Box 143 Complex transmission cycles Ross River virus

The epidemiology of Ross River virus (RRv) disease illustrates the varying effect of climatic phenomena on a complex infectious disease transmission cycle. RRv disease is the most prevalent vector-borne disease in Australia, and has also been reported in several Pacific island countries. The virus causes a non-fatal epidemic polyarthritis, with arthritic symptoms that range from mild to severe and debilitating, and which can last several years in some people. There is no cure, and treatment is palliative.

The disease is caused by an alphavirus that can be transmitted by more than 30 different mosquito species. Mosquitoes such as Ochlerotatus camp-torhynchus and O. vigilax breed in inter-tidal wetlands, and are the main vectors in coastal regions. Culex annulirostris is the main inland vector: it breeds in vegetated fresh water, and is common in both tropical and temperate regions that are subject to flooding or irrigation during summer. Other species, such as O. notoscriptus, are important vectors in semi-rural and urban areas. The main natural vertebrate hosts for the virus are marsupials (kangaroos and wallabies), with other animals also implicated (notably possums and horses).

The primary enzootic cycle of the virus is between the non-immune reservoir host and a mosquito vector. When immunity in the host population is low, and climatic conditions are suitable, massive amplification of the virus occurs in the host and mosquito populations. In this situation the abundance of mosquitoes typically results in transmission of the virus to humans, when infected mosquitoes are forced to seek blood meals outside their natural targets. Changes in climate strongly influence the replication of this virus (Kay and Aaskov, 1989), the breeding, abundance and survival of the mosquito vectors (Lee et al., 1989), and the breeding cycle of the natural hosts (Caughley et al., 1987). The epidemiology of the disease reflects this, with different seasonal and inter-annual patterns being observed between the broad climatic regions of the Australian continent (Russell, 1994; Tong and Hu, 2001; Woodruff, 2005). In the northern tropical region the disease is endemic, and cases occur in most months of every year. In the southern temperate and inland arid parts of the country the pattern is sporadic, with wide variation between years in the number of reported cases.

RRv disease is one of the few infectious diseases that can be predicted by climate-based early warning systems (WHO, 2004). Weather conditions at relatively coarse temporal and spatial resolutions have been used to predict epidemics with sufficient accuracy and advance notice for public health planning. In the dry temperate south-eastern part of the country, Woodruff and colleagues have shown that sustained winter/spring rainfall (i.e. the total number of rain days) and warm late spring temperatures, in conjunction with low rainfall in the spring of the preceding year, increased the risk of summertime RRv epidemics (Woodruff et al., 2002). They speculated there are two linked mechanisms that lead to epidemic potential in this region. First, flood-water Aedes species maintain the natural cycle of the virus by transovarial transmission through embryonated eggs (Lindsay et al., 1993). These mosquitoes "overwinter" as drought-resistant eggs in mud flats and creek beds (Marshall, 1979). After heavy winter rainfall, the females emerge and infect the vertebrate hosts (Lindsay et al., 1993). Substantial rainfall from late winter enables early and prolific breeding of Aedes populations and an extended period of virus build-up, thus increasing the transmission potential. The period of prolonged heavy rainfall also acts to raise the water table across this flat region, reducing absorption and runoff. As a consequence, pools of water remain on the ground into summer (even if there is low summer rainfall). This provides breeding sites for the summer breeding Culex mosquitoes, which preferentially bite both humans and kangaroos - thus extending the infection beyond the natural cycle to humans.

The second mechanism relates to rainfall in the spring of the year before an epidemic, and to its role in host-virus population dynamics. High spring rainfall supports large numbers of mosquitoes. When this occurs, a greater proportion of kangaroo hosts become infected (the period of viraemia lasting about one week) and then immune for life. This results in a reduction in the pool of susceptible kangaroos in the following year, and consequently minimal viral amplification and a lower probability of human cases. Conversely, several years of low spring rainfall dramatically raises the proportion of susceptible kangaroos so that in subsequent years - if climatic conditions are suitable - the probability of a large outbreak becomes very high.

sequence of climatic and ecological changes that created optimum conditions for the proliferation and spread of the virus (Engelthaler et al., 1999). Six preceding years of drought appear to have reduced the populations of natural predators -birds and snakes, in particular - of the white-footed mouse, which naturally harbors the virus. In early 1993, heavy rainfall resulted in an abundance of pinon nuts and grasshoppers upon which rodents feed. The resulting rapid expansion of the mouse population caused a huge increase in the amount of mouse-excreted virus entering the local environment, drying, and then blowing around in the wind. Human exposure increased greatly, and the apparently first-ever outbreak of hantavirus pulmonary syndrome occurred in North America.

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