Difference between revisions of "Bluetongue Virus"

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Also known as: '''''BTV — Bluetongue
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{{unfinished}}
  
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==Introduction==
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==Description==
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Bluetongue is a non-contagious, [[:Category:Arthropods|arthropod]]-borne disease of ruminants, caused by bluetongue virus (BTV). The clinical severity of disease is variable, but is characterised by inflammation of mucous membranes, haemorrhages and oedema<sup>1</sup>. Although cattle are the main reservoir of infection, sheep are more severely affected and can suffer a cyanotic tongue, lending the disease name. The virus has been isolated from hosts and vectors on all continents (excluding Antartica)<sup>2</sup>, despite being initially recognised in Africa in the late 19th and early 20th centuries<sup>3</sup>. Originally thought to be a disease of tropical and sub-tropical regions, bluetongue has shown a propensity to become established in temperate areas, and in recent years has spread North, through the Mediterranean Basin, to become endemic in many European countries including the UK. Although BTV's transmission and epidemiology is dependent on insect vectors, bluetongue greatly influences the global trade of ruminants as it is included on the Office International des Epizooties List A of animal diseases<sup>4</sup>.
 
  
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==Virus Characteristics==
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Bluetongue is a non-contagious, arthropod-borne disease of ruminants, caused by bluetongue virus (BTV). The clinical severity of disease is variable, but is characterised by inflammation of mucous membranes, haemorrhages and oedema<sup>1</sup>. Although cattle are the main reservoir of infection, sheep are more severely affected and often suffer a cyanotic tongue, lending the disease its name. The virus has been isolated from hosts and vectors on all continents(excluding Antartica)<sup>2</sup>, despite being initially recognised in Africa in the late 19th and early 20th centuries<sup>3</sup>. Originally thought to be a disease of tropical and sub-tropical regions, bluetongue has shown a propensity to become established in temperate areas, and in recent years has spread North, through the Mediterranean Basin, to become endemic in many European countries including the UK. Although BTV's transmission and epidemiology is dependent on insect vectors, bluetongue greatly influences the global trade of ruminants as it is included on the Office International des Epizooties List A of animal diseases<sup>4</sup>.
 +
 
 +
==Aetiology==
 
[[Image:Bluetongue Virus.gif|thumb|right|150px|Bluetongue virus particle. Source: Wikimedia Commons; Author: CDC (2007)]]
 
[[Image:Bluetongue Virus.gif|thumb|right|150px|Bluetongue virus particle. Source: Wikimedia Commons; Author: CDC (2007)]]
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Bluetongue virus is a species of the genus Orbivirus, within the [[:Category:Reoviridae|Reoviridae]] family. The Reoviridae are non-enveloped and possess a double-stranded RNA genome contained in an outer-shelled icosohedral capsid. The BTV genome is arranged into 10 segments and encodes 7 structural and 4 non-structural viral proteins<sup>2</sup>. The BTV receptor is currently unknown, but is proposed to included sialic acid and junctional adhesion molecules. After interaction with this receptor, the virus enters an endolysosome where the capsid is partially digested to allow the genome into the cell. Replication begins at this partially uncoated stage since the virus particles contain all the necessary enzymes<sup>5</sup>. First, the dsRNA is transcribed to form positive sense RNA, of which some is delivered to cytoplasm for ribosomal translation and the remainder is packaged into partially assembled virions. Complementary negative sense RNA is then formed in the virions, to give a dsRNA genome. Complete virus particles are released from the cell.
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Bluetongue virus is a species of the genus Orbivirus, within the Reoviridae family. The Reoviridae are non-enveloped and possess a double-stranded RNA genome contained in an outer-shelled icosohedral capsid. The BTV genome is arranged into 10 segments and encodes 7 structural and 4 non-structural viral proteins<sup>2</sup>. The BTV receptor is currently unknown, but is proposed to included sialic acid and junctional adhesion molecules. After interaction with this receptor, the virus enters an endolysosome where the capsid is partially digested to allow the genome into the cell. Replication begins at this partially uncoated stage since the virus particles contain all the necessary enzymes<sup>5</sup>. First, the dsRNA is transcribed to form positive sense RNA, of which some is delivered to cytoplasm for ribosomal translation and the remainder is packaged into partially assembled virions. Complementary negative sense RNA is then formed in the virions, to give a dsRNA genome. Complete virus particles are released from the cell.
  
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All BTVs share group antigens, which can be demonstrated by agar gel diffusion tests, fluorescent antibody tests and the group
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All BTV’s share group antigens, which can be demonstrated by agar gel diffusion tests, fluorescent antibody tests and the group
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reactive [[ELISA testing|ELISA]]<sup>1</sup>. There are 24 distinct serotypes, which are distinguished by epitopes on the outer capsid protein VP2<sup>4</sup>, encoded by L2, the only serotype-specific BTV gene. Serotypes are differentiated using serum neutralisation tests, although there is some degree of cross-reactivity between serotypes<sup>1</sup>. Numerous strains of bluetongue virus also exist, and these are characterised by molecular analysis.
+
reactive ELISA<sup>1</sup>. There are 24 distinct serotypes, which are are distinguished by epitopes on the outer capsid protein VP2<sup>2</sup>, encoded by L2, the only serotype-specific BTV gene. Serotypes are differentiated using serum neutralisation tests, although there is some degree of cross-reactivity between serotypes<sup>1</sup>. Numerous strains of bluetongue virus also exist, and these are characterised by molecular analysis.
  
 
==Hosts==
 
==Hosts==
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All ruminants are susceptible to bluetongue virus infection, including sheep, goats, cattle, deer, buffaloes, camels and antelopes. Sheep are most severely affected, and disease is occasionally seen in goats. Although cattle BTV infection is significant in the epidemiology of disease, the condition is generally subclinical in this host. Mortalities in white-tailed deer due to bluetongue have been reported in the USA<sup>1</sup>.
 
  
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Pigs and horses do not become infected with BTV, but may act as a food source for the [[Ceratopogonidae|''Culicoides'']] midges that transmit bluetongue virus to ruminants. Their habitats may also provide areas suitable for vector breeding.
+
All ruminants are susceptible to bluetongue virus  infection, including sheep, goats, cattle, deer, buffaloes, camels and antelopes. Sheep are most severely affected, and disease is occasionally seen in goats. Although cattle BTV infection is significant in the epidemiology of disease, the condition is generally subclinical in this host. Mortalities in white-tailed deer due to bluetongue<sup>1</sup>.
 +
 
 +
Pigs and horses do not become infected with BTV, but may act as a food source for the Culicoides midges that transmit bluetongue virus to ruminants. Their habitats may also provide areas suitable for vector breeding.
  
 
==Transmission and Epidemiology==
 
==Transmission and Epidemiology==
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BTV is transmitted by biting insects. Although vertical and venereal transmission between ruminant hosts can occur, it is insignificant in the overall epidemiology of bluetongue.
 
  
 
===Vectors===
 
===Vectors===
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The arthropod vector for bluetongue virus is the [[Ceratopogonidae|''Culicoides'']] biting midge. These are biological vectors of BTV, so the virus replicates in insect tissue after feeding on an infected host<sup>6</sup>. It takes 10-14 days for the virus to disseminated from the insect's gut to its salivary glands, after which bluetongue virus may be transmitted to a new, susceptible ruminant host. This incubation period may be reduced when ambient temperatures are higher<sup>2</sup> and once infected, midges maintain BTV infection for life.
 
  
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Classically, the major vector for BTV is ''Culicoides imicola''. This midge is found throughout Africa, the
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The arthropd vector for bluetongue virus is the ''Culicoides'' biting midge. These insects take blood meals from vertebrate host and breed in damp, dung-enriched soil enriched, and so are abdunant in the vicinity of domestic livestock. The activity of ''Culicoides'' varies with the time of day: the midges are most active at night, from an hour before sunset to an hour after sunrise. Activity is decreased by windy conditions, and increased during the day when the weather is dull. ''Culicoides'' generally avoid entering buildings and other closed spaces.
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Middle East, southern Asia, Portugal, Greece, Corsica, Sardinia, Sicily and areas of Italy<sup>1</sup>, and its distribution appears to be extending northwards. However, ''C. imicola'' has not yet been demonstrated in the United Kingdom.  
+
 
 +
3.2 Culicoides species have a normal insect complete metamorphosis life cycle –
 +
egg, four larval instars, pupa and adult. In temperate and cool regions they
 +
“overwinter” at the fourth larval instar stage. Some species enter diapause when the
 +
number of daylight hours declines below a threshold level but others are more
 +
influenced by temperature which affects their activity levels. The adult populations in
 +
Britain tend to fall dramatically from mid to late October. From December adults are
 +
usually either not at all detectable or only in very small numbers, depending upon the
 +
prevailing temperature, until April-May. These periods may be even longer in northern
 +
Britain. The life span of adults is usually about 10 days, but in cooler conditions their
 +
metabolism slows and they may survive for periods of more than a month.
  
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===Vector Competence===
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Most species require a blood meal before laying eggs, although C. impunctatus (the
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Certain information can help inferences be made regarding BTV vectors in Britain. Both ''C. obsoletus'' and ''C. pulicaris'' have been implicated in transmission before. Previously, BTV has been isolated from ''C. obsoletus'' in Cyprus, and [[African Horse Sickness|African horse sickness virus]] (another Orbivirus) in Spain. ''C. obsoletus'' and ''C. pulicaris'' were also the most abundant ''Culicoides'' species detected in the 1999 BTV epizootic in Greece and Bulgaria, and so are strongly suspected of acting as vectors in this case. They may also have mediated outbreaks in Serbia, FYR Macedonia, Croatia and Bosnia in 2001-2002, where ''C. imicola'' has not been recorded. Both species are therefore contenders to transmit bluetongue virus in the UK<sup>1</sup>.
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Scottish highland biting midge), a member of the C. pulicaris group, does not require a
 +
blood meal for maturation of the first egg batch. This enables this midge to persist in
 +
areas with few mammalian hosts.
 +
3.3 Different Culicoides species have different preferences for breeding sites
 +
ranging from damp dung, damp soil to tree holes, streamsides and the edges of ponds.
 +
The C. obsoletus group breeds in damp soil and composted organic material such as
 +
old manure heaps common around stables and animal housing. The C. pulicaris group
 +
prefers to breed in wet soil, sphagnum marsh and bogs.
 +
3.4 Culicoides imicola is the major vector of BTV in the Old World. It is one of the
 +
most widely distributed of Culicoides species. It occurs throughout most of Africa, the
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Middle East, southern Asia, much of Portugal, south-west Spain and the Balearics,
 +
many Greek Islands, substantial parts of the Greek mainland, Corsica, Sardinia, Sicily
 +
and wide areas of southern and central mainland Italy.
 +
C. imicola appears to be expanding its range both northwards and westwards but is
 +
still restricted in Europe to southern parts. C. imicola has not been recorded in Great
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Britain.
 +
3.5 Culicoides obsoletus is probably one of the commonest Culicoides species
 +
across the whole of central and northern Europe. Similarly, C. pulicaris is also
 +
common throughout central and northern Europe. Both of these species are widespread
 +
throughout most of the British Isles.
 +
3.6 In practice, the usual reference to C. obsoletus really relates to a complex of
 +
closely related species (C. obsoletus, C. dewulfi, C. scoticus, C. chiopterus, C.
 +
montanus) the females of which are difficult or impossible to separate. In Bulgaria, C.
 +
obsoletus and C. scoticus, at least, co-exist. Since it is the females that are the vectors
 +
of BTV, it is not always possible to determine the identity of the vector when
 +
undertaking virus isolation from midges. In the UK, C. obsoletus, C. dewulfi, C.
 +
scoticus and C. chiopterus occur. These C. obsoletus group species belong to a larger
 +
grouping (subgenus Avaritia) that includes C. imicola (the major European and
 +
African BTV vector) and C. brevitarsis (the major Australian BTV vector). A similar
 +
taxonomic situation exists with C. pulicaris which is a complex of morphologically
 +
similar species, eight of which occur in the UK and with C. nubeculosus, a European
 +
species which is closely related to the North American BTV vector C. sonorensis (= C.
 +
variipennis).
 +
3.7 The distributions of C. obsoletus and C. pulicaris group midges in UK are not
 +
well understood. Observations of both have been made in many parts of the British
 +
Isles. When observations have not been recorded in certain areas it usually means that
 +
efforts have not been made to collect rather than the species is absent there. Generally,
 +
the insects congregate where there are breeding sites and hosts upon which to feed.
  
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A British population of ''C. obsoletus'' has been shown to have and oral susceptibility rate of less than 2%<sup>1</sup>, suggesting that ''C. obsoletus'' is likely to be an inefficient or minor vector of BTV in the UK. However, it is possible that a high abundance or survival rate may compensate for this low vector competence. Indeed, ''C. brevitarsis'', the major Australian vector of BTV, has an extremely low experimental competency yet is an effective vector in the field.
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Thus, the highest concentrations of C. obsoletus and/or C. pulicaris group midges are
 +
found where cattle, horses, pigs and, to a lesser extent, sheep populations are highest.
 +
If domestic animals are removed from a site, over several months the midge
 +
population reduces significantly, by a factor of ten to twenty times, but will usually
 +
persist at the lower level if other ecological factors are favourable, by feeding on wild
 +
hosts and/or humans.Vector numbers are likely to be low in hill sites where sheep are
 +
at low densities and where the climatic conditions are likely to be more extreme.
 +
3.8 Studies of Culicoides spp. in Britain are being expanded under a DEFRAfunded
 +
project out of the Institute of Animal Health, Pirbright. Monitoring is being
 +
expanded to twenty-five or more sites, one of the aims being to determine the species
 +
list, species distribution, seasonal incidence and vector competency of the various
 +
species.
  
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Two other ''Culicoides'' species, ''C. nuberculous'' and ''C. impunctatus'', exist in mainland Europe and the UK, and have been experimentally infected with bluetongue virus.
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===Vector Competency===
 +
3.9 The C. obsoletus group has long been suspected of being a vector, mainly on
 +
the basis of BTV isolations from this species made in Cyprus, and African horse
 +
sickness virus (AHSV) isolations made from mixed pools of C. obsoletus and C.
 +
pulicaris in Spain. In this context it should be borne in mind that BTV and AHSV tend
 +
to utilise the same Culicoides species as vectors.
 +
3.10 It is strongly suspected that C. obsoletus and/or C. pulicaris group midges acted
 +
as BTV vectors in northern Greece and southern Bulgaria during the 1999 BTV
 +
epizootic, as they were by far the most abundant and most prevalent detected. It is
 +
similarly suspected that these species may also have mediated the BT outbreaks in
 +
Serbia, western and southern Bulgaria, FYR Macedonia, Croatia and Bosnia during the
 +
period 2001-2002. C. imicola has not been recorded in these regions.
 +
3.11 Vector competence studies on a British population of C. obsoletus have
 +
recorded oral susceptibility rates of less than 2% in comparison with a known major
 +
vector C. sonorensis (19.5%). This initially suggested that C. obsoletus is likely to be
 +
only a minor or inefficient vector of BTV. Nevertheless, the high abundance and
 +
survival rates of C. obsoletus as exhibited in Bulgaria in 1999, and as seen on farms
 +
and around stables in South East England, could compensate for its low levels of
 +
vector competence. Observations of cattle exposed to midges have shown up to ten
 +
thousand bites per hour. It should be noted that C. brevitarsis, the major vector of BTV
 +
in Australia, has an experimental competency of only 0.3 percent when feeding on
 +
sheep although it is quite an effective vector in the field.
 +
3.12 Vector competence for a particular virus is a hereditary trait and populations of
 +
a vector species with high, low or intermediate levels of competence can be derived by
 +
selective breeding.
 +
Technical Review - Bluetongue: The Virus, Hosts and Vectors
 +
___________________________________________________________________________
 +
6.
 +
Version 1.5; 21 November 2002
  
 
===Epidemiology===
 
===Epidemiology===
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Although bluetongue virus is capable of infecting any ruminant, cattle are the main amplifying and maintenance hosts and are most abundantly fed on by ''Culicoides'' vectors. Infection of sheep with BTV is therefore usually preceded by widespread infection of cattle and an increase in vector density<sup>1</sup>.
 
  
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Although vertical and venereal transmission of bluetongue is possible, only to the presence of competent insect vectors influences the epidemiology of BTV<sup>2</sup>. This is illustrated by the fact that bluetongue virus is limited to geographical areas where competent vectors are present and that transmission only occurs at times of the year when conditions are favourable for vector activity<sup>1</sup>. In Britain, transmission occurs mainly in late summer and autumn. Once bluetongue virus is transmitted to a vertebrate host, there are two possible outcomes: either the host dies, or an immune response is mounted against the virus and the host is rendered resistant to re-infection. Either way, animals quickly become "unavailable" for BTV infection as the virus spreads, particularly where livestock populations are small. This presents a hurdle that must be surmounted if bluetongue virus is to persist in an area. By movement of infected vectors or viraemic animals, BTV can become established in new locations with naive hosts in order to overcome this obstacle. This means that even in zones where bluetongue virus is endemic, persistence is dynamic and comprises perpetually shifting "hot spots" of infection<sup>1</sup>. Creation of an enzootic zone is only possible in locations where adult midges are present throughout the year since bluetongue cannot be maintained through vertebrate-vertebrate or vector transovarial transmission. Any points where vectors are absent from the system must not exceed the maximum duration of viraemia in the ruminant host, otherwise the last infected vertebrate will have died or recovered by the time new vectors are available for onwards transmission.
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===Impact of Global Warming===
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3.13 Vector competence of Culicoides vectors for Orbiviruses is partly influenced by
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In some areas, bluetongue can occur in annual bouts. This may be due to new introduction of virus each year from adjacent areas where the disease is endemic, via the transportation of ''Culicoides'' on the wind for up to 100 kilometres. Alternatively, this could be the manifestation of low-level persistence.  
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temperature. Orbivirus development in Culicoides vectors is unable to occur at
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temperatures below about 10°C to 15°C depending on the Orbivirus species and
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Introduction of bluetongue virus to a new area has the potential to occur in several ways. Firstly, infected animals may be transported to the region, and local insect vectors could spread and perpetuate BTV infection within naive animals. It is also possible that local vectors could acquire BTV from infected animals in neighbouring areas, where there is a cross-over in the distribution of ''Culicoides'' species. Finally, infected vectors can be acquired from areas where bluetongue infection exists. ''Culicoides'' can be transported considerable distances on the wind, and it is also conceivable that the distribution of competent vectors may expand to colonise previously unpopulated areas under the influence of climate change.
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serotype. Furthermore, there needs to be a minimum amount of time at suitable
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temperatures (expressed as “day degrees or hour degrees”) for completion of the
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Bluetongue virus infection was first confirmed in the UK in September 2007 when a veterinarian spotted suspicious clinical signs on a cattle holding near Ipswich<sup>7</sup>. It is believed that BTV-laden vectors were dispersed to the UK on the wind, since meteorological conditions on 4th August 2007 were capable of carrying midges from northern Europe to East Anglia. This would be expected to produce disease at a point that would coincide with the first case, given the time necessary for clinical detection to occur.
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development cycle in the Culicoides vector before virus transmission can occur. This
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“physiological” time is the cumulative product of virus development time multiplied
 +
by the temperature in degrees above the threshold for virus replication. Increasing
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environmental temperature (climate change) will also extend the vector season.
 +
Combined, these conditions may result in Orbivirus development within Culicoides
 +
being able to take place over a greater proportion of the year and over a wider
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geographical area. In addition, within the range of temperatures over which Orbivirus
 +
development can occur, the levels of vector competence of a Culicoides vector
 +
population for some Orbivirus serotypes increases linearly with temperature and so the
 +
impact of warmer temperatures may be even greater.
 +
3.14 Temperature can also affect the competence of ‘non-vector’ Culicoides species.
 +
For example, C. nubeculosus generally is considered to be incapable of transmitting
 +
BTV due to a midgut infection barrier. However, exposure of the immatures to rearing
 +
temperatures close to their upper lethal limit (33-35°C) can result in >10% of adults
 +
becoming competent to transmit BTV. It is likely that the integrity of the gut wall of
 +
some adults is damaged by the extreme rearing temperatures, thereby allowing virus
 +
particles to bypass the midgut barriers, enter the haemocoel and develop as in a normal
 +
vector. The increase in frequency and intensity of extremely warm days predicted to
 +
occur with climate change will enhance the chances of this phenomenon occurring in
 +
non-vector Culicoides species and hence could increase the number of BTV competent
 +
adults within populations.
 +
3.15 The vectorial capacity of a Culicoides population (and hence the potential for
 +
virus transmission) is affected by (a) the number of adult midges in the population and
 +
(b) the proportion of adults capable of transmitting the virus, and is greatest when
 +
these factors are at a peak.
 +
3.16 Within favourable limits, the development rate of Culicoides from egg to adult
 +
is directly related to temperature. Thus increasing temperatures coupled with an
 +
extension in the developmental season may result in a greater number of generations
 +
(and therefore adults) per year. In addition, the overwintering ability of adult
 +
Culicoides is likely to improve, as winters become both warmer and shorter. Improved
 +
overwintering success is also likely to increase the spring population input, which in
 +
turn could result in even larger populations during the summer
 +
Technical Review - Bluetongue: The Virus, Hosts and Vectors
 +
___________________________________________________________________________
 +
7.
 +
Version 1.5; 21 November 2002
 +
3.17 The proportion of adult Culicoides capable of transmitting virus is dependent
 +
on (a) vector competence (the capacity for the virus to develop in and be transmitted
 +
by the vector), (b) adult survival, (c) the blood-feeding interval and (d) the extrinsic
 +
incubation period (EIP; development time of the virus in the vector). In order to
 +
transmit virus Culicoides must not only be vector competent, but also survive long
 +
enough to blood-feed after the completion of the viral EIP. Culicoides vectors are
 +
more likely to satisfy these criteria at high temperatures (e.g. 27-30°C), because,
 +
although adult survival is reduced at high temperatures, this is more than compensated
 +
for by the accompanying decrease in duration of the EIP and blood-feeding interval.
 +
Consequently, it is likely that warmer temperatures as a result of climate change will
 +
increase the likelihood that Culicoides will survive long enough to transmit virus.
 +
3.18 Changes in weather (temperature, precipitation, humidity and wind) and climate
 +
from global warming could produce both wider distribution of vectors towards the
 +
poles or upwards in elevation and increased vectorial capacity (the ability of a vector
 +
population to transmit virus to a vertebrate population) of Culicoides vector
 +
populations, resulting in increased prevalence of BTV in Europe. The present BT
 +
outbreak in the Mediterranean Basin is already the most serious epizootic on record.
 +
3.19 An expansion in the range of C. imicola will increase the areas of Europe at risk
 +
from BTV. Also, the extended distribution of C. imicola could bring BTV into the
 +
range of C. obsoletus group and C. pulicaris group midges much more frequently and
 +
this could result in even greater areas of Europe being affected by BTV.
 +
3.20 The impact of climate change on the vectorial capacity of Culicoides
 +
populations will have three main effects on BTV transmission in the Mediterranean
 +
basin:
 +
· the greater abundance of adult Culicoides combined with the increased proportion
 +
of adults capable of transmitting the virus will increase the likelihood and severity
 +
of an epizootic, following the introduction of BTV into an area. The greatest risk
 +
will be at times of the year when temperatures reach approximately 25-30°C (i.e.
 +
when conditions are optimal for Culicoides development and virus transmission
 +
· as temperatures will be conducive for both viral and Culicoides development for a
 +
greater proportion of the year, the length of the viral transmission season will
 +
increase.
 +
· the enhanced overwintering success of adult Culicoides combined with the
 +
extension in the Culicoides development season will prolong the seasonal
 +
occurrence of adult midges and hence improve the overwintering chances of BTV.
 +
3.21. Studies are needed to correlate the day degrees required for BTV development
 +
in the potential vectors against British climate data to establish the risk of
 +
establishment of a BTV infection under present climatic conditions and with global
 +
warming.
  
 
==Pathogenesis==
 
==Pathogenesis==
−
The pathogenesis of BTV infection has been shown to be similar in sheep and cattle, and is assumed to be similar in other species of ruminants<sup>8, 9, 10</sup>. However, the severity of disease varies greatly with species and cattle in particular express very few signs.
+
*Transfer occurs through blood from viremic animals via biting midges ('''Culicoides spp.''')
 +
*Replication in haematopoietic and endothelial cells of blood vessels
 +
*Clinical signs vary between species, with sheep most severely affected
 +
**Pyrexia
 +
**Ocular and nasal discharge
 +
**Drooling from mouth uclers
 +
**Swelling of the mouth, head and neck
 +
**Lameness
 +
**Subdural hemorrhages
 +
**Inflammation of the coronary band
 +
*Cattle as the main reservoir
 +
*A blue tongue is rarely seen as as a clinical sign of infection
 +
*Resulting loss of condition, reduction in wool an meat production, which can be followed by death
  
−
When a BTV-infected midge takes a blood meal from a ruminant host, innoculated virus spreads from the skin to replicate in the regional lymph nodes, tonsils and spleen<sup>11</sup>. A secondary cell-associated viraemia then carries the virus to many tissues where further replication occurs in macrophages and endothelial cells. In the process of reproducing, bluetongue virus causes endothelial cell injury and necrosis<sup>10</sup> which can increase vascular permeability to cause oedema. Endothelial damage can also give thrombosis, leading to tissue infarction. In sheep and deer a [[Disseminated Intravascular Coagulation|consumptive coagulopathy]] may occur<sup>2</sup>.
+
==Diagnosis==
  
−
Several factors can influence the presentation of disease. Firstly, each virus strain is associated with its own particular virulence and thus clinical manifestation<sup>10</sup>. Host factors are also important: breed<sup>3, 12</sup>, stress, nutritional status and age<sup>12, 13</sup> can all affect bluetongue presentation.
+
The typical clinical signs of bluetongue enable a presumptive diagnosis, especially in areas where the disease is endemic. Suspicion is confirmed by the presence of petechiae, ecchymoses, or hemorrhages in the wall of the base of the pulmonary artery and focal necrosis of the papillary muscle of the left ventricle. These highly characteristic lesions are usually obvious in severe clinical infections but may be barely visible in mild or convalescent cases. These lesions are often described as pathognomonic for bluetongue, but they have also been observed occasionally in other ovine diseases such as heartwater, pulpy kidney disease, and Rift Valley fever. Hemorrhages and necrosis are usually found where mechanical abrasion damages fragile capillaries, such as on the buccal surface of the cheek opposite the molar teeth and the mucosa of the esophageal groove and omasal folds. Other autopsy findings include subcutaneous and intermuscular edema, skeletal myonecrosis, myocardial and intestinal hemorrhages, hydrothorax, hydropericardium, pericarditis, and pneumonia. In many areas of the world, bluetongue in sheep, and especially in other ruminants, is subclinical and, therefore, laboratory confirmation based on virus isolation in embryonated chicken eggs, susceptible sheep, or cell cultures, or the identification of viral RNA by PCR is necessary. The identity of isolates may be confirmed by the group-specific antigen-capture ELISA, immunofluorescence, immunoperoxidase, serotype-specific virus neutralization tests, or hybridization with complementary gene sequences of group- or serotype-specific genes. For virus isolation, blood (10-20 mL) is collected as early as possible from febrile animals into an anticoagulant such as heparin, sodium citrate, or EDTA and transported at 4°C to the laboratory. For longterm storage where refrigeration is not possible, blood is collected in oxalate-phenol-glycerin (OPG). Blood to be frozen should be collected in buffered lactose peptone and stored at or below -70°C. Blood collected at later times during the viremic period should not be frozen, as lysing of the RBC or thawing releases the cell-associated virus, which may then be neutralized by early humoral antibody. The virus does not remain stable for long at -20°C. In fatal cases, specimens of spleen, lymph nodes, or red bone marrow are collected and transported to the laboratory at 4°C as soon as possible after death. A serologic response in ruminants can be detected 7-14 days after infection and is generally lifelong. Current recommended serologic techniques for the detection of bluetongue virus antibody include agar gel immunodiffusion and competitive ELISA. The latter is the test of choice and does not detect cross-reacting antibody to other orbiviruses, especially anti-EHDV (epizootic hemorrhagic disease virus) antibody. Various forms of virus neutralization test, including plaque reduction, plaque inhibition, and microtiter neutralization can be used to detect type-specific antibody.
−
 
 
−
==Diagnosis==
 
−
Where animals present with clinical signs of bluetongue a presumptive diagnosis may be made, especially in regions where bluetongue is endemic. Post-mortem examination can be used to confirm the diagnosis. However, many cases of bluetongue are mild or subclinical and so laboratory confirmation of disease is required. Cattle in particular show few clinical signs.
 
  
 
===Clinical Signs===
 
===Clinical Signs===
−
Bluetongue is primarily a disease of '''sheep''', and in the face of infection these animals can display clinical signs ranging from acute to subclinical<sup>1, 14</sup>. Acute disease follows an incubation period of about one week, which may depend on the infectious dose of virus received. Signs begin with pyrexia of around 40.5-42°C, and hyperaemia of the oral and nasal mucosa is seen 24-36 hours later accompanied by hypersalivation and a serous nasal discharge. The nasal discharge quickly becomes mucopurulent and potentially blood-tinged, and dries to form a crust around the nostrils. Oedema of the head occurs, which particularly affects the lips and tongue but may also spread to include the ears and submandibular areas. In a few cases the tongue becomes severely swollen and cyanotic, lending the disease its name. Petechial haemorrhages appear on the still-hyperaemic mucosae, and areas of necrosis appear on the gums, cheeks and tongue 5-8 days after the onset of fever. Covered by a diphtheritic membrane, these necrotic lesions heal slowly and contribute to inappetance, dysphagia and hypersalivation. In some cases, profuse bloody diarrhoea is seen. Erythema and petechiation of the coronary band can cause lameness, and sheep stand with an arched back, reluctant to move. In advanced disease, skeletal muscle is necrosed and contributes to rapid weight loss, along with inappetance. Animals in the late stage may also suffer torticollis. In pregnant ewes, infection with BTV may lead to abortions, foetal mummification, or the birth of stillborn or weak lambs, which may suffer congenital defects.
+
The course of the disease in sheep can vary from peracute to chronic, with a mortality rate of 2-30%. Peracute cases die within 7-9 days of infection, mostly as a result of severe pulmonary edema leading to dyspnea, frothing from the nostrils, and death by asphyxiation. In chronic cases, sheep may die 3-5 wk after infection, mainly as a result of bacterial complications, especially pasteurellosis, and exhaustion. Mild cases usually recover rapidly and completely. The major production losses include deaths, unthriftiness during prolonged convalescence, wool breaks, and possibly reproductive loss. In sheep, bluetongue virus causes vascular endothelial damage, resulting in changes to capillary permeability and subsequent intravascular coagulation. This results in edema, congestion, hemorrhage, inflammation, and necrosis. The clinical signs in sheep are typical. After an incubation period of 4-6 days, a fever of 105-107.5°F (40.5-42°C) develops. The animals are listless and reluctant to move. Clinical signs in young lambs are more apparent, and the mortality rate is higher (up to 30%). About 2 days after onset of fever, additional clinical signs such as edema of lips, nose, face, submandibular area, eyelids, and sometimes ears; congestion of mouth, nose, nasal cavity, conjunctiva, and coronary bands; and lameness and depression may be seen. A serous nasal discharge is common, later becoming mucopurulent. The congestion of nose and nasal cavity produces a “sore muzzle” effect, the term used to describe the disease in sheep in the USA. Sheep eat less because of oral soreness and will hold food in their mouths to soften before chewing. They may champ to produce a frothy oral discharge at the corners of the lips. On close examination, small hemorrhages can be seen on the mucous membranes of the nose and mouth. Ulceration develops where the teeth come in contact with lips and tongue, especially in areas of most friction. Some affected sheep have severe swelling of the tongue, which may become cyanotic (‘blue tongue”) and even protrude from the mouth. Animals walk with difficulty as a result of inflammation of the hoof coronets. A purple-red color is easily seen as a band at the junction of the skin and the hoof. Later in the course of disease, lameness or torticollis is due to skeletal muscle damage. In most affected animals, abnormal wool growth resulting from dermatitis may be observed.  
−
 
+
The pathogenesis of bluetongue in cattle seems to differ from that in sheep and is based on immediate IgE hypersensitivity reactions. Clinical signs in cattle are rare but may be similar to those seen in sheep. They are usually limited to fever, increased respiratory rate, lacrimation, salivation, stiffness, oral vesicles and ulcers, hyperesthesia, and a vesicular and ulcerative dermatitis. Susceptible cattle and sheep infected during pregnancy may abort or deliver malformed calves or lambs. The malformations include hydranencephaly or porencephaly, which results in ataxia and blindness at birth. White-tailed deer and pronghorn antelope develop severe hemorrhagic disease leading to sudden death. Pregnant dogs abort or give birth to stillborn pups and then die in 3-7 days.
−
Considering all cases, including those which are subclinical, mortality due to bluetongue in sheep ranges between 2% and 30%<sup>14</sup>. Death can occur up to a month after the onset of clinical signs, or a protracted recovery may follow acute infection. Recovery in mild cases is often much more rapid.
 
−
 
 
−
Disease is most often sub-clinical in '''cattle''' despite its epidemiological significance in this species: it has been reported that only 0.01% of infected cattle show signs of bluetongue<sup>1</sup>. Clinical signs, when seen, can include inflammation or erosions of the oral and nasal mucosae and a stiff gait. Similar signs to sheep may also occur: pyrexia, tachypnoea, lacrimation, salivation and an ulcerative dermatitis are all possibilities. In cattle in early gestation, embryonic death and resorption can result from BTV infection.
 
  
 
===Laboratory Tests===
 
===Laboratory Tests===
−
In the United Kingdom, bluetongue is a notifiable disease and so samples from suspected cases should be submitted to the Institute for Animal Health (Pirbright) for laboratory diagnosis. Samples are collected from sheep with raised temperatures and include jugular blood collected into a plain tube to provide serum for an antibody test, and a heparinised blood sample to be used for PCR. Serum from in-contact ruminants is also submitted, as well as spleen and lymph node from all post-mortem cases. All samples should be stored at 4&deg;C and never frozen. Paired serology may be necessary.
 
−
 
−
There is an array of laboratory tests available for the diagnosis of bluetongue, and a table published by DEFRA<sup>1</sup> summarises these:
 
−
 
−
 
−
{| class="wikitable collapsible" width="75%" align="center"
 
−
| <center> <u> '''Test''' </u> </center>         
 
−
| <center><u>'''Specimen Required'''</u> </center>       
 
−
|<center><u>'''Test Detects'''</u> </center>       
 
−
|<center><u>'''Timescale'''</u> </center>         
 
−
|-
 
−
|<u>'''Virus Isolation'''</u>
 
−
|<center>Whole EDTA blood</center>
 
−
|<center>Virus</center>
 
−
|<center>1 - 3 weeks</center>
 
−
|-
 
−
|<U>'''Antigen Detection'''</U> <BR>Sandwich ELISA <BR>PCR <BR>Serum Neutralisation<BR> 
 
−
|<center><BR>Whole heparin or EDTA blood; tissues <BR>Whole EDTA blood; tissues <BR>Whole heparin or EDTA blood; tissues<BR>  </center>
 
−
|<center><BR>Antigen - group specific <BR>Viral RNA - group specific<BR>Serotype<BR>  </center>
 
−
|<center><BR>Blood: 5 - 14 days; Tissues: 4 hours <BR>2 days <BR>2 - 4 weeks<BR>  </center>
 
−
|-
 
−
|<U>'''Antibody Detection'''</U> <BR> Competition ELISA <BR> Serum Neutralisation <BR> Pathogenicity Testing in Sheep <BR>
 
−
|<center><BR>Serum <BR>Serum <BR> Virus isolate <BR>  </center>
 
−
|<center><BR>Antibody - group specific <BR>Antibody - serotype specific <BR>Virulence<BR>  </center>
 
−
|<center><BR>3 hours <BR>2 - 4 weeks <BR>2 weeks<BR>  </center>
 
−
|-
 
−
|}
 
−
 
 
===Pathology===
 
===Pathology===
−
A haemorrhagic gross pathology of BTV infection reflects the endothelial damage responsible for disease pathogenesis<sup>1, 4, 10, 12</sup>. Certain lesions have been described as "pathognomic" for bluetongue: these include necrosis of the papillary muscle in the left ventricle, and haemorrhage in pulmonary arterial wall. However, these lesions may be difficult to visualise in mild or recovering cases and may occasionally occur in other diseases such as [[Pulpy Kidney|pulpy kidney]] disease or [[Rift Valley Fever]].  
+
Complete loss of integrity of epithelium. Uncommon.
−
 
+
*Characteristic of Bluetongue Virus,  
−
In addition to these characteristic lesions, the oral mucosa is found to be hyperaemic and oedematous and occasionally cyanotic on post-mortem examination, and petechial or ecchymotic haemorrhages may be present. The ruminal pillars and omasal folds can also appear hyperaemic, and abrasions may be seen on the lips, dental pad, tongue and cheeks. These are sometimes covered by grey necrotic material. Moderate lymphomegaly and splenomegaly are apparent, and there are areas of necrosis in the skeletal musculature. Pulmonary oedema and catarrhal inflammation of the upper respiratory tract is seen in some cases.
+
*Epithelium lost and haemorrhage produces blue / black discoloration of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]], hence the name.
−
 
 
−
Histologically, endothelial damage in capillaries and minor arterioles causes thrombus formation and vascular occlusion, leading to tissue infarction. Haemorrhage, necrosis and mononuclear cell infiltration may be seen in the myocardium.
 
−
 
 
−
==Control==
 
−
 
 
−
There is no efficient treatment for bluetongue, and so the emphasis is on prophylaxis and control.
 
−
 
 
−
===Vaccination===
 
−
Vaccines against BTV are available, and in different situations may be used to prevent or control outbreaks of bluetongue. Initially, modified live BTV vaccines were used, particularly in Africa, the United States and southern Europe<sup>4</sup>. Although useful for the control of disease, these vaccines have the potential to introduce novel strains of virus into the environment, which could lead to vector infection and reversion to virulence by evolution or genome reassortment with wild-type viruses. Foetal infection and teratogenesis are also possible. Killed, adjuvanted vaccines for some serotypes are now available, which are much safer. It is this type of product that has been used in recent years for control of BTV-8 in the UK.
 
  
−
===Vector Control===
 
−
As the cycle of bluetongue transmission involves a ''Culicoides'' vector, elements of disease control can be targetted at controlling midges. This can involve the use of insecticides on ''Culicoides'' breeding grounds to reduce midge numbers, and insect repellants on livestock to limit feeding on potential BTV hosts. Animals can also be housed indoors at dawn and dusk, when midges are most active. So far, little evidence has supported the value of these control measures, and the practicalities of implementing these strategies may preclude them from widespread use.
 
  
−
===Surveillance===
 
−
Surveillance is a key component to controlling the spread of bluetongue. As well as vigilance in the face of a bluetongue outbreak to determine the extent of disease spread, ongoing surveillance is required to limit the possibility of BTV entering areas where the virus is not already circulating. The UK currently achieves ongoing surveillance through two mechanisms<sup>15</sup>. Firstly, bluetongue is a notifiable disease, and so it is a legal requirement for livestock holders to report all new cases of bluetongue on their premises. This allows new midge-transmission from the continent and any re-emergence of disease to be assessed. Secondly, every susceptible animal imported from Continental Europe, where bluetongue is currently circulating, is post-import tested for all serotypes of bluetongue virus. This ensures infected animals are not introduced to the country.
 
  
−
===Controlling Spread of Bluetongue in Europe===
 
−
Although some factors influencing the introduction of bluetongue to an area are outwith human control, such as transportation of ''Culicoides'' on the wind, certain measures can be taken to help avoid BTV becoming established in an area. This involves designation of areas where bluetongue is circulating as restricted (or protection) zones for the specific serotype, and imposing movement limitations within and between these areas. Animals in protection zones may be moved within the zone, and to confluent protection zones for the same serotype. However, they may not be moved to free zones (BTV-free areas), although animals from free zones may be moved without restriction. A map of the current restriction/protection zones in Europe is available from the [http://ec.europa.eu/food/animal/diseases/controlmeasures/bt_restrictedzones-map.jpg European Commission Website].
 
  
−
Since animals may be moved freely between protection zones for the same serotype, a protection zone which does not currently have circulating BTV is at risk of becoming re-infected.  This fact has lead to the designation of lower risk zones. Vaccination is only normally permitted within protection zones, but livestock holders in lower risk zones are able to vaccinate their animals. There are also more stringent regulations on bringing in animals from confluent protection zones. Therefore, the risk of re-introducing bluetongue is reduced and the area can move towards BTV freedom more confidently. A further advantage of lower risk zones is that fewer limitations apply to the export of livestock to free zones or areas with other BTV serotypes.
+
*Grossly:
 +
**Infarctions -> necrosis
 +
**Haemorrhage
 +
*Histologically:
 +
**Necrosis -> calcification or regeneration (depends on age of lesion)
  
−
===Control in the UK===
+
==Treatment==
−
In 2007, BTV-8 was confirmed in the UK and control measures implemented. However, the last BTV-8 infected premise was confirmed in the UK in November 2008, and since this date the situation has remained unchanged. No imported ruminants have tested positive for BTV-8 and there is no evidence that the disease has been circulating since this point. On 12th June 2010 the UK's status was changed from a protection zone for BTV-8 to a lower risk zone (LRZ). This status continues to allow vaccination against BTV, and imposes stricter restrictions on importing animals from zones with the same BTV serotype. The aim of this is to help prevent bluetongue re-entering the country. Up-to-date information on the current UK bluetongue situation can be found on the [http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bluetongue/latest/index.htm DEFRA Bluetongue: Latest situation] webpage. At this point in time (Autumn 2010), vaccination is voluntary within the UK.
 
  
−
In the UK, Bluetongue is a notifiable disease and so cases must be reported to the local AHO. There are also further obligations for notification: within 24 hours of confirmation of bluetongue in the UK, the Chief Veterinary Officer must inform the European Commission and the OIE Central Bureau. There are several broad principles of disease control when a bluetongue outbreak occurs in the UK<sup>16</sup>. Firstly, premises suspected of having the disease are inspected by a veterinary surgeon, and a ban is placed on moving animals on and off the site. Once it has been confirmed that bluetongue is circulating (i.e. there is not a single, isolated case of disease, for example due to importation), a restricted zone is imposed around the infected premises. A restricted zone is the overall area where restrictions apply and is composed of a protection zone (100km radius) surrounded by a surveillance zone (50km radius). The sizes of these zones are dictated by EU legislation for bluetongue control. The restricted zone may also contain control zones of tighter restrictions in the immediate vicinity (20km) of infected premises. Movements are permitted within protection and suveillance zones, and from the surveillance zone to the protection zone. Animals from neighbouring BTV-free areas may move into either the surveillance or protected zones. However, the converse of any of these movements is not permitted unless animals are travelling to slaughter. No movements are permitted within, to, or from the control zone.  
+
*BTV is '''NOTIFIABLE'''
 +
*Vigilance in recognizing clinical signs
 +
*Restriction of movement:
 +
**Protection Zone: 100km radius around infected premises, movement within zone allowed but not in or out
 +
***Vaccination within PZ using appropriate serotype is encouraged but still voluntary
 +
**Surveillance Zone: 50km radius beyond PZ
 +
*Vector control: ectoparasiticides, etc.
  
−
In addition to movement restrictions, surveillance for disease and vectors is implemented as necessary in an outbreak, and relevant communications are made to livestock owners and veterinary surgeons to advise of the measures in place. The aim at all times is to tightly control disease, with an aim to eradication, and vaccination will normally play a large part in this according to plans laid out by DEFRA. A test and slaugher policy is not used, because BTV is not transmitted directly between susceptible animals.
+
Prophylactic immunization of sheep remains the most effective and practical control measure against bluetongue in endemic regions. Three polyvalent vaccines, each comprising 5 different bluetongue virus serotypes attenuated by serial passage in embryonated hens’ eggs followed by growth and plaque selection in cell culture, are widely used in southern Africa and elsewhere, should epizootics of bluetongue occur. A monovalent modified live virus vaccine propagated in cell culture is available for use in sheep in the USA. Live-attenuated vaccines should not be used during Culicoides vector seasons because they may transmit the vaccine virus(es) from vaccinated to nonvaccinated animals, eg, other ruminant species. This may result in reassortment of genetic material and give rise to new viral strains. Abortion or malformation, particularly of the CNS, of fetuses may follow vaccination of ewes and cows with attenuated live vaccines during the first half and the first trimester of pregnancy, respectively. Passive immunity in lambs usually lasts 4-6 mo. The control of bluetongue is different in areas where the disease is not endemic. During an outbreak, when one or a limited number of serotypes may be involved, vaccination strategy depends on the serotype(s) that are causing infection. Use of vaccine strains other than the one(s) causing infection affords little or no protection. The vector status, potential risk from vaccine virus reassortment with wild-type viral strains, virus spread by the vectors to other susceptible ruminants, and reversion to virulence of vaccine virus strains or even the production of new serotypes also should be considered. Although a number of noninfectious vaccines are in development, they are not yet commercially available. Control of vectors by using insecticides or protection from vectors by moving animals into barns during the evening hours lowers the number of Culicoides bites and subsequently the risk of exposure to bluetongue virus infection.
−
 
 
−
{{Learning
 
−
|flashcards = [[Cattle Medicine Q&A 06]]
 
−
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=title:(Bluetongue)+OR+(%22Blue+tongue%22)&occuring1=freetext&rowId=2&options2=AND&q2=&occuring2=freetext&rowId=3&options3=AND&q3=&occuring3=freetext&publishedstart=2000&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all&x=42&y=4 Bluetongue publications since 2000]
 
−
}}
 
  
 
==Links==
 
==Links==
  
 
*[http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bluetongue/index.htm Defra - Bluetongue]
 
*[http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bluetongue/index.htm Defra - Bluetongue]
−
*[http://www.oie.int/eng/maladies/fiches/a_A090.htm Office International des Epizooties (World Organisation for Animal Health) - Bluetongue]
 
 
*[http://www.bluetongue-info.co.uk BTV Control in Cattle and Sheep (Intervet)]
 
*[http://www.bluetongue-info.co.uk BTV Control in Cattle and Sheep (Intervet)]
 
*[http://www.iah.ac.uk/disease/bt_aw.shtml Institute for Animal Health - Bluetongue]
 
*[http://www.iah.ac.uk/disease/bt_aw.shtml Institute for Animal Health - Bluetongue]
Line 136: Line 261:
 
==References==
 
==References==
  
−
#DEFRA (2002) [http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/documents/bluetongue_technical.PDF Technical Review - Bluetongue : The Virus, Hosts and Vectors.]  
+
#Defra (2002) [http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/documents/bluetongue_technical.PDF Technical Review - Bluetongue : The Virus, Hosts and Vectors.]  
 
#Gibbs, E P J and Geiner, E C (1994) The Epidemiology of Bluetongue. ''Comparative Immunology, Microbiology and Infectious Diseases'', '''17(3-4)''', 207-220.
 
#Gibbs, E P J and Geiner, E C (1994) The Epidemiology of Bluetongue. ''Comparative Immunology, Microbiology and Infectious Diseases'', '''17(3-4)''', 207-220.
 
#Spreull, J (1905) Malarial catarrhal fever (bluetongue) of sheep in South Africa. ''Journal of Comparative Pathology and Therapeutics'', '''18''', 321-337.
 
#Spreull, J (1905) Malarial catarrhal fever (bluetongue) of sheep in South Africa. ''Journal of Comparative Pathology and Therapeutics'', '''18''', 321-337.
 
#MacLachlan, N J (2004) Bluetongue: A Review and Global Overview of the Only OIE List a Disease that is Endemic in North America. ''Proceedings of the 55th Annual Meeting of the American College of Veterinary Pathologists (ACVP) and 39th Annual Meeting of the American Society of Clinical Pathology (ASVCP)'', p1237.
 
#MacLachlan, N J (2004) Bluetongue: A Review and Global Overview of the Only OIE List a Disease that is Endemic in North America. ''Proceedings of the 55th Annual Meeting of the American College of Veterinary Pathologists (ACVP) and 39th Annual Meeting of the American Society of Clinical Pathology (ASVCP)'', p1237.
 
#Carter, G R and Wise, D J (2005) '''A Concise Review of Veterinary Virology''', ''IVIS''.
 
#Carter, G R and Wise, D J (2005) '''A Concise Review of Veterinary Virology''', ''IVIS''.
−
#Mellor, P S (2000) Replication of arboviruses in insect vectors. ''Journal of Comparative Pathology'', '''123''', 231-247.
 
−
#IAH (2008) [http://www.iah.ac.uk/disease/bt_aw.shtml Institute for Animal Health - Bluetongue Research Programme]
 
−
#Barratt-Boyes, S M and MacLachlan, N J (1995) Pathogenesis of bluetongue virus infection of cattle. ''Journal of the American Veterinary Medical Association'', '''206(9)''', 1322-1329.
 
−
#MacLachlan, N J (1994) The pathogenesis and immunology of bluetongue virus infection of ruminants. ''Comparative Immunology, Microbiology and Infectious Diseases'', '''17(3-4)''', 197-206.
 
−
#Mahrt, C R and Osburn, B I (1986) Experimental bluetongue virus infection of sheep; effect of vaccination: pathologic, immunofluorescent, and ultrastructural studies. ''American Journal of Veterinary Research'', '''47''', 1198-1203.
 
−
# Pini, A (1976) Study on the pathogenesis of bluetongue: replication of the virus in the organs of infected sheep. ''Onderstepoort Journal of Veterinary Researh'', '''43''', 159-164.
 
−
#Parsonson, I M (1991) Overview of bluetongue virus infection of sheep. '''Bluetongue, African Horse Sickness and Related Orbiviruses''', ''CRC Press''.
 
−
#Thomas, A D and Neitz, W O (1947) Further observations on the pathology of bluetongue in sheep. ''Onderstepoort Journal of Veterinary Science and Animal Industry'', '''22''', 27-40.
 
−
#Mullens, B A et al (1995) Effects of temperature on virogenesis of bluetongue virus serotype 11 in Culicoides variipennis sonorensis. ''Medical and Veterinary Entomology'', '''9''', 71-76.
 
−
#[http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bluetongue/control/index.htm www.defra.gov.uk - Bluetongue: Surveillance and control.]
 
−
#DEFRA (2008) [http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/documents/bluetongue-control-strategy081201.pdf UK Bluetongue Control Strategy.]
 
−
#Gould, A R and Hyatt, A D (1994) The orbivirus genus: diversity, structure, replication and phylogenetic relationships. ''Comparative Immunology, Microbiology and Infectious Diseases'', '''1''', 163-188.
 
 
#Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''', ''Merial''.
 
#Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''', ''Merial''.
 
#Dal Pozzo, F et al (2009) Bovine infection with bluetongue virus with special emphasis on European serotype 8. ''The Veterinary Journal'', '''182(2)''', 142-151.
 
#Dal Pozzo, F et al (2009) Bovine infection with bluetongue virus with special emphasis on European serotype 8. ''The Veterinary Journal'', '''182(2)''', 142-151.
 
#MacLachlan, N J et al (2009) The Pathology and Pathogenesis of Bluetongue. ''Journal of Comparative Pathology'', '''141(1)''', 1-16.
 
#MacLachlan, N J et al (2009) The Pathology and Pathogenesis of Bluetongue. ''Journal of Comparative Pathology'', '''141(1)''', 1-16.
 +
#Barratt-Boyes, S M and MacLachlan, N J (1995) Pathogenesis of bluetongue virus infection of cattle. ''Journal of the American Veterinary Medical Association'', '''206(9)''', 1322-1329.
 
#Afshar, A (2004) Bluetongue: Laboratory Diagnosis. ''Comparative Immunology, Microbiology and Infectious Diseases'', '''17(3-4)''', 221-242.
 
#Afshar, A (2004) Bluetongue: Laboratory Diagnosis. ''Comparative Immunology, Microbiology and Infectious Diseases'', '''17(3-4)''', 221-242.
 
#Gould, E A and Higgs, S (2009) Impact of climate change and other factors on emerging arbovirus diseases. ''Transactions of the Royal Society of Tropical Medicine and Hygiene'', '''103(2)''', 109-121.  
 
#Gould, E A and Higgs, S (2009) Impact of climate change and other factors on emerging arbovirus diseases. ''Transactions of the Royal Society of Tropical Medicine and Hygiene'', '''103(2)''', 109-121.  
 +
#MacLachlan, N J (1994) The pathogenesis and immunology of bluetongue virus infection of ruminants. ''Comparative Immunology, Microbiology and Infectious Diseases'', '''17(3-4)''', 197-206.
  
  
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{{review}}
+
[[Category:Orbiviruses]][[Category:Cattle]][[Category:Sheep]][[Category:Pig]]
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[[Category:Orbiviruses]][[Category:Cattle Viruses]][[Category:Sheep Viruses]][[Category:Goat Viruses]][[Category:Camelids]]
+
[[Category:Tongue_-_Pathology]][[Category:To_Do_-_Lizzie]]
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[[Category:Tongue_-_Pathology]] [[Category:Brian Aldridge reviewing]]
 
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[[Category:Oral Diseases - Cattle]][[Category:Oral Diseases - Sheep]][[Category:Oral Diseases - Goat]]
 
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[[Category:Respiratory Diseases - Sheep]][[Category:Viral Myositis]]
 

Revision as of 13:12, 20 August 2010


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Description

Bluetongue is a non-contagious, arthropod-borne disease of ruminants, caused by bluetongue virus (BTV). The clinical severity of disease is variable, but is characterised by inflammation of mucous membranes, haemorrhages and oedema1. Although cattle are the main reservoir of infection, sheep are more severely affected and often suffer a cyanotic tongue, lending the disease its name. The virus has been isolated from hosts and vectors on all continents(excluding Antartica)2, despite being initially recognised in Africa in the late 19th and early 20th centuries3. Originally thought to be a disease of tropical and sub-tropical regions, bluetongue has shown a propensity to become established in temperate areas, and in recent years has spread North, through the Mediterranean Basin, to become endemic in many European countries including the UK. Although BTV's transmission and epidemiology is dependent on insect vectors, bluetongue greatly influences the global trade of ruminants as it is included on the Office International des Epizooties List A of animal diseases4.

Aetiology

Bluetongue virus particle. Source: Wikimedia Commons; Author: CDC (2007)

Bluetongue virus is a species of the genus Orbivirus, within the Reoviridae family. The Reoviridae are non-enveloped and possess a double-stranded RNA genome contained in an outer-shelled icosohedral capsid. The BTV genome is arranged into 10 segments and encodes 7 structural and 4 non-structural viral proteins2. The BTV receptor is currently unknown, but is proposed to included sialic acid and junctional adhesion molecules. After interaction with this receptor, the virus enters an endolysosome where the capsid is partially digested to allow the genome into the cell. Replication begins at this partially uncoated stage since the virus particles contain all the necessary enzymes5. First, the dsRNA is transcribed to form positive sense RNA, of which some is delivered to cytoplasm for ribosomal translation and the remainder is packaged into partially assembled virions. Complementary negative sense RNA is then formed in the virions, to give a dsRNA genome. Complete virus particles are released from the cell.

All BTV’s share group antigens, which can be demonstrated by agar gel diffusion tests, fluorescent antibody tests and the group reactive ELISA1. There are 24 distinct serotypes, which are are distinguished by epitopes on the outer capsid protein VP22, encoded by L2, the only serotype-specific BTV gene. Serotypes are differentiated using serum neutralisation tests, although there is some degree of cross-reactivity between serotypes1. Numerous strains of bluetongue virus also exist, and these are characterised by molecular analysis.

Hosts

All ruminants are susceptible to bluetongue virus infection, including sheep, goats, cattle, deer, buffaloes, camels and antelopes. Sheep are most severely affected, and disease is occasionally seen in goats. Although cattle BTV infection is significant in the epidemiology of disease, the condition is generally subclinical in this host. Mortalities in white-tailed deer due to bluetongue1.

Pigs and horses do not become infected with BTV, but may act as a food source for the Culicoides midges that transmit bluetongue virus to ruminants. Their habitats may also provide areas suitable for vector breeding.

Transmission and Epidemiology

Vectors

The arthropd vector for bluetongue virus is the Culicoides biting midge. These insects take blood meals from vertebrate host and breed in damp, dung-enriched soil enriched, and so are abdunant in the vicinity of domestic livestock. The activity of Culicoides varies with the time of day: the midges are most active at night, from an hour before sunset to an hour after sunrise. Activity is decreased by windy conditions, and increased during the day when the weather is dull. Culicoides generally avoid entering buildings and other closed spaces.

3.2 Culicoides species have a normal insect complete metamorphosis life cycle – egg, four larval instars, pupa and adult. In temperate and cool regions they “overwinter” at the fourth larval instar stage. Some species enter diapause when the number of daylight hours declines below a threshold level but others are more influenced by temperature which affects their activity levels. The adult populations in Britain tend to fall dramatically from mid to late October. From December adults are usually either not at all detectable or only in very small numbers, depending upon the prevailing temperature, until April-May. These periods may be even longer in northern Britain. The life span of adults is usually about 10 days, but in cooler conditions their metabolism slows and they may survive for periods of more than a month.

Most species require a blood meal before laying eggs, although C. impunctatus (the Scottish highland biting midge), a member of the C. pulicaris group, does not require a blood meal for maturation of the first egg batch. This enables this midge to persist in areas with few mammalian hosts. 3.3 Different Culicoides species have different preferences for breeding sites ranging from damp dung, damp soil to tree holes, streamsides and the edges of ponds. The C. obsoletus group breeds in damp soil and composted organic material such as old manure heaps common around stables and animal housing. The C. pulicaris group prefers to breed in wet soil, sphagnum marsh and bogs. 3.4 Culicoides imicola is the major vector of BTV in the Old World. It is one of the most widely distributed of Culicoides species. It occurs throughout most of Africa, the Middle East, southern Asia, much of Portugal, south-west Spain and the Balearics, many Greek Islands, substantial parts of the Greek mainland, Corsica, Sardinia, Sicily and wide areas of southern and central mainland Italy. C. imicola appears to be expanding its range both northwards and westwards but is still restricted in Europe to southern parts. C. imicola has not been recorded in Great Britain. 3.5 Culicoides obsoletus is probably one of the commonest Culicoides species across the whole of central and northern Europe. Similarly, C. pulicaris is also common throughout central and northern Europe. Both of these species are widespread throughout most of the British Isles. 3.6 In practice, the usual reference to C. obsoletus really relates to a complex of closely related species (C. obsoletus, C. dewulfi, C. scoticus, C. chiopterus, C. montanus) the females of which are difficult or impossible to separate. In Bulgaria, C. obsoletus and C. scoticus, at least, co-exist. Since it is the females that are the vectors of BTV, it is not always possible to determine the identity of the vector when undertaking virus isolation from midges. In the UK, C. obsoletus, C. dewulfi, C. scoticus and C. chiopterus occur. These C. obsoletus group species belong to a larger grouping (subgenus Avaritia) that includes C. imicola (the major European and African BTV vector) and C. brevitarsis (the major Australian BTV vector). A similar taxonomic situation exists with C. pulicaris which is a complex of morphologically similar species, eight of which occur in the UK and with C. nubeculosus, a European species which is closely related to the North American BTV vector C. sonorensis (= C. variipennis). 3.7 The distributions of C. obsoletus and C. pulicaris group midges in UK are not well understood. Observations of both have been made in many parts of the British Isles. When observations have not been recorded in certain areas it usually means that efforts have not been made to collect rather than the species is absent there. Generally, the insects congregate where there are breeding sites and hosts upon which to feed.

Thus, the highest concentrations of C. obsoletus and/or C. pulicaris group midges are found where cattle, horses, pigs and, to a lesser extent, sheep populations are highest. If domestic animals are removed from a site, over several months the midge population reduces significantly, by a factor of ten to twenty times, but will usually persist at the lower level if other ecological factors are favourable, by feeding on wild hosts and/or humans.Vector numbers are likely to be low in hill sites where sheep are at low densities and where the climatic conditions are likely to be more extreme. 3.8 Studies of Culicoides spp. in Britain are being expanded under a DEFRAfunded project out of the Institute of Animal Health, Pirbright. Monitoring is being expanded to twenty-five or more sites, one of the aims being to determine the species list, species distribution, seasonal incidence and vector competency of the various species.

Vector Competency

3.9 The C. obsoletus group has long been suspected of being a vector, mainly on the basis of BTV isolations from this species made in Cyprus, and African horse sickness virus (AHSV) isolations made from mixed pools of C. obsoletus and C. pulicaris in Spain. In this context it should be borne in mind that BTV and AHSV tend to utilise the same Culicoides species as vectors. 3.10 It is strongly suspected that C. obsoletus and/or C. pulicaris group midges acted as BTV vectors in northern Greece and southern Bulgaria during the 1999 BTV epizootic, as they were by far the most abundant and most prevalent detected. It is similarly suspected that these species may also have mediated the BT outbreaks in Serbia, western and southern Bulgaria, FYR Macedonia, Croatia and Bosnia during the period 2001-2002. C. imicola has not been recorded in these regions. 3.11 Vector competence studies on a British population of C. obsoletus have recorded oral susceptibility rates of less than 2% in comparison with a known major vector C. sonorensis (19.5%). This initially suggested that C. obsoletus is likely to be only a minor or inefficient vector of BTV. Nevertheless, the high abundance and survival rates of C. obsoletus as exhibited in Bulgaria in 1999, and as seen on farms and around stables in South East England, could compensate for its low levels of vector competence. Observations of cattle exposed to midges have shown up to ten thousand bites per hour. It should be noted that C. brevitarsis, the major vector of BTV in Australia, has an experimental competency of only 0.3 percent when feeding on sheep although it is quite an effective vector in the field. 3.12 Vector competence for a particular virus is a hereditary trait and populations of a vector species with high, low or intermediate levels of competence can be derived by selective breeding. Technical Review - Bluetongue: The Virus, Hosts and Vectors ___________________________________________________________________________ 6. Version 1.5; 21 November 2002

Epidemiology

Impact of Global Warming

3.13 Vector competence of Culicoides vectors for Orbiviruses is partly influenced by temperature. Orbivirus development in Culicoides vectors is unable to occur at temperatures below about 10°C to 15°C depending on the Orbivirus species and serotype. Furthermore, there needs to be a minimum amount of time at suitable temperatures (expressed as “day degrees or hour degrees”) for completion of the development cycle in the Culicoides vector before virus transmission can occur. This “physiological” time is the cumulative product of virus development time multiplied by the temperature in degrees above the threshold for virus replication. Increasing environmental temperature (climate change) will also extend the vector season. Combined, these conditions may result in Orbivirus development within Culicoides being able to take place over a greater proportion of the year and over a wider geographical area. In addition, within the range of temperatures over which Orbivirus development can occur, the levels of vector competence of a Culicoides vector population for some Orbivirus serotypes increases linearly with temperature and so the impact of warmer temperatures may be even greater. 3.14 Temperature can also affect the competence of ‘non-vector’ Culicoides species. For example, C. nubeculosus generally is considered to be incapable of transmitting BTV due to a midgut infection barrier. However, exposure of the immatures to rearing temperatures close to their upper lethal limit (33-35°C) can result in >10% of adults becoming competent to transmit BTV. It is likely that the integrity of the gut wall of some adults is damaged by the extreme rearing temperatures, thereby allowing virus particles to bypass the midgut barriers, enter the haemocoel and develop as in a normal vector. The increase in frequency and intensity of extremely warm days predicted to occur with climate change will enhance the chances of this phenomenon occurring in non-vector Culicoides species and hence could increase the number of BTV competent adults within populations. 3.15 The vectorial capacity of a Culicoides population (and hence the potential for virus transmission) is affected by (a) the number of adult midges in the population and (b) the proportion of adults capable of transmitting the virus, and is greatest when these factors are at a peak. 3.16 Within favourable limits, the development rate of Culicoides from egg to adult is directly related to temperature. Thus increasing temperatures coupled with an extension in the developmental season may result in a greater number of generations (and therefore adults) per year. In addition, the overwintering ability of adult Culicoides is likely to improve, as winters become both warmer and shorter. Improved overwintering success is also likely to increase the spring population input, which in turn could result in even larger populations during the summer Technical Review - Bluetongue: The Virus, Hosts and Vectors ___________________________________________________________________________ 7. Version 1.5; 21 November 2002 3.17 The proportion of adult Culicoides capable of transmitting virus is dependent on (a) vector competence (the capacity for the virus to develop in and be transmitted by the vector), (b) adult survival, (c) the blood-feeding interval and (d) the extrinsic incubation period (EIP; development time of the virus in the vector). In order to transmit virus Culicoides must not only be vector competent, but also survive long enough to blood-feed after the completion of the viral EIP. Culicoides vectors are more likely to satisfy these criteria at high temperatures (e.g. 27-30°C), because, although adult survival is reduced at high temperatures, this is more than compensated for by the accompanying decrease in duration of the EIP and blood-feeding interval. Consequently, it is likely that warmer temperatures as a result of climate change will increase the likelihood that Culicoides will survive long enough to transmit virus. 3.18 Changes in weather (temperature, precipitation, humidity and wind) and climate from global warming could produce both wider distribution of vectors towards the poles or upwards in elevation and increased vectorial capacity (the ability of a vector population to transmit virus to a vertebrate population) of Culicoides vector populations, resulting in increased prevalence of BTV in Europe. The present BT outbreak in the Mediterranean Basin is already the most serious epizootic on record. 3.19 An expansion in the range of C. imicola will increase the areas of Europe at risk from BTV. Also, the extended distribution of C. imicola could bring BTV into the range of C. obsoletus group and C. pulicaris group midges much more frequently and this could result in even greater areas of Europe being affected by BTV. 3.20 The impact of climate change on the vectorial capacity of Culicoides populations will have three main effects on BTV transmission in the Mediterranean basin: · the greater abundance of adult Culicoides combined with the increased proportion of adults capable of transmitting the virus will increase the likelihood and severity of an epizootic, following the introduction of BTV into an area. The greatest risk will be at times of the year when temperatures reach approximately 25-30°C (i.e. when conditions are optimal for Culicoides development and virus transmission · as temperatures will be conducive for both viral and Culicoides development for a greater proportion of the year, the length of the viral transmission season will increase. · the enhanced overwintering success of adult Culicoides combined with the extension in the Culicoides development season will prolong the seasonal occurrence of adult midges and hence improve the overwintering chances of BTV. 3.21. Studies are needed to correlate the day degrees required for BTV development in the potential vectors against British climate data to establish the risk of establishment of a BTV infection under present climatic conditions and with global warming.

Pathogenesis

  • Transfer occurs through blood from viremic animals via biting midges (Culicoides spp.)
  • Replication in haematopoietic and endothelial cells of blood vessels
  • Clinical signs vary between species, with sheep most severely affected
    • Pyrexia
    • Ocular and nasal discharge
    • Drooling from mouth uclers
    • Swelling of the mouth, head and neck
    • Lameness
    • Subdural hemorrhages
    • Inflammation of the coronary band
  • Cattle as the main reservoir
  • A blue tongue is rarely seen as as a clinical sign of infection
  • Resulting loss of condition, reduction in wool an meat production, which can be followed by death

Diagnosis

The typical clinical signs of bluetongue enable a presumptive diagnosis, especially in areas where the disease is endemic. Suspicion is confirmed by the presence of petechiae, ecchymoses, or hemorrhages in the wall of the base of the pulmonary artery and focal necrosis of the papillary muscle of the left ventricle. These highly characteristic lesions are usually obvious in severe clinical infections but may be barely visible in mild or convalescent cases. These lesions are often described as pathognomonic for bluetongue, but they have also been observed occasionally in other ovine diseases such as heartwater, pulpy kidney disease, and Rift Valley fever. Hemorrhages and necrosis are usually found where mechanical abrasion damages fragile capillaries, such as on the buccal surface of the cheek opposite the molar teeth and the mucosa of the esophageal groove and omasal folds. Other autopsy findings include subcutaneous and intermuscular edema, skeletal myonecrosis, myocardial and intestinal hemorrhages, hydrothorax, hydropericardium, pericarditis, and pneumonia. In many areas of the world, bluetongue in sheep, and especially in other ruminants, is subclinical and, therefore, laboratory confirmation based on virus isolation in embryonated chicken eggs, susceptible sheep, or cell cultures, or the identification of viral RNA by PCR is necessary. The identity of isolates may be confirmed by the group-specific antigen-capture ELISA, immunofluorescence, immunoperoxidase, serotype-specific virus neutralization tests, or hybridization with complementary gene sequences of group- or serotype-specific genes. For virus isolation, blood (10-20 mL) is collected as early as possible from febrile animals into an anticoagulant such as heparin, sodium citrate, or EDTA and transported at 4°C to the laboratory. For longterm storage where refrigeration is not possible, blood is collected in oxalate-phenol-glycerin (OPG). Blood to be frozen should be collected in buffered lactose peptone and stored at or below -70°C. Blood collected at later times during the viremic period should not be frozen, as lysing of the RBC or thawing releases the cell-associated virus, which may then be neutralized by early humoral antibody. The virus does not remain stable for long at -20°C. In fatal cases, specimens of spleen, lymph nodes, or red bone marrow are collected and transported to the laboratory at 4°C as soon as possible after death. A serologic response in ruminants can be detected 7-14 days after infection and is generally lifelong. Current recommended serologic techniques for the detection of bluetongue virus antibody include agar gel immunodiffusion and competitive ELISA. The latter is the test of choice and does not detect cross-reacting antibody to other orbiviruses, especially anti-EHDV (epizootic hemorrhagic disease virus) antibody. Various forms of virus neutralization test, including plaque reduction, plaque inhibition, and microtiter neutralization can be used to detect type-specific antibody.

Clinical Signs

The course of the disease in sheep can vary from peracute to chronic, with a mortality rate of 2-30%. Peracute cases die within 7-9 days of infection, mostly as a result of severe pulmonary edema leading to dyspnea, frothing from the nostrils, and death by asphyxiation. In chronic cases, sheep may die 3-5 wk after infection, mainly as a result of bacterial complications, especially pasteurellosis, and exhaustion. Mild cases usually recover rapidly and completely. The major production losses include deaths, unthriftiness during prolonged convalescence, wool breaks, and possibly reproductive loss. In sheep, bluetongue virus causes vascular endothelial damage, resulting in changes to capillary permeability and subsequent intravascular coagulation. This results in edema, congestion, hemorrhage, inflammation, and necrosis. The clinical signs in sheep are typical. After an incubation period of 4-6 days, a fever of 105-107.5°F (40.5-42°C) develops. The animals are listless and reluctant to move. Clinical signs in young lambs are more apparent, and the mortality rate is higher (up to 30%). About 2 days after onset of fever, additional clinical signs such as edema of lips, nose, face, submandibular area, eyelids, and sometimes ears; congestion of mouth, nose, nasal cavity, conjunctiva, and coronary bands; and lameness and depression may be seen. A serous nasal discharge is common, later becoming mucopurulent. The congestion of nose and nasal cavity produces a “sore muzzle” effect, the term used to describe the disease in sheep in the USA. Sheep eat less because of oral soreness and will hold food in their mouths to soften before chewing. They may champ to produce a frothy oral discharge at the corners of the lips. On close examination, small hemorrhages can be seen on the mucous membranes of the nose and mouth. Ulceration develops where the teeth come in contact with lips and tongue, especially in areas of most friction. Some affected sheep have severe swelling of the tongue, which may become cyanotic (‘blue tongue”) and even protrude from the mouth. Animals walk with difficulty as a result of inflammation of the hoof coronets. A purple-red color is easily seen as a band at the junction of the skin and the hoof. Later in the course of disease, lameness or torticollis is due to skeletal muscle damage. In most affected animals, abnormal wool growth resulting from dermatitis may be observed. The pathogenesis of bluetongue in cattle seems to differ from that in sheep and is based on immediate IgE hypersensitivity reactions. Clinical signs in cattle are rare but may be similar to those seen in sheep. They are usually limited to fever, increased respiratory rate, lacrimation, salivation, stiffness, oral vesicles and ulcers, hyperesthesia, and a vesicular and ulcerative dermatitis. Susceptible cattle and sheep infected during pregnancy may abort or deliver malformed calves or lambs. The malformations include hydranencephaly or porencephaly, which results in ataxia and blindness at birth. White-tailed deer and pronghorn antelope develop severe hemorrhagic disease leading to sudden death. Pregnant dogs abort or give birth to stillborn pups and then die in 3-7 days.

Laboratory Tests

Pathology

Complete loss of integrity of epithelium. Uncommon.

  • Characteristic of Bluetongue Virus,
  • Epithelium lost and haemorrhage produces blue / black discoloration of the tongue, hence the name.



  • Grossly:
    • Infarctions -> necrosis
    • Haemorrhage
  • Histologically:
    • Necrosis -> calcification or regeneration (depends on age of lesion)

Treatment

  • BTV is NOTIFIABLE
  • Vigilance in recognizing clinical signs
  • Restriction of movement:
    • Protection Zone: 100km radius around infected premises, movement within zone allowed but not in or out
      • Vaccination within PZ using appropriate serotype is encouraged but still voluntary
    • Surveillance Zone: 50km radius beyond PZ
  • Vector control: ectoparasiticides, etc.

Prophylactic immunization of sheep remains the most effective and practical control measure against bluetongue in endemic regions. Three polyvalent vaccines, each comprising 5 different bluetongue virus serotypes attenuated by serial passage in embryonated hens’ eggs followed by growth and plaque selection in cell culture, are widely used in southern Africa and elsewhere, should epizootics of bluetongue occur. A monovalent modified live virus vaccine propagated in cell culture is available for use in sheep in the USA. Live-attenuated vaccines should not be used during Culicoides vector seasons because they may transmit the vaccine virus(es) from vaccinated to nonvaccinated animals, eg, other ruminant species. This may result in reassortment of genetic material and give rise to new viral strains. Abortion or malformation, particularly of the CNS, of fetuses may follow vaccination of ewes and cows with attenuated live vaccines during the first half and the first trimester of pregnancy, respectively. Passive immunity in lambs usually lasts 4-6 mo. The control of bluetongue is different in areas where the disease is not endemic. During an outbreak, when one or a limited number of serotypes may be involved, vaccination strategy depends on the serotype(s) that are causing infection. Use of vaccine strains other than the one(s) causing infection affords little or no protection. The vector status, potential risk from vaccine virus reassortment with wild-type viral strains, virus spread by the vectors to other susceptible ruminants, and reversion to virulence of vaccine virus strains or even the production of new serotypes also should be considered. Although a number of noninfectious vaccines are in development, they are not yet commercially available. Control of vectors by using insecticides or protection from vectors by moving animals into barns during the evening hours lowers the number of Culicoides bites and subsequently the risk of exposure to bluetongue virus infection.

Links

References

  1. Defra (2002) Technical Review - Bluetongue : The Virus, Hosts and Vectors.
  2. Gibbs, E P J and Geiner, E C (1994) The Epidemiology of Bluetongue. Comparative Immunology, Microbiology and Infectious Diseases, 17(3-4), 207-220.
  3. Spreull, J (1905) Malarial catarrhal fever (bluetongue) of sheep in South Africa. Journal of Comparative Pathology and Therapeutics, 18, 321-337.
  4. MacLachlan, N J (2004) Bluetongue: A Review and Global Overview of the Only OIE List a Disease that is Endemic in North America. Proceedings of the 55th Annual Meeting of the American College of Veterinary Pathologists (ACVP) and 39th Annual Meeting of the American Society of Clinical Pathology (ASVCP), p1237.
  5. Carter, G R and Wise, D J (2005) A Concise Review of Veterinary Virology, IVIS.
  6. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
  7. Dal Pozzo, F et al (2009) Bovine infection with bluetongue virus with special emphasis on European serotype 8. The Veterinary Journal, 182(2), 142-151.
  8. MacLachlan, N J et al (2009) The Pathology and Pathogenesis of Bluetongue. Journal of Comparative Pathology, 141(1), 1-16.
  9. Barratt-Boyes, S M and MacLachlan, N J (1995) Pathogenesis of bluetongue virus infection of cattle. Journal of the American Veterinary Medical Association, 206(9), 1322-1329.
  10. Afshar, A (2004) Bluetongue: Laboratory Diagnosis. Comparative Immunology, Microbiology and Infectious Diseases, 17(3-4), 221-242.
  11. Gould, E A and Higgs, S (2009) Impact of climate change and other factors on emerging arbovirus diseases. Transactions of the Royal Society of Tropical Medicine and Hygiene, 103(2), 109-121.
  12. MacLachlan, N J (1994) The pathogenesis and immunology of bluetongue virus infection of ruminants. Comparative Immunology, Microbiology and Infectious Diseases, 17(3-4), 197-206.
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