21 Sunday July 2019
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Overview of Rift Valley Fever:

   Overview of Rift Valley FeverOverview of Rift Valley Fever2


Rift Valley fever (RVF) is a peracute or acute zoonotic disease of domestic ruminants in Africa, Madagascar, and the Arabian Peninsula.

Signs of the disease tend to be nonspecific, rendering it difficult to recognize individual cases. Infections may also be inapparent or mild.

During epidemics, the occurrence of numerous abortions and deaths among young animals, together with an influenza-like disease in humans, tends to be characteristic.

Etiology and Epidemiology:


  1. RVF virus belongs to the genus Phlebovirus and is a typical Bunyavirus. It has a 3-segmented, single-stranded, negative-sense RNA genome with a molecular weight of 4–6 × 106, and each of the segments, L (large), M (medium), and S (small), is contained in a separate nucleocapsid within the virion.
  2. No significant antigenic differences have been demonstrated between RVF isolates from many countries and outbreaks, but differences in pathogenicity are seen.
  3. The disease is endemic in tropical regions of mainly eastern and southern Africa, although West Africa and the drier North Africa are also affected. An epidemic was also reported in 2000 in Saudi Arabia and Yemen.
  4. Cyclic epidemics have occurred at 5- to 20-yr intervals in drier areas. The cycles are normally associated with periods of abnormally heavy rainfall. In the periods between epidemics, the virus is believed to be dormant in eggs of the floodwater-breeding mosquito Aedes mcintoshi in the dry soil of grassland depressions (dambos).
  5. Although transovarial transmission is believed to be the most important interepidemic survival strategy of the virus, inapparent cycling of disease may occur at forest edge habitats.
  6. RVF may spread by windborne mosquitoes or movement of viremic animals. With adequate rainfall, the infected maintenance mosquitoes develop and infect ruminants, which amplify the virus.
  7. The virus is spread by many species of mosquitoes or mechanically by other insects characteristic of different regions.
  8. The incidence of RVF peaks in late summer. After the first frost, both the disease and vectors may disappear. In warmer climates where insect vectors are present continuously, seasonality is not seen.
  9. Humans are also readily infected through blood aerosols from infected animals during ritual slaughter, or by exposure to infected animal tissues, aborted fetuses, mosquito bites, and laboratory procedures.
  10. Humans can act as amplifying hosts and introduce the disease (via mosquitoes) to animals in uninfected areas.


Clinical Findings:


  1. The incubation period is 12–36 hr in lambs. A biphasic fever of up to 106°F (41°C) may develop. Affected animals are listless and reluctant to move or feed and may show signs of abdominal pain. Lambs usually die within 2 days.
  2. Older animals may die acutely or develop an inapparent infection. Sick animals may regurgitate and develop a bad-smelling diarrhea and icterus, which is common in cattle. Sometimes, abortion may be the only sign of infection.
  3. In pregnant ewes, the mortality and abortion rates vary from 5 to almost 100% in different outbreaks and on different farms.
  4. The rates in cattle are usually <10%.



  1. The hepatic lesions are similar in all species and vary mainly with the age of the affected individual.
  2. The most severe lesions seen in aborted fetuses and newborn lambs moderately to greatly enlarged, soft, friable livers with irregular congested patches. Numerous grayish white necrotic foci are invariably present but may not be clearly visible.
  3. Hemorrhage and edema of the wall of the gallbladder and mucosa of the abomasum are common.
  4. Intestinal contents are dark chocolate-brown. In all animals, the spleen and peripheral lymph nodes are enlarged and edematous and may show petechiae. In humans, RVF is usually inapparent or associated with a moderate to severe, nonfatal influenza-like illness.
  5. A minority may develop severe disease with ocular lesions, encephalitis, or severe hepatic lesions with hemorrhages.



  1. RVF should be suspected when abnormally heavy rains and flooding are followed by the widespread occurrence of abortions and mortality among newborn animals characterized by necrotic hepatitis, concurrent with hemorrhages and influenza-like disease in people handling animals or their products. Histopathologically, the liver lesions in lambs are severe and extensive.
  2. The virus can readily be isolated from tissues of aborted fetuses and the blood of infected animals.
  3. The viral titer in these tissues is often high enough to use organ suspensions as antigen for a rapid diagnosis in neutralization, complement fixation, ELISA, agar gel diffusion tests, or staining of organ impression smears; however, these tests should be supplemented by isolation in suckling mice or hamsters injected intracerebrally or in cell cultures such as baby hamster kidney (BHK21), monkey kidney (Vero), CER and mosquito cells, or primary kidney and testis cell cultures of lambs. Detection of viral nucleic acid by PCR is possible, and reverse
  4. transcriptase-PCR tests have been described.
  5. All conventional serologic tests can be used to detect antibody against RVF virus and are helpful in epidemiologic studies.
  6. In some areas, however, serologic surveys may be complicated by cross-reactivity between RVF virus and other phleboviruses.
  7. An IgM ELISA can demonstrate recent infection using a single serum sample.


Control and Prevention:

  1. Control of vectors, movement of stock to high-lying areas, and confinement of stock in insect-proof stables are usually not practical, instituted too late, and of little value. Immunization remains the only effective way to protect livestock.
  2. The mouse neuro-adapted Smithburn strain of RVF virus can readily be produced in large quantities, is inexpensive, and induces a durable immunity 6–7 days after inoculation.
  3. It should normally not be used for the protection of pregnant animals because it may cause abortion, congenital defects, and hydrops amnii in the ewe; however, its use may be contemplated during an outbreak when possible adverse effects may be outweighed by the dangers of a natural infection. Although not proved, it is theoretically possible for the attenuated virus to revert to virulence.
  4. A small-plaque variant and a mutagen-induced strain have been investigated as potential vaccine candidates but have not been accepted as replacements for the Smithburn strain. Outbreaks of RVF cannot be predicted and are usually of sudden onset.
  5. Therefore, routinely immunizing lambs at 6 mo of age, which should afford lifelong protection, is advisable.
  6. The offspring of susceptible ewes can be immunized at any age. It is not advisable to use live, attenuated vaccines in nonendemic countries; subunit DNA vaccines are being developed and will offer a better alternative.
  7. Pregnant ewes and cattle should be vaccinated with a formalin-inactivated vaccine, which elicits a better immunity in cattle and is safe in pregnancy.
  8. Revaccination after 3 mo is advisable to induce an immunity that will last ∼1 yr and to confer colostral immunity to the offspring.


Zoonotic Risk:

People involved in the livestock industry should be made aware of the potential dangers of exposure to RVF-infected animals and tissues.