Climaterelated human behavior and infectious disease occurrence

In addition to the direct influence of climate on pathogen proliferation and the lifecycles of vectors and intermediate hosts, climatic conditions can also affect infectious disease transmission indirectly by changing human physiology or behavior. For example, a child's susceptibility to respiratory syncytial virus infection may be increased if there is an alteration in the mucociliary activity of the respiratory epithelium or mucosa thickness. This has been hypothesized to occur in response to increasing dryness and cold (Chan et al., 2002). Another example is cerebrospinal meningitis, which typically occurs world-wide in seasons and regions of low absolute humidity (Besancenot et al., 1997). The natural habitat of the meningococcus is the throat, the lining of which is likely to deteriorate in susceptible people during periods of low humidity.

These relationships may, at least partly, be explained by seasonally-related change in patterns of children's play and person-to-person contact (see also Chapter 6). Children who spend more time indoors in cold weather may inadvertently increase their exposure to indoor air pollutants, such as tobacco smoke, smoke from wood fires, and nitrogen dioxide emitted from un-flued gas heaters, depending on the amount of ventilation, which could confound the association between infections and cold temperatures (Jones, 1998).

Prolonged close proximity to other infectious children can increase the opportunity for transmission of infectious agents (Sennerstam and Moberg, 2004). The well-known seasonality of influenza in elderly people, with epidemic outbreaks occurring in winter, has generally been attributed to indoor crowded conditions. The strong inverse association between cases of pneumococcal disease and temperature (with peaks in midwinter and troughs in midsummer) may relate to the coincident high concentration of circulating viruses in winter (such as respiratory syncytial virus, influenza virus, and adenovirus). Infection with such viruses predisposes to otitis media, which becomes suppurative and leads to pneumo-coccal bacteremia or meningitis (Kim et al., 1996).

However, social behaviors, and, in particular, increased contact with other people, cannot explain all variations and outbreaks of infectious diseases. For example, several studies have found that the time-pattern of respiratory syncytial virus epidemics is not consistent with increased social contact among children during school time. Meanwhile, there is increasing evidence that infectious disease emergence, reactivation, and spread reflect the various large-scale environmental changes that are now arising in response to the burgeoning human pressures on the world's environment. Widespread deforestation, other land-use changes, water-damming and irrigation, biodiversity losses that occur because of those and other reasons, more intensive and extensive trading patterns, and increased human crowding (especially in peri-urban shanty towns and slums) are all likely to influence patterns of infectious disease occurrence. As humans encroach further into previously uncultivated environments, new contacts between wild fauna, insect vectors, and humans and their livestock increase the risk of cross-species infection.

The recent emergence of the Nipah virus, a highly virulent paramyxovirus, as a human-infecting pathogen illustrates the interplay between social, behavioral, and environmental influences in generating a new circumstance for infectious disease emergence - in this case, more specifically, the interplay between climatic conditions, deforestation, wild species disturbances, and intensive livestock production (Chua et al., 2002; Chua, 2003; Weiss and McMichael, 2004). The first recorded Nipah virus outbreak followed the establishment of commercial piggeries in conjunction with fruit orchards located close to the tropical forest in northern Malaysia. The causal constellation underlying this emergent infectious disease remains uncertain, and almost certainly complex. The following are likely components. During the 1980s and 1990s, the forest habitat of the local fruit bats (Pteropus species - the natural host of the virus) had been reduced by deforestation for pulpwood and industrial plantation. Then, in 1997-1998, slash-and-burn deforestation escalated and resulted in the formation of a severe haze that blanketed much of the region. This was exacerbated by a drought and associated forest fires, driven by a severe El NiƱo event in the same year (see Box 14.4). Forest fruit yields declined, and hungry food-seeking bats encroached into cultivated fruit orchards. Pigs are thought to have been infected via the eating of shared fruits (and bat droppings), and this new mammalian host then infected the pig farmers. This zoonosis ultimately infected several hundred Malaysian rural workers, causing a fatal encephalitic disease in approximately half of them (Daszak et al., 2000, 2006).

0 0

Post a comment