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International Notes Crimean-Congo Hemorrhagic Fever -- Republic of South Africa
During August and September 1984, eight cases of Crimean-Congo hemorrhagic fever (CCHF) occurred in a hospital in Capetown, Republic of South Africa. Two patients died.
The index case was a 26-year-old man from the Vredenburg district, approximately 120 kilometers north of Cape Town. Although he had no evidence of a recent tick bite, he had had regular contact with farm animals. His illness began on August 28, with a sore throat, muscle pains, and pyrexia. Four days later, he had slight hematemesis, followed by a massive gastrointestinal hemorrhage the next day. After resuscitation at a peripheral hospital, he was transferred to a hospital in Cape Town, late on September 3.
On admission, the patient was in a severe hemorrhagic state requiring rapid transfusion to maintain blood volume. He was transferred to an intensive-care unit, where hemorrhagic fever was suspected. Although the bleeding was controlled, the patient died of multiple organ failure on September 8. The diagnosis was confirmed by isolation of the CCHF virus from blood taken on September 4 and from liver tissue removed immediately after death. No antibodies were detected.
Patients 2, 3, and 4 were nurses who had cared for the index patient during his first few hours in the intensive-care unit and before the institution of isolation procedures. Five days after initial contact, they developed pyrexia, muscle pain, sore throat, conjunctivitis, and upper abdominal tenderness. Four days after the onset of symptoms, a bleeding tendency was noted, and their platelet counts fell dramatically.
Patients 5 and 6 were nurses who had no direct contact with the index patient but came in contact with contaminated material during the setting up of isolation procedures. Five days after this contact, they developed symptoms similar to those of patients 2, 3, and 4. Purpura and bleeding also began on the fourth day of illness.
CCHF was confirmed in patients 2-6 by isolation of the virus and a rising antibody titer.
Patient 7 was a 37-year-old surgeon who had had no known direct contact with the index patient but had visited the intensive-care unit before isolation. Headache and pyrexia began 5 days later, followed by severe thrombocytopenia and bleeding after an additional 5 days. CCHF was not initially suspected, but the virus was isolated from his blood. Despite intensive supportive measures, he died 8 days after onset of illness. As with patient 1, there was no antibody response.
Patient 8 was a senior member of the nursing staff who had contact with all the other CCHF patients. Her probable mode of infection was an unintentional needle prick while nursing patient 3. Prophylactic treatment with antibody-rich plasma, ribavirin, and interferon was begun, but she developed headache, weakness, jaundice, and elevated liver enzymes. Her illness was milder than those of the other patients, and she did not develop thrombocytopenia. Although the antibody titer rose during her illness, no virus was isolated.
Treatment was mainly supportive. Multiple platelet transfusions were essential to maintain hemostasis. Convalescent anti-CCHF plasma was administered to patients 2-5. Patients 2-6 did not develop major hemorrhages and were discharged 10-12 days after onset of symptoms.
The hospital is a 2,000-bed teaching hospital. The correct diagnosis was suspected 12 hours after admission and barrier nursing had begun on the index patient. Stringent isolation procedures, including use of protective clothing and goggles, were instituted 36 hours after admission. Laboratory confirmation of the diagnosis was received only 2 days after the patient died.
During the first 24 hours, numerous blood specimens were handled in various hospital laboratories without precautions. Fully equipped laboratories were later set up in the isolation area for blood cross-matching and hematologic and chemical investigations. Virologic studies were carried out in the high security (P4) laboratory of the National Institute of Virology in Johannesburg.
Altogether, 35 persons came in contact with the index patient while in the hospital, including students, technicians, and cleaning staff. Patient 8 was the only tertiary case, among the numerous contacts with patient 7. Reported by WL Michell, MD, JJ Groenewald, PJ van Eeden, MD, Tygerberg Hospital and University of Stellenbosch, JW Moodie, University of Cape Town, R Swanepoel, AE Sheperd, PA Leman, SP Sheperd, National Institute of Virology, Johannesburg, Republic of South Africa; Div of Viral Diseases, Center for Infectious Diseases, CDC.
Editorial Note: CCHF was first reported in South Africa in 1981 (1). Subsequently, a number of cases have occurred (2), but secondary cases have not previously been reported in South Africa. CCHF has resulted in hospital epidemics in several other countries (3,4).
CCHF is caused by a Bunyavirus of the arbovirus group (5). Widespread occurrence of the antibodies in wild and domestic animals in South Africa has been documented (6). Transmission to humans is thought to be primarily via the Hyalloma genus of tick or contact with the blood of infected animals (6).
CCHF is being reported with increasing frequency from South Africa. Unlike previous South African cases, which have all been associated with exposure to ticks or livestock, the present outbreak was due to nosocomial spread of virus. Nosocomial infections with CCHF have occurred in other countries, including Iraq, the Soviet Union, and Pakistan (3,5,7). Contact with bloody secretions appeared to be the means of transmission in those outbreaks, although airborne transmission has been neither proven nor disproven (5). Similarly, in the South African outbreak, five of the six secondary cases and the tertiary case had direct contact with either a patient or contaminated material. Of particular interest is patient 7, the only secondary case to die, who had no known direct contact with a patient or with contaminated material. As in this outbreak, tertiary cases are often mild, perhaps because of a low infective dose or of attenuation of the virus after human passage (3).
Treatment of CCHF is mainly supportive. The role of prophylactic plasma, ribavirin, and interferon in reducing the severity of illness could not be evaluated in this situation. The four patients who received CCHF antibody-rich plasma had relatively mild disease. Although its efficacy is not firmly established, some reports suggest a beneficial role for plasma therapy, especially when adminstered early in the course of illness (5). Antiviral drugs, such as ribavirin, are of potential use in the treatment of CCHF, but they have yet to undergo clinical trials.
CCHF, as well as other viral hemorrhagic fevers, such as Ebola virus disease, Marburg virus disease, and Lassa fever, have the potential to spread in a hospital setting. Patients are often hospitalized with a severe illness, but the nonspecific nature of their signs and symptoms may not suggest a viral hemorrhagic fever (8). Furthermore, even simple isolation procedures, such as barrier nursing on open wards, can effectively halt transmission of these viruses (9). Thus, it is imperative that a diagnosis of a viral hemorrhagic fever be considered in any patient with an unknown febrile disease who either resides in or traveled to an endemic area within 3 weeks of the onset of symptoms. If other, more common causes of the fever, such as malaria or sepsis, can be reasonably excluded, measures for isolation of the patient should be taken immediately.
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