Rift Valley fever is an arthropod-borne viral disease that affects various mammals. It is characterized by abortions in pregnant animals and liver damage. The disease was first described in Kenya in 1931. It is endemic in many African and Middle Eastern countries. Transmission occurs via mosquito bites or contact with infected animal tissues. Symptoms in animals include fever, vomiting, and abortions. The virus can be diagnosed by isolating it from blood or tissues of infected hosts. Controlling mosquito populations and vaccinating susceptible animal species are important for prevention.

1. Rift Valley Fever
Dr.Tariq Mustafa Mohamed Ali,
Department of Municipalities and Agriculture,
Agriculture Sector,
Veterinary Laboratory , Al Ain

2. Definition
 Rift Valley fever (RVF) is an arthropod-borne viral
disease affecting wide variety of mammals .
 characterized by abortions among pregnant animals,
high mortality in neonates, and hepatic necrosis.
 The Human beings are highly susceptible to the
disease .
 The Disease Classified as an OIE List A disease
(A080)

3. Geographic Distribution
RVF has been recognised as an exclusive
disease in African countries, with an
underlying association with high rainfall and
dense populations of vector mosquitoes.

4. History of the disease
 First described by Daubny in 1931 in Rift
valley area In kenya .
 Antibodies recorded in human cases from
Central africa and the virus isolated from
animals raised in Uganda ,Mali, Congo and
Gabon by 1936

5. History of the disease (Cont.)
 In 1951 reported in South Africa
 In 1954 reported in French Equatorial Africa
 In 1956 reported in Cattle in Kenya
 In 1957 reported in Cattle in Togo
 In 1958 reported in Rhodesia (Nambia)
 In 1973 in sudan in Kosti District

6. History of the disease (Cont.)
 The only epizootic outbreaks of RVF outside
sub-Saharan Africa were recorded in animals
and humans in Egypt in 1977-78,
 Mauritania in 1987 and again in Egypt in
1993.

7. History of the disease (Cont.)
The first confirmed Rift Valley fever outbreak
outside Africa was reported in September
2000, in the Arabian Peninsula

8. History of the disease (Cont.)
Laboratory infections have been recorded in
other parts of the world

13. Current situation of the disease

15. Current situation of the disease
( Cont.)
Endemic Countries
Gambia, Senegal, Mauritania, Namibia, South
Africa, Mozambique, Zimbabwe, Zambia,
Kenya, Sudan, Egypt, Madagascar, Saudi
Arabia, Yemen

17. Epidemiology ( Cont.)
Countries known to have some cases with
periodic virus isolation
Botswana, Angola , Democratic Republic of
the Congo, Congo, Gabon, Cameroon,
Nigeria, Central African Republic, Chad,
Niger, Burkina Faso, Mali, Guinea, Tanzania,
Malawi, Uganda, Ethiopia, Somalia

19. Epidimiology in 2005 1st half

20. Epidimiology in 2005 2nd half

21. Epidimiology in 2006 1st half

22. Epidimiology in 2006 2nd half

23. AETIOLOGY
RFV virus belongs to family Bunyaviridae ,
genus Phlebovirus.

24. Family Bunyaviridae
 The largest family of viruses.
 It includes the most arthropod-born
viruses
 It include more than 350 membres with
large diversity
 Genetic reassortment in infected
mosquitoes migt be the cause of this
diversity.

25. Bunyaviruses
Group V: (-)sense RNA Viruses
Genus Type Species Hosts
Family
Orthobunyavirus Bunyamwera virus Vertebrates
Hantavirus Hantaan virus Vertebrates
Nairobi sheep disease
Bunyaviridae Nairovirus Vertebrates
virus
Sandfly fever Sicilian
Phlebovirus Vertebrates
virus , RFV
Tomato spotted wilt
Tospovirus Plants
virus

26. Cryptogram of RVF virus
R/1: Σ 3 6 / L- : Se/ E : I,V/C,I,Ve(C)/Ac,Di

27. Cryptogram
R/1: Σ 3 6 / L- :Se/ E :I,V/C,I,Ve(C)/Ac,Di
 RNAV , SS,
 3 molecules/ - ve strand
 Spherical,elongated NC / Enveloped
 90 - 100 um , heat labile , ether sensitive .
 All isolates are serologically similar
 Host range /mode of transmission / kind of vector
if present

28. Micrograph of RVFV
 The virion is budding into
membrane vesicles of Golgi
vesicles in the cytoplasm of
a liver cell of an infected rat.
The virion is about
100 nm (nanometer)

29. NA of RVF virus
 Single-stranded RNA
 Negative sense / ambi-sense
 Each virion contains, 3 linear segments :
 L 2.7 X 10 6
 M 1.6 X 10 6
 S 0.6 X 10 6
 Not present in equimolar amounts
 5' ends not capped; 3' ends not
polyadenylated;
 Genomic RNA not infectious.

31. Protein structure of RFV
 L ~8.5kb / RNA dep.RNA polymerase
( Transcriptase)
 M ~5.7kb / G1, G2, NSM
 S ~0.9kb / N, NSS

32. Effect of Temperature
 The virus can remain viable for up to 4
months at 4o C.
 Specimens stored below 0o C will retain
infectivity for 8 years .
 The virus in serum, inactivated by 56°C for
120 minutes
 Rift Valley fever virus in aerosols has a half-
life in excess of 77 minutes at 25o C and 30
percent relative humidity .

33. Effect of Chemical factors on RFV
virus
Rift Valley fever virus is inactivated by lipid
solvents (ether and chloroform ),
detergents, and low pH.
.

34. Effect of Chemical factors on RFV
virus ( Cont.)
 At neutral or alkaline pH in the presence of
protein such as serum, the virus can remain
viable for up to 4 months at 4o C.
 Solutions having a pH of 6.2 (acetic acid) or
lower are also effective.

35. Effect of Disinfectants
Inactivated by strong solutions of sodium or
calcium hypochlorite (residual chlorine should
exceed 5000 ppm)

36. Survival
The RVFV survives in dried discharges and multiplies in
some arthropod vectors.

37. Host range
 Rift Valley fever virus infects many species of
animals and humans .
 Sheep and cattle are the primary species
affected and the primary amplifiers of the
virus.

38. Host Range
 Neonatal lambs, kids, calves, and puppies
are highly susceptible and have a high
mortality.

39. Human being
 Humans are highly susceptible to RVF virus
infection and are readily infected by
mosquitoes and aerosols.
 Humans develop a sufficient viremia to be a
source of infection for mosquitoes and thus
could introduce the disease into uninfected
areas.

40. Transmission
 Haematophagous mosquitoes of many genera
(Aedes, Anopheles, Culex, Eretmapodites, Mansonia,
etc.) can transmit fever as biological, competent
vectors.
 Can replicate extensively in insects - transovarian
passage allows overwintering.
 Mosquitoes (Aedes) migt be the reservoir host
 Direct contamination: occurs in humans when
handling infected animals and meat

41. Transmission (Cont.)
Historically, explosive outbreaks of the disease
have occurred simultaneously over a wide
area of Africa at 5 to 15 year intervals

42. Infection of human being
 Direct and indirect contact with infected
animals through nasal discharge, blood,
vaginal secretions after abortion in animals,
mosquitoes, and infected meat.
 Aerosol and consumption of raw milk is also
possible

44. Incubation Period
 Experimentally, the incubation period in
newborn lambs, kids, calves, and puppies, is
about 12 hours.
 In adult sheep, cattle, goats, and dogs the
incubation period may be as long as 3 days.
 In humans, the incubation period is 4 to 6
days.

45. Gross Lesions
Severe illness , Mortality , Severe
Refractive to
Abortion & Mortality illness Viremia &
Infection & Viremia infection
Abortion
Sheep Monkeys Horses Guinea pigs
Cattle Camels Cats Rabbits
Goats Rats Dogs Pigs
Water buffalo Gray squirrels Monkeys Hedgehogs
Humans Tortoises
Frogs
Chickens
Canaries
Pigeons
Parakeets

46. Morbidity and Mortality in an Outbreak
Susceptibl Morbdity Mortality Case
Species Cases Deaths
e cases rate rate fatality rate
Sheep 9000 1500 105 16.7% 1.2% 7%
Goats 10000 1500 95 15% 0.95% 6.3%
Cattle 4000 500 30 13% 0.75% 6%
Camelidae 4000 500 5 13% 0.13% 1%
Animals belong to different herds.70 people have died

47. Clinical Signs in cattle
 Adults: fever (40-41°C), excessive salivation,
anorexia, weakness, fetid diarrhoea, fall in
milk yield.
 Calves: fever (40-41°C), depression. Mortality
rate: 10-70%
 Abortion may reach 85% in the herd.
 Mortality rate is usually less than 10%

48. Fetuses can be aborted at any stage of
gestation.

49. Clinical Signs in adult sheep & goats
 Fever (40-41°C), mucopurulent nasal
discharge, vomiting .
 Abortion may reach 100% in pregnant ewes
 Mortality rate may reach 20-30%

50. Clinical signs

52. Clinical Signs in lambs and Kids
 fever (40-42°C), anorexia, weakness, death
within 36 hours after inoculation.
 Mortality rate: for animals under 1 week of
age - up to 90%; for animals over 1 week of
age - up to 20%

53. Clinical Signs in other animals
Inapparent infections are quite frequent in other
species than sheep

54. PM lesions.
Focal or generalised hepatic necrosis (white
necrotic foci of about 1 mm in diameter)

58. PM Lesions ( cont.)
Congestion, enlargement, and discoloration of
liver with subcapsular haemorrhages

61. PM Lesions ( cont.)
 Brown-yellowish colour of liver in aborted
fetuses

63. PM Lesions ( cont.)
Widespread cutaneous haemorrhages,
petechial to ecchymotic haemorrhages on
parietal and visceral serosal membranes

68. PM Lesions ( cont.)
 Enlargement, oedema, haemorrhages and
necrosis of lymph nodes

71. PM Lesions ( cont.)
 Congestion and cortical haemorrhages of
kidneys and gallbladder

72.  Severe hemorrhagic
and edematous biliary
cystitis.

74. PM Lesions ( cont.)
 Haemorrhagic enteritis

76. PM Lesions ( cont.)
Icterus (low percentage)

77. The yellow appearance and petechial hemorrhages
are characteristic of hepatic necrosis

79. Focal necrosis and multifocal
degeneration

80. Specimens for Laboratory
 Heparinised or clotted blood
 Plasma or serum
 Tissue samples of liver, spleen, kidney, lymph
node, heart blood and brain from aborted
fetus.
 Specimens should be submitted preserved in
10% buffered formalin and in glycerol/saline
and transported at 4°C

81. Differential Diagnosis
1. Bluetongue
2. Wesselsbron disease
3. Enterotoxemia of sheep
4. Ephemeral fever
5. Brucellosis
6. Vibriosis
7. Trichomonosis
8. Nairobi sheep disease
9. Heartwater
10. Ovine enzootic abortion
11. Towic plants
12. Bacterial septicaemias
13. Rinderpest and Peste des petits ruminants

82. Laboratory diagnosis
 Virus isolation:
 Inoculation of mice or hamsters - preferred
method
 Inoculation of 1-2-day-old lambs
 Inoculation of embryonated chicken eggs
 Tissue culture inoculation (Vero, CER, BHK-
21, mosquito line cells or primary calf, lamb
and goat kidney and testis cells)

83. Laboratory diagnosis (cont.)
Viral antigen detection by :
1. Immunofluorescence in cryostat sections or
in impression smears of liver, spleen and
brain.
2. Complement fixation and immunodiffusion
on tissue suspensions

84. Laboratory diagnosis (cont.)
Antigen detection in blood by :
1. Immunodiffusion
2. ELISA

85. Laboratory diagnosis by Serological tests
 Enyzme-linked immunosorbent assay - IgG and IgM
and for Ag.detection
 Virus neutralisation
 Fluorescent antibody test
 Haemagglutination inhibition
 Plaque reduction neutralisation
 Complement fixation
 Immunodiffusion

86. Control and Eradication
 Vaccination is the only practical method of
preventing low-level losses.
 Animal movement of from endemic areas to
RVF-free areas should be discouraged.
 Mosquito control during an epizootic is logical
but not practical for large areas;
 Slaughter of sick animals is not
recommended

87. Vaccination
 Vaccination of all susceptible animals to
prevent infection of amplifying hosts and thus
infection of vectors is the only way to prevent
infection of animals and man
 Inactivated vaccine containing saponin or
peanut oil

88. Public Health