History, Disease definition, Transmission, Clinical symptom, Epidemiology, Pathogenesis, Diagnosis, Treatment, Prevention and Control

1. Viral Diseases
BLUE TONGUE
Faculty of Veterinary Medicine & Animal
Husbandry
Somali National University
Mogadishu, Gaheyr Campus
Oct. 29. 2023

3. Blue Tongue is a non-contagious, insect-borne,
seasonal viral disease affecting sheep, characterized
by congestion of the buccal and nasal mucosa and
the coronary tissue of the hooves, and stiffness due
to muscle degeneration. Bluetongue virus is a
notifiable disease in many countries.

4. The disease is caused by an Orbivirus of the
Reoviridae family. 24 bluetongue virus
serotypes are currently recognized. The virus is
remarkably stable and can remain infective for
many years.
Etiology

5. Bluetongue has been known in Africa for over a hundred
years and has probably been endemic in wild ruminants in
sub-Saharan Africa. The disease was initially called “fever”
or “epizootic catarrh”, but was later referred to as “malarial
catarrhal fever of sheep”, due to the mistaken belief that the
disease was caused by an intracorpuscular parasite
The disease was later renamed “bluetongue” (1905), with
reference to the characteristic cyanotic tongues that were
occasionally observed in infected sheep

6. Viruses of the family Reoviridae (Reo = Respiratory,
Enteric, Orphan) infect vertebrates, invertebrates, higher
plants, fungi and bacteria.
They are unique in that they possess a linear, double-
stranded, segmented RNA genome. A number are
important veterinary pathogens.

7. Historically, bluetongue virus has been confined to tropical
and subtropical areas. Bluetongue is widespread in Africa
and the Middle East occurring when the climate is warm
and wet.
More recently, climate change and trade patterns have seen
increasing outbreaks in temperate regions (including
Northern Europe)

8. Map: Bluetongue restricted zones in Europe as of the 18th of April 2018.

9. The sheep is the only animal which is clinically
affected but in cattle, goats, camels and African
antelopes there is an inapparent infection.
Indigenous African sheep rarely show any
clinical signs.

10. BTV affects sheep, cattle, deer, goats and camelids
Humans are not affected.
Species Affected
There is no public health risk associated
with BT.

11. Natural transmission is by blood-sucking insects, the proven
vectors being Culicoides spp. The disease may sometimes be
spread mechanically by mosquitoes. It cannot be transmitted
by contact, and in the absence of insect vectors, infected and
non-infected animals can remain in the closest contact
without spread of the disease.
Transmission

12. Bluetongue usually appears shortly after the beginning of
the rainy season when insect vectors start to become
abundant. Sheep of all ages are susceptible, except lambs
of immune dams. The highest mortality in endemic areas
occurs in yearlings, the older sheep usually being
immune following recovery from an earlier attack.
Clinical Features

13. The incubation period is about one week and the first
sign usually observed is a rise in temperature.
The fever is accompanied by unwillingness to feed,
rolling movements of the tongue and licking of the lips,
followed in 24 hours by nasal discharge and salivation.

14. The nasal discharge is at first thin and watery, but soon
becomes mucopurulent. Later, the discharges dry up and
encrust the nostrils. The nasal mucosa is congested and
may ulcerate. Blood then appears in the nasal discharge.

15. The lips become swollen, very tender, and bleed
readily when handled, especially where the skin and
mucosa meet. The mucosa of the mouth is congested
and often cyanotic. There is a great tendency to
excoriation, and superficial ulcers form very readily.

16. Deeper ulcers filled with white necrotic debris appear at
any site where there is irritation. The cheek papillae
become congested and their lips are often necrotic.
Oedema of the face, ears, or submaxillary region, is not
uncommon.

17. Shortly after the mouth lesions have fully developed,
lameness or stiffness is often observed. In mild outbreaks
this may be the only sign. The lameness is due to a
coronitis manifested by the development of a red or
purplish band which travels down the hoof with the growth
of the horn. The skin in the interdigital cleft may be
reddened or show a purplish discoloration.

18. Sheep. There are multiple erosions and crusts on the muzzle and lips.

19. Sheep, mouth. Most of the dental pad is eroded; the remaining pale
mucosa is necrotic.

20. Bovine, mammary gland. There is extensive coalescing ulceration
of the teat skin.

21. Sheep, foot. There are multiple petechiae in the hoof wall, and
there is marked hyperemia of the coronary band.

22. Sheep, tongue. The lateral mucosa contains several ulcers that
are covered by exudate and surrounded by zones of hyperemia

23. Sheep, skeletal muscle. There is a focus of hemorrhage on the
left; pale areas are consistent with myodegeneration.

24. Sheep, rumen. There are multiple mucosal hemorrhages centered
on the pillars.

25. The stiffness is due to degeneration of the skeletal
muscle fibres. Sick animals frequently exhibit
torticollis. Secondary infections of the respiratory
system commonly occur, affected sheep showing signs
of pneumonia soon after the development of the mouth
lesions. Diarrhea, which may be blood-stained, is
sometimes seen.

26. The mortality rate is very variable ranging from nil to 90
per cent according to the strain of virus and breed of
sheep involved.
Death usually occurs within six days of the first
appearance of the disease.

27. Prognosis is difficult since many very sick animals
make complete recoveries while other milder cases
which seem to be recovering collapse and die at any
time during convalescence.
Recovered animals are usually emaciated, take a long
time to recover condition, and may shed the fleece.

28. Apart from the excoriation and ulceration observed in the
nasal and buccal mucosa, the chief pathological changes
are a gelatinous infiltration of the subcutaneous tissues
and intermuscular fasciae, numerous small hemorrhages
in the muscle tissue and a degeneration of the fibres of
the skeletal muscles.
Pathology

29. The symptom are highly suggestive. A useful aid to field
diagnosis is the presence of petechiae in the shoulder
muscles. Confirmation of the diagnosis requires the
isolation and identification of the virus. The whole flock
should be examined and blood should be collected in
anticoagulant solution from febrile animals, that have not
yet developed typical signs. Blood samples should be
forwarded to the laboratory on ice.
Diagnosis

30. Difficulties in differential diagnosis occur with foot-and-
mouth disease, peste des petits ruminants, and contagious
pustular dermatitis.
Careful clinical examination will aid differentiation.
Moreover bluetongue, unlike the others, is not contagious.

31. Mouth lesions may be treated symptomatically.
It is important to keep infected animals in the shade as
sunlight appears to aggravate the condition.
Treatment

32. There are several distinct antigenic types of the virus.
Recovery is followed by immunity against the
homologous strain which lasts for over a year.
The virus has been attenuated in chick embryos and a
polyvalent vaccine containing the 16 main immunogenic
types is available.
Recently a tissue culture vaccine has been produced.
Both vaccines protect for about one year.
Immunology

33. In endemic areas control consists of annual vaccination
of all sheep with polyvalent vaccine at least a month
before the rains so that stock will be immune before the
vectors appear.
Non-pregnant ewes should be vaccinated at least three
weeks before mating because vaccination may interfere
with estrus.
Control

34. Pregnant ewes should never be vaccinated in early
pregnancy otherwise there is a high risk of causing
congenital abnormalities.
The situation in lambs is complicated because the
colostral immunity which lasts for up to six months may
be adequate to interfere with vaccinal strains though not
with natural infection.

35. Infection can be avoided by moving stock during the
rains to high, well-drained ground where there are no
Culicoides, or by housing at night.
Smoke fires at night and dipping in insecticides are useful
methods of vector control.

36. Segregation of sick animals is of little use in
controlling spread, since the disease is not contagious.
Eradication would appear impracticable as Culicoides
cannot be eliminated

37. To prevent the introduction of the disease, importation
of sheep and cattle and possibly other ruminants from
countries where the disease is endemic should be
prohibited and the interior of aircraft which have landed
in endemic areas should be sprayed with insecticide after
take-off

38. The fact that the infection is widespread in Africa and the
Middle East should be taken into account if it is decided
to import highly susceptible sheep into these areas for
improvement of the local animals.