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Congo-Crimean Hemorrhagic Fever -- Republic of South Africa

Seven cases of Congo-Crimean hemorrhagic fever (CCHF) have recently been reported from the Republic of South Africa (Figure 3). Four of these patients were exposed to a single ill cow; the fifth, to two additional ill cows from the same farm. The other two cases are unrelated. Brief case reports follow.

Cases 1-5: A 23-year-old farm laborer became ill May 1, 1984, with severe headache, fever, and dizziness. On May 4, he was in a confused state, and by May 9, he became comatose. A concussion was diagnosed, and surgery was performed for intracranial bleeding and hydrocephalus. The man did not regain consciousness and died May 27. Serum taken May 17 had an immunofluorescence assay (IFA) titer of 1:128 to CCHF, with a positive anti-immunoglobulin M (IgM) conjugate.

The second and third patients, who worked on the same farm, became ill May 3 and May 5, respectively, with severe headaches, backaches, and fever. One had rash and melanic stools. Severe symptoms lasted only a few days, but full recovery was slow. IFA titers were positive in both cases.

The fourth patient owned the farm in Frankfort, Orange Free State province, on which the other three patients worked. He became ill May 8, with sudden onset of severe headache, fever, and rigors. Within a few days, he developed mental confusion, hematemesis, epistaxis, and a petechial rash. He gradually recovered but continued to suffer from mild mental confusion when discharged May 26.

The fifth patient, a 70-year-old laborer, became ill several days after assisting a veterinarian in autopsies of two cows. He recovered but could remember neither the date of onset nor the duration of his illness. CCHF was confirmed on May 18 by IFA. No other farm residents developed antibodies.

The farm owner had purchased 46 cows on January 17, and January 31, 1984, from the southern Cape province, an area presumed free of CCHF. Two became ill and died March 13. Autopsies were performed by the veterinarian whom the fifth patient had assisted; he diagnosed anaplasmosis, a tick-borne disease. A third cow became ill and died April 29. The veterinarian diagnosed foreign-body reticulitis/pericarditis, but no autopsy was performed. All three of the laborers who subsequently became ill had handled the third cow the day of its death and recalled soiling their hands with blood-tinged discharge from the cow's nose. The farmer had not handled the dead cow but had given it intravenous treatments several days earlier. Shortly before his illness, he had found a tick on his sock; the tick had not bitten him, but he had crushed it between his fingers.

Twenty of the 46 new cows were bled on May 18. Seventeen had IFA antibodies against CCHF ranging in titer from 1:16 to 1:4096; five of 20 cows tested from the farmer's original herd had demonstrable antibodies ranging in titer from 1:32 to 1:512. No Hyalomma ticks (common carriers of CCHF virus) were seen on cattle in May, but partially engorged Rhipicephalus evertsi and Boophilus decoloratus were removed from the cattle and are being tested for the presence of virus.

Cases 6 and 7: A 46-year-old man became ill in November 1983 with fever, severe headache, rash, and epistaxis. IFA testing of his serum confirmed the diagnosis of CCHF. The patient lived in Germiston, near Johannesburg, but kept cattle at a farm near Bronkhorstspruit, northeast of Pretoria. Shortly before onset of illness, he had been involved in dehorning and castrating cattle. He did not recall being bitten by ticks.

The last patient, a 32-year-old farmer from Danielskuil, west of Kimberley in the Cape province, became ill on February 2, 1984, with a severe influenza-like illness and rash. Sera obtained on March 14 and March 23 demonstrated respective IFA titers to CCHF of 1:1024 and 1:4096. The patient had slaughtered sheep shortly before his illness began. Reported by R Swanepoel, AJ Shepherd, MJ Erasmus, National Institute for Virology, Dept of Health and Welfare, Transvaal, Dr MPJ van Rensburg, R Wessels, Regional Health Svcs, Orange Free State, Dr S Hattingh, Professor BD Middlecote, Bloemfontein; Dr Schutte, Dr van der Lingen, Dr van Rensburg, Dr Venter, Frankfort, Dr D van Coller, Germiston; Dr JD van Rensburg, Kimberley; Dr B Miller, Rietfontein Hospital, Johannesburg, Dr KD McDonald, Dr SP Taylor, Dr HGV Kustner, National Epidemiological Svc, Pretoria, Republic of South Africa; Special Pathogens Br, Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: The first indigenous case of CCHF in South Africa was reported in 1981. CCHF antibodies have since been found to be common in cattle but not in man, in the interior of the country. In a serosurvey, only 17 of 1,108 sera from people who had spent their entire lives on farms in the interior were positive (1).

CCHF is a distinct clinical entity caused by a tick-borne member of the Bunyaviridae family. The disease, which occurs in eastern Europe, central Asia, the Middle East, and Africa, has a relatively short incubation period (3-6 days) and an abrupt onset characterized by fever, chills, headache, myalgia, abdominal pain, nausea, liquid stools, and anorexia. Conjunctivitis, enanthema of the oral mucosa, leukopenia, and severe thrombocytopenia may also be present. Hemorrhagic manifestations may occur by the fourth day, followed by hypotension and shock. Mortality ranges from about 10% to about 50%. Diagnosis is confirmed by serology or by isolation of virus from blood or tissues obtained at autopsy (2). CCHF is classically transmitted by the bite of an ixodid tick, most often of the Hyalomma genus. The virus seems to be maintained in nature by trans-ovarial and trans-stadial (from larva to nymph to adult) passage among ticks and by transmission from ticks to asymptomatic wild and domestic mammals, such as cattle, sheep, goats, camels, hares, and hedgehogs (2-4). Agricultural workers are at highest risk for contracting CCHF. Contacts of patients have also contracted the disease, either in homes or in hospitals via blood or bloody discharges.

CCHF virus, the presence of which was unrecognized in South Africa before 1981, now appears to be widespread in animal reservoirs throughout much of the country (1,5). It is still uncommon among humans, and immunity appears to be rare. Thus, there is a large susceptible population, and the risk of infection exists for livestock workers, veterinarians, and others who live, work, or play in rural environments.

All seven patients reported here had exposure to cattle or sheep, and none could claim with certainty any tick bites. Although transmission via infected material from domestic mammals is known to occur (2), it appears to be the most common mechanism in South Africa. Reports in the literature have associated viremia with clinical illness and abortion in cattle and other domestic mammals (2,6). Although viral isolation or serology was not attempted, at least two of the three cows that died on the farm in Frankfort probably had CCHF viremia. Whether their clinical illness was due to CCHF is unclear. Furthermore, 17 of 20 cows from a nonendemic area were seropositive when tested in an endemic area. Presumably, these cows seroconverted between January, when they were first brought to the endemic area, and May, when they were tested. This presumed seroconversion may have been associated with viremia and possibly shedding of virus in other fluids, such as saliva and urine.

Persons who come in close contact with these animals, which may not have clinical symptoms, are in danger of acquiring the virus. The importation of nonimmune cattle--and perhaps other domestic animals--into an endemic area may be an important means by which CCHF virus is ultimately transmitted to humans.


  1. Swanepoel R, National Institute for Virology, Department of Health and Welfare, Republic of South Africa. Personal communication.

  2. Hoogstraal H. The epidemiology of tick-borne Crimean-Congo hemorrhagic fever in Asia, Europe, and Africa. J Med Entomol 1978;15:307-417.

  3. Burney MI, Ghafoor A, Saleen M, Webb PA, Casals J. Nosocomial outbreak of viral hemorrhagic fever caused by Crimean hemorrhagic fever-Congo virus in Pakistan, January 1976. Am J Trop Med Hyg 1980;29:941-7.

  4. Suleiman MN, Muscat-Baron JM, Harries JR, et al. Congo/Crimean haemorrhagic fever in Dubai. An outbreak at the Rashid Hospital. Lancet 1980;II:939-41.

  5. Swanepoel R, Struthers JK, Shepherd AJ, McGillivray GM, Nel MJ, Jupp PG. Crimean-Congo hemorrhagic fever in South Africa. Am J Trop Med Hyg 1983;32:1407-15.

  6. Woodall JP, Williams MC, Simpson DI. Congo virus: a hitherto undescribed virus occurring in Africa. II. Identification studies. E Afr Med J 1967;44:93-8.

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