Crimean-Congo hemorrhagic fever
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IdentityTop of page
Preferred Scientific Name
- Crimean-Congo hemorrhagic fever
Other Scientific Names
- Crimean-Congo haemorrhagic fever
International Common Names
- English: Congo virus disease; Crimean haemorrhagic fever; viral haemorrhagic fever; viral tick-borne haemorrhagic fever disease
- French: fievre hemorragique Crimee-Congo
Local Common Names
- Turkey: Kirim-Kongo Kanamali Atesi
OverviewTop of page
Crimean-Congo haemorrhagic fever (CCHF) is a severe haemorrhagic fever viral disease that affects humans. It was initially described in 1944 in the Crimean peninsula of the USSR when several hundred Soviet troops developed an acute febrile illness accompanied by severe bleeding and shock (Chumakov, 1945). Further outbreaks occurred in the USSR, principally in many southern Soviet republics, with many thousands of clinical cases. In 1956, the virus (then called Congo virus) was isolated from a patient in the Belgian Congo (now Democratic Republic of the Congo) in Africa (Simpson et al., 1965) and has subsequently been found throughout most of the continent. Many outbreaks of disease were initially reported in Middle Eastern countries (Hoogstraal, 1979; Burney et al., 1980), but the disease is now known to occur across a huge geographic area from western China to the Middle East and southeastern Europe and throughout most of Africa (Whitehouse, 2004; Bente et al., 2013). Although this disease is not manifested in livestock, domesticated stock may act as important reservoirs of infection and source of virus for tick vectors.
Hosts/Species AffectedTop of page
CCHF disease occurs only in humans. A wide variety of mammals including domesticated and wild ruminants, insectivores, small lagomorphs, rodents and some carnivores have been shown to be infected with the virus and are important hosts for Hyalomma and other ixodid ticks that transmit CCHF ( Hoogstraal, 1979; Whitehouse, 2004; Nalca and Whitehouse, 2007). Larval and nymphal stages of Hyalomma and other ixodid (hard) ticks frequently take their blood meals from various ground-feeding bird species, which have been incriminated in Africa and Europe as amplifying hosts for CCHF (Hoogstraal, 1979; Camicas et al., 1994).
DistributionTop of page
CCHF was first recognized in 1944 in the Crimea in the southern Soviet Union and subsequently in Bulgaria. An identical viral agent was isolated in the Belgian Congo in 1956 and initially named ‘Congo virus.’ The disease is known throughout a large region of Africa, with the majority of cases being reported from Mauritania, South Africa, Uganda, and Sudan. However, significantly more cases have occurred throughout many countries in eastern and central Asia and the Middle East and Turkey (Bente et al., 2013). For instance, Turkey has experienced an unprecedented emergence in the disease over the past 15 years, with over 5000 human infections diagnosed since the first cases were identified in that country in 2002.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||Present||1998||Bente et al., 2013|
|Armenia||No information available||OIE, 2009|
|Azerbaijan||Disease never reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||Disease never reported||OIE, 2009|
|Bhutan||Disease never reported||OIE, 2009|
|Cambodia||No information available||OIE, 2009|
|China||Present||1965||Bente et al., 2013|
|-Hong Kong||No information available||OIE, 2009|
|India||Present||2011||Patel et al., 2011|
|Indonesia||No information available||OIE, 2009|
|Iran||Present||2000||Bente et al., 2013|
|Iraq||Present||1979||Bente et al., 2013|
|Israel||Disease never reported||OIE, 2009|
|Japan||No information available||OIE, 2009|
|Jordan||No information available||OIE, 2009|
|Kazakhstan||Present||1948||WHO, 2001; Bente et al., 2013|
|Korea, Republic of||Disease never reported||OIE, 2009|
|Kuwait||Disease never reported||OIE, 2009|
|Kyrgyzstan||Present||Bente et al., 2013|
|Laos||Disease never reported||OIE, 2009|
|Lebanon||Disease never reported||OIE, 2009|
|Malaysia||Disease never reported||OIE, 2009|
|Mongolia||No information available||OIE, 2009|
|Myanmar||Disease never reported||OIE, 2009|
|Nepal||Disease never reported||OIE, 2009|
|Oman||Present||1995||WHO, 2001; Bente et al., 2013|
|Pakistan||Present||1976||Burney et al., 1980; WHO, 2001; OIE, 2009; Bente et al., 2013|
|Philippines||Disease never reported||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||No information available||OIE, 2009|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||Disease never reported||OIE, 2009|
|Tajikistan||Present||1943||Bente et al., 2013|
|Thailand||No information available||OIE, 2009|
|Turkey||Present||2002||Bente et al., 2013|
|United Arab Emirates||Present||1979||Bente et al., 2013|
|Vietnam||No information available||OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Algeria||No information available||OIE, 2009|
|Angola||No information available||OIE, 2009|
|Benin||No information available||OIE, 2009|
|Botswana||Disease never reported||OIE, 2009|
|Burkina Faso||No information available||OIE, 2009|
|Chad||No information available||OIE, 2009|
|Congo||No information available||NULL||WHO, 2001; OIE, 2009|
|Congo Democratic Republic||Present||1956||WHO, 2001; Bente et al., 2013|
|Djibouti||No information available||OIE, 2009|
|Egypt||No information available||OIE, 2009|
|Eritrea||No information available||OIE, 2009|
|Ethiopia||No information available||OIE, 2009|
|Gabon||No information available||OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||No information available||OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||Present||2000||Bente et al., 2013|
|Lesotho||Disease never reported||OIE, 2009|
|Madagascar||Disease never reported||OIE, 2009|
|Malawi||No information available||OIE, 2009|
|Mali||No information available||OIE, 2009|
|Mauritania||Present||1983||Bente et al., 2013|
|Mauritius||Disease never reported||OIE, 2009|
|Morocco||No information available||OIE, 2009|
|Mozambique||No information available||OIE, 2009|
|Namibia||Disease not reported||OIE, 2009|
|Nigeria||Disease never reported||OIE, 2009|
|Rwanda||Disease never reported||OIE, 2009|
|Senegal||Present||2003||Camicas et al., 1994; Bente et al., 2013|
|South Africa||Present||1981||Swanepoel et al., 1983; Bente et al., 2013|
|Sudan||Present||2008||Bente et al., 2013|
|Swaziland||Disease never reported||OIE, 2009|
|Tanzania||No information available||OIE, 2009|
|Togo||No information available||OIE, 2009|
|Tunisia||Disease never reported||OIE, 2009|
|Uganda||Disease never reported||OIE, 2009|
|Zambia||Disease never reported||OIE, 2009|
|Zimbabwe||Disease not reported||OIE, 2009|
|Canada||Disease never reported||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease not reported||OIE, 2009|
|USA||Disease never reported||OIE, 2009|
Central America and Caribbean
|Belize||Disease never reported||OIE, 2009|
|Costa Rica||Disease never reported||OIE, 2009|
|Cuba||Disease never reported||OIE, 2009|
|Dominican Republic||Disease never reported||OIE, 2009|
|El Salvador||No information available||OIE, 2009|
|Guadeloupe||No information available||OIE, 2009|
|Guatemala||Disease never reported||OIE, 2009|
|Haiti||Disease never reported||OIE, 2009|
|Honduras||Disease never reported||OIE, 2009|
|Jamaica||No information available||OIE, 2009|
|Martinique||Disease never reported||OIE, 2009|
|Nicaragua||Disease never reported||OIE, 2009|
|Panama||Disease never reported||OIE, 2009|
|Argentina||Disease never reported||OIE, 2009|
|Bolivia||Disease never reported||OIE, 2009|
|Brazil||Disease never reported||OIE, 2009|
|Chile||Disease never reported||OIE, 2009|
|Colombia||Disease never reported||OIE, 2009|
|Ecuador||Disease never reported||OIE, 2009|
|French Guiana||No information available||OIE, 2009|
|Peru||Disease never reported||OIE, 2009|
|Uruguay||Disease never reported||OIE, 2009|
|Venezuela||Disease never reported||OIE, 2009|
|Albania||Present||2001||Papa et al., 2002|
|Austria||No information available||OIE, 2009|
|Belarus||No information available||OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Croatia||Disease never reported||OIE, 2009|
|Cyprus||Disease never reported||OIE, 2009|
|Czech Republic||Disease never reported||OIE, 2009|
|Denmark||Disease never reported||OIE, 2009|
|Estonia||No information available||OIE, 2009|
|Finland||Disease never reported||OIE, 2009|
|Former USSR||Present||Chumakov, 1945; Chumakov, 1974|
|France||Disease never reported||OIE, 2009|
|Germany||Disease never reported||OIE, 2009|
|Greece||Present||2008||Papa et al., 2010|
|Hungary||Disease never reported||OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease never reported||OIE, 2009|
|Italy||No information available||OIE, 2009|
|Latvia||Disease never reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease not reported||OIE, 2009|
|Luxembourg||Disease never reported||OIE, 2009|
|Macedonia||Disease never reported||OIE, 2009|
|Malta||Disease never reported||OIE, 2009|
|Montenegro||Disease never reported||OIE, 2009|
|Netherlands||Disease never reported||OIE, 2009|
|Norway||Disease never reported||OIE, 2009|
|Poland||No information available||OIE, 2009|
|Portugal||Disease never reported||OIE, 2009|
|Romania||No information available||OIE, 2009|
|Russian Federation||Present||WHO, 2001; OIE, 2009; Bente et al., 2013|
|Serbia||Present||1995||Bente et al., 2013|
|Slovakia||Disease never reported||OIE, 2009|
|Slovenia||Disease never reported||OIE, 2009|
|Spain||Disease never reported||OIE, 2009|
|Sweden||Disease never reported||OIE, 2009|
|Switzerland||Disease never reported||OIE, 2009|
|UK||Disease never reported||OIE, 2009|
|Ukraine||Disease never reported||OIE, 2009|
|Yugoslavia (Serbia and Montenegro)||Present||WHO, 2001|
|Australia||Disease never reported||OIE, 2009|
|French Polynesia||Disease never reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease never reported||OIE, 2009|
Disease CourseTop of page
Clinical disease occurs only in humans; for information on this see the Zoonoses and Food Safety section.
EpidemiologyTop of page
CCHF is characteristically seen in the steppe and floodplain regions of Southern Europe and Asia, and in the drier bush savannah grasslands and semi-deserts of Africa. The foothills of the steppes in Asia and Europe with juniper and other tree cover are another biotope enzootic for CCHF. The most important tick genus involved in the transmission of CCHF is Hyalomma; these are the most common ticks affecting wild and domestic animals in the above biotopes (Hoogstraal, 1979; Bente et al., 2013). Thus, the geographic distribution of CCHF largely reflects that of Hyalomma ticks.
The virus is transmitted in tick populations from larvae to nymphs to adults (transstadial transmission), from adult females to their eggs (vertical transmission), or from male ticks to female ticks during copulation (venereal transmission) (Turell, 2007). The virus is thus well adapted to the tick host, which serves as its reservoir in nature, in addition to its vector. CCHFV has been detected in more than 30 species of ticks, including both hard and soft ticks (Turell, 2007). However, only a subset of these ticks has been definitely shown to be competent vectors of the virus experimentally in the laboratory. Those that have include several members of the genus Hyalomma, but also members of the genera Amblyomma, Rhipicephalus, and Dermacentor. The enzootic maintenance cycle of the virus involves ticks, birds, and other vertebrate hosts. For instance, larvae and nymphs of Hyalomma ticks, in particular, aggressively feed on a variety of hosts, including hedgehogs, hares, and ground-feeding birds, while the adults actively seek out sheep, cattle, and other large mammals. Most birds that are fed upon by CCHFV-infected ticks do not become viremic, but can play a role in the spread of these virus-infected ticks to new geographic areas (Leblebiciogul et al., 2014).
Predisposing factors for CCHF outbreaks include variations in tick populations, which can change from year to year depending on various factors including availability of vertebrate hosts, weather conditions, climate change, changes in vegetation or other factors that alters the success of molting and egg production of the ticks. Mild warm winter conditions, which favour the survival of large proportions of the larval ticks, have been associated with CCHF epizootics, whereas severe prolonged cold spells have a negative effect upon larval and nymphal tick populations (Estrada-Pena et al., 2012).
Human socio-economic changes are also important in disease transmission dynamics. Population movements may bring susceptible human populations into contact with the cryptic enzootic maintenance cycle for CCHF (Hoogstraal, 1979; Linthicum and Bailey, 1994). In particular, war results in displacement of population groups with their animals. There is a marked growth in vegetation following depopulation and this favours increases in small mammal populations and of the ticks, which find abundant hosts on which to feed. Under these conditions, tick populations can increase 10,000-1,000,000-fold. A return of humans to such areas is inevitably followed by greater contact with infected tick populations and higher risk of CCHF. This occurred during the original CCHF outbreak in Crimea in 1944 when soldiers sent to reclaim abandoned farms were exposed to large numbers of ticks infesting a markedly expanded wild hare population and is thought to play a role in the more recent emergence of CCHF in Central Turkey when residents returned to farms abandoned during civil conflict (Bente et al., 2013).
Impact: EconomicTop of page
The disease only occurs in humans, thus there are no significant economic losses to agriculture.
Zoonoses and Food SafetyTop of page
Those people living in enzootic areas who are associated with livestock are at greatest risk of infection. Herders, milkers, shearing staff, slaughtering staff, farm labourers and forestry workers are all at increased risk of contracting CCHF. In addition, medical personnel having direct contact with CCHF patients are at particularly high risk of infection (Whitehouse, 2004). While many human infections result from tick bites, others result from direct exposure to tissues, blood, and other bodily fluids from infected animals. Principally among those at increased risk include abattoir workers and others involved in the skinning and slaughter of animals.
A real danger exists to all personnel dealing with CCHF patients both in the home and at hospitals and clinics; nosocomial spread of CCHF is a well-documented phenomenon (Whitehouse, 2004). Person-to-person transmission can occur through contact with the virus-containing body fluids of a patient during the first 7-10 days of illness. However, standard barrier nursing methods are sufficient to prevent the transmission of CCHF in the patient care setting.
In humans, clinical disease occurs following an incubation period that ranges from 1-5 days following tick bite to 5-7 days following contact with infected blood or tissues (Ergonul, 2006). Disease symptoms can vary greatly. Some patients experience only a mild, nonspecific febrile illness, while others develop severe haemorrhagic disease. Patients can experience a sudden onset of fever, headache, muscle pains, vomiting, swelling of the face, a haemorrhagic rash, and bleeding from the nasopharynx, gastrointestinal tract and other sites. In some cases, cerebral haemorrhage, as well as bleeding from the vagina, may occur (Ergonul, 2006). In fatal cases, death occurs from 5-14 days after infection and results from haemorrhage, multi-organ failure, and shock. Case fatality rate can be as high as 30%.
CCHF should be suspected when a person with an appropriate exposure history (tick bite or contact with animal tissue/fluids) becomes acutely ill with malaise, fever, and other flu-like symptoms. CCHF patients are usually viremic during the first 7-10 days of illness. Thus, a specific diagnosis can be made by testing a serum specimen for viral RNA by RT-PCR. Testing for virus-specific IgM and/or IgG by ELISA or other methods can also be performed. Virus-specific IgM becomes detectable by the end of the first week, with IgG appearing shortly thereafter (Bente et al., 2013). The isolation of virus in culture has been long considered the “gold standard’ for diagnosis, but for CCHFV, it requires Biosafety Level-4 biocontainment, which is not available in most of the CCHF-endemic countries. In view of its speed, sensitivity, and safety, RT-PCR should be considered the standard diagnostic method for CCHF (Bente et al., 2013).
Current medical management of CCHF is largely supportive including volume replacement with intravenous fluids, careful monitoring to prevent the development of pulmonary edema, and treatment of coagulation abnormalities by giving the patient fresh frozen plasma and/or platelets. In severe cases of haemorrhagic disease with significant blood loss, a blood transfusion may be required. The antiviral drug, ribavirin, has been used for the treatment of CCHF since the mid-1980s. It is generally thought that ribavirin therapy is beneficial as long as it is initiated early in the course of illness. However, in a randomized clinical trial, ribavirin treatment was unable to significantly alter the course of the disease (Koksal et al., 2010). Type I interferon inhibits CCHFV replication in culture, but showed no benefit when given to 6 patients during an outbreak in South Africa (van Eeden et al., 1985).
Prevention and ControlTop of page
The control of tick populations is not normally thought to be a cost-effective strategy of disease control. In general, it is believed that control of CCHF through the application of chemical acaricides to livestock is impractical; however, aerial spraying and dipping of livestock has been practised in outbreak situations. Other methods of tick control include the use of biological control, which typically involves the deliberate introduction of predators, parasites, or pathogens to control populations of a vector species. An innovative method to attempt to control ticks has been the use of tick pheromones in conjunction with acaricides. Many of these strategies incorporate a pheromone-acaricide-impregnated device (a so-called “tick decoy”), which is used to lure and kill host-seeking ticks (Sonenshine, 2006). Although many of these biocontrol methods hold promise, further research is needed to determine whether they can be effective under field conditions.
The most effective means of preventing infection is to educate those populations of individuals at the highest risk for contracting the disease regarding ways to avoid contact with the virus. Important risk groups include healthcare workers and persons working outdoors in endemic areas, particularly those with direct contact with large domestic animals. Those individuals who work outdoors should take appropriate precautions to avoid exposure to ticks. Others including farmers, veterinarians, and workers at abattoirs and slaughterhouses should take measures to reduce their exposure to animal blood and other body fluids.
A suckling mouse brain-derived, formalin-inactivated vaccine was used in parts of Eastern Europe and the former Soviet Union in the 1970s with apparent success. However, the vaccine is not widely available, and given the relatively small target population of persons at risk for contracting the disease, the large-scale development and production of a CCHF vaccine by modern standards seems unlikely (Whitehouse, 2007).
ReferencesTop of page
Bente DA, Forrester NL, Watts DM, McAuley AJ, Whitehouse CA, Bray M, 2013. Crimean-Congo hemorrhagic fever: history, epidemiology, pathogenesis, clinical syndrome and genetic diversity. Antiviral Research, 100(1):159-189. http://www.sciencedirect.com/science/journal/01663542
Burney ML, Ghafoor A, Saleen M, Webb PA, Casals J, 1980. Nosocomial outbreak of viral haemorrhagic fever caused by Crimean Congo haemorrhagic fever virus in Pakistan, January 1976. American Journal of Tropical Medicine and Hygiene, 29:941-947.
Camicas JL, Cornet JP, Gonzalez JP, Wilson ML, Adam F, Zeller HG, 1994. Crimean-Congo haemorrhagic fever in Senegal. Latest results on the ecology of CCHF virus. Bulletin de la Société de Pathologie Exotique, 87(1):11-16; 22 ref.
Chumakov MP, 1945. A New Viral Tick Borne haemorrhagic fever disease in the Crimea. In: Krymskaya gemoragicheskaya likhoradka Simpheropol, 13-43. [in Russian].
Chumakov MP, 1974. Contribution to 30 years of investigation of Crimean haemorrhagic fever. In: Chumakov MP, ed. Medical Virology, Vol. 22. Trudy Inst. Polio Virus Research. Entsef. Akad. Med. Nauk. SSSR, 5-18. [English translation NAMRU 3-T950].
Eeden PJ van, Eeden SF van, Joubert JR, King JB, Wal BW van de, Michell WL, 1985. A nosocomial outbreak of Crimean-Congo haemorrhagic fever at Tygerberg Hospital. Part II. Management of patients. South African Medical Journal, 68:718-721.
Estrada-Peña A, Ayllón N, Fuente Jde la, 2012. Impact of climate trends on tick-borne pathogen transmission. Frontiers in Physiology, 3:64.
Flick R, 2007. Molecular biology of the Crimean-Congo hemorrhagic fever virus. In: Crimean-Congo hemorrhagic fever: a global perspective [ed. by Ergonul, O.\Whitehouse, C. A.]. Heidelberg, Germany: Springer Berlin, 35-44. http://www.springerlink.com/content/?k=isbn%3a(978-1-4020-6106-6)
Hoogstraal H, 1979. The epidemiology of tick borne Crimean Congo Haemorrhagic fever in Asia, Europe and Africa. Journal of Medical Entomology, 15:307-417.
Koksal I, Yilmaz G, Aksoy F, Aydin H, Yavuz I, Iskender S, Akcay K, Erensoy S, Caylan R, Aydin K, 2010. The efficacy of ribavirin in the treatment of Crimean-Congo hemorrhagic fever in Eastern Black Sea region in Turkey. Journal of Clinical Virology, 47(1):65-68. http://www.sciencedirect.com/science/journal/13866532
Leblebicioglu H, Eroglu C, Erciyas-Yavuz K, Hokelek M, Acici M, Yilmaz H, 2014. Role of migratory birds in spreading Crimean-Congo hemorrhagic fever, Turkey. Emerging Infectious Diseases, 20(8):1331-1334. http://wwwnc.cdc.gov/eid/article/20/8/pdfs/13-1547.pdf
Linthicum KJ, Bailey CL, 1994. Ecology of Crimean-Congo haemorrhagic fever. In: Sonenshine DE, Mather TN, ed. Ecological Dynamics of Tick Borne zoonoses. New York, USA: Oxford University Press, 392-437.
Nalca A, Whitehouse C, 2007. Crimean-Congo hemorrhagic fever virus infection among animals. In: Crimean-Congo hemorrhagic fever: a global perspective [ed. by Ergonul, O.\Whitehouse, C. A.]. Heidelberg, Germany: Springer Berlin, 155-165. http://www.springerlink.com/content/?k=isbn%3a(978-1-4020-6106-6)
OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
Papa A, Bino S, Llagami A, Brahimaj B, Papadimitriou E, Pavlidou V, Velo E, Cahani G, Hajdini M, Pilaca A, Harxhi A, Antoniadis A, 2002. Crimean-Congo hemorrhagic fever in Albania, 2001. European Journal of Clinical Microbiology & Infectious Diseases, 21(8):603-606.
Papa A, Dalla V, Papadimitriou E, Kartalis GN, Antoniadis A, 2010. Emergence of Crimean-Congo haemorrhagic fever in Greece. Clinical Microbiology and Infection, 16(7):843-847. http://www.blackwell-synergy.com/loi/clm
Patel AK, Patel KK, Minesh Mehta, Parikh TM, Harsh Toshniwal, Kamlesh Patel, 2011. First Crimean-Congo hemorrhagic fever outbreak in India. Journal of the Association of Physicians of India, 59(September):585-589. http://www.japi.org/september_2011/10_CR_First_Crimean-congo.pdf
Simpson DIH, Williams MC, Woodall JP, 1965. Four cases of human infection with the Congo agent. Report East African Virus Research Institute, (1963-64), 14:27-28.
Swanepoel R, Struthers JK, Shepherd AJ, McGillivray GM, Nel MJ, Jupp PG, 1983. Crimean-Congo hemorrhagic fever in South Africa. American Journal of Tropical Medicine and Hygiene, 32(6):1407-1415; [1 fig.]; 24 ref.
Turell M, 2007. Role of ticks in the transmission of Crimean-Congo hemorrhagic fever virus. In: Crimean-Congo hemorrhagic fever: a global perspective [ed. by Ergonul, O.\Whitehouse, C. A.]. Heidelberg, Germany: Springer Berlin, 143-154. http://www.springerlink.com/content/?k=isbn%3a(978-1-4020-6106-6)
Watt DM, Ksiazek TG, Linthicum KJ, Hoogstraal H, 1988. Crimean-Congo haemorrhagic fever. In: Monath TP, ed. The Arboviruses: epidemiology and ecology, Vol. 2. Boca Raton, Florida, USA: CRC Press, 177-260.
Whitehouse C, 2007. Risk groups and control measures for Crimean-Congo hemorrhagic fever. In: Crimean-Congo hemorrhagic fever: a global perspective [ed. by Ergonul, O.\Whitehouse, C. A.]. Heidelberg, Germany: Springer Berlin, 273-280. http://www.springerlink.com/content/?k=isbn%3a(978-1-4020-6106-6)
WHO, 2001. Crimean-Congo haemorrhagic fever. www.who.int/m/topics/crimean-congo_haemorrhagic_fever/en/index.html.
ContributorsTop of page
26/02/15 Updated by:
Chris A. Whitehouse, U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, Maryland 21702, USA.
Distribution MapsTop of page
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