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Trypanosomes—A millstone for the developing world and an insidious threat to Australian livestock

Bruce Watt, Central Tablelands Local Land Service, Bathurst NSW

'Pathogenic forms of trypanosomes are the major constraint to livestock production in much of Africa and also cause losses in South America and Asia. In Australia, the species found in livestock are not obviously associated with disease' (Callow 1984).

'With a wide vertebrate host range, including livestock, dogs and wild animals, T evansi has the potential to enter Australia unnoticed and become established (Callow 1984).

Posted Flock & Herd March 2015


Trypanosomes affect people and livestock in Africa, Asia and South America. The species of greatest veterinary importance are Trypanosoma congolense and T. vivax (both affecting a wide range of domestic mammals but particularly cattle), T. brucei subspecies brucei (affecting most domestic mammals especially goats, sheep, horses and donkeys) and T. evansi (the cause of surra and infecting a wide range of mammals including cattle, pigs, horses and donkeys). T. suis affects only pigs while T. simiae, is primarily a parasite of pigs. T.equiperdum is transmitted venereally in horses and donkeys (Connor accessed 2014).

Two further subspecies of T. brucei, T. brucei rhodesiense and T. brucei gambiense, affect people, causing East African and West African sleeping sickness respectively. Humans are the main reservoir for T. brucei gambiense while wild game animals are the main reservoir for T. brucei rhodesiense.

In sub Saharan Africa, 50 million people are exposed to trypanosomiasis while tsetse transmitted trypanosomes endanger 30% of about 150 million cattle and similar numbers of small ruminants. Trypanosomes causes such severe disease that livestock are excluded from large areas of Africa, while in other areas trypanosomiasis contributes to poverty and food shortages, depressing every aspect of livestock production, increasing mortality and reducing fertility, growth rates and milk production. Losses are also incurred through decreased draught power and manure (used for fuel and fertilizer). Meat production losses alone are estimated at US$5 billion (International Livestock Research Institute, accessed 2015).


Trypanosomes are single celled flagellated protists and are characterised by possessing a kinetoplast, a large mass of DNA, within a single mitochondrion at the base of the flagellum. They include organisms of major human and veterinary significance (Ladiges et al. 2006). The trypanosomes reproduce asexually by mitosis and are divided into two groups based on their mode of transmission. The Salivaria develop in anterior part of the vector's digestive system and accumulate in and are transmitted from the salivary glands. The Stercoraria develop in the lower bowel of vectors and are passes in their faeces. They transmit via ingestion or wound contamination aided in some cases when the host rubs the irritated bite site (Chernin 2000).


The classic trypanosome infection, human sleeping sickness, is caused by the salivarians T. brucei rhodesiense and T. brucei gambiense, spread by the tsetse fly (Glossina spp.). An infected fly injects saliva contaminated with trypanosomes into the tissues and bloodstream of a susceptible host. A local inflammatory reaction develops then resolves spontaneously but organisms proliferate in the bloodstream and invade other tissues. Trypanosomes provoke an immune response leading to hypergammaglobulinaemia, lymphadenopathy and splenomegaly but they are able to evade this immune response by spontaneously changing their coat of identical surface glycoproteins. It is estimated that T brucei for example, has a repertoire of 300-1000 variable antigenic types, thwarting both the host's immune response and vaccine development. This ongoing battle between the parasite and the immune system produces intermittent parasitaemia, enhancing transmission and leading to chronic infection of increased pathogenicity, exacerbated by immune suppression.

In sleeping sickness, organisms also invade other tissues including endocrine organs resulting in thyroid, adrenal and pituitary dysfunction and they eventually cross the blood-brain barrier, provoking a marked meningoencephalitis. Untreated cases succumb to coma, organ failure and death.

In animals, trypanosomiasis is characterised by weight loss, infertility, abortions, anaemia and increased mortality in the acute stages of the disease. Survivors may recover spontaneously or remain chronically infected with a fluctuating parasitaemia. However, the clinical manifestation of trypanosomiasis is influenced by the interaction of host susceptibility and species or strain pathogenicity (Nantulya 1990).

Horses with surra are usually fatally affected, dying within two weeks in acute cases to 4 months in chronic cases. They show weakness, lethargy and an intermittent fever before death. Camels are highly susceptible with similar signs to horses. Cattle and buffaloes are most often chronically affected, showing intermittent pyrexia, anaemia, emaciation, hind limb weakness and oedema of the brisket. Surra is usually rapidly fatal in cats and dogs although dogs may show neurological signs suggestive of rabies (Geering 1987).


Trypanosomiasis is confirmed by demonstrating parasites in the body fluids of clinically affected animals. However, Connor cautioned that;

'the diagnosis of trypanosomiasis is notoriously difficult. Not only are there no specific clinical signs, but the intermittent and usually low parasitaemias make detection of the trypanosomes difficult. Furthermore, infection is not synonymous with disease: many sub clinically affected animals live in delicate balance with potentially pathogenic trypanosomes. An element of clinical judgement, therefore, enters into the diagnosis of trypanosomiasis (Connor accessed 2014).'


Trypanosoma evansi, the cause of surra, poses the most significant threat to Australian livestock. In a study conducted in northeastern Australia, twelve tabanid species with potential to transmit T. evansi were identified. However, some such as Tabanus pallipennis were considered to be more likely vectors because of their feeding behaviour and host preference. Surra could infect a wide range of species with pigs and macropods identified as potential reservoirs. Of concern, macropod blood was frequently detected in five tabanid species, even where macropod populations were less dense than other potential hosts. It was concluded that the large populations of feral pigs and wallabies in northern Australia constitute 'an important risk factor for the rapid spread of surra and would present a major challenge for effective control of the disease (Muzari 2010).'

Surra has occurred in Australia. In 1907 it was diagnosed at Port Hedland in imported camels. The camels were destroyed and the disease has not been seen since (Geering 1987).

Australia has several endemic trypanosomes including T. theileri (a benign blood parasite of cattle) and the presumed extinct T. melophagium. Both T theileria and T. melophagium are stercorarian trypanosomes despite the vectors being blood sucking tabanid flies and sheep ked (Melophagus ovinus) respectively. Early Australian studies showed that sheep became infected with T. melophagium after they ingested infected keds or their faeces (Turner and Murnane 1930 cited by Callow 1984).


AUSVETPLAN (2006) outlines a comprehensive plan to manage an incursion of surra, the trypanosomal infection of most risk to Australia. Surra in horses is an OIE listed disease and is therefore is notifiable internationally. Surra is a Category 4 emergency animal disease in Australia, meaning that costs of control are to be shared 80% by industry and 20% by government under the Government and Livestock Industry Cost Sharing Deed In Respect of Emergency Animal Disease Responses (EAD Response Agreement).

An outbreak of surra would cause production losses, disease and mortality and could affect trade in the beef and dairy industries and would hamper the horse industry. Surra would have an unknown effect on our native and feral animal populations.

As outlined by AUSVETPLAN, the intention is to eradicate surra if possible. However, (again as mentioned in the plan), the practicality of eradication is vastly different if the infection is discovered early in a southern horse stud compared to a northern cattle property with large numbers of feral and native animals. Factors that need to be considered in determining the practicality of eradication include; the extent of the infection prior to diagnosis, the location of the outbreak, the species involved (especially feral or native mammals) and the effect of the disease on trade.


  1. AUSVETPLAN Disease Strategy Surra Version 3.0, 2006, available online, www.animalhealthaustralia.com.au accessed February 2015
  2. Callow LL (1984). Animal Health in Australia, Vol 5, Protozoal and Rickettsial Diseases, pp 249-251
  3. Connor RJ The diagnosis, treatment and prevention of animal trypanosomiasis under field conditions. FAO corporate document repository www.fao.org accessed 28 December 2014
  4. Chernin J (2000). Parasitology, p 52
  5. Geering (1987). Animal Health in Australia, volume 9, Exotic diseases, pp 202-3
  6. International Livestock Research Institute, Trypanosomiasis
    http://www.ilri.org/InfoServ/Webpub/fulldocs/Ilrad88/Trypanosomiasis.htm; accessed 21 February 2015
  7. Muzari, Mutizwa Odwell (2010). Tabanid flies and potential transmission of Trypanosoma evansi in Queensland. PhD thesis, James Cook University, researchonline.jcu.edu.au abstract available online, accessed 28 December 2014
  8. Nantulya VM (1990). Trypanosomiasis in domestic animals: the problems of diagnosis, Rev. sci. tech. Off. int. Epiz., 1990, 9 (2), 357-367
  9. Ladiges P, Evans B, Saint R and Knox B (2006) Biology, an Australian Focus. Chapter 35 The Protists, pp 849-51


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