three day sickness disease seen in large ruminants

1. Ephemeral fever

2. i. Rhabdo viridae: ss, negative sense, RNA virus
ii. Bullet to blunt cone shaped
iii. Diameter: 73 nm
iv. Length: 70-183 nm
v. Shorter bullets & conical forms are defective
particles, interfere virus growth in tissue
culture.
vi. Readily inactivated @ pH <5 & >10
vii. No evidence of immunogenic diversity
viii.Antigenic variation demonstrated

3. BEFD
• It is a non contagious arthropod disease.
• It is characterized by fever, lameness, stiffness.
• It is caused by ephemero virus of
rhabdoviridae

5. • It is an ancient disease of cattle and buffalo in Asia and
Africa.
• Now, the disease became more evident and economically
important, wherever cattle populations increase or
production systems intensify.
• In Pacific countries, where the introduction of cattle
followed European settlement, the disease is more recent.
• Fat cattle, lactating cows in late pregnancy, bulls and steers
in heavy condition suffer more severely than non-lactating
thin or young animals.
• Draught cattle or buffaloes need rest for at least a week
after recovery or they may die.

6. Host range
• Disease reported only in cattle & water buffalo
• Neutralizing antibodies found in domesticated
deer & goats
• Antibodies can be produced in small laboratory
animals following i/v or s/c injection of BEFV
• Wild animals:
(VN & liq.phase ELISA done for serological survey)
Wild animals: Cape buffalo,water buck, antelope,
giraffe, wildebeest, hartebeest, kudu, eland,
impala, topi and tsessebe

7. 1. The fattest animals and the best milkers suffers
the worst.
2. Heavy bulls and feedlot cattle in very fat
condition suffer the highest mortality.
3. Cows in the eighth or ninth month of pregnancy
may abort (Uren et al., 1987).
4. Very hot weather increases mortality, probably
due to the effects of dehydration. Many fevered
animals will not drink, even if offered water (St-
George, 1994).

8. epidemiology
• Ephemeral fever was first described in South
Africa in 1906.
• It was clearly recognized in Egypt in 1895 and
1924.
• The disease is now known to exist in a broad belt
of tropical, subtropical, and temperate countries
in Africa, Asia, and Australia
• Israel, Syria, Iraq, Iran, Pakistan, India,
Bangladesh, southern and central China, and
southern Japan through Southeast Asia to
Australia- disease is highly prevalent

9. Distribution
• The vectors of bovine ephemeral fever (BEF) virus in Kenya are
highly dependent on temperature and rainfall or river flooding, so
that the prevalence varies greatly from sporadic to massive
epidemics in different years.
• The virus has been isolated from Culicoides imicola and C.
coarctus in Zimbabwe , from a mixed pool of biting midges in Kenya,
comprising C. kingi, C. nivosis, C. bedfordi and C. pallidipennis , and
from C. puncticollis in Turkmenistan .
• In Australia, there have been isolations from C.
brevitarsis , Anopheles bancroftii mosquitoes and a mixed pool of
mosquitoes that included Culex, Uranotaenia and Aedes spp.
• North and South America and most of Europe are free of infection
or disease

10. • Africa, Asia & Australia: subtropical & temperate climates
• In summer & autumn months, disappear in winter( temp.
changes)

11. Countries in which BEF is known to occur or from which the disease
has been reported historically shown in blue
Peter J. Walker et al. 2015

12. • Vectors and Intermediate Hosts
• Pattern analogous with other vector borne
diseases
i. Arthropod transmission not demonstrated but epidemeological
data suggests that it is so.
ii. No reports of vertical or horizontal transmission
iii. BEFV isolated from culicine & anopheline mosquitoes in Australia
and from biting midge( G: culicoides) in Africa & Australia
iv. Disease can only be reproduced in cattle by i/v inoculation of virus
v. Virus is absent in lymph during early viremia
vi. Mosquitoes are currently favoured as the major vectors, other
arthropod species also must be involved

13. Incubation period
• 29 hours-10 days ( 3-5 days)
depends on strain & dose of virus
• Viremia detected 24 hours before the onset of
fever and lasts for 4-5 days, maximum upto 13
days.
• No evidence of virus carrier status in cattle

14. • In an epizootic, the cases usually occur
approximately 1 week before the main
wave of infection within a herd
• The course of the disease in the herd may
range from 3-6 weeks
• Single, double or even triple bouts of
disease have been reported within a
single epidemic, but reason not clear.

15. • Mosquito inject virus into a venule
• Viraemia develops with localization &
inflammation in mesodermal tissues-
joints, lymphnodes& muscles
• Virus does not damage host tissue directly
• Host response is due to the high level of interferons
(interleukins ) triggered by the virus
• The interferons in turn cause inflammatory response
• Wide range of hematological & biochemical changes will
occur
• Hypocalcaemia , rise in blood pH lowers the level of
available calcium
• Calcium deficit is responsible for muscle fasiculation,
ruminal stasis and paralysis
• In all cases, there is an early neutrophilia with an
abnormal level of immature neutrophils in the
circulation (“left shift”)

16. Rapid respiration leads to decrease in CO2 levels which causes a rise in plasma pH.
It causes lower availability of calcium in the plasma, leads to hypocalcaemia

17. • Fever is in 2 or more phases:
in 1st febrile stage when interleukins predominate, the
clinical signs are milder .
the febrile stages may be completely distinct with a
period of apparent normality for 3 to 26 h or merge
into each other.
in the later phases clinical signs are severe, lasting 2to
4 days.
recovery follows the disappearance of interferons
from the circulation.

18. pathology
• Pathology is that of a generalised inflammatory disease.
• There is an increase in permeability of small blood vessels with an escape
of neutrophils into the tissues.
• Joint capsules, pleural, peritoneal cavities and the pericardial sac contain
straw coloured fibrinous fluid.
• There may be lung congestion or pneumonia.
• In some rare cases with prolonged paralysis, Wallerian degeneration is
found high in the spinal cord
• It is also possible to see lesions in the upper cervical region of the spinal
cord.
(Hill and Schultz, 1977; Murphy et al., 1986)
• limb lesions may occur.
• Serofibrinous inflammation of the limb joints, polysinovitis, polyarthritis,
polytendinitis, cellulites and focal necrosis of skeletal muscles has been
observed.
• Subcutaneous emphysema over the thorax has been frequently observed
in cattle following BEF infection in Africa.

19. Clinical signs
• Course of disease
I. Onset of fever( 12 hrs)
sudden, peak of 40-42⁰C, within few hrs, lasting for 12-24 hrs
fall in milk production
appetite is normal
ii. Period of disability(1-2 days)
anorexia, depression & nasal discharge, sub mand. Edema
shifting lameness, muscle stiffness
increased heart & resp. rate
milk production virtually ceased
sternal recumbency
loss of swallowing reflex, bloat
lateral recumbency with further loss of reflex, coma & death

20. iii. Recovery
gradual or dramatic @ 3rd day
fever subsides
in lactating cows & fat steers more time for recovery
iv. Sequelae
complications: aspiration pneumonia, abortion
temporary infertility
hind quarter paralysis
10-15% loss of production persists
if forced to over work or subjected to severe stress; die

21. Clinical symptoms
Mild Cases
• Usually seen in animals less than 18 months
old.
• Fever
• slight ocular and nasal discharge
• loss of appetite
• lameness in one or more limbs
• with recovery in 1-2 days

22. Moderate Cases
• Fever and severe depression
• animals in sternal recumbency, some may rise if stimulated.
• Serous ocular and nasal discharges, which may become cloudy.
• Salivation and dehydration occur if swallowing reflex is lost.
• There is rapid respiration in episodes.
• Tachycardia,
• Swelling of leg joints with lameness or refusal to bear weight,
• Ruminal atony and sometimes bloat, and constipation.
• Milk secretion falls suddenly and is often (with fever) the first
presenting sign of the disease,
(Theodoridis et al., 1973b; Davis et al., 1984)
• Recovery occurs abruptly after 2-4 days.
• Abortion may follow if illness occurs in the eighth or ninth month of
pregnancy
(St-George et al., 1986)

24. Animals suffering are unable to
swallow, suffer from constipation and
remain lying down

25. Severe Cases
• The signs progress to lateral recumbency, paralysis and progressive
loss of reflexes.
• A high respiration rate and tachycardia become continuous.
• Swelling with crepitation due to a subcutaneous emphysema may
be felt under the skin of the backline after 3-4 days of fever
(Theodoridis and Coetzer, 1979)
• Death may occur or recovery may be rapid or slow.
• Residual paresis may remain after fever has resolved and the animal
is eating and drinking normally.
• The paresis may resolve in days, weeks or never.

26. Post mortem lesions
• Serofibrinous polysynovitis
• Polytenovaginitis
• Polyarthritis
• Cellulitis
• Focal necrosis of skeletal muscles
• Fluid mixed with fibrin clots present in
pericardial, pleural, and peritoneal cavities.
• Generalized edema of lymph nodes
• Lungs with patchy edema, lobular
congestion, atelectasis and interstitial
emphysema

27. diagnosis

28. • Based on clinical signs and history of fever and
symptoms of lameness
• In endemic areas, antibody titre is high so,
laboratory confirmation is necessary.

29. iv. Differential Diagnosis
(The sudden onset of fever and fall in milk yield)
Rift Valley fever
Blackleg
Botulism
parturient hypocalcaemia
Babesiosis
Anaplasmosis
limb damage due to trauma
 hoof infections

30. 2) Laboratory daignosis
 Sero-conversion: paired serum
– SN test
– ELISA
 Tests to detect and quantify the G protein-encoding gene of BEFV.
 The virus can be identified by immunofluorescent or other immuno-
staining techniques
 by serum virus-neutralisation.
 FA staining of blood smears prepared during viremia.
 IC inoculation of suckling mice.
 Virus isolation can be attempted (from the leukocyte fraction of the
blood) in tissue cultures but is not very efficient.
 Blood clot contraction is interfered with from the second day of
fever in BEF infections for 2-4 days.

31. Treatment:-
• Recovery with no treatment usually
• Nothing should be given by mouth unless the
swallowing reflex is observed to be working
• In severe cases
– Anti-inflammatory drugs
– Fluid therapy
– calcium borogluconate
– Broad spectrum antibiotics.
– Recovery period 3-4 wks.
– Rest is essential during illness and for atleast a week after
recovery

32. vaccination
• Attenuated live virus vaccine
#in South Africa, Japan, and Australia
#These vaccines appear to protect against severe laboratory challenge,
# but evidence of their effectiveness in the field in the face of an epizootic is
variable.
• Live vaccines with adjuvant confer at least 12 months protection after 2 doses
given 4 weeks apart
• Live-attenuated vaccines have been prepared by serial passage of BEFV in
suckling mice and/or in cell cultures, including baby hamster kidney (BHK-
21), hamster lung (HmLu-1) or African green monkey kidney (Vero) cells
• Many of these live-attenuated vaccines have been administered with
aluminum hydroxide or Freund’s incomplete adjuvant and require volumes
of up to 12 mL/dose.

33. • Killed vaccine
• Inactivated BEF vaccines have been prepared by
treatment with formalin, β-propriolactone , binary
ethyleneimine or ultraviolet light.
• Heat-inactivation of the virus resulted in failure to induce a
neutralising antibody response after vaccination
• Most early inactivated vaccines used either aluminium gel
or Freund’s incomplete adjuvant
• Killed vaccines provide 6 months protection when given in
2 doses, 4 weeks apart
• Animal vaccinated from 6 months of age and should be
revaccinated annually to ensure continued immunity

34. • subunit vaccine
• protects against laboratory and field
challenge
• Vaccination experiments have also been
conducted using the BEFV G protein delivered
in recombinant virus vectors
• The vaccine has not yet been manufactured.

35. Control of cattle movements
• As viraemia is brief (3–5 days) and occurs soon
after infection, the risks associated with the
movement of infected cattle pertains mostly to
rapid transport across relatively short distances
and a brief quarantine period in a vector-free
area should be sufficient to eliminate the risk of
introduction of BEFV with imported cattle.
• Although BEF is not an OIE-listed disease, some
countries require that live cattle or bovine semen
to be imported are tested and shown to be free
of BEFV-neutralising antibodies

36. Thank you

37. References
• Walker. J.P and Klement. E Epidemiology and control of
bovine ephemeral fever Veterinary Research 2015 46:124
• Maiti S, Chakravarty P, Garai S, Bandyopadhyay S &
Chouhan VS, Ethno-veterinary practices for ephemeral
fever of Yak: A participatory assessment by the Monpa tribe
of Arunachal Pradesh Indian Journal of Traditional
Knowledge Vol. 12 (1), January 2013, pp. 36-39
• St. George TD, Uren MF, Zakrzewski H, 1986. The
pathogenesis and treatment of bovine ephemeral fever.
Arbovirus research in Australia. Proceedings Fourth
Symposium May 6-9, 1986, Brisbane, Australia, 303-307;
[Discussion pp.313-315]

38. • Davies F.G., Walker A., The isolation of ephemeral
fever virus from cattle and culicoides midges in
Kenya, Vet. Rec. 95, 1974, 63 – 64
• Patel, P. R.Suthar,B. H.Soni, V. K.Dangaria, A.
Prajapati, C. B Bovine ephemeral fever and
related rhabdoviruses. Proceedings of the 1st
International Symposium held in Beijing, PRC, 25-
27 August 1992
• UREN, M. (1989), Bovine ephemeral fever.
Australian Veterinary Journal, 66: 233–236.

39. • Theodoridis A, Boshoff S, Botha MJ, 1973a.
Studies on the development of a vaccine
against bovine ephemeral fever.
Onderstepoort Journal of Veterinary Research,
40:77-82.
• Theodoridis A, Coetzer J, 1979. Subcutaneous
and pulmonary emphysema as complications
of bovine ephemeral fever. Onderstepoort
Journal of Veterinary Research, 46:125-127.