ReviewTrypanosoma evansi and T. equiperdum: distribution, biology, treatment and phylogenetic relationship (a review)
Introduction
Trypanosoma evansi is a widely-distributed haemoflagellate of veterinary importance that infects a variety of larger mammals including horses, mules, camels, buffalo, cattle and deer. It causes epidemics of a disease called surra, which is of great economic importance in Africa, Asia and South America, where thousands of animals die from T. evansi infection each year. The infection is mechanically transmitted by blood-sucking insects of the genera Tabanus, Stomoxys, Atylotus and Lyperosia. Trypanosoma equiperdum also infects equines under natural conditions, and causes a venereally transmitted disease called dourine. However, though T. equiperdum has a wide geographical distribution (Hoare, 1972; Stephen, 1986), cases of dourine are rarely reported possibly due to the difficulty of diagnosis. Based on the differences in the mode of transmission, the host range, the pathogenicity, and the location of the parasite in its host, these two trypanosomes were classified as different species (Hoare, 1972). However, biochemical and molecular biological data indicate that T. evansi and T. equiperdum are much more closely related to each other than to Trypanosoma brucei brucei. In this review, the biology, distribution, pathogenicity, treatment as well as biochemical and molecular characteristics of T. evansi and T. equiperdum are compared and discussed.
Section snippets
Morphology and ultrastructure
Morphologically, T. evansi and T. equiperdum cannot be distinguished from the slender forms of T. brucei brucei or the human pathogenic subspecies T. brucei rhodesiense and T. brucei gambiense. Although pleomorphism may appear to some extent, generating stumpy and intermediate forms in some strains, T. evansi is generally monomorphic, assuming a long slender form. Strains from different geographical areas and various host sources are morphologically indistinguishable (Hoare, 1972; Stephen, 1986
Susceptibility of mammalian hosts
T. evansi has a wide range of hosts and is pathogenic for most domestic, wild and laboratory mammals. However, equines, camels, dogs, deer and Asian elephants are more frequently found infected by this trypanosome species than buffalo and cattle (Hoare, 1972; Lun et al., 1993). Infection in pigs can occur, but is either asymptomatic or associated with only light clinical signs. Goats experimentally infected with T. evansi showed chronic infection even with CNS involvement (Zweygarth, 1992),
In
The route of transmission
Many blood-sucking insects, especially horseflies (Tabanus spp.) and stableflies (Stomoxys spp.) can mechanically transmit T. evansi from one infected host to another, however, their role as vectors may vary under different conditions. For example, horseflies and stableflies are the most efficient vectors for transmission of this parasite in China and in Indonesia (Luckins, 1988; Lun et al., 1993). In Africa, the tsetse fly (Glossina spp), like other blood-sucking flies, can act as a mechanical
Pathogenicity
T. evansi is pathogenic to most domestic and many wild mammals, but its effect on the host varies according to the virulence of the strain of trypanosome, the species of the host, unspecific factors affecting the animal such as other infections and general stress, and the local epizootiological conditions (Hoare, 1972). The clinical signs of surra in most domestic and wild animals infected with T. evansi are characterized by fever and anaemia, followed by emaciation, oedema, cachexia and
Diagnosis and treatment
Diagnosis of T. evansi is based on demonstrating either the parasite or parasite antigens, or antibodies directed against the trypanosomes. For the direct demonstration of the parasite, the techniques used for the diagnosis of sleeping sickness or Nagana can be employed: (1) haematocrit centrifugation, (2) mini anion-exchange chromatography with DEAE-cellulose, (3) inoculation of laboratory mice. The demonstration of specific antibodies for the diagnosis of T. evansi infections in camels has
In vitro cultivation
The bloodstream forms of T. evansi isolates can be cultivated in vitro at 37°C in minimum essential medium (MEM) with Earle's salts, supplemented with 15–20% horse serum in the presence of a mammalian feeder layer (Brun and Jenni, 1987). Axenic culture is also possible in MEM supplemented according to Baltz et al. (1985)and the addition of 15% heat-inactivated horse serum. Chinese T. evansi isolates could be directly grown axenically starting from bloodstream forms isolated from an infected
Biochemical and molecular characteristics
Isoenzyme analysis has widely been used to group morphologically similar or identical forms in a variety of parasitic protozoa, especially among the trypanosomes (Gibson et al., 1980; Boid, 1988; Lun et al., 1992a; Stevens et al., 1992). More recently, analysis of small or large subunit ribosomal RNA sequences (Johnson and Baverstock, 1989; Qu et al., 1990; Hide and Tait, 1991), restriction fragment length polymorphisms (RFLPs) in DNA (Borst et al., 1981; Gibson et al., 1985; Paindavoine et
Conclusions
All the biological, clinical, morphological and molecular evidence (as summarized in Table 1) strongly supports the notion that T. evansi and T. equiperdum are sister taxa that arose from a common ancestor that descended from T. brucei. What, then, are the phylogenetic relationships among these three species, which vary in the mode of transmission, life cycle and the presence or absence of maxicircles? As mentioned in Section 4, bloodstream forms of T. equiperdum are rarely found in nature. It
Acknowledgements
This work was supported in part by a grant from the National Education Committee of PR China to ZRL. Thanks to Dr. G. Scheidegger for assistance with the electron micrographs, and to Drs. W. Gibson, R. Kaminsky, T. Smith and Mrs. J. Jenkins for critical reading of the manuscript.
References (59)
- et al.
The use of enzyme linked immunosorbent assays to investigate the prevalence of Trypanosoma equiperdum in Ethiopian horses
Vet. Parasitol.
(1997) - et al.
Malic enzyme type VII isoenzyme as an indicator of suramin resistance in Trypanosoma evansi
Exp. Parasitol.
(1989) - et al.
Quantitation of genetic differences between Trypanosoma brucei gambiense, rhodesiense and brucei by restriction enzyme analysis of kinetoplast DNA
Mol. Biochem. Parasitol.
(1981) - et al.
Drug sensitivity of Chinese Trypanosoma evansi and Trypanosoma equiperdum isolates
Vet. Parasitol.
(1994) - et al.
The kinetoplast DNA of Trypanosoma equiperdum
Biochim. Biophys. Acta
(1980) - et al.
Numerical analysis of enzyme polymorphism: A new approach to the epidemiology and taxonomy of trypanosomes of subgenus Trypanozoon
Adv. Parasitol.
(1980) - et al.
Further analysis of intra-specific variation in Trypanosoma brucei using restriction site polymorphisms in the maxi-circle of kinetoplast DNA
Mol. Biochem. Parasitol.
(1985) - et al.
Rapid ribosomal RNA sequencing and the phylogenetic analysis of protists
Parasitology Today
(1989) - et al.
Cymelarsan in the treatment of buffaloes naturally infected with Trypanosoma evansi in South China
Acta Trop.
(1991) - et al.
Trypanosomiasis of domestic animals in China
Parasitology Today
(1993)