease. Because the lack of knowledge still prevails, still gap can be filled in near future by research.

References

Mass-Coma et al, Climate change effects on trematodiasis, with emphasis on zoonotic fascioliasis and schistosomiasis. Veterinary Parasitology 163(2009) 264-280.

Nardone et al, effects of climate change on animal production and sustainability of livestock systems. Livestock science 130(2010) 57-69

Thornton et al, the impacts of climate change on livestock and livestock systems in developing countries: A review of what we know and what we need to know. Agricultural systems 101(2009) 113-127

Gubler et al, resurgent vector-borne diseases as a global health problem. Emerging infectious disease4(1998) 442-450

Githeko et al, climate change vector borne diseases: a regional analysis. Bull.WHO 78(2000) 1136-1147

Patz et al. Effect of environmental change on emerging parasitic diseases. International journal of parasitology 30(2000)1395-1405

IPCC (Inter Governmental Panel on Climate Change: AR4).2007.The Inter governmental Panel on Climate Change 4th Assesment Report. www.ipcc.ch/

Baylis et al, The effects of climate change on infectious diseases of animals. Report for the Foresight Project on Detection of Infectious disease.2006 UK 35pp

Sutherst, Implications of global change and climate variability for vector!borne diseases] generic approaches to impact assessments. International Journal for Parasitology 28(1998) 935-945

De La Rocque et al, 2008. Climate change: effects on animal disease systems and implications for surveillance and control. In: De La Rocque, S., Hendrickx, G., Morand, S. (Eds.), Climate Change: Impact on the Epidemiology and Control of Animal Diseases. World Organization for Animal Health (OIE), Paris. Sci. Tech. Rev. 27 (2), 309–317

Lacetera, N., Bernabucci, U., Ronchi, B., Nardone, A., 1996. Body condition score, metabolic status and milk production of early lactating dairy cows exposed to warm environment. Riv. Agric. Subtrop. Trop. 90, 43–55.

Nardone, A., Villa, E., 1997. Characterization, utilization and conservation of cattle germoplasm in the Mediterranean Area. EAAP Publication No. 85, pp. 109–122.

Ronchi, B., Bernabucci, U., Lacetera, N., Nardone, A., Bertoni, G., 1995. Effetti dello stress termico sullo stato metabolico di vitelle di razza Frisona. Zoot. Nutriz. Anim. 21, 209–221.

Ronchi, B., Bernabucci, U., Lacetera, N., Nardone, A., 1997. Effetti dello stress termico sullo stato metabolico-nutrizionale di vacche Frisone in lattazione. Zoot. Nutriz. Anim. 22, 351–363.

Ronchi, B., Bernabucci, U., Lacetera, N., Verini Supplizi, A., Nardone, A., 1999. Distinct and common effects of heat stress and restricted feeding on metabolic status in Holstein heifers. Zoot. Nutriz. Anim. 25, 71–80.

Ronchi, B., Stradaioli, G., Verini Supplizi, A., Bernabucci, U., Lacetera, N., Accorsi, P.A., Nardone, A., Seren, E., 2001. Influence of heat stress and feed restriction on plasma progesterone, estradiol-17β LH, FSH, prolactin and cortisol in Holstein heifers. Liv. Prod. Sci. 68, 231–241.

Moore, C.E., Kay, J.K., VanBaale, M.J., Collier, R.J., Baumgard, L.H., 2005. Effect of conjugated linoleic acid on heat stressed Brown Swiss and Holstein cattle. J. Dairy Sci. 88, 1732–1740.

Itoh, F., Obara, Y., Rose, M.T., Fuse, H., Hashimoto, H., 1998a. Insulin and glucagon secretion in lactating dairy cows during heat exposure. J. Anim. Sci. 76, 2182–2189.

Itoh, F., Obara, Y., Rose, M.T., Fuse, H., 1998b. Heat influences on plasma insulin and glucagon in response to secretogogues in non-lactating dairy cows. Dom. Anim. Endocrinol. 15, 499–510.

Sano, H., Takahashi, K., Ambo, K., Tsuda, T., 1983. Turnover and oxidation rates of blood glucose and heat production in sheep exposed to heat. J. Dairy Sci. 66, 856–861.

Sano, H., Ambo, K., Tsuda, T., 1985. Blood glucose kinetics in whole body and mammary gland of lactating goats exposed to heat. J. Dairy Sci. 68, 2557–2564.

Beard, C.W., Mitchell, B.W., 1987. Influence of environmental temperatures on the serologic responses of broiler chickens to inactivated and viable Newcastle disease vaccines. Avian Dis. 31, 321–326.

Regnier, J.A., Kelley, K.W., 1981. Heat- and cold-stress suppresses in vivo and in vitro cellular immune responses of chickens. Am. J. Vet. Res. 42, 294–299.

Regnier, J.A., Kelley, K.W., Gaskins, C.T., 1980. Acute thermal stressors and synthesis of antibodies in chickens. Poult. Sci. 59, 985–990.

Baumgard, L.H., Wheelock, J.B., O’Brien, M., Shwartz, G., Zimbelman, R.B., Sanders, S.R., VanBaale, M.J., Collier, R.J., Rhoads, M.L., Rhoads, R.P., 2007. The differential effects of heat stress vs. underfeeding on production and post-absorptive nutrient partitioning. Proc. of the Southwest Nutrition and Management Conference, The university of Arizona, Tucson, February 23rd.

Wheelock, J.B., Sanders, S.R., Shwartz, G., Hernandez, L.L., Baker, S.H., McFadden, J.W., Odens, L.J., Burgos, R., Hartman, S.R., Johnson, R.M., Jones, B.E., Collier, R.J., Rhoads, R.P., VanBaale, M.J., Baumgard, L.H., 2006. Effects of heat stress and rbST on production parameters and glucose homeostasis. J. Dairy Sci. 89 (Suppl. 1), 290–291 (abst.).

Lin, H., Decuypere, E., Buyse, J., 2006. Acute heat stress induces oxidative stress in broiler chickens. Comp. Biochem. Physiol. A. Integr. Physiol. 144, 11–17.

Soper, F., Muscoplat, C.C., Johnson, D.W., 1978. In vitro stimulation of bovine peripheral blood lymphocytes: analysis of variation of lymphocyte blastogenic response in normal dairy cattle. Am. J. Vet. Res. 39, 1039–1042.

Bonnette, E.D., Kornegay, E.T., Lindemann, M.D., Hammerberg, C., 1990. Humoral and cell-mediated immune response and performance of weaned pigs fed four supplemental vitamin E levels and housed at two nursery temperatures. J. Anim. Sci. 68, 1337–1345.

Donker, R.A., Nieuwland, M.G., van der Zijpp, A.J., 1990. Heat-stress influences on antibody production in chicken lines selected for high and low immune responsiveness. Poult. Sci. 69, 599–607.

Kelley, K.W., Osborne, C.A., Evermann, J.F., Parish, S.M., Gaskins, C.T., 1982. Effects of chronic heat and cold stressors on plasma immunoglobulin and mitogen-induced blastogenesis in calves. J. Dairy Sci. 65, 1514–1528.

Lacetera, N., Bernabucci, U., Ronchi, B., Scalia, D., Nardone, A., 2002. Moderate summer heat stress does not modify immunological parameters of Holstein dairy cows. Int. J. Biometeorol. 46, 33–37.

Elvinger, F., Hansen, P.J., Natzke, R.P., 1991. Modulation of function of bovine polimorphonuclear leukocytes and lymphocytes by high temperature in vitro and in vivo. Am. J. Vet. Res. 52, 1692–1698.

Kamwanja, L.A., Chase, C.C., Gutierrez, J.A., Guerriero, V., Olson, T.A., Hammond, A.C., Hansen, P.J., 1994. Responses of bovine lymphocytes to heat shock as modified by breed and antioxidant status. J. Anim. Sci. 72, 438–444.

Morrow-Tesch, J.L., McGlone, J.J., Salak-Johnson, J.L., 1994. Heat and social effects on pig immune measures. J. Anim. Sci. 72, 2599–2609.

Wittmann, E.J., Mellor, P.S., Baylis, M., 2001. Using climate data to map the potential distribution of Culicoides imicola (Diptera: Ceratopogonidae) in Europe. Rev. Sci. Tech. 20, 731–740.

Thornton P K, Robinson T P, Kruska R L, Jones P G, McDermott J Reid R S (2006). Cattle trypanosomiasis in Africa to 2030. Report for the Foresight Project on Detection of Infectious Diseases, Department of Trade and Industry, UK Government, 11 pp.

Kovats R.S., Campbell-Lendrum D.H., McMichael A.J., Woodward A. & Cox J.S. (2001). – Early effect of climate change: do they include changes in vector-borne disease? Philos. Trans. roy. Soc. Lond., B, biol. Sci., 356, 1057-1068.

White, N., Sutherst, R.W., Hall, N., Whish-Wilson, P., 2003. The vulnerability of the Australian beef industry to impacts of the cattle tick (Boophilus microplus) under climate change. Climatic Change 61, 157–190.

Randolph S E 2010. To what extent has climate change contributed to the recent epidemiology of tick-borne diseases? Veterinary Parasitology 167 92-4.

Rogers D J, 1996. Changes in disease vector distributions. In: Hulme, M. (Ed.) Climate Change and Southern Africa: an exploration of some potential impacts and implications in the SADC region. Climatic Research Unit, University of East Anglia, Norwich, 49-55.

Harvell C D, Kim K, Burkholder J M, Colwell R R, Epstein P R, Grimes D J, Hofmann E E, Lipp E K, Osterhaus A, Overstreet R M, Porter J W, Smith G W and Vasta G R, 1999. Review: Marine ecology – Emerging marine diseases – Climate links and anthropogenic factors. Science 285, 1505-1510.

Harvell C D, Mitchell C E, Ward J R, Altizer S, Dobson A P, Ostfeld R S and Samuel M D, 2002. Ecology – Climate warming and disease risks for terrestrial and marine biota. Science 296, 2158-2162.

Hay S I, Tatem A J, Guerra C A and Snow R W, 2006. Foresight on population at malaria risk in Africa: 2005, 2015 and 2030. Online at http://www.foresight.gov.uk/

WHO, 1996. Climate Change and Human Health. World Health Organisation: Geneva.

Cook G, 1992. Effect of global warming on the distribution of parasitic and other infectious diseases: a review. Journal of the Royal Society of Medicine 85, 688-691

Full Text Read : 3692 Downloads : 476
Previous Next

Open Access Policy

Close