Rift valley fever natural history, complications and prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aakash Hans, MD[2]

Overview

Natural History, Complications and Prognosis

Rift Valley fever (RVF) is caused by a virus belonging to the Bunyaviridae family and Phlebovirus genus, known as Rift Valley fever virus (RVFV). Majority of humans experience fever which subsides on its own, while a few go on to develop neurological symptoms, clot formation, hemorrhage or vision abnormalities.

  • Natural History
    • Febrile Illness :
      • The patient does not develop symptoms until 4 to 5 days after exposure.
      • Symptoms of fever develop all of a sudden and include generalized weakness, feeling cold, headaches, nausea and a feeling of heaviness in the righty upper abdomen.[1]
      • Next, the patient develops high body temperatures 101.8 to 103.1 F along with body aches, sensitivity to light and low blood pressure. [2]
      • Various other manifestations like vomiting accompanied with abdominal pain, loss of sense of taste, nosebleeds and loose stools may also be seen in some individuals.[3]
      • After three to four days since the onset of illness, symptoms begin to subside and body temperatures drop back to normal.
      • Some individuals may experience repeat episodes of fever and headache one to three days following recovery.[4]
      • Once the body temperature becomes normal some patients develop clots in their coronary vessels or have severe pain in the abdomen or lower limbs.
      • The virus is detected in the blood until third day of illness while antibodies begin to appear in the blood from the fourth day onward.[5]
  • Complications
    • Neurological manifestations :
    • Hemorrhage :
    • Clot formation:
      • A case was reported which developed several clots after being infected with RVFV. [12]
      • After the patient’s fever subsided, he developed patches on his lower limbs around the fifth day of illness.
      • This was followed by inflammatory changes in the patient’s popliteal vein by the twelfth day followed by formation of pulmonary infarcts at various locations from twentieth day onwards.
      • The patient developed a pulmonary embolus on the 45th day of illness which proved to be fatal.
      • No liver involvement was observed during postmortem examination.
    • Ophthalmological manifestations :
      • Individuals can present with symptoms at variable intervals after the disease onset.
      • Loss of peripheral vision or blurred vision is commonly reported after infection.
      • Unilateral or bilateral eyes may be involved with features of edema in the macula, retinal bleeding or loss of transparency in the vitreous.[13]
      • Majority of cases do not regain complete eye function, even after the viral infections subsides.[14]
  • Prognosis
    • Majority of individuals develop a mild to moderate course of fever and body aches, from which they recover spontaneously.
    • Complications are seen rarely with ocular problems occurring in about 1 to 2% cases, while encephalitis and hemorrhage developing in approximately 1% cases or less. [15]
    • Hemorrhagic fever is associated with a high fatality rate of 50%, while the fatalities reported overall are only around 1% of total cases.
    • Only 1 to 10% of cases with ocular manifestations continue to have lifelong, irreversible impairment of vision.

References

  1. Findlay GM, Daubney R. The virus of rift valley fever or enzootic hepatitis. Lancet. 1931;221:1350–1351
  2. Kitchen SF. Laboratory infections with the virus of rift valley fever. Am J Trop Med. 1934;14:547–564
  3. Mundel B, Gear J. Rift valley fever; i. The occurrence of human cases in johannesburg. S Afr Med J. 1951;25:797–800.
  4. Rift Valley fever; accidental infections among laboratory workers.SMITHBURN KC, MAHAFFY AF J Immunol. 1949 Jun; 62(2):213-27.
  5. Rift Valley fever; accidental infections among laboratory workers.SMITHBURN KC, MAHAFFY AF J Immunol. 1949 Jun; 62(2):213-27.
  6. Maar SA, Swanepoel R, Gelfand M. Rift valley fever encephalitis. A description of a case. Cent Afr J Med. 1979;25:8–11.
  7. Alrajhi AA, Al-Semari A, Al-Watban J. Rift valley fever encephalitis. Emerg Infect Dis. 2004;10:554–555
  8. Laughlin LW, Girgis NI, Meegan JM, Strausbaugh LJ, Yassin MW, Watten RH. Clinical studies on rift valley fever. Part 2: Ophthalmologic and central nervous system complications. J Egypt Publ Health Assoc. 1978;53:183–184
  9. van Velden DJ, Meyer JD, Olivier J, Gear JH, McIntosh B. Rift valley fever affecting humans in south africa: A clinicopathological study. S Afr Med J. 1977;51:867–871.
  10. Yassin W. Clinico-pathological picture in five human cases died with rift valley fever. J Egypt Publ Health Assoc. 1978;53:191–193.
  11. Al-Khuwaitir TS, Al-Moghairi AM, Sherbeeni SM, Al-Ghamdi AS. Rift valley fever hepatitis complicated by disseminated intravascular coagulation and hepatorenal syndrome. Saudi Med J. 2004;25:528–531
  12. Schwentker FF, Rivers TM. Report of a fatal laboratory infection complicated by thrombophlebitis. J Exp Med. 1933;59:305–313
  13. Siam AL, Meegan JM, Gharbawi KF. Rift valley fever ocular manifestations: Observations during the 1977 epidemic in egypt. Br J Ophthalmol. 1980;64:366–374
  14. Ayoub M, Barhoma G, Zaghlol I. Ocular manifestations of rift valley fever. Bull Ophthalmol Soc Egypt. 1978;71:125–133.
  15. https://www.nj.gov/agriculture/divisions/ah/diseases/riftvalley.html

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