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bluetongue

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bluetongue

Summary

  • Last modified
  • 27 June 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • bluetongue
  • Overview
  • Bluetongue is an arthropod-borne, non-contagious viral disease of domestic and wild ruminants that induces variable clinical signs depending on the host species and breed (Maclachlan...

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Pictures

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PictureTitleCaptionCopyright
Severe depression and lameness, oedema of the ears and face, inflammation of the nose and lips.
TitleSymptoms
CaptionSevere depression and lameness, oedema of the ears and face, inflammation of the nose and lips.
CopyrightGeoffrey P. Gard
Severe depression and lameness, oedema of the ears and face, inflammation of the nose and lips.
SymptomsSevere depression and lameness, oedema of the ears and face, inflammation of the nose and lips.Geoffrey P. Gard
Swollen cyanotic tongue, oedema and inflammation of the face, nose and lips
TitleSymptoms
CaptionSwollen cyanotic tongue, oedema and inflammation of the face, nose and lips
CopyrightGeoffrey P. Gard
Swollen cyanotic tongue, oedema and inflammation of the face, nose and lips
SymptomsSwollen cyanotic tongue, oedema and inflammation of the face, nose and lipsGeoffrey P. Gard
A sheep infected with bluetongue virus: conronitus (haemorrhage of the coronary band), causing lameness.
TitleSymptoms
CaptionA sheep infected with bluetongue virus: conronitus (haemorrhage of the coronary band), causing lameness.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus: conronitus (haemorrhage of the coronary band), causing lameness.
SymptomsA sheep infected with bluetongue virus: conronitus (haemorrhage of the coronary band), causing lameness.Philip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
TitleSymptoms
CaptionA sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
SymptomsA sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.Philip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
TitleSymptoms
CaptionA sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
SymptomsA sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.Philip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
TitleSymptoms
CaptionA sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.
SymptomsA sheep infected with bluetongue virus, serotype 3: oedema of the muzzle and excessive salivation.Philip Mellor/Institute for Animal Health, Pirbright, UK
Sheep with bluetongue showing facial oedema.
TitleBluetongue. Symptoms.
CaptionSheep with bluetongue showing facial oedema.
CopyrightR. Paul Kitching
Sheep with bluetongue showing facial oedema.
Bluetongue. Symptoms.Sheep with bluetongue showing facial oedema.R. Paul Kitching
Sheep with bluetongue showing coronitis.
TitleBluetongue. Symptoms.
CaptionSheep with bluetongue showing coronitis.
CopyrightR. Paul Kitching
Sheep with bluetongue showing coronitis.
Bluetongue. Symptoms.Sheep with bluetongue showing coronitis.R. Paul Kitching
(a) Normal brain: (b) Brain with cerebellar hypoplasia resulting from a congenital Bluetongue infection.
TitlePathology. Bluetongue.
Caption(a) Normal brain: (b) Brain with cerebellar hypoplasia resulting from a congenital Bluetongue infection.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
(a) Normal brain: (b) Brain with cerebellar hypoplasia resulting from a congenital Bluetongue infection.
Pathology. Bluetongue.(a) Normal brain: (b) Brain with cerebellar hypoplasia resulting from a congenital Bluetongue infection.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
A sheep infected with bluetongue virus, serotype 3: oedema of the tongue and muzzle.
TitleSymptoms
CaptionA sheep infected with bluetongue virus, serotype 3: oedema of the tongue and muzzle.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: oedema of the tongue and muzzle.
SymptomsA sheep infected with bluetongue virus, serotype 3: oedema of the tongue and muzzle.Philip Mellor/Institute for Animal Health, Pirbright, UK
Lameness of a sheep suffering from bluetongue virus infection.
TitleSymptoms
CaptionLameness of a sheep suffering from bluetongue virus infection.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
Lameness of a sheep suffering from bluetongue virus infection.
SymptomsLameness of a sheep suffering from bluetongue virus infection.Philip Mellor/Institute for Animal Health, Pirbright, UK
A cow infected with bluetongue virus: excoriation of the teats.
TitleBluetongue symptoms
CaptionA cow infected with bluetongue virus: excoriation of the teats.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A cow infected with bluetongue virus: excoriation of the teats.
Bluetongue symptomsA cow infected with bluetongue virus: excoriation of the teats.Philip Mellor/Institute for Animal Health, Pirbright, UK
A cow infected with bluetongue virus: 'burnt muzzle' - a result of necrosis of the muzzle epithelium.
TitleBluetongue symptoms
CaptionA cow infected with bluetongue virus: 'burnt muzzle' - a result of necrosis of the muzzle epithelium.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A cow infected with bluetongue virus: 'burnt muzzle' - a result of necrosis of the muzzle epithelium.
Bluetongue symptomsA cow infected with bluetongue virus: 'burnt muzzle' - a result of necrosis of the muzzle epithelium.Philip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: conjunctivitis, resulting from haemorrhage and engorgement of the conjunctiva.
TitleBluetongue symptoms
CaptionA sheep infected with bluetongue virus, serotype 3: conjunctivitis, resulting from haemorrhage and engorgement of the conjunctiva.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A sheep infected with bluetongue virus, serotype 3: conjunctivitis, resulting from haemorrhage and engorgement of the conjunctiva.
Bluetongue symptomsA sheep infected with bluetongue virus, serotype 3: conjunctivitis, resulting from haemorrhage and engorgement of the conjunctiva.Philip Mellor/Institute for Animal Health, Pirbright, UK
A cow infected with bluetongue virus: 'burnt muzzle' - a result of necrosis of the muzzle epithelium.
TitleSymptoms
CaptionA cow infected with bluetongue virus: 'burnt muzzle' - a result of necrosis of the muzzle epithelium.
CopyrightPhilip Mellor/Institute for Animal Health, Pirbright, UK
A cow infected with bluetongue virus: 'burnt muzzle' - a result of necrosis of the muzzle epithelium.
SymptomsA cow infected with bluetongue virus: 'burnt muzzle' - a result of necrosis of the muzzle epithelium.Philip Mellor/Institute for Animal Health, Pirbright, UK
Congested, oedematous lung and marked hydrothorax.
TitleGross pathology
CaptionCongested, oedematous lung and marked hydrothorax.
CopyrightGeoffrey P. Gard
Congested, oedematous lung and marked hydrothorax.
Gross pathologyCongested, oedematous lung and marked hydrothorax.Geoffrey P. Gard
Haemorrhage at the base of the pulmonary artery and a congested oedematous lung.
TitleGross pathology
CaptionHaemorrhage at the base of the pulmonary artery and a congested oedematous lung.
CopyrightGeoffrey P. Gard
Haemorrhage at the base of the pulmonary artery and a congested oedematous lung.
Gross pathologyHaemorrhage at the base of the pulmonary artery and a congested oedematous lung.Geoffrey P. Gard
Haemorrhages and inflammation in the region of the reticulo-omasal groove.
TitleGross pathology
CaptionHaemorrhages and inflammation in the region of the reticulo-omasal groove.
CopyrightGeoffrey P. Gard
Haemorrhages and inflammation in the region of the reticulo-omasal groove.
Gross pathologyHaemorrhages and inflammation in the region of the reticulo-omasal groove.Geoffrey P. Gard
Congested, oedematous lung with the trachea opened to show froth.
TitleGross pathology
CaptionCongested, oedematous lung with the trachea opened to show froth.
CopyrightGeoffrey P. Gard
Congested, oedematous lung with the trachea opened to show froth.
Gross pathologyCongested, oedematous lung with the trachea opened to show froth.Geoffrey P. Gard
Haemorrhage and congestion of tunica media of the pulmonary artery.
TitleHistopathology
CaptionHaemorrhage and congestion of tunica media of the pulmonary artery.
CopyrightGeoffrey P. Gard
Haemorrhage and congestion of tunica media of the pulmonary artery.
HistopathologyHaemorrhage and congestion of tunica media of the pulmonary artery.Geoffrey P. Gard
Alveolar congestion and oedema of the lung.
TitleHistopathology
CaptionAlveolar congestion and oedema of the lung.
CopyrightGeoffrey P. Gard
Alveolar congestion and oedema of the lung.
HistopathologyAlveolar congestion and oedema of the lung.Geoffrey P. Gard
Degeneration and necrosis of the skeletal muscle.
TitleHistopathology
CaptionDegeneration and necrosis of the skeletal muscle.
CopyrightGeoffrey P. Gard
Degeneration and necrosis of the skeletal muscle.
HistopathologyDegeneration and necrosis of the skeletal muscle.Geoffrey P. Gard
Early inflammatory lesion in skeletal muscle.
TitleHistopathology
CaptionEarly inflammatory lesion in skeletal muscle.
CopyrightGeoffrey P. Gard
Early inflammatory lesion in skeletal muscle.
HistopathologyEarly inflammatory lesion in skeletal muscle.Geoffrey P. Gard
Myocardium, showing inflammatory and necrotic changes.
TitleHistopathology
CaptionMyocardium, showing inflammatory and necrotic changes.
CopyrightGeoffrey P. Gard
Myocardium, showing inflammatory and necrotic changes.
HistopathologyMyocardium, showing inflammatory and necrotic changes.Geoffrey P. Gard
Swelling and exudate on the nostrils and lips.
TitleExternal symptoms
CaptionSwelling and exudate on the nostrils and lips.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Swelling and exudate on the nostrils and lips.
External symptomsSwelling and exudate on the nostrils and lips.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)

Identity

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Preferred Scientific Name

  • bluetongue

International Common Names

  • English: anomalies in the calf due to in-utero bluetongue; blue tongue; bluetongue in ruminants; hydranencephaly with or without cerebellar lesions in ruminants
  • Spanish: lengua azul
  • French: fievre catarrhale du mouton

English acronym

  • BT

Overview

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Bluetongue is an arthropod-borne, non-contagious viral disease of domestic and wild ruminants that induces variable clinical signs depending on the host species and breed (Maclachlan, 2009), as well as camelids, and some other herbivores (such as elephants). The disease is caused by bluetongue virus (BTV) which is the type species of the genus Orbivirus within the family Reoviridae.

BTV is transmitted through bites from adult females of certain species of Culicoides (biting midges). The distribution and seasonal activity of the vector determines the distribution and the occurrence of the disease (Mellor, 2000). Bluetongue is most common in certain breeds of sheep whereas asymptomatic BTV infection of cattle is typical in enzootic regions. Bluetongue in cattle can be a feature of specific outbreaks, notably the current epizootic in Europe caused by BTV serotype 8 (Maclachlan, 2009). White-tailed deer, pronghorn (Dubay, 2006) and desert bighorn sheep in North America can get the disease, and in goats clinical disease is rare, and, when present, is much milder than in sheep (Verwoerd and Erasmus, 1994).

Bluetongue was first described in South Africa after Merino sheep from Europe were introduced in the late eighteenth century (Verwoerd and Erasmus, 1994). The disease was considered confined to South Africa and for many years research efforts on the virus and the disease were exclusively undertaken in that country, mostly at the Onderstepoort Veterinary Institute. The viral nature of the disease was established, as was its insect spread and multiple virus serotypes (Howell, 1960; 1970). There are now 24 serotypes of BTV recognized worldwide.

BTV is the type species of the genus Orbivirus in the family Reoviridae (sub family Sedoreovirinae). The BTV genome consists of 10 double stranded RNA segments that are packaged within an icosahedral nucleocapsid composed of seven structural proteins (Roy, 2006). The inner capsid, forming the core, is made up by two major (VP7 and VP3) and three minor (VP1, VP4 and VP6) viral proteins, which are relatively conserved amongst members of the BTV serogroup. The outer capsid is composed of two proteins, VP2 and VP5, which show a high degree of sequence variation both between and within each serotype (Mertens 2007). The serotype is determined mainly by VP2, which contains most of the neutralizing epitopes of the virus.

This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. For further information on this disease from OIE, see the website: www.oie.int.

Host Animals

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Animal nameContextLife stageSystem
Bos indicus (zebu)Domesticated hostCattle & Buffaloes: All Stages
Bos taurus (cattle)Domesticated hostCattle & Buffaloes: All Stages
Bubalus bubalis (Asian water buffalo)Domesticated hostCattle & Buffaloes: All Stages
Camelus dromedarius (dromedary camel)Domesticated host, Wild hostOther: All Stages
Capra hircus (goats)Domesticated hostSheep & Goats: All Stages
CervidaeDomesticated hostOther: All Stages
ElephantidaeWild hostOther: All Stages
GallusExperimental settingsPoultry: Embryo
Mus musculus (house mouse)Experimental settingsOther: Juvenile
Ovis aries (sheep)Domesticated hostSheep & Goats: All Stages
RuminantiaWild hostOther: All Stages

Hosts/Species Affected

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Bluetongue is an arbovirus, infecting vertebrates and invertebrates cyclically.

Bluetongue virus naturally infects domestic and wild ruminants, camelids and some other herbivores such as elephants. Historically, the primary cycle may have involved species of African antelope, but this role has now been taken over by cattle (Erasmus, 1990).

Midges of the genus Culicoides act as biological vectors of bluetongue virus. Of the approximately 1400 species of Culicoides world-wide, less than 20 are considered actual or possible vectors (OIE, 1998; Mellor, 1990). The most well-studied vector species are C. variipennis and C. insignis in the USA, C. fulvus, C. wadai, C. actoni and C. brevitarsis in Australia, and C. imicola in Africa and the Middle East (Erasmus, 1990). It is possible that additional vector species will be identified in countries such as China and Bulgaria where bluetongue has been recognized only recently.

Systems Affected

Top of page blood and circulatory system diseases of large ruminants
blood and circulatory system diseases of small ruminants
bone, foot diseases and lameness in large ruminants
bone, foot diseases and lameness in small ruminants
digestive diseases of large ruminants
digestive diseases of small ruminants
multisystemic diseases of large ruminants
multisystemic diseases of small ruminants
nervous system diseases of large ruminants
nervous system diseases of small ruminants
reproductive diseases of large ruminants
reproductive diseases of small ruminants
respiratory diseases of large ruminants
respiratory diseases of small ruminants
skin and ocular diseases of large ruminants
skin and ocular diseases of small ruminants

Distribution

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Transmission of the BTV is by the bite of adult females of certain Culicoides species, and the distribution and seasonal activity of the vector determines both the distribution and occurrence of the disease.

Until recently bluetongue was confined mainly to tropical and temperate regions between latitudes 40oN and 35oS (Mellor 2000). The disease is found in Africa, Americas, Australia, and parts of Asia (Walton 2004). Between 1998 and 2007, several BTV strains of five serotypes (BTV-1, BTV-2, BTV-4, BTV-9, and BTV-16) have been circulating in Europe around the Mediterranean (Saegerman, 2008). From 2006, two main changes occurred in the European epidemiology of BT: (i) the appearance of exotic BTV strains belonging to several serotypes, and (ii) the emergence further north than ever before of a BTV serotype.circulating in the Mediterranean area.(Vandenbussche 2009). In August 2006, BTV emerged for the first time northern Europe and quickly spread to Netherlands, Luxembourg, Belgium, Northern France and Germany (Vandenbussche 2009). This outbreak was caused by BTV-8, (which had not before in Europe, but which did occur in sub-Saharan Africa), and was transmitted by endogenous midges including Culicoides obsoletus, C. dewulfi and C. chiopterus (Saegerman 2008). The BTV-8 re-emerged in 2007 spreading to the UK (OIE report id6259) and extending its range in the countries infected the year before. As a result of serious economic loss, a vaccination campaign against BTV-8 was started in 2008 in most western European countries. In 2008 BTV was found in Czech Republic, Switzerland, and Sweden as well as in most of the countries that had the virus the year before.

From 1998 to 2005 at least 6 strains of BTV of 5 serotypes (1, 2, 4, 9 and 16)  have been circulating in the Mediterranean area. In July 2007, BTV-1 was introduced from Morocco to Spain, and from there it spread quickly to Portugal and south-west France. In spring 2009, BTV-1 was isolated in north-east france, indicating that the virus was still spreading. In October 2008, a strain of BTV-6 was identified in the Netherlands and in Germany. Also in 2008 a strain identified as BTV-11 was identified in north Belgium (Vandenbussche, 2009).  

In endemic areas such as South Africa, serotypes are distributed randomly and the dominant serotypes at any particular time are largely determined by herd immunity. Monitoring Culicoides  for BTV at various sites in South Africa over 6 years (1979-1984) showed that 14-18 different serotypes were found each year although at very different frequencies.The dominat serotypes were usually replaced by others the following season. These seroptypes posess a high epidemic potential , and include sertypes 1-6, 8, 11, and 24 (Erasmus, 1994).

For current information on disease incidence, see OIE's WAHID Interface

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AfghanistanNo information availableOIE, 2009
ArmeniaDisease not reportedOIE, 2009
AzerbaijanDisease never reportedOIE, 2009
BahrainDisease never reportedOIE, 2009
BangladeshDisease not reportedOIE, 2009
BhutanDisease never reportedOIE, 2009
Brunei DarussalamDisease not reportedOIE Handistatus, 2005
CambodiaNo information availableOIE, 2009
ChinaNo information availableNULLOIE, 2004a; Chen et al., 1996; Zhou WeiHan, 1996; Zhu et al., 1996; OIE, 2009
-AnhuiWidespreadZhou WeiHan, 1995; Zhou WeiHan, 1996
-GansuLocalisedHuang et al., 1996
-GuangxiWidespreadChen et al., 1996
-Hong KongNo information availableOIE, 2009
-JiangsuLocalisedZhu et al., 1996
-Nei MengguWidespreadGuo et al., 1996; Mo et al., 1996; Zhang et al., 1996
-ShanxiLocalisedLei et al., 1996
-XinjiangWidespreadQin et al., 1996; Zhang et al., 1996
-YunnanWidespreadBi et al., 1996; Zhang et al., 1996
Georgia (Republic of)Disease not reportedOIE Handistatus, 2005
IndiaRestricted distributionNULLOIE, 1999; OIE, 2009
-Andhra PradeshWidespreadMehrotra, 1992; Sreenivasulu et al., 1999
-GujaratWidespreadMehrotra, 1992
-HaryanaWidespreadJain et al., 1986; Jain et al., 1992
-Indian PunjabPresentSharma et al., 1981
-Jammu and KashmirWidespreadMehrotra, 1992
-KarnatakaWidespreadMehrotra, 1992
-Madhya PradeshWidespreadMehrotra, 1992
-MaharashtraWidespreadKukarni et al., 1992; Mehrotra, 1992
-OdishaPresentPrasad et al., 1987
-RajasthanWidespreadMehrotra, 1992
-Tamil NaduWidespreadMehrotra, 1992; Aruni et al., 1997
-Uttar PradeshWidespreadMehrotra, 1992
IndonesiaDisease not reportedNULLOIE, 1999; OIE, 2009
-JavaWidespreadSendow et al., 1986; Sendow et al., 1991
-KalimantanWidespreadSendow et al., 1986
-Nusa TenggaraWidespreadSendow et al., 1986
-SulawesiWidespreadSendow et al., 1986
-SumatraWidespreadSendow et al., 1986
IranPresentNULLOIE, 1999; OIE, 2009
IraqNo information availableNULLHafez, 1978; OIE, 2009
IsraelPresentNULLHassan, 1992a; Dafni, 1966; Braverman and Galun, 1973; Shimshony et al., 1988; OIE, 2003; OIE, 2009
JapanDisease not reported200602Gard, 1996; Goto et al., 1996; OIE, 1999; OIE, 2009
JordanDisease not reportedNULLOIE, 1999; OIE, 2009
KazakhstanDisease not reportedOIE, 2009
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofDisease never reportedOIE, 2009
KuwaitDisease never reportedOIE, 2009
KyrgyzstanDisease never reportedOIE, 2009
LaosDisease never reportedOIE, 2009
LebanonDisease not reportedOIE, 2009
MalaysiaDisease not reportedOIE, 2009
-Peninsular MalaysiaDisease not reportedHassan, 1992b; Sharifah et al., 1995; OIE Handistatus, 2005
-SabahLast reported1999OIE, 1999; OIE Handistatus, 2005
-SarawakSerological evidence and/or isolation of the agentOIE Handistatus, 2005
MongoliaAbsent, reported but not confirmedOIE, 2009
MyanmarDisease never reportedOIE, 2009
NepalNo information availableOIE, 2009
OmanDisease never reportedNULLHassan, 1992a; OIE, 2009
PakistanRestricted distributionNULLHawkes, 1996; OIE, 2009
PhilippinesNo information availableOIE, 2009
QatarNo information availableOIE, 2009
Saudi ArabiaPresentNULLHafez and Taylor, 1985; Abu et al., 1992; OIE, 2009
SingaporeDisease not reportedOIE, 2009
Sri LankaDisease never reportedOIE, 2009
SyriaDisease not reportedNULLTaylor et al., 1985; OIE, 2009
TaiwanLast reported2003OIE, 2003; OIE Handistatus, 2005
TajikistanDisease never reportedOIE, 2009
ThailandDisease never reportedNULLApiwatnakorn et al., 1996; OIE, 2009
TurkeyDisease not reported200008Taylor et al., 1985; Burgu et al., 1992; OIE, 1999; OIE, 2009
TurkmenistanDisease never reportedOIE Handistatus, 2005
United Arab EmiratesDisease not reportedOIE, 2009
UzbekistanDisease never reportedOIE Handistatus, 2005
VietnamDisease never reportedOIE, 2009
YemenNo information availableNULLStanley, 1990; OIE, 2009

Africa

AlgeriaPresentNULLOIE Reports; OIE Reports; OIE Reports; OIE, 2009
AngolaDisease never reportedOIE, 2009
BeninNo information availableOIE, 2009
BotswanaDisease not reported20080131Mushi et al., 1992; OIE, 2009
Burkina FasoNo information availableOIE, 2009
BurundiDisease not reportedOIE Handistatus, 2005
CameroonDisease never reportedEkue et al., 1985; Lefèvre and Calvez, 1986; OIE Handistatus, 2005
Cape VerdeDisease never reportedOIE Handistatus, 2005
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableNULLLefèvre and Calvez, 1986; OIE, 2009
CongoNo information availableOIE, 2009
Congo Democratic RepublicDisease not reportedLefèvre and Calvez, 1986; OIE Handistatus, 2005
Côte d'IvoireDisease not reportedFormenty et al., 1994; OIE Handistatus, 2005
DjiboutiDisease not reportedOIE, 2009
EgyptDisease not reported1974Hilmy Zaki, 1965; Ayoub and Singh, 1970; Soliman et al., 1972; Hafez and Ozawa, 1973; Barsoum, 1992; OIE, 2009
EritreaNo information availableOIE, 2009
EthiopiaNo information availableNULLLefèvre and Calvez, 1986; OIE, 2009
GabonDisease never reportedNULLLefèvre and Calvez, 1986; OIE, 2009
GambiaNo information availableNULLGoossens et al., 1998; OIE, 2009
GhanaNo information availableOIE, 2009
GuineaNo information availableNULLKonstantinov et al., 1990; Butenko, 1996; OIE, 2009
Guinea-BissauNo information availableOIE, 2009
KenyaDisease not reportedNULLDavies and Walker, 1974; Davies et al., 1992; OIE, 1999; OIE, 2009
LesothoPresentNULLOIE, 1999; OIE, 2009
LibyaDisease never reportedOIE Handistatus, 2005
MadagascarDisease never reportedNULLFerreira and Rosinha, 1986; OIE, 2009
MalawiAbsent, reported but not confirmedNULLHaresnape et al., 1988; OIE, 1999; OIE, 2009
MaliNo information availableNULLMaiga and Sarr, 1992; OIE, 2009
MauritaniaNo information availableLefèvre and Calvez, 1986
MauritiusDisease never reportedOIE, 2009
MoroccoDisease not reported200711OIE, 2004d; Hawkes, 1996; OIE, 2009
MozambiqueDisease not reported200512Kanhai and Silva, 1981; OIE, 2009
NamibiaDisease not reported200806OIE, 2004e; OIE, 1999; OIE, 2009
NigerDisease not reportedMariner et al., 1989; Weitzman et al., 1991
NigeriaDisease never reportedNULLBida and Eid, 1974; Moore and Kemp, 1974; Taylor and McCausland, 1976; Obi et al., 1983; OIE, 2009
RéunionLast reported2003Barré et al., 1985; Charton et al., 1991; OIE, 2003; OIE Handistatus, 2005
RwandaDisease never reportedOIE, 2009
Sao Tome and PrincipeDisease not reportedOIE Handistatus, 2005
SenegalNo information availableNULLLefevre and Taylor, 1983; OIE, 2009
SeychellesDisease not reportedOIE Handistatus, 2005
SomaliaNo information availableHussein et al., 1985; OIE Handistatus, 2005
South AfricaPresentNULLNevill et al., 1992; OIE, 1999; OIE, 2009
SudanDisease not reported198908Pillai, 1961; Abu Elzein, 1985; Elfatih et al., 1987; Fayza et al., 1990; OIE, 2009
SwazilandDisease not reportedOIE, 2009
TanzaniaNo information availableNULLHyera and Lyaruu, 1995; OIE, 2009
TogoNo information availableOIE, 2009
TunisiaDisease not reported200806OIE, 1999; OIE, 2009
UgandaDisease not reportedOIE, 2009
ZambiaNo information availableNULLMweene et al., 1996; OIE, 2009
ZimbabweAbsent, reported but not confirmedNULLJorgensen et al., 1989; Anderson and Rowe, 1998; OIE, 2009

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaDisease not reported198809Hawkes, 1996; OIE, 2009
-British ColumbiaLocalisedDulac et al., 1992
GreenlandDisease never reportedOIE, 2009
MexicoPresentNULLHoman et al., 1992; OIE, 1999; OIE, 2009
USARestricted distributionOIE, 2009
-AlabamaLocalisedPearson et al., 1992; Tomori et al., 1992
-ArizonaWidespreadPearson et al., 1992; Tomori et al., 1992
-ArkansasLocalisedPearson et al., 1992; Tomori et al., 1992
-CaliforniaWidespreadPearson et al., 1992; Tomori et al., 1992
-ColoradoWidespreadPearson et al., 1992; Tomori et al., 1992
-FloridaPresentPearson et al., 1992; Tomori et al., 1992
-GeorgiaPearson et al., 1992; Tomori et al., 1992
-IdahoPresentPearson et al., 1992; Tomori et al., 1992
-IllinoisPresentPearson et al., 1992
-IowaLocalisedPearson et al., 1992; Tomori et al., 1992
-KansasPresentPearson et al., 1992; Tomori et al., 1992
-KentuckyLocalisedPearson et al., 1992; Tomori et al., 1992
-LouisianaPresentPearson et al., 1992; Tomori et al., 1992
-MississippiWidespreadPearson et al., 1992; Tomori et al., 1992
-MissouriWidespreadPearson et al., 1992; Tomori et al., 1992
-MontanaPresentPearson et al., 1992; Tomori et al., 1992
-NebraskaPresentPearson et al., 1992; Tomori et al., 1992
-NevadaPresentPearson et al., 1992; Tomori et al., 1992
-New MexicoWidespreadPearson et al., 1992; Tomori et al., 1992
-North CarolinaLocalisedPearson et al., 1992; Tomori et al., 1992
-OklahomaWidespreadPearson et al., 1992; Tomori et al., 1992
-OregonPresentPearson et al., 1992; Tomori et al., 1992
-South CarolinaLocalisedPearson et al., 1992; Tomori et al., 1992
-South DakotaLocalisedPearson et al., 1992; Tomori et al., 1992
-TennesseeLocalisedPearson et al., 1992; Tomori et al., 1992
-TexasWidespreadPrice and Hardy, 1954; Pearson et al., 1992; Tomori et al., 1992
-UtahWidespreadPearson et al., 1992; Tomori et al., 1992
-VirginiaLocalisedPearson et al., 1992; Tomori et al., 1992
-WashingtonPresentPearson et al., 1992; Tomori et al., 1992
-WyomingPresentPearson et al., 1992; Tomori et al., 1992

Central America and Caribbean

Antigua and BarbudaDisease never reportedHoman et al., 1992
BahamasDisease not reportedGibbs and Greiner, 1985
BarbadosSerological evidence and/or isolation of the agentThompson et al., 1992; OIE, 1999; OIE Handistatus, 2005
BelizeDisease not reportedOIE, 2009
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease not reportedOIE Handistatus, 2005
Costa RicaPresentNULLThompson et al., 1992; OIE, 2009
CubaRestricted distributionOIE, 2009
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicPresentNULLThompson et al., 1992; OIE, 1999; OIE, 2009
El SalvadorDisease not reported1997Thompson et al., 1992; OIE, 2009
GrenadaDisease never reportedHoman et al., 1992
GuadeloupePresentOIE, 2009
GuatemalaDisease not reported1998Thompson et al., 1992; OIE, 2009
HaitiDisease never reportedOIE, 2009
HondurasDisease not reported2004Thompson et al., 1992; OIE, 2009
JamaicaDisease never reportedNULLThompson et al., 1992; OIE, 2009
MartiniquePresentOIE, 2009
NicaraguaNo information availableNULLThompson et al., 1992; OIE, 2009
PanamaNo information availableNULLThompson et al., 1992; OIE, 1999; OIE, 2009
Puerto RicoReported present or known to be presentThompson et al., 1992
Saint Kitts and NevisDisease never reportedHoman et al., 1992; OIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease never reportedOIE Handistatus, 2005
Trinidad and TobagoLast reported2003Thompson et al., 1992; OIE Handistatus, 2005

South America

ArgentinaPresentNULLOIE, 1999; OIE, 2009
BoliviaAbsent, reported but not confirmedOIE, 2009
BrazilDisease not reported200203Hawkes, 1996; OIE, 2009
-AmapaWidespreadViegas de Abreu, 1983
-AmazonasWidespreadViegas de Abreu, 1983
-Minas GeraisWidespreadSilva et al., 1988; Castro et al., 1992
-ParaWidespreadViegas de Abreu, 1983
-ParaibaLocalisedMelo et al., 2000
-Rio de JaneiroWidespreadCunha et al., 1988
-RoraimaWidespreadViegas de Abreu, 1983
ChileDisease never reportedNULLTamayo et al., 1985; OIE, 2009
ColombiaDisease not reported1975Homan et al., 1992; OIE, 1999; OIE, 2009
EcuadorDisease never reportedOIE, 2009
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaDisease not reportedNULLLancelot et al., 1989; OIE, 2009
GuyanaDisease never reportedGibbs and Greiner, 1985; OIE Handistatus, 2005
ParaguayNo information availableOIE, 1999; OIE Handistatus, 2005
PeruDisease not reportedNULLRosadio et al., 1984; OIE, 2009
SurinameWidespreadGibbs and Greiner, 1985
UruguayDisease never reportedOIE, 2009
VenezuelaNo information availableNULLPérez et al., 1995; OIE, 1999; OIE, 2009

Europe

AlbaniaDisease not reportedOIE, 2009
AndorraDisease never reportedOIE Handistatus, 2005
AustriaPresentOIE, 2009
BelarusDisease never reportedOIE, 2009
BelgiumPresentOIE, 2009
Bosnia-HercegovinaLast reported2003OIE Handistatus, 2005
BulgariaDisease not reported200803OIE, 1999; OIE, 2009
CroatiaDisease not reported200411OIE, 2004b; OIE, 2009
CyprusDisease not reportedNULLTaylor et al., 1985; Papadopoulos, 1992; OIE, 1999; OIE, 2009
Czech RepublicPresentOIE, 2009
DenmarkPresentOIE, 2009
EstoniaDisease never reportedOIE, 2009
FinlandDisease never reportedOIE, 2009
FrancePresentOIE, 2009
-CorsicaLast reported2004NativeOIE, 2004c
GermanyPresentOIE, 2009
GreecePresentNULLPapadopoulos, 1992; OIE, 1999; OIE, 2009
HungaryPresentOIE, 2009
IcelandDisease never reportedOIE, 2009
IrelandDisease never reportedOIE, 2009
Isle of Man (UK)Disease never reportedOIE Handistatus, 2005
ItalyRestricted distributionOIE, 2009
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE, 2009
LiechtensteinAbsent, reported but not confirmedOIE, 2009
LithuaniaDisease never reportedOIE, 2009
LuxembourgPresentOIE, 2009
MacedoniaDisease not reportedOIE, 2009
MaltaDisease not reportedOIE, 2009
MoldovaDisease never reportedOIE Handistatus, 2005
MontenegroDisease not reportedOIE, 2009
NetherlandsPresentOIE, 2009
NorwayDisease never reportedOIE, 2009
PolandDisease never reportedOIE, 2009
PortugalPresentNULLOIE, 2005; OIE, 2009
RomaniaDisease never reportedOIE, 2009
Russian FederationPresentOIE, 2009
SerbiaDisease not reportedOIE, 2009
SlovakiaDisease never reportedOIE, 2009
SloveniaDisease never reportedOIE, 2009
SpainPresentOIE, 2009
-Balearic IslandsLast reported2003OIE, 2003
SwedenPresentOIE, 2009
SwitzerlandPresentOIE, 2009
UKPresentOIE, 2009
-Northern IrelandDisease never reportedOIE Handistatus, 2005
UkraineDisease never reportedOIE, 2009
Yugoslavia (former)Last reported2001OIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Last reported2002OIE Handistatus, 2005

Oceania

AustraliaPresentNULLOIE, 1999; OIE, 2009
-Australian Northern TerritoryLocalisedDella-Porta et al., 1983; Tomori et al., 1992
-New South WalesLocalisedDella-Porta et al., 1983; Burton and Littlejohns, 1988; Tomori et al., 1992
-QueenslandLocalisedDella-Porta et al., 1983; Tomori et al., 1992
-Western AustraliaLocalisedDella-Porta et al., 1983; Tomori et al., 1992
French PolynesiaDisease never reportedOIE, 2009
New CaledoniaDisease never reportedOIE, 2009
New ZealandDisease never reportedOIE, 2009
Northern Mariana IslandsSerological evidence and/or isolation of the agentOIE, 1999
Papua New GuineaSerological evidence and/or isolation of the agentDella-Porta et al., 1983; Tomori et al., 1992; Puana, 1996
SamoaDisease never reportedOIE Handistatus, 2005
Solomon IslandsWidespreadTomori et al., 1992
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathology

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All of the pathology of bluetongue can be assigned to vascular endothelial damage resulting in changes to capillary permeability and fragility, with subsequent disseminated intravascular coagulation and necrosis of tissues supplied by damaged capillaries. These changes result in oedema, congestion, haemorrhage, inflammation and necrosis.

In animals dying acutely, the oral mucosa is hyperaemic and petechiae or ecchymoses may be present. Excoriations may be in areas subject to mechanical abrasion; the edges of lips, dental pad, tongue and cheeks opposite the molar teeth. There may be hyperaemia in the fore-stomachs. The lungs may be hyperaemic with severe alveolar and interstitial oedema, froth in the bronchi, and excess fluid in the thoracic cavity. The pericardial sac may have petechiae and excess fluid. A variable sized haemorrhage in the tunica media near the base of the pulmonary artery is almost pathognomonic. Subepicardial and subendothelial haemorrhages, particularly involving the left ventricle, are common. Generalized damage to the cardiovascular system is evidenced by widespread hyperaemia, oedema and haemorrhage (Erasmus, 1990).

Animals that die later than 14 days after infection often show dramatic degeneration and necrosis of the skeletal musculature. Muscles lose pigmentation and the inter-muscular fasciae are infiltrated with a clear gelatinous fluid (Erasmus, 1990).

Microscopic examination of mucosal lesions shows mononuclear cell infiltration, degeneration and necrosis of epithelial cells in which large acidophilic intra-cytoplasmic masses accumulate. Affected muscles have oedema, haemorrhage, hyaline degeneration and necrosis. Infiltration by neutrophils, macrophages and lymphocytes is present in acute cases (Verwoerd and Erasmus, 1994).

Diagnosis

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Diagnosis can be on the basis of clinical and pathological findings, but requires confirmation by a specialist laboratory. There is a summary of recommended procedures for bluetongue serology and virus isolation (Afshar and Gard, 1995), while Afshar (1994) provides details of the diagnostic methods. The isolation and identification of bluetongue virus is also described in detail by Clavijo et al. (2000).

Various techniques have been used to detect antibodies against bluetongue virus (BTV). These include agar gel immunodiffusion (AGID), haemagglutination-inhibition, complement fixation and ELISA, which are serogroup-specific and serum neutralization, which is serotype-specific. Although all these assays are available, only AGID and competitive-ELISA are recommended as prescribed tests for international trade in the OIE Manual of Standards for Diagnostic Tests and Vaccines (OIE, 2004f). Competitive ELISA is becoming more popular because of its greater accuracy and adaptation to conventional laboratory rapid testing and reading technology (OIE, 2004f).

Rapid and reliable confirmation of BTV and serotype differentiation is essential at the start of an outbreak to allow for the early selection of vaccine. Historically, laboratory confirmation of the BTV serotype depended on the isolation and amplification of virus by inoculation of washed and lysed sheep red blood cells (RBC) or homogenized tissue into embryonated chicken eggs and/or cell cultures (BHK21, Vero and insect cells), and the subsequent serotyping of the virus using the virus neutralization test (VNT) (OIE, 2004f). The identification of the virus in the culture medium of infected cells could be performed by serogroup-specific antigen capture ELISA (Thevasagayam, 1996). Molecular tools, such as the RT-PCR, have and are being developed and evaluated for the rapid detection and serotype identification of BTV based on nucleotide sequences of different genome segments in BTV-infected cell cultures and/or infected tissues of ruminants (Wade-Evans et al., 1990; McColl and Gould, 1991; Pearson et al., 1991; Katz et al., 1993; Koumbati et al., 1999; MacLachlan et al., 1994; Harding et al., 1995; Parsonson and McColl, 1995; Pritchard et al., 1995; Shad et al., 1997; Aradaib et al., 1998; Koumbati et al., 1999; Johnson et al., 2000; Billinis et al., 2001; Zientara et al., 2002; Breard et al., 2003; Aradaib et al., 2003; Breard et al., 2005). These assays can also be used to differentiate between natural infection and vaccination (Breard et al., 2003; Orru et al., 2004).

Differential diagnosis should include contagious ecthyma, foot and mouth disease, photosensitization, pneumonia, polyarthritis, footrot, foot abscesses, plant poisonings, peste des petits ruminants, coneurosis and epizootic haemorrhagic disease of deer.

List of Symptoms/Signs

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SignLife StagesType
Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate Sheep & Goats:All Stages Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sheep & Goats:All Stages Diagnosis
Digestive Signs / Bloody stools, faeces, haematochezia Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Sign
Digestive Signs / Congestion oral mucous membranes, erythema, redness oral mucosa Sheep & Goats:All Stages Diagnosis
Digestive Signs / Diarrhoea Sign
Digestive Signs / Difficulty in prehending or chewing food Sheep & Goats:All Stages Sign
Digestive Signs / Dysphagia, difficulty swallowing Sign
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Diagnosis
Digestive Signs / Malformation of jaw, brachygnathia, prognathia Cattle & Buffaloes:Calf Sign
Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Diagnosis
Digestive Signs / Tongue protrusion Sheep & Goats:All Stages Sign
Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears Sheep & Goats:All Stages Diagnosis
Digestive Signs / Vomiting or regurgitation, emesis Sign
General Signs / Ataxia, incoordination, staggering, falling Sign
General Signs / Ataxia, incoordination, staggering, falling Sign
General Signs / Cyanosis, blue skin or membranes Sheep & Goats:All Stages Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Exercise intolerance, tires easily Sheep & Goats:All Stages Sign
General Signs / Fever, pyrexia, hyperthermia Cattle & Buffaloes:All Stages,Other:All Stages,Sheep & Goats:All Stages Diagnosis
General Signs / Forelimb lameness, stiffness, limping fore leg Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Diagnosis
General Signs / Generalized lameness or stiffness, limping Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Diagnosis
General Signs / Generalized weakness, paresis, paralysis Sheep & Goats:All Stages Sign
General Signs / Haemorrhage of any body part or clotting failure, bleeding Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Sheep & Goats:All Stages Diagnosis
General Signs / Hindlimb lameness, stiffness, limping hind leg Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Diagnosis
General Signs / Inability to stand, downer, prostration Sheep & Goats:All Stages Sign
General Signs / Lack of growth or weight gain, retarded, stunted growth Sheep & Goats:All Stages Sign
General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes Sheep & Goats:All Stages Sign
General Signs / Opisthotonus Sign
General Signs / Oral cavity, tongue swelling, mass in mouth Sheep & Goats:All Stages Diagnosis
General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass Sheep & Goats:All Stages Sign
General Signs / Petechiae or ecchymoses, bruises, ecchymosis Sheep & Goats:All Stages Diagnosis
General Signs / Reluctant to move, refusal to move Sheep & Goats:All Stages Diagnosis
General Signs / Sudden death, found dead Sign
General Signs / Torticollis, twisted neck Sheep & Goats:All Stages Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sheep & Goats:All Stages Sign
General Signs / Weight loss Sheep & Goats:All Stages Sign
Musculoskeletal Signs / Abnormal forelimb curvature, angulation, deviation Cattle & Buffaloes:Calf Sign
Musculoskeletal Signs / Abnormal hindlimb curvature, angulation, deviation Cattle & Buffaloes:Calf Sign
Musculoskeletal Signs / Contracture fore limb, leg Cattle & Buffaloes:Calf Sign
Musculoskeletal Signs / Contracture hind limb, leg Cattle & Buffaloes:Calf Sign
Musculoskeletal Signs / Decreased mobility of forelimb joint, arthrogryposis front leg Cattle & Buffaloes:Calf Sign
Musculoskeletal Signs / Decreased mobility of hindlimb joint, arthrogryposis rear leg Cattle & Buffaloes:Calf Sign
Nervous Signs / Abnormal behavior, aggression, changing habits Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sheep & Goats:All Stages Diagnosis
Nervous Signs / Tremor Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling Sign
Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature Sign
Ophthalmology Signs / Conjunctival, scleral, redness Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Ophthalmology Signs / Nystagmus Sign
Ophthalmology Signs / Purulent discharge from eye Sign
Pain / Discomfort Signs / Forefoot pain, front foot Sheep & Goats:All Stages Diagnosis
Pain / Discomfort Signs / Hindfoot pain, rear foot Sheep & Goats:All Stages Diagnosis
Pain / Discomfort Signs / Mouth, oral mucosal or tongue pain Sheep & Goats:All Stages Diagnosis
Pain / Discomfort Signs / Pain, head, face, jaw, ears Sheep & Goats:All Stages Sign
Pain / Discomfort Signs / Skin pain Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Sheep & Goats:All Stages Sign
Reproductive Signs / Agalactia, decreased, absent milk production Sign
Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Sign
Reproductive Signs / Female infertility, repeat breeder Sign
Reproductive Signs / Heat on palpation scrotum, testes Sheep & Goats:All Stages Sign
Reproductive Signs / Lack of libido or erection Sheep & Goats:All Stages Sign
Reproductive Signs / Male infertility Sign
Reproductive Signs / Mummy, mummified fetus Sign
Reproductive Signs / Vulval ulcers, vesicles, erosions, tears, cuts, pustules, papules Sign
Reproductive Signs / Warm mammary gland, hot, heat, udder Sheep & Goats:All Stages Sign
Respiratory Signs / Abnormal breath odor, foul odor mouth Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sheep & Goats:All Stages Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sheep & Goats:All Stages Diagnosis
Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages Diagnosis
Respiratory Signs / Mucoid nasal discharge, serous, watery Sheep & Goats:All Stages Diagnosis
Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules Sheep & Goats:All Stages Diagnosis
Respiratory Signs / Purulent nasal discharge Sheep & Goats:All Stages Sign
Skin / Integumentary Signs / Alopecia, thinning, shedding, easily epilated, loss of, hair Sign
Skin / Integumentary Signs / Cracked skin, fissure Sign
Skin / Integumentary Signs / Heat, nail, claw, hoof, hot, warm Sheep & Goats:All Stages Diagnosis
Skin / Integumentary Signs / Nail, claw, hoof sloughing, separation Sign
Skin / Integumentary Signs / Skin crusts, scabs Sign
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin erythema, inflammation, redness Sheep & Goats:All Stages Diagnosis
Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene Sign
Skin / Integumentary Signs / Skin scales, flakes, peeling Sign
Skin / Integumentary Signs / Skin ulcer, erosion, excoriation Sign
Skin / Integumentary Signs / Warm skin, hot, heat Sheep & Goats:All Stages Diagnosis

Disease Course

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Natural bluetongue infection is usually subclinical and the occurence of disease is the result of a complex interaction between the animal, the virus and the environment. Bluetongue is almost exclusively a disease of sheep, with European breeds most susceptible. Most breeds of sheep, especially in regions where the virus is endemic, are resistant to disease though there is increasing information that native breeds in India and China can be clinically affected. Outbreaks of disease typically occur either when susceptible sheep are introduced to endemic areas, or when infected midges carry the virus from endemic regions to adjacent areas containing populations of immunologically-naïve, susceptible sheep.

Many strains of bluetongue virus appear incapable of causing significant disease following natural or experimental infection of breeds of sheep known to be susceptible to disease. Experimental reproduction of disease can be inconsistent, except with the most virulent strains of virus. This could be because exposure of the virus to sunlight can have a marked influence on the severity of disease (Erasmus, 1990). Also, passage of virulent field virus in cell cultures rapidly reduces virus virulence (Gard, 1987).

After introduction by the bite of an infected midge, bluetongue virus first replicates in the local lymph nodes and subsequently induces a primary viraemia which seeds other lymph nodes, spleen, lung and vascular endothelium (Gibbs and Greiner, 1988). Circulating virus associates with blood cells, mostly with erythrocytes and platelets, though virus associated with mononuclear cells is critical for dissemination of virus throughout the animal. Later in viraemia, the virus is exclusively associated with erythrocytes (MacLachlan, 1994). Virus particles appear to be sequestered in invaginations of the erythrocyte membrane, allowing prolonged viraemia in the presence of neutralizing antibodies (OIE, 1998).

Fever is usual but not invariable. Other common clinical signs include oedema (of lips, nose, face, submandibulum, eyelids and sometimes ears), congestion (of mouth, nose, nasal cavity, conjunctiva, skin and coronary bands), lameness and depression. The oedema of lips and nose can give the sheep a 'monkey-face' appearance. There is frequently a serous nasal discharge, later becoming mucopurulent. The congestion of the nose and nasal cavity produces a 'sore muzzle' effect, the term used to describe the disease seen in sheep in the USA before its bluetongue virus aetiology was realized. The mouth is sore and the sheep may champ to produce a frothy oral discharge. Sheep are not strictly anorexic, but eat less because of oral soreness and will hold food in their mouths to soften it before chewing. Affected sheep occasionally have swollen, congested, cyanotic tongues, which gave rise to the name Bluetongue. Lameness, due to coronary band congestion, may occur early in the disease and lameness or torticollis, as a result of skeletal muscle damage, may occur later (OIE, 1998).

If fever occurs, sheep are first pyrexic 4-10 days after infection. The other clinical signs soon follow with acute deaths occurring during the second week following infection. Many of these deaths are the result of pulmonary oedema and/or cardiac insufficiency. Further sheep may die from chronic disease 3 to 5 weeks after infection with bacterial complications, especially pasteurellosis. Under-nutrition arising from lameness and depression may be contributing factors. The production loss due to bluetongue may be the result of deaths, unthriftiness during prolonged convalescence, wool breaks and possibly reproductive wastage (OIE, 1998).

Although the frequency of infection of cattle with bluetongue virus is generally higher than in sheep, disease in cattle is rare. Clinical disease is actually a hypersensitivity reaction, characterised by fever, stiffness or lameness and increased respiratory rate. There may be lacrimation and increased salivation. The skin of the muzzle is often inflamed, and may crack and peel. The lips and tongue may be swollen, with ulcers on the oral mucosa. Similarly, the skin of the neck, flanks, perineum, and teats may be affected (Erasmus, 1990).

Hydranencephaly and congenital deformities may develop in bovine and sheep foetuses of bluetongue virus-infected dams, the severity of lesions depending on the stage of gestation. Foetuses seem to be most susceptible during the period of active brain development (Erasmus, 1990). It is clear that cell culture-adapted virus more readily crosses the placenta than unadapted virus, suggesting that the occasional instances of natural virus-induced teratogenesis may be due to strains of virus derived from live virus vaccines (MacLachlan, 1994).

Bluetongue in dogs associated with use of a contaminated vaccine was reported by Akita et al. (1994). Only pregnant bitches were affected.

Epidemiology

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Bluetongue virus is an arbovirus that has evolved a life cycle where alternate cycles of virus replication in vertebrate and invertebrate hosts are essential for virus persistence. There is no evidence of vertical transmission of the virus in the invertebrate host. Observations on the placental transmission of virus in the vertebrate host are contradictory (Roberts, 1990) and therefore any vertical transmission in vertebrates is considered to be of no consequence to virus ecology. There is little evidence of direct or indirect contact transmission in either host, other than rare instances of transmission via semen in vertebrates (OIE, 1998). The virus cannot be spread by meat, milk or dairy products. Cattle are the primary vertebrate hosts (Erasmus, 1990) and a small number of species of Culicoides midges are the only insect hosts (Mellor, 1990). The rare recovery of bluetongue virus from other insects is of no ecological significance.

The insect vectors of bluetongue virus breed in moist conditions in a variety of habitats, particularly damp, muddy areas and in faecal and plant matter. They have nocturnal feeding habits, preferring still, warm conditions, pastures and open pens. At least some species preferentially feed on cattle. Females take a blood meal prior to egg laying, feed at roughly 4-day intervals and live for about 2 to 3 weeks. The eggs hatch in 2 to 3 days and depending on the temperature, the larval stage lasts 12 to 16 days. Adults emerge 2 to 3 days after pupation and take a blood meal 1 day later and they also mate during this time (Roberts, 1990). The activities of the midge are influenced by temperature and the optimum lies between 13o and 35oC (Sellers, 1981).

As summarized by Gibbs and Greiner (1994), bluetongue is a common, generally subclinical infection of ruminants throughout the tropics and subtropics, within a number of separate ecosystems. Seasonal incursions of the virus into more temperate latitudes, sometimes accompanied by disease, may occur under favourable climatic conditions at certain key locations. There is evidence that infected midges are carried on the wind for long distances (Sellers, 1981). It has been postulated that the major epidemics of bluetongue, in regions where disease occurs only sporadically, can often be traced to windborne carriage of infected Culicoides from distant areas (Gibbs and Greiner, 1988).

Critical in the understanding of the epidemiology of bluetongue is knowledge of the ability of the Culicoides species in different ecosystems to carry the virus, which is known as vector competency. However, vector competency research is a very specialised discipline. Not only may different populations of a species of midge have varying susceptibilities to a strain of virus, but a single strain of the vector may have differing susceptibility to different virus serotypes (Mellor, 1990).

Competent midges become infected when biting viraemic vertebrates. The chance of infection depends in part on the genotype of the midge, the strain of virus, the level of viraemia, and environmental factors (Mellor et al., 2000). The period between feeding on infected blood and the appearance of virus in the saliva of the midge (the extrinsic incubation period) is 1-2 weeks.

The USA vector, C. variipennis, is able to ingest approximately 10-4ml of blood (Mellor, 1990), whereas the most widely distributed Australian vector, C. brevitarsis, has a blood meal volume of around 10-4.5ml (Muller et al., 1982). Therefore viraemia must be of the order of 104 infectious units of virus per ml or greater for feeding midges to have much chance of infection. OIE (1998) summarized reported peak levels of viraemia, in virus infectious units per ml of blood, as 104.4 to 106.3 for cattle, 106.4 to 108.0 for sheep and 106.0 for goats, though levels reached are mostly much lower. Viraemia peaks in the first two weeks after infection, before the appearance of serum antibody. Virus titres then drop rapidly and are very low if infections persist for a month or more.

The durationof viraemia in the infected vertebrate is an important factor in the transmission of bluetongue virus to biting, competent midges. Bluetongue is no longer considered a persistent infection of ruminants, especially cattle (MacLachlan, 1994). Singer et al. (2001) analyzed a large volume of existing data on the length of bluetongue viraemia of cattle and concluded that this was equal to or less than 9 weeks in >99% of adults. OIE (1998) report the viraemia of most cattle as less than 4 weeks with fewer than 1% exceeding 8 weeks. The maximum duration of viraemia reported for sheep is 54 days (Koumbati et al., 1999).

Impact: Economic

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Bluetongue can be a costly infection for several reasons. The clinical disease in sheep can be severe, resulting in deaths, weight loss and wool break. In some countries where disease is endemic (South Africa and some States of the USA), vaccination is a recurring cost. However the greater cost of bluetongue is to infected countries which export live animals, germplasm and some animal products such as foetal calf serum. Here the presence of bluetongue virus, even if wholly subclinical, causes loss of trade due to restrictions on the source of animals, and the costs of health testing. It has been estimated that in the late 1970s, the ban on US cattle semen exports resulted in an annual loss of $24 million (Gibbs and Greiner, 1988).

Bluetongue is included in the OIE List A diseases, largely because of dramatic outbreaks of disease in Cyprus in 1943 and Portugal and Spain in 1956. The Cyprus outbreak was due to a particularly virulent strain of the virus causing between 60 and 70% losses in some flocks (Gambles, 1949). The Iberian outbreaks were also spectacular. Within the first 4 months 46,000 sheep had died in Portugal and 133,000 in Spain (Roberts, 1990). However, these outbreaks wre exceptional, and normally there is a minimal or unrecognised loss. This listing of bluetongue in the most serious of animal diseases exacerbates the trade sensitivity and associated costs to countries with the infection, and has been challenged by some (Gibbs and Greiner, 1994).

Zoonoses and Food Safety

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Bluetongue is not a zoonosis.

Disease Treatment

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There is no treatment for bluetongue disease. The recovery of affected animals will be aided by the provision of shade, water, feed and shelter. Anti-inflammatory and pain relief medications can be used to limit clinical signs.

Prevention and Control

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Bluetongue is a disease of sheep, but cattle are the principal vertebrate reservoirs of the virus. Once established, it is impossible to eradicate bluetongue virus. The virus will circulate, generally subclinically, in cattle and other ruminants, and in midges. In countries marginally suitable for virus persistence, the virus may be maintained for several years before dying out. Since 1998, six strains of bluetongue virus have spread across 12 European countries and 800 km further north in Europe than had previously been reported. It has been suggested that this spread has been driven by recent changes in European climate that have allowed increased virus persistence during winter, the northward expansion of Culicoides imicola, the main bluetongue virus vector, and, beyond this vector's range, transmission by indigenous European Culicoides species (Purse et al., 2005).

The bluetongue virus cycle could be interrupted by the immunization of vertebrate hosts, especially cattle, removal of vectors or prevention of vector attack. Understandably, the cost of immunization of animals that will not suffer from the disease is not acceptable to farmers. The control of midges by the application of insecticides and larvicides to insect resting and breeding sites, or systemically to cattle, has not been fully investigated but is likely to have local success only. Protecting sheep from exposure to midges is a more practical approach and can be achieved by moving sheep from insect resting and breeding sites, stabling animals overnight or the use of insect repellents. Mixing cattle with sheep will draw vectors with a host preference for cattle from sheep, but may raise the virus infection level of the midge population.

Prophylactic immunization of sheep is the most practical and effective control measure. However, multiple serotypes of virus are usual in endemic situations (Hawkes, 1996), requiring multivalent vaccines because bluetongue vaccines are serotype specific. Multivalent vaccines have problems resulting from interference between virus strains, differences in immunogenicity and growth rates between various strains, as well as differences in the response of individual animals to the components of such vaccines (Verwoerd and Erasmus, 1994). Additionally, there is growing concern by some scientists (Murray and Eaton, 1996; Mellor and Wittmann, 2002) about the use of live attenuated bluetongue vaccines. They summarized concerns in four areas. These areas are: the known teratogenicity of attenuated virus for the developing foetus; the propensity for vaccine virus to be excreted in the semen of bulls and rams; the possibility that vaccine virus will infect vectors and establish in the environment; and the generation of recombinant progeny virus with novel genetic and biological properties after the reassortment of genes from wild and vaccine virus in the vaccinated animal or the vector. Consequently, these live vaccines are perceived to have significant drawbacks so that some authorities prohibit their use. However, live attenuated bluetongue vaccines have wide use in South Africa, Italy, Morocco, Spain and France, and more limited use in USA and a few other countries. The vaccines are compromises between attenuation and immunogenicity and may have residual pathogenicity for some vaccinated sheep. The application of the vaccines has to be well managed. Colostral immunity in young sheep can interfere with the development of active immunity to the vaccine and breeding ewes and rams should be vaccinated before mating.

European projects have contributed to the development of an efficacious first generation inactivated vaccine for BTV2 and BTV4. Initial tests show very good efficacy and safety. Industrial level production has already started and the vaccines are now being applied in affected EU countries.

Alternatives to live attenuated or inactivated vaccines are under investigation. Genetic engineering offers a variety of approaches to producing viral vaccines. An exciting advance in this field is the ability to construct virus-like particles (VLPs) or recombinant core-like particles (CLPs) that resemble their natural counterparts but lack genetic information. To develop a rationally designed vaccine for bluetongue disease of sheep, individual BTV proteins, VLPs and CLPs have been synthesized using baculovirus expression systems (Roy, 2002). An alternative method is to clone the gene of interest into a host-restricted living carrier organism such as leporipox or capripox viruses. The immunogenicity, safety and efficacy of these new vaccines are being evaluated under controlled trial conditions. However, if a commercial product of any of these is achieved, it will undoubtedly cost considerably more than a live attenuated or inactivated vaccine.

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Links to Websites

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Bluetongue. Agriculture and Agri-Food, Canada, 1996http://hoshi.cic.sfu.ca/epix/topics/animal/bluetung.htm
Bluetongue. Office International des Epizooties, 2000http://www.oie.int/eng/maladies/fiches/a_A090.htm

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