- Summary of Invasiveness
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- History of Introduction and Spread
- Risk of Introduction
- Pathogen Characteristics
- Vectors and Intermediate Hosts
- Economic Impact
- Environmental Impact
- Risk and Impact Factors
- Gaps in Knowledge/Research Needs
- Links to Websites
- Principal Source
- Distribution Maps
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IdentityTop of page
Preferred Scientific Name
- Trypanosoma evansi (Steel, 1885) Balbiani, 1888
Other Scientific Names
- Spirochaeti evansi Steel, 1885
- Trypanosoma brucei evansi
Summary of InvasivenessTop 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.
Taxonomic TreeTop of page
- Domain: Eukaryota
- Kingdom: Protista
- Phylum: Protozoa
- Subphylum: Sarcomastigophora
- Order: Kinetoplastida
- Family: Trypanosomatidae
- Genus: Trypanosoma
- Species: Trypanosoma evansi
Notes on Taxonomy and NomenclatureTop of page
Trypanosomes are protozoan parasites of the blood and sometimes tissues of many animal species. They are taxonomically assigned to the order Kinetoplastida, family Trypanosomatidae, and genus Trypanosoma. The name is derived from the Greek trypano (borer) and soma (body) because of the corkscrew-like motion of some trypanosomatid species. The genus Trypanosoma is known from fossils in Dominican amber represented by the extinct species T. antiquus (Poinar, 2005). T. evansi belongs to the T. brucei group within the subgenus Trypanozoon (Desquesnes et al., 2013). In fact, recent whole genome sequencing and analysis support the idea that T. evansi should be classified as a subspecies of T. brucei (Carnes et al., 2015). Desquesnes et al. (2013) discussed this and concluded that, as the genetic evidence was not unequivocal, and T. evansi shows strong biological, ecological and medical differences from T. brucei, it was advisable to retain the name T. evansi. T. equinum, affecting horses in South America, was previously regarded as a separate species but is now considered to be a dyskinetoplastic variant of T. evansi (Stevens and Brisse, 2004).
Infection with T. evansi causes a disease named ‘surra’ in India, El debab, El gafar, Tabourit or Mbori in North Africa and Mal de Caderas or Murrina in Latin America (OIE, 2012). The origin of 'surra' is from the Marathi sūra, meaning “the sound of heavy breathing through the nostrils”. A parasite that would later be named T. evansi was first identified and described as the causative agent of surra by Griffith Evans in 1880 while working in India. A young veterinarian named J.H. Steel, believing that the causative organisms were spirochaetes, named them Spirochaeti evansi. Several years later, the taxonomic error was corrected, and they were placed in the genus Trypanosoma (Fallis, 1986).
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.
History of Introduction and SpreadTop of page
Trypanosoma evansi was first described in 1880 from India. However, it is thought to be derived from the African T. brucei brucei, which is restricted to the tsetse fly belt of Africa. T. evansi is no longer able to undergo its cycle in the tsetse fly (Glossina sp.) due to the loss of the maxicircles of mitochondrial DNA; however, it is not known when this phenomenon occurred. Historical data suggests that surra was already present in India at least several centuries B.C. (Desquesnes et al., 2013). Apparently the parasite ultimately spread eastward from India, but the date of this initial spread is unknown. The westward extension of T. evansi is more recent, however. It is thought to have been introduced into Latin America in the 16th century with the Arabian horses belonging to the Spanish conquistadores (Hoare, 1965). It was described for the first time on the Island of Marajo at the mouth of the Amazon River in Brazil in 1827; and was further observed in Paraguay in 1847; in the Pantanal, Brazil in 1850; and Mato Grosso, Brazil in 1860, before further spreading into Bolivia, Venezuela, Guyana, and Colombia (Hoare, 1972).
In Europe, there have been recent introductions of T. evansi in the Canary Islands (Spain) (Gutiérrez et al., 1998) and the Spanish mainland (Tamarit et al., 2010), and a single epizootic in France in 2006 resulting from infected camels imported from the Canary Islands (Desquesnes et al., 2008).
Risk of IntroductionTop of page
Due to its wide host range, Trypanosoma evansi has the potential to invade new geographical areas, as shown by the recent incursions in continental Spain and France. Europe, North America and Australia might potentially be at risk (Desquesnes et al., 2013).
Pathogen CharacteristicsTop of page
Trypanosoma evansi is classified within the genus Trypanosoma, subgenus Trypanozoon, along with T. brucei brucei (cause of nagana in livestock), T. brucei rhodesiense and T. brucei gambiense (cause of human African sleeping sickness), and T. equiperdum (cause of a sexually transmitted disease in horses). When observed microscopically in fresh blood samples, T. evansi appears small with a thin posterior extremity and free flagellum. There is also a highly visible undulating membrane. When observed on a Giemsa stained thin smear, T. evansi is described as a monomorphic thin trypomastigote parasite (Desquesnes et al., 2013). By comparison with T. brucei, it shows mostly slender forms with a long free flagellum and thin posterior extremity with subterminal small kinetoplast, but some intermediate (shorter free flagellum and posterior extremity) and rare “stumpy” forms have been reported.
The mean length of the parasite is 24 ± 4 µm, which does not vary sustainably with geographical, host, or strain origin, but can change in relation to the growing conditions of the parasite and the immune response of the host (Tejero et al., 2008). Like all pathogenic trypanosomes, T. evansi is covered by a dense protein layer consisting of a single protein called the variable surface glycoprotein (VSG) (Richards, 1984).
Two key, and related, biological features distinguish T. evansi from the T. brucei group. First, its transmission is independent from the tsetse fly as an obligatory vector. Second, all strains of T. evansi investigated so far are akinetoplastic or dyskinetoplastic, that is lacking all or critical parts, respectively, of the mitochondrial or kinetoplast DNA (kDNA). T. brucei has a complex life cycle involving a vertebrate bloodstream stage and a procyclic stage in the tsetse fly. In T. 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. 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 T. evansi, along with T. equiperdum, to become one of the pathogenic trypanosomes with the widest geographical distribution.
Surra, the disease associated with this pathogen, is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). Animal Health and Production Compendium users can refer to the AHPC library for further information from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Vectors and Intermediate HostsTop of page
Economic ImpactTop 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) place a permanent constraint on raising livestock throughout much of Asia and Latin America.
Environmental ImpactTop 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.
Risk and Impact FactorsTop of page Invasiveness
- Proved invasive outside its native range
- Has a broad native range
- Host damage
- Negatively impacts agriculture
- Negatively impacts animal health
- Negatively impacts livelihoods
- Difficult to identify/detect in the field
- Difficult/costly to control
Gaps in Knowledge/Research NeedsTop of page
An effective vaccine against surra is sorely needed to control this disease. This has not been possible to date due to the rapid turnover of the parasite’s outer surface glycoprotein (VSG), which also occurs in other animal and human pathogenic trypanosomes. More research is needed to develop ways to stop or control this antigenic variation and/or develop new vaccine targets.
Another important area for future research is the development of new anti-trypanosome therapeutics, and drug resistance. The major constraint to chemotherapeutic control of Trypanosoma evansi is the development of drug resistance. There are only a limited number of drugs available for the treatment of trypanosomiasis, and an even more limited number suitable for treatment of T. evansi infection in camels due to the toxicity of some of the available drugs in camels. In addition, these drugs have been in use over many decades, including use as prophylaxis, which can lead to increased drug resistance.
ReferencesTop of page
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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
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