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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
Taxonomic TreeTop of page
- Domain: Eukaryota
- Kingdom: Protista
- Phylum: Protozoa
- Subphylum: Sarcomastigophora
- Order: Kinetoplastida
- Family: Trypanosomatidae
- Genus: Trypanosoma
Pathogen CharacteristicsTop of page
Trypanosomes are microscopic unicellular protozoan flagellates in the genus Trypansoma. They are obligatory parasites of vertebrates, and infect fish and amphibian species, reptiles, birds and mammals. The morphology and life cycle of trypanosomes have been described by Itard (1989). Trypanosome nutrition has been reviewed by Igbokwe (1995).
A trypanosome is an elongated flattened cell, with an undulating membrane and a free flagellum at the anterior end. There is a kinetoplast at the base of the flagellum, located towards the posterior end. The structures of the different constituents of the trypanosomes have been determined by electron microscopy.
The trypanosomes are transmitted from one host to another through haematophagous insects, in which the parasite multiplies (by binary fission) and develops in the gut. The stercorarian trypanosomes develop in the posterior part of the insect gut and the metatrypanosomes are deposited along with the faeces of the insect vector onto the skin or mucous membrane of the host, after which the infective forms penetrate into the tissue. T. cruzi, a typical stercorarian trypanosome, is transmitted by the Triatominae bugs. The metatrypanosomes of this species multiply in the mammalian host, in the amastigote form, inside cells of the reticulo-endothelial system and later in other tissues such as skeletal muscles, heart, liver, nervous tissue and reproductive organs. These intracellular forms divide several times before producing the trypomastigotes, which enter the bloodstream. The bloodstream forms later re-invade the tissue in the anastigote form.
Another stercorarian trypanosome of veterinary importance, T. theileri, is transmitted by biting insects such as Tabanidae (horse flies), Stomoxys, ticks, Simulium and mosquitoes, and has a similar life cycle to T. cruzi.
The salivarian trypanosomes develop in the anterior part of the gut (midgut, proventriculus, proboscis, salivary gland) of the tsetse fly (Glossina spp). The development of Dutonella species is confined to the proboscis of the tsetse fly, where the trypanosomes attach to the walls of the labial cavity and transform into epimastigote forms. They multiply rapidly and later detach to invade the hypopharynx where they transform into preinfective trypomastigotes before becoming infective metatrypanosomes. Transmission occurs through inoculation when the tsetse injects its saliva through a bite before a blood meal.
The development of Nannomonas species in the tsetse fly occurs in the midgut and proboscis. The trypanosomes in the blood-meal multiply actively in the midgut where they remain for 2 months. They move to the proventriculus and then to the oesophagus and the proboscis, where they attach to the wall and transform into epimastigotes. They finally penetrate the anterior end of the hypopharynx and become infective metatrypanosomes.
The development of Trypanozoon species occurs in the midgut, hypopharynx and salivary gland. The short forms in the blood meal are transformed in the crop of the tsetse fly into procyclic forms, which become trypomastigotes. They multiply actively and later move to the proventriculus, where they become thinner, and longer and finally invade the salivary glands. The trypomastigotes transform into epimastigotes in the salivary glands. After multiplication, the epimatigotes produce the infective metatrypanosomes, which are injected into the bloodstream of the host by tsetse bites. The development of the Pycnomonas species is similar to that of Trypanozoon species.
Trypanosomes depend on the host’s supplies of carbohydrates, proteins, lipids and some micronutrients. During periods of high parasitaemia, the parasites may deplete these supplies and release metabolites that may have adverse effects on the host, as has been reviewed previously (Seed and Hall, 1985).
Trypanosomes have very small polysaccharide stores and glucose is the most important exogenous substrate used by the bloodstream forms of the parasite for energy (Gutteridge and Coombs, 1977). Energy is generated primarily during glycolysis, in specialized microbodies called glycosomes (Fairlamb and Opperdoes, 1986). Transitional forms of trypanosomes have the ability to use a-ketoglutarate to generate energy, perhaps through substrate-level and oxidative phosphorylation (Bienen et al., 1991). The products of aerobic energy metabolism are mainly pyruvate, but also glycerol, acetate and carbon dioxide (Gutteridge and Coombs, 1977).
Trypanosomes have been shown to take up and digest protein molecules in their organelles (Brown et al., 1965; Langreth and Balber, 1975). They also take up free plasma amino acids, although they are capable of synthesizing some amino acids from carbohydrates (Gutteridge and Coombs, 1977). They catabolize tyrosine, phenylalanine and tryptophan to produce some biologically active metabolites, as reviewed by Seed and Hall (1985).
Mellors and Samad (1989) reviewed the acquisition of exogenous lipids by bloodstream trypanosomes. The parasites reportedly have a limited ability to synthesize fatty acids de novo. They have been shown to incorporate, to a limited extent, exogenous glucose, acetate, glycerol and fatty acids into their lipids. They take up large amounts of fatty acids such as palmitic and linoleic acid. Trypanosomes do not metabolize exogenous phosphatidylcholine (PC) or phosphatidyl-ethanolamine (PE), but can readily take up exogenous lyso-PC and lyso-PE. The exogenous lyso-PC can be acylated to form PC, which the trypanosomes incorporate into their membranes. Some of the micronutrients that trypanosomes may take up from exogenous sources are p-aminobenzoic acid, vitamins such as thiamine, folic acid, riboflavin, cobalamin, ascorbic acid and nicotinamide (von Brand, 1973) and nucleotide precursors such as hypozanthine and thymidine (Baltz et al., 1985).
Vectors and Intermediate HostsTop of page
ReferencesTop of page
Baltz T; Baltz D; Giroud C; Crockett J, 1985. Cultivation in a semi-defined medium of animal infective forms of Trypanosoma brucei, T. equiperdum, T. evansi, T. rhodesiense and T. gambiense.. EMBO Journal, 4(5):1273-1277; 22 ref.
Bienen EJ; Saric M; Pollakis G; Grady RW; Clarkson ABJr, 1991. Mitochondrial development in Trypanosoma brucei brucei transitional bloodstream forms. Molecular and Biochemical Parasitology, 45(2):185-192; 26 ref.
Brown KN; Armstrong JA; Valentine RC, 1965. The ingestion of protein molecules by blood forms of Trypanosoma rhodesiense. Experimental Cell Research, 39:129-135.
Gutteridge WE; Coombs GH, 1977. Biochemistry of Parasitic Protozaa. London, UK: Macmillan Press.
Itard J, 1989. African animal trypanosomoses. In: Manual of tropical veterinary parasitology [ed. by Troncy, P. M. \Itard, J. \Morel, P. C.]. Wallingford, UK: CAB International, 177-297.
Langreth SG; Balber AE, 1975. Protein uptake and digestion in bloodstream and culture forms of Trypanosoma brucei. Journal of Protozoology, 22:40-53.
von Brand T, 1973. Biochemistry of Parasites. New York, USA: Academic Press.