MicrobiologyBytes

Aedes (Stegomyia) aegypti (Linneaus) is an important vector of dengue and other arboviruses. Despite its limited flight dispersal capability, its close association with humans and its desiccation-resistant eggs have facilitated many long distance dispersal events within and between continents, allowing it to expand its range globally from its origin in Africa. Its global emergence and resurgence can be attributed to factors including urbanisation, transportation, changes in human movement, and behaviour, resulting in dengue running second to malaria in terms of human morbidity and mortality. Global historical collections and laboratory experiments on this well studied vector have suggested its distribution is limited by the 10°C winter isotherm, while a more recent and complex stochastic population dynamics model analysis suggests the temperature’s limiting value to be more towards the 15°C yearly isotherm. While historical surveys in Australia have indicated that Ae. aegypti occurred over much of the continent, its range has receded from Western Australia, the Northern Territory and New South Wales (NSW) over the last 50 years. It is now only found in Queensland, although recent incursions into the Northern Territory have required costly eradication strategies. The significant reduction in vector distribution has been attributed to a combination of events including the introduction of reticulated water, which reduced the domestic water storage requirements of households that had provided stable larval sites, as well as the removal of the railway-based water storage containers hypothesised as being responsible for the long distance dispersal.

“Drought-proofing” Australia’s urban regions by installing large domestic water tanks may enable the dengue mosquito Ae. aegypti to regain its foothold across the country and expand its range of possible infections. A new paper challenges the common assumption that climate change will drive the spread of this mosquito, suggesting instead that the real driver is human behavior. The study combines current and forecasted climate change conditions with historical epidemics to reveal the risk of dengue infections in all capital cities around Australia by 2050. Researchers developed and critically assessed their models to project the distribution of the mosquito in 2030 and 2050. Currently, dengue fever occurs in Queensland only. However, the implementation of new water tanks, combined with already warm summer temperatures, could enable the mosquito to re-emerge and further its current reach. Dengue risks will not be driven directly by warmer temperatures or changes in rainfall patterns. Australian summers already provide ideal conditions for dengue transmission around the country, but the introduction of government-subsidized water storage devices now adds the ideal breeding ground for the dengue mosquito to re-emerge. While research is properly focused on the impact of anthropogenic climate change, this study highlights the need to look also at our responses to those changes and the outcomes they generate. The current dengue fever epidemic in far north Queensland is approaching 1,000 reported cases over the summer of 2008-2009.

Australia’s Dengue Risk Driven by Human Adaptation to Climate Change. 2009 PLoS Negl Trop Dis 3(5): e429
The reduced rainfall in southeast Australia has placed this region’s urban and rural communities on escalating water restrictions, with anthropogenic climate change forecasts suggesting that this drying trend will continue. To mitigate the stress this may place on domestic water supply, governments have encouraged the installation of large domestic water tanks in towns and cities throughout this region. These prospective stable mosquito larval sites create the possibility of the reintroduction of Ae. aegypti from Queensland, where it remains endemic, back into New South Wales and other populated centres in Australia, along with the associated emerging and re-emerging dengue risk if the virus was to be introduced. Having collated the known distribution of Ae. aegypti in Australia, we built distributional models using a genetic algorithm to project Ae. aegypti’s distribution under today’s climate and under climate change scenarios for 2030 and 2050 and compared the outputs to published theoretical temperature limits. Incongruence identified between the models and theoretical temperature limits highlighted the difficulty of using point occurrence data to study a species whose distribution is mediated more by human activity than by climate. Synthesis of this data with dengue transmission climate limits in Australia derived from historical dengue epidemics suggested that a proliferation of domestic water storage tanks in Australia could result in another range expansion of Ae. aegypti which would present a risk of dengue transmission in most major cities during their warm summer months. In the debate of the role climate change will play in the future range of dengue in Australia, we conclude that the increased risk of an Ae. aegypti range expansion in Australia would be due not directly to climate change but rather to human adaptation to the current and forecasted regional drying through the installation of large domestic water storing containers. The expansion of this efficient dengue vector presents both an emerging and re-emerging disease risk to Australia. Therefore, if the installation and maintenance of domestic water storage tanks is not tightly controlled, Ae. aegypti could expand its range again and cohabit with the majority of Australia’s population, presenting a high potential dengue transmission risk during warm summers.

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Bluetongue is a highly infectious virus disease of ruminants. Cattle and goats are major hosts of the virus, but in these species infection is usually asymptomatic despite high virus levels, allowing the disease to circulate in the absence of any symptoms. Sheep and deer are usually the only species to exhibit symptoms of infection. Bluetongue infections are marked by a high fever, excessive salivation, swelling of the face and tongue and cyanosis of the lips and tongue (turning blue). Infected animals become lame and listless. Ulcers appear around the mouth, nose and eyes. Then the neck may start to swell, followed by the head. The animal becomes lame, starts bleeding internally and breathing becomes difficult. The incubation period for bluetongue is 5-20 days. The mortality rate is normally low, but infected animals lose condition and there is a high mortality rate of 70% or more in susceptible breeds of sheep (due to secondary bacterial infections). While infected animals can recover, productivity is reduced with milk yields in dairy herds dropping by about 40%.

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Bluetongue virus (BTV) is a Reovirus of the genus Orbivirus. The virus is transmitted by midges, in particular Culicoides imicola and a few other species. Of more than 1,400 species of midges known world-wide, only around 20 culicoid species are known to be involved in transmission of bluetongue virus. Bluetongue can also be transmitted directly from one animal to another through semen and transplacentally. Bluetongue occurs in Australia, the USA, Africa, the Middle East, Asia and Europe, generally between latitudes 35°S and 50°N. It occurs around the Mediterranean in summer, subsiding when temperatures drop in winter. In Europe the disease has been spreading north since October 1998, possibly as a result of climate change. In August 2006 bluetongue spread to the Netherlands, then Belgium, Germany, Holland, and Luxembourg. The first ever case of bluetongue in the UK was reported in Suffolk on 23rd September 2007. On 28th September 2007 Defra confirmed that bluetongue is now endemic in the UK.

Unlike foot and mouth disease, bluetongue cannot be controlled by culling of infected livestock alone. Since midges form a reservoir of infection in endemic areas, you would also need to kill all the midges to eradicate the disease. Another complication is there are at least 24 distinct serotypes of the virus (based on the lack of cross neutralisation). Vaccination against one serotype does not usually confer protection against any of the other serotypes. The antigenic diversity of Bluetongue virus is due to both antigenic drift (accumulation of point mutations) and antigenic shift (reassortment of individual gene segments). The virus which has affected northern Europe and the UK is known as BTV8.

Live attenuated BTV vaccines containing a weakened form of the live virus are cheap, easy to produce and can be administered in a single dose. They are effective in controlling clinical outbreaks of bluetongue. However, the disadvantages of attenuated BTV vaccines are:

• Risk of reassortment with virulent wild viruses which potentially could give rise to new virulent strains.
• Potential for reversion to virulence both in the vertebrate host and in vector insects.
• Attenuated BTV can cross the placenta and pregnant ruminants vaccinated with attenuated vaccines may suffer foetal loss.
• Existing vaccines are designed for sheep; there is little data on their safety and effectiveness in other species.

There have been attempts to develop inactivated (killed) whole virus vaccines for BTV for the past 25 years, but none have yet been produced commercially. Inactivated vaccines are they more expensive to produce than attenuated vaccines and also require at least two doses with an adjuvant to generate a protective immune response. Bluetongue virus is not usually contagious for humans, and meat and dairy products pose no hazard. However, there is some concern over the potential spread via blood from infected people.

Bluetongue: Latest News

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• Will bluetongue come to the UK on the wind in 2007?
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