What is the shape of the trypanosome


English: trypanosome

1 definition

Trypanosomes are mobile, flagellated single cells of the genus Trypanosoma in the order of the Trypanosomatida. All representatives of this genus are obligate heteroxene parasites with a host change between vertebrates and arthropods (mostly insects).

2 background

Trypanosomes have a variably shaped, usually slender cell body and have exactly one flagellum, also called a flagellum. In addition, like all trypanosomatids, they have, as an independent substructure of the mitochondrion, a kinetoplast that is always located near the base of the flagellum, an organelle that contains a large number of linked DNA cycles with autonomous replication.

Trypanosomes multiply through longitudinal and multiple division. In vertebrates they occur in their main trypomastigotic form - especially in the liquid tissues of their hosts, e.g. in the blood, in the lymph, in the liquor or in the pericardial fluid.

3 taxonomy

The trypanosomes, more precisely the genus "Trypanosoma", can be classified taxonomically as follows:

  • Domain: Eukaryota
    • Without rank: Excavata
      • Tribe: Euglenozoa
        • Sub-stem: Mastigophora

Trypanosomes are still referred to as protozoa or flagellates in the literature. Both groups, which are characterized by similarities in external characteristics, have, however, been shown to be polyphyletic in phylogenetic studies and are no longer used in more recent taxonomies.

4 forms

Many trypanosomes come in different forms because they change shape over the course of their life cycle. Above all, the length of the cell and the position of the flagellum outlet relative to the cell nucleus vary. One differentiates:

  • Trypomastigote form: the flagella emerges in the rear area of ​​the cell behind the nucleus. This shape is characteristic of the extracellular occurrence.
  • Epimastigote form: the flagella emerges in the middle of the cell in front of the nucleus. Epimastigotes live extracellularly and occur only in the arthropod host.
  • Amastigote form: no free scourge is visible. This form occurs intracellularly in the vertebrate host in some species of trypanosomes.

In the trypomastigote and epimastigote form, the flagella lies laterally on the cell surface with several attachment points after it emerges in the direction of movement and is extended forward, swinging freely. As with all morphological forms of trypanosomatids (except for the amastigote), the free swinging last section of the flagellum is always located at the front end (front), the position "front" being defined by the direction of movement. So it is a pulling scourge.

5 trypanosoma sections

Trypanosomes, which infect humans and domestic animals or farm animals, can be divided into several sub-genres, which in turn can be assigned to 2 sections (as a rank between genus and sub-genus). Pathogen of the section Salivaria (e.g. Trypanosoma brucei) develop and multiply in the middle or foregut of the arthropod and are transmitted with the mouth parts (bite or sting) via the saliva. Pathogen of the section Stercoraria (e.g. Trypanosoma cruzi), on the other hand, develop and multiply in the rectum of the arthropod and are introduced into the vertebrate's body with the faeces (via small wounds or mucous membranes).

There are other Trypanosoma sections, the species of which infest rodents, birds and amphibians or fish.

6 pathogen species of trypanosomiasis diseases

Under the term Trypanosomiasis are grouped together infectious diseases caused by trypanosomes.

There are a large number of trypanosome species or subspecies, but only a few of them are pathogenic for humans. These include:[1], P. 149

Trypanosomiasis Another name Pathogen vectorReservoir host
African trypanosomiasis West African sleeping sicknessTrypanosoma brucei gambiense (Salivaria) Glossina palpalis (Habitat: rainforests, anthropophilic) Human (main host), dogs, pigs
East African sleeping sicknessTrypanosoma brucei rhodesiense (Salivaria) Glossina morsitans (Habitat: savanna, only very weakly anthropophilic) Bushbuck, hartebeest, sheep, goats, cattle, rarely: humans
American trypanosomiasis Chagas diseaseTrypanosoma cruzi (Stercoraria) Predatory bugHumans and around 150 species of mammals
Glossina = generic name of the tsetse flies

For West African sleeping sickness, humans are the main vertebrate reservoir host.

Due to the very weak anthropophilic vector Glossina morsitans, humans are rarely attacked by the pathogen Trypanosoma brucei rhodesiense, the East African sleeping sickness. However, if an infection does occur, the disease is the most severe of all known vertebrate hosts.

The infectious cycle of the pathogens of both African and American trypanosomiasis is known in detail today. Infection via the vector (tsetse fly, predatory bug) occurs via the metacyclic trypomastigote subform of the metamorphosis of the respective pathogen.

Most trypanosomes cause animal diseases, including the Nagana disease. The most important representatives for mammalian pathogens and the infested mammals (without mentioning reservoir hosts with only mild diseases) are:[1], P. 149

  • Salivaria
    • Trypanosoma brucei gambiense (sleeping sickness)
    • Trypanosoma brucei rhodesiense (sleeping sickness)
    • Trypanosoma brucei brucei (Nagana in horses, donkeys, dogs)
    • Trypanosoma vivax (Nagana in cattle, sheep, goats, horses)[1], P. 148
    • Trypanosoma congolense (Nagana in cattle, sheep, goats, horses)[1], P. 147
    • Trypanosoma simiae (affects pigs, infectious disease is sometimes also referred to as Nagana)
    • Trypanosoma evansi (surra for horse, camel, water buffalo, dog)[1], P. 150
    • Trypanosoma equinum (Mal de Caderas / paralyzes in horses)
    • Trypanosoma equiperdum (stallion disease in horses)
  • Stercoraria
    • Trypanosoma cruzi (Chagas disease, affects more than 150 species of mammals)
    • Trypanosoma theileri (attacks cattle)
    • Trypanosoma melophagium (attacks sheep)
    • Trypanosoma lewisii (affects rats)
    • Trypanosoma rangeli (affects various mammals)

Due to Nagana diseases, cattle breeding is only possible to a very limited extent on around half of the cultivable land in Sub-Saharan Africa (Tsetse Belt).[1], P. 148

7 infection

Trypanosomes are usually transmitted by vectors in which various developmental processes are carried out, e.g. by tsetse flies or predatory bugs. These include all species pathogenic to humans.

In Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense, for example, after being bitten by a tsetse fly, they first multiply at the puncture site and form a swelling here, the so-called trypanosome chancre. After about two weeks, the pathogens enter the blood and lymphatic system and cause swelling of the lymph nodes and periodic attacks of fever. After weeks or years, they finally invade the CNS by overcoming the blood-brain barrier and trigger meningitis. The CNS offers the pathogens the ideal refuge, as they only have a limited repertoire of immune reactions.

In Trypanosoma cruzi, edema at the entry point of the feces of the predatory bugs is followed by an acute phase with fever, urticaria-like skin changes and lymph node swellings in a third of the infected. After a latency phase of several years, the chronic phase, due to an enlarged heart and the destruction of nerve cells in the digestive tract, mainly leads to a palpitations and reduced performance under stress, as well as progressive paralysis of the gastrointestinal tract.

Some trypanosome species that are pathogenic for domestic animals or livestock (e.g. Trypanosoma evansi, Trypanosoma equinum, Trypanosoma equiperdum) have decoupled from their arthropod hosts during evolution. They are only transmitted via contact infection, live exclusively in vertebrate hosts and have completely or partially lost their kinetoplast, which is only essential for life in arthropods.[1], P. 149 These species can only be assigned to the Salivaria because of their close phylogenetic relationship to Trypanosoma brucei.

8 specialty

Trypanosomes have a proteoglycan coat that constantly changes its antigenic properties. Thus they evade the immune defense.

9 source

  1. 1,01,11,21,31,41,51,6Lucius / Loos-Frank, Biology of Parasites, Springer 2008, accessed on March 20, 2017