Classification: Taxonomic ranks under review (cf. Illustrated Guide to Protozoa, 2000. Allen Press)

Protista (unicellular eukaryotes)
Sarcomastigophora (with pseudopodia and/or flagella)
Mastigophora (flagellates)
Zoomastigophora (zooflagellates, without chloroplasts)
Kinetoplastida (presence of extranuclear DNA, kinetoplast)

Family: Trypanosomatidae
All species are characterized by the possession of a kinetoplast, a unique structure formed by massed DNA (circles or lattice) within the single large mitochondrion closely associated with the flagellar basal body. Four main developmental stages are formed: trypomastigotes (with a posterior kinetoplast and an emergent flagellum forming a long undulating membrane); epimastigotes (with an anterior kinetoplast and an emergent flagellum forming a short undulating membrane); promastigotes (with an anterior kinetoplast and a short emergent flagellum, but no undulating membrane); and amastigotes (with a kinetoplast but no emergent flagellum or undulating membrane). Many trypanosome species are parasitic only in insects whereas others are transmitted by insect vectors to a wide range of vertebrate hosts. Three main groups infect the blood and/or tissues of humans and animals causing severe clinical diseases:



salivarian trypanosomes which undergo anterior station (foregut) development in the insect vector and are transmitted via saliva to the blood of vertebrate hosts (e.g. tsetse flies transmit T. brucei which causes sleeping sickness in humans and nagana in cattle)



stercorarian trypanosomes which undergo posterior station (hindgut) development in vectors and are transmitted via faecal contamination of bite site to infect blood and tissues of vertebrate hosts (e.g. reduviid bugs transmit T. cruzi which causes Chagas’ disease in humans)



leishmanias which develop in foregut of insect vectors and are transmitted via bite to the tissues of vertebrate hosts (e.g. sandflies transmit Leishmania spp. causing 3 types of leishmaniasis in humans and animals)

Trypanosoma brucei
[this species causes sleeping sickness in humans and nagana in cattle]

Parasite morphology: The parasite forms trypomastigotes in vertebrate hosts and epimastigotes in the insect vector. The trypomastigotes (with posterior kinetoplast and long undulating membrane) are pleomorphic in size ranging from 16-42µm in length by 1-3µm in width. They occur as elongate slender dividing forms (with long free flagellum) or stumpy non-dividing infective (metacyclic) forms (with no free flagellum). The epimastigotes (with anterior kinetoplast and short undulating membrane) are also variable in size ranging from 10-35µm in length by 1-3µm in width.

Host range: Salivarian trypanosomes are confined to tropical Africa, corresponding in distribution with their tsetse fly vectors. Three closely-related subspecies are found: Trypanosoma brucei brucei (T. b. brucei) which is primarily parasitic in native antelopes and other wild ruminants (asymptomatic carriers, trypanotolerant) but infects introduced domestic animals; T. b. rhodesiense which causes acute disease in humans in East Africa; and T. b. gambiense which produces a much more chronic disease in humans in West Africa.

Trypanosoma species

Mastigote length

Vertebrate hosts


Insect vector


CYCLIC TRANSMISSION (parasite development within vector)

SALIVARIA (anterior station development)

T. b. gambiense


man, domestic animals

sleeping sickness

tsetse fly

West Africa

T. b. rhodesiense


man, some ruminants

sleeping sickness

tsetse fly

East Africa

T. b. brucei


ruminants, monogastrics


tsetse fly

tropical Africa

T. congolense


cattle, domestic animals


tsetse fly

tropical Africa

T. vivax


ruminants, horses


tsetse fly

tropical Africa

T. simiae


pigs, some ruminants

virulent trypanosomiasis

tsetse fly


STERCORARIA (posterior station development)

T. cruzi


man, domestic/wild animals

Chagas’ disease

reduviid bugs


T. theileri




tabanid flies


T. melophagium




sheep ked


T. lewisi




rat fleas


T. rangeli


man, rats


reduviid bugs

Sth America

NON-CYCLIC TRANSMISSION (no parasite development within vector)

MECHANICA (mechanical transmission)

T. evansi


ruminants, horses, dogs

surra, murrina

biting flies/bats

Asia, America

T. equinum


horses, ruminants

mal de caderas

biting Diptera


T. equiperdum






Site of infection: Trypomastigotes are found extracellularly in the blood and lymph of infected individuals (including lymph nodes and spleen) but may invade the central nervous system and other tissues.

Pathogenesis: The disease is known as Old World (African) trypanosomiasis. Although there are many regional common names given depending on the parasite subspecies and hosts involved, the disease is often called sleeping sickness in humans, and nagana in animals. Parasites injected into the host by the insect vector first cause an inflammatory reaction characterized by a localized tender reddish swelling (known as a chancre). Trypanosomes then multiply in the plasma and interstitial fluid causing acute to subacute febrile illness. A classic sign of T. b. gambiense infection is the enlargement of the cervical lymph glands at the back of the neck (known as Winterbottom’s sign). T. b. rhodesiense infections in humans usually cause acute systemic disease with haemolymphatic involvement, swollen lymph nodes, fever and rapid weight loss. T. b. gambiense usually causes chronic disease with neurological involvement, meningoencephalitis, lethargy and coma (hence ‘sleeping’ sickness). Parasite development occurs in cyclic waves moderated by host immune responses. Trypanosomes have a glycoprotein coat on the outer surface of the cell membrane which is highly antigenic and leads to the production of host antibodies which act, together with complement, to lyse parasites. Trypanosomes, however, repeatedly change the molecular arrangement of the coat so some individuals avoid immune destruction and divide to produce a new wave of infection. This antigenic variation is under genetic control and while synthesis of successive variant surface glycoproteins does not occur in a fixed sequence, it is not entirely random. The repeated cycles of host antibody production and parasite destruction leads to cyclic fevers, macroglobulinemia, microvascular damage, coagulopathy, and perivascular inflammation. When parasites penetrate the blood-brain barrier (within weeks for T. b. rhodesiense or up to years for T. b. gambiense), they cause encephalitis, coma and death. The clinical course of T. b. brucei infections depends on the susceptibility of the host species. Horses and dogs are particularly susceptible and may succumb within 2-3 weeks Cattle and pigs are more refractory to disease and may survive for several months. Clinical signs include anaemia, fever, oedema and progressive paralysis. Native animal species (antelope and other wild ruminants) are trypanotolerant and may act as asymptomatic carriers.

Mode of transmission: All salivarian trypanosomes are transmitted by tsetse fly vectors (Glossina spp.). Metacyclic trypomastigotes ingested during feeding transform into procyclic trypomastigotes in the midgut. These stages migrate through gut membranes and invade the salivary glands where they transform into epimastigotes which undergo anterior station development to produce infective metacyclic trypomastigotes which are injected during feeding.

Differential diagnosis: Infections were conventionally diagnosed by the direct detection of parasites in blood, bone marrow or cerebrospinal fluid by microscopic examination before or after centrifugation. In vitro cultivation has proven difficult and in vivo inoculation into laboratory animals yields variable results. More recently, a variety of immunoserological tests have been developed to detect host antibodies using fluorescent, agglutination or enzyme markers. Card-agglutination and dot-spot tests are available for field use. Molecular characterization techniques utilizing polymerase chain reaction (PCR) amplification of parasite DNA have yielded good results in species/strain differentiation with certain genes (e.g. SRA gene, serum-resistant-associated).

Treatment and control: Historically, arsenical drugs have been used despite major toxicity problems. Melarsoprol and trypursamide are used to treat chronic infections (involving CNS signs). Other drugs have proven more effective against systemic infections (suramin, pentamidine) and neurological infections (berenil, eflornithine, difluoromethylornithine). Prevention involves avoiding being bitten by tsetse flies, but this can be difficult as they are persistent daytime feeders and can bite through thin clothing. Control measures based on vector eradication (using insecticidal sprays, fly traps, or clearing vegetation) and managing wild game reservoirs of infection (by fencing, culling or creating wildlife corridors) have only proven partially effective. Some recent success has been recorded in breeding trypanotolerant domestic livestock (e.g. Ndama cattle).


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