- Hosts/Species Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Impact: Environmental
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Principal Source
- Distribution Maps
Don't need the entire report?
Generate a print friendly version containing only the sections you need.Generate report
IdentityTop of page
Preferred Scientific Name
International Common Names
- English: surra, trypanosoma evansi, in cattle - exotic; surra, trypanosoma evansi, in pigs - exotic; Trypanosoma evansi infection
- Spanish: mal de caderas; murrina
Local Common Names
- North Africa: el debab ; el gafar ; mbori; tabourit
OverviewTop of page
Trypanosoma evansi is a protozoan parasite that is the causative agent of the animal disease surra. The disease occurs in a wide area from the northern part of Africa through the Middle East to Southeast Asia; it is thought to have been introduced to the Americas in the 16th century and is now found in much of Latin America except the southernmost parts. It is not known to occur in North America (except Mexico), Australia, Europe (except for rare introductions into Spain and France), or northern Russia. It affects a very large range of domestic and wild animals; only one case of human infection has been reported. It has a significant economic and animal health impact on cattle, camels and other livestock in many countries. T. evansi is mechanically transmitted primarily by several species of haematophagous flies (mainly Tabanids and Stomoxes), but in Latin America the vampire bat (Desmodus rotundus) is a vector and reservoir host. Clinical manifestations of disease include fever, anaemia, loss of appetite, weight loss, nervous signs, abortion, cachexia, and potentially death. No vaccine is available. Several chemotherapeutic drugs are used for the prophylaxis and treatment of surra; however, drug resistance is known to occur. Surra is on the OIE list of notifiable diseases. For further information on this disease from OIE, see the website: www.oie.int.
Hosts/Species AffectedTop of page
Trypanosoma evansi has one of the widest host ranges among the trypanosomes. While almost all mammalian species are susceptible to infection with T. evansi, only certain ones develop significant clinical signs and play a role in its epidemiology. Their susceptibility, however, varies greatly depending on host geography, host species, and parasite strain (Desquesnes et al., 2013). In Africa and the Middle East, T. evansi is mainly a parasite of camels, but it is also highly pathogenic in the Equidae (horses, asses, mules, and donkeys). In Asia, it is a major parasite for water buffaloes (Bubalus bubalis) (in contrast, it is not pathogenic in the African buffalo Syncerus caffer). Surra is also considered to be an economically important disease in cattle, pigs, and goats in many parts of Asia. T. evansi has also been found in elephants in India and Thailand. In Australia, Europe, and the New World, T. evansi is an important threat to horses, cattle, pigs, camels (in Australia), and other livestock species. In addition to domestic hosts, T. evansi has been found in a wide range of wildlife species around the world (Desquesnes et al., 2013). In Central and South America, it has been found in various marsupials, primates, lagomorphs, rodents, perissodactyls, and artiodactyls; however, their epidemiological importance, if any, has not been fully established (Herrera et al., 2004). Note that only a selection of hosts is shown in the Host Animals table.
The Latin American vampire bat (Desmodus rotundus) is an interesting example of a species simultaneously being a host, reservoir, and a vector -- it can mechanically transmit the parasite in its saliva, and also act as a true reservoir, maintaining the parasite in the bat colony in the absence of other hosts (Hoare, 1965).
DistributionTop of page
Trypanosoma evansi has the widest geographical distribution among the trypanosomes. In the Eastern Hemisphere, its geographical distribution is continuous from the northern part of Africa through the Middle East to Southeast Asia. In Africa, it is present in all countries where camels are present. It is found in sub-Saharan and Mediterranean climates, as well as in arid deserts and semiarid steppes. It is present in the Arabian Peninsula, Turkey, Afghanistan, Pakistan, and has been occasionally reported from Bulgaria (Desquesnes et al., 2013). It is also present throughout southern Asia, including India, China, Mongolia, parts of Russia, Bhutan, Nepal, Myanmar, Laos, Vietnam, Cambodia, Thailand, Malaysia, the Philippines, and Indonesia (Luckins, 1988). Its presence was suspected in Papua New Guinea, but not confirmed, and it is so far absent from Australia (Reid, 2002) (it was briefly introduced there in the early 20th century but was soon eradicated -- Desquesnes et al., 2013, citing Hoare, 1972). In Latin America, it is present in much of South America other than the southernmost parts, and it is uncertain how far north through Central America its range extends -- some reports suggest Mexico, but this is not certain (Desquesnes, 2004). In Europe, there have been recent introductions of T. evansi in the Canary Islands (Spain) (Gutiérrez et al., 1998), the Spanish mainland (Tamarit et al., 2010), and a single epizootic in France resulting from infected camels imported from the Canary Islands (Desquesnes et al., 2008). The parasite is absent from North America, northern Europe, and northern Russia (Desquesnes et al., 2013).
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.
PathologyTop of page
Anaemia is a common feature of clinical trypanosomiasis with Trypanosoma evansi. It appears to be predominantly haemolytic, associated with decreased life span of erythrocytes and extensive erythrophagocytosis (Habila et al., 2012). The onset of anaemia is related to the appearance of trypanosomes in the blood, and the severity is associated with the level and initial wave of parasitaemia. Haemolytic factors such as free fatty acids, immunologic mechanisms, haemodilution, coagulation disorders, depression of erythrogenesis and release of trypanosomal sialidase have all been implicated in the development of anaemia in trypanosomiasis (Habila et al., 2012). The anaemia in both human and animal trypanosomiases is, however, predominantly the result of haemolytic crises in which the erythrocytes are destroyed by an expanded mononuclear phagocytic system (Igbokwe and Mohammed, 1991). The destruction of erythrocytes is in part due to the action of sialidase, which cleaves sialic acids on the cell surface and exposes galactosyl residues. These residues are then recognized by D-galactose-specific lectins on macrophages, leading to erythrophagocytosis and subsequently anaemia (Sallau et al., 2008).
Another of the important aspects of T. evansi infection and surra is immunosuppression. Primarily, this allows the trypanosomes to survive and multiply in extracellular fluids, especially in the blood. The best-known immune “escape” mechanism developed by trypanosomes is the antigenic variation caused by their variant surface glycoproteins (VSGs) (Cross, 1975; Vickerman, 1969). VSGs are the main antigenic determinant for the host immune system, and so antigenic variation in T. evansi appears to be the primary mechanism for evasion of the hosts’ immune responses (Habila et al., 2012). The key features underlying successful immune evasion are clone-specific singular VSG expression combined with switching from one VSG to another (Horn, 2014). The VSG coat accounts for about 10% of the total protein of the parasite, and the genome contains approximately 1000 VSG genes, which are randomly switched on and off at each generation (Habila et al., 2012). Significantly, this antigenic variation in the VSG has prevented development of a protective vaccine and permits reinfections when animals are exposed to a new antigenic type.
DiagnosisTop of page
The general clinical signs of Trypanosoma evansi infection are not sufficiently pathognomonic for diagnosis. Therefore, laboratory methods for detecting the parasite are required. The classical direct parasitological methods for the diagnosis of trypanosomiasis, namely microscopic examination of blood or lymph node material, are useful, particularly in resource-limited countries, but they are not highly sensitive. However, sensitivity can be increased significantly by using various concentration or amplification procedures (OIE, 2012). Concentration procedures basically consist of centrifugation of heparinized capillary tubes of the suspected animal’s blood. Trypanosomes concentrate at the junction between the buffy coat and the plasma, which can be observed under the microscope either directly through the glass capillary tube (Woo’s technique) or in a wet preparation using phase-contrast or dark-ground microscopy (Murray’s technique). These methods have the added benefit of allowing the degree of anaemia (i.e., the haematocrit) to be estimated.
Laboratory animals may be used to reveal subclinical infections in domesticated animals. T. evansi has a broad spectrum of infectivity for small rodents so rats and mice can be used. Rodent inoculation using buffy coat material can detect as few as 1.25 T. evansi/ml blood (Reid et al., 2001).
In regions where other Trypanosoma spp. occur, specific identification by microscopy is not possible, and molecular methods are needed to specifically identify T. evansi. Specific DNA probes have been used to detect trypanosome DNA in infected blood or tissue but are not routinely applied as further evaluation needs to be performed. Polymerase chain reaction techniques are generally preferred and are routinely used in many laboratories. The sensitivity of PCR is dependent on the amount of DNA in the sample, which is proportional to the level of parasitaemia. In addition, DNA preparation is an important step that determines the success and the sensitivity of the PCR. The test can be performed on whole blood, or preferably, on the buffy coat to increase the sensitivity. Needle biopsy material or tissues of lungs, liver, or kidney obtained post mortem can also be used. Numerous primer sets for both standard and real-time PCRs have been developed and evaluated for the detection of T. evansi DNA (OIE, 2012).
Similarly, many different serological tests have been developed to detect specific antibodies to trypanosomal antigens. These include direct and indirect agglutination tests, complement fixation tests, indirect fluorescence antibody tests, and the trypanolysis test (OIE, 2012). However, many of these tests are either useful only for small-scale surveys or are no longer used. More recently, they have been replaced by the more sensitive and more easily standardized techniques of enzyme linked immunosorbent assay (ELISA) and the card agglutination test (CATT). Evaluations of ELISA and CATT have been carried out in camels, horses, cattle, buffaloes, and pigs (Desquesnes et al., 2009; Diall et al., 1994; Holland et al., 2005; Reid and Copeman, 2003; Verloo et al., 2000).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Sign|
|General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia||Sign|
|General Signs / Pale mucous membranes or skin, anemia||Sign|
|General Signs / Petechiae or ecchymoses, bruises, ecchymosis||Sign|
|General Signs / Swelling mass penis, prepuce, testes, scrotum||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Sign|
|Skin / Integumentary Signs / Skin papules||Sign|
|Skin / Integumentary Signs / Skin pustules||Sign|
|Skin / Integumentary Signs / Skin vesicles, bullae, blisters||Sign|
Disease CourseTop of page
The clinical signs of Trypanosoma evansi infection can vary dramatically depending on host species. Even within a host species, there can be variability in clinical signs in different geographical areas. However, in general, disease signs include fever, anaemia, loss of appetite, weight loss, nervous signs, abortion, cachexia, and death. Surra is primarily a disease of camelids and equines, in which the typical clinical disease course is described here.
In camels, signs of illness begin with intermittent fever (41°C) for about one week. The animals appear dull and listless and become progressively weaker with loss of appetite and weight, develop oedema (particularly of the udder or scrotum), become anaemic, and develop petechial or ecchymotic haemorrhages. Nervous signs are sometimes observed, including periodic convulsions. The disease can be fatal, sometimes within a few months; however it is more often chronic and can frequently last 2-3 years (in parts of its rage it has been called Tibarsa, which means “three years disease” -- Desquesnes et al., 2013).
In horses, the incubation period is 1-4 weeks (sometimes up to 8 weeks), after which fever develops with high peaks (up to 44°C) corresponding to parasitaemia levels. Other signs, such as weakness, lethargy, anemia, and severe weight loss follow. Additionally, petechial haemorrhages on the eyelids and vulvar and vaginal mucosa can occur, as can haemorrhaging into the anterior chamber of the eye. As in camels, abortion, nervous signs, and oedema of the abdomen, testicles or udder are clinical signs of surra in horses. Other equines, such as donkeys, asses, and mules can become infected with T. evansi, but appear to have lower susceptibility compared to horses (Desquesnes et al., 2013).
EpidemiologyTop of page
In contrast to the complex life cycle of Trypanosoma brucei, involving a vertebrate bloodstream stage and a procyclic stage in the tsetse fly, in Trypanosoma evansi a total or partial loss of kDNA has “locked” the trypanosome in the bloodstream form resulting in the elimination of the need for the tsetse fly vector, enabling mechanical transmission by a variety of vectors. This has resulted in its ability to leave the African tsetse fly belt and spread to other continents (Lai et al., 2008; Lun and Desser, 1995), allowing it, along with T. equiperdum, to become one of the pathogenic trypanosomes with the widest geographical distribution. Several species of haematophagous flies, including tabanids (Tabanus spp., Chrysops spp., and Haematopota spp.) and Stomoxes (Stomoxys spp.), are implicated in mechanically transferring infection from host to host. Flies in the genera Musca, Haematobia, and Atylotus can also serve as vectors, but tabanids (horse flies) are the most significant arthropod vectors. The Latin American vampire bat (Desmodus rotundus) is mainly responsible for disseminating the parasite in Latin America. The vampire bat is an interesting example of a species simultaneously being a host, reservoir, and a vector -- it can mechanically transmit the parasite in its saliva, and also act as a true reservoir, maintaining the parasite in the bat colony in the absence of other hosts (Hoare, 1965). Carnivores may become infected after ingesting infected meat, and transmission in milk and during coitus has been documented (OIE, 2013).
Impact: EconomicTop of page
Several economically important animals, including camels, horses, buffaloes, and cattle, are particularly affected by surra (OIE, 2012). Camels, for example, are a major part of the economies of many African and Middle East countries, being used for nomadic pastoralism, transportation, racing, and production of milk, wool and meat. According to the United Nations Food and Agriculture Organization, the total world camel population is approximately 23 million animals (FAO, 2016), and surra is considered the most important single cause of morbidity and mortality in camels (OIE, 2013). In addition to camels, Trypanosoma evansi and other livestock trypanosomes threaten 48 million cattle in 37 African countries and are responsible for major losses in the production of milk, meat, and manure fertilizer (Desquesnes et al., 2013). In addition to Africa, T. evansi (and other animal trypanosomes) places a permanent constraint on raising livestock throughout much of Asia and Latin America.
Impact: EnvironmentalTop of page
While Trypanosoma evansi infects a wide range of domestic and wild animals, clinical disease (surra) mainly affects domestic livestock. Although infected wildlife can become reservoir hosts (i.e. asymptomatic carriers), the impact of T. evansi on biodiversity and the environment is minimal.
Zoonoses and Food SafetyTop of page
In general, Trypanosoma evansi is thought to be a strictly animal pathogen and not considered to be a zoonotic concern. However, in 2005 the first case of human trypanosomiasis caused by T. evansi was reported (Joshi et al., 2005). The patient was a cattle farmer from a small village in central India. He had intermittent fever associated with chills and sweating for 15 days. He then developed signs of sensory deficit, and was disoriented and agitated with violent behavior. It was speculated that the patient was probably contaminated through a wound on his finger when exposed to blood of infected cattle. There was no central nervous system invasion by the parasites, and the patient was successfully treated with suramin. Follow-up serological survey of the local population surrounding the patient’s village found 81 of 1806 (4.4%) people tested to be seropositive to T. evansi, suggesting exposure to the parasite in the study area (Shegokar et al., 2006).
While there is some epidemiological evidence that some carnivores, especially dogs, may be infected with T. evansi by eating contaminated meat (Desquesnes et al., 2013), there is no evidence suggesting that humans have been infected via contaminated food. Because of this, and the rarity of human infection in general, T. evansi is not considered a food safety concern.
Disease TreatmentTop of page
Several drugs can be used for the prophylaxis and treatment of surra. Prophylactic drugs include quinapyramine dimethylsulfate, prothridium and isometamidium chloride, and in some cases suramin. As therapeutic treatments, quinapyramine sulfate, suramin, and diminazene aceturate can be used (OIE, 2013; Petersen and Grinnage-Pulley, 2015). Only a few drugs, including melarsomine (Cymelarsan), quinapyramine sulfate (Triquin), and isometamidium chloride (Trypamidium-Samorin), have been approved for use in camelids (Wernery and Kaaden, 2002). Many of the drugs used for cattle are either not curative or are too toxic for camels. Overdosing quinapyramines, for example, can cause side effects in camels such as tremors, salivation and collapse leading to death (Wernery and Kaaden, 2002). Drug resistance occurs and should be considered in refractory cases (Petersen and Grinnage-Pulley, 2015). Thus, monitoring for drug resistance is important and should be employed when suspicion of resistance arises.
Prevention and ControlTop of page
Control of surra is difficult for a number of reasons. Effective control of the disease is hampered by the lack of vector specificity and the wide range of hosts affected. Due to the lack of vector specificity, control measures are often aimed at the host rather than the vector. These can include detection and treatment of infected animals, prophylactic treatment of susceptible animals (although drug resistance is a continuing concern), and protection of animals from biting flies and (in Latin America) vampire bats (OIE, 2013).
There is no vaccine available for this disease. Development of an effective vaccine is not likely in the near future due to the ability of the parasite to rapidly change its surface glycoproteins to avoid the host immune response.
ReferencesTop of page
Carnes, J., Anupama, A., Balmer, O., Jackson, A., Lewis, M., Brown, R., Cestari, I., Desquesnes, M., Gendrin, C., Hertz-Fowler, C., Imamura, H., Ivens, A., Korený, L., Lai DeHua, MacLeod, A., McDermott, S. M., Merritt, C., Monnerat, S., Moon, W. J., Myler, P., Phan, I., Ramasamy, G., Sivam, D., Lun ZhaoRong, Lukeš, J., Stuart, K. (et al), 2015. Genome and phylogenetic analyses of Trypanosoma evansi reveal extensive similarity to T. brucei and multiple independent origins for dyskinetoplasty. PLoS Neglected Tropical Diseases, 9(1), e3404. http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0003404 doi: 10.1371/journal.pntd.0003404
Cross, G. A. M., 1975. Identification, purification and properties of clone-specific glycoprotein antigens constituting the surface coat of Trypanosoma brucei. Parasitology, 71(Pt 3), 393-417. doi: 10.1017/S003118200004717X
Desquesnes, M., 2004. Livestock trypanosomoses and their vectors in Latin America, [ed. by Desquesnes, M. ]. Paris, France: OIE (World Organisation for Animal Health).ix + 174 pp. https://www.oie.int/doc/ged/D9818.PDF
Desquesnes, M., Bossard, G., Patrel, D., Herder, S., Patout, O., Lepetitcolin, E., Thevenon, S., Berthier, D., Pavlovic, D., Brugidou, R., Jacquiet, P., Schelcher, F., Faye, B., Touratier, L., Cuny, G., 2008. First outbreak of Trypanosoma evansi in camels in metropolitan France. Veterinary Record, 162(23), 750-752. http://veterinaryrecord.bvapublications.com/archive/
Desquesnes, M., Bossard, G., Thévenon, S., Patrel, D., Ravel, S., Pavlovic, D., Herder, S., Patout, O., Lepetitcolin, E., Hollzmuller, P., Berthier, D., Jacquiet, P., Cuny, G., 2009. Development and application of an antibody-ELISA to follow up a Trypanosoma evansi outbreak in a dromedary camel herd in France. Veterinary Parasitology, 162(3/4), 214-220. http://www.sciencedirect.com/science/journal/03044017 doi: 10.1016/j.vetpar.2009.03.033
Desquesnes, M., Holzmuller, P., Lai DeHua, Dargantes, A., Lun ZhaoRong, Jittaplapong, S., 2013. Trypanosoma evansi and surra: a review and perspectives on origin, history, distribution, taxonomy, morphology, hosts, and pathogenic effects. BioMed Research International, 2013, Article ID 194176. http://www.hindawi.com/journals/bmri/2013/194176/
Diall O, Bajyana Songa E, Magnus E, Kouyate B, Diallo B, Van Meirvenne N, Hamers R, 1994. Evaluation of a direct serologic card agglutination test for the diagnosis of camel trypanosomiasis caused by Trypanosoma evansi. (Evaluation d'un test sérologique d'agglutination directe sur carte dans le diagnostic de la trypanosomose caméline à Trypanosoma evansi). Revue Scientifique et Technique, 13(3): 793-800
Fallis AM, 1986. Griffith Evans 1835-1935: Discoverer of the first pathogenic trypanosome. Canadian Veterinary Journal, 27(9): 336-338
FAO, 2016. FAOSTAT: Food and Agriculture Data. Rome, Italy: FAO. http://www.fao.org/faostat
Gutiérrez, C., Montoya, J. A., Padron, M., Corbera, J. A., Juste, M. C., Molina, J. M., 1998. Description of a case of trypanosomiasis due to Trypanosoma evansi in a dromedary in the Canary Islands. (Descripción de un caso de tripanosomosis en el dromedario por T. evansi en Canarias). Medicina Veterinaria, 15(6), 356-357.
Habila, N., Inuwa, M. H., Aimola, I. A., Udeh, M. U., Haruna, E., 2012. Pathogenic mechanisms of Trypanosoma evansi infections. Research in Veterinary Science, 93(1), 13-17. http://www.sciencedirect.com/science/journal/00345288 doi: 10.1016/j.rvsc.2011.08.011
Herrera, H. M., Dávila, A. M. R., Norek, A., Abreu, U. G., Souza, S. S., D'Andrea, P. S., Jansen, A. M., 2004. Enzootiology of Trypanosoma evansi in Pantanal, Brazil. Veterinary Parasitology, 125(3/4), 263-275. doi: 10.1016/j.vetpar.2004.07.013
Holland, W. G., Thanh, N. G., Do, T. T., Sangmaneedet, S., Goddeeris, B., Vercruysse, J., 2005. Evaluation of diagnostic tests for Trypanosoma evansi in experimentally infected pigs and subsequent use in field surveys in North Vietnam and Thailand. Tropical Animal Health and Production, 37(6), 457-467. http://springerlink.metapress.com/link.asp?id=103008 doi: 10.1007/s11250-005-1217-y
Horn, D., 2014. Antigenic variation in African trypanosomes. Molecular and Biochemical Parasitology, 195(2), 123-129. http://www.sciencedirect.com/science/article/pii/S0166685114000590 doi: 10.1016/j.molbiopara.2014.05.001
Igbokwe, I. O., Mohammed, A., 1991. The reticulocyte response to the anaemia in goats caused by experimental Trypanosoma brucei infection. Veterinary Research Communications, 15(5), 373-377. doi: 10.1007/BF00366994
Joshi, P. P., Shegokar, V. R., Powar, R. M., Herder, S., Rahul Katti, Salkar, H. R., Dani, V. S., Aradhana Bhargava, Jannin, J., Truc, P., 2005. Human trypanosomiasis caused by Trypanosoma evansi in India: the first case report. American Journal of Tropical Medicine and Hygiene, 73(3), 491-495.
Lai DeHua, Hashimi, H., Lun ZhaoRong, Ayala, F. J., Lukeš, J., 2008. Adaptations of Trypanosoma brucei to gradual loss of kinetoplast DNA: Trypanosoma equiperdum and Trypanosoma evansi are petite mutants of T. brucei. Proceedings of the National Academy of Sciences of the United States of America, 105(6), 1999-2004. http://www.pnas.org/ doi: 10.1073/pnas.0711799105
Lun, Z. R., Desser, S. S., 1995. Is the broad range of hosts and geographical distribution of Trypanosoma evansi attributable to the loss of maxicircle kinetoplast DNA?. Parasitology Today, 11(4), 131-133.
Misra, K. K., Roy, S., Choudhury, A., 2016. Biology of Trypanosoma (Trypanozoon) evansi in experimental heterologous mammalian hosts. Journal of Parasitic Diseases, 40(3), 1047-1061. http://link.springer.com/article/10.1007/s12639-014-0633-1 doi: 10.1007/s12639-014-0633-1
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties
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. Trypanosoma evansi infection (Surra) (Chapter 2.1.21). In: Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: OIE, 314-328. http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.01.21_TRYPANO_SURRA.pdf
OIE, 2013. Trypanosoma evansi infections (including surra). Paris, France: OIE, 4 pp. http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/Disease_cards/TRYPANO_EVANSI.pdf
Petersen C, Grinnage-Pulley TL, 2015. Trypanosomiasis. In: MSD Veterinary Manual. Kenilworth, New Jersey, USA: Merck Sharp & Dohme. http://www.merckvetmanual.com/mvm/circulatory_system/blood_parasites/trypanosomiasis.html
Poinar, G., Jr., 2005. Triatoma dominicana sp. n. (Hemiptera: Reduviidae: Triatominae), and Trypanosoma antiquus sp. n. (Stercoraria: Trypanosomatidae), the first fossil evidence of a triatomine-trypanosomatid vector association. Vector Borne and Zoonotic Diseases, 5(1), 72-81. doi: 10.1089/vbz.2005.5.72
Reid, S. A., Copeman, D. B., 2003. The development and validation of an antibody-ELISA to detect Trypanosoma evansi infection in cattle in Australia and Papua New Guinea. Preventive Veterinary Medicine, 61(3), 195-208. doi: 10.1016/j.prevetmed.2003.07.004
Reid, S. A., Husein, A., Copeman, D. B., 2001. Evaluation and improvement of parasitological tests for Trypanosoma evansi infection. Veterinary Parasitology, 102(4), 291-297. doi: 10.1016/S0304-4017(01)00539-8
Sallau AB, Ibrahim MA, Salihu A, Yusuf IA, 2008. Bloodstream form of Trypanosoma evansi contains galactosidase. Middle East Journal of Science Research, 3: 49-52
Shegokar, V. R., Powar, R. M., Joshi, P. P., Aradhana Bhargava, Dani, V. S., Ravindra Katti, Zare, V. R., Khanande, V. D., Jannin, J., Truc, P., 2006. Human trypanosomiasis caused by Trypanosoma evansi in a village in India: preliminary serologic survey of the local population. American Journal of Tropical Medicine and Hygiene, 75(5), 869-870. http://www.ajtmh.org
Stevens, J. R., Brisse, S., 2004. Systematics of trypanosomes of medical and veterinary importance. In: The trypanosomiases, [ed. by Maudlin, I., Holmes, P. H., Miles, M. A.]. Wallingford, UK: CABI Publishing. 1-23. http://www.cabi.org/cabebooks/ebook/20043124834 doi: 10.1079/9780851994758.0001
Tamarit, A., Gutierrez, C., Arroyo, R., Jimenez, V., Zagalá, G., Bosch, I., Sirvent, J., Alberola, J., Alonso, I., Caballero, C., 2010. Trypanosoma evansi infection in mainland Spain. Veterinary Parasitology, 167(1), 74-76. http://www.sciencedirect.com/science/journal/03044017 doi: 10.1016/j.vetpar.2009.09.050
Tejero, F., Roschman-González, A., Perrone-Carmona, T. M., Aso, P. M., 2008. Trypanosoma evansi: a quantitative approach to the understanding of the morphometry-hematology relationship throughout experimental murine infections. Journal of Protozoology Research, 18(1), 34-47.
Verloo, D., Holland, W., My, L. N., Thanh, N. G., Tam, P. T., Goddeeris, B., Vercruysse, J., Büscher, P., 2000. Comparison of serological tests for Trypanosoma evansi natural infections in water buffaloes from north Vietnam. Veterinary Parasitology, 92(2), 87-96. doi: 10.1016/S0304-4017(00)00284-3
Wernery U, Kaaden OR, 2002. Infectious diseases in camelids (2nd ed.). Blackwell
OrganizationsTop of page
Japan: National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho Nishi 2-13 , Obihiro, Hokkaido 080-8555 , http://www.obihiro.ac.jp/~protozoa/eng/index-eng.html
France: World Organization for Animal Health (OIE), Paris, http://www.oie.int
Italy: Food and Agriculture Organization of the United Nations (FAO), Rome, http://www.fao.org
Principal SourceTop of page
Draft datasheet under review
ContributorsTop of page
20/01/2016 Original text by:
Chris Whitehouse, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702-5011, USA.
Distribution MapsTop of page
Unsupported Web Browser:
One or more of the features that are needed to show you the maps functionality are not available in the web browser that you are using.
Please consider upgrading your browser to the latest version or installing a new browser.
More information about modern web browsers can be found at http://browsehappy.com/