Rift Valley Fever

Dr.Tariq Mustafa Mohamed Ali,

Department of Municipalities and Agriculture,

Agriculture Sector,

Veterinary Laboratory , Al Ain

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)

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.

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

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

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.

History of the disease (Cont.)

The first confirmed Rift Valley fever outbreak outside Africa was reported in September

2000, in the Arabian Peninsula

History of the disease (Cont.)

Laboratory infections have been recorded in other parts of the world

Current situation of the disease

Current situation of the disease ( Cont.)

Endemic Countries

Gambia, Senegal, Mauritania, Namibia, South Africa, Mozambique, Zimbabwe, Zambia, Kenya, Sudan, Egypt, Madagascar, Saudi

Arabia, Yemen

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

Epidimiology in 2005 1st half

Epidimiology in 2005 2nd half

Epidimiology in 2006 1st half

Epidimiology in 2006 2nd half

AETIOLOGY

RFV virus belongs to family Bunyaviridae , genus Phlebovirus.

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.

Bunyaviruses

Group V: (-)sense RNA Viruses

Family Genus Type Species Hosts

Bunyaviridae

Orthobunyavirus

Bunyamwera virus Vertebrates

Hantavirus Hantaan virus Vertebrates

Nairovirus Nairobi sheep disease virus

Vertebrates

Phlebovirus Sandfly fever Sicilian virus , RFV

Vertebrates

Tospovirus Tomato spotted wilt virus

Plants

Cryptogram of RVF virus

R/1: 3 6 / L- : Se/ E : I,V/C,I,Ve(C)/Ac,Di

CryptogramR/1: 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

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)

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.

Protein structure of RFV

L ~8.5kb / RNA dep.RNA polymerase ( Transcriptase)

M ~5.7kb / G1, G2, NSM

S ~0.9kb / N, NSS

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 .

Effect of Chemical factors on RFV virus

Rift Valley fever virus is inactivated by lipid solvents (ether and chloroform ),

detergents, and low pH.

.

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.

Effect of Disinfectants

Inactivated by strong solutions of sodium or calcium hypochlorite (residual chlorine should

exceed 5000 ppm)

Survival

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

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.

Host Range

Neonatal lambs, kids, calves, and puppies are highly susceptible and have a high mortality.

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.

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

Transmission (Cont.)

Historically, explosive outbreaks of the disease have occurred simultaneously over a wide

area of Africa at 5 to 15 year intervals

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

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.

Gross Lesions

Severe illness , Abortion & Mortality

Mortality , Severe illness Viremia &

AbortionInfection & Viremia

Refractive to infection

Sheep

Cattle

Goats

Water buffalo

Humans

Monkeys

Camels

Rats

Gray squirrels

Horses

Cats

Dogs

Monkeys

Guinea pigs

Rabbits

Pigs

Hedgehogs

Tortoises

Frogs

Chickens

Canaries

Pigeons

Parakeets

Morbidity and Mortality in an Outbreak

SpeciesSusceptible cases

Cases DeathsMorbdity rate

Mortality rate

Case 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

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%

Fetuses can be aborted at any stage of gestation.

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%

Clinical signs

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%

Clinical Signs in other animals

Inapparent infections are quite frequent in other species than sheep

PM lesions.

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

PM Lesions ( cont.)

Congestion, enlargement, and discoloration of liver with subcapsular haemorrhages

PM Lesions ( cont.)

Brown-yellowish colour of liver in aborted fetuses

PM Lesions ( cont.)

Widespread cutaneous haemorrhages, petechial to ecchymotic haemorrhages on parietal and visceral serosal membranes

PM Lesions ( cont.)

Enlargement, oedema, haemorrhages and necrosis of lymph nodes

PM Lesions ( cont.)

Congestion and cortical haemorrhages of kidneys and gallbladder

Severe hemorrhagic and edematous biliary cystitis.

PM Lesions ( cont.)

Haemorrhagic enteritis

PM Lesions ( cont.)

Icterus (low percentage)

The yellow appearance and petechial hemorrhages

are characteristic of hepatic necrosis

Focal necrosis and multifocal degeneration

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

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

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)

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

Laboratory diagnosis (cont.)

Antigen detection in blood by :

1. Immunodiffusion

2. ELISA

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

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

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

Public Health