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International Notes Rift Valley Fever -- Egypt, 1993

In June 1993, several persons in Aswan Governorate (1993 population: 952,000) in southern Egypt sought medical care for acute loss of vision following an illness characterized by fever, headache, retro-orbital pain, and myalgias. Ophthalmologists who examined these persons noted paramacular retinal hemorrhages and edema, and Rift Valley fever (RVF) was suspected; serologic studies of these patients confirmed the diagnosis of acute RVF (1,2). In August 1993, serologic surveys were conducted in two villages to estimate the prevalence of RVF virus (RVFV) antibody among persons residing in selected rural communities in Aswan Governorate. This report summarizes the findings of these serosurveys and two nested epidemiologic studies conducted in the same villages 2 weeks later.

All persons aged greater than 1 year in households randomly chosen for survey were interviewed, and a blood specimen was obtained with informed consent (with parents as proxy for children aged less than 10 years). Specimens were analyzed for immunoglobulin M (IgM) and immunoglobulin G (IgG) antibody by enzyme-linked immunosorbent assay (3).

In one village (population: 2400) that was chosen for survey because a fatal case of RVFV encephalitis occurred there, 39 (12%) of 326 persons in 42 households were seropositive for RVFV IgM antibody. In a nested case-control study with 20 RVFV IgM seropositive persons (cases) and three sex-, age- (plus or minus 10 years), and neighborhood-matched seronegative persons (controls) per case, acute RVF was associated with contact with the blood of a slaughtered animal during the preceding 6 months (matched odds ratio {OR}=11.3; 95% confidence interval {CI}=1.3-102.7) and with sleeping outdoors every night (OR=9.3; 95% CI=1.7-52.6).

In the second village (population: 2600), 30 (8.4%) of 359 persons in 52 households were seropositive for RVFV IgM antibody. In a retrospective cohort study nested in the original survey, the risk for IgM seropositivity was associated with attending the slaughtering of an animal (relative risk {RR}=2.5; 95% CI=1.2-5.1), sleeping outdoors every night (RR=2.7; 95% CI=1.3-5.6), and having a history of schistosomiasis (RR=3.6; 95% CI=1.8-7.1). Of those children aged less than 13 years and born at least 2 years after the 1977 epidemic in Egypt, 28 (13%) of 215 had serologic evidence of RVFV infection (i.e., IgM or IgG antibody). Four of these children had no evidence of recent infection (i.e., only IgG).

To monitor the potential spread of RVF from southern Egypt (i.e., Aswan) to the Nile Delta region of northern Egypt in 1993, RVF surveillance was conducted at fever hospitals, among persons in high-risk occupational groups (e.g., abattoir and veterinary workers), and in selected animal populations. In October 1993, RVFV was isolated from a 17-year-old woman with fatal hemorrhagic disease hospitalized in Sharkiya in the Nile Delta. In 1993, RVF was documented among persons residing in the governorates of Dakhla, Damietta, Gharbiya, Giza, Ismailia, Kafr al-Sheikh, Minufiya, Port Said, Qena, and Sharkiya. Reported by: MS El Sharkawy, DPH, Director General (retired), Communicable Diseases Control Dept, Ministry of Health; S Abdel Raheem, DPH, First Undersecretary (retired), Preventive Sector, Ministry of Health; S Oun, DPH, Director General, Preventive Sector, Ministry of Health, Aswan Governorate; AM Abd El-Ghafar, MBBCh, M Khalifa, MBBCh/MSc, MH El Sakka, MBBCh, MF Abdel-Wahab, MBBCh, SA Abdel-Rahman, MBBCh, MF Ahmed, MBBCh, A El-Sheikh, MBBCh, FM Abdeen, MBBCh, Egyptian Counterpart, IZE Imam, MD, Technical Advisor, E Mansour, MD, Director, Field Epidemiology Training Program, Child Survival Project, Ministry of Health. RR Arthur, PhD, BAM Botros, PhD, CM Calamaio, DVM, JR Campbell, PhD, SE Cope, PhD, CE Cummings, MD, RG Hibbs, MD, S Presley, PhD, GR Rodier, MD, AW Salib, AK Soliman, DVM, TA Tantawy, PhD, US Naval Medical Research Unit No. 3, Cairo. JC Morrill, DVM, US Army Medical Research Institute of Infectious Diseases/Consultant, World Health Organization. A Gad, PhD, MA Darwish, MD, Ain Shams Univ Faculty of Medicine, Cairo. Div of Communicable Diseases, World Health Organization, Geneva. Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; International Br, Div of Field Epidemiology, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: RVF, an acute febrile illness often with hemorrhagic manifestations (4), is caused by an RNA-containing virus of the Bunyaviridae family. RVF epizootics are characteristically associated with domesticated ruminants (e.g., sheep, cattle, buffalo, goats, and camels) and humans living in close proximity. The reservoir for RVFV is unknown. RVFV initially was detected in Kenya during the 1930s when a febrile illness, characterized by spontaneous abortions in ewes and high death rates in lambs, also caused fever and myalgias in veterinarians investigating the outbreak (5). During 1977-78, the first epidemic of RVF reported in Egypt and the largest recorded thus far was associated with approximately 18,000 cases and 598 deaths in humans (4,6). With the exception of the two outbreaks in Egypt, RVFV is known to circulate only in sub-Saharan Africa; outbreaks previously have been reported in Cameroon, Central African Republic, Madagascar, Mali, Mauritania, Mozambique, Nigeria, Senegal, South Africa, Sudan, Tanzania, Zambia, and Zimbabwe (7,8).

Retrospective serosurveys have indicated that RVFV was not present in Egypt before the 1977-78 epidemic (4,6). In the 1993 studies of RVF, among children born after the 1977 outbreak, nearly all those with RVFV antibody had serologic evidence of recent infection, suggesting that RVFV probably was not circulating in the study areas during the interepidemic period. Ongoing surveillance is being conducted at fever hospitals, among persons in high-risk occupational categories, and in sentinel animal populations. After the outbreak in Egypt was recognized in 1993, vaccination of livestock with killed RVFV vaccine was intensified. In 1994, live-attenuated RVFV vaccine was used to vaccinate nearly 6 million domesticated animals throughout Egypt. Because RVF cases continued to occur 3-4 years after the 1977 epidemic began, additional human cases may be expected during the next several years, particularly among persons at high risk, despite reported widespread animal vaccination with live attenuated vaccine.

The nested epidemiologic studies in this report indicated that sleeping outdoors every night could possibly be a risk factor for exposure to mosquito vectors. Similarly, the slaughter-related factors may be proxies for exposure(s) to infected animals. The findings in this report are among the first published studies systematically analyzing various risk factors for human RVFV infection in rural populations in Africa (8).

The species of several genera of mosquitoes (including Aedes, Anopheles, Culex, Erethmapodites, and Mansonia) are capable of transmitting RVFV and may be important vectors during epizootics (4,6-9). Although widespread aerial insecticide application could decrease mosquito vectors, this strategy is expensive and difficult to implement. Human transmission may occur following exposure to either the blood or viscera of infected animals (e.g., during slaughtering) or to instruments, needles, or laboratory specimens contaminated with the virus (8,10). RVFV vaccine for humans is not commercially available.

Because of the epizootic nature of RVF, human infection occurs primarily among persons living in small villages and rural areas with exposure to potentially infected livestock or infected arthropod vectors (i.e., mosquitoes) or among persons in high-risk occupations (e.g., veterinarians and slaughterhouse workers). RVF infection has not been documented in either tourists or foreign nationals living in Egypt. Personal measures that may decrease RVF transmission include use of bednets and/or effective mosquito repellents containing diethyl metatoluidine (if available) and minimizing exposures to blood or tissues (e.g., viscera, abortus, and retained placenta) of animals potentially infected with RVF. Universal precautions during the handling of blood, blood products, medical instruments, or syringes should minimize the risk for disease among workers in health facilities or laboratories.


  1. El Sharkawi SA, Sobhy AR. Highlights on some epidemiologic points in Rift Valley fever outbreaks in Aswan, Egypt. Presented at the World Health Organization Conference, Teramo, Italy, September 14-15, 1993; publication no. WHO/IZST Consultation/WP/93.5.1.

  2. Arthur RR, El-Sharkawy MS, Cope SE, et al. Recurrence of Rift Valley fever in Egypt. Lancet 1993;342:1149-50.

  3. Niklasson B, Peters CJ, Grandien M, Wood O. Detection of human immunoglobulins G and M antibodies to Rift Valley fever virus by enzyme-linked immunosorbent assay. J Clin Microbiol 1984;19:225-9.

  4. Meegan JM. The Rift Valley fever epizootic in Egypt 1977-78: description of the epizootic and virologic studies. Trans R Soc Trop Med Hyg 1979;73:618-23.

  5. Daubney R, Hudson JR, Garnham PC. Enzootic hepatitis or Rift Valley fever: an undescribed virus disease of sheep, cattle, and man from East Africa. J Path & Bact 1931;34:545-79.

  6. Imam IZE, El-Karanmany R, Omar F, El-Kafrawy O. Rift Valley fever in Egypt. J Egypt Public Health Assoc 1981;56:356-83.

  7. Gear JHS, Monath TP, Bowen GS, Kemp GE. Arboviruses of Africa. In: Textbook of pediatric infectious diseases. 2nd ed. Philadelphia: WB Saunders, 1987:1480-1.

  8. Wilson ML, Chapman LE, Hall DB, et al. Rift Valley fever in rural northern Senegal: human risk factors and potential vectors. Am J Trop Med Hyg 1994;50:663-75.

  9. Hoogstraal H, Meegan JM, Khalil GM, Adham FK. The Rift Valley fever epizootic in Egypt, 1977-78: ecological and entomological studies. Trans R Soc Trop Med Hyg 1979;73:624-9. 

  10. Ghoneim NJ, Woods GT. Rift Valley fever and its epidemiology in Egypt: a review. J Medicine 1983;14:55-79.

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