Bluetongue is an infectious arthropod-borne viral disease primarily of domestic and wild ruminants. Infection with bluetongue virus (BTV) is common in a broad band across the world, which until recently stretched from ~35°S to 40°–50°N. Bluetongue virus is the type-species of the genus Orbivirus in the family Reoviridae. The geographic restriction is in part related to the climatic and environmental conditions necessary to support the Culicoides vectors.

1. BLUE TONGUE
(SORE MUZZLE, PSEUDO FOOT-AND-MOUTH
DISEASE, MUZZLE DISEASE)
Submitted by
Ranjini Manuel

2. INTRODUCTION
 Bluetongue(BTV) is an insect borne viral disease of
domestic and wild ruminants, especially sheep.
 The name refers to the blue discoloration of the
tongue and mucous membranes, due to cyanosis.
 BTV is classified as an OIE list A disease/ multiple
species and is therefore notifiable.

3. HISTORY
 First described in South Africa in 1881 “epizootic
catarrh”, Malarial catarrhal fever (Spruell, 1905).
 He proposed a method of immunization
inoculation of immune serum and virulent whole
blood.
 Theiler -unable to confirm Spreull’s work,
introduced another method -only infected blood -
been attenuated for sheep by several serial
passages in the same species.
 Vaccine prepared by Theiler’s formula 2 was
employed for nearly 40 years

4.  In 1933 it was first diagnosed in cattle (Bekker et al., 1934) -clinical signs
were similar – FMD-it was called pseudo-FMD, or sore-mouth
 The name blue tongue originated from the Dutch word“blaau tong”
means mouth sickness
 It was also called bloutong by south African farmers

5. INDIA
 The disease was first reported in India in 1964
(Sapre S.N.,1964) Southdown, Rambouillet,
Russian Merino and Corriedale
 First report of BT - Maharashtra
 In 1974 BT was reported in the Dorset breed in
Andhra Pradesh.
 In 1981 BT was widely spread in Southern India.

6. ETIOLOGY
 Family Reoviridae, 10ds RNA segments
 Genus Orbivirus
 24 serotypes worldwide
 non-enveloped virus,
 90 nm in diameter
 Non-contagious
 Insect-borne viral disease
 Ruminants: Primary host is sheep
 Others infected: Cattle, goats, deer
 Cattle – reservoir and amplification host

7. RESISTANCE TO PHYSICAL & CHEMICAL
ACTION
 Temperature: Inactivated by 50°C/3 hours; 60°C/15 minutes.
 pH: Sensitive to pH 8.0.
 Chemicals/Disinfectants: Inactivated by ß-propiolactone; iodophores and phenolic
compounds.
 Survival: Very stable in the presence of protein (e.g. has survived for years in blood
stored at 20°C)

8. EPIDEMIOLOGY
 BT is endemic in many parts of India and its outbreak in 22 serotypes are recorded in India out of 24
serotypes of BTV.
 Morbidity and mortality – High in Sheep, low in Goats
 Seroprevalence of 27.97% in Bidar district of Karnataka
(Bhoyar et. al.,2004)
 Higher prevalence of Bluetongue in goats (58.01%) has also been reported from Goa
(Barbuddhe et. al., 2005)

9.  The disease was recorded regularly in Tamil Nadu
where a total of 258 outbreaks were reported
between 1986 and 1995
 In Tamil Nadu during the monsoon season of 1997–98
BT caused the death of 300,000 sheep and goats.

10.  Erode District of Tamilnadu- During 2004–2008- morbidity -
1388 among Sheeps. Mortality of 239 sheeps. Sheep was
highly prone to bluetongue with a mortality rate of 17.2 %
when compared to cattle and goat. Outbreak occurred
the month of November and December, when heavy rainfall
conditions makes congenial environment for the
multiplication of vectors Culicoides sp.
 (R. Yasothai 2008)

12. Andhra Pradesh

13. KERALA
 2005, Seroprevalence of BTV – sheep and goat- sera samples
were collected from 14 districts out of which 12 confirmed the
presence of group specific BTV antibodies by dot ELISA and
reconfirmed with c-ELISA
 Seroprevalence – 5.1%
 2014, seroprevalence of BTV among domestic ruminants in
northern kerala samples were collected from wayanad,
Kozhikode and Palakkad- cELISA was used-
 seroprevalence – 9.3%

14. MORTALITY & MORBIDITY
 Sheep
Severity of disease varies with Breed, Strain of virus, Environmental stress
 Morbidity: as high as 100%
 Mortality: usually 0 to 30%
 Cattle, goats
 Morbidity: up to 5%
 Mortality low

15. RISK FACTORS
 Monsoon
 Poor flock nutrition
 High parasitic burden
 Lack of affordable veterinary care
 Poor immunogenicity of the inactivated vaccines
(Ilango et.al 2006)

16. TRANSMISSION
 A vector borne disease.
 Principal vector  Culicoides insects are the major vectors of BTV.
 They are most active from about one hour before sunset until one hour
after sunrise (Mellor et al., 2000)
South India
 Culiciodes brevitarsis
Culicoides imicola (Ilango et.al 2006)
North India
Culicoides oxistoma
Culicoides monocoli (Maheswari, 2012)

17. Replicates in
digestive tract
Progeny virus
released in to the
haemocoel
Salivary glands
are infected
The whole cycle from
infection to transmission
takes between 10 to 15
days at 25 °C and
individual vectors once
infected usually remain so
for life (Chandler et al.,
1985; Eaton et al., 1990;
Mellor, 1990, 2000, 2004).

18. TRANSMISSION
 Isolated from some arthropods, e.g., sheep ked (Melophagus
ovinus) (Luedke et al., 1965)
 some species of ticks
(Stott et al., 1985; Bouwknegt et al., 2010)
 mosquitoes
 However, these are mechanical vectors with only a negligible
role in disease epidemiology (Radostits et al., 1994).
(Melophagus
ovinus)
Ixodes ricinus
mosquito

19. TRANSMISSION
 Bull semen can also transfer the virus, but it can be infected
only when the bull is viraemic (Bowen and Howard, 1984;
Howard et al., 1985; Osburn, 1994; Kirkland et al., 2004) and
when semen contains red or white blood cells with which
the virus is associated (Osburn, 1994; Wilson et al., 2008).

20. TRANSMISSION
 The passage of BTV across the placenta is another mode of
transmission. It has been recorded in cattle
(Gibbs et al., 1979; Thomas et al., 1986; De Clercq et al., 2008;
Desmecht et al., 2008; Menzies et al., 2008; Backx et al., 2009; Darpel
et al., 2009; Lewerin et al., 2010; Santman-Berends et al., 2010)
 In an experimental study it was possible to infect a newborn calf
with BTV-contaminated colostrum (Backx et al., 2009).

21. PATHOGENESIS
transported by dendritic cells
from the skin local lymph
nodes
spreads to the blood
circulation inducing a primary
viraemia (blood elements)
Seeds other lymphoid
organs, spleen & lungs
The virus replicates in
vascular endothelial cells,
macrophages and
lymphocytes
Virus particles, sequestered in
invaginations of the RBC
membrane-prolonged
viremia

22. cell necrosis, apoptosis by
activating the p38MAP kinase,
the virus  vascular
permeability
induces the production of TNFα, IL-1, IL-8, IL-6, IFN-I and
cyclooxygenase-2, and enhances plasma concentration of prostacyclin
and thromboxane, which frequently leads to an excessive inflammatory
response and subsequent damage to the cells and tissues
BTV-infected endothelial cells  damage to the endothelium, interfere
with its function &  vascular permeability, DIC  this leads to the
development of edema, inflammation, congestion, necrosis and effusions

24. CATTLE & WILD RUMINANTS
 Endothelial cell damage is minimal.
 The viremia in cattle is highly cell associated, particularly with
erythrocytes and platelets.
 Although the virus does not replicate in the erythrocytes and
infected erythrocytes are likely to circulate for their life span.
 In cattle, viraemia may last as long as 60 or, even 100 days
(Sellers and Taylor, 1980), which makes this animal an important
host from the epidemiological point of view.

25. Viraemia and immune response
 Viraemia in infected animals has a prolonged course, but is not persistent
 Duration depends on the longevity of erythrocytes to which virus is bound (MacLachlan et al.,
2009)
 Viraemia lasts -14 to 54 days in sheep,Goats- 19 to 54 days (Barzilai and Tadmor, 1971; Luedke
and Anakwenze, 1972; Koumbati et al., 1999).

26.  The infected animals react to BTV with interferon production and humoral and cell-
mediated immune responses (MacLachlan and Thomson, 1985; MacLachlan, 1994).
 The sera of infected ruminants also contain serogroup-specific antibodies induced
by the VP7 protein, as well as antibodies against other structural and non-structural
proteins (MacLachlan et al., 1987; Richards et al., 1988; MacLachlan, 2004).

27. CLINICAL SIGNS
 SHEEP
 Incubation period- 5-20 days
 High fever (after 48hrs of fever) nasal discharge, with
reddening of the buccal and nasal mucosae & salivation
 Nasal discharge- mucopurulent and often blood stained
 Oral erosions and ulcerations, Hyperemic oral mucosa.

28. CLINICAL SIGNS
 Excoriation of the buccal mucosa- offensive odor.
 Tongue- Swollen, protruding, Cyanotic
 Feet- Sore hooves, lameness, Coronitis
 Fragile wool and diarrhoea.
 Abortion, foetal mummification & congenital defects

29. Salivation Facial swelling
Mucopurulent
Nasal Discharge

30. Coronitis
Hemorrhages at the
coronary band
Painful
hooves
Hooves may eventually
slough off

32. Wryneck, with twisting of the head and
neck to one side, occurs in a few cases,
appearing suddenly around day 12.
apparently attributable to the direct action of
the virus on muscle tissue, which is severe enough
to prevent eating

33. CONVALESCENCE
 Partial or complete loss of the fleece is common and
causes great financial loss for the farmer.
 During convalescence include separation /cracking of
the hooves
 Although the subsequent birth of lambs with
porencephaly and cerebral necrosis is usually
recorded after vaccination with attenuated virus, it
also occurs rarely after natural infections.

34.  Cattle and goats
 Most infections are in apparent, although serotype 8,
are highly virulent in cattle.
 Usually subclinical.
 Lethargic, anorexic and shows weakness
 Erosions, crusts around muzzle and teats
 Coronitis.
 Reproductive failure, deformities & abortion observed
if the infection is contracted in early gestation.
 ‘‘The Dancing Disease’’.

35. CLINICAL PATHOLOGY
  PCV and initial leukopenia followed by leucocytosis.
 The skeletal myopathy that occurs in this disease is
reflected by creatinine phosphokinase
 Hyperaemia, or occasionally cyanosis, of the oral mucosa
with petechiae and ecchymoses.
Focally extensive area of
haemorrhage - cattle

36.  The spleen, lymphatic nodes and tonsils are enlarged and haemorrhagic,
occasionally with petechiae.
 The tongue root, pericardial sac, kidney, gut (particularly at the iliocaecal junction)
and subcutaneous tissues may have petechiae.
 inflammation of the upper respiratory tract, pulmonary oedema, pleuritis,
pericarditis or enteritis may be present

37. SAMPLES
 Living animals: blood in heparin
 Freshly dead animals: spleen, liver, red bone marrow, heart blood, lymph
nodes
 Aborted and congenitally infected new born animals: pre-colostrum
serum plus same samples as for freshly dead animals
 All samples have to be preserved at 4°C, and not frozen
(As per OIE)

38. DIAGNOSIS
 Identification of BTV in blood or tissue samples - (RT-PCR) method and can detect BTV RNA in
samples as late as 6 months after infection (Katz et al., 1994; MacLachlan et al., 1994).
 The identification of a BTV serotype is carried out in the virus neutralisation test ( gold standard).
Other available diagnostic methods include antigen-capture ELISA, immunospot and
immunofluorescence tests
 Virus identification from cell cultures can then be conducted by methods such as
immunofluorescence and immunoperoxidase assays using BTV-specific monoclonal antibodies.

39.  CFT – Compliment fixation test
 Agar gel immunodiffusion test(AGID), easy to perform, inexpensive but
relatively insensitive and detects cross-reacting antibodies to other orbiviruses.
 Competitive ELISA (c-ELISA) – commonly used in labs, ideal to monitor
efficiency of vaccination campaign in non infected animals
 serum neutralization (SNT)- highly sensitive, specific, expensive and time
consuming
BTV – electron microscope

40. VIRUS ISOLATION
 Embryonated eggs, 9-12 days old, are used for BTV isolation and
intravenously inoculated with the material examined.
 The material obtained from embryonated eggs can either be
further propagated in cell culture or directly examined using
molecular methods (PCR or in situ hybridisation) (Schoepp et al.,
1991; Katz et al., 1994; Wang et al., 1988; Clavijo et al., 2000).

41. VIRUS ISOLATION
 Bluetongue virus can also be isolated in cell lines of insect origin, such as the KC line derived
from Culicoides sonorensis cells or the C6/36 line from Aedes albopictus (AA) cells; the
mammalian BHK-21, CPAE or Vero cell lines can also be used (Wechsler and McHolland,
1988; Mecham, 2006).
 The cytopathic effect produced by BTV is observed only on cell lines of mammalian origin at
3 to 5 days after inoculation and appears as foci of rounded and refractile cells

42. DIFFERENTIAL DIAGNOSIS
 Foot-and-mouth disease
 PPR
 Epizootic hemorrhagic disease (wild ruminants)
 Contagious ecthyma (sheep)
 Sheep pox (sheep)
 Bovine viral diarrhoea/mucosal disease (cattle)
 Malignant catarrhal fever (cattle)
 Acute photodermatitis (cattle)

43. TREATMENT
 Symptomatic and supportive treatment
 Local irrigations with mild disinfectant solutions may afford some relief.
 Affected sheep should be housed and protected from weather,
particularly hot sun
 fluid and electrolyte therapy and treatment to control secondary
infection may be desirable.

44. vaccination
 Vaccination is the only satisfactory control
procedure once the disease has been
introduced into an area.
 Successful in keeping losses to a very low
level
 An immediate ban on animal import from
countries with bluetongue is the priority
measure, followed by the monitoring of
farms

45.  Bluetongue vaccines are serotype-specific
 Two types of vaccines, inactivated and live attenuated, are currently available
 Live attenuated vaccine – used in endemic regions, 1 dose assure protection for a year,
production is inexpensive, low efficiency at high temperatures over 35 °C
 May show clinical signs, malformation of foetus, poor semen quality, decreased milk
production
 recommended to vaccinate ewes 9 to 15 weeks before mating, and rams after the mating period

47. RAKSHA-BLU
 First vaccine for Blue tongue in India. Protect the animals against five
strains of the ‘bluetongue’ virus.
 Result of collaborative efforts of IIL, TANUVAS (Tamil Nadu University of
Veterinary and Animal Sciences) and ICAR (Indian Council of Agricultural
Research). The vaccine was developed in three years.
 Active Ingredient(s): Contains bluetongue vaccine modified live virus, type
10.
 Given to 3 months old lambs, will be followed by a booster dose- three
months and annual vaccination
 Penicillin and streptomycin are added as preservatives.
 Per dose -expense of 5 rupees.

48. INACTIVATED VACCINE
 Inactivated vaccine
 Today monovalent vaccines against BTV-1, BTV-8 and BTV-9 are available
 Bluevac BTV8 is licensed for both cattle and sheep, and can be used during pregnancy.
All animals should be given a primary course of two injections under the skin, three
weeks apart. The immunity afforded by the vaccine lasts for a year after completion of
the primary course.

49. INACTIVATED VACCINE
 Zulvac 8 Bovis is licensed for use in cattle whereas the Zulvac 8 Ovis vaccine
should be used in sheep. Both vaccines prevent viraemia. The vaccines can be
used in cattle from three-months-old and sheep aged six-weeks. Each species
require two 2ml doses administered intramuscularly in cattle and subcutaneously
in sheep, three weeks apart. Provides immunity for 12 months.

50.  Well inactivated vaccines can prevent the development of clinical
disease in susceptible hosts, reduce direct economic losses due
to infection, facilitate safe trading in animals and prevent the
development of viraemia
 Recombinant vector vaccines, sub-unit vaccines and others
which would offer advantages such as no risk – very expensive

51. CONTROL
 Reducing the risk of exposure is attempted by spraying cattle
and sheep with repellents and insecticides and housing sheep at
night
 Bi weekly application of permethrin
 During transmission periods, avoidance of low, marshy areas or
moving sheep to higher altitudes may reduce risk.

52.  There is a high mortality in Culicoides that fed on cattle that have been
treated with anthelmintic dose of ivermectin
 It is sensitive to 3% NaOH, organic iodine complex, phenol and b-
propiolactone (Radostits, 1994; Anonymous, 2009a).
 protection of animals in stables can be improved by door and window
screens made of a fine mesh or a coarse fabric impregnated with
insecticide (Radostits et al., 1994; Calvete et al., 2010).