IPCC Report.pdf - Adam Curry

Case StudiesChapter 9are typically indirect and are mediated by a constellation of factors, asopposed to the direct health impacts of severe weather, for example,traumatic injuries resulting directly from exposure to kinetic energyassociated with storms (Noji, 2000).Commonly, underdeveloped health and other infrastructure, poverty,political instability, and ecosystem disruptions interact with weather toimpact health adversely, sometimes to a disastrous degree (Myersand Patz, 2009). For example, cholera is an infectious disease that isperpetuated by poverty and associated factors, though outbreaks arecommonly associated with rainy season onset. Research in the lastdecade has demonstrated that cholera is also sensitive to climatevariability (Rodó et al., 2002; Koelle et al., 2005a; Constantin de Magnyet al., 2007). Assuming persistence of these vulnerability factors, choleraoutbreaks may become more widespread as the climate continues tochange (Lipp et al., 2002) due to the projected likely increase in frequencyof heavy precipitation over many areas of the globe, and tropicalregions in particular (see Table 3-1). Insights into the disease’s ecology,however, including its climate sensitivity, may one day inform early warningsystems and other interventions that could blunt its disastrous impact.Equally, if not more important, poverty reduction and improvements inengineering, critical infrastructure, and political stability and transparencycan reduce vulnerability among exposed populations to the degree thatcholera could be contained.9.2.7.2. BackgroundCholera has a long history as a human scourge. The world is in the midstof the seventh global pandemic, which began in Indonesia in 1961 andis distinguished by continued prevalence of the El Tor strain of the Vibriocholerae bacterium (Zuckerman et al., 2007; WHO, 2010). Primarily drivenby poor sanitation, cholera cases are concentrated in areas burdened bypoverty, inadequate sanitation, and poor governance. Between 1995 and2005, the heaviest burden was in Africa, where poverty, water sourcecontamination, heavy rainfall and floods, and population displacementwere the primary risk factors (Griffith et al., 2006).V. cholerae is flexible and ecologically opportunistic, enabling it to causeepidemic disease in a wide range of settings and in response to climateforcings (Koelle et al., 2005b). Weather, particularly seasonal rains, haslong been recognized as a risk factor for cholera epidemics.Cholera is one of a handful of diseases whose incidence has been directlyassociated with climate variability and long-term climate change (Rodóet al., 2002). One driver of cholera’s presence and pathogenicity is theEl Niño-Southern Oscillation (ENSO), which brings higher temperatures,more intense precipitation, and enhanced cholera transmission. ENSOhas been associated with cholera outbreaks in coastal and inlandregions of Africa (Constantin de Magny et al., 2007), South Asia(Constantin de Magny et al., 2007), and South America (Gil et al., 2004).There is concern that climate change will work synergistically withpoverty and poor sanitation to increase cholera risk.As with other disasters, the risk of disastrous cholera epidemics can bedeconstructed into hazard probability, exposure probability, and populationvulnerability, which can be further broken down into populationsusceptibility and adaptive capacity. As noted in the introduction, somedisastrous cholera epidemics are not associated with discrete extremeweather events, but extreme impacts are triggered instead by exposureto a less dramatic weather event in the context of high populationvulnerability. We focus on factors affecting exposure and vulnerability ingeneral, then apply this discussion to the Zimbabwe cholera epidemicthat began in 2008.9.2.7.2.1. ExposureCholera epidemics occur when susceptible human hosts are broughtinto contact with toxigenic strains of V. cholerae serogroup O1 orserogroup O139. A host of ecological factors affect V. cholerae’senvironmental prevalence and pathogenicity (Colwell, 2002) and thelikelihood of human exposure (Koelle, 2009). In coastal regions, there isa commensal relationship between V. cholerae, plankton, and algae(Colwell, 1996). Cholera bacteria are attracted to the chitin of zooplanktonexoskeletons, which provide them with stability and protect them frompredators. The zooplankton feed on algae, which bloom in response toincreasing sunlight and warmer temperatures. When there are algalblooms in the Bay of Bengal, the zooplankton prosper and cholerapopulations grow, increasing the likelihood of human exposure.Precipitation levels, sea surface temperature, salinity, and factors affectingmembers of the marine and estuarine ecosystem, such as algae andcopepods, affect exposure probability (Huq et al., 2005). Many of thesefactors appear to be similar across regions, although their relativeimportance varies, such as the association of V. cholerae with chitin(Pruzzo et al., 2008) and the importance of precipitation and sea level(Emch et al., 2008). For example, marine and estuarine sources were thesource of pathogenic V. cholerae strains responsible for cholera epidemicsin Mexico in recent El Niño years (Lizarraga-Partida et al., 2009).Other variables are associated with increased likelihood of exposure,including conflict (Bompangue et al., 2009), population displacement,crowding (Shultz et al., 2009), and political instability (Shikanga et al.,2009). Many of these factors are actually mediated by the moreconventional cholera risk factors of poor sanitation and lack of accessto improved water sources and sewage treatment.9.2.7.2.2. Population susceptibilityPopulation susceptibility includes both physiological factors that increasethe likelihood of infection after cholera exposure, as well as social andstructural factors that drive the likelihood of a severe, persistent epidemiconce exposure has occurred. Physiologic factors that affect cholera riskor severity include malnutrition and co-infection with intestinal parasites(Harris et al., 2009) or the bacterium Helicobacter pylori. Infections aremore severe for people with blood group O, for children, and for those508