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 disease of ruminants caused by Bluetongue virus (BTV) and it is transmitted by biting midges. In sheep, clinical signs of BTV infection can include fever, vasodilation, swelling and, in severe cases, death, although the severity of symptoms varies with the breed of sheep, the individual animal and the strain of virus involved. Cattle are a major reservoir host for BTV infection, primarily because of the less obvious clinical signs in these animals. After an exhaustive search for a natural agent of transmission, Culicoides midges were shown to be the vectors for Bluetongue virus (Culicoides and the emergence of bluetongue virus in northern Europe. Trends Microbiol 2009 17(4): 172-178).

Although BTV infection was initially centred in Africa, the virus was first detected in Greece in 1989, from where it has spread steadily north. Since the disease is spread exclusively by insects, and because the virus is quite specific about which midge species can be used as vectors, predictions about the spread of the disease were based on known ranges of different midge species, which in turn depends on climate. However, midges can sometimes be carried over very long distances by weather systems, or by ships or aircraft.

Despite widespread speculation regarding the exact origin of BTV-8 as the strain of the virus found in northern Europe, no single convincing hypothesis has been proposed. Although future full-genome sequencing might assist this task (as was the case in the incursion of West Nile virus into North America), the small number of reference strains of BTV-8 from areas of potential origin collected before the incursion into northern Europe makes it unlikely that this approach will provide unambiguous evidence. As long as our understanding of the potential routes of virus introduction remains poor, we will be unable to accurately estimate the potential for future introductions of BTV, as has been illustrated by the more recent detection of BTV-6 in Europe, or of other midge-borne arboviruses, such as African horse sickness virus (AHSV).

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Although the technology to produce safe, effective, inactivated vaccines existed, no coordinated action was taken by any Member State of the European Union (EU) to begin production of a BTV-8 vaccine until late 2007, when the full damage began to become evident. This was in part due to the assumption that the virus would not overwinter under northern European conditions (despite the fact that BTV had been documented overwintering successfully in other areas with far cooler winter temperatures). In the absence of an available vaccine, knowledge concerning the entomology of the insects involved in BTV transmission became paramount.

The spread of BTV has provided a severe test of the way in which the movement of vector-borne pathogens is predicted, identified and controlled in Europe. There are many arobovirus diseases (spread by arthropod vectors such as midges, mosquitos and ticks), affecting human as well as animal health. Whether BTV represents a herald for future incursions by other arboviruses into Europe remains difficult to know. It is clear that there exists a similar potential for emergence of other insect-borne pathogens on grounds of climate alone, but where different vectors are used – for example, in the case of AHSV – the dynamics of the current BTV outbreak cannot easily be used to estimate risk. What has been shown by this outbreak is that arbovirus–vector relationships are highly dynamic and extremely difficult to combat. Unless regions that are potentially at risk of transmission are prepared to invest the resources required to provide adequate information regarding vectors and suitable control methods, this will remain the case.

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An international research team has found the first clear example of how climate extremes, such as increased frequency of droughts and floods expected with global warming, can create conditions in which diseases that are tolerated one at a time may converge and cause mass die-offs of livestock or wildlife. The study suggests that extreme climatic conditions are capable of altering normal host-pathogen relationships and causing a “perfect storm” of multiple infectious outbreaks that could trigger epidemics with catastrophic mortality. Led by scientists at the University of California, Davis, the University of Illinois, and the University of Minnesota, the research team examined outbreaks of canine distemper virus (CDV) in 1994 and 2001 that resulted in unusually high mortality of lions of Tanzania’s Serengeti National Park and Ngorongoro Crater. CDV cycles periodically within these ecosystems; numerous epidemics have occurred without decreasing lion populations. But the virus outbreaks of 1994 and 2001 were both preceded by extreme drought conditions, which led to debilitated populations of Cape buffalo, a major prey of lions. After the rains returned, the buffalo suffered heavy tick infestations, resulting in high levels of a tick-borne blood parasite in the lion population. (The parasites are normally present in lions at harmless levels.) The canine distemper virus further suppressed the lions’ immunity, which was already challenged by the high level of blood parasites. This allowed the tick-borne disease to reach fatally high levels, leading to mass die-offs of lions. In 1994, the number of lions in the Serengeti study area dropped by over 35 percent after the double infection. Similar losses occurred in the Crater die-off in 2001. Lion populations recovered quickly – within years after each event, but most climate change models predict increasing frequency of droughts in East Africa. The study illustrates how ecological factors can produce unprecedented mortality events and suggests that co-infections may lie at the heart of many of the most serious die-offs in nature.

Climate Extremes Promote Fatal Co-Infections during Canine Distemper Epidemics in African Lions. PLoS ONE 2008 3(6): e2545
Extreme climatic conditions may alter historic host-pathogen relationships and synchronize the temporal and spatial convergence of multiple infectious agents, triggering epidemics with far greater mortality than those due to single pathogens. Here we present the first data to clearly illustrate how climate extremes can promote a complex interplay between epidemic and endemic pathogens that are normally tolerated in isolation, but with co-infection, result in catastrophic mortality. A 1994 canine distemper virus (CDV) epidemic in Serengeti lions (Panthera leo) coincided with the death of a third of the population, and a second high-mortality CDV epidemic struck the nearby Ngorongoro Crater lion population in 2001. The extent of adult mortalities was unusual for CDV and prompted an investigation into contributing factors. Serological analyses indicated that at least five “silent” CDV epidemics swept through the same two lion populations between 1976 and 2006 without clinical signs or measurable mortality, indicating that CDV was not necessarily fatal. Clinical and pathology findings suggested that hemoparsitism was a major contributing factor during fatal epidemics. Using quantitative realtime PCR, we measured the magnitude of hemoparasite infections in these populations over 22 years and demonstrated significantly higher levels of Babesia during the 1994 and 2001 epidemics. Babesia levels correlated with mortalities and extent of CDV exposure within prides. The common event preceding the two high mortality CDV outbreaks was extreme drought conditions with wide-spread herbivore die-offs, most notably of Cape buffalo (Syncerus caffer). As a consequence of high tick numbers after the resumption of rains and heavy tick infestations of starving buffalo, the lions were infected by unusually high numbers of Babesia, infections that were magnified by the immunosuppressive effects of coincident CDV, leading to unprecedented mortality. Such mass mortality events may become increasingly common if climate extremes disrupt historic stable relationships between co-existing pathogens and their susceptible hosts.

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The Past:
Plague has given rise to at least three major pandemics. The first (the Justinian plague) spread around the Mediterranean Sea in the 6th century AD, the second (the Black Death) started in Europe in the 14th century and recurred intermittently for more than 300 years, and the third started in China during the middle of the 19th century and spread throughout the world. Purportedly, each pandemic was caused by a different biovar of Yersinia pestis, respectively, Antiqua (still found in Africa and Central Asia), Medievalis (currently limited to Central Asia), and Orientalis (almost worldwide in its distribution).

The Present:
Given this history, plague is often classified as a problem of the past. However, it remains a current threat in many parts of the world, particularly in Africa, where both the number of cases and the number of countries reporting plague have increased during recent decades. Following the reappearance of plague during the 1990s in several countries, plague has been categorised as a re-emerging disease.

The Future:
Plague cannot be eradicated, since it is widespread in wildlife rodent reservoirs. Hence, there is a critical need to understand how human risks are affected by the dynamics of these wildlife reservoirs. For example, the likelihood of a plague outbreak in North American and Central Asian rodents, and the resulting risk to humans, is known to be affected by climate. Recent analysis of data from Kazakhstan shows that warmer springs and wetter summers increase the prevalence of plague in its main host, the great gerbil. Such environmental conditions also seem to have prevailed during the emergence of the Second and Third Pandemics – conditions that might become more common in the future.
Plague may not match the so-called “big three” diseases (malaria, HIV/AIDS, tuberculosis; see for example) in numbers of current cases, but it far exceeds them in pathogenicity and rapid spread under the right conditions. It is easy to forget plague in the 21st century, seeing it as a historical curiosity. But in our opinion, plague should not be relegated to the sidelines. It remains a poorly understood threat that we cannot afford to ignore.

Plague: Past, Present, and Future. 2008 PLoS Med 5(1): e3

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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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In 2006, over 2000 cases of bluetongue were recorded in northern Europe. The disease, which has been more typically associated with Mediterranean areas, is believed to have become established hundreds of kilometres to the north of its traditional area, probably as a consequence of the hottest summer/autumn period since records began. In this special article, John Gloster and colleagues describe the meteorological conditions surrounding the 2006 outbreak, and investigate the possibility of bluetongue virus (BTV) spreading on the wind to the UK in 2007. For this to happen there would need to be a source of windborne virus, together with a susceptible population of ruminants in the vicinity of the coast. Evidence from outbreaks in the Mediterranean Basin suggests that long-distance transport of BTV-infected vectors has already occurred, at least in that region. The overall likelihood of this occurring in northern Europe depends critically on whether the virus overwinters on the near continent; this will not be known until around May 2007. The 2006 outbreak has highlighted the importance of understanding the impact of climate change on animal disease.

Will bluetongue come on the wind to the United Kingdom in 2007?
Vet Rec. 2007 160: 422-426