T.W. Jonesa, R. C. Payne*, I.P. Sukanto & S. Partoutomob
aCentre for Tropical Veterinary Medicine, University of Edinburgh, Easter Bush, ROSLIN, Midlothian, Scotland, UK, EH25 9RGbBalai Penelitian Veteriner, (BALITVET), Jl. Martadinata, BOGOR 16114, Indonesia
* Current address National Veterinary Research Centre, Kikuyu, Kenya
Acknowledgements.
References
Trypanosoma evansi is believed to have been introduced into South East Asia in livestock imported from India (Hoare, 1972). The disease Surra was first reported in Indonesia, in 1897, when a group of horses on Java was found to be infected, with further outbreaks being reported in buffalo and cattle in East Java. Attempts were made to control the spread of the disease. These included isolation and slaughter of infected animals and lighting bonfires to drive away the flies which, even at that time, were thought to be associated with the disease. These efforts were ineffective and a decade later surra was reported to be enzootic throughout the low lying plains of Java (Doeve, 1917).
Extensive movements of livestock within Java and between the islands of the archipelago have sustained the continuing dissemination of T. evansi whilst the abundance of haematophagous flies probably facilitated transmission to susceptible hosts when infected animals were moved into disease free areas. Since the first report of surra, outbreaks of the disease have been recorded in many different areas of the country and the parasite is probably present on most of the major islands of the archipelago (Adiwinata and Dachlan, 1969). Recently serological studies have confirmed the widespread endemicity of T. evansi throughout Indonesia (Payne et al., 1991a).
Host species affected.
T. evansi has been reported to occur in a variety of hosts the most economically important being horses, buffalo and cattle but it has also been reported from sheep and goats, pigs, dogs, cats and a range of wild animals. Of these horses are most severely affected, often dying within weeks infection.
Disease outbreaks.
An important feature of T. evansi infections in Indonesia is the sporadic nature of disease outbreaks which are often localised but with high mortality rates and attributed to moving infective animals into areas previously free from infection (Payne et al., 1990) or moving disease free animals into endemic areas (Payne et al., 1991b). Work, food and environmental stresses have also been associated with surra epizootics.
Enzootic stability
The widespread endemicity of T. evansi infection throughout most of the Indonesian archipelago and the sporadic nature of disease outbreaks suggests that some form of enzootic stability has developed between the parasite and most of its hosts (apart from horses), as has been described for other protozoa such as Babesia (Mahoney, 1977). In the case of T. evansi the mechanism for such stability is unknown but could be coupled to the apparent restricted antigenic diversity seen in this trypanosome (Jones and McKinnell, 1985) which could result in a build up of immunity over time in an area.
Transmission of T. evansi.
A wide range of haematophagous diptera have been implicated in the transmission of T. evansi (Foil, 1989). In Indonesia, transmission is principally attributed to tabanid flies Tabanus, Haematopota, Chrysops and is considered to be mechanical with no evidence of development or multiplication in any fly species that have been examined for vector potential. Transmission by other flies such as Stomoxys, Musca, Haematobia however, could also occur when stocking densities and fly numbers are high.
Control of T. evansi.
Early control regimes included isolation or slaughter of infected animals, confinement of all healthy animals in stables during the day in order to discourage tabanids, which prefer to feed in sunlight, and prohibition of livestock movements. The introduction of suramin in the 1920's resulted in a relaxation of the official control measures and gradually chemotherapy superceded other methods of control. In the event of serious outbreaks of disease, however, the precaution of restricting livestock movement is still applied (Payne et al., 1990). Suramin continues to be the drug of choice although there are reports of suramin resistant stocks of T. evansi appearing in Indonesia. Other trypanocidal drugs, however, have not proven to be as effective against T. evansi in Indonesia as they have in other areas. Isometamidium chloride only provides a temporary reduction in parasitaemia in cattle and buffalo and diminazine aceturate gives unpredictable results. Recently trials at BALIVET to evaluate the efficacy of Cymelarsan (Rhone Merieux, France) indicated that the drug was effective against T. evansi infections in cattle at a dose rate of 0.75 mg/kg (Payne et al., 1994) but has not yet been approved for the treatment of cattle or buffalo
Future prospects.
Control of T. evansi is likely to remain heavily dependent on chemotherapeutic intervention principally with Suramin The short to medium-term outlook for this approach, however, is now uncertain as commercial production of suramin has ceased, therefore, future disease control will depend on the availability of new trypanocidal drugs. At present there is very little information on vector ecology that could be used as an alternative or part of integrated control regimes, although there is ample evidence that link disease outbreaks with conditions that lead to high population densities of (potential) vectors.
This paper is based on a post-project review manuscript prepared by one of the authors (RCP) on completion of a collaborative research program on T. evansi infection in Indonesia carried out between CTVM and BALITVET and funded by the Overseas Development Administration, Foreign & Commonwealth Office, London. Much of the early literature, referring to studies on Trypanosoma evansi in Indonesia, was originally published in Dutch and was translated into English for us by Dr E. F. Dieleman.
Adiwinata, R. T. and Dachlan, A., 1969. A brief note on surra in Indonesia. Elveka, Folia Veterinariea, 3: 11-15.
Doeve, W. C. A., 1917. Hededeelingen betreffende surra. Veeartsenjkundeige bcaden V. Nederl-Indie., 29: 4-15.
Foil, L. D., 1989. Tabanids as vectors of disease agents. Parasitology Today, 5: 88-96.
Hoare, C. A., 1972. The Trypanosomes of Mammals. A Zoological Monograph. Blackwell Scientific Publications, pp 555-593.
Jones, T. W. and McKinnell, C. D., 1985. Antigenic variation in Trypanosoma evansi: a comparison of the predominant variable antigenic type repertoire of stocks from the Sudan. Trop. Med. Parasitol, 36: 205-209.
Mahoney, D. F., 1977. Babesia of domestic animals. In: J. P. Krier (Editor), Parasitic Protozoa, Vol. VI. Academic Press, New York, pp 1-52.
Payne, R. C., Sukanto, I. P., Djauhari, D., Partoutomo, S., Wilson, A. J., Jones, T. W., Boid, R. and Luckins, A. G., 1991. Trypanosoma evansi infection in cattle, buffaloes and horses in Indonesia. Vet. Parasitol, 38: 109-119.
Payne, R. C., Sukanto, I. P., Graydon, R., Saroso, H. and Jusif, S. H., 1990. An outbreak of trypanosomiasis caused by Trypanosoma evansi on the island of Madura, Indonesia. Trop. Med. Parasitol, 41:445-446.
Payne, R. C., Waltner-Toewes, D., Djauhari, D. and Jones, T. W., 1991. Trypanosoma evansi infection in swamp buffalo imported into Central Java. Prev. Vet. Med., 11: 105-114.
Payne, R.C., Sukanto, I.P., Partoutomo, S., Jones, T.W., Luckins, A.G., and Boid, R.,1994. Efficacy of Cymelarsen (Rhone Merieux, France) in Friesian Holstein Calves infected with Trypanosoma evansi. Trop. Anml. Hlth Prod., 26: 219-226.
