Box 145 A tale of two vibrios cholerae and parahaemolyticus

Outbreaks of cholera, caused by Vibrio cholerae, show an association with coastal water warming, as part of the El Niño cycle, in both Bangladesh and Peru. An American scientist, Rita Colwell (1996), has argued that the proliferation of phytoplankton and zooplankton in warmer water provides a biological culture medium for proliferation of this vibrio, whose natural home is in coastal waters, estuaries, and rivers. The proliferating vibrio then enters the aquatic food web, and reaches humans via fish that are caught and eaten.

Other more recent research (Long et al., 2005) has found that, as water temperatures warm, the inhibition of proliferation of the cholera vibrio exerted by other bacterial species wanes and the vibrio becomes an increasingly dominant bacterium within that ecosystem. Support for one or both of these mechanisms is evident in the very strong correlation between the observed incidence of cholera in Matlab, near coastal Bangladesh, and the incidence predicted on the basis of sea-surface temperature and planktonic blooms during 2000-04 (Willcox and Colwell, 2005). These findings suggest that warming ocean waters will increase the risk of cholera outbreaks, particularly in vulnerable populations around the world.

Meanwhile, another temperature-sensitive vibrio inhabits some of the world's coastal waters. Vibrio parahaemolyticus is the main cause of seafood-associated food poisoning in the US. A major outbreak occurred on a cruise ship off northern Alaska in summer 2004, after passengers had eaten oysters (McLaughlin et al., 2005). The record showed that mean coastal water temperatures had increased by 0.2°C per year since 1997 - and, most interestingly, that 2004 was the only year in which the temperature exceeded the critical temperature of 15°C throughout the July-August oyster harvest season. The authors concluded that: "Rising temperatures of ocean water seem to have contributed to one of the largest known outbreaks of V parahaemolyticus in the US." They suggested that, with global warming, this elevated risk will persist in future.

Several recent reports are nevertheless suggestive of how climate change may affect the transmission of infectious agents. For example, tick-borne (viral) encephalitis (TBE) in Sweden appears to have increased in both its (northern) geographic range and, in Stockholm County, its annual incidence in response to a succession of warmer winters during the 1980s and 1990s (Lindgren 1998; Lindgren et al., 2000). During that time there was evidence of an inter-annual correlation between winter-spring temperatures and the incidence of TBE in

Stockholm County. The geographic range of the ticks that transmit this disease extended northwards in Sweden during the 1980s and 1990s (Lindgren et al., 2000). The range of the ticks has also increased in altitude in the Czech Republic (Danielova, 1975), in association with a recent warming trend (Zeman, 1997). However, these interpretations have been contested, including in relation to climatic influences on the complex seasonal dependence of the three life-stages of the tick (Randolph and Rogers, 2000).

There has been much interest in whether or not recent regional warming in parts of eastern and southern Africa has been the cause of increases in malaria incidence in the highlands, or whether human influences (such as habitat alteration or drug-resistant pathogen strains) were responsible. For the moment, the evidence remains equivocal. Several studies have noted an increase in highland malaria in recent decades (Loevinsohn, 1994; Lindblade et al., 1999; Ndyomugyenyi and Magnussen, 2004), with some such increases occurring in association with local warming trends (Tulu, 1996; Bonora et al., 2001). Two studies concluded that there had been no statistically significant trends in climate in those same regions (Hay et al., 2002; Small et al., 2003), although the medium-resolution climate data (New et al., 1999) that were used in those two studies were subsequently deemed not well suited to research at this smaller geographical scale (Patz et al., 2002). A recent re-analysis of the study that found no evidence of a temperature effect, updated to the present from 1950 to 2002 for four high-altitude sites in East Africa where malaria has become a serious public health problem, found evidence for a significant warming trend at all sites (Pascual et al., 2006). It is most likely that the expansion of anti-malarial drug resistance and failed vector control programs, in addition to climate, are also important factors driving recent malaria expansions in these regions (Harvell et al., 2002).

Recent studies in China indicate that the increase in incidence of schis-tosomiasis over the past decade may incorporate an influence of the warming trend. The critical "freeze line" limits the survival of the intermediate host (Oncomelania water snails) and hence the transmission of the parasite Schistosomiasis japonica. This has moved northwards, and now an additional 20 million people are at risk of schistosomiasis (Yang et al., 2005).

Depending on the temperature preferences of pathogen and host, it is plausible to imagine that the season for proliferation of infections would expand or contract in future, with implications for the length of climate-sensitive infectious diseases. Donaldson (2006) and others have observed that the season associated with laboratory isolation of respiratory syncytial virus, and RSV-related emergency department admissions, now ends 3.1 and 2.5 weeks earlier, respectively, per 1°C increase in annual central England temperatures (P = 0.002 and 0.043, respectively). They conclude that climate change may be shortening the RSV season.

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