Bluetongue Disease And The Link To Climate Change Biology Essay

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Bluetongue (BT), also known as sore mouth, soremuzzle or ovine catarrhal fever, is a serious disease of ruminants caused by bluetongue virus (BTV). Although the virus has the capacity to replicate in virtually all ruminants, the severe form of the disease is restricted to particular sheep breeds, especially "fine wool and mutton breeds that are common in Europe" (Purse et al, 2005). The disease has far reaching socioeconomic implications - directly, BT causes severe morbidity and mortality in sheep, particularly lambs. Furthermore, BT indirectly interrupts trade in ruminants, ruminant products and associated germ plasm. In the United States alone, annual economic loss from BT is estimated to reach US$125 million (Purse et al, 2005), and globally has been estimated at US$3 billion (Tabachnik et al, 1996). Historically, BT has been restricted to eastern and southern Africa, parts of Asia and the European Mediterranean fringe, primarily due to the geographical range of BTVs traditional Afro-Asian vector, the biting midge Culicoides imicola. Recently however, the disease has been reported some 800km further north in Europe than ever before (Purse et al, 2005), and it has been hypothesised that climate change in Europe is a primary driver of this spread. This essay will summarise the main arguments for this case, and posit potential future research that could use this essay for inspiration.

Bluetongue virus and bluetongue disease

Bluetongue virus (BTV) is the Orbovirus type species of the family Reoviridae, and exists as 24 distinct serotypes (Mellor et al, 2008) and multiple infectious strains. The disease caused by BTV, bluetongue (BT), is a clinical infection of certain ruminant species, most notably sheep, and presents with "fever, erosions, crusting and cyanosis around the mouth, oedema of head and neck, sometimes pulmonary oedema and lameness due to involvement of hooves and to muscle damage" (Andrews et al, 1978). Mortality from BT varies by area between 5% and 30% (Andrews et al, 1978). Current research suggests the disease has caused the deaths of over 1.5 million sheep since 1998 (Purse et al, 2007), as well as the socioeconomic damage mentioned previously.

Pathogenically, BTV serotypes differ greatly in virulence, and affect ruminants with varying intensity of clinical signs. The most virulent strains can seriously affect other ruminants aside from sheep, such as cattle, goats, yak and some species of deer (Mellor et al, 2008). Less virulent strains can cause subclinical infection, particularly in cattle which can experience prolonged viraemia of the virus for up to 100 days after first exposure (Purse et al, 2005). The majority of transmission of BTV therefore occurs 'silently' from inapparently-infected BTV-resistant animals, who act as significant reservoirs for the virus. Interestingly, BTV has high genetic diversity due primarily to both drift and shift mutations, so "pathogenicity even within a serotype may be highly variable" (Saegerman et al, 2008). Currently, out of 24 BTV serotypes, 1, 2, 3, 4, 6 and 10 are recognised to be the most pathogenic and to have the greatest epidemic potential (Dungu et al, 2004).

The disease has historically been endemic to sub-Saharan Africa and Asia, but has been identified in the southern and western United States in white-tailed deer and other wild ruminants. It was first observed in the US in 1948 (Hardy and Price, 1952, cited by Andrews et al, 1978) but may have gone unrecognized before this.

Historic BT vectors and BTV epidemiology

The vast majority of BTV transmission is through vector species, specifically certain species of nocturnal biting midge of the genus Culicoides (research has also incriminated the sheep ked Melophagus ovinus in BTVs transmission, although it remains unclear whether virus multiplication takes place inside this vector i.e transmission is mechanical, not biological [Luedke et al, 1965]). Less than 1% of Culicoides species are competent vectors for BTV (Purse et al, 2005), and consequently the virus and thus disease are constrained to habitats where these species occur. Historically, this was "the tropical and subtropical parts of the world, between latitudes 35°S and 40°N" (Purse et al, 2005) - see figure 1 for more details.

Fig. 1 - map showing the current global distribution of BTV and Culicoides vector species. Adapted from Purse et al, 2005.

In the Old World the traditional vector for BTV is Culicoides imicola, and is usually restriced to sub-Saharan Africa parts of Asia. BT has thus historically been restricted to these Old World locales, reflecting Culicoides distributions and the temperature necessary for BTV replication inside its vector. However, since C. imicola is a weak flyer, passive dispersal from wind over distances of hundred of kilometres is a realistic possibility, especially over large areas of water such as the Mediterranean where wind speed is generally higher than on land (Sellers, 1992). This, coupled with ongoing livestock trade through traditional routes such as the 'Ruminant Street', which connects Afghanistan, Iran and Pakistan to southern Europe through Turkey, has meant that several serotypes of BTV have been scattered around the southern fringe of Europe, particularly the Greek Islands and Turkey, since the 1970s (Mellor et al, 2008). Countries where C. imicola currently occurs are highlighted in dark-green in figure 1.

Culicoides/BTV and climate change

3.1) European climate change

By and large, mean daily temperatures across the European region increased by approximately 1.2°C between 1900 and 2000 - see figure 2. The effect of this warming is more intensive at night and in winter (Klein Tank and Konnen, 2003). In addition, between 1946 and 1999, European mean annual precipitation also increased, although this was localised to northern alpine regions of Europe (Klein Tank and Konnen, 2003).

Fig. 2 - graph showing the observed annual temperature deviations across the European region over 150 years compared with the 1961-1990 European average (°C). Superimposed is the 10-year trend of these averages in dark pink. Adapted from Purse et al, 2005.

3.2) Sensitivity of Culicoides/BTV to climate change - temperature

Temperature has a pronounced effect on Culicoides life cycles. Survival rates of both larvae and adults over winter are increased by higher winter temperatures, an effect of climate change mentioned previously (Klein Tank and Konnen, 2003), and this naturally enhances recruitment of the vector to adult populations.

Increased temperature also has a direct influence on vector competence and virogenesis rates within adult vectors - "this is partly because in vitro synthesis (which is dependent on the activity of the RNA-dependent RNA polymerase) is optimal at 28-29°C, but is inhibited below 10°C" (Van Dijk and Huismans, 1982).

Temperature may also affect heritable mechanisms in Culicoides vectors that would otherwise limit the dissemination of

3.3) Sensitivity of Culicoides/BTV to climate change - precipitation

3.4) Current BTV occurrence in Europe

History of change of BT in Europe - then Implications for climate change on bluetongue vectors, sensitivity of BTV to climate change - split into 3 areas as per Beth 05 - extending distributions/climatic envelopes, involvement of novel vectors as per para 2, over-wintering of BTV in cool regions (Takamatsu et al, 2003)

Changing patterns of BTV in Europe

Implications for future research, Culicoides also in African Horse sickness. emergence of other vector borne pathogens, effective risk management of bluetongue and other diseases - bring in my thesis question in all its glory