Changes in human diseases or epidemiological transitions have always occurred during shifts in human social organisations and many scientists propose that we are about to enter another as a result of globalisation and ecological disruption (mcMichael 2001). Habitat complexity influences the composition, abundance and distribution of animals that play a role in the transmission cycles of many common human infectious diseases such as malaria and schistosomiasis. As a result, habitat and biodiversity loss influences transmission cycles by affecting the abundance, behaviour and condition of hosts or vectors (Keesing 2010).

Biodiversity affects the abundance of the host or vector organisms involved in disease transmission. For example, plants growing in experimental fields not hosts for fungal pathogens decreased the pathogen load of species that are hosts by reducing host density through competition (Mitchell 2002). 

Furthermore, the behaviour of host, vectors and parasites can change as a result of biodiversity loss affecting rates of transmission and prevalence in human populations. In more diverse habitats, a parasite is more likely to end up in an unsuitable intermediate host reducing the probability of infecting a human. This was demonstrated by studies on parasitic worms that cause schistosomiasis (Laracuente 1979).

Finally, biodiversity loss and human led habitat alteration clearly involves changing conditions. This can lead to increased encounter rates between pathogens and hosts when the host species has not undergone declines.  Furthermore, another plant study comparing genetically diverse and non diverse experimental fields found that those growing in species rich conditions had dryer leaves as a result of changes in microclimatic conditions and as a result had lower prevalence of a fungus. (Keesing 2010)

As ecosystem health and transmission processes are so nuanced, it is difficult to separate individual mechanisms to find direct cause and effect. Clearer patterns emerge when considering different infectious diseases independently. Malaria, one of the most damaging infectious diseases, resulting in 1 million deaths in 2007 alone is caused by one of four Plasmodium species via the female anopheles mosquito. Habitat alteration, particularly deforestation, is having a huge influence on transmission rates. Deforestation acts to raise surface water availability through the formation of puddles and pools that act as new breeding sites for the mosquito. Furthermore, microclimates as mentioned above are also affected. Larvas may be exposed to greater sunlight raising temperatures which cause mosquitos to digest more quickly so feed more often and lay more eggs. Higher temperatures affect the adult mosquito by reducing development time. In addition to this human factors clearly play a great role. Globalisation changes migration patterns and leads to the emigration of non immune individuals into high malaria risk areas affecting incidence and transmission (Pongsiri et al 2009).

As the links between ecosystems, biodiversity and disease occupy varying temporal and spatial realms and across political boundaries nuanced research is needed.  Furthermore, this is a relatively new field of study so there is far more to be discovered. Policy informed by this evidence can then be formulated that acts to preserve both human life and local and global habitats. 

Sources:

Keesing et al. 2010. Impacts of biodiversity on the emergence and transmission of infectious disease. Nature. Vol 468 (7324). pp 647- 652.  

Laracuente, A. 1979. Comparison of four species of snails as

potential decoys to intercept schistosome miracidia. Am. J. Trop. Med. Hyg. Vol 28. pp

99–105

McMichael, A. 2002. Population, environment, disease and survival: past patterns, uncertain futures. The Lancet. Vol 359. pp 1145-1148. 

Mitchell, C et al. 2002. Effects of grassland plant species diversity, abundance, and composition on foliar fungal disease. Ecology. Vol 83. pp1713–1726

Pongsiri et al. 2009. Biodiversity loss affects global biodiversity. Bioscience. Vol 59(11). pp 945-954.