Preferred Scientific Name
- camel pox
International Common Names
- English: camel pox
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Camelpox is a contagious viral disease of camels that occurs throughout the camel-breeding countries of northern Africa, the Middle East, and Asia (Balamurugan et al., 2013). Camelpox virus (CMLV) naturally infects only the dromedary camel (Camelus dromedarius) and the Bactrian camel (Camelus bactrianus) (Wernery and Kaaden, 2002). Clinical manifestations of disease range from local and mild (pock lesions) to severe [mortality rate 10-28% in adults and 25-100% in young animals (Balamurugan et al., 2013)]. The disease occurs more frequently and more severely in young animals and pregnant females. A CMLV-based vaccine is available, but it is not widely used and only calves more than 6 months of age are protected (Duraffour et al., 2011).
CMLV is considered to solely naturally infect Old World camelids, which includes the dromedary camel (Camelus dromedarius) and the Bactrian camel (C. bactrianus). While experimental infection of guanacos (Lama guanicoe), a camelid native to South America, with CMLV has been successful (Wernery et al., 2000), natural infection of New World camelids has never been reported (Duraffour et al., 2011). Since 1972, there have been several attempts to infect animals others than camels with CMLV in order to define its host range. Horses, sheep, goat, cattle, rats, and guinea pigs all appeared to be refractory to CMLV infection (Duraffour et al., 2011). It is interesting to note, however, that a study in Saudi Arabia demonstrated that sheep and goats have prevalence rates of 6% and 10%, respectively, of anti-CMLV neutralizing antibodies (Housaw, 2007). These data might suggest the potential adaptation of CMLV to hosts other than camels in countries where the disease is enzootic; however, more research in this area needs to be done to support this hypothesis. Notably, two strains of CMLV have been shown to be pathogenic to rhesus monkeys. Strain etha-78 administered intradermally induced typical pox lesions (Falluji et al., 1979). Strain CM-G2 has also been shown to be pathogenic in monkeys, although no generalized rash was observed (Baxby, 1972). In contrast, strain CP/Nw/92/2 did not induce any reaction when administered intradermally to monkeys; however, the dose of virus given was not stated (Khalafalla and Mohamed, 1998). Clearly, further experiments are required to clarify the pathogenicity of CMLV for nonhuman primates.
The role for an arthropod vector in the transmission of camelpox has long been suspected. This idea is supported by the isolation of CMLV from Hyalomma dromedarii ticks during an outbreak of disease in the United Arab Emirates in 1995-1996 (Wernery et al., 1997a,b). H. dromedarii is the predominant tick species infesting camels. However, the question remains to be determined whether ticks are a true vector (or reservoir) of the virus or if they can only mechanically transmit the virus. Much work is need to determine what role, if any, ticks play in the epidemiology of camelpox.
Camelpox occurs in almost every region where camel breeding is practiced. Outbreaks of disease have been reported in many countries of the Middle East, Asia, Africa and southern Russia. These have included Iraq, Iran, Kazakhstan and Turkmenistan, India, United Arab Emirates, Saudi Arabia, Somalia, Ethiopia, Kenya, Sudan, Egypt, Niger, Mauritania, Morocco, and Syria (Wernery and Kaaden, 2002; Duraffour et al., 2011). Of note, camelpox has never been reported from Australia even though there are feral populations of dromedary camels and camel farming is practiced (Wernery and Kaaden, 2002). Similarly, disease has not been observed in llama and related species (New World camelids) of South America (Balamurugan et al., 2013).
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.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Botswana||Absent, No presence record(s)|
|Eritrea||Absent, No presence record(s)|
|Lesotho||Absent, No presence record(s)|
|Madagascar||Absent, No presence record(s)|
|Mauritania||Present||1989||Original citation: Nguyen-Ba-Vy, et al. (1989)|
|Mauritius||Absent, No presence record(s)|
|Mozambique||Absent, No presence record(s)|
|Niger||Present||1989||Original citation: Nguyen-Ba-Vy, et al. (1989)|
|Uganda||Absent, No presence record(s)|
|Zimbabwe||Absent, No presence record(s)|
|Azerbaijan||Absent, No presence record(s)|
|Bangladesh||Absent, No presence record(s)|
|Bhutan||Absent, No presence record(s)|
|China||Absent, No presence record(s)|
|Israel||Absent, No presence record(s)|
|Jordan||Absent, No presence record(s)|
|Kuwait||Absent, No presence record(s)|
|Laos||Absent, No presence record(s)|
|Lebanon||Absent, No presence record(s)|
|Malaysia||Absent, No presence record(s)|
|Nepal||Absent, No presence record(s)|
|Qatar||Absent, No presence record(s)|
|Singapore||Absent, No presence record(s)|
|Sri Lanka||Absent, No presence record(s)|
|Tajikistan||Absent, No presence record(s)|
|Thailand||Absent, No presence record(s)|
|United Arab Emirates||Present||1995|
|Yemen||Absent, No presence record(s)|
|Albania||Absent, No presence record(s)|
|Belgium||Absent, No presence record(s)|
|Bulgaria||Absent, No presence record(s)|
|Croatia||Absent, No presence record(s)|
|Cyprus||Absent, No presence record(s)|
|Czechia||Absent, No presence record(s)|
|Denmark||Absent, No presence record(s)|
|Finland||Absent, No presence record(s)|
|Germany||Absent, No presence record(s)|
|Hungary||Absent, No presence record(s)|
|Iceland||Absent, No presence record(s)|
|Ireland||Absent, No presence record(s)|
|Latvia||Absent, No presence record(s)|
|Liechtenstein||Absent, No presence record(s)|
|Lithuania||Absent, No presence record(s)|
|Luxembourg||Absent, No presence record(s)|
|Malta||Absent, No presence record(s)|
|Montenegro||Absent, No presence record(s)|
|Netherlands||Absent, No presence record(s)|
|North Macedonia||Absent, No presence record(s)|
|Norway||Absent, No presence record(s)|
|Portugal||Absent, No presence record(s)|
|Russia||Absent, No presence record(s)|
|Serbia||Absent, No presence record(s)|
|Slovakia||Absent, No presence record(s)|
|Slovenia||Absent, No presence record(s)|
|Spain||Absent, No presence record(s)|
|Sweden||Absent, No presence record(s)|
|Switzerland||Absent, No presence record(s)|
|Ukraine||Absent, No presence record(s)|
|United Kingdom||Absent, No presence record(s)|
|Belize||Absent, No presence record(s)|
|Canada||Absent, No presence record(s)|
|Costa Rica||Absent, No presence record(s)|
|Cuba||Absent, No presence record(s)|
|Dominican Republic||Absent, No presence record(s)|
|Greenland||Absent, No presence record(s)|
|Guadeloupe||Absent, No presence record(s)|
|Guatemala||Absent, No presence record(s)|
|Haiti||Absent, No presence record(s)|
|Martinique||Absent, No presence record(s)|
|Mexico||Absent, No presence record(s)|
|Nicaragua||Absent, No presence record(s)|
|Panama||Absent, No presence record(s)|
|United States||Absent, No presence record(s)|
|Australia||Absent, No presence record(s)|
|French Polynesia||Absent, No presence record(s)|
|New Zealand||Absent, No presence record(s)|
|Argentina||Absent, No presence record(s)|
|Bolivia||Absent, No presence record(s)|
|Brazil||Absent, No presence record(s)|
|Chile||Absent, No presence record(s)|
|Colombia||Absent, No presence record(s)|
|Ecuador||Absent, No presence record(s)|
|Peru||Absent, No presence record(s)|
|Uruguay||Absent, No presence record(s)|
|Venezuela||Absent, No presence record(s)|
The CMLV usually enters through skin or via the oro-nasal route. After local replication and development of a primary skin lesion, the virus spreads to the local lymph nodes, which leads to a leukocyte-associated viraemia. Widespread secondary skin lesions appear a few days after the onset of viraemia and new lesions continue to appear for 2-3 days until viraemia subsides. The histopathology of skin lesions reveals characteristic cytoplasmic swelling, vacuolation and ballooning of the keratinocytes of the outer stratum spinosum of the epidermis. The rupture of these cells produces vesicles and localized oedema associated with perivascular cuffing of mononuclear cells, neutrophils and eosinophils. Marked epithelial hyperplasia may also occur at the borders of the skin lesions. The lung lesions are usually characterized by hydropic degeneration, proliferation of the bronchial epithelial cells associated with proliferative alveolitis and bronchiolitis infiltrated by macrophages, necrosis and fibrosis, which leads to obliteration of normal architecture (Balamurugan et al., 2013).
|General Signs / Fever, pyrexia, hyperthermia||Other:All Stages||Sign|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Other:All Stages||Sign|
|Skin / Integumentary Signs / Skin papules||Other:All Stages||Sign|
|Skin / Integumentary Signs / Skin pustules||Other:All Stages||Sign|
|Skin / Integumentary Signs / Skin vesicles, bullae, blisters||Other:All Stages||Sign|
The disease is characterized by an incubation period of 9-13 days, followed by fever, enlarged lymph nodes, skin lesions, and prostration. Eruptions are mainly localized on the head, lips, nostrils, eyelids, and oral cavity. In general, the lesions heal in 4-6 weeks. However, in the more severe general form of the disease, lesions may spread over the body and even multiple lesions can be found on the mucous membranes of the mouth and respiratory and digestive tracts. Severely affected camels also develop proliferative poxviral lesions in the bronchi and lungs (Kinne et al., 1998). This form of the disease is often fatal (Pfeffer et al., 1998a). Additionally, pregnant animals may abort and mortality in affected animals can be exacerbated by septicaemia caused by secondary bacterial infections (Wernery and Kaaden, 2002).
Camelpox is a common highly contagious disease of Old World camelids (Camelus dromedarius and C. bactrianus); however, New World camelids are also susceptible. The disease occurs throughout the camel-breeding areas of Africa, the Middle East and Asia, including southern Russia and parts of the former Soviet Union. Infections are common among the camel herds of the nomadic pastoralists in the semi-desert zones of these countries. The disease has not been observed, however, in the introduced dromedary camel in Australia or the tylopoda (llama and related species) in South America (Balamurugan et al., 2013). A severe form of the disease is most often seen in young calves under the age of four years. These animals can experience a generalized form of disease with high morbidity (up to 92%) and mortality (up to 28%) rates (Jezek et al., 1983; Duraffour et al., 2011). In addition to young calves, pregnant females appear to be more susceptible to camelpox. Abortion rates can reach as high as 87%, as evidenced in Syria (Al-Zi'abi et al., 2007). The incidence and mortality rates are mostly higher in male, as opposed to female camels. In addition, various studies have demonstrated that the incidence and severity of outbreaks increased during the rainy season, while milder disease occurred during the dry season (Wernery et al., 1997a,b; Khalafalla and Ali, 2007). There are several hypotheses for these observations. It could be that CMLV strains of different virulence many explain the differences in pathogenicity seen between wet and dry seasons, although this has not been examined before (Duraffour et al., 2011). Another, perhaps more likely, possibility could be the involvement of arthropod vector populations that vary depending on the season (see hosts/vectors sections).
According to the United Nations Food and Agriculture Organization, the total world camel population is approximately 23 million animals (http://faostat.fao.org). Camels are a major part of the economy in many countries. They are used for nomadic pastoralism, transportation, racing, and production of milk, wool and meat (Wernery and Kaaden, 2002; Balamurugan et al., 2013). Thus, camelpox is a socio-economic concern as it incurs considerable loss in terms of morbidity, mortality, loss of weight and reduction in milk yield for the animal, in addition to economic losses to the camel racing and transportation industries.
During the time of the smallpox eradication campaign, the question arose as to whether camels could serve as an animal reservoir for variola virus and whether camelpox virus could be transmitted to humans. Various observations suggested that human infections with camelpox virus were rare. Based in part on these observations, Baxby concluded that camelpox virus was significantly different from variola virus and incapable of infecting man (Baxby, 1972). However, rare human cases of camelpox have been reported. It was reported that people drinking milk from camelpox-affected animals developed ulcers on the lips and in the mouth; however, these reports were unable to be confirmed (Davies et al., 1975). Additional studies sought to assess the risk of camelpox virus infections in humans. Of 465 camel herdsmen handling affected camels, only one camel handler, who was not vaccinated against smallpox, developed pock-like lesions on his arm and seroconverted for orthopoxvirus, but again, the exact cause of the infection was not determined by specific diagnostic tests (Jezek et al., 1983).
The first conclusive evidence of zoonotic camelpox virus infection in humans occurred during an outbreak of disease in camels in India during 2009. During this outbreak, three human cases (who were camel handlers) were reported having clinical manifestations of camelpox, including papules, vesicles, ulceration, and ultimately scabs over their fingers and hands (Bera et al., 2011). Serum samples of the three suspected cases showed neutralizing antibodies against camelpox virus. Furthermore, in one of the three cases, viral DNA could be detected by PCR specific for camelpox virus genes (Bera et al., 2011). Nevertheless, the paucity of human cases reported in the more than 45 years since the virus was first isolated suggests that zoonotic human camelpox is very rare.
Given the increased concerns over the past decade that orthopoxviruses, including smallpox and monkeypox viruses, could be used as biological weapons, there has been increased efforts in the development of antivirals active against poxviruses (Prichard and Kern, 2012). Many of these could be envisaged for the treatment of camelpox. In particular, three of the most active anti-poxvirus drugs include cidofovir (Vistide; Gilead, CA, USA), its lipid derivative brincidofovir (CMX001; Chimerix Inc., NC, USA), and ST-246 (SIGA Inc., OR, USA) (Duraffour et al., 2011). Cidofovir and brincidofovir are active against a broad range of DNA viruses, including poxviruses, and both compounds target the viral DNA polymerase. Cidofovir is already marketed for the treatment of cytomegalovirus retinitis in HIV-infected humans. It is not orally bioavailable and thus must be given by intravenous injection. In addition, cidofovir is nephrotoxic in humans. As a consequence, a lipid derivative of cidofovir, brincidofovir or CMX001, was developed that has been shown to be orally bioavailable and did not show any toxicity in mice (Ciesla et al., 2003) or in humans undergoing a Phase I clinical study (http://www.chimerix.com/). It was previously reported that in cell culture, cidofovir inhibited 50% of CMLV replication (Smee et al., 2002; Duraffour et al., 2007a). The antiviral activity of brincidofovir against CMLV has not been reported. In contrast, ST-246 is a unique compound that blocks a late step in virus assembly by preventing intracellular virus formation and subsequent virus egress from the cell (Jordan et al., 2010). ST-246 is a potent inhibitor that is specific to orthopoxviruses. It is oral bioavailable, and has been shown to have a good safety profile in both humans and monkeys. In the case of CMLV, the activity of ST-246 has only been evaluated in vitro; however, the antiviral activity was very potent (EC50 value of 0.01 µM in Vero cells) (Duraffour et al., 2007b). While potent inhibitors of CMLV and other orthopoxviruses, none of these drugs have been evaluated for use in the treatment of camelpox in camels
Over the years, outbreaks of camelpox have resulted in major economic losses in several Middle Eastern countries (Duraffour et al., 2011). As a result, much research has focused on the development of prophylactic vaccines to contain the spread of camelpox. To date four camelpox vaccines have been developed and evaluated. They are all made from the CMLV and include the Jouf-78 strain (Hafez et al., 1992), VD47/25 strain (Nguyen et al., 1996), Ducapox 298/89 (Wernery and Zachariah, 1999), and the CMLV-T8 strain (El Harrak and Loutfi, 2000). The Jouf-78 strain is an attenuated CMLV strain that has been passaged 80 times in cell culture and has been shown to offer full protection from CMLV challenge. Based on field studies, a single dose of vaccine ranging from 103 to 104 TCID50 provides full protection. The attenuated strain VD47/25, also passaged 80 times in cell culture, was evaluated in experiments in Mauritania. This strain was found to be innocuous in camels at a dose of 104.7 TCID50 given subcutaneously and fully protected camels from an otherwise lethal CMLV infection (Nguyen et al., 1996). In the United Arab Emirates, a modified live CMLV vaccine obtained from passaging the strain CaPV298-2 in Vero cells was used. The vaccine named Ducapox for “DUbai CAmelPOX” vaccine is produced by Highveld Biological of South Africa. It was used for field vaccination just before the onset of a large camelpox outbreak in Dubai in 1993-1994. Among 2000 vaccinated camels, seven developed disease, but it was not known if these animals were infected before vaccination or if they were true vaccination failures (Pfeffer et al., 1996). Furthermore, in was shown in two animals that protection lasted for 6 years (Wernery and Zachariah, 1999). Vaccine efficacy was also demonstrated in new world camelids against an otherwise lethal CMLV challenge (Wernery et al., 2000). In Morocco, a vaccine containing an inactivated CMLV (strain T8), combined with an adjuvant, is manufactured and distributed by Biopharma (El Harrak and Loutfi, 2000). The T8 strain was isolated from scabs during an outbreak in Morocco in 1984. The vaccine has been shown to be safe in young and adult camels and elicits neutralizing antibodies (El Harrak and Loutfi, 2000). However, it requires a second injection after one month for efficient protection.
Due to the immaturity of the immune system, it is generally recommended to give any vaccine to camels that are at least 6 months old, and a second vaccination might be necessary for young calves (Duraffour et al., 2011). Antivirals could play a role in preventing the spread of the disease in animals that are younger than 6 months old.
Azwai SM; Carter SD; Woldehiwet Z; Wernery U, 1996. Serology of Orthopoxvirus cameli infection in dromedary camels: analysis by ELISA and Western blotting. Comparative Immunology, Microbiology and Infectious Diseases, 19(1):65-78.
Bera BC; Shanmugasundaram K; Sanjay Barua; Venkatesan G; Nitin Virmani; Riyesh T; Gulati BR; Bhanuprakash V; Vaid RK; Kakker NK; Malik P; Manish Bansal; Gadvi S; Singh RV; Yadav V; Sardarilal; Nagarajan G; Balamurugan V; Hosamani M; Pathak KML; Singha RK, 2011. Zoonotic cases of camelpox infection in India. Veterinary Microbiology, 152(1/2):29-38. http://www.sciencedirect.com/science/journal/03781135
Bray M; Babiuk S, 2011. Camelpox: target for eradication? Antiviral Research, 92(2):164-166.
Ciesla SL; Trahan J; Wan WB; Beadle JR; Aldern KA; Painter GR; Hostetler KY, 2003. Esterification of cidofovir with alkoxyalkanols increases oral bioavailability and diminishes drug accumulation in kidney. Antiviral Research, 59(3):163-171.
Duraffour S; Snoeck R; Krecmerová M; Oord Jvan den; Vos Rde; Holy A; Crance JM; Garin D; Clercq Ede; Andrei G, 2007. Activities of several classes of acyclic nucleoside phosphonates against camelpox virus replication in different cell culture models. Antimicrobial Agents and Chemotherapy, 51(12):4410-4419. http://aac.asm.org/
Duraffour S; Snoeck R; Vos Rde; Oord JJvan Den; Crance JM; Garin D; Hruby DE; Jordan R; Clercq EDe; Andrei G, 2007. Activity of the anti-orthopoxvirus compound ST-246 against vaccinia, cowpox and camelpox viruses in cell monolayers and organotypic raft cultures. Antiviral Therapy, 12(8):1205-1216.
El-Harrak M; Loutfi C, 2000. Camel pox in dromedary calves in Morocco. Identification of the isolated virus. Vaccine development and prophylaxis. (La variole du dromadaire chez le jeune au Maroc. Isolement et identification du virus. Mise au point du vaccin et application à la prophylaxie.) Revue d'Élevage et de Médecine Vétérinaire des Pays Tropicaux [Proceedings of the International Workshop on the Camel Calf, Ouarzazate, Morocco, 24-26 October 1999.], 53(2):165-167.
Elliot H; Tuppurainen E, 2010. Camelpox. In: Manual of Diagnostic Tests and Vaccines for Terrestrial Animal. Paris, France: World Organisation for Animal Health (OIE), 1177-1184.
Housawi FMT, 2007. Screening of domestic ruminants sera for the presence of anti-camel pox virus neutralizing antibodies at Al-Hassa District of Saudi Arabia. Assiut Veterinary Medical Journal, 53(115):101-105.
Jordan R; Leeds JM; Tyavanagimatt S; Hruby DE, 2010. Development of ST-246(R) for Treatment of Poxvirus Infections. Viruses, 2(11):2409-2435.
Khalafalla AI; Al-Busada KA; El-Sabagh IM, 2015. Multiplex PCR for rapid diagnosis and differentiation of pox and pox-like diseases in dromedary camels. Virology Journal, 12(102):(7 July 2015). http://www.virologyj.com/content/12/1/102
Khalafalla AI; Ali YH, 2007. Observations on risk factors associated with some camel viral diseases. In: Proceedings of the 12th International Conference of the Association of Institutions for Tropical Veterinary Medicine (AITVM), Montpellier, France, 20-22 August, 2007. Does control of animal infectious risks offer a new international perspective? [ed. by Camus, E.\Cardinale, E.\Dalibard, C.\Marinez, D.\Renard, J. F.\Roger, F.]. Paris, France: Centre de Coopération Internationale en Recherche Agronomique pour le Développement (CIRAD), 101-105.
Leese AS, 1909. Two diseases of young camels. Journal of Tropical Veterinary Science, 4:1-7.
Moss B, 2013. Poxviridae. In: Fields Virology (6th edition) [ed. by Knipe, D. M. \Howley, P. M.]. Philadelphia, USA: Lippincott Williams & Wilkins, 2129-2159.
Nguyen-Ba-Vy; Guerre L; Saint-Martin G, 1996. Preliminary study of the safety and immunogenicity of the attenuated VD<sub>47/25</sub> strain of camelpox virus. (Étude préliminaire de l'innocuité et du pouvoir immunogène de la souche atténuée VD<sub>47/25</sub> de camelpoxvirus.) Revue d'Élevage et de Médecine Vétérinaire des Pays Tropicaux, 49(3):189-194.
Nguyen-Ba-Vy; Richard D; Gillet JP, 1989. Properties of a strain of orthopoxvirus isolated from dromedaries in Niger. (Propriétés d'une souche d'orthopoxvirus isolée des dromadaires du Niger.) Revue d'Élevage et de Médecine Vétérinaire des Pays Tropicaux, 42(1):19-25.
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
OIE, 2012. World Animal Health Information Database. Version 2. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home
Prichard MN; Kern ER, 2012. Orthopoxvirus targets for the development of new antiviral agents. Antiviral Research, 94(2):111-125.
Rheinbaden FV; Gebel J; Exner M; Schmidt A, 2007. Environmental resistance, disinfection, and sterilization of poxviruses. In: Poxviruses [ed. by Schmidt, A. A. \Weber, A. \Mercer, O.]. Basel, Switzerland: Birkhauser Verlag, 397-405.
Sadykov RG, 1970. Cultivation of camelpox virus in chick embryos. Virusng Bolezni Skh. Zhi'ootnykh Part I:55.
Smee DF; Sidwell RW; Kefauver D; Bray M; Huggins JW, 2002. Characterization of wild-type and cidofovir-resistant strains of camelpox, cowpox, monkeypox, and vaccinia viruses. Antimicrobial Agents and Chemotherapy, 46(5):1329-1335.
Vinayagamurthy Balamurugan; Gnanavel Venkatesan; Veerakyathappa Bhanuprakash; Singh RK, 2013. Camelpox, an emerging orthopox viral disease. Indian Journal of Virology, 24(3):295-305. http://link.springer.com/article/10.1007%2Fs13337-013-0145-0
Vinayagamurthy Balamurugan; Veerakyathappa Bhanuprakash; Madhusudhan Hosamani; Jayappa KD; Gnanavel Venkatesan; Bina Chauhan; Singh RK, 2009. A polymerase chain reaction strategy for the diagnosis of camelpox. Journal of Veterinary Diagnostic Investigation, 21(2):231-237.
Wernery U; Kaaden OR, 2002. Camel pox. In: Infectious Diseases in Camelids, Second Edition [ed. by Wernery, U. \Kaaden, O. R.]. Vienna, Austria: Blackwell Science Berlin, 176-185 pp.
Azwai S M, Carter S D, Woldehiwet Z, Wernery U, 1996. Serology of Orthopoxvirus cameli infection in dromedary camels: analysis by ELISA and Western blotting. Comparative Immunology, Microbiology and Infectious Diseases. 19 (1), 65-78. DOI:10.1016/0147-9571(95)00023-2
CABI, Undated. Compendium record. Wallingford, UK: CABI
El-Harrak M, Loutfi C, 2000. Camel pox in dromedary calves in Morocco. Identification of the isolated virus. Vaccine development and prophylaxis. (La variole du dromadaire chez le jeune au Maroc. Isolement et identification du virus. Mise au point du vaccin et application à la prophylaxie.). Revue d'Élevage et de Médecine Vétérinaire des Pays Tropicaux. 53 (2), 165-167.
Hafez S M, Al-Sukayran A, Cruz D dela, Mazloum K S, Al-Bokmy A M, Al-Mukayel A, Amjad A M, 1992. Development of a live cell culture camelpox vaccine. Vaccine. 10 (8), 533-539. DOI:10.1016/0264-410X(92)90353-L
OIE, 2009. World Animal Health Information Database - Version: 1.4., Paris, France: World Organisation for Animal Health. https://www.oie.int/
OIE, 2012. World Animal Health Information Database. Version 2., Paris, France: World Organisation for Animal Health. https://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home
06/04/17 Original text by:
Chris A. Whitehouse, 1425 Porter Street, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, MD 21702, USA
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